DISEASES OF
                     CATTLE, SHEEP, GOATS AND SWINE


                                    By

                                G. MOUSSU

    PROFESSOR AT THE VETERINARY COLLEGE OF ALFORT; DOCTOR OF MEDICINE;
                         DOCTOR OF SCIENCE, ETC.

                                   AND

         JNO. A. W. DOLLAR, M. R. C. V. S., F. R. S. E., M. R. I.

 PRESIDENT OF THE ROYAL COLLEGE OF VETERINARY SURGEONS; VICE-PRESIDENT OF
    THE ROYAL INSTITUTE OF PUBLIC HEALTH; CORRESPONDING MEMBER OF THE
    CENTRAL SOCIETY OF VETERINARY MEDICINE OF PARIS; ASSOCIATE OF THE
   SOCIETY OF VETERINARY MEDICINE OF BRABANT (BELGIUM); LIFE MEMBER OF
                  ROYAL ITALIAN SOCIETY OF HYGIENE, ETC.


                  AMERICAN VETERINARY PUBLISHING COMPANY
                                 CHICAGO
                                PUBLISHER
                                   1920

                          (All Rights Reserved)




                                PREFACE.


No apology seems called for in presenting to English-speaking veterinary
surgeons and students a treatise on the diseases of cattle. To those
entrusted with the onerous task of preventing or curing disease in
cattle, sheep, and swine the scantiness of permanent literature dealing
with the subject must always have proved a matter of some embarrassment,
while to teachers and students alike the want of a concise and modern
textbook has long been a difficulty of the first order. It is hoped that
the present volume may go some way towards remedying this state of
affairs.

As on previous occasions, the writer has freely availed himself of
foreign sources of information. Two years ago he purchased the literary
rights in Professor Moussu’s “Maladies du Bétail,” which had even then
attained an European reputation, and which forms the backbone of the
present volume. To obtain further information, the more important German
treatises have been laid under contribution, while all accessible
English, American, and Colonial literature of recent date has been
referred to. (The references practically extend up to the moment of
writing—the latest being June, 1905.) In this way the work may in some
degree claim to have assumed an international character. The extent of
the additions is indicated by an increase in the number of illustrations
of 140, and of the text of nearly 50 per cent.

Professor McQueen has performed the greatly-valued service of reading
proof sheets and advising the writer as the book passed through the
press.

To Dr. Salmon, of the United States Department of Agriculture, special
thanks are due for his generous permission to quote from the annual
reports of that body.

Other acknowledgments will be found in the text.

Once again the writer, who on this occasion chances also to be the
President of the Royal College of Veterinary Surgeons, appeals for
lenient judgment on work performed under no common stress of duties,
professional and political.

                                                      JNO. A. W. DOLLAR.

  56, NEW BOND STREET,
          LONDON, ENGLAND,
                  _June, 1905_.




                               CONTENTS.


                               SECTION I.
                  DISEASES OF THE ORGANS OF LOCOMOTION.

 CHAP.                                                              PAGE
       METHODS OF EXAMINATION                                          1

    I. DISEASES OF BONES                                               3
          GENERAL DISEASES                                             4
             Rachitis                                                  4
             Osseous Cachexia                                          7

          LOCAL AFFECTIONS                                            20
             Fractures                                                20
             Fractures of the horns                                   21
             Detachment of the horns                                  23
             Fissuring of the horns                                   24
             Fractures of the horns                                   25

          EXOSTOSES                                                   27
             Spavin in the ox                                         27
             Ring-bone                                                28
             Suppurating ostitis                                      29
             Bone tumours                                             30

   II. DISEASES OF THE FOOT                                           31
             Congestion of the Claws                                  31
             Contusions of the sole                                   31
             Laminitis                                                32
             Sand crack                                               34
             Pricks and stabs in shoeing                              36
             Picked-up nails, etc. (“Gathered nail”)                  37
             Inflammation of the interdigital space (Condylomata)     38
             Canker                                                   40
             Grease                                                   41
             Panaritium—Felon—Whitlow                                 41
             Foot rot                                                 43

  III. DISEASES OF THE SYNOVIAL MEMBRANES AND OF THE ARTICULATIONS    45
          I. SYNOVIAL MEMBRANES AND ARTICULATIONS                     45
             Synovitis                                                45
             Inflammation of the patellar synovial capsule            45
             Distension of the synovial capsule of the hock joint     46
             Distension of tendon sheaths in the hock region          46
             Distension of the synovial capsule of the knee joint     47
             Distension of the synovial capsule of the fetlock
               joint                                                  48
             Distension of tendon sheaths                             48
             Distension of tendon sheaths in the region of the knee   49
             Distension of the bursal sheath of the flexor tendons    49
             Traumatic synovitis—“Open synovitis”                     49
             Traumatic tendinous synovitis                            50
             Traumatic articular synovitis—Traumatic
               arthritis—“Open arthritis”                             51

          II. STRAINS OF JOINTS                                       52
             Strain of the shoulder                                   52
             Strain of the knee                                       53
             Strain of the fetlock                                    54
             Strain of the stifle joint                               54
             Strain of the hock joint                                 55

          III. LUXATION OF JOINTS                                     56
             Luxation of the femur                                    56
             Luxation of the patella                                  58
             Luxation of the femoro-tibial articulation               61
             Luxation of the scapulo-humeral joint                    63

          IV. HYGROMAS                                                64
             Hygroma of the knee                                      65
             Hygroma of the haunch                                    67
             Hygroma of the trochanter of the femur                   67
             Hygroma of the stifle                                    67
             Hygroma of the point of the hock                         68
             Hygroma of the point of the sternum                      69

   IV. DISEASES OF MUSCLES AND TENDONS                                70
             Rupture of the external ischio-tibial muscle (Biceps
               femoris)                                               70
             Rupture of the flexor metatarsi                          72

          PARASITIC DISEASES OF MUSCLES                               73
             Cysticercus disease of the pig                           73
             Beef measles                                             79
             Trichiniasis—Trichinosis                                 84

    V. RHEUMATISM                                                     89
          Articular rheumatism                                        89
          Muscular rheumatism                                         92

          INFECTIOUS FORMS OF RHEUMATISM OR PSEUDO-RHEUMATISM         94
             Infectious rheumatism in young animals                   94
             Infectious pseudo-rheumatism in adults                   99
             Scurvy—Scorbutus                                        104

                               SECTION II.
                  DISEASES OF THE DIGESTIVE APPARATUS.
       SEMIOLOGY OF THE DIGESTIVE APPARATUS                          106

    I. DISEASES OF THE MOUTH                                         121
          Stomatitis                                                 121
             Simple stomatitis                                       121
             Catarrhal stomatitis in sheep                           122
             Necrosing stomatitis in calves                          123
             Mycotic stomatitis in calves                            124
             Ulcerative stomatitis in sheep                          125
             General catarrhal stomatitis in swine                   126
             Ulcerative stomatitis in swine                          127
             Mercurial stomatitis                                    128
          Glossitis                                                  130
             Superficial glossitis                                   130
             Acute deep-seated glossitis                             131
             Chronic glossitis                                       132

   II. DISEASES OF THE SALIVARY GLANDS, TONSILS AND PHARYNX          134
          Parotiditis (Parotitis)                                    134
             Acute parotiditis                                       134
             Chronic parotiditis—Parotid fistula                     136
          Inflammation of the submaxillary salivary gland            137
          Tonsilitis in pigs                                         138
          Pharyngitis                                                138
             Pseudo-membranous pharyngitis in cattle                 141
             Pseudo-membranous pharyngitis in sheep                  142
          Pharyngeal polypi                                          143

  III. DISEASES OF THE ŒSOPHAGUS                                     145
          Œsophagitis                                                145
          Stricture of the œsophagus                                 148
          Dilatation of the œsophagus                                149
          Œsophageal obstructions                                    152
          Ruptures and perforations of the œsophagus                 157

   IV. DEPRAVED APPETITE—THE LICKING HABIT—INDIGESTION               158
          Depraved appetite in the ox                                158
          Depraved appetite in calves and lambs                      160
          Colic in the ox                                            162
             Colic due to ingestion of cold water—Congestive colic   162
             Colic due to invagination                               163
             Colic as a result of strangulation                      167
          Diseases of the stomach                                    169
          Indigestion                                                170
             Gaseous indigestion                                     170
             Impaction of the rumen—Indigestion as a result of
               over-eating                                           175
             Impaction of the omasum (third stomach)                 179
             Abomasal indigestion                                    182
             Acute gastric indigestion in swine                      185

    V. INFLAMMATION OF THE GASTRIC COMPARTMENTS                      186
          Rumenitis—Reticulitis—Gastritis                            186
             Acute gastritis                                         188
             Catarrhal gastritis in swine                            190
             Ulcerative gastritis                                    191
             Chronic tympanites                                      194
             Gastric disturbance due to foreign bodies               198
             Tumours of the gastric compartments                     202

   VI. ENTERITIS                                                     203
          Acute enteritis                                            203
          Hæmorrhagic enteritis                                      206
          Chronic enteritis (Chronic diarrhœa)                       207
          Dysentery in calves                                        210
          Diarrhœic enteritis in calves                              212

  VII. POISONING                                                     215
          Poisoning due to food                                      215
          Poisoning by caustic alkalies                              216
          Poisoning by caustic acids                                 217
          Poisoning by common salt                                   217
          Poisoning by the nitrates of potash and soda               217
          Poisoning by tartar emetic                                 218
          Poisoning by arsenic                                       218
          Phosphorus poisoning                                       219
          Mercurial poisoning                                        219
          Lead poisoning: Saturnism                                  220
          Copper poisoning                                           221
          Carbolic acid poisoning                                    221
          Poisoning by aloes                                         221
          Iodoform poisoning                                         222
          Iodine poisoning: iodism                                   222
          Strychnine poisoning                                       222
          List of plants poisonous to stock                          223
          Colchicum poisoning                                        256
          Poisoning by annual mercury                                256
          Poisoning by bryony                                        256
          Poisoning by castor oil cake                               257
          Poisoning by cotton cake                                   257
          Poisoning by molasses refuse                               258
          Diseases produced by distillery and sugar factory pulp     259

 VIII. PARASITES OF THE DIGESTIVE APPARATUS                          263
          Gastro-intestinal strongylosis in sheep                    263
          Lumbricosis of calves                                      267
          Strongylosis of the abomasum in the ox                     268
          Parasitic gastro-enteritis, diarrhœa, and anæmia in
            cattle, sheep and lambs                                  268
          Intestinal coccidiosis of calves and lambs
            (Psorospermosis, hæmorrhagic enteritis, bloody flux,
            dysentery, etc.)                                         271
          Intestinal helminthiasis in ruminants                      275

   IX. DISEASES OF THE LIVER                                         279
          Congestion of the liver                                    280
          Nodular necrosing hepatitis                                280
          Cancer of the liver and bile ducts                         282
          Echinococcosis of the liver                                283
          Suppurative echinococcosis                                 288
          Cysticercosis                                              290
          Distomatosis—Liver fluke disease—Liver rot                 293

                              SECTION III.
                         RESPIRATORY APPARATUS.

    I. EXAMINATION OF THE RESPIRATORY APPARATUS                      311

   II. NASAL CAVITIES                                                319
          Simple coryza                                              319
          Gangrenous coryza                                          320
          Tumours of the nasal cavities                              325
          Purulent collections in the nasal sinuses. Nasal gleet     326
          Purulent collections in the frontal sinus                  327
          Purulent collections in the maxillary sinus                329
          Œstrus larvæ in the facial sinuses of sheep                330

  III. LARYNX, TRACHEA AND BRONCHI                                   333
          Laryngitis                                                 333
             Acute laryngitis                                        333
             Pseudo-membranous laryngitis                            333
          Tumours of the larynx                                      335
          Bronchitis                                                 336
             Simple acute bronchitis                                 337
             Chronic bronchitis                                      337
             Pseudo-membranous bronchitis                            339
             Verminous bronchitis in sheep and cattle (Husk, hoose,
               etc.)                                                 340

   IV. LUNGS AND PLEURÆ                                              343
          Pulmonary congestion                                       343
          Simple pneumonia                                           343
          Pneumonia due to foreign bodies—Mechanical pneumonia       347
             Pneumonia due to the migration of foreign bodies from
               the reticulum                                         348
          Pneumomycosis due to Aspergilli                            350
          Gangrenous broncho-pneumonia due to foreign bodies         351
          Infectious broncho-pneumonia                               354
          Broncho-pneumonia of sucking calves                        356
          Sclero-caseous broncho-pneumonia of sheep                  358
          Pulmonary emphysema                                        359
          Diseases of the pleura                                     361
             Acute pleurisy                                          361
             Chronic pleurisy                                        362
          Pneumo-thorax                                              362
          Hydro-pneumo-thorax and pyo-pneumo-thorax                  366

    V. DISEASES OF STRUCTURES ENCLOSED WITHIN THE MEDIASTINUM        368
          Tumours of the Mediastinum                                 369

                               SECTION IV.
                       THE ORGANS OF CIRCULATION.

       SEMIOLOGY OF THE ORGANS OF CIRCULATION                        370

    I. CARDIAC ANOMALIES                                             374
          Ectopia of the heart                                       374

   II. PERICARDITIS                                                  375
          Exudative pericarditis due to foreign bodies               376
          Chronic pericarditis                                       389
          Pseudo-pericarditis                                        390

  III. ENDOCARDITIS                                                  394

   IV. DISEASES OF BLOOD-VESSELS                                     396
          Phlebitis                                                  396
             Accidental phlebitis                                    396
             Internal infectious phlebitis (Utero-ovarian
               phlebitis)                                            398
             Umbilical phlebitis of new-born animals                 399
             Umbilical phlebitis or omphalo-phlebitis                402

    V. DISEASES OF THE BLOOD                                         406
          Septicæmia of new-born animals                             406
          Takosis: a contagious disease of goats                     412
          Blood poisoning (Malignant œdema) in sheep and lambs in
            New Zealand                                              415
          Piroplasmosis                                              416
             Bovine piroplasmosis                                    416
             Bovine piroplasmosis in France                          424
             Ovine piroplasmosis                                     425
          Diseases produced by trypanosomata                         426
          Louping-ill                                                429
             Suggested measures for prevention                       435
          Braxy                                                      435
          Bilharziosis in cattle and sheep                           439
          Heat stroke—Over-exertion                                  442

   VI. DISEASES OF THE LYMPHATIC SYSTEM                              444
          The lymphogenic diathesis                                  448
          Caseous lymphadenitis of the sheep                         453
          Goitre in calves and lambs                                 453

                               SECTION V.
                             NERVOUS SYSTEM.
          Cerebral congestion                                        456
          Meningitis                                                 456
          Encephalitis                                               458
          Cerebral Tumours                                           459
          Insolation                                                 460
          Post-partum paralysis—Milk fever—Mammary
            toxæmia—Parturient apoplexy—Dropping after calving       461
          Cœnurosis (Gid, sturdy, turn-sick)                         467
          “Trembling,” or Lumbar prurigo, in sheep                   475

                               SECTION VI.
            DISEASES OF THE PERITONEUM AND ABDOMINAL CAVITY.

    I. PERITONITIS                                                   478
          Acute peritonitis                                          478
          Chronic peritonitis                                        481
          Ascites                                                    483
          Peritoneal cysticercosis                                   485

   II. HERNIÆ                                                        487
          Congenital herniæ                                          487
             Perineal hernia of young pigs                           487
             Umbilical hernia                                        488
          Acquired herniæ                                            489
          Hernia of the rumen                                        490
          Hernia of the abomasum                                     493
          Hernia of the intestine                                    494
          Treatment of herniæ                                        495
          Diaphragmatic hernia                                       496
          Eventration                                                499
          Fistulæ of the digestive apparatus                         500

                              SECTION VII.
                         GENITO-URINARY REGIONS.

       DISEASES OF THE URINARY APPARATUS                             502

    I. POLYPI OF THE GLANS PENIS AND SHEATH                          506
          Inflammation of the sheath                                 506
          Persistence of the urachus                                 508

   II. DISEASES OF THE BLADDER                                       511
          Acute cystitis                                             511
          Chronic cystitis                                           513
             Urinary lithiasis. Calculus formation                   514
             Calculi in bovine animals                               515
          Urinary calculi in sheep                                   518
          Paralysis of the bladder                                   519
          Eversion of the bladder                                    519
          Hæmaturia                                                  520

  III. DISEASES OF THE KIDNEYS                                       527
          Congestion of the kidneys                                  527
          Acute nephritis                                            528
          Chronic nephritis                                          530
          Hydro-nephrosis                                            531
          Infectious pyelo-nephritis                                 533
          Suppurative nephritis and perinephritis                    537
          The kidney worm (_Sclerostoma pinguicola_) of swine        539

   IV. GENITAL APPARATUS                                             542
          Vaginitis                                                  543
             Acute vaginitis                                         544
             Contagious vaginitis                                    545
             Croupal vaginitis                                       545
             Chronic vaginitis                                       546
          Metritis                                                   547
             Septic metritis                                         547
             Acute metritis                                          550
             Chronic metritis                                        552
          Epizootic abortion in cows                                 553
          Salpingitis—Salpingo-ovaritis                              555
          Torsion of the uterus                                      556
          Tumours of the uterus                                      559
          Tumours of the ovary                                       559
          Genital malformations                                      560
          Imperforate vagina                                         560
          Nympho-mania                                               562

    V. DISEASES OF THE MAMMARY GLANDS                                565
          Physiological anomalies                                    567
          Wounds or traumatic lesions                                568
             Chaps and cracks                                        568
          Milk fistulæ                                               569
          Inflammatory diseases                                      570
             Congestion of the udder                                 570
          Mammitis                                                   571
             Acute mammitis                                          573
             Contagious mammitis in milch cows                       580
             Chronic mammitis                                        581
             Gangrenous mammitis of milch ewes                       583
             Gangrenous mammitis in goats                            584
          Cysts of the udder                                         585
          Tumours of the udder                                       585
          Verrucous papillomata of the udder                         586

   VI. DISTURBANCE IN THE MILK SECRETION AND CHANGES IN THE MILK     587
          Microbic changes in milk. Lactic ferments                  588

  VII. MALE GENITAL ORGANS                                           594
          Tumours of the testicle                                    594
          Accessory glands of the genital apparatus                  597

                              SECTION VIII.
        DISEASES OF THE SKIN AND SUBCUTANEOUS CONNECTIVE TISSUE.

    I. ECZEMA                                                        599
          Acute eczema                                               599
          Chronic eczema                                             600
          Sebaceous or seborrhœic eczema                             601
          Eczema due to feeding with potato pulp                     603
          Impetigo in the pig                                        605
          Acne in sheep                                              606
          Fagopyrism (Buckwheat poisoning)                           606

   II. PHTHIRIASIS                                                   608

          SCABIES—SCAB—MANGE                                         611
          Scabies in sheep                                           611
             Sarcoptic scabies                                       612
             Psoroptic mange—Sheep scab                              614
             The tobacco-and-sulphur dip                             626
             Lime-and-sulphur dips                                   627
             Arsenical dips                                          632
             Carbolic dips                                           633
             Chorioptic mange—Symbiotic mange—Foot scab              636
          Mange in the ox                                            638
             Sarcoptic mange                                         638
             Psoroptic mange                                         639
             Chorioptic mange                                        640
          Mange in the goat                                          641
             Sarcoptic mange                                         641
             Chorioptic mange                                        642
          Mange in the pig                                           642
          Demodecic mange                                            643
             Demodecic mange in the ox                               644
             Demodecic mange in the goat                             644
             Demodecic mange in the pig                              644
          Non-psoroptic forms of acariasis                           645
          Hypodermosis in the ox (warbles)                           646

  III. RINGWORM                                                      649
          Ringworm in the sheep, goat, and pig                       653

   IV. WARTS IN OXEN                                                 655
          Urticaria in the pig                                       656
          Scleroderma                                                657

    V. SUBCUTANEOUS EMPHYSEMA                                        659

                               SECTION IX.
                          DISEASES OF THE EYES.
          Foreign bodies                                             661
          Conjunctivitis and keratitis                               662
          Verminous conjunctivitis                                   662
          Verminous ophthalmia of the ox                             663

                               SECTION X.
                          INFECTIOUS DISEASES.
          Cow-pox—Vaccinia                                           665
             Cow-pox and human variola—Preparation of vaccine        669
             Tetanus                                                 670
             Actinomycosis                                           672
             Actinomycosis of the maxilla                            673
             Actinomycosis of the tongue                             674
             Actinomycosis of the pharynx, parotid glands and neck   675
          Tuberculosis                                               682
             Tuberculosis of the respiratory apparatus               690
             Tuberculosis of the serous membranes                    694
             Tuberculosis of lymphatic glands                        696
             Tuberculosis of the digestive tract                     699
             Tuberculosis of the genital organs                      700
             Tuberculosis of bones and articulations                 701
             Tuberculosis of the brain                               702
             Tuberculosis of the skin                                703
             Acute tuberculosis—Tuberculous septicæmia               704
          Swine fever—Verrucous endocarditis and pneumonia of the
            pig                                                      710
             Swine fever                                             710
             Verrucous endocarditis of the pig                       713
             Pneumonia of the pig                                    714
          Hæmorrhagic septicæmia in cattle                           716

                               SECTION XI.
                               OPERATIONS.

    I. CONTROL OF ANIMALS                                            720
          Control of oxen                                            720
             Partial control                                         720
             Control of the limbs                                    720
             General control                                         722
             Control by casting                                      723
          Control of sheep and goats                                 725
          Control of pigs                                            725
          Anæsthesia                                                 726

   II. CIRCULATORY APPARATUS                                         727
          Bleeding                                                   727
             Bleeding in sheep                                       727
             Bleeding in the pig                                     728
          Setons, rowels, plugs, or issues                           728

  III. APPARATUS OF LOCOMOTION                                       730
          Surgical dressing for a claw                               730
          Amputation of the claw or of the two last phalanges        730

   IV. DIGESTIVE APPARATUS                                           734
          Ringing pigs                                               734
          Œsophagus                                                  734
             Passing the probang                                     735
             Crushing foreign bodies in the œsophagus                735
             Œsophagotomy                                            736
             Sub-mucous dissection of the foreign body               736
          Rumen                                                      737
             Puncture of the rumen                                   737
          Gastrotomy                                                 739
          Laparotomy                                                 740
          Herniæ                                                     741
             Inguinal hernia in young pigs                           741
             Imperforate anus                                        742
             Prolapsus and inversion of the rectum                   743

    V. RESPIRATORY APPARATUS                                         745
          Trephining the facial sinuses                              745
             Trephining the horn core                                745
             Frontal sinus                                           745
             Maxillary sinus                                         745
          Tracheotomy                                                746

   VI. GENITO-URINARY ORGANS                                         747
          Urethrotomy in the ox                                      747
             Ischial urethrotomy                                     747
             Scrotal urethrotomy                                     748
          Passage of the catheter and urethrotomy in the ram         749
          Passage of the catheter in the cow                         750
          Castration                                                 751
             Castration of the bull and ram                          751
             Bistournage                                             751
             Martelage                                               756
             Castration by clams                                     756
             Castration by torsion                                   757
             Castration with the actual cautery                      758
             Castration by the elastic ligature                      758
             Castration of the ram                                   759
             Castration of boars and young pigs                      759
             Castration of cryptorchids                              760
             Female genital organs                                   760
             Castration of the cow                                   761
             Castration of the sow                                   765
          Suture of the vulva                                        768
          Trusses                                                    769
          Section of the sphincter of the teat                       770
          Dilatation of the orifice of the teat                      770
          Ablation of the mammæ                                      771




              DISEASES OF CATTLE, SHEEP, GOATS AND SWINE.




                               SECTION I.
                 DISEASES OF THE ORGANS OF LOCOMOTION.


                        METHODS OF EXAMINATION.

Accidental and local diseases of the apparatus of locomotion are matters
of less urgency in the case of cattle than in that of the horse. On the
other hand, general affections, such as rheumatism and osseous cachexia,
demand a larger share of attention, and are of the utmost importance.

As the accurate diagnosis of any disease demands careful and systematic
examination, the practitioner usually observes a certain order in his
investigations, as indicated below:—

(1.) =Inspection=, from the side, from the front and from behind,
reveals the existence of deformities of bones, limbs, muscles and
joints, articular displacements, and irregularities of conformation or
of gait.

By inspection of an animal as it walks various forms of lameness, and
their particular characteristics, are rendered visible.

(2.) =Palpation and pressure= will detect changes in local sensibility,
the softness or hardness of tissues, the existence of superficial or
deep fluctuation, œdematous swelling, and abnormal growths like
ring-bones and exostoses, as well as the exact character of articular
enlargements.

(3.) =Percussion= is of little value in examining the apparatus of
locomotion. Nevertheless, percussion of the claws, and of certain bones
of the limbs, or of flat bones, may afford valuable information in cases
of laminitis, ostitis, and periostitis. Percussion along the
longitudinal axes of the limb bones is also useful in diagnosing
intra-articular fractures, subacute arthritis, osteomyelitis, etc.

(4.) =The gait.= Lame animals should be made to move, in order to assist
both in discovering the cause, and in estimating the gravity of the
condition. Sometimes it is advisable to turn the animal loose, but most
frequently it is moved in hand, either in straight lines or in circles.

Information so obtained should always be supplemented by local
manipulation and by passive movement, such as flexion, extension,
abduction, adduction and rotation of the joints.

A knowledge of the characteristics of normal movement in any given
joint, renders it comparatively easy to detect abnormality, such as
increased sensibility, articular crepitation or friction, and to
diagnose fractures with or without displacement, ruptures of tendons or
ligaments, etc.




                               CHAPTER I.
                           DISEASES OF BONES.


The diseases affecting bony tissues may broadly be divided into local
and general. Local diseases like ostitis, periostitis, necrosis,
fracture, etc., are somewhat rare, and are less important in cattle than
such general diseases as rachitis and osseous cachexia.

Rachitis is a disease of young animals, and occurs during the growing
period. Osseous cachexia is a disease of adults. Nevertheless, there is
a relationship between these two morbid conditions, for they frequently
co-exist in one family. Moreover, brood mares and cows suffering from
osseous cachexia give birth to foals and calves, which, if left with
their mothers, almost inevitably become rachitic.

The general characteristic common to both rachitis and osseous cachexia
consisting in diminution in the normal proportion of mineral salts
entering into the constitution of the bone, numerous theories have been
advanced to explain this irregularity in nutrition.

=The theory of insufficiency= is one of the oldest. It presupposes that
the young animals’ food contains insufficient mineral salts necessary
for building up the skeleton, hence rachitis; or again, that the daily
food of the adults does not afford sufficient mineral salts to
compensate for the normal transformation which is continually going on
within the organism, and for the direct losses which occur through the
medium of the urine, milk, etc.

This extremely simple theory appears perfectly logical, but
unfortunately does not fit in with all the observed facts. In reality,
rachitis attacks children whose supply of milk, from a chemical point of
view, leaves nothing to be desired. The same is true of animals,
particularly of young pigs. The so-called “acid theory” has therefore
been advanced to explain the points left obscure by its predecessor.

=The acid theory.= According to this theory, the food may contain more
than sufficient mineral material without, however, preventing the
development of rachitis or of osseous cachexia.

In animals suffering from digestive disturbance the alimentary tract may
become the seat of excessive fermentation or of changes in secretion.
There is thus produced an excess of lactic acid which passes into the
circulation and accumulates in the tissues, checking the processes which
end in ossification or, in the case of adults, even leading to
decalcification.

It seems fairly well established that experimental administration of
lactic acid to animals causes diminution in the quantity of calcium
salts contained in the bones (Siedamgrotsky, Hofmeister). On the other
hand however Arloing and Tripier failed to produce rachitis
experimentally.

Bouchard revived this theory in a somewhat modified form. He considers
that calcium salts are absorbed as carbonates and chlorides and
phosphoric acid as phospho-glyceric acid. The reaction which these
compounds undergo within the organism ends in the formation of the
phosphate of calcium necessary to ossification, but this “phosphate of
ossification” cannot be deposited if the organism contains an excess of
lactic acid.

=Theory of inflammation.= A third theory which until now has received
very little support is that called the theory of inflammation. The
general lesions which characterise rachitis are regarded as resulting
from primary attacks of ostitis and osteo-periostitis. The cause of
these forms of inflammation is not suggested.

To the above views may be added that more recently emitted by Dr.
Chaumier, according to which rachitis is of an infectious nature.
Unfortunately no proof of this has yet been adduced.


                           GENERAL DISEASES.


                               RACHITIS.

Rachitis is a disease of youth, and is common both to the human species
and to all domestic animals. It is characterised by irregularities in
development and by imperfect consolidation of the bones. The boundary
between rachitis and osseous cachexia is difficult to define and in fact
at the present moment the two diseases can scarcely be defined with
exactitude. Rachitis again is often complicated with softening of the
bones, disease of the limbs, arrested development, etc., but it must not
be forgotten that although the irregularities in ossification and
development of the skeleton are the symptoms most striking to the eye,
they do not stand alone, and that from the point of view of development
all the tissues, including the muscles, are more or less affected and
that most of the physiological functions such as digestion and the
secretion of urine are deranged.

=Etiology.= One of the principal causes suggested is that of heredity,
and so far as human beings are concerned, one seldom fails to discover
the rachitic taint. Certainly the offspring of individuals marked by any
debilitating disease like alcoholism, tuberculosis, syphilis, etc., are
poorly equipped for their future development. Their tissues lack the
necessary qualities and, _cæteris paribus_, their physiological
functions are performed less perfectly than are those of normal
individuals.

It is difficult to apply such information to domestic animals, because
badly developed subjects are not used for reproduction and the
importance assigned to heredity can therefore scarcely be sustained. The
conditions of life, on the contrary, have an unquestionable influence,
and if rachitis is so frequent in young animals living near towns, for
example, it is undoubtedly due to that want of air, light and liberty,
which first affects the mother’s health and later that of her offspring.

The same may be said of insufficient and improper food; for in this
connection quality is of even greater importance than quantity. Even
free feeding is insufficient if the fodder does not contain the material
necessary for sustaining and building up the developing frame, a point
which readily explains the occurrence of rachitis when young animals
receive a diet deficient in certain chemical constituents.

This occurs in young lambs and pigs where the mothers are given too
little variety or too small a quantity of food.

In calves and foals rachitis is rare but occurs when the mothers are
exhausted or cachectic or are debilitated by chronic wasting diseases
like tuberculosis or osseous cachexia. The milk is then no longer of
normal chemical constitution.

One fact appears to dominate the whole subject of the causation of
rachitis, viz., the failure to assimilate sufficient of the mineral
salts required in building up the skeleton. This failure to assimilate
may be caused by too meagre feeding, but even when the food is
sufficiently rich, some digestive disturbance may reduce the amount
absorbed below normal. This appears the only plausible explanation
unless we admit Dr. Chaumier’s theory that the disease is of an
infectious character.

=Symptoms.= The onset is absolutely insidious and the diagnosis of
rachitis is never made until nutrition has long been abnormal.

This disturbance of nutrition is revealed by irregularity and
abnormality in appetite, by difficulty in rising and moving about, and
by the animals lying down for long periods. The subjects are feeble,
sluggish and badly developed.

Next supervenes the second phase characterised by deformity of bones.
This is of two kinds—deformity in the neighbourhood of joints (deformity
or enlargement of the epiphyses) and deformity of the diaphyses. The
former results from irregularity in ossification of the articular
cartilages. The latter is followed by loss of rigidity in the bones of
the limbs which, under the influence of the body weight and of muscular
contraction, bend in different directions.

The bones appear of increased thickness principally towards the
articulations. The latter are deformed, and on palpation are found to be
surrounded by uneven and irregular growths.

The front limbs are distorted. In young pigs, lambs, and less frequently
in foals, calves and dogs, the jaws become deformed, and mastication is
rendered difficult.

The vertebral column may also be affected, and lordosis (bending
downwards of the back) or skoliosis (lateral bending of the back) is
somewhat frequent.

Cyphosis, or upward bending of the back, seldom occurs, and when seen,
sometimes results from disease other than rachitis.

[Illustration: $1]

General development is always interfered with and the young creatures
are generally dwarfed.

The digestive apparatus is disordered, the appetite is irregular and
sometimes depraved, while indigestion, gastritis, and enteritis are not
exceptional. Physiological and pathological research has shown that the
quantity of phosphoric acid eliminated in twenty-four hours in a
rachitic child is double the quantity passed by a healthy infant. The
amount of urea in the urine (which is a criterion of nutrition, and
usually varies in proportion to the amount of food ingested) is, on the
contrary, diminished even when highly nitrogenous food is given, thus
suggesting diminution in nutrition.

=Lesions.= The lesions are represented by abnormal and irregular
thickening around the interarticular cartilages. The cartilage is
thickened, compressible, very spongy and without regular ossification.
Diffused periostitis exists principally towards the extremities of the
bone. Beneath the periosteum the surface of the bone appears rough and
softened. On section the medullary canals are seen to be enlarged and
filled with marrow of a gelatinous character. The Haversian canals are
dilated, and the entire tissue appears very vascular. Chemical analysis
proves that the mineral constituents of the bone, particularly the
phosphates, have diminished by one-half; the organic constituents on the
other hand are increased in a similar ratio, but the ossein is abnormal.
Ossification has, in a word, been incomplete.

=Diagnosis.= Diagnosis presents no difficulty except in the early stages
before deformity has occurred.

Rachitis can scarcely be mistaken for any other condition except perhaps
infectious rheumatism, but the rapid course of the disease in the latter
case, the persistence of fever and the swelling of the joint cavities
sufficiently differentiate the conditions provided care is exercised.

=Prognosis.= From an economic point of view the prognosis is very grave
for if the lesions are extensive there is nothing to be gained by
keeping the animal.

=Treatment.= Treatment differs very little, whether the animals are
still being suckled or have been weaned. In the former case it is
necessary to improve the quality and chemical constitution of the
mother’s milk by giving food, richer both in mineral salts and in
nitrogenous material.

Cooked grains, milk, and forage of good quality should be given freely.
When the mothers are exhausted and anæmic it is better to feed the
little animals artificially or to change them to a foster-mother. Those
already weaned should be given good rich milk, eggs, boiled gruel, and
drugs, such as the phospho-chlorate of lime, 1 to 1½ drachms per day
(for a calf); lacto-phosphate of lime, 1 to 1½ drachms; bi-phosphate of
lime, 1 drachm, or simply ordinary phosphate of lime. Oil containing 1
per cent. of dissolved phosphorus may be given in doses of 1 to 2½
drachms, according to the size of the calves, but its use calls for much
care, and it should only be given for alternate periods of a fortnight.
The glycerophosphates are not very active. Beef meal in doses of 6
drachms to 1½ ounces and chloride of ammonium in doses of 30 to 60
grains have also been used advantageously. The above drugs, but
particularly the bi-phosphate of lime and chloride of ammonium,
stimulate nutrition and diminish the quantity of phosphoric acid
eliminated.


                           OSSEOUS CACHEXIA.

“Osseous cachexia” is a general disease which develops slowly and
progressively, producing its most marked effects on the bony tissues. It
has received a great many different names, such as osteoporosis,
osteoclastia, osteomalacia, fragilitas ossium, enzootic ostitis, bone
softening, etc., but none of these appears so appropriate as the term
osseous cachexia, suggested by Cantiget.

All the above-mentioned names are applicable to some phase of the
disease, but none to the disease in its complete development. Thus the
name “osteoporosis,” accepted by German authors, is quite applicable to
the phase of rarefying ostitis seen at the commencement, but this
condition occurs in other diseases. The expressions “osteoclastia” and
“fragilitas ossium” suggest the fragility of the bones and the
commonness of fracture. The term “osteomalacia” is warranted during the
period of bone softening. The term “gout,” though in practice confusing,
has been held to be justified by the frequent appearance of synovitis
and arthritis; while that of “enzootic ostitis” indicates the appearance
of the disease in all the stables in one district, without however
pointing to its nature. It is possible that under certain circumstances
the train of symptoms might be incomplete, and then the terms above
indicated would be quite inappropriate. “Osseous cachexia,” on the other
hand, is very comprehensive, and appears to cover the entire development
of the disease, for which reason it here receives preference.

Law defines the disease as “a softening and fragility of the bones of
adult animals, in connection with solution and removal of the earthy
salts.” He describes it as an enzootic disease of mature animals—mainly
cows—in which the decalcifying process proceeds most actively in the
walls of the Haversian canals and cancelli of the affected bones. In
consequence of the removal of the earthy salts the bones become soft and
more or less fragile.

The disease has been observed in England, Scotland, United States,
France, Belgium, and Jutland, and generally in districts with low-lying
damp pastures. It attacks cows which are heavy milkers. Susceptibility
appears to increase with advancing age.

=History.= Having been described by Vegetius, the disease was again
observed about 1650 in Norway where it was treated by the administration
of crushed bones. It is fairly frequent in some parts of Germany and
Belgium. In France it was studied in 1825 by Roux, and in 1846 by
Dupont, but Zundel in 1870 was the first who gave a good description of
it, founded partly on the authority of German authors and partly on
observations made by himself in the Valley of the Lower Rhine. Since
that time it has successively been reported in the Yonne by Thierry, in
the Nièvre by Vernant, in the Aube by Collard and Henriot (1893), in the
Indre by Cantiget, as well as in La Vendée by Tapon in 1893. In that and
the succeeding year Moussu also saw numerous cases in the districts of
Indre-et-Loire, Loire-et-Cher, Berry, Sologne, and in some parts of
Beauce.

=Symptoms.= The first symptoms are difficult to detect and interpret,
especially at the commencement of an outbreak and in parts where the
disease is rare they may lead to confusion and errors in diagnosis. On
the other hand, in regions where the disease is common the practitioner
will be able to form his diagnosis from the appearance of the first
signs.

To render clear the mode in which the symptoms develop we may divide the
progress of the disease into four phases, though this grouping is
somewhat arbitrary.

=1. The initial phase= is not well marked, and is announced by digestive
disturbance and by wasting. The former of these symptoms may be referred
to some other cause, but consists in irregularity, diminution and
sometimes perversion of the appetite. These earlier signs are soon
followed by loss of spirits, and some interference with movement, but
the symptoms only become of importance or attain their full development
when the animals remain lying for a long period in the stable.

[Illustration: $1]

=2. The second phase= is characterised by more precise signs, which
become almost pathognomonic. Difficulty in rising is added to the
already existing tendency to remain lying, and to the interference with
movement.

When lying down the patient no longer responds to the trifling stimulus,
which a healthy animal needs to cause it to rise. It remains languid and
apparently lazy, though in reality it experiences pain and difficulty on
attempting to get up. The least muscular effort when lying down often
causes it to moan, as do efforts to change its position or to walk. Even
when standing still, it may appear to be in pain, and patients often
assume a position similar to that of a horse suffering from laminitis.

At the end of this second phase, swellings appear, due to synovitis or
arthritis of the extremities, synovitis of the sesamoid or navicular
sheaths or to inter-phalangeal arthritis or arthritis of the fetlock
joint. Weakness becomes marked, and the appetite is very irregular.

Secretion of milk diminishes or ceases and abortion is not uncommon.

=3. The third phase= is characterised by fractures, and it is this
peculiarity of the disease which has procured for it the names of
fragilitas ossium, and osteoclastia. These fractures may affect any
portion of the skeleton. Animals so suffering sometimes break a leg
whilst trotting or the pelvis in simply jumping over a ditch; a
collision with a fixed object like the jamb of the stable door, or a
fall on the ground, may result in the fracture of one or several ribs.

[Illustration: $1]

Such shocks would be of no importance to a healthy animal, but to one
suffering from osseous cachexia, any violence, or even the slightest
muscular effort may be followed by fracture of the gravest character,
involving even the vertebral column. In cows the pelvis, femur, and
tibia are most frequently injured.

In horses, particularly in riding horses, fractures are commonest in the
region of the forearm, cannon bone, and anterior phalanges. So extremely
fragile are the bones at this stage that the horse represented herewith
broke twelve ribs at one time by simply falling on its side. It is
interesting to note that such fractures are never accompanied by any
extensive bleeding. They have little tendency to repair, no real callus
formation occurs, and on post-mortem examination one often finds the
ends unconnected by temporary callus, worn, and rounded by reciprocal
friction.

At this stage but under other circumstances, the animals show great
reluctance to rise, remaining down for twelve to twenty-four hours
without shifting their position. If forced to get up, they stand as
though fixed in one position, the respiration and circulation become
rapid, and they soon grow tired and fall.

=4. The fourth phase=, or period of osteomalacia, _i.e._ softening of
the bones, is also the last. It is rarely seen in large animals like
horses and oxen, because accidents so often accompany the preceding
stages and necessitate slaughter; but it is common in goats and pigs.

In this phase the bones become elastic, soft and depressible, yielding
to the pressure of the operator’s fingers.

[Illustration: $1]

The flat bones are particularly liable to this change, which is common
to domesticated animals. The bones of the head are the first to suffer;
later those of the pelvis. The lower jaw becomes swollen, particularly
about the centre of the branches which may attain three, four, or five
times, their normal thickness.

The depression in the submaxillary space disappears. The upper jaw
undergoes similar changes, becoming deformed and thickened until the
cavities of the sinuses and the hollow appearance of the palate are
lost, while the face is so changed that it cannot be recognised as that
of a horse, goat, etc.

The molar teeth are almost buried, their tables alone being visible at
the bottom of a depression, the edges of which rise above the
neighbouring parts (pig).

Mastication is clearly impossible, the jaws appear paralysed, the
muscles powerless, and only swallowing is possible, a fact which
explains why life is only prolonged to this stage in animals which can
be fed with a spoon or bottle (pigs and goats). The bones of the
cranium, although greatly changed in texture, are always less deformed
than those of the face.

The changes are such that it is often easy with a mere post-mortem knife
to cut the head completely in two. Osseous tissue, properly so-called,
has disappeared.

All the constituent tissues, with the exception of the skin and muscles,
_i.e._, the bone, periosteum and aponeuroses, have the appearance and
consistence on section of the fibro-lardaceous tissue seen in chronic
inflammation.

The following is a condensed description of the disease as given by
Law:—

=Symptoms.= Poor condition or even emaciation, with very visible
projection of the bones. The coat is rough, skin tense, inelastic and
hidebound, appetite variable, sometimes impaired, and nearly always
perverted (or depraved) so that the patient will lick the manger
continually or pick up and chew all sorts of objects: bones, leather,
clothing, wood or iron, stones, etc. The amount of food consumed may,
however, be up to the normal. The most marked feature is the difficulty
and stiffness of locomotion.... Temperature and yield of milk may remain
normal.

“Later, appetite and milk secretion fail, temperature rises a degree or
two, the animal refuses to rise, remaining down twelve to twenty-four
hours at a time, and ... when rising ... remaining on the knees for a
time, moaning and indisposed to exert itself further. At this stage many
cases begin to improve and may get well in five or six weeks. Some will
remain down for several weeks and finally get up and recover. With
constant decubitus, however, the animal falls off greatly, becoming
emaciated and weak, the appetite may fail altogether, and the patient is
worn out by the persistent fever, nervous exhaustion and poisoning from
the numerous bed-sores ... which are common over the bony prominences.
It is in these last conditions, above all, that fractures and
distortions of the pelvic bones, and less frequently of the bones of the
legs occur.”

[Illustration: $1]

“The disease may advance for two or three months, and in case of pelvic
fractures and distortions, there may be permanent lameness, and
dangerous obstruction to parturition, even though the bones should
acquire their normal hardness through the deposition of lime salts.”

In horses, the different phases of the disease develop precisely as in
bovines. The apparent differences between affected horses and cattle
result in reality from differences in their capacity for continuing
work. In the first phase, horses are incapable of work, their movements
being badly co-ordinated. They are inclined to stumble, and appear as
though suffering from strain of the lumbar muscles.

In the second phase pain referable to the bones sets in. Lameness
develops without visible lesions and is rapidly followed by synovitis
and arthritis in the lower portions of the limbs, and by wasting and
anæmia.

The animals seem unable to move rapidly, or if forced to do so may
sustain fractures even at a trot: the limb bones sometimes break or
ligamentous insertions in the neighbourhood of joints are torn away,
resulting in sudden falls on the ground and fracture of ribs or even of
the vertebral column. This corresponds to the third phase, osteoclastia,
in oxen.

[Illustration: $1]

From then onwards, horses become useless and, if not destroyed, may,
after a few weeks or months, develop the condition known as
osteomalacia, in which the flat bones become softened, the head, the
branches of the lower jaw and the face become deformed, while
mastication and other functions are impeded.

Germain gives the above symptoms as characteristic of the mode of
development of the disease in French and Algerian horses imported into
Tonquin, and his description, written several years ago, is fully
confirmed by more recent observations. Since Tonquin was taken over by
the French, however, improved methods of culture have resulted in the
production of better cereals and forage; the fodder plants have been
vastly improved, to the great benefit of imported animals.

In the goat, the disease shows some slight peculiarities. Thus, in the
second phase, during which goats and sheep suffer so markedly from
lameness and pain in the bones, goats often walk on the knees. The
disease, however, is uncommon in these animals. The phase of
osteoclastia is also less marked and fractures are rare, because the
animals weigh less and also because they are less exposed to falls and
violent shocks. The bones, nevertheless, are extremely fragile and
fractures may be produced at will.

Osteomalacia, on the other hand, is always well marked.

Regarding the development of the disease in pigs, we may repeat what has
just been said respecting the goat. Walking on the knees is often one of
the first signs, fractures are somewhat rare, and the period of
softening and deformity is always very noticeable.

=Course.= The development of the disease is slow, lasting from one to
three months as a rule, and is little influenced by hygienic conditions.
Good milking cows, however, seem to be most frequently attacked,
probably because of the great losses of nutritive material which occur
through the milk. The calves borne by such animals are often rachitic.
Oxen are less commonly attacked. Horses rarely suffer from the disease
in France, but frequently in Tonquin. Pigs reared on very poor soil
seldom escape attack.

[Illustration: $1]

If treated from the beginning, or even before the second phase has
become well developed, the disease may be cured, but after this period
little improvement need be expected.

=Causation.= The problem of why osseous cachexia occurs has naturally
given rise to numerous explanations, some plainly inadmissible, others,
however, of greater or less plausibility.

The fact which, from the earliest times, appears to have attracted most
attention is the relation defective nourishment bears to development of
the disease. In Norway, as early as the year 1650, the plant known as
sterregraes (which renders animals dull and heavy) was thought to be the
cause of the disease; two centuries later, in 1846, the _Anthericum
ossifragum_ was similarly regarded. Zundel, in 1870, claimed that the
Germans first referred the development of the disease to chemically
incomplete forms of nourishment. This opinion seems fully confirmed by
the remarkable observations of Germain on European horses imported into
Cochin-China, and it is finally placed beyond question by the work of
Cantiget. Basing his researches on analysis of the soil, he proved that
osseous cachexia only occurs in cattle depastured on land which is too
poor in phosphoric acid and calcium phosphate, and that it can be
banished by enriching the soil with suitable manures up to a point when
the proportion of phosphoric acid becomes normal. In good land, suitable
for raising cattle, the proportion of phosphoric acid, according to the
best exponents of agricultural chemistry, should not fall below 4,000
kilograms to the hectare. Cantiget and Brissonet have shown that where
the soil contains less than 1,500 kilograms to the hectare, osseous
cachexia is almost permanently present. As soon, however, as this
proportion is raised above 2,000 kilograms by suitable culture, the
losses diminish, and the cachexia finally disappears.

This view was greatly strengthened by fodder analyses, which showed that
in all cases where the soil is poor in calcium phosphate, the forage is
poor in phosphoric acid, and _vice versâ_. The food is too poor in
mineral salts, firstly for normal development; and secondly for the
proper nutrition of the skeleton.

Germain is of a similar opinion with regard to the occurrence of osseous
cachexia in horses in Cochin-China, where the soil is very poor in lime.
The fodder and cereals are poor in mineral salts, and even when given in
large quantities do not furnish proper (chemical) nutrition. Clear proof
of the correctness of this view is afforded by the fact that feeding
with forage and cereals obtained from France or Algeria prevents the
disease appearing, or diminishes and finally removes the previously
existing symptoms. Furthermore, Germain shows that Europeans, living
solely on the products of the country, to some extent suffer like the
horses.

This theory though based on sufficiently solid foundations to carry
conviction, has been questioned, and it may be desirable to record
briefly the criticisms advanced against it.

One of the most important is as follows:—

As osseous cachexia of oxen occurs in certain well-defined districts in
France, and seems due to the feeding, why does it not attack horses in
the same regions in an enzootic form? The answer appears to be that
horses receive a greater amount of rich food, particularly of cereals,
which contain much larger amounts of mineral salts, including
phosphates, than does ordinary forage.

The most serious objection was made by Tapon, who states that in 1893 he
saw osseous cachexia in oxen on farms in La Vendée where superphosphate
had been used for years, whilst the disease did not exist on other farms
where such chemical manures were not employed. Before attaching much
weight to this objection, however, it would be necessary to know the
richness in phosphoric acid of the soil on the respective farms, for it
is possible that, in consequence of natural conditions and in spite of
the use of certain mineral manures, the richness of the soil on the
first-mentioned farms, though manured with superphosphates, was still
below that of the others which had received no artificial, manure.

The system of culture is also of importance, for at the present day,
even with the use of artificial manures, cropping would rapidly
impoverish soils which were not suitably and sufficiently enriched.
Abundance or apparent richness of food signifies nothing if quality is
lacking.

It may also be asked: if the question of nourishment is of such prime
importance why are animals of European origin in Cochin-China affected,
whilst the indigenous races prove immune? The answer would appear to be
that, in addition to the defective quality of food, other factors, such
as adaptation to environment and relative digestive power, play a
considerable part in the production of the disease.

=Favouring causes.= Whilst conceding that the disease is due to one
determining cause, viz. the food, it is unquestionable that other causes
may favour its appearance. Abundant milking is one, so that the disease
most frequently appears six to eight weeks after calving. Gestation may
also determine an attack. The disease is rarer in oxen than in milch
cows. Starvation and bad hygienic conditions also have a certain
influence; it is well known that during dry years, particularly when
fodder is scarce, osseous cachexia makes the greatest ravages. Law
states that the disease has been attributed to excess of organic matter
in the soil, to succulent watery foods, as rank watery grasses,
potatoes, turnips and other roots deficient in nutritious solids. Some
agent—microbe or toxin—swallowed with the food has been suspected but
not yet isolated.

Other explanations have been advanced but up to the present time they
scarcely deserve to be regarded even as hypotheses. Thus Anacker in 1865
declared that the disease commenced as muscular rheumatism, was
succeeded by destructive or atrophic ostitis, and ended as osteoporosis.
So far as the order of the osseous lesions is concerned, this view is
quite correct, but the ossific changes are consequences and not causes.

The idea that the disease was due to an infectious agent has been
advocated by Leclainche, without, however, having been proved. Pétrone
is the only person who has hitherto suggested that osteomalacia in man
is due to infection with a nitric ferment (_Micrococcus nitrificans_).
According to him, pure cultures of this organism injected into dogs,
produce osteomalacia. These statements, however, require confirmation.

=Lesions.= The chief lesions are to be found in the bones. They consist
in rarefaction of the compact tissue, increase in size of the medullary
cavity and Haversian canals, and enlargement of the areolæ of the spongy
tissue. The bone marrow loses its fatty constituents, appears red and
gelatinous, and contains a greatly exaggerated number of blood-vessels.
When heated, the bones do not yield oil as in healthy subjects, and when
dry, they seem abnormally porous. In the osteoclastic phase, the bones
become very friable and even the shafts assume a spongy appearance. They
diminish in density. These changes correspond to the stages of eccentric
rarefying ostitis and osteoporosis of German authors.

The flat bones often show well-marked periostitis, but the great
thickening sometimes seen in certain of the bones of the head appears to
be the result of a special osteo-periostitis. It is quite certain that
the disease is due to something more than a mere want of mineral
constituents in the bone, and poverty in this respect certainly does not
explain the hypertrophic changes. The nutrition of the bones as a whole
is disturbed, resulting in alterations both in the ossein and in the
mineral salts, the whole process being accompanied by symptoms of
osteo-periostitis.

[Illustration: $1]

The fractures which occur so frequently during the osteoclastic phase
have well-marked peculiarities. The extravasation of blood is trifling,
and no callus forms, even when the ends of the bones are immobilised by
external aid; if the ends are left free, they soon become worn and
polished by rubbing against one another.

In the neighbourhood of the articulations and ligamentous insertions the
periosteum soon undergoes change, and it is not uncommon to find
sub-periosteal and intra-osseous extravasations of blood.

Germain has also noted in horses the disappearance of the intervertebral
and articular cartilages, and the frequent occurrence of anchylosis,
true or false.

In the final stages, the bones may be cut with a knife, and a time
arrives when bony tissue seems completely to have disappeared; thus, as
shown in Fig. 8 herewith, it was possible to cut the entire head of a
pig into thin slices without the slightest difficulty. All parts of the
head had been affected by the softening change.

From the chemical point of view, the diminution in mineral salts and in
phosphate of calcium has long been recognised, but the degree of this
change varies according to the phase. In human beings the proportions
have been estimated as follows: Normal bone, 50 to 80 per cent. of
phosphate of calcium; bone in persons suffering from osteomalacia, 5 to
20 per cent. of phosphate of calcium. The changes in the ossein have not
been carefully studied. We only know that histologically the ossein
becomes fibrillar, and that chemically it no longer retains its normal
composition.

=The diagnosis= is difficult, particularly on the first occasion of
seeing the disease, and especially if this is of an enzootic character.
The practitioner may also have some hesitation in diagnosing isolated
cases in regions where the disease seldom occurs.

Otherwise, diagnosis is usually easy, as soon as lameness or synovitis,
or arthritis of the lower regions of the limbs appears. Only in isolated
cases are the lesions likely to be mistaken for accidental injuries, and
it is also fairly easy to differentiate them from the localised lesions
of rheumatism. The latter disease seems more frequently to attack the
upper joints of the limbs, and is often accompanied by intense fever and
cardiac disturbance.

=Prognosis.= In a general sense the disease is very grave, because it
appears as an enzootic, and, in dry years and those during which there
is a scarcity of forage, inflicts enormous losses on the breeders of
certain countries. When advice is sought towards the end of the second
phase of the disease the prognosis is therefore very grave. Under such
circumstances it is often better to slaughter rather than to treat,
provided that the affected animals, like cows, pigs, or goats are still
of some value.

=The prognosis= is much more hopeful if treatment is attempted at an
early stage, when improved diet and the use of suitable drugs sometimes
lead to recovery.

=Treatment.= We know that in the Middle Ages this disease was often
treated by the administration of crushed bones, and even at the present
day ground bones are frequently recommended. Treatment must be
subordinated to proper feeding, no system of medication being of any
value whatever unless the food is suitable.

Germain states that imported horses in Cochin-China recover if simply
returned to their former diet, _i.e._ to cereals and forage obtained
from France or Algeria. Cantiget shows that such improvements in
cultivation as the free distribution of superphosphate manures on
impoverished soils modify the chemical composition of the forage, and
render it capable of building up and sustaining the organism and bony
tissues; treatment should therefore be essentially prophylactic in
character.

Animals suffering from osseous cachexia should be fed on cereals and
forage obtained from rich districts where the disease has never
occurred; but, as in times of scarcity questions of expense almost
always receive first consideration, it may be necessary to substitute
bran for such products, or give oats, maize, beans, rice, and oil or
cotton cake, etc., all of which can be obtained commercially, and are of
sufficient nutritive richness. It is often advantageous to give such
food cooked and slightly salted.

Commercial ground bones and calcium phosphate (bi- or tri-basic), in
doses of 1 ounce per day for oxen and 1¼ to 2 drachms for pigs or goats,
have given excellent results in the hands of most practitioners. Some
recommend the addition of iron salts or bitter tonics like gentian or
nux vomica in doses of 2½ drachms per day for a full-grown ox.

Law declares that the treatment should be varied “with the predominance
of the causes, essential or accessory.... Green clover, alfalfa, and
other leguminous products, ground oats, beans, peas, linseed or rape
cake ... and vetches may be especially recommended.... The free access
to common salt and a liberal supply of bone meal are helpful....
Apomorphia is especially valuable in correcting the perverted appetite
and stimulating digestion. A change of pasture is always advisable. In
all cases where possible the water should be changed as well as the
food. Attention to the housing, grooming, and general care of the
animals should not be neglected. Finally, every drain upon the system
should be lessened or stopped. The milk may be dried up, and the animal
should not be bred.”

Meat meal also renders good service, but the use of cod liver oil,
suggested by Zundel, is too expensive, and phosphorised oil is too
dangerous to be adopted in ordinary treatment.

Local treatment for synovitis and arthritis has been recommended. It is
ineffective unless accompanied by good feeding and internal medication.
On the other hand, the lesions often diminish rapidly or totally
disappear under the influence of general medication alone.


                           LOCAL AFFECTIONS.


                               FRACTURES.

Although oxen, sheep, goats, and pigs are much less subject to fractures
than the horse and dog, nevertheless, they do suffer from such
accidents. Repair is perfectly possible, but the cases are often not
worth treating, unless the subjects are young or of considerable value.
On the other hand, in fat and heavy subjects, it is difficult to fix the
parts in position. Slinging produces bad results, and generally should
not be encouraged.

Apart from fractures accompanying general chronic diseases, like
rachitis and osseous cachexia, the vertebræ, the pelvis, the ribs, or
any of the limb bones, may be fractured in consequence of accident.

Such fractures may be either complete or incomplete (fissures), simple
or compound.

The general signs which indicate fracture are always the same, viz.,
loss of function, local pain, abnormal mobility, crepitation, due to
rubbing together of the ends of the bones, and deformity of the part.
Diagnosis is generally easy; prognosis on the other hand is very
variable.

The vertebral column may be accidentally fractured in the region of the
neck in consequence of the animal falling on its head; in the
dorsolumbar region, from falling into ditches or ravines, or, in the
case of bulls fighting, from violent muscular efforts. Fractures of the
first kind are immediately fatal; those of the second result in
paraplegia of the hind limbs, and necessitate immediate slaughter.

=Fractures= of the =pelvis= comprise:—

1. Fractures of the angle of the haunch, resulting from external
violence and characterised by sinking of the external angle of the
ilium, deformity of the hip, and lameness without specially marked
characters. This fracture is rarely complicated. The symptoms of
lameness diminish with rest, but deformity continues.

2. Fractures of the floor of the pelvis, usually extending from the
anterior margin of the pubis to the foramen ovale and from the posterior
margin of the foramen ovale to the end of the symphysis. They result
from obstetrical manipulation, as in forcibly removing a fœtus which is
too large, or a monstrosity. As a rule, the animals cannot rise, or if
they succeed in doing so, are incapable of moving. Diagnosis is made by
exploration through the rectum. Such fractures always necessitate
slaughter.

Fractures of the neck of the ilium and of the base of the cotyloid
cavity, even in cases of dislocation, are rare despite what has been
said to the contrary.

In the fore limb, fractures of the scapula and humerus are usually of
traumatic origin, are seldom accompanied by marked displacement, and are
capable of uniting if a long rest at grass is allowed. Pitch bandages
should be applied to the surface, covering all the surrounding regions,
viz. the withers, upper portion of the forearm, girth and chest, to
assist in immobilising the region of fracture, and to promote union.

Fractures of the forearm are more difficult to treat, because the
bandage applied must extend as far as the hoof. In this case
displacement often occurs. It is therefore necessary, firstly, to reduce
the fracture, and bring the ends in perfect contact, for which purpose
it may be requisite to cast the animal, and give an anæsthetic; and,
secondly, to apply a pitch plaster in the form of a shallow gutter,
leaving the inner surface of the limb uncovered along a line about two
inches wide following the course of the veins of the forearm.

Fractures of the metacarpus and metatarsus usually heal well in all
animals of moderate weight, such as heifers, steers, goats or sheep,
provided a simple plaster bandage, covering the entire limb or
preferably with an opening in the position above indicated, is applied
and continued downwards as far as the claws.

In sheep and goats it is sometimes even sufficient to use a splint
formed of straw-boards, and in the case of oxen, of wood, applied over a
cotton-wool padding and retained in position by straps, or in the case
of the heavier animals by dextrine or pitch bandages.

In the hind limb, fractures of the femur are more serious, because the
apparatus that can be used to secure immobility is seldom or never
effective; excepting in young animals, it is therefore usually better to
slaughter.

Fractures of the tibia are treated like those of the forearm when it
appears desirable to keep the animals alive.

Plaster bandages can very easily be prepared by saturating tarlatan in a
mixture of equal parts of thoroughly dry plaster and water. Six to ten
thicknesses of tarlatan, arranged alternately longitudinally and
transversely, are sufficient. When adjusted they can be kept in position
until the plaster has hardened by means of dry bandages applied from
below upwards, which can be removed after a lapse of half an hour to an
hour.


                        FRACTURES OF THE HORNS.

=Anatomy of the horns.= The horns form organs of defence, and project on
either side of the frontal bone at the poll. Each consists firstly of a
bony basis generally known as the horn core; secondly, of a
horn-secreting membrane; thirdly, of a horny sheath, the horn properly
so called.

(1.) The horn core projecting from the frontal bone does not develop
until after birth. About the third month a little prominence appears
under the skin, which, as it develops, assumes a conical shape, and may
be seen to be covered with a horny substance. In proportion as the horn
core grows, there develops within it a cavity which may either be of a
simple character or divided by a longitudinal partition. This
communicates with the frontal sinus, a fact which explains the
collection of pus in the sinuses as a result of injuries to the horns.
The sinus of the horn core does not exist in young animals, and is not
completely developed before the third or fourth year of life.

[Illustration: $1]

(2.) The horn-secreting membrane is formed by the skin, which undergoes
special development around the base of the horn and comes to resemble
that of the coronary band, from which the hoof or claw is secreted. The
band is about one-fifth of an inch in breadth. The papillæ of the dermis
are specially developed at this point, and the epithelium which they
secrete eventually forms the horn.

The internal surface of the growing horn is adherent to the horn core
through the medium of another tissue formed by a specially
differentiated periosteum which is continuous with the periosteum
covering the frontal bone. It is not a true periosteum, but a vascular
tissue formed of papillary layers analogous to those of the podophyllous
tissue of the ox’s claw or horse’s hoof.

This keratogenous membrane receives a rich vascular supply from the
arterial circle formed at the base of the horn core by a division of the
external carotid, the blood conveyed by which is freely distributed to
the enlarged papillæ. The great vascularity of these parts explains why
lesions of the horns are often followed by such profuse bleeding.

(3.) The horn secreted by the papillæ of the horn band (which is
analogous to that of the coronary band of the horse) forms a cone
varying in its curve in various breeds. Its base is hollow, and contains
little depressions holding the papillæ from which the horn is secreted.
From its base up to the end of the horn core the walls progressively
increase in thickness. From this point it is solid; in a fully-grown
horn the bone does not extend more than one-half or two-thirds of the
entire length.

In the adult, the development of the horns varies with different breeds
and is affected by sex. In the bull the horns are short, but in the cow
and ox long. Short and fine in animals of improved breed like the
Durham, they are long and thick in breeds of working oxen.

Injuries affecting the horns are of three classes, determined by the
part affected.

1. Detachment of the horn or sheath.

2. Laceration:—

  (_a_) Of the horny sheath alone.

  (_b_) Of the horny sheath and of the horn core.

  (_c_) Of the horn core alone, the horny sheath remaining intact.

3. Fractures:—

  (_a_) Of the terminal half of the horn.

  (_b_) Of the lower half.

  (_c_) Of the base.


                        DETACHMENT OF THE HORNS.

When the yoke is badly fitted or padded, it is liable to cause a
continual strain or a succession of shocks producing chronic
inflammation of the keratogenous membrane. Should the end of the horn
then be struck heavily, it is quite possible that the horn will either
partially or wholly be detached. In this case it falls away without
there necessarily being any important lesion of the horn core.

Such accidents are not infrequently caused by the driver striking the ox
on the horn with the yoke in order to keep it quiet while it is being
harnessed.

=The prognosis= of this condition is not grave, except for the fact that
working animals cannot be used until the horn is completely regrown.

=The treatment= simply consists in thoroughly cleansing and disinfecting
the horn core and then applying a protective dressing. The bony basis is
surrounded with a mass of tow saturated with an antiseptic solution,
like 2 per cent. creolin or carbolic acid solution, which is kept in
position by a spiral bandage passed around the horn, and secured in a
figure of 8 on the opposite horn. Instead of applying such a dressing,
some practitioners content themselves with using an antiseptic ointment
or even a simple dressing of tar.


                        FISSURING OF THE HORNS.

=Causation.= In a general sense fissures may result from any violence
affecting the centre portion of the horns, such as blows with the yoke
or accidental bruises inflicted by the animals themselves in fighting
with their neighbours.

=Symptoms.= Whether the fissure is confined to the horny covering itself
or whether it extends to both the portions constituting the horn, that
is, the horny covering and the horn core, two very noticeable symptoms
are always present: 1. A straight fissure resembling a sand crack, and
appearing usually on the convexity of the horn, and, 2. A very trifling
hæmorrhage, which does not appear until some hours or even a day after
the accident.

=Diagnosis.= If the lesion only affects the horn core, diagnosis is
always difficult, for one can hardly perceive any sensitiveness of the
horn near the fissure.

=Prognosis.= Provided that the horn core is not injured, the prognosis
is favourable; but in the contrary case, it should be reserved; for
hæmorrhage extending to the interior of the frontal sinus not
infrequently causes suppuration in that cavity.

=Treatment.= Attempts should first be made to check hæmorrhage by
applying masses of tow saturated with cold water and frequently wetted
with slightly antiseptic solutions, such as 2 per cent. creolin or
carbolic acid. If hæmorrhage persists in spite of this simple treatment,
astringents may be employed, which, by causing the formation of a clot,
mechanically arrest further extravasation of blood. These astringents
vary considerably in value, and we should particularly warn
practitioners against perchloride of iron, which causes necrosis of the
tissues, and later, formation of pus. A 5 per cent. solution of gelatine
is hæmostatic and excellent for the purpose named, as also is hydroxyl
solution. When once hæmorrhage is arrested, the keratogenous membrane
rapidly heals in consequence of its vascularity, and soon secretes fresh
horn.


                        FRACTURES OF THE HORNS.

=Etiology.= Fractures of the horns, like fissures, are produced by
violence, but of a more marked character. They are termed complete or
incomplete, according as the entire thickness of the horn or only a
portion of that thickness is involved.

The fracture may affect either the terminal half or the basilar half;
or, again, it may have its seat in the frontal bone below the origin of
the horn core, in which case a flake of bone will be detached. Such
fractures assume varying forms, and may either be deeply excavated,
oblique, smooth, regular or dentated.

[Illustration: $1]

=Symptoms.= The symptoms are extremely simple. They consist mainly in
the mobility of the fractured end, and such phenomena as sensitiveness,
hæmorrhage, etc. When the fracture extends to the frontal bone,
crepitation may also be noted.

=Prognosis.= The prognosis is not grave unless the fracture extends to
the basilar half of the horn or affects the frontal bone.

=Treatment.= (1.) If the fracture is confined to the horn core, it is
only necessary to bring the fragments into regular apposition, after
having removed the broken end of the horn itself.

(2.) In treating a fracture affecting the middle portion of the horn or
in treating animals destined for the butcher, the best method is to make
a simple wound by dividing the parts with a saw below the fracture. This
is a painful operation, necessitating anæsthesia, and requiring the
animal to be cast or firmly fixed to a post or placed in a trevis. To
diminish the painful stage of the operation, it was formerly recommended
to make a circular incision extending through the entire thickness of
the horn proper, and then to remove with a fine, very sharp saw the
portion of the horn core. This, however, is scarcely practicable, and it
is much better to make a direct section. Hæmorrhage is checked with
compresses, moistened with cold water, after which a dressing known as
the “Maltese cross dressing” (Fig. 10) is applied according to general
principles.

The surface of the section, after washing with an antiseptic solution,
is powdered with iodoform or a mixture of iodoform and boric acid,
covered with a mass of tow or cotton wool, saturated with liquid
antiseptic, and then surrounded with a flat pad of wadding, which
extends completely around the horn as far as its base. A second pad of
larger size, intended to protect the wound against external violence, is
arranged around the free extremity of the horn. This is kept in position
by two small cross bandages. Another bandage, the loop of which is fixed
to the base of the opposite horn, is then applied in spiral turns,
completely enveloping the former pads and extending from the base to the
point. Arriving at the free end, the operator reverses the bandage,
draws it tight, and continues down to the base of the horn, fixing it by
figure of 8 turns passed around the base of both horns.

[Illustration: $1]

(3.) In dealing with fractures of the lower third of the horn in working
oxen, it is necessary to seek consolidation of the horn by callus
formation, so that the animals may again become useful in the yoke. Very
great difficulty accompanies attempts to immobilise the horn in such
cases, since the least shock to the extremity of the horn destroys the
union, on account of the length of the lever represented by the horn
itself.

The first method of treatment consists, after the wound has been
carefully disinfected, in fixing the ends in place by tightly applied
pads, surrounded by splints, curved to fit to the horn. These are
supported by several turns of a spiral bandage.

Were one certain of the cleanliness of the wound and of its perfectly
aseptic condition, it would be better at once to have recourse to a
fixed bandage, strengthened by plaster or silicate of soda.

These bandages are applied longitudinally and should extend a
considerable distance on either side of the fractures. If the horn is
long and thick, it is best to use a fixed dressing of this kind secured
by bandages in the form of a Maltese cross.

All these methods, however, are more or less inconvenient, and the most
practical procedure often consists in removing the horn. Treatment
should only be attempted when the owner specially requests it in order
to render the animal useful for working or show purposes.

Moreover, however strong the dressing, accidents are frequent, for
accidental shocks to the fractured horn interfere with the co-aptation
of parts, and diminish the chance of perfect union. To avoid these
drawbacks, the apparatus shown in Fig. 11 has been invented.

This apparatus consists of a splint, the middle of which fits the back
of the animal’s poll, the sides being gouged out to receive the lower
half of the horn and notched, to enable the fractured horn to be well
supported by bandages.

[Illustration: $1]

(4.) Fractures of the base of the horn are more serious, because a
fragment of the frontal bone is usually torn away with the horn core. As
a rule, the fracture is subcutaneous or without external wound. The horn
is displaced, and swings loosely. On examination, a characteristic
crepitation sound is easily detected. In such fractures hæmorrhage is
subcutaneous and often extends to the frontal sinus, in consequence of
which it is not uncommon for pus to form in the sinus as a complication.

Treatment includes reduction of the fracture, and the application of a
fixed plaster or silicate bandage covering the fronto-occipital and
superior auricular regions.

When a skin wound exists, it is better to remove the horn and bony
fragment, and to apply an antiseptic dressing in order to prevent
infection of the frontal sinus.


                               EXOSTOSES.


                           SPAVIN IN THE OX.

Exostoses are somewhat uncommon in the bovine species, and when they
occur are rarely of great clinical interest. Nevertheless, in cows and
old working oxen one sometimes sees metatarsal spavin. Its gravity,
however, appears to be very much less than in the horse, on account of
its position. Very commonly there is only trifling lameness.

Treatment by application of biniodide of mercury ointment or the actual
cautery gives good results. The principal precaution required is to
prevent the animals licking the parts.


                               RING-BONE.

Ring-bones only occur in working oxen, and particularly in aged animals
used in hilly regions. They result almost exclusively from wounds,
ligamentous and tendinous strains, and articular injuries.

[Illustration: $1]

They are preceded (as can usually be proved by dissection of limbs) by
fibrous or fibro-cartilaginous induration in or about the coronet or one
of the phalanges. These thickenings increase the diameter of the pastern
in all directions. Ring-bones are seldom very large; but as they
partially or entirely surround the insertions of the lateral ligaments,
inter-phalangeal articulations or insertions of the digital extensors,
they are painful, and produce lameness of varying intensity.

=Diagnosis= is easy, partly because the tension of the skin and the
fibrous thickening render palpation painful.

=Prognosis= is grave, because the effect of ring-bone is sometimes to
render working animals useless.

[Illustration: $1]

[Illustration: $1]

=Treatment.= To relieve the diseased claw of pressure due to its bearing
on the ground, the shoe should be removed and the claw freely pared. If
necessary, the healthy claw of the same foot may be raised by placing a
piece of thick leather between the sole and the shoe. It is advisable at
once to apply an energetic plaster, or, better still, to resort to
firing in points.


                          SUPPURATING OSTITIS.

In addition to the changes in bone resulting from rachitis, osseous
cachexia, tuberculosis, and actinomycosis, one sometimes sees cases of
periostitis or ostitis pure and simple. As a result of external injury
or direct wounds, the bone may be contused and injured, becoming the
seat of diffused periostitis, necrosis, suppurating ostitis or
osteomyelitis. Open fractures may produce the same results.

=Treatment= comprises disinfection of wounds, antiseptic injection of
fistulæ, the application of antiseptic pencils, curettage, the removal
of sequestra, and vesicant or resolvent complications. When such
conditions extend to neighbouring joints and produce suppurative
arthritis, the animals ought to be killed.


                             BONE TUMOURS.

The only bone tumours of real importance from a practical point of view
are malignant growths represented by rapidly spreading epitheliomata or
sarcomata, originating in the periosteum. Fortunately such tumours are
rare.

They are not difficult to diagnose, as they develop rapidly, are
accompanied by pain and lameness ending in diminution or loss of the
power of movement, and frequently attack neighbouring lymphatic glands.
Even when in good condition, animals lose flesh and appetite, and
finally die of general wasting. The =diagnosis= is sufficiently guided
by the deformity of the parts, the bosselated appearance of the tumours,
the absence of fluctuation, the hæmorrhage which follows exploratory
puncture, the character of the little fragments of tissue removed
through these punctures, and finally the leukocytosis, which accompanies
the development of malignant tumours.

=The prognosis= is grave, for it is usually difficult or out of the
question to have recourse to removal, resection or amputation, when the
tumours have acquired any considerable size. Success is impossible
unless intervention is early, and the growth is in a readily accessible
part. In other circumstances early slaughter is indicated.




                              CHAPTER II.
                         DISEASES OF THE FOOT.


                        CONGESTION OF THE CLAWS.

Congestion of the claws is not infrequently confused with contusion of
the sole. It is, however, essentially different, and presents closer
analogies with laminitis. The condition is characterised by congestion
of the entire vascular system of the claw and principally of the velvety
tissue. Like laminitis, it affects all four limbs; in rare cases the two
front or two hind.

Congestion of the claw results almost exclusively from enforced movement
on hard, dry and hot ground. It is commoner in animals unaccustomed to
walking, and in heavy beasts which have been travelled considerable
distances to attend fairs or markets. It is commonest in the bovine and
porcine species, and less common in sheep.

The =symptoms= appear after animals return from a long journey by road.
They are characterised by unwillingness to bear weight on the feet and
difficulty in movement. Standing is painful, and the animals resist
being moved; as soon as released they lie down.

=Diagnosis= presents no difficulty, though the condition is sometimes
mistaken for slight laminitis.

=Prognosis= is favourable.

Absolute and prolonged rest is always followed by recovery, no internal
medication being necessary, though this result is promoted by enveloping
the claws in wet compresses or by using cold foot baths, etc.


                        CONTUSIONS OF THE SOLE.

Contusions of the sole are only seen in animals which work without shoes
or in such as are badly shod.

Work on rocky ground, movement over newly metalled roads, and wounds
produced by sharp stones, are the principal causes of contusion of the
sole. Badly applied shoes, flat or slightly convex on their upper
surfaces, may also produce bruising in the region of the sole. The
anterior angle of the claw is rarely affected.

Lameness is the first symptom to attract attention. It is slightly
marked, unless the bruising has been overlooked until suppuration has
set in. It affects only one or two limbs, and is rarely accompanied by
general disturbance, such as loss of appetite, fever, exhaustion during
work, etc.

Locally the claw or claws affected are abnormally sensitive to
percussion of the wall, and particularly to compression of the sole.

The parts are hot to the hand, and thinning the sole with a knife shows
little perforations, irregular points and crevices in the horn. One may
also find softening, infiltration and hæmorrhage within the horn similar
to those of corn in the horse, undermining of the sole over limited
areas, and sometimes suppuration, if the animals have been forced to
work when lame.

Complications like necrosis of the velvety tissue or of the bone, though
comparatively common in the horse, are rare in oxen.

=Diagnosis= is not difficult provided the history of the case is known.
Confusion with laminitis is scarcely possible, for the gait of this
lameness and the local symptoms are all different. Examination of the
sole will usually dispel any remaining doubt.

=Prognosis.= The prognosis is favourable. When the horn is simply
softened and a blackish liquid transudes, the lesion is trifling; if the
discharge is reddish grey the lesion is graver, and implicates all the
velvety tissue; finally, separation of the horn from the secreting
membrane and the discharge of true pus point to death of the
keratogenous tissue or of the bone.

=Treatment= should be commenced by carefully thinning the sole around
the wound and applying moist antiseptic dressings or cold affusions.
Removal of loose portions of horn hastens repair by allowing discharge,
which has accumulated between the living tissues and the horn itself, to
escape freely. The extirpation of necrotic tissue and the application of
surgical dressings are only called for in specially grave cases.

This treatment usually gives good results. The acute complications which
are so common and so dangerous in the horse seldom occur in the ox.

Most of these operations can be performed without casting, provided the
animal is placed in a trevis or is sufficiently secured.


                               LAMINITIS.

Laminitis is characterised by congestion, followed by inflammation of
the horn-secreting tissues of the foot. It is now rare in oxen and very
seldom assumes an acute form. The slow pace at which animals of the
bovine species move may sufficiently explain this rarity; nevertheless,
prolonged travel on stony roads with heavy vehicles, rapid and repeated
marches to towns or important fairs, are sufficient to produce attacks.
Before the days of railways, and for some time after their introduction,
in Britain cattle were travelled by road, and laminitis was common.

Long journeys in crowded railway trucks may also produce the disease,
although the animal has not been forced to walk. Persons engaged in
exhibiting cattle at shows are well aware of this. Prolonged maintenance
of the standing position will produce the trouble, to which the joltings
of the railway journey may also contribute their share. Prolonged
standing on board ship may induce laminitis.

“Show condition” and the consumption of highly nitrogenous, and
particularly of farinaceous, foods favour the occurrence of laminitis.

Breed is also considered to have some influence, and laminitis is said
to occur more frequently in animals raised in flat districts, because in
their case the space between the digits is larger than in mountain-bred
cattle. In this connection the body weight may perhaps play a certain
part.

=The symptoms= vary somewhat, depending on whether laminitis is general
and affects all four feet, or restricted to the two front or the two
hind feet.

The internal claws always seem more severely affected and more sensitive
than the external. In very rare cases the animal remains standing, but
usually it lies down, and will only rise under strong compulsion.

When standing, the symptoms are similar to those noted in the horse; the
animal appears as though absolutely incapable of moving. If all four
feet are affected the animal assumes a position as though just about to
rise; if the front feet alone are affected the animal kneels in front
whilst it stands on its hind legs, a very unusual position for the ox to
assume; finally, if the hind feet alone are affected, the animal seems
to prefer a position with the feet under the body both in front and
behind. (See _Veterinarian_, 1894, case by Bayley, and note by Nunn.)

It is always difficult to make the animal move. Walking seems painful,
and most weight is thrown on the heels. The body swings from side to
side as the limbs are advanced, and each limb is moved with a kind of
general bodily effort.

The claws are hot, sensitive to the slightest touch, and painful on
percussion.

Throughout the development of laminitis the general symptoms are very
marked. The appetite falls off early, fever soon appears, and in grave
cases the temperature rises to 105° or to 106° Fahr. Thirst is marked,
and the animal seems to prefer cold drinks. The muzzle is dry, the face
anxious and expressive of pain. Wasting is rapid.

The ordinary termination is in resolution, which occurs between the
eighth and fifteenth day, provided the patient has been suitably
treated. The disease rarely becomes chronic. On the other hand, the claw
occasionally separates, as a consequence of hæmorrhage or suppuration,
between the horn proper and its secreting membrane. Should this
complication threaten, the pastern becomes greatly swollen, the
extremities become intensely congested, and separation commences at the
coronet. Loss of the claws, however, like suppuration, is rare.

=Diagnosis.= Congestion of the sole, the early stage of infectious
rheumatism and osseous cachexia may, at certain periods of their
development, be confused with laminitis; but the history and the method
of development of the above-mentioned diseases always allow of easy
differentiation.

It should, however, be added that, in certain exceptional conditions
(suppurating echinococosis, producing chronic intoxication, tumours of
the liver, and tumours of the pericardium and mediastinum), symptoms may
be shown that suggest the existence of laminitis, although it is not
really present. In these cases pain may possibly be felt in the bones of
the extremities.

=The prognosis= is usually favourable, but necessarily depends on the
intensity of the disease. Fat stock always suffer severely.

=The treatment= varies in no important particular from that prescribed
for the horse, and is usually followed by rapid improvement. The chief
indications are free bleeding from the jugular, the application of a
mustard plaster over the chest, and the administration of a smart
purgative (1 to 2 lbs. of sulphate of soda, according to the size of the
animal) at first, followed by laxatives. This treatment may be completed
by giving salicylate of soda _per os_ in doses of 5 to 8 drams, or
arecoline in subcutaneous injection, 1 to 1½ grains. Local treatment
consists in cold affusions or poultices to the feet.

Failing cold baths, clay plasters applied to the feet are useful. To
ensure success all these methods should be utilised simultaneously. In
cases of separation of the claw, antiseptic dressings, with a thick pad
of tow placed under the sole, become necessary.

Chronic laminitis may perhaps occur in the ox as in the horse, but, as a
rule, oxen are slaughtered before the disease can assume this form. In
dealing with fat, or even with fairly well-nourished, oxen it would
clearly be more economical to slaughter early, and so prevent wasting
and the resulting loss from disease.


                              SAND CRACK.

Sand crack—that is to say, the occurrence of vertical fissures in the
wall of the claw—is not absolutely rare in bovines. It is commonest in
working oxen drawing heavy loads, though in very exceptional cases it
affects animals which have never worked. (Moussu describes one case in a
young ox where four sand cracks existed simultaneously.) It may also
result from injuries to the coronet. In contrast to the case of the
horse, and owing to the different conditions under which the ox performs
its work, the disease is commoner in front than in hind feet. In
drawing, the ox’s front limbs play the principal part, and the animal
pivots, so to speak, on the claws of the front limbs.

The position of the crack may vary. It is commonest on the inner surface
of the claw, rare at the toe, and still rarer at the quarter. It is
often superficial and complete, extending throughout the entire height
of the claw, but not throughout its thickness; sometimes it is complete
and profound, the fissure then extending to the podophyllous tissue.

=The symptoms= are purely local in the case of superficial lesions. When
the injury is deep seated, or when it originates in a wound of the
coronet, lameness is present. Intense lameness, swelling of the coronet,
and blood-stained or purulent discharge point to grave injury and
probable complications.

=Diagnosis= is easy. The =prognosis= naturally varies with the symptoms.
It is favourable when the fissure is merely superficial, but becomes
grave when it is deep seated and the animal is exclusively used for
heavy draught.

=Treatment.= When the lesion is superficial and unaccompanied by
lameness, no surgical interference is necessary. Rest or very light work
is alone required. As soon as lameness appears, rest is obligatory. The
application of antiseptic poultices, containing 2½ to 3 per cent. of
carbolic acid, creolin, etc., usually alleviates pain in a short time,
and facilitates healing in the depth of the fissure.

In exceptional cases, where complications have occurred in consequence
of suppuration beneath the fissure, suppuration in the coronary region,
or necrosis of the podophyllous tissues, an operation becomes necessary,
and is of exactly similar character to that performed under like
circumstances in the horse.

Over a space of 1 to 1½ inches on either side of the fissure the horn is
thinned “to the blood,” and the subjacent dead tissue removed. The claw
is then thoroughly cleansed with some antiseptic solution, the wound
freely dusted with equal parts of iodoform, tannin and boric acid, and
covered with pads of tow or cotton wool, fixed in position by
appropriate bandages. After such operations a long rest is essential for
complete recovery, during which, however, the animal may be fattened.

The object of operation is to prevent complications, like chronic
suppuration and necrosis, which would endanger the animal’s life, rather
than to effect perfect restoration of usefulness for the work previously
done.


                      PRICKS AND STABS IN SHOEING.

The wall of the ox’s claw is so thin that shoeing is always somewhat
difficult, more especially as nails can only be inserted in the external
wall. Moreover, as very fine nails must be used, they are apt to bend,
penetrate the podophyllous tissue, and cause injuries of varying
importance. The ox is often very restless when being shod, and, even
though firmly fixed, usually contrives to move the foot every time the
nail is struck. The farrier, therefore, may easily overlook the injury
which he has just caused, and by proceeding and ignoring it may
transform a simple stab into a much more dangerous wound.

=Symptoms.= In most cases lameness appears immediately the animal leaves
the trevis, but, although this is more difficult to explain, lameness is
sometimes deferred until the day after, or even two days after, shoeing.
Though little marked at first, lameness may become so severe that the
animal cannot bear the pain caused by the foot touching the ground. When
this stage is reached general disturbance becomes marked, fever sets in,
rumination stops, and appetite is lost.

These symptoms point to the occurrence of suppuration. The pus, confined
within the horny covering of the foot, causes very acute suffering and
sometimes grave general disturbance; later it burrows in various
directions, separating the podophyllous tissue from the horn, and ends
by breaking through “between hair and hoof” in the region of the
coronet. In exceptional cases, complications such as necrosis of the
podophyllous tissue extending to the bone, and suppuration of its spongy
tissue, may be observed.

=Diagnosis.= When the farrier suspects he has pricked an animal the
immediate withdrawal of the nail will remove any doubt, because bleeding
usually follows. If the condition is only detected at a later stage, the
early lameness having been misinterpreted, examination of the claw and
tapping the clenches of the nails will cause the animal to show pain at
a given point, thus indicating the penetration of the nail. Removal of
the offending nail is painful, and is often followed by discharge of pus
or blood-stained fluid, which clearly points to the character of the
injury. In obscure cases the shoe should not be reapplied.

When the horn wall is separated from the sensitive structures, there is
marked general disturbance, and pus is discharging at the coronet, it is
practically impossible to err in diagnosis.

=Prognosis.= In cases of simple nail puncture the prognosis is hopeful,
provided that the condition is at once diagnosed. The longer it remains
unrecognised, particularly if complication like necrosis has occurred,
the graver becomes the outlook.

=Treatment.= In cases of simple puncture the nail should immediately be
withdrawn and the animal placed on a perfectly clean bed to prevent the
wound becoming soiled or infected. If lameness appear and become
aggravated, the shoe should be removed and antiseptic poultices applied.
In the majority of cases the lameness will then diminish, and in a few
days completely disappear.

In cases of discovery within the first few days the same treatment is
applicable, and is often sufficient. If, on the contrary, pus is
discharging at the coronet, if lameness is intense and the general
symptoms marked, it may be needful to operate.

The stages of operation comprise: thorough thinning of the horn in the
shape of an inverted =V= over the affected portion of the wall, removal
of the loose necrosed parts, disinfection of the wound, and the
application of a surgical dressing covering the entire claw.


                PICKED-UP NAILS, Etc. (“GATHERED NAIL.”)

Penetrating wounds of the plantar region are, as in the horse, usually
included under the heading of “Picked-up Nails.” They are only seen in
oxen or cows which are not shod. Pointed objects, like nails, harrow
teeth, sharp fragments of wood or glass, etc., may produce injuries of
the character of that now in question.

In considering the position of such wounds we may for convenience divide
the plantar region into two zones, one extending from the toe of the
claw to the point of insertion of the perforans tendon, the other
comprising the region between this insertion and the bulb of the heel.

=Symptoms.= Lameness occurs immediately, and varies with the intensity
of the existing pain. If the offending body has not remained fixed in
the wound, this lameness may in a few moments disappear, either for good
or merely for a time. The recurrence of lameness on the following day or
a couple of days later marks the commencement of inflammatory changes in
the deeper seated tissues. This lameness in many instances is
accompanied by a movement suggestive of stringhalt, the foot being kept
on the ground only for a very short time, or sometimes not being brought
into contact with the ground at all.

The depth to which the offending object has penetrated, and the
direction it has taken, may sometimes be discovered by a mere casual
examination of the sole. In other cases only the orifice by which it has
penetrated can be found. If the injury has existed for several days, the
discharge from the puncture will be thin and blackish, purulent, or
blood-stained, according to the case. Fever and general systemic
disturbance suggest an injury of a grave character.

=Diagnosis.= The diagnosis is easy, inasmuch as the lameness almost
directs examination to the foot.

=Prognosis= is rarely grave. The direction, the situation and mode of
insertion of the flexor tendon, which forms the plantar aponeurosis,
ensure this aponeurosis being rarely injured by objects penetrating from
without. The points of the offending bodies usually pass either forwards
to the phalanx or backwards in the direction of the plantar cushion.

=Treatment.= The first stage in treatment consists in removing the
foreign body and thoroughly thinning the neighbouring horn. An
antiseptic poultice consisting of linseed meal saturated with 3 per
cent. carbolic acid or creolin solution is then applied. Considerable
and progressive improvement usually takes place in a few hours. If
lameness persists, surgical interference becomes necessary; in the
anterior zone it is confined to removing any dead portions of the
velvety tissue and to extirpating the fragment of bone which has
undergone necrosis. In the posterior zone the sinus must be probed and
laid open, so that all the diseased parts can be treated as an open
wound.

If, as happens in exceptional cases, the plantar aponeurosis is found to
be severely injured, the complete operation for picked-up nail, as
practised in the horse, may be performed, or the claw may be amputated.
In the former operation the horn covering the sole is first thinned “to
the blood.”

The stages of operation are as follows:—

(1.) Ablation of the anterior portion of the plantar cushion. Transverse
vertical incision at a distance of 1¼ inches in front of the heel;
excision of the anterior flap.

(2.) Transverse incision and ablation of the plantar aponeurosis by the
same method.

(3.) Curettage of the point of implantation of the aponeurosis into the
bone.

(4.) Antiseptic dressing of the claw.

Finally, if the primary lesion, wherever it may have started, has become
complicated by arthritis of the inter-phalangeal joint, it will be
necessary to remove the claw, or, better still, to remove the two last
phalanges, the latter operation being easier than the former, and
providing flaps of more regular shape and better adapted for the
production of a satisfactory stump.


                INFLAMMATION OF THE INTERDIGITAL SPACE.

(CONDYLOMATA.)

Condylomata result from chronic inflammation of the skin covering the
interdigital ligament. Any injury to this region causing even
superficial damage may result in chronic inflammation of the skin and
hypertrophy of the papillæ, the first stage in the production of
condylomata.

Injuries produced by cords slipped into the interdigital space for the
purpose of lifting the feet when shoeing working oxen are also fruitful
causes.

Inflammation of the interdigital space is also a common complication of
aphthous eruptions around the claws and in the space between them.
Continual contact with litter, dung and urine favour infection of
superficial or deep wounds, and by causing exuberant granulation lead to
hypertrophy of the papillary layer of the skin. When the animal stands
on the foot the claws separate under the pressure of the body weight and
the condylomata are relieved of pressure. When, however, the limbs are
rested, the claws mutually approach, compress the abnormal vegetations,
flatten, excoriate, and irritate them, thus favouring their further
development.

[Illustration: $1]

The symptoms are easy to detect. The animals appear in perfect health,
but have difficulty in walking, and show pain. They walk as though on
sharp, rough ground, and lameness is sometimes severe. Locally, the
anterior surface of the claws and the interdigital space are markedly
congested and sensitive, or painful on pressure. The growths are of
varying size, isolated or confluent, bleeding, excoriated, or covered
with horn, and are visible between the claws when the animal stands on
the limb. In many cases they form a perfect cast of the vertical
interspace. When the superficial layers have undergone conversion into a
horn-like material, lameness diminishes or disappears.

=Diagnosis= presents no difficulty.

=Prognosis= is only grave in so far as the condition interferes with
animals working, but it may render working oxen entirely useless.

=Treatment= in the early stages is of a preventive character, and
consists in placing animals which have been accidentally injured or
attacked with foot-and-mouth disease on a perfectly clean bed.

Surgical treatment is the only reliable method in cases where
hypertrophy of the papillary layer is well marked, and is extremely
simple.

The animal should be fixed in the trevis, the foot to be operated on
separately secured, and the growths completely removed with sharp
scissors or with a bistoury and forceps. When bleeding has subsided the
wound is covered with a mixture of equal parts of iodoform, tannin, and
powdered boric acid, and an interdigital dressing is applied. The
dressing is removed after five to ten days, according to circumstances.
If the cicatrix shows signs of exuberant growth it is dusted with
powdered burnt alum, and the parts are treated as an open wound. When
the growths are covered with horn and no longer painful it is not
desirable to interfere with them.


                                CANKER.

Canker—_i.e._, chronic suppurative inflammation of the podophyllous or
velvety tissue—is accompanied by hypertrophy of the papillæ and
progressive separation of the horn of the sole. It is much rarer in the
ox than in the horse, although it occasionally occurs.

Prolonged retention in dirty stables, where the bedding is mixed with
manure and continually moistened with urine, is the principal cause of
the disease. Individual predisposition and the action of some specific
organism may also have some influence.

Canker in oxen, like the same disease in horses, is recognised by
softening and separation of the horn of the sole, and by progressive
extension of the process towards neighbouring parts. The usual course
consists in invasion of the podophyllous tissue, separation of the wall
and of the heels, and pathological hypertrophy of the horn-forming
tissues, producing condylomata.

The new growths do not attain the same dimensions as in the horse, but,
on the other hand, the disease very frequently takes a progressive
course, involving the whole of the claw. A trifling accidental injury
may be followed by infection of the subungual tissues, and thus become
the point of origin for canker.

Canker may attack only one claw; on the other hand, it may extend to
both claws of one foot, or to the claws of more than one foot in the
same animal.

=Diagnosis.= Diagnosis is easy. The separation of the horn, the presence
of a caseous, greyish-yellow and offensive discharge between the
separated parts and the horn-secreting tissues, the appearance of the
exposed living tissues, etc., leave no room for doubt.

=Prognosis.= The prognosis is grave; for, as in the horse, the disease
is obstinate.

=Treatment= consists in scrupulously removing all separated horn, so as
fully to expose the tissues attacked by the disease. The parts should
then be thoroughly disinfected with a liquid antiseptic, and a
protective pressure dressing applied.

As a rule, cauterisation with nitric acid, followed by applications of
tar or of mixtures of tannin and iodoform, iodoform and powdered burnt
alum, etc., effect healing, without such free use of the knife as has
been recommended in the horse during the last few years.


                                GREASE.

Grease in the ox seems only to have been described by Morot and Cadéac,
and even in these cases the descriptions appear rather to apply to
elephantiasis or fibrous thickening of the skin than to grease proper.
The descriptions are not sufficiently clear, and the symptoms described
differ too much from the classical type seen in the horse to convince us
without further confirmation of the occurrence of the disease.


                       PANARITIUM—FELON—WHITLOW.

Any injury in the interdigital space or flexure of the pastern may,
under unfavourable circumstances, be complicated by death of the skin,
necrosis of the interdigital ligament, of the fibro-fatty cushion in the
flexure of the pastern, and of the terminal portions of the tendons.

These lesions are sometimes regarded as panaritium. In reality, they
correspond exactly to what, in the horse, are known as “cracked heels”
and “quittor.” The primary injury becomes infected with organisms which
rapidly cause death of the skin or the formation of a deep-seated
abscess and necrosis of the invaded tissues.

=Causation.= Neglect of sanitary precautions and filthy stables
constitute favouring conditions, the feet being continually soiled and
irritated by the manure and urine. Animals reared on plains, and having
broad, flat, widely-separated claws, are more predisposed than animals
from mountainous regions, in which the interdigital ligament is stronger
and the separation of the claws less marked. Any injury, abrasion, or
cut may serve as a point of origin for such complications.

Panaritium may even occur as an enzootic with all the characters noted
in isolated cases. In Germany it has received the name of “contagious
foot disease.” These enzootic outbreaks of panaritium follow epizootics
of foot-and-mouth disease, with lesions about the claws. Through the
superficial aphthous lesions the parts become inoculated with bacteria,
and the severity of the resulting injury is in some measure an
indication of the virulence of the infecting organism.

=Symptoms.= The first important symptom consists in intense local pain,
rapidly followed by marked lameness. The affected region soon becomes
swollen; the coronary band appears congested; the skin of the
interdigital space projects both in front and behind; the claws are
separated, and all the lower portion of the limb appears congested and
œdematous. The engorgement usually extends as high as the fetlock, and
the parts are hard and extremely sensitive. The patient is feverish,
loses appetite, and commences to waste. After five to ten days sloughing
occurs at some point—if the ligament is affected, in the interdigital
space; if the tendons, or the fibro-fatty cushions, the slough appears
in the flexure of the pastern. The dead tissue may separate and fall
away, or remain in position macerated in pus. Separation is generally
slow, requiring from twelve to fifteen days, and, unless precautions are
taken, complications occur. If only the interdigital ligament or
fibro-fatty cushion be necrotic, recovery may be hoped for; but, on the
other hand, if the tendons, tendon sheaths, ligaments, or bones are
affected, complications like suppurating synovitis, suppurating ostitis,
arthritis, etc., supervene, with fatal results. Death may occur from
purulent infection, unless the animal is slaughtered early.

=The diagnosis= is easy. The intensity of the lameness, separation of
the claws, swelling of the pastern region, sensitiveness of the swollen
parts, and absence of lesions in the ungual region sufficiently indicate
the nature of the condition.

=The prognosis= is grave, for complications may result, in spite of
proper treatment.

=Treatment.= Treatment consists, first of all, in thoroughly cleansing
the affected limb and placing the animal on a very clean bed. The parts
are next subjected to antiseptic baths containing carbolic acid,
creolin, sulphate of zinc, or sulphate of copper. It is often more
convenient, and quite as efficacious, to apply antiseptic poultices to
the foot and pastern, and to allow them to remain for some days, being
moistened several times daily with one of the solutions indicated. The
effects are: rapid diminution of the pain, delimitation of the necrotic
tissues is hastened, and the abscess is more readily opened.

Many practitioners recommend early intervention in the form of deep
scarification in the interdigital space or pastern region. The local
bleeding, and the drainage which takes place through the wounds so made,
is said to hasten recovery or to prevent complications.

When the abscess has opened, and the dead tissue separated, the abscess
cavity or wound should be regularly washed out with a disinfecting
solution, to prevent complications, in case fragments of necrotic tissue
have been retained. If, however, complications have occurred, no
hesitation should be felt in freely incising the parts, and, if
necessary, in removing one or both phalanges. When both joints of one
foot are affected, and arthritis threatens to or has set in, there is no
object in treating the animal, and early slaughter is to be recommended.

In cases where the disease follows foot-and-mouth disease, and threatens
to become enzootic, it can generally be prevented spreading by keeping
the foot-and-mouth subjects on very clean beds, and frequently washing
the feet with antiseptic solutions. Disinfection of the sheds is also
very desirable.


                               FOOT ROT.

Foot rot is a disease of sheep, and, like canker, is confined to the
claws.

Thanks to the progress of hygiene, it tends to become rarer, but is
still seen in the enzootic form in some portions of England and
Scotland, in the mountains of Vivarais, the Cévennes, and the Pyrenees.

It affects large numbers of animals at once, animals belonging to one
flock or to neighbouring flocks in one locality, and when it invades a
sheep farm, all the animals may successively be attacked at intervals,
according to the local conditions.

=Symptoms.= The disease develops rather insidiously, and the patients
always retain an excellent appetite. It begins with lameness, which is
at first slight, later becomes accentuated, and in the last periods is
very intense. On examination, the coronet and lower part of the limb as
high as the fetlock are found to be swollen. Palpation reveals
exaggerated sensibility, and on direct examination, a fœtid discharge is
discovered in the interdigital space. This discharge, which is peculiar
to the onset of the disease, only continues for a week or two, and is
succeeded by a caseous exudate which is always offensive, which moistens
and macerates the horn, the skin, the tissues in the interdigital space,
and the region of the heels. From the 20th to the 30th day after onset
the claw separates above in the interdigital space. The separation
extends towards the heel, then to the toe, exposing ulceration of the
subjacent podophyllous tissue.

From this time the patients experience very severe pain, and, as in
other diseases of the feet, remain lying for long periods. Movement
becomes extremely painful, and the animals frequently walk on the knees.
The subungual lesions become aggravated, separation of the claw extends,
necrosis of the podophyllous tissue and of subjacent tissue becomes more
extensive, and the inter-phalangeal ligaments and the extensor or flexor
tendons become involved. Finally, the claws are lost, and synovitis and
arthritis are added to the complications already existing.

In an infected locality the development is always the same. The animals
lose flesh, become anæmic, and, unless vigorously treated, soon die. The
ordinary duration of the disease is from five to eight months, sometimes
more. If, however, patients are isolated and well treated they recover.

=Causation.= The specific cause of foot rot still remains to be
discovered, although everything points to the conclusion that it
consists in an organism capable of cultivation in manure, litter, etc.,
for foot rot is transmissible by cohabitation, by mediate contagion
through infected pasture, by direct contact and by inoculation.

The chief favouring influences are bad drainage, filthy condition of the
folds, and herding in marshy localities.

=Diagnosis.= The condition can scarcely be mistaken, for the sheep
suffers from no other disease resembling it, excepting, perhaps,
foot-and-mouth disease.

=Prognosis.= The prognosis is grave, for the disease usually assumes a
chronic course, affects entire flocks, and the patients require
individual attention.

=Treatment.= The primary essential to success in treatment consists in
separating and isolating the diseased animals in a scrupulously clean
place and providing a very dry bed.

In the early stages the disease may be checked by astringent and
antiseptic foot baths. It is then sufficient to construct a foot-bath at
the entrance to the fold, containing either milk of lime, 4 per cent.
sulphate of iron, copper sulphate, creolin, etc. Through this the sheep
are passed two or three times a week. These precautions rarely suffice
when the feet are already extensively diseased; and when the horn is
separated to any considerable extent, surgical treatment is
indispensable. All loose portions of horn should be removed and
antiseptic applications made to the parts.

When a large number of sheep are affected the treatment is very
prolonged, but it is absolutely indispensable, and the numerous
dressings required necessarily complicate the treatment. It would be
valuable to experiment with small leggings, which would retain the
dressings in position, and, at the same time, shelter the claws from the
action of the litter, while favouring the prolonged action of the
antiseptic.

When the lesions are not extensive, a daily dressing is sufficient.

Among the materials most strongly recommended are antiseptic and
astringent ointments containing carbolic acid, iodoform, or camphor.
Vaseline with 5 per cent. of iodine is very serviceable, and much to be
preferred to applications like copper sulphate, iron sulphate, etc. Its
greatest drawback is its expense.




                              CHAPTER III.
      DISEASES OF THE SYNOVIAL MEMBRANES AND OF THE ARTICULATIONS.


                I.—SYNOVIAL MEMBRANES AND ARTICULATIONS.


                               SYNOVITIS.

Inflammation of the synovial membranes, or synovitis, may affect the
synovial sacs either of the joints or of the tendon sheaths. It may be
acute or chronic and occur either idiopathically or follow the
infliction of an injury. Its two chief forms are simple, or “closed,”
synovitis and suppurative, or “open,” synovitis, the essential
distinction between which is that in the latter microorganisms are
present, whilst in simple synovitis they are absent. In all cases the
disease is characterised by distension of the sac affected.

Synovitis produced by a wound communicating with the outer air may be
complicated by suppuration, and if the synovial membrane of a joint be
involved the primary synovitis is almost always followed by traumatic
arthritis.

The commonest forms of chronic simple synovitis are:—


             INFLAMMATION OF THE PATELLAR SYNOVIAL CAPSULE.

Inflammation of the synovial membrane of the femoro-patellar joint is
most commonly seen in working oxen as a consequence of strains during
draught. It is also found in young animals which have injured the
synovial capsule through falls, slips, or over-extension of the limb.

=Symptoms.= Development is slow and progressive, and injury may not be
discovered until the lameness which follows has become fairly marked.
This lesion is characterised by swelling in the region of the stifle. On
palpation, fluctuation may readily be noted both on the outer and inner
surfaces of the joint. The exudate is sometimes so abundant and
distension so great that the straight ligaments, the neighbouring bony
prominences, and the ends of the tendons are buried in the liquid
swelling.

Lameness, which is at first marked, often diminishes with exercise. The
length of the step is lessened.

=Diagnosis.= The diagnosis presents no difficulty, but the lesions must
be distinguished from those due to tuberculosis in this region,
rheumatic arthritis, and the specific arthritis seen in milch cows.

=The prognosis= is grave, for the disease renders animals useless for
work.

=Treatment.= Rest, cold moist applications, and massage constitute the
best treatment in the early stages. Should swelling persist, one may
afterwards apply a smart blister or even tap the joint aseptically,
drawing off the fluid and then applying the actual cautery. Irritant
injections must be avoided.


         DISTENSION OF THE SYNOVIAL CAPSULE OF THE HOCK JOINT.

                        _Bog Spavin in the Ox._

Bog spavin is frequent in working oxen and in oxen from three to five
years old. It is due to strain in draught or to strain produced in
rearing up at the moment of covering. Old bulls, heavy of body, and
stiff in their limbs are predisposed to it.

=Symptoms.= The symptoms usually develop gradually and without lameness,
but sometimes declare themselves more rapidly with lameness, accompanied
by marked sensitiveness on palpation. At first the hock shows a
generalised doughy swelling, soon followed by dilatation of the
articular synovial sac. Somewhat later four different swellings
appear—two in front, separated by the tendons of the common extensor and
flexor metatarsi, and two at the back, extending inside and outside to
the flexure of the hock.

=Diagnosis.= The only precaution required in diagnosis is to avoid
confusion with articular rheumatism.

=Prognosis.= The prognosis is rather grave in the case of working oxen,
and even of bulls; often slaughter is preferable to treatment.

=Treatment= differs in no respect from that of distension of the stifle
joint. In young bulls aseptic puncture and drainage of the joint,
followed by the application of the actual cautery, probably give the
best results.


            DISTENSION OF TENDON SHEATHS IN THE HOCK REGION.

Like the preceding, this condition is rarely seen except in bulls and
working oxen. It is characterised by dilatation of the upper portion of
the tarsal sheath, one swelling appearing on the outer side, the other
on the inner.

The differential =diagnosis= is based on the position of these synovial
sacs, which are quite close to the insertion of the tendo-Achillis, and
on the absence of any swelling in front of the joint.

=Treatment= is identical with that indicated in the last condition.

Massage and cold water applications should be employed at first, to be
followed by aseptic puncture and withdrawal of fluid, supplemented if
necessary by firing in points.


         DISTENSION OF THE SYNOVIAL CAPSULE OF THE KNEE JOINT.

[Illustration: $1]

[Illustration: $1]

This is one of the rarest conditions now under consideration, because
the synovial membranes of the knee joint are everywhere strongly
supported by very powerful ligaments. The synovial capsules of the
carpo-metacarpal and inter-carpal joints are incapable of forming sacs
of any size. On the other hand, the radio-carpal may become moderately
prominent in front, especially towards the outside above the superior
carpal ligament. When weight is placed on the limb, the excess of
synovia is expelled from the joint cavity towards this little sac, which
then becomes greatly distended. If, on the other hand, the knee is bent,
the sac shrinks or disappears.

=Treatment.= Treatment is restricted to the application of a blister or
to firing in points.


        DISTENSION OF THE SYNOVIAL CAPSULE OF THE FETLOCK JOINT.

The synovial capsule of the fetlock joint in the ox is strongly
supported in front and at the sides, but may protrude under the anterior
ligament, producing a swelling behind the metacarpus under the five
branches of division of the suspensory ligament and slightly below the
sesamoid bones. These distensions, like bursal swellings, are commoner
in hind limbs and in old working oxen. Their development is always
followed in time by a certain degree of knuckling over. At first the
metacarpus and phalanges come to form a straight line, but later the
fetlock joint itself is thrust forward.

=The diagnosis= necessitates careful manual examination of the region of
the fetlock joint.

=The prognosis= is somewhat grave, for the disease sooner or later
necessitates the destruction of certain animals.

=Treatment= is practically identical with that used in all such
conditions: friction with camphorated alcohol, cold affusions and
massage in the earlier stages, followed if needful by blisters or firing
in points.


                     DISTENSION OF TENDON SHEATHS.

Distension of the synovial capsule which surrounds the superior
suspensory ligament, like distension of the articular capsule of the
fetlock, occurs in working animals, and most commonly affects the front
limbs. It is indicated by two swellings, one situated on either side of
and behind the branches of division of the suspensory ligament and in
front of the flexor tendons. These two swellings extend higher than the
articular swellings, which, however, they sometimes accompany. The
surface of the fetlock is then swollen, doughy on pressure, and somewhat
painful.

These enlargements may produce more or less marked lameness and cause
knuckling.

=The diagnosis= is clear from local examination.

=The prognosis= is unfavourable, as the animals after a time become
useless for work.

=Treatment.= The beginning of the disease may often be cured by baths of
running water, combined with massage. At a later stage, local
stimulants, blisters, or firing are necessary. The best treatment
probably consists in puncturing the parts with antiseptic precautions,
washing out the synovial cavity with an antiseptic, and immediately
afterwards lightly firing the surface of the region in points.


        DISTENSION OF TENDON SHEATHS IN THE REGION OF THE KNEE.

Any of the numerous tendon sheaths which facilitate the gliding of
tendons in the neighbourhood of the knee may become inflamed and give
rise to a chronic synovial swelling. The commonest of such swellings is
due to distension of the sheath of the extensor metacarpi magnus, which
appears as a vertical line in front of the knee, extending from the
lower third of the forearm and slightly to the outer side of the central
line. This synovial enlargement arises in oxen working on broken roads,
in clay or marshy soils, where the animals are liable to stick fast, and
are often obliged to struggle vigorously in order to extricate
themselves.

=The diagnosis= is based on the position and direction of the dilated
synovial sheath.

=Treatment= is identical with that of other cases of chronic synovitis.


         DISTENSION OF THE BURSAL SHEATH OF THE FLEXOR TENDONS.

This condition is rare. It is announced, as in the horse, by a
dilatation of semi-conical form, the apex of which is situated opposite
the lower margin of the carpal sheath, the base extending as high as the
infero-posterior third of the radius.

The dilatation is more marked on the inner than on the outer side of the
limb.

Distension of the synovial sheath of the common extensor of the digits
in the fore limb and of the extensor of the external digit is still
rarer than the preceding conditions.


                 TRAUMATIC SYNOVITIS—“OPEN SYNOVITIS.”

When an injury in the neighbourhood of a joint penetrates deeply, it may
implicate either the synovial sheath of a tendon or the synovial
membrane of a joint. If the body inflicting the wound is aseptic, a
condition which in accidental wounds is rare, the wound may have no
grave consequences. Usually, however, the body producing the injury is
infected, and the infection rapidly extends throughout the tendon sheath
or synovial sac. In the first case, traumatic suppurating synovitis of a
tendon sheath is the result; in the second, a suppurating articular
synovitis arises, which soon becomes complicated with injury of the
articular cartilages, ligaments, etc. (traumatic arthritis).

The primary lesion may only affect the periarticular region, not
directly extending to the synovial membranes, and only after an interval
of some days may symptoms of suppurating synovitis or suppurating
arthritis appear, in consequence of progressive invasion of the parts by
specially virulent microbes.


                     TRAUMATIC TENDINOUS SYNOVITIS.

Suppurative inflammation of the synovial bursæ of tendons in consequence
of wounds most commonly affects the sesamoid sheaths of the front or
hind limbs; more rarely, the tendon sheaths of the hock or knee; and,
exceptionally, the small synovial sheaths of the extensors of the
metacarpus and phalanges, etc.

Such inflammation follows injuries with forks, harrow teeth, or any
sharp foreign body. It is characterised by the existence of a fistula or
wound, indicating the course taken by the body inflicting the injury,
from which at first normal synovia escapes. Later, however, the
discharge becomes turbid, and after the second day gives place to a
clotted, serous, or purulent fluid.

A diffuse, œdematous, warm, painful swelling very rapidly develops
around the injury. The animal is more or less feverish and lame. The
swelling soon extends throughout the entire length of the infected
synovial sheath. The patient loses appetite, and unless treatment is
promptly undertaken, complications supervene which often necessitate
slaughter. The prognosis is always grave.

=Treatment.= Continuous irrigation has long been recommended. It is
worthy of trial, but in the majority of cases occurring in current
practice it cannot be carried out.

Moussu prefers a form of treatment which he claims has always succeeded
in horses and oxen—viz., irrigation of the parts, followed by injection
of sublimate glycerine solution.

He first washes out the infected synovial cavity with boiled water
cooled to 100° Fahr. A counter-opening may become necessary, and the
washing should be continued until the escaping water appears perfectly
clear. Immediately after each such irrigation he injects from 7 to 14
drams of glycerine containing 1 part in 1,000 of corrosive sublimate. He
repeats this treatment daily.

By reason of its affinity for water and for the liquids in the tissues
or suppurating cavities into which it is injected, the glycerine
penetrates in all directions, reaching the finest ramifications of the
synovial sacs, a fact which explains its superiority over aqueous
antiseptic solutions.

Suppuration is rapidly checked and repair becomes regular. The pain and
lameness progressively diminish, and recovery may be complete.

It is advisable to assist this internal antiseptic treatment by external
stimulants and by the use of a blister. Solutions of greater strength
than 1 part of sublimate to 500 of glycerine are only required during
the first few days of treatment and until suppuration diminishes. Later,
they prove irritant, and interfere with healing.


  TRAUMATIC ARTICULAR SYNOVITIS—TRAUMATIC ARTHRITIS—“OPEN ARTHRITIS.”

[Illustration: $1]

It has been described above how primary inflammation of the articular
synovial membrane produced by a wound may rapidly develop into
suppurating arthritis.

=Symptoms.= The pain is very marked at the moment when the accident
occurs, but this pain, due to the mechanical injury inflicted,
diminishes or completely disappears after some hours. Soon, however,
synovial discharge sets in, announcing the onset of traumatic synovitis.
At first limpid, it soon becomes turbid, then curdled, and finally
grumous, purulent and greyish in colour.

Pain then returns, rapidly becomes intense, continuous and lancinating.
It produces lameness, sometimes so severe that no weight whatever can be
borne on the limb. A diffuse, œdematous, warm and extremely sensitive
swelling then rapidly develops around the whole of the injured joint.
General disturbance, with fever and loss of appetite, appears,
indicating a very alarming condition.

It is sometimes a little difficult to differentiate between this
condition and that due to injury of a tendon sheath, but as a rule
diagnosis is easy.

=Prognosis= is very grave. Life is threatened, and wasting occurs very
rapidly. Infection of the synovial membrane is soon followed by necrosis
and erosion of the articular cartilages, as well as by softening and
inflammatory change in the ligaments, etc.

[Illustration: $1]

=Treatment.= Should the patient be in reasonably good condition, but
otherwise of no particular value, it should at once be slaughtered. If,
on the other hand, it possess a special value, and the owner wish to
preserve its life, the same antiseptic treatment should be adopted as
was indicated in dealing with suppurating synovitis of tendon sheaths.
The loss of the articular cartilage of the joint is followed by free
granulation and union of the apposed surfaces of bone resulting in
anchylosis of the joint and qualified recovery. Such results, however,
are only likely to follow in relatively light animals which are capable
of standing for considerable periods.


                         II.—STRAINS OF JOINTS.

When, in consequence of muscular contraction or external violence, the
bony surfaces constituting a joint are displaced so as to stretch,
lacerate, or partially tear the ligaments, synovial capsule or tendons
supporting the joint, so-called sprain, or strain, or wrench results.
The articular surfaces are not sufficiently displaced to cause luxation,
but a series of periarticular injuries result, and are followed by the
symptoms which we recognise as those of strain. Joints in which movement
is restricted within narrow limits, such as the hock or fetlock, are
most liable to such injuries, which also occur in very freely movable
articulations like the shoulder and stifle.


                        STRAIN OF THE SHOULDER.

This accident is produced by the animal falling on its side, by slipping
at the moment of landing, the limb being extended and in contact with
the ground, by the foot slipping at the moment when it is leaving the
ground and the limb is at its extreme limit of backward extension, by
side slips, etc. The periarticular lesions will then be found on the
front, back, or internal surface of the articulation, depending on the
manner in which the accident has occurred. According to some authors,
violent muscular efforts, as well as work in soft clay soil, bogs and
rice swamps, are also capable of causing strain of the shoulder.

=Symptoms.= At first moving appears difficult, the patient lies down a
great deal, then lameness becomes characteristic. Movement of the
scapulo-humeral joint being painful, the patient endeavours as far as
possible to avoid it; the limb is advanced stiffly in an abducted
position and with a mowing movement. This semi-circular movement avoids
the necessity of flexing the scapulo-humeral angle, but diminishes the
length of the stride.

Locally, the region of the scapulo-humeral angle is swollen, doughy, and
extremely sensitive on manual examination. If the practitioner
endeavours to flex it by lifting the limb the animal flinches.

=Diagnosis.= The diagnosis is not very difficult, although the peculiar
mowing movement is also seen in other cases, such as cracked heels and
mallenders.

=Prognosis.= The prognosis is favourable, for, provided there has been
only a moderate strain of the tendons or isolated injury to the muscles,
recovery is almost certain.

=Treatment.= Treatment consists in resting the animal and in assisting
repair.

The parts can be immobilised by the application of a vesicant or mild
blister. A week or ten days later dry friction, muscular and
periarticular massage are indicated, and gentle exercise should be
commenced. The same treatment may be employed in strain of the elbow
joint and in strains of muscles or tendons in the neighbourhood of
joints. Such lesions are, however, very rare in the ox.


                          STRAIN OF THE KNEE.

Strain of the knee is commoner in the ox than in the horse, because of
the special conformation of the knee in the ox and the mode of working
under a yoke. This mode of working gives less individual liberty to the
fore quarters, and sometimes interferes with the animal’s efforts when
moving a load. Strains of ligaments and periarticular injuries occur as
a general rule on the inner side of the limb.

=The symptoms= consist in lameness, exaggerated sensibility on pressure,
pain on forced flexion of the knee, and swelling of the entire
periarticular region.

=The prognosis= is somewhat serious in working oxen.

=Treatment=, when applicable, should consist of stimulant dressings,
massage, and douches.


                         STRAIN OF THE FETLOCK.

This is one of the commonest accidents of draught oxen.

=Causation.= Working on rough, irregular, rocky ground, or on roads with
deep ruts, is the commonest cause of this condition. When the animal
moves on irregular surfaces the two claws do not bear an equal share of
weight; sometimes the whole weight is for a moment thrown on one claw.

The phalanges, therefore, are displaced inwards or outwards, or are
twisted around their vertical axis, causing the fetlock joint and its
supporting ligaments to be more or less severely strained. The internal
or external ligaments of the joint or the suspensory ligament or flexor
tendons may even be lacerated.

The fetlock may also be strained by the animal making violent efforts to
free the claws or pastern which have become fixed in a hole in the
ground, in bogging, in hobbling, or in leaping a fence.

=Symptoms.= Lameness is noticeable from the beginning, but is
unaccompanied by any visible lesion. On examination of the limb, the
entire region from the fetlock downwards is found to be sensitive to
pressure, and painful when forcibly extended or flexed from side to
side. This sensitiveness is particularly marked when the phalanges are
rotated on the shank. A few days later the entire fetlock becomes the
seat of diffused swelling.

=Diagnosis= is facilitated by the fact that the fetlock has an entirely
different appearance from that seen when tendon sheaths or the synovial
capsules of joints are distended.

=Prognosis.= The prognosis varies considerably, according to the extent
to which deep-seated structures are involved, and the gravity of the
lesions is usually proportioned to the intensity of the symptoms.

=Treatment.= Frequent cold applications, cold foot baths for an hour or
two night and morning, and even cold poultices are useful. When the pain
has somewhat diminished, which usually occurs in from three to four
days, vesicants may be employed, and, at a later stage, massage. Failing
improvement by these methods, the injured region may be fired in points.

Strain of the hind fetlock occurs under precisely similar conditions to
those above described in the case of front limbs.


                      STRAIN OF THE STIFLE JOINT.

Strain of the stifle joint results from over-extension of ligaments
without displacement of the patella, and also (and probably more
frequently) from injuries to the aponeurosis and tendons of insertion of
the abductor muscles of the femur and tibia.

=Causation.= Strain of the stifle may follow violent collisions, such as
occur in entering or leaving the stable, from falls on rough ground,
from direct blows, from slips, etc., or even from the sudden and violent
contraction of the muscles of the antero-external surface of the
quarter.

=Symptoms.= Lameness follows immediately or soon after the accident, and
is of a peculiar character; to avoid using the injured joint, the animal
advances the hind limb with a mowing movement.

The injured region exhibits diffuse inflammatory swelling, which impedes
palpation, and makes it difficult to determine the exact nature of the
local lesion. The thigh at the stifle is painful.

=Diagnosis and prognosis.= Diagnosis presents no considerable
difficulty. The prognosis must be based on the intensity of the
symptoms, and becomes grave if the tendons or aponeurotic insertions be
injured, or extensive damage have been done to ligaments.

=Treatment.= At first, continued cold applications, douches, and massage
are most useful; blisters are more effective in the grave cases, and
comprise not only the ordinary blisters, but the powerful mixed blister
containing tartar emetic, powdered hellebore, bichromate of potash, etc.
If for any special reason it is of importance to preserve the animal’s
life, the parts may be fired; but for economic reasons it is usually
better to fatten it for the butcher.


                       STRAIN OF THE HOCK JOINT.

=Causation.= Strain of the hock joint is commonest in young oxen which
are being trained to work. Their hind quarters are necessarily more or
less free, and the animals are apt to make side movements to avoid the
goad, thus exposing the hock to irregular strain.

The internal ligaments are more frequently strained than the external, a
fact due to the conformation of the hocks.

=Symptoms.= Strain is accompanied by lameness, most marked when the
animals endeavour to turn, by exaggerated sensibility of the entire hock
region, and, in grave cases, by subcutaneous œdema.

=Diagnosis and prognosis.= Diagnosis is simple. The prognosis is
sometimes grave, because a spavin or a permanent chronic enlargement of
the capsule of the true hock joint may form.

=Treatment.= It is often desirable at once to apply an extensive blister
over the whole hock and to supplement this at a later stage by cold
applications, or by continuous cold irrigation for half an hour or more
both night and morning.

In exceptional cases the use of the actual cautery becomes necessary.


                        III.—LUXATION OF JOINTS.

Luxation consists of permanent displacement of the bony surfaces forming
a joint, and may follow violent mechanical injury or any other cause.

Luxations have been divided into congenital, _i.e._, such as exist from
the time of birth; spontaneous, _i.e._, those which result from some
defect of conformation or constitution; and acquired or accidental,
which occur as results of falls, wounds, accidents, etc.

From the point of view of their duration, luxations are termed temporary
when they do not necessitate reduction, progressive when the tendency is
towards greater and greater displacement of the surfaces, or permanent
when reduction is impossible.

Those commonest in bovines are luxations of the femur, luxation of the
patella, femoro-tibial luxation, and luxation of the scapulo-humeral
joint.


                         LUXATION OF THE FEMUR.

Luxation of the head of the femur with displacement beyond the cotyloid
cavity is very frequently congenital. The condition also occurs with
some frequency in adults or aged animals in consequence of relaxation of
the articular ligaments and the absence of the subpubic ligament
(pubio-femoral ligament).

=Causation.= Luxation may be congenital, the head of the femur being
displaced backwards and carried above the cotyloid cavity. This form is
of no practical interest, because the animals are not usually reared.
More frequently in young or adult animals it assumes the spontaneous
progressive form, in consequence of degenerative changes in and
relaxation of the coxo-femoral interosseous ligament. The head of the
femur presses on the upper margin of the cotyloid cavity, which it
injures, and eventually becomes lodged in the neighbourhood of the neck
of the ilium, in the great sciatic notch.

This luxation is also found as a purely accidental occurrence in animals
which have suffered from falls and from slipping of the hind limbs
backwards or sidewards, as occasionally follows awkward leaping
movements. The slipping outwards of the limbs, which causes this form of
luxation, is comparatively easy, because of the absence of the
pubio-femoral ligament. The accident may also be followed merely by
subluxation, that is to say, tearing of the inner portion of the
capsular ligament and rupture of some portion of the adductor muscles of
the thigh without rupture of the interosseous fibres, the head of the
femur not quitting the cotyloid cavity. This accident occurs in stables
with smooth, slippery floors, and in railway trucks. It may affect one
side or both. The latter condition is exceptional.

Finally, luxation may be either complete (in which case the capsular and
interosseous ligaments are both ruptured) or incomplete. In the former
case, the head of the femur becomes displaced upwards and forwards
towards the great sciatic notch, more rarely backwards in the direction
of the ischium, and in exceptional cases downwards and inwards below the
pubis into the foramen ovale.

=Symptoms.= The symptoms vary, depending on whether the luxation is of
the spontaneous, progressive order or, on the contrary, is accidental.
In progressive luxation, the animals are able to rise and walk with
difficulty. The affected limb swings when the animal is advancing, not
as though it were paralysed, but simply as though displaced at its upper
part. Pain is exhibited when weight is placed on the limb, and there is
difficulty in movement. The limb appears shorter than its neighbour when
the animal stands on it, and the prominence representing the trochanter
is more marked. When a false joint has formed, the limb is rigid, is
moved stiffly and abducted, and the stride is shortened.

[Illustration: $1]

In accidental luxations, either of one or both limbs, the attitude
assumed by the animal is often characteristic. One of the limbs is
extended at right angles to the longitudinal axis of the body, and
sometimes both limbs assume this position, an attitude which would be
absolutely impossible under normal conditions. The animal cannot rise.
It lifts the front part of the body by rising on its knees, but the hind
quarters do not follow. The ruptured adductor muscles are unable to
bring and hold the limb parallel to the longitudinal axis of the body;
the abductors act unopposed, and at the moment when the animal makes its
greatest effort to rise the limb (or limbs) is carried outwards and the
body comes to the ground on the udder or groin.

Inspection discovers a depression where the great trochanter should be.
On applying the open hand over the hip joint, whilst an assistant who
grasps the pastern moves the limb in different directions, one can feel
and hear, in spite of the mass of muscle covering the part, a modified
crepitation due to sero-sanguinolent effusion in and around the joint.
This crepitation can also be detected by pushing the hand as high up as
possible on the internal surface of the thigh, and thus exploring the
neighbourhood of the luxation.

=Diagnosis.= The position which the animal assumes when one endeavours
to make it rise is characteristic. Diagnosis of progressive luxation,
however, is more difficult.

=Prognosis.= The prognosis is extremely grave; for, even though
reduction can be effected, one is practically unable to ensure that the
parts shall remain in position.

=Treatment.= Treatment comprises reduction of the luxation and fixation
of the parts. Reduction can be effected without very much difficulty by
casting the animal on the affected side, placing a block of wood, or a
pail, between the thighs, and manœuvring the limb in the desired
direction. As, however, subluxation is the condition most commonly seen,
there is frequently no reduction to effect. Moreover, fixation of the
joint after reduction is almost impossible in such heavy subjects, and
luxation is very liable to recur. From an economic standpoint, slaughter
is advisable or imperative.


                        LUXATION OF THE PATELLA.

Luxation of the patella is not uncommon in working oxen, and is
occasionally seen in cows as the result of a slip when entering or
leaving the byre, the reason being the peculiar anatomical arrangement
of the femoro-patellar articulation.

The internal lip of the trochlea of the femur is very high, the
external, on the other hand, being only slightly developed. The patella
itself is smaller than that of the horse, and possesses a small
cartilaginous prolongation, principally on its inner face, in marked
contrast with the large cartilage found in the horse. As in the latter
animal, the outward displacement of the patella is only prevented by the
internal patellar ligament and the femoro-patellar aponeurosis. Under
the influence of varying causes to which the joint is exposed, these
supporting structures often prove insufficient to prevent the patella
being displaced outwardly.

=Causation.= From an anatomical standpoint, luxation inwards seems
impossible. It certainly must be very rare and be preceded by rupture of
the external ligament. On the other hand, as in the horse, it seems
possible that the patella may be caught on the summit of the internal
lip of the trochlea, especially if the trochlea happens to present a
flattening at that point.

Outward luxation may be spontaneous or accidental. It is termed
spontaneous, when produced by relaxation of the ligaments of attachment
or by irregular muscular action; accidental, when resulting directly
from any external mechanical cause. Violent contraction of the triceps
cruralis, by lifting the patella beyond its normal limit of travel,
helps, or at least permits, the patella to be displaced outwardly at the
moment when the muscle relaxes.

Pathological relaxation of the ligaments and muscles, by allowing the
patella to descend too far on the trochlea, also renders displacement
possible, hence spontaneous luxation sometimes occurs even while the
animal is at rest in the stable. This luxation is certainly only of a
temporary character, or perhaps only of the nature of subluxation, and
is often reduced by mere muscular contraction when the animals are
forced to move.

Should the hind limb slip in a backward direction the angle of the joint
becomes more obtuse and the lips of the trochlea are turned downwards,
thus greatly favouring lateral displacement of the patella, which under
these circumstances is no longer immobilised on the trochlear pulley;
displacement outwards then occurs, constituting the condition termed
luxation.

Various forms of mechanical violence, like blows, collisions of the
stifle with the jambs of doors, falls, etc., may also bring about this
luxation.

=The symptoms= of fully-developed accidental luxation are
characteristic. Immediately the accident occurs, the limb is immobilised
in a state of complete extension; neither the stifle nor the hock joint
can be flexed, and only the fetlock joint retains any degree of
mobility.

Movement is very difficult. The hind limb appears rigid, as though
formed of one bone. The pastern is directed backwards and dragged along
the ground, and when weight is placed on the limb the anterior surface
of the pastern may almost be in touch with the ground. The limb is
advanced, but the foot cannot be placed properly on the ground.

Locally the patella is found to be outside the external lip of the
trochlea, and its internal ligaments are extremely tense.

If the luxation is spontaneous and of muscular origin, or a consequence
of relaxation of the tendons, it is usually noticeable immediately the
animal leaves the stall. The animal cannot move without great
difficulty. It grows steadily worse with the lapse of time, because the
synovial membrane becomes irritated and chronic arthritis is set up.

The symptoms are identical with those of traumatic luxation, but are
only temporary.

=Diagnosis.= The position of the limb and the displacement of the
patella are sufficiently distinctive to render diagnosis fairly easy,
and to allow of this accident being differentiated from luxation of the
femoro-tibial joint or hooking of the patella in the ischio-tibial
muscle.

=Prognosis.= The prognosis varies greatly. If the luxation is of
traumatic origin and the accompanying symptoms are not grave, reduction
may be followed by permanent recovery. On the other hand, in spontaneous
luxation recurrence is almost inevitable.

=Treatment=. The indications for treatment may be comprised in a single
phrase: reduction, with immobilisation of the parts for a sufficient
time. To effect reduction, a strip of webbing is fixed around the
pastern of the affected limb, passed over the withers, in front of the
shoulder of the opposite side, and brought round in front of the neck or
between the front limbs. By means of this an assistant exercises strong
traction on the limb until the fetlock is raised as high as the elbow of
the same side. The operator then applies strong inward pressure to the
patella, which usually slips back on to the gliding surface of the
trochlea at the first or second effort.

[Illustration: $1]

After-treatment comprises the application of a smart blister, producing
œdematous infiltration of all the tissues around the joint, and thus
impeding movement and recurrence of luxation. For this purpose various
preparations are used—_e.g._, cantharides, biniodide of mercury, croton
oil, etc. It is also advisable to fix the animal so that for a time it
cannot lie down, and to secure the pastern to the neck by means of a
side-line.

As an experiment, cases of simple fixation of the patella on the summit
of the internal lip of the trochlea might be treated by Bassi’s
method—_i.e._, subcutaneous division of the internal lateral ligament of
the patella which holds the bone in its abnormal position.

Finally, in spontaneous luxation, occurring in young animals in which
blisters have been ineffectually tried after reduction, Bénard’s bandage
may be used, though it is not generally regarded as very practical. It
consists of a piece of cloth of elongated lozenge form about four feet
in length, six inches in breadth at its centre and two inches at its
ends. Its centre is pierced by a transverse opening intended to surround
the patella, and carries a loop for the purpose of supporting the turns
of bandage. A second longitudinal opening is situated about eight inches
from the centre.

Reduction being effected, the whole region of the stifle joint is
covered with Burgundy or ordinary pitch and the bandage then applied.
The patella projects through the central opening. The end A is passed
backwards around the thigh, and through the aperture B; the two cross
ends are then brought forward, crossed again at the end, the loop over
the patella carried a second time backwards, again crossed, and finally
fixed in front under the patella. The bandage should be firmly applied,
without, however, being so tight as to interfere with circulation, and
must be left in place from eight to ten days.

[Illustration: $1]

Van Denmoegdenberg recommends placing the patient on an inclined plane,
with the hind quarters a foot higher than the front, so as to cause
permanent contraction of the anterior muscles of the quarter, and thus
immobilise the patella. Simple cold baths, frequently repeated, friction
with camphorated alcohol or essence of turpentine, complete this
original but somewhat questionable treatment, and are said to result in
recovery in a fortnight.


              LUXATION OF THE FEMORO-TIBIAL ARTICULATION.

This form of luxation is rare, a fact explained by the strength of the
lateral ligaments of the joint, and of the cruciform interosseus
ligaments. It may assume different forms, according as the head of the
tibia is displaced in front of, behind, to the inside, or to the outside
of the lower extremity of the femur. In all, therefore, it may appear in
four different forms. The commonest is backward luxation.

=Causation.= With the sole exception of luxations or subluxations due to
tuberculosis (lateral luxations, either inwardly or outwardly, occurring
during tubercular arthritis, with more or less marked destruction of the
condyles), these luxations are always accidental or the result of
mechanical violence.

They result from leaping into hollows, falling into deep ditches or
ravines, or galloping through broken or steep places. Any violent shock
affecting the femur, either in front or from the outside, is capable of
causing luxation backwards or inwards.

[Illustration: $1]

=Symptoms.= The most frequent condition is backward luxation of the
upper extremity of the tibia. Movement becomes difficult, the limb is
held rigidly, and all the lower part of the leg is extended. None of the
joints can be flexed. The leg is dragged forward, without the animal
being able to place the foot flat on the ground, and the claws are
trailed over the litter or the toe grazes the soil.

On local examination the stifle is seen to be deformed. The lower
extremity of the femur and the patella appear prominent. The upper part
of the tibia is thrust backwards, and seems to have disappeared, leaving
a depression below the femoro-patellar region. The muscles forming the
back of the thigh at this level are thrust out of position, and appear
to project abnormally.

Viewed from behind, the inner line of the thigh appears more or less
convex when the upper extremity of the tibia is luxated inwardly. On
local examination the displacement of the bones can be readily detected.
In luxation forwards the prominence of the stifle is caused by the
summit of the tibial crest and by the patella, whilst the lower
extremity of the femur cannot be felt. In outward luxation the upper
extremity of the tibia forms an abnormal prominence, above which a
horizontal digital depression appears.

=Diagnosis.= Provided that the examination is made soon after the
occurrence of the accident, little difficulty will be found in coming to
a conclusion, but the diagnosis necessitates more care when examination
is deferred for two or three days, because extensive effusion then
exists. Luxations or subluxations of tuberculous origin are generally
consecutive to old-standing destructive tuberculous arthritis.

=The prognosis= is grave—firstly, because reduction is difficult; and,
secondly, because it is often impossible to maintain the reduction and
to preserve complete immobilisation of the injured joint.

=Treatment= should not be undertaken except in young animals which have
not yet attained full development.

In attempting to reduce outward or inward luxation of the tibia the
animal should be cast on the side opposite to the lesion.
Counterextension is practised by passing a length of webbing around the
limb in the region of the groin; extension in the direction of the
length of the femur by means of a loop of webbing fixed to the cannon
bone: the operator uses both hands in endeavouring to replace the head
of the tibia.

In forward luxation of the tibia counter-extension is effected by means
of a loop of webbing passed above the hock and drawn forward. Extension
is made backwards in an oblique direction, the operator again being left
free to effect reduction with both hands.

Reduction of backward luxation of the tibia is still more difficult, in
consequence of the contraction of the mass of muscle at the back of the
thigh.

Plaster bandages are the most convenient means of immobilising the parts
after reduction.


                 LUXATION OF THE SCAPULO-HUMERAL JOINT.

This luxation, like that of the femoro-tibial articulation, is
exceptional. It may assume one of two forms, depending on whether the
head of the humerus is displaced inwardly, or towards the back of the
glenoid cavity; but as a rule luxation occurs inwardly. Forward luxation
of the head of the humerus is almost impossible, in consequence of the
resistance offered by the tendons of the flexor brachii and antea
spinatus muscles. Similarly, luxation outwards is very difficult, the
tendon of the postea spinatus being very powerful and offering enormous
resistance.

Inwardly, on the other hand, the insertion of the subscapularis is much
less powerful, and there is no real opposition to movement of the head
of the humerus.

=Causation.= Violent mechanical shocks transverse to the upper third of
the arm may, by sheer force, displace the head of the humerus in an
inward direction, causing rupture of the internal wall of the capsular
ligament and of the subscapularis muscle. Jumping from high to low
ground and falling on the front limbs tend to displace the glenoid
cavity in front of the head of the humerus, and often result in luxation
of the bone in a backward direction, a luxation, however, which almost
always assumes a postero-internal direction. The commonest causes of
these luxations are the sideward falls of animals which have attempted
to cover others. Whether the subject be a bull or a cow, if the
stationary animal suddenly moves to one side, or if the moving animal is
frightened by the appearance of a dog, one of the front limbs may be
violently dragged away from the body; the resistance of the capsular
ligament and internal muscles of the shoulder may be overcome and
luxation produced.

=Symptoms.= Symptoms are immediately apparent: no weight can be placed
on the injured limb, and the animal moves on three legs. All muscular
action is avoided, the limb is slightly shortened as a consequence of
the head of the humerus slipping behind the shoulder, which is held
rigidly during movement; the points of the claws are dragged along the
ground.

On local examination the point of the shoulder appears to be deformed
and outwardly displaced, in consequence of the pressure exercised by the
displaced head of the humerus. Below the glenoid cavity and coracoid
process lies a depression, at the base of which the displaced humerus
can be felt. This depression, however, is soon filled up by the
sero-sanguinolent effusion consequent on luxation.

=Diagnosis.= Bearing in mind the conditions to which the accident is
due, the diagnosis presents no great difficulty.

=Prognosis.= The prognosis is grave, for although it is relatively easy
to reduce the displacement, it is very difficult to keep the joint fixed
in position.

=Treatment.= To effect reduction, the animal should be cast on the sound
side, and a loop of webbing passed under the arm, in order to provide
for counter-extension. The limb is extended by direct traction on the
cannon bone or fetlock, whilst the operator endeavours to effect
reduction with one hand placed in front and one behind the joint.

In young animals of trifling weight immobilisation may be attempted, the
best method being the application of pitch plasters. If, on the other
hand, the subject is heavy, there is so great a chance of displacement
when lying down and rising, that such cases are usually sent to the
butcher, or abandoned to chance. Relative recovery, sufficient to permit
of growth or fattening, may take place without professional assistance.


                             IV.—HYGROMAS.

Hygromas result from chronic inflammation of serous bursæ, naturally
existing, or of serous bursæ which form at prominent points where the
skin is exposed to repeated friction, blows, shocks, or over-extension.

They usually develop slowly, without producing marked pain or alarming
symptoms, and therefore the practitioner is seldom consulted until the
swelling has attained a considerable size.

The hygroma is usually characterised by its non-painful character and by
regular fluctuation throughout. The walls of the serous bursæ are merely
thickened, so that palpation is easy.

Should the hygroma become infected and inflamed, it assumes the same
characters as an abscess: it becomes highly sensitive, is surrounded by
œdematous infiltration, shows more marked fluctuation at some
specialised point, and eventually breaks, discharging pus.

Long-standing hygromas often have thickened fibro-cartilaginous and
extremely hard walls, which render examination more difficult.

[Illustration: $1]

Where the hygroma is much exposed to friction the skin covering it
undergoes complete transformation, the layers of epidermis becoming
converted into a substance resembling horn. The entire substance of the
wall of the hygroma then undergoes change, and is often infiltrated with
lime salts or encrusted with plates of bone of varying thickness.


                          HYGROMA OF THE KNEE.

This condition is very common in bovines, a fact explained by the manner
in which these animals rise. Whilst the hind limbs are being lifted, the
entire burden of the body weight is transmitted to the knees and the
tissues covering them; so that, if the ground is rough, the skin may be
sufficiently displaced to produce laceration of the subcutaneous
connective tissue, serous effusion in the layers of connective tissue,
and the immediate production of an hygroma beneath the skin and in front
of the synovial sheaths of the extensor tendons.

Hygroma is principally caused by falls on the knees, roughness of the
stable floor, prolonged decubitus during the course of a serious
disease, or after an attack of foot-and-mouth disease.

Hygromas may be no larger than a turkey’s egg or a man’s clenched fist,
but sometimes assume the dimensions of a child’s head. Calcification and
ossification of the walls and cornification of the skin are commonest in
old hygromas of the knee.

The sensibility and uniform fluctuation make mistakes in diagnosis
difficult. The condition can only be confused with distension of the
synovial sheath of the extensor metacarpi magnus; but this (synovial)
swelling extends in the same direction as the tendon, _i.e._,
vertically, attains the lower third of the radius, and is broadest
above. Hygromas must also be distinguished from tumours. Moussu only
mentions a single case of this kind, the tumour being very slightly
bosselated and, naturally, revealing no fluctuation.

=The prognosis= is not grave, though the condition may prove
troublesome, because the original injuries may be continued even during
treatment and prevent recovery.

[Illustration: $1]

=Treatment.= Success rarely follows cold applications or blistering,
which are only of value at the commencement. It is better to puncture
the cavity aseptically, remove the fluid contents, and fire the growth
in points. Free opening of the lowest portion of the swelling is
followed by discharge of liquid, but almost inevitably by infection at a
later stage, and by suppuration. Recovery certainly may occur, a slight
thickening of the anterior surface of the knee remaining; but the
process is often very prolonged. Some authors prefer to pass a seton or
drain vertically through the swelling. The results are identical with
those following free opening and drainage, suppuration being
unavoidable.

If the animal be sufficiently valuable to warrant surgical intervention,
the entire hygroma, together with its indurated wall, may be excised. An
elliptical fragment of skin is removed from the front of the swelling,
and the whole mass separated by dissecting away or tearing through the
connective tissue. Considerable care is necessary to avoid injuring the
synovial sheaths of the extensor tendons. This treatment, which is only
applicable in valuable animals, is completed by firmly suturing the lips
of the wound, and applying an antiseptic surgical dressing or a plaster
bandage similar to that used in operating on broken knees in horses.[1]
The animal must be prevented from lying down until the wound has firmly
united.

Footnote 1:

  See Dollar’s “A Surgical Operating Table for the Horse.” (London: Gay
  and Bird.)


                         HYGROMA OF THE HAUNCH.

With the exception of hygroma of the knee, hygromas are commoner on hind
than on front limbs. That of the haunch is limited to the external angle
of the ilium. It follows violent falls or collisions with door posts,
and results from laceration of the layers of subcutaneous connective
tissue and separation of the skin from subjacent parts.

The effusion is often of a sero-sanguinolent character. It is more
frequent in animals occupying narrow or irregularly shaped stalls, the
hygroma being developed through repeated collision of the angle of the
haunch with the wall. Finally, it may follow prolonged decubitus.

=Diagnosis= is easy, but the =prognosis= has a certain element of
gravity, because, should suppuration occur, it may be succeeded by
necrosis of the aponeurosis inserted into the external angle of the
ilium.

=Treatment= should first be directed to removing the cause. Of the
various modes of intervention, the best probably consists in
disinfecting the parts, puncturing the swelling, and injecting some
irritant of an antiseptic character, or simply washing out the cavity.
Iodine and carbolic solutions are most commonly employed. Firing is
contra-indicated.


                HYGROMA OF THE TROCHANTER OF THE FEMUR.

This condition is rare, except in thin milch cows kept under bad
hygienic conditions and insufficiently supplied with bedding. Continual
bruising of the prominences of the quarters whilst the animal is lying
is the usual cause.

This hygroma forms a hemispherical swelling covering the trochanteric
prominence. Movement is interfered with, and the stride is shortened.

The condition can only be confused with the diffuse swellings due to
periarthritis in the coxo-femoral region, which frequently occur in cows
suffering from infectious pseudo-rheumatism.

=The prognosis= is somewhat grave, for in case of suppuration the
insertions of tendons and fascia into the summit of the trochanter may
become necrotic.

=Treatment.= The first point is to supply the animal with ample clean
bedding. The swelling may be repeatedly blistered. If considered
necessary, a puncture may be made under antiseptic precautions, the
fluid drawn off, and the cavity washed out; but it is better to avoid
opening the parts with a bistoury, on account of the danger of
suppuration and of necrosis of the tendons and aponeurotic tissues in
the neighbourhood.


                         HYGROMA OF THE STIFLE.

Hygroma of the stifle or of the patella appears under the skin, outside
the external ligament of the femoro-tibial articulation. It usually
follows repeated abrasion when lying down, especially if the paving of
the stalls is rough or irregular.

The swelling varies in size from a hen’s egg up to that of a child’s
head, and exhibits fluctuation throughout.

[Illustration: $1]

=The prognosis= is somewhat serious, for here again complications may
result from necrosis of neighbouring aponeuroses.

Some authors recommend passing a seton dressed with some irritant
material through the swelling. Aseptic puncture, however, seems
preferable, followed by washing out of the cavity and the application of
a blister.


                   HYGROMA OF THE POINT OF THE HOCK.

This hygroma usually results from blows with the ox-goad, which cause
inflammation of the subcutaneous connective tissue and œdematous
infiltration extending down the leg. Afterwards the slightest injury, or
even the friction due to the animal lying down, causes liquid to collect
and an hygroma to form.

[Illustration: $1]

This hygroma is readily infected and often suppurates; it then becomes
very sensitive, producing intense lameness. More frequently, however,
under the influence of prompt treatment, the liquid is absorbed, the
layers of subcutaneous connective tissue become hardened, and undergo
more or less extensive induration.


                  HYGROMA OF THE POINT OF THE STERNUM.

Hygroma of the point of the sternum is a rarity. It only occurs in thin
animals in which the point of the sternum is prominent, and which are
confined to stables with rough floors and provided with insufficient
bedding.

The swelling should not be opened, for the tissues in front of the
sternum readily become the seat of suppuration.

If treatment is desirable, the fluid may be drained off by means of an
aseptic puncture.




                              CHAPTER IV.
                    DISEASES OF MUSCLES AND TENDONS.


     RUPTURE OF THE EXTERNAL ISCHIO-TIBIAL MUSCLE (BICEPS FEMORIS).

The biceps femoris muscle extends from the superior spinous process of
the sacrum to the region of the patella and the external surface of the
thigh. Above, it is inserted into the sacrum and the posterior margin of
the ischium, below into the supero-external surface of the tibia. It
completely covers the coxo-femoral articulation, and its passage over
the summit of the trochanter is lubricated by a serous bursa. The whole
of its anterior margin is connected with the fascia lata by an
aponeurotic expansion. From varying causes this aponeurotic layer may
become fissured; during the backward and forward movements of the limb
the summit of the trochanter may enter the fissure and become fixed
there by the tension and resistance of neighbouring tissues. This
accident has been described as “displacement or rupture of the biceps
femoris muscle.”

According to Cruzel, fixation of the biceps femoris may occur, in very
thin animals, without rupture of the musculo-aponeurotic layer, the
process being then simply confined to stretching of the aponeurotic
layer over the summit of the trochanter. Under such circumstances the
musculo-aponeurotic layer presents a cup-like depression, into which the
summit of the trochanter fits, and thus effectually prevents movement of
the muscle.

Whether the accident is due to an actual fissure, or only to stretching
of the aponeurosis, the symptoms are the same.

=Causes.= The principal predisposing causes are thin condition and
malformation of the limbs (turning outward of the hind toes).

The accident may occasionally be caused by a slip backwards, or by
extreme efforts in draught when ascending hills.

=Symptoms.= Immediately the accident occurs the limb becomes fixed in a
position of maximal extension. The trochanter being caught, the femur
can no longer be flexed, and the lower joints are also fixed in such a
way that the limb can only be moved as a whole. The claws are dragged
along the ground, and the affected limb, which can never be completely
advanced, is brought forward with a mowing movement.

On local examination, the trochanter appears to be very prominent, and
situated directly above a rigid cord which extends parallel with the
anterior margin of the affected muscle.

If the accident consists merely in the formation of a depression in the
muscle, in which the summit of the trochanter is fixed, and if there is
no fissuring, the muscle and the femur are certainly immobilised, but
the limb can be moved to a certain extent, the “mowing” movement is less
marked, and there is no well-defined rigid cord along the anterior
margin of the muscle.

[Illustration: $1]

=Diagnosis.= The condition can only be confused with luxation of the
patella; but manual examination of the affected parts revealing the
presence of a rigid cord below the trochanter at once removes any doubt.

=Prognosis.= The prognosis is only grave in working animals. Moreover,
the accident is now much rarer than formerly, if only because animals
are better looked after and better fed.

=Treatment.= If the accident results simply from the formation of a
depression in the musculo-aponeurotic layer which replaces the muscle at
the point where it passes over the trochanter, there is nothing to be
done. Reduction will occur spontaneously, and entire liberty of action
will be regained. Cruzel states that it is sometimes sufficient to force
the animal to move down a slope, in order to withdraw the trochanter
from the depression in which it has been lodged, and to restore its
normal mobility.

Rest and good feeding favour the deposition of fat, and soon alter the
conditions responsible for the accident; the muscles of the quarter
become surrounded with fat, the external ischio-tibial muscle (biceps
femoris) is thrust outwards on account of its superficial position, and
then cannot be ruptured by the summit of the trochanter. If, on the
other hand, the musculo-aponeurotic layer is fissured and the summit of
the trochanter firmly fixed in the opening, operation becomes necessary.
This consists in incising the anterior margin of the muscle over the
afore-mentioned rigid cord. The margins of the wound retract, the
tension of the cord is diminished, the trochanter released, and the
normal play of the limb restored.

Numerous methods of operation have been described and a number of
special instruments invented. The earlier methods consisted in simple
subcutaneous section of the rigid cord formed by the musculo-aponeurotic
layer and the muscle. Subcutaneous section is carried out exactly like
tenotomy, using straight and curved tenotomes. The seat of operation is
about three inches below the summit of the trochanter. In the absence of
tenotomes, section may be performed with a bistoury introduced from
below the muscle by means of a grooved director, which has been inserted
through a cutaneous puncture made at the point indicated over the
anterior margin of the prominent cord.

In better nourished subjects, in which this cord is less prominent, the
operator may, to ensure greater accuracy, make a vertical incision an
inch or two in length at the point selected over the anterior margin of
the muscle, isolate this muscle by means of the director, and afterwards
perform the section. Considerable hæmorrhage occasionally follows
division of some small muscular vessel, but is of no consequence unless
the wound has been infected.


                    RUPTURE OF THE FLEXOR METATARSI.

The rupture of this tendon-muscle is exceptional, and, according to the
description given by Furlanetto, is attended by the same symptoms as in
the horse—_i.e._, flexion of the stifle joint is not accompanied by
flexion of the hock or of the metatarsus on the tibia. The cannon bone
hangs vertically when the limb is moved.

Recovery follows prolonged rest.

Wounds and sections of tendons in the region of the cannon bone,
sections of the tendo-Achillis, etc., have been seen and described. All
such injuries may heal under antiseptic treatment and after aseptic
suture of the divided ends, provided the sutures and dressings are
applied immediately. If, on the other hand, suppuration, infection,
necrosis of tendons, synovitis or arthritis occur as complications, such
injuries become extremely serious, and from an economic standpoint
render it better to sacrifice the animal rather than attempt treatment.


Strains of tendons and tendinitis occur in the front limbs of oxen,
particularly of those used in carts. The chief indications are swelling
in the region of the cannon bone and fetlock, uneven contour of the
flexor tendons, sensibility on pressure, and lameness of varying
intensity.

=Treatment= consists in continuous cold irrigation, massage, the
application of a blister or even of the actual cautery. As a rule,
however, it is better to rest and fatten the animal.

A frequent complication of such injuries of tendons consists in
knuckling over at the fetlock.


                     PARASITIC DISEASES OF MUSCLES.


                       INFECTION WITH CYSTICERCI.

Infection of the connective and muscular tissues with cysticerci results
from the entry into the body of embryos of _Tænia solium_ and _Tænia
saginata_ of man. It occurs in man and almost all animals, but is only
of grave clinical importance in the pig and ox.

The following table shows the chief cystic (cestode) parasites of
animals, though the cysts are not always confined to muscular
structures:—

 ┌─────────────────────────┬───────────────────────────────────────────┐
 │         Adult.          │                   Larva.                  │
 ├───────────────────┬─────┼───────────────────────┬───────────────────┤
 │       Name.       │Host.│         Name.         │       Host.       │
 ├───────────────────┼─────┼───────────────────────┼───────────────────┤
 │_Tænia saginata_   │Man  │_Cysticercus bovis_    │Cattle.            │
 │_Tænia solium_     │Man  │_Cysticercus cellulosæ_│Swine and man.     │
 │_Tænia marginata_  │Dogs │_Cysticercus           │Cattle, sheep, and │
 │                   │     │  tenuicollis_         │  swine.           │
 │_Tænia cœnurus_    │Dogs │_Cœnurus cerebralis_   │Cattle and sheep.  │
 │_Tænia             │Dogs │_Echinococcus          │Cattle, sheep,     │
 │  echinococcus_    │     │  polymorphus_         │  swine, man, etc. │
 └───────────────────┴─────┴───────────────────────┴───────────────────┘


                    CYSTICERCUS DISEASE OF THE PIG.

This disease of the pig is due to _Cysticercus cellulosæ_, the cystic
form of the _Tænia solium_ or _Tænia armata_ of man. As a disease of the
pig it has been recognised from the most ancient times, and is stated to
be the cause of Moses and Mohammed having prohibited the consumption of
pork by their disciples. In the Middle Ages it formed the subject of
legislation. It was, however, only when the investigations of Van
Beneden and Kuchenmeister had completed those of the zoologists of the
seventeenth and eighteenth centuries that the evolution of tæniæ became
well known and the importance of the cystic phase clearly established.

[Illustration: $1]

[Illustration: $1]

=Causation.= The cause of cysticercus disease in the pig may be summed
up in one phrase—viz., ingestion of eggs or embryos of _Tænia solium_.

Young animals alone seem to contract the disease. After the age of eight
to ten months they appear almost entirely proof against it.

It is very rare in animals reared in confinement, but is relatively
common in those roaming at liberty; because they are much more likely to
discover human excrement and the embryos of tænia. The eggs having been
swallowed, the six-hooked embryos are set at liberty in the intestine,
perforate the tissues, enter the vessels, and are carried by the blood
into all parts of the body. Those alone develop well which reach the
interstitial and intermuscular connective tissue. The others in the
viscera usually disappear. Their presence in the depths of the muscles
produces slight general disturbance and signs of local irritation, due
to the development of the cyst itself. At the end of a month the little
vesicle is large enough to be visible to the naked eye; in forty to
forty-five days it is as large as a mustard seed, and in two months as a
grain of barley. Its commonest seats are the abdominal muscles, muscular
portions of the diaphragm, the psoas, tongue, heart, the muscles of
mastication, intercostal and cervical muscles, the adductors of the hind
legs, and the pectorals.

[Illustration: $1]

=Symptoms.= The symptoms of invasion are so little marked as usually to
pass undetected. Occasionally, when large quantities have been ingested,
signs of enteritis may occur, but these are generally ascribed to some
entirely different cause. In some cases there is difficulty in moving,
and the grunt may be altered.

Certain authors declare that the thorax is depressed between the front
limbs, but this symptom is of no particular value, and is also common to
osseous cachexia and rachitis. Paralysis of the tongue and of the lower
jaw is of greater importance. In exceptional cases, where the cysticerci
are very numerous and penetrate the brain, signs of encephalitis,
vertigo, and turning sickness (gid, sturdy) may be produced. These
signs, however, disappear, and the cysticerci undergo atrophy.
Interference with movement may give rise to suspicion when the toes of
the fore and hind limbs are dragged along the ground, and thus become
worn. This peculiarity is due to the presence of cysts in the muscles of
the limbs, but it occurs in an almost identical form in osseous
cachexia.

[Illustration: $1]

One symptom alone is pathognomonic, and it appears only at a very late
stage—viz., the presence of cysts under the thin mucous membranes which
are accessible to examination, such as those of the tongue and eye.

[Illustration: $1]

Visual examination then reveals beneath these mucous membranes the
presence of little greyish-white, semi-transparent grains the size of a
grain of barley, or even larger. Unfortunately, in an animal so
difficult to handle as the pig, this visual examination is decidedly
troublesome, and is usually replaced by palpation. In many instances the
disease does not attract attention during the patient’s life, and is
only discovered on slaughter in consequence of the lesions by which it
is characterised.

=Diagnosis.= As the characteristic lesions of cysticercus disease are to
be found in the depths of the muscular and connective tissues, and as
the external symptoms may be regarded as of doubtful significance, the
diagnosis can only be confirmed during life by manual examination of the
tongue. This examination of the tongue has been practised since the
earliest times. Aristophanes even speaks of it, and in the Middle Ages
it was performed under sworn guarantees. The regulations concerning the
inspection of meat have finally led to the suppression of this calling.

In this method of examining the tongue, the operator commences by
throwing the animal on its side, usually on the right side, and holding
it in this position by placing his left knee on its neck. He then passes
a thick stick between the jaws and behind the tusks, opens the mouth
obliquely, raising the upper jaw by manipulating the stick. Finally he
fixes one end of this last by placing his foot upon it, and holds the
other extremity by slipping it under his left arm. In this position he
is able to grasp the free end of the tongue and by digital palpation to
examine the tongue itself, the gums, the free portions of the frænum
linguæ, etc.

[Illustration: $1]

If he discovers cysts, the diagnosis is confirmed, but failure to do so
by no means disposes of the possibility of infection. Railliet declares
that about one animal in four or five shows no cysts beneath the tongue,
and, moreover, fraud is possible in this connection, it being quite
possible to prick the little cysts with a needle so that the liquid
contents escape, and examination gives no positive result. For these
reasons _intra-vitam_ examination alone is now discounted, and the chief
reliance is placed on post-mortem search.

=Prognosis.= The prognosis is very grave, not on account of danger to
the lives of the infected, but because infected meat may be offered for
human consumption. Should such meat, in an insufficiently cooked
condition, be eaten by man, its ingestion is followed by the development
of _Tænia solium_. If cooking were always perfect it would destroy the
cysticerci, but the uncertainty in this respect should prevent such meat
being consumed. The cysticerci are killed at a temperature of 125° to
130° Fahr.

[Illustration: $1]

=Lesions.= The lesions are represented by cysts alone—_i.e._, by
semi-transparent bladders, each of which contains a scolex or head armed
with four suckers and a double crown of hooks. The little bladders are
most commonly found in the muscles, lodged in the interfascicular
tissue, which they slightly irritate.

[Illustration: $1]

The number present varies extremely, depending on the intensity of
infestation and the number of eggs swallowed. Whilst in some cases
difficult to discover, in others they are so numerous that the tissues
appear strewn with them.

They are commonest in the muscles of the tongue, neck, and shoulders, in
the intercostal and psoas muscles, and in those of the quarter.

The viscera—viz., the liver, kidneys, heart, lungs, etc.—are less
commonly infested, and in these organs the cysts degenerate very
rapidly. In animals which have been infested for a long time, the cysts
may even have undergone caseo-calcareous degeneration, the liquid being
absorbed and the lesions presenting the appearance of little oblong firm
nodules.

On cutting through masses of muscle the vesicles protrude from between
the bundles.

In young animals, infestation with cysticerci causes wasting and
ill-health; subsequently the patients improve in appearance, later on
fatten, and gain marketable condition.

Of the carcases examined in Prussian slaughter-houses between 1876–82,
one in every 305 was found infested; between 1885–93, one in every 537.

=Treatment.= There is no curative treatment. Only preventive measures
are of value. These are confined to rendering it impossible for animals
to ingest eggs of the _Tænia solium_.

Cysticercus disease is rare in the north, centre, and east of France,
and in districts where animals are reared in confinement. It is commoner
where pigs are at liberty, such as Limousin, Auvergne, and Perigord. It
is frequent in North Germany, where the custom of eating half-cooked
meat contributes to the propagation of _Tænia solium_. It is also
frequent it Italy.

[Illustration: $1]


                             BEEF MEASLES.

=Causation.= The disease of beef measles is due to the penetration into
the connective and muscular tissues of embryos of the _Tænia saginata_,
or unarmed tænia of man.

This disease, unlike that of the pig, has only been recognised within
comparatively recent times, and only after Weisse’s experiments (St.
Petersburg, 1841) on feeding with raw flesh was attention drawn to it,
although as early as 1782 the _Tænia saginata_ had been described by
Goëze.

Measles in the ox is rarely seen in France, but is common in North and
East Africa. Alix has found it in Tunis, Dupuys and Monod in Senegal,
and it is common in the south of Algeria. The disease is due simply to
oxen swallowing eggs or embryos of the unarmed tænia, a fact which
explains the frequency of the disease in places where the inhabitants
are of nomad habits, and consequently disregard the most elementary
rules of public and general hygiene.

[Illustration: $1]

[Illustration: $1]

Furthermore, cattle in the Sahara, in Senegal and in the Indies, have a
very marked habit of eating ordure, and as no attempts are made to
prevent it, the risk to these animals is greatly increased.

As in the pig, the embryos which reach the stomach and intestine
penetrate into the circulatory system, and are thereby distributed
throughout the entire organism.

The development of the cysticercus is complete in forty days, and if
swallowed by man in infected meat after this period it again gives rise
to the _Tænia saginata_.

The age of the animals seems of less importance than in the case of the
pig, for Ostertag and Morot have seen cases of beef measles in animals
of ten years old.

=Symptoms.= The symptoms are still less marked than in the pig, and in
ordinary cases of infection always escape observation. Stiles, however,
gives the following account of a case experimentally infected:—

[Illustration: $1]

“Symptoms. Four days after feeding segments of _T. saginata_ to a
healthy three-months-old calf, the patient showed a higher temperature
(the normal temperature was 39·2° C.). The calf ate but little on that
day, showed an accelerated pulse, swollen belly, staring coat, and upon
pressure on the sides showed signs of pain. The next day the animal was
more lively, ate a little, and for nine days later did not show any
special symptoms except pain on pressure of the abdominal walls, and a
slight fever. Nine days after the infection the temperature was 40·7°
C., pulse 86, respiration 22; the calf laid down most of the time, lost
its appetite almost entirely, and groaned considerably. When driven it
showed a stiff gait and evident pain in the side. The fever increased
gradually, and with it the feebleness and low-spiritedness of the calf,
which now retained a recumbent position most of the time, being scarcely
able to rise without aid, and eating only mash with ground corn.
Diarrhœa commenced, the temperature fell gradually, and on the
twenty-third day the animal died. The temperature had fallen to 38·2° C.
During the last few days the calf was unable to rise; in fact, it could
scarcely raise its head to lick the mash placed before it. Pulse was
reduced by ten beats. On the last day the heart-beats were very much
slower, yet firm, and could be plainly felt. Several days before death
the breathing was laboured, and on the last day there was extreme
dyspnœa.”

[Illustration: $1]

=Diagnosis.= In forming a diagnosis we meet with the same difficulty as
in the case of the pig. It is always easy to examine the tongue; but
when visible lesions are absent diagnosis in the case of the ox remains
doubtful and problematical even more than in the pig.

In the carcase, diagnosis is much easier. The cysts are sought for, as
in the pig, by making sections of muscle, those usually selected being
the pterygoid, cervical, cardiac, and psoas muscles, and those of the
quarters.

=Prognosis.= The prognosis is grave, not indeed for the infected
animals, which seem little injured by the parasite, but for human
beings, who run the risk of contracting _Tænia inermis_ by eating
insufficiently-cooked meat.

A temperature of 115° to 120° Fahr. destroys the cysticerci, but in
roast meats the central temperature of the mass always remains below
this figure.

Salting for fifteen to twenty days destroys the vitality of the
parasite.

=Lesions.= The lesions are confined to the presence of the cyst and of
two little zones of chronic inflammation immediately surrounding it.
Unless heavily infested the subjects fatten just as well as others.

The vesicles are semi-transparent, ³⁄₁₆ inch to ¼ inch in length,
slightly ovoid in form, and contain a tænia head with four suckers, but
without hooks.

In seven to eight months the cysts undergo degeneration, the liquid is
absorbed, and calcium salts are deposited throughout the mass. The
lesions which remain have, in the ox, the appearance of interstitial
disseminated tuberculosis.

There is no curative treatment. The infested animal recovers
spontaneously with the lapse of time, for the cysticerci undergo
degenerative processes, but the flesh of such animals is of little
commercial value.

From a preventive standpoint we can only hope to improve matters by a
gradual and progressive change in social and public hygienic conditions.

[Illustration: $1]

When the life of the nomad shall have been entirely replaced by that of
the highly-civilised European and private hygienic precautions have
rendered it impossible for animals to obtain access to segments or eggs
of the _Tænia saginata_, beef measles will disappear.

At present, in the countries where the disease is common, one
experiences a feeling of astonishment that it is not far more frequent;
for experiment has shown that a person infected with one unarmed
tapeworm expels with the fæces an average of four hundred proglottides
per month, each proglottis or segment of the worm containing about
30,000 eggs, each of which is capable of developing into a tapeworm.

Beef measles is rather common in Germany, but rare in France,
Switzerland, and Italy.


                       TRICHINIASIS—TRICHINOSIS.

Trichinosis is a disease caused by the entrance into the body of the
_Trichina spiralis_. This parasite is swallowed in the larval form, and
undergoes sexual changes in the intestine, at first producing intestinal
trichinosis, which represents the first phase in the development of the
disease.

The trichinæ breed rapidly. The embryos penetrate into or are directly
deposited in the blood-vessels, which convey them to all parts of the
body, thus setting up the second phase of the disease, known as muscular
trichinosis.

[Illustration: $1]

[Illustration: $1]

Trichinosis as a disease has long been recognised. Peacock in 1828 and
J. Hilton in 1832 mentioned the existence of the cysts of trichinæ; Owen
in 1835 gave the name of _Trichina spiralis_ to the parasites contained
in the cysts. Trichinosis being common in Germany at that time, Virchow
and Leuckart undertook its investigation, but mistook other nematodes of
the intestine for the _Trichina spiralis_. In 1847 Leydy recognised that
trichinosis occurred in American pigs.

In 1860 Zenker found muscular and intestinal trichinosis on post-mortem
examination of a girl who had been suspected of suffering from typhoid
fever, and a carefully conducted inquiry revealed the fact that this
girl had some time previously eaten a quantity of raw ham. Virchow and
Leuckart returned to their investigations, and the life history of the
parasite soon became definitely known.

=Causation.= Trichinosis is capable of attacking all mammifers without
exception, from a man to a mouse; and most animals which can be made the
subjects of experiment contract the disease in varying degrees.

The intestinal form is seen in birds, but the muscles do not become
infested by the embryos.

Cold-blooded animals are proof against the disease.

[Illustration: $1]

After the ingestion of meat containing cysts of the parasite, the
processes of gastric and intestinal digestion set the larvæ at liberty.
These larvæ become sexual at the end of four to five days, and the
females, which are usually twice as numerous as the males, begin laying
eggs from the sixth day, continuing for a month to six weeks. Each
female lays approximately from 10,000 to 15,000 eggs. The embryos
perforate the intestinal walls, pass into the circulation, and are
hurried into all parts of the system. This period of infestation
constitutes the first phase of the disease.

Askanazy, in 1896, suggested that it was not the embryos which
perforated the intestinal walls and thus reached the blood-vessels, but
the fertilised female trichinæ themselves, which entered the terminal
chyle vessels and laid their eggs directly within them.

This observation is of great interest, for it contradicts the view held
by Leuckart and proves that treatment is useless even in the first
phase.

The males are about ¹⁄₁₆ inch in length, the females ⅛ inch to ⁵⁄₃₂
inch, and are ovoviviparous.

=Symptoms.= The symptoms lack precise character, even when the disease
is known to be developing, and moreover they have only been carefully
observed in experimental cases. As soon as the laying period begins,
signs of intestinal disturbance may be observed, possibly due to embryos
perforating the intestinal walls (if we accept Leuckart’s view), or,
according to Askanazy, to adult females penetrating the chyle vessels
and disturbing intestinal absorption.

These symptoms are only appreciable in cases of “massive” infestation.
If slight, the disturbance passes unperceived. In severe cases the
symptoms consist of diarrhœa, loss of appetite, grinding of the teeth,
abdominal pain in the form of dull colic, and sometimes irritation of
the peritoneum. The embryos carried by the circulation then escape into
the tissues and, like the cysticerci, become encysted, preferably in the
muscles, in the interfascicular connective tissue towards the ends of
the bundles. Each (asexual) parasite plays the part of a foreign body,
causing infiltration of serum and exudation of leucocytes in its
neighbourhood, and soon becoming encysted in the interior of a little
ovoid space surrounded by a fibro-fatty wall. Fat granules accumulate at
each end of the cyst.

[Illustration: $1]

[Illustration: $1]

[Illustration: $1]

The parasite, which at first appeared straight, soon assumes a bent
form, then that of a figure “6,” then of a figure “3,” and preserves a
latent vitality throughout the entire period of encystment. These cysts
are of very small dimensions, invisible to the naked eye, and their
discovery necessitates the use of the microscope. They are about ¹⁄₆₄th
inch in length and ¹⁄₁₂₀th inch in width. Very frequently two or three
cysts may be found arranged in line, presenting the appearance of beads
on a string: more rarely two parasites may be found in one cyst;
exceptionally, as many as six or seven. The appearance of “beads on a
string” is due to the fact that the parasites follow the interfascicular
capillaries.

In animals which are kept for a long time and fattened the cyst walls
undergo fatty infiltration. The change is commonest in pigs. In the same
way calcareous infiltration sometimes occurs, but only when the
parasites have lost their vitality. This calcareous degeneration
consists in the deposit of carbonate and phosphate of lime in the walls
of the cyst; it never begins before the seventh or eighth month after
infestation, and is sometimes much longer delayed.

No man or animal ever becomes infested except by the ingestion of meat
or drink containing larval trichinæ. The pig and small rodents are most
frequently attacked. Man contracts trichinosis by eating insufficiently
cooked infected pork. The fact that small rodents, particularly rats,
eat the bodies of their kind explains the persistence of trichinosis in
certain regions. Pigs roaming at large, and thus liable to find and eat
the dead bodies of such rodents, may contract trichinosis in this way or
from eating ordure.

For some weeks after the larvæ have penetrated the muscular tissues the
animals show stiffness of the limbs, difficulty in moving, and in
mastication, etc., but these troubles disappear in a short time.

The above facts explain why trichinosis in the pig is almost unknown in
France, Italy, and Spain. It is commoner in Germany and in certain
States of Europe, such as Holland and Russia, although investigations
had previously shown that in Paris about 7 per cent. of the sewer rats
were sufferers from trichinosis and that in Germany the percentage rose
as high as 15 to 20. In Chicago and Cincinnati, U.S.A., the proportion
of rats suffering from trichinosis has been as high as 50 to 70 per
cent., and as in some of the Northern States pigs were bred in complete
freedom, it follows that at one time very large numbers of American pigs
must have suffered from trichinosis.

In consequence of sanitary precautions this proportion has since greatly
diminished.

=Diagnosis.= During the animal’s life diagnosis is a difficult matter,
though, on the other hand, simple microscopic examination of suspected
meat is sufficient at once to settle the question. In dealing with the
living animal, however, it is necessary, as in examining suspected meat,
to obtain a fragment of muscle in order to submit it to microscopic
examination. This fragment can be obtained by the method known as
“harpoonage,”—a trocar provided with a cutting hook, or a trocar the
canula of which has a sharp-edged opening near its end, being thrust
into the muscle. On removing the trocar the elasticity of the tissues
causes a fragment to project into the opening in the canula, and on
withdrawing the latter a fragment sufficient for examination is
obtained. One may proceed in the same way by harpoonage when examining
large masses of suspected meat the surface of which reveals no lesion.

The specimen having been obtained, a few fragments of the muscular
fasciculi are crushed between two glasses and examined with a low power.

The trichinæ will be found towards the ends of the muscle near the
region of the tendons; few or none exist in the fat. These parasites are
most readily discovered in the diaphragm, in the muscles of the
shoulders and quarters, and in the psoas muscles.

=Prognosis.= The prognosis is relatively favourable so long as
infestation is only moderate. But it is very grave from the point of
view of public hygiene, on account of the possibility of persons
becoming infected by eating the diseased meat.

=Treatment.= There is no curative treatment. Formerly it was believed
that, provided the condition were early diagnosed, the intestinal form
might possibly be cured by administering purgatives and vermifuges so as
to prevent the embryos penetrating the system.

After Askanazy’s discoveries this view had to be abandoned, and the
practitioner is necessarily powerless in dealing with the muscular form.
Time alone effects improvement and a relative cure by causing
caseo-calcareous degeneration of the cysts. With a prophylactic object,
every precaution should be taken to prevent the possibility of pigs
being contaminated. This question particularly interests America,
because of the extreme prevalency of pig trichinosis there.

From the point of view of public hygiene all infected meat should be
seized and destroyed, despite the fact that perfect cooking destroys the
vitality of the parasites, which perish at 120° Fahr.

Ordinary salting but slightly affects their vitality, which explains why
from time to time the importation of meat has to be prohibited and why
meat should always be scrupulously inspected.




                               CHAPTER V.
                              RHEUMATISM.


In bovine pathology the term “Rheumatism” is applied to a number of
different morbid conditions, the sole connection between which is that
they seriously affect the organs of locomotion. This reason may perhaps
be accepted as sufficient for including the study of rheumatism amongst
diseases affecting locomotion.

The disease is of considerable importance, and for this reason the study
of rheumatism itself necessarily precedes the description of
pseudo-rheumatism, secondary rheumatism, or infectious rheumatism in
young and adult animals.


                         ARTICULAR RHEUMATISM.

Acute rheumatism has a clearly marked predilection for the
articulations. Sometimes the great serous membranes are simultaneously
affected (pleura, pericardium, endocardium), but only in very
exceptional circumstances are they primarily attacked. That form of
rheumatism known as visceral is as a general rule secondary in
comparison with articular rheumatism. Several joints and tendon sheaths
may be attacked at the same time. Under such circumstances rheumatism
may be defined as a febrile disease, probably of an infectious nature,
revealing itself by simple or multiple inflammation of joints and the
tissues surrounding them, and capable of becoming complicated with
inflammation of the pleura, pericardium, endocardium, meninges of the
brain, etc.

=Causation.= All authors agree in recognising the influence of heredity,
of wet and cold, of sudden changes in temperature, draughts in the
stable, prolonged exposure to low temperatures, or the chilling of
animals saturated with perspiration. These are and cannot be otherwise
than occasional causes; but the determining cause remains at present
unknown.

In human pathology it has been proved beyond dispute that a certain
relationship exists between arthritism, or the “uric acid diathesis,”
and rheumatism. This fact is so well recognised that doctors have said
that rheumatism was to arthritism what scrofula is to tuberculosis.
That, however, does not advance our knowledge of the question in the
smallest degree, and it may simply be that arthritism represents one of
the principal favouring conditions in the development of rheumatism.

In domestic animals the uric acid diathesis is little known, renal
lithiasis is no more a rarity than gravel; but at the present time no
one appears clearly to have established the relationship between these
diseases and the development of rheumatism. What, however, we must all
admit is that rheumatism exhibits all the phases of development of a
rapidly progressive infectious disease.

Numerous attempts have been made by doctors during the last few years to
discover the presence of a microscopic agent and to demonstrate its
pathological characteristics. Several microbes have been described, but
one is forced to confess that the results have until now been very
contradictory and uncertain; and yet there is little room to doubt that
the disease is of an infectious character.

=Symptoms.= The symptoms are generally well defined and well developed.
The onset is sudden; an animal which one day before appeared perfectly
well is attacked in one or several joints. Usually the upper joints of
the limb are involved—the shoulder, elbow, knee, haunch, stifle, hock.

Nevertheless, invasion is probably not as sudden as it appears to be,
and, as in the human species, the subject begins by feeling erratic
pains, which, however, pass unnoticed. The animal moves with difficulty,
as though it were suffering from laminitis, and has pain when placing
weight on the limb, while the joint attacked soon shows a swelling which
extends to the tendon sheaths and the neighbouring serous bursæ. The
local temperature is higher than that of surrounding parts, sensibility
becomes very marked, and pain attends the slightest pressure on, or even
movement of, the affected joint. Intense lameness follows, which may
even at first give rise to the suspicion of fracture. The animals remain
lying for long periods, groan from time to time, and suffer great pain
when rising.

In some cases the local manifestations appear to be transferred from one
joint to another.

These local symptoms are accompanied by high fever. The temperature
rises to 105° or 106° Fahr., the pulse to 80 or 90, and the breathing is
enormously accelerated if the patients are forced to move.

Loss of appetite is very marked. Rumination may be suspended, and these
grave symptoms are accompanied by constipation, rapid wasting, cessation
or marked diminution of the milk supply, decrease in the quantity of
urine passed, etc.

A few days after the onset, visceral complications may occur, though
fortunately such complications are far from being constant. Auscultation
and percussion sometimes reveal the lesions of pleurisy, endocarditis,
pericarditis, etc.

The development of articular rheumatism varies greatly, and may
occasionally continue for weeks or months, the condition of one joint
improving only to be followed by inflammation of another.

The visceral lesions rarely disappear completely, and it is not uncommon
to note symptoms of chronic valvular endocarditis. Relapses are somewhat
frequent, and the disease may continue in a chronic form after the acute
symptoms have disappeared.

=Lesions.= The joint itself is not alone affected. All the tissues
surrounding it are congested, swollen and painful, particularly the
sheaths and insertions of the tendons. Within the inflamed synovial
capsules of the joints an increased quantity of turbid synovia
accumulates, distending the joint and producing a condition of
hydrarthrosis.

In animals slaughtered during the course of the disease one finds
congestive infiltration of the limbs.

The temperature of the parts near the affected joints is higher than
that of neighbouring regions. Sensibility is much more acute, and the
slightest external pressure gives rise to pain.

In favourable cases the joint may appear scarcely injured. The principal
symptoms are those of pain. In old-standing cases certain permanent
changes may occur, such as thickening and hardening of the wall of the
synovial capsule, fibrous infiltration of the tissues around the joint,
or even diffuse and irregular calcareous infiltration.

Cases of false or true anchylosis are rare, the animals usually being
slaughtered before such conditions can develop.

=Complications.= The commonest complications are endocarditis
and pericarditis. Valvular endocarditis localised in the
auriculo-ventricular valves is revealed by a systolic sound, and by
tumultuous or irregular beating of the heart when the animals are forced
to move. Pericarditis, which seems rare in bovine animals, is much
commoner in sheep. This pericarditis, however, produces none of the
external signs of pericarditis due to a foreign body. Like tuberculous
pericarditis, it is only accompanied by a trifling amount of exudate,
and is recognised by increased cardiac dulness and diminution in the
cardiac sounds on auscultation.

Simple pleurisy associated with pericarditis is frequent in sheep, but
unknown or little known in the ox.

If in animals other visceral complications occur, affecting the
peritoneum, meninges of the brain or intestines, they are at present
little recognised.

=Diagnosis.= Articular rheumatism can only be confused with osseous
cachexia or laminitis. Osseous cachexia, however, possesses symptoms
peculiar to itself, and generally extends to an entire district, whilst
rheumatism appears in an isolated form. Again, the arthritis peculiar to
osseous cachexia most commonly affects the joints of the extremities
(fetlock and phalanges). The disease may be differentiated from
laminitis by simply manipulating the joints, which are painful in
rheumatism but not in laminitis, and by percussing the claws, which are
painful in laminitis but not in rheumatism, and by noting the character
of the gait.

=Prognosis.= The prognosis is grave, as in all acute diseases which are
capable of assuming a protracted chronic form. It is also necessary to
take into account the loss of condition, the possibility of relapse, and
the complications due to prolonged decubitus.

=Treatment.= The first indication is to place the patients in a nearly
constant temperature, to supply bedding generously, and to arrange for
the animal being undisturbed. Among drugs salicylate of soda gives the
best results if administered in sufficient doses—6 to 7 drams per day
for oxen or cows of medium size, 45 to 75 grains for sheep.

Diuretics, like bicarbonate of soda, nitrate of potash and hay tea or
infusion of couch grass, pellitory, etc., also give good results.

The joints attacked may be blistered, but it is often preferable to use
mild ointments, containing camphor or belladonna, because, as soon as
pain diminishes, moderate massage of the affected parts, which favours
rapid absorption of the effusions, can then at once be resorted to. The
diet should consist of easily digested food and of lukewarm hay tea,
etc. When the animals are suffering from kidney disease in any form
salicylate of soda is contra-indicated.

Antipyrin may also be of service in doses of 45 to 75 grains for bovines
and 15 grains for sheep. Preparations of methyl salicylate can only be
used for animals of value.


                          MUSCULAR RHEUMATISM.

Muscular rheumatism is due to causes similar to those of articular
rheumatism. The symptoms, moreover, often occur simultaneously, or may
alternate with the articular manifestations, with which they are seldom
entirely unconnected.

Moist cold seems to be the predetermining cause, whether it acts
indirectly on the nerve trunks or affects the capillary circulation in
the muscles, through the medium of the vaso-motor supply. The results
are revealed by the development of neuralgia, neuritis or interstitial
myositis; and these diseases, by producing more or less intense pain,
cause difficulty in movement or distinct lameness. Attempts have been
made to explain the development of these lesions by ascribing a certain
action to the uric acid (which is said to be in excess in the body), and
to the lactic acid, which accumulates in the muscular tissue after
fatigue or over-exertion, and may occasionally produce temporary
myositis. Up to the present time, no satisfactory proof has been
furnished enabling us to identify the myositis of rheumatism with the
myositis of over-exertion, which, moreover, appears to differ from it in
essential particulars.

=Symptoms.= Muscular rheumatism is often ill-recognised in veterinary
medicine, and closer observation would appear to suggest that it is much
less frequent than has been stated. Generalised muscular rheumatism is
rare; patients stand stiffly as though incapable of moving; the limbs
and the back appear rigid, and the animal seems only capable of changing
its position by a single movement of its whole body. One might readily
believe at first sight that the case was one of generalised laminitis or
slight generalised tetanus. The animal has difficulty in rising; when
moving the limbs are dragged, and the patient is cautious in lying down.

Most frequently the disease is localised in one region, such as the
shoulder, the loins, or the quarters. The affected part is stiff, tense,
painful, hard, and as though in a state of cramp. Palpation and pressure
reveal the presence of very exaggerated sensibility, which varies within
wide limits, according to circumstances, changes in atmospheric
conditions, etc. These local signs are accompanied by a general reaction
of varying severity, somewhat resembling that seen in articular
rheumatism. Appetite is diminished or suppressed, as is rumination; the
muzzle is dry and hot; the temperature may rise as high as 103° or 104°
Fahr.

=Lesions.= The lesions are imperfectly recognised, because those who
might most easily observe and study them have often neither the means
nor the leisure for the purpose. Possibly one would at times discover
lesions of neuritis; but in any case it is not so very rare to discover
lesions of interstitial sclerosing myositis in the depths of the muscles
of the quarter, loins, shoulders, etc., a condition rarely found in any
other disease. Naturally these are only the ultimate lesions of muscular
rheumatism; for slight attacks leave no traces visible to external
examination.

=Diagnosis.= The commonest error is that of mistaking the condition for
laminitis of all four limbs. The history often suffices to eliminate
this disease from consideration, while palpation and percussion of the
claws remove any remaining doubt.

=The prognosis= is not usually grave, and recovery sometimes follows the
adoption of good hygienic conditions. On the other hand, certain
patients lose flesh rapidly.

=Treatment.= Salicylate of soda and antipyrin still form the two most
efficacious drugs, particularly the first, which may almost be regarded
as a veritable specific in rheumatism. The doses vary with the size of
the patients, from 2½ to 7 drams per day. These doses are continued for
six to eight days consecutively. Some authors prefer salicylic acid,
which, however, is more irritant, in doses of 15 to 75 grains. Tartar
emetic, in doses of 2½ to 4 drams per day until purgation is
established, is also said to have proved of great value in the hands of
the older practitioners. Local treatment comprises stimulating frictions
with camphorated alcohol, ammonia, and oil of turpentine. Such
applications are usually of great service, particularly when associated
with methodical massage of the affected parts. These modes of treatment
should be supplemented with a proper dietary and the administration of
tepid, diuretic fluids as required.


          INFECTIOUS FORMS OF RHEUMATISM OR PSEUDO-RHEUMATISM.

Under the head of infectious rheumatism or pseudo-rheumatism may be
grouped joint diseases of a rheumatic type accompanying various general
or local diseases in young animals and adults: diseases of the
umbilicus, rachitis, peripneumonia, retention of the fœtus, dysentery,
etc. These diseases are characterised by articular symptoms, which
sometimes appear early, sometimes only when the disease itself is
declining, and develop suddenly or gradually, the joint cavities
themselves either being directly invaded by the agents of the primary
disease or remaining exempt. These pseudo-rheumatic attacks are due to
the localised action of microbic toxins on the articular synovial
membranes. Sometimes the serous membranes of the large body cavities are
also implicated.

This theory explains the development of acute arthritis without the
presence of gonococci during the course of an attack of blenorrhagia in
man, and may be applied in respect of certain forms of arthritis or
synovitis without the presence of microbes in domestic animals.


                INFECTIOUS RHEUMATISM IN YOUNG ANIMALS.

=Causation.= To explain the occurrence of infectious rheumatism in young
animals a variety of causes has been invoked, such as bad feeding, the
absence of that purgation which usually follows the action of the
mother’s first milk (_i.e._, colostrum), and clears the bowel of
meconium, the effect of heredity, of chills, of insufficient food, and
of unduly abundant or very rich food, which has been said to produce
indigestion and its various complications.

All these causes may play a certain part in favouring the development of
infectious rheumatism, but none constitutes the direct cause.

Lecoq and Loiset in their investigations regarding this disease in colts
mentioned the almost invariable existence of lesions in the umbilical
region. Bollinger in 1869 recognised the possibility of infection by way
of the umbilical vein. Röll and Guillebeau are of the same opinion, and
Morot’s excellent study shows that here must be sought the most frequent
point of origin of the articular symptoms. In animals born in dirty
stables the umbilical cord becomes infected at the time of birth, or its
cicatrix a few days later. The result is the development of rapidly
fatal septicæmia, suppuration in the wound, omphalitis,
omphalo-phlebitis, or umbilical arteritis; and to this infection are due
the various complications, which may appear almost immediately, as in
the case of septicæmia of calves, or may be deferred for a shorter or
longer interval, for so long indeed that the umbilicus may appear to
have healed externally (infectious pneumonia and endocarditis,
infectious arthritis, etc.). The umbilical cord and the tissues
surrounding the cicatrix form excellent culture grounds for those
microorganisms which always exist in such abundance in litter and
manure; and there is, therefore, no difficulty in understanding why in
dirty stables infection so readily occurs. The infective agents may be
of very varying kinds, a fact which explains the difference in the
symptoms which follow umbilical infection; although ovoid bacteria,
streptococcus pyogenes, and the bacilli of necrosis seem most common.

Omphalitis and omphalo-phlebitis are not the only diseases capable of
producing infectious rheumatism in young animals. Certain infections
resembling dysentery and diarrhœic enteritis are also its frequent
forerunners. In young animals even rachitis, which is accompanied by
various digestive disorders, may serve as the point of origin for
infectious rheumatism and all its complications.

In older animals—_i.e._, in animals from five to six months, or even
twelve to fifteen months—infectious rheumatism may occur without a
clearly defined cause. It then develops with the symptoms and lesions of
that condition known as “osteomyelitis of adolescence” in human
pathology. These forms of osteomyelitis are due to infection with
streptococci and staphylococci. In veterinary medicine the pathogeny has
not yet been accurately ascertained.

=Symptoms.= Infectious rheumatism in young animals assumes one of two
clinical appearances, possibly due to different causes, viz.—plastic or
suppurative arthritis following umbilical infection, and simple
exudative arthritis. In the former variety symptoms appear soon after
birth, rarely after the age of two months, and as an exception in
animals of six to eight months affected with rachitis. The onset is
sometimes sudden; the patient, though healthy on the previous evening,
is unable next morning to rise or move. Hence in France this disease has
received the titles, amongst others, of laminitis and paralysis of the
newly born.

Certain joints, often a pair, appear swollen, hot and painful. The
synovial sacs are distended, and in the upper joints of the limb appear
much more prominent than in the lower. When the patients are still able
to move they walk on three legs, but usually they remain lying
permanently, and if aroused show great difficulty in rising and very
acute pain in moving.

[Illustration: $1]

[Illustration: $1]

General disturbance is also very marked; the temperature varies between
103° and 105° Fahr. The animals are dull, have no appetite, and exhibit
intense thirst. The pulse rate and respirations are increased, and not
uncommonly symptoms of grave visceral complications, such as
endocarditis, pleurisy, pneumonia, etc., can be detected. Diarrhœic
enteritis sometimes appears as a secondary development.

The animals remain permanently lying down. They can only be induced to
rise with difficulty, and, when moved, exhibit very acute pain.

In many cases the disease then takes a rapid course and ends fatally.
Death is the usual termination whenever any of the above-mentioned
visceral complications exist. Recovery is exceptional. In certain lucky
cases, sometimes without any treatment whatever, the symptoms become
less acute, the appetite persists or improves, fever diminishes, the
condition of the joints remains stationary, and after the lapse of
several weeks there is ground for anticipating recovery. In all cases,
however, the convalescents remain thin and sickly, exhibit pain and
capricious appetite, and in very few cases indeed is there any economic
reason for keeping them alive.

More frequently infectious rheumatism terminates by abscess formation in
the joints. The articular cavity becomes filled with pus, the tissues
covering one of the synovial sacs soften, and the abscess opens,
discharging fibrinous clots, thin watery pus mixed with synovia, and
_débris_ of articular cartilages or ligaments. Pyæmia is the final
complication when the patients are not slaughtered.

In the cases comprised under the second heading the symptoms appear more
slowly and develop insidiously, the chief, viz., a tendency to remain
lying and difficulty in movement, long preceding the appearance of
exudative arthritis. The course depends chiefly on the nature of the
infective agent. In calves suffering from peripneumonia, calves from
stables in which epizootic abortion rages, rachitic calves or calves
suffering from severe diarrhœic enteritis, the joints do not become the
seat of suppuration.

In such cases the arthritis is of a simple exudative character, but
without microbic infection of the joint cavity. This form is less
dangerous, and is often curable provided the original cause be kept in
mind.

=Lesions.= The lesions are always very marked, and are quite different
from those of simple rheumatism. The synovial membranes and the
periarticular tissues are always thickened, injected, inflamed, and
infiltrated.

In more benign cases the synovial exudate from the joint cavities is
simply cloudy, contains no infectious germs, and proves sterile on
attempts at cultivation. In such cases there is no abscess formation.
But most frequently this stage of serous exudation is only temporary,
and the articular fluid, which at first seems sterile, may, when tested
some days later by means of cultures, reveal the presence of organisms.
The synovia accumulated within the joint sometimes contains fibrinous
flocculi, which are at first small, but later form veritable coagula,
filling up and thickly coating all the prominences of the joint and
moulding themselves on the extremities of the bones constituting the
articulation. Sometimes the cartilages undergo very rapid ulceration,
the subjacent layers of bone become inflamed, and the osteoarthritis
which develops is so severe and painful that the patients are forced to
remain absolutely still, and are quite incapable of rising. The lesions
may remain stationary at this point. In other cases suppuration occurs
in the articulation itself, the wall of the synovial cavity, the
periarticular tissues, and the skin soften; then the abscess breaks,
giving rise to open suppurating arthritis. Animals are rarely kept long
enough to become so gravely affected; many die before this stage, and
the others are usually slaughtered. Moreover, they rapidly perish from
exhaustion and from visceral complications of a pyæmic character.

[Illustration: $1]

In many cases post-mortem examination reveals nothing whatever in the
region of the umbilical cord (through which infection has occurred), but
the germs of infection may be found in the blood or general circulation;
or again, careful investigation may show ulceration of the umbilicus,
lesions of omphalitis, of ascending umbilical arteritis in consequence
of infection of the thrombus, of umbilical phlebitis, or of infective
peritonitis, etc. The infectious agent reaches the liver through the
blood-vessels, then attains the posterior vena cava, after which the
infection assumes the gravest possible character, producing
complications like arthritis and purulent infection, with the formation
of multiple abscesses in the depths of the viscera.

The _Staphylococcus aureus_ and various streptococci are the most
frequent but not the only causes of these infections.

=The diagnosis= is not difficult, provided the disease be not mistaken
for true rheumatism. As true rheumatism is very rare in young animals,
and as, on the other hand, attention is aroused by the presence of
lesions of the umbilicus and by the existence of diarrhœic enteritis,
rachitis, etc., there is seldom room for doubt.

=Prognosis.= The prognosis is extremely grave whenever the case results
from infection of the umbilicus. French statistics place the mortality
at 90 per cent. and German at 75 per cent.

Curative =treatment= can only be attempted with any chance of success in
the simple exudative form. Even then it is necessary to simultaneously
treat the primary disease, such as rachitis or diarrhœic enteritis.

The recommendations of former practitioners as to the use of saline
purgatives, cream of tartar, etc., were probably due to their having
recognised that diarrhœa is sometimes the primary cause.

Moussu has seen simple exudative arthritis in rachitic subjects
disappear, together with the rachitis, under proper treatment.

The indications therefore are, firstly, to take measures against the
primary disease, treating the local lesions separately with blisters,
douches, or simply cold applications and massage. Provided the general
condition can be improved, recovery may follow.

Unfortunately, this treatment is useless against infectious rheumatism
with suppurative arthritis resulting from infection of the umbilicus. In
such cases treatment, if undertaken, should be directed towards
perfectly disinfecting the umbilical wound or any existing sinuses.

Injections of strong carbolic solution, the application of antiseptic
ointments or of antiseptic pencils containing iodoform, salol, etc.,
into the sinuses, followed by a surgical dressing covering the
umbilicus, form the basis of this primary treatment, which, it need
scarcely be said, has little chance of checking the course of already
existing arthritis. The use of internal antiseptics and of antipyretics
like camphor, salicylate of soda, etc., is worthy of trial. On the other
hand, prophylactic treatment in an infected area has every chance of
succeeding. The use of dry, clean litter under the mother and the
new-born calf, thorough cleansing of the umbilical cord or umbilical
cicatrix, and the application to the umbilicus of a small surgical
dressing or even a smear of tar, almost always suffice to prevent the
occurrence of these forms of arthritis.


                INFECTIOUS PSEUDO-RHEUMATISM IN ADULTS.

The infectious pseudo-rheumatism of adults differs from infectious
rheumatism in young animals in that it never becomes complicated with
suppurative arthritis, and rarely affects more than one joint at a time.
The hind limbs are the parts usually attacked, and the joints seem
predisposed to disease in the following order of frequency: the
femoro-tibial, coxo-femoral, and hock joints.

On account of its greater frequency in cows, it has been termed
“arthritis of milch cows” and “infectious arthritis of milch cows,” etc.
In reality it may also attack bulls and oxen, but such cases are
exceptional.

=Causation.= First mentioned by Coulbeaux in 1824, and by Pauleau in
1832, this disease has been well studied by Ph. Heu. Old works mention
it as attacking good milkers in the best dairies around Paris, and Heu
declares it to be the most deadly disease after peripneumonia and
tuberculosis.

This form of arthritis usually appears in an insidious form after
abortion, retention of the fœtus, or post-partum metritis. In cases of
epizootic abortion infectious rheumatism sometimes assumes an epizootic
form, and completes the devastation begun by abortion. Under other and
much rarer circumstances it may follow enteritis of adults or attacks of
mammitis, etc. The pathogeny of these forms of arthritis is not
difficult to understand, for in the greater number of instances they
form delayed consequences of local uterine infection.

[Illustration: $1]

The soluble products secreted by infectious organisms multiplying within
the uterus are absorbed by the uterine mucous membrane, causing slow
intoxication; and in consequence of the special elective affinity which
the toxins show for the articular serous membranes, and in many cases
also for the visceral serous membranes, the special characteristics are
developed. Under certain circumstances the joint cavity may even become
the seat of true microbic infection.

=Symptoms.= The appearance of the first symptoms is difficult to
identify, for many cows abort, fail to “cleanse,” or become affected
with metritis without infectious rheumatism supervening. It is a
long-delayed condition, which may be postponed for weeks or even for
several months after an abnormal parturition, and to a time when the
symptoms of metritis have almost entirely disappeared. The onset is
characterised by difficulty in rising, and soon afterwards by lameness,
or by the animal failing to place weight on one of the hind limbs. The
affected joint, usually one of the articulations of the stifle, appears
markedly enlarged, is not appreciably hot to the touch, but reveals a
certain amount of painful sensibility on pressure. The periarticular
tissues are infiltrated and the synovial sacs slightly distended.

[Illustration: $1]

[Illustration: $1]

After a few days, a week or two at most, the periarticular swelling
diminishes, and the condition appears to remain stationary.

Appetite is normal or only diminished. The pain continues, and causes
progressive wasting and diminution in the yield of milk.

If at this time the practitioner makes a careful digital examination of
the diseased region, he may find one of two conditions. In the first,
the synovial sacs appear distended, fluctuating and in exactly the same
condition as in ordinary bog spavin. This is what has been termed the
exudative form of infectious arthritis. In the second, the enlarged
joint remains very sensitive, the walls of the synovial sac are
thickened, fluctuation is either absent or only slightly marked, but
induration is very manifest. This constitutes the plastic form.

[Illustration: $1]

Exudative arthritis is the form usually seen at first. It may preserve
its primary characteristics, but only too often proves to be the
forerunner of the plastic form, which develops with the lapse of time.
If nothing is done wasting becomes more marked, and is accompanied by
cachexia. The animals are unable to rise, the complications inseparable
from decubitus occur, and wasting or secondary purulent infection sets
in.

=Lesions.= In the exudative form the changes are confined to
inflammation and thickening of the synovial membranes, intra-articular
exudation, and sometimes grooving of the cartilages without ulceration
of the articular surfaces and without disorganisation of the joint.

The plastic form, on the other hand, leads to destruction of the
cartilages, ligaments, and sub-cartilaginous bony layers, induration and
calcification of the walls of the synovial cavity, and even periostitis
of the ends of the bones, with the formation of false joints. The
internal surface of the inflamed synovial membranes begins to granulate,
the fibrous clots distending the articular dilatations are perforated by
these extending granulations, and fibrous tracts soon develop even in
the articulation itself, undergo calcification, and produce complete
anchylosis.

=Diagnosis.= The diagnosis is easy. The animal’s history and symptoms,
and the stationary character of the pain in the earlier stages are
sufficient to prevent any error.

=Prognosis.= The prognosis is grave, but not fatal. In the exudative
form recovery may follow early treatment. In the plastic form, however,
the chances of success are extremely meagre.

=Treatment.= It is easier to prevent than cure, particularly in these
forms of arthritis. The means are simple, and consist in always treating
the post-partum infection as soon as it is recognised. The animals can
be effectively safeguarded against later articular complications by the
free use of intra-uterine antiseptic injections, until the uterine
injuries have wholly healed, and by the administration of saline
purgatives and diuretics.

When infectious arthritis is diagnosed, it is still necessary to resort
to the same methods if the uterine symptoms persist, and to complete the
treatment by local applications.

The best method of local treatment seems to consist in puncturing the
articulation aseptically, removing almost all of the liquid exudate, and
immediately thereafter firing the skin covering the joint in points or
lines.

If treatment has been invoked too late, if plastic arthritis with the
formation of fibrous bands within the joint and destruction of the
cartilages and calcification of ligaments, etc., already exists, there
is no economic object in undertaking treatment. Fattening may be
attempted, or the animals may be handed over to the butcher, if wasting
is not too far advanced.

The use of cold douches, plaster bandages, blisters containing nitrate
of mercury, painting with sulphuric acid, etc., are too inconvenient and
too inefficient to be recommended in actual practice. Similarly, the
salicylate of soda, which is so useful in simple rheumatism, has no real
superiority over diuretics in this condition.


                           SCURVY-SCORBUTUS.

=Definition.= “Scurvy is a subacute or chronic trophic disorder
characterised by debility, inanition, anæmia, swelling and bleeding of
the gums, gingival ulceration, dropping of the teeth, and petechial or
more extensive hæmorrhages and exudations in the skin, serosa, and solid
tissues.”

=Causes.= “Among the lower animals, pigs especially suffer, when kept in
close, foul quarters and fed on a monotonous and insufficient ration.
Formerly scurvy ... was attributed to an exclusive diet of salt food; to
excess of sodium and deficiency of potassium salts; to the absence of
fresh vegetables; to tainted food, etc. In pigs the food and environment
are usually chiefly at fault, the subjects have been kept ... in foul
buildings, in a hot, moist atmosphere, and with an uniform diet of maize
or other unvarying and insufficient ration. Röll attaches great
importance to putrid food. Benion has found the affection mainly in
obese swine, the forced feeding and intestinal fermentations manifestly
operating as factors. Hess and others attribute the disease in pigs to
the germ of erysipelas. Stengel has produced purpuric disease in animals
by inoculation of the extravasated blood from human scurvy patients.
Muller and Babès found a slender bacillus and streptococci in the
tissues of scorbutic gums.... There is considerable presumption of the
existence of a microbian cause, the efficiency of which is dependent on
the unhygienic conditions above stated, while these unwholesome
conditions are equally non-pathogenic in the absence of the microbe.”

=Lesions.= “The blood is black and incoagulable or clots loosely, rigor
mortis is slight, changes may be found in the number and character of
the white and red blood globules, but are not constant; there is usually
an excess of sodium salts and deficiency of potassium ones, and there is
marked petechiation of the skin, mucosæ and serosæ. The bone marrow may
be abnormally red and the bones fractured at the epiphyses, or
carious.... The gums are softened, swollen, red and uneven, with
hæmorrhagic discoloration, erosions, necrotic areas and ulcers.”

=Symptoms.= “Anorexia or fastidious appetite, prostration, debility and
sluggish, indifferent movements, are followed by the local lesions on
the skin and gums. On the skin appear petechiæ and extravasations, which
often implicate the bristles, so that they may be shed or pulled out
with ease, the bulbs appearing dark and blood-stained (bristle rot).
These may be followed by necrotic sloughs, and deep ulcers that are slow
to heal. The gums are red and swollen, with hæmorrhagic spots, and bleed
on the slightest touch. Erosions, sores, and ulcers are not uncommon;
the tongue is dry and furred, and the mouth exhales a fœtid odour. The
teeth may become loose in their sockets. Swelling of the joints ... may
be noticed, and lameness or stiffness from muscular or intermuscular
extravasation. Blood effusions into ... the eye have been noticed, and
paralytic or comatose symptoms from similar effusions on the brain. In
the absence of improvement the patient becomes more and more debilitated
and exhausted, and death may be preceded by profuse exhausting
diarrhœa.”

“=Prognosis= is unfavourable in advanced cases, and when the faulty
regimen cannot be corrected.”

=Treatment.= “The first consideration is to correct the unwholesome
conditions of life, purify the building and its surroundings, and allow
a free range on pasture. Subject each patient to a thorough soapy wash,
and if possible allow clean running water in which a bath may be taken
at will. Access to green food and invertebrates (slugs, larvæ, etc.) is
important, or a varied diet of grain, middlings, bran, roots, fruits,
tubers, cabbage, silage, etc., must be furnished. Iron and bitters
(gentian, nux vomica) are useful, and sometimes small doses of arsenite
of soda solution or cream of tartar are useful. Acorns or
horse-chestnuts are recommended. For the mouth a wash of potassium
chlorate, soda biborate, or potassium permanganate may be resorted
to.... In the case of fat pigs it is more profitable to butcher at once,
as soon as early symptoms appear.” From Law’s “Veterinary Medicine,” p.
558, Vol. III.




                              SECTION II.
                  DISEASES OF THE DIGESTIVE APPARATUS.


                 SEMIOLOGY OF THE DIGESTIVE APPARATUS.

The group of diseases which affect the digestive apparatus is one of the
most important in bovine pathology, because almost all animals of the
bovine species are bred with the object of utilising to the full their
powers of digestion and assimilation.

Whether we consider adult fat animals, calves intended for slaughter or
milch cows, the object sought is always the same—_i.e._, to secure the
greatest possible economic return through the medium of the digestive
functions.

Even although in working oxen there is no tendency to overfeeding, the
animals remain none the less predisposed to diseases of the digestive
apparatus; the meal times are often too short, and rumination has to be
performed under the yoke or during work—in a word, under unfavourable
physiological conditions.

=Semiology.= To ensure correct diagnosis it is necessary here, perhaps
more than in any other department of pathology, to be capable of
grasping the symptoms or syndromes and signs afforded by the different
parts of the digestive apparatus; to know how to co-ordinate and group
them so as logically to deduce the final synthesis, the diagnosis. The
diagnosis proving correct, the prognosis becomes easy, and this is the
chief object from the economic standpoint. The practitioner who
undertakes treatment knows how to deal with the case, and the owner
likewise knows what he undertakes to do.

Although this classification may appear arbitrary, we shall consider
successively diseases of the mouth, of the pharynx, œsophagus, stomach,
intestines, etc., firstly describing the symptoms characterising these
diseases. At the same time we should state that many symptoms are common
to a large number of diseases and in themselves have absolutely nothing
characteristic. They are simply sign-posts capable of showing the way.

=Mouth.= External examination reveals the condition of the muzzle, the
lips and their commissures, and the surroundings of the buccal opening,
and detects the existence of any desquamation, rents, eruptions,
ulcerations, etc., which may be present.

In quiet animals the practitioner can examine the cavity of the mouth
single-handed, but in troublesome animals it becomes necessary to have
an assistant, who seizes the muzzle with one hand and the tongue with
the other, or who simply fixes the animal’s head. In exceptional cases
it will be necessary to secure the patient to a post, tree, or wall. The
mere attempt at examination will show whether there is trismus or
absolute freedom of movement in the jaws.

[Illustration: $1]

By introducing the fingers between the commissures and applying them to
the bars or to the free portion of the tongue, the practitioner will be
able approximately to estimate the local and general temperature. The
sensations experienced will also inform him of the degree of moisture or
dryness of the mouth and of its sensibility.

On separating the jaws, he will note the odour exhaled and its possible
abnormalities—its acid, sourish, fœtid, or putrid character. He will
directly observe any anæmia or hyperæmia of the mucous membrane, from
the inner surface of the lips and cheeks up to the soft palate, although
owing to the thickness of the buccal epithelium it is not always easy to
estimate anæmia or hyperæmia in the ox. The surface of the tongue should
also be examined, and a note made whether it appear dry, pasty, dusty,
sooty, etc., though these appearances are occasionally apt to lead one
astray. The observer should also inquire regarding want of appetite,
depraved or exaggerated appetite, etc.

Even the manner in which the animal picks up its food will serve to
direct his attention to the development, or possible existence, of some
disease of the mouth, although want of appetite is not always
characteristic of a lesion in the pharynx or œsophagus, but sometimes of
a lesion in its neighbourhood, like hypertrophy of the retro-pharyngeal
or bronchial lymphatic glands.

This examination will also detect the existence on the lips of wounds,
cuts, injuries or specific eruptions (aphtha, tuberculous ulcerations,
the ulcerations of gangrenous coryza, etc.) on the gums indications of
gingivitis, periostitis, mercurial poisoning, actinomycosis of the
maxilla, and ulcerations of all kinds; on the tongue, of wounds, of
simple or specific inflammatory eruptions (aphtha, the ulcerations of
actinomycosis, tuberculosis, gangrenous coryza, etc.), as well as the
swellings due to superficial or deep-seated glossitis. By the same
method of examination, though with somewhat more difficulty, one can
detect abnormal mobility, irregularity of development, caries, etc., of
the teeth, the condition of the excretory ducts of the salivary glands,
the state of the hard and soft palate, and the existence of fissures,
vegetations, polypi and tumours.

[Illustration: $1]

=Salivary glands.= The salivary glands, particularly the parotid and
submaxillary, should be examined by direct inspection and palpation.

Direct inspection reveals the existence of swellings, deformity of
parts, increase in salivation, or ptyalism, which sometimes occur in
conjunction with foot-and-mouth disease, actinomycosis, acute stomatitis
and mercurial poisoning, as well as increase in size of the salivary
ducts.

Palpation reveals the degree of sensibility of the parts, the existence
of œdema, induration, cysts, and, more frequently, distension of the
salivary ducts as well as the presence of calculi, tumours, the
direction of fistulæ, etc.

Difficulties may occur, particularly when the submaxillary and parotid
glands are affected; but methodical and complete examination will
usually enable one to differentiate the conditions.

=Pharynx.= The pharynx may be examined externally by inspection and
palpation, and internally by direct digital palpation. Inspection
reveals possible deformities of the region of the gullet, palpation the
condition of the tissues as well as abnormal sensibility and
infiltration. Internally, digital examination must be cautiously
conducted, and after a strong gag has been securely inserted in the
mouth. Under such conditions it is without danger. The hand being
inserted exactly in the median line will detect obstructions which may
already have been partly identified by external palpation, as well as
the existence of inflammation with or without the formation of false
membranes, and of ulcerations, polypi, etc.

=Œsophagus.= In consequence of its anatomical formation, situation and
course, the œsophagus may be divided into two distinct parts—viz., the
cervical, which can be examined from the outside, and the thoracic,
which cannot so be examined.

The cervical part may be examined by inspection, by palpation from one
side, or by palpation with both hands and from both sides.

[Illustration: $1]

Inspection leads to the detection of changes in the shape of the
œsophagus and of the jugular furrow. In fat subjects, however, it is of
little value. As the position and the course of the œsophagus are known,
unilateral palpation, or, better still, bilateral palpation, employing
both hands, is of very much greater service. These methods reveal the
presence of swellings, infiltrations, changes in shape and sensibility,
the presence of foreign bodies, the existence of dilatations or
contractions of the tube, etc.

Auscultation and percussion, though recommended by some practitioners,
are not of much service.

Inability to swallow, due to change in the œsophagus, is also detected
by inspection. Its existence suggests a number of possible conditions,
such as fissure or ulceration of the œsophagus, compression in the
mediastinal region as a result of tuberculous or other disease,
contraction or dilatation of the œsophagus, etc. Furthermore, inspection
will betray the existence of dilatation of the tube, to which vomiting
and regurgitation of food are sometimes due.

Internal exploration is the only method of detecting changes in the
thoracic portion, and may also be utilised to locate lesions in the
cervical region. It is practised by passing a sound of small calibre or
any flexible cylindrical object, such as a cart rope, etc. The patient
must be fixed with the head extended on the neck and a proper gag or
speculum introduced into the mouth. Exploration assists us in
recognising the existence of inflammation of the œsophagus, true or
false contraction, dilatation and the presence of obstructions.

In animals of the bovine species all these lesions—viz., inflammation of
the œsophagus, fissuring and ulceration, obstructions, compressions,
dilatations and contractions of the tube—although not very frequent, are
nevertheless from time to time encountered.

=Stomach.= Exploration of the stomach or of the different gastric
compartments presupposes an exact knowledge of the respective positions
of the different reservoirs. Topographical anatomy shows that the rumen
is situated in the left flank, and that it occupies the whole of the
left abdominal region from the diaphragm to the pelvic cavity. As a
consequence, it may be explored from the region of the twelfth rib; it
is inclined slightly from above downwards, and from left to right, its
extreme right border extending as far as, or a little beyond, the white
line.

The reticulum, the smallest of the four reservoirs, is situated in the
sub-ensiform region at right angles to the median plane of the body. On
the left it touches the rumen and the diaphragm; on the right side it is
in contact in front with the diaphragm, above with the omasum, and to
the right and towards the rear with the abomasum. The omasum is situated
above the reticulum and conical right portion of the rumen; in front it
touches the liver, and towards the back and left the rumen. The abomasum
is situated obliquely in the right hypochondriac region, its anterior
surface resting on the lower wall of the abdomen towards the middle and
right side of the body, its pyloric portion extending upwards, behind
the right hypochondriac region.

=Rumen.= The rumen can be examined by inspection, palpation, percussion,
and auscultation. The use of the œsophageal sound and of the trocar and
canula is also of value in diagnosis.

Inspection affords information of a varying character, according to the
moment when it is practised, even in a condition of health. It only
extends to the condition of the flank before or after a meal, etc.,
emptiness of the rumen being accompanied by hollowness of the flank, and
distension, following an abundant meal, by fulness in this region.

When digestion is not proceeding normally, the flank may be distended
unduly by gaseous accumulations or by the presence of solid food. In
abdominal and mediastinal tuberculosis and in gastro-enteritis there may
be simple tension or slight dilatation. When indigestion or enteritis is
entering on a favourable stage, the flank may appear hollow, and in
cases of chronic diarrhœa it may appear retracted.

[Illustration: $1]

Digital examination or palpation may be practised over the entire region
of the flank. It shows whether the rumen is full or empty, reveals the
consistence of the contained food in cases of chronic indigestion, the
sensibility of the walls, and the rate and order of the muscular
contractions. Direct or indirect percussion may be carried out on a
horizontal line from the twelfth rib as far back as the flank, and
vertically from the lumbar vertebræ to the white line. In health one
discovers in young animals an upper zone of normal resonance due to gas,
a zone of semi-dulness and an inferior zone of absolute dulness, due to
the liquids in the rumen. The spleen, which is attached to the
supero-anterior surface of the left side of the rumen, does not
seriously restrict the area open to percussion.

In pathological conditions percussion from above downwards may produce a
tympanitic sound, due to gaseous indigestion or a clear sound throughout
the greater portion of the vertical diameter suggestive of acute
gastro-enteritis with the formation of gas in the rumen, or of adhesive
peritonitis preventing the rumen from collapsing. Indigestion due to
excess of solid food, on the contrary, is characterised by a dull sound
throughout the entire region from above downwards. Percussion along a
horizontal line permits of the delimitation of certain zones which vary
a great deal in area, according to the case.

Auscultation is more instructive than percussion. Like percussion, it
may be practised throughout the entire depth of the abdomen, from the
transverse processes of the lumbar vertebræ as far as the white line,
and in a horizontal direction from the eleventh rib to the region of the
flank.

Auscultation of the upper zone enables one to detect sounds of
deglutition, gurgling sounds (glou-glou), and a sound resembling falling
water, due to the movement of solids or liquids in the rumen and
reticulum. The sounds heard vary in different cases, and depend on the
state of repletion or of emptiness of the rumen.

Auscultation of the middle zone reveals:

Firstly, a very special crepitation sound, which may be compared to the
deflagration of a handful of salt thrown on burning coal. It is believed
to result from the bursting of bubbles in the contents of the rumen
under the action of normal digestion.

Secondly, a churning sound produced by the rhythmic peristaltic
contractions of the rumen, by which the substances ingested are very
intimately mixed. By applying the ear over the flank region or by
palpation the rhythmic contractions of the rumen, two per minute in most
cases, can readily be perceived.

In practice examination of the rumen is confined to these four methods.

=Puncture.= From an exclusively scientific point of view, exploration of
the rumen also comprises analysis of the gas collected through puncture
and analysis of the liquids removed by aspiration (first stages of
gastric digestion). Normally, these gases, in the order of their
abundance in the mixture, consist of the following: Carbonic acid,
carburetted hydrogen and nitrogen.

In disease, and in most cases of abnormal fermentation, the carburetted
hydrogen is greatly in excess of the carbonic acid. In chronic
gastro-enteritis, ammonium sulphide and other offensive gases are found
in addition.


=Chemical analysis.= In the rumen the ingested food is macerated in an
alkaline liquid at a temperature of 100° to 101° Fahr. (the alkalinity
is due to the saliva). This process markedly modifies the composition of
the ingested matter. Nevertheless, the upper portion in contact with the
gas sometimes presents a slightly acid reaction, probably due to
carbonic acid. The sugary and fatty materials contained in the food
respectively undergo lactic and butyric fermentation. Only a small
quantity of the starch, however, is transferred into sugar. In the calf,
and in very young animals, the reaction of the rumen is acid throughout
the entire period of sucking. In disease, when rumination has long been
suspended and chronic loss of appetite or gastro-enteritis exists, the
reaction is generally acid. The sugars, gums, and soluble salts of
forage, roots, etc., are dissolved in the rumen, but fatty materials
undergo no modification.

The reticulum, which is the smallest of the gastric compartments, is
situated in the sub-ensiform and retrodiaphragmatic regions, extending
right and left of the middle line to a nearly equal distance. Above and
to the left it communicates freely with the rumen, to the right with the
omasum.

In practice it can only be examined in two ways: inspection and
palpation.

By inspection changes in the configuration of the ensiform region may
sometimes be detected. Such changes are rare, and must be distinguished
from congenital deformity. They sometimes accompany inflammation of the
reticulum produced by a foreign body, when the lower abdominal wall is
directly perforated by such body.

In cases of inflammation of the reticulum due to foreign bodies, abscess
formation, perforation, etc., it is possible to detect œdematous
infiltration, abnormal sensibility, fluctuation and increased heat,
etc., by manipulating the parts with the fingers or the clenched fist.

If the evidence pointing to the presence of a foreign body in the
reticulum is considered sufficient, gastrotomy may be performed and the
interior of the viscus examined with the hand, but although the
operation is possible it is very rarely practised.

=Omasum.= The omasum occupies, so to speak, a position inverse to that
of the reticulum, lying deep down on the right side, behind the
diaphragm, under the hypochondrium, and above the abomasum and
reticulum.

It is the only gastric compartment which cannot be examined, although
when impacted it may be felt on the right side.

=Abomasum.= The abomasum is lodged in the lower part of the right flank
under the circle of the hypochondrium. It extends obliquely from below,
upwards from the sub-ensiform to the sublumbar region. The smaller
curvature is turned towards the rumen on the left side; the larger
curvature is in contact with the abdominal wall. In spite of what has so
often been stated by those who have never seen it, the abomasum can be
examined and is accessible along the circle of the hypochondrium.

In adults useful information can rarely be obtained by inspection; but
in sucking calves the abomasum, if distended by indigestion,
gastro-enteritis, etc., sometimes appears prominently in the right
abdominal region. Palpation with the fingers or with the fist will
detect exaggerated sensibility, irritation, inflammation, or distension.

Percussion and auscultation furnish no very precise information. The
information obtained by the above-described examination of the stomach
is in practice amplified by a search for certain symptoms which are
usually easy to detect. They comprise:

(_a_) Suppression or irregularity of rumination. This very important
symptom suggests the degree of gravity of the digestive disturbance, and
to some extent the gravity of the general condition. Suppressed
rumination is a common symptom in many diseases, some of which are
purely digestive, though all are not. It is, however, a grave sign in
most cases.

(_b_) Eructation, which is usually frequent, may be regarded as normal
provided the exhaled gas preserves the fresh odour of grass or of the
food swallowed, like brewers’ grains, turnips, etc. Sometimes the gas is
sour, acid, fœtid, or putrid, all of which conditions indicate disease.

(_c_) Yawning is not common. It becomes frequent and attracts attention
in certain abnormal conditions; in others, again, it may be completely
suppressed.

(_d_) Nausea and vomiting are rare. Vomiting is commoner in calves, and
results from inability to digest the milk, or simply to over-distension
of the abomasum. The matter vomited by adults usually consists of partly
masticated food, and is derived from the rumen; while the contents of
the abomasum are occasionally rejected, in which case the material is of
pulpy consistence and has an acid smell.

(_e_) Digestive disturbance is sometimes accompanied by various
modifications in the breathing, such as immobilisation of the
hypochondriac region and of the diaphragm; abnormal sensibility and
reflex coughing on palpation, and, in inflammation of the reticulum due
to foreign bodies, costal respiration.

[Illustration: $1]

It is by methodically observing, grouping, and classifying the symptoms
presented that one is enabled to detect the links connecting them.

=Intestine.= The intestinal mass is contained in the right half of the
abdomen above the compartment of the stomach. The large intestine
occupies the upper zone, corresponding externally with the hollow of the
flank from the thirteenth rib to the haunch. The small intestine
occupies the middle zone from the thirteenth rib to the entrance to the
pelvis and the stifle region; the inferior zone is occupied by the rumen
and abomasum, and in pregnant females by the gravid uterus.

Notwithstanding these indications it is somewhat difficult to examine
the mass of the large intestine, separated as it is from the abdominal
wall by the =U=-shaped inflection of the duodenal loop, of which the
deep retrograde branch is in contact with the terminal portion of the
floating colon.

Inspection of the right flank furnishes no information of value in
diseases of the intestine, nor is auscultation of much service beyond
enabling one to detect the frequency, diminution, or absence of
borborygmus. Palpation alone is really of service. Practised gently and
superficially with the tips of the fingers it detects abnormal
sensibility in acute cases of enteritis; when with more energy,
palpation reveals whether the bowel be full or empty, provided that the
muscular resistance be not too marked.

=Colic.= In colic the clinical signs, their varieties, and the lesions
which give rise to them are of much more importance. When it results
from intestinal congestion _à frigore_ (due, for example, to the
ingestion of cold water), colic is usually violent, sudden, and of
relatively short duration. In other cases it is violent and prolonged
for several hours, a whole day, or even two days, and may be followed by
coma and suppressed peristalsis; it then indicates invagination,
volvulus, or strangulation. Sometimes, on the contrary, it remains dull
and is slow and continued (acute gastro-enteritis, hæmorrhagic
gastro-enteritis, etc.).

Finally, colic of the latter character may, in addition, be accompanied
by icterus, in cases of retention of bile, biliary calculi, hepatitis,
etc.

=Anus.= Examination of the anus is easy. Simple inspection reveals its
presence or absence, and consequently the existence of congenital rectal
atresia, which is somewhat common in calves and colts. Digital
exploration is, however, sometimes useful, for in occasional cases an
anus may exist, which externally appears normal, but terminates in a
sac, the rectum being closed by a membranous partition.

Nothing is easier to recognise than tenesmus; it occurs in cases of
profuse diarrhœa, diarrhœa of calves, and dysentery in newly-born
animals.

[Illustration: $1]

=Rectal exploration.= Exploration of the rectum is a last and most
valuable means of confirming the diagnosis in all visceral diseases of
the pelvis and abdomen. To utilise this method to the full, the rectal
pouch should first be thoroughly emptied by the free use of enemata, the
subsequent examination being made with great care. The animal’s hind
legs being secured, the operator smears his hand and forearm with some
fatty substance, and, forming the fingers into a cone, introduces them
with gentle pressure through the anus, the palm of the hand being turned
downwards. Passing the hand gently along the rectum, the operator will
be able to distinguish the conical posterior pouches of the rumen, the
loop of the duodenum, the mass of convolutions of the small intestines
and of the colon, etc. Next, he will examine the vagina, uterus,
bladder, ureters, kidneys, aorta, and the pelvic and sublumbar lymphatic
glands. He may be able to recognise distension of the rumen with food,
twists of the intestine, herniæ, mesenteric or diaphragmatic
invagination or volvulus of the bowel, etc.

In other cases he may be able to discover lesions of the kidney, of the
uterus, of the broad uterine ligaments, of the ovaries, or of vessels.

In all cases it is desirable to make a methodical and complete
examination, whatever the primary object may have been. Such an
examination may be carried out as follows: The operator having
introduced his hand into the rectum, begins by examining the state of
the pelvic organs, the rectum, base of the vagina, the body and horns of
the uterus, the bladder and the lymphatic glands and ligaments of the
pelvis.

By laying the hand flat in the rectum and pressing gently downwards the
anterior border of the pubis may be felt, somewhat more deeply placed.
The rectum is then thrust slightly to the right, and the ascending
branch of the right ilium, as high as the sacro-iliac articulation, and
the lower surface of the sacrum, are directly examined; lastly, the hand
is directed towards the left, gliding down the left ilium, and returning
to the point of departure. In this way the state of the pelvic floor, of
the arteries, veins, and lymphatic glands, etc., the degree of mobility,
tension, or fulness of the uterus, as well as the condition of the broad
ligaments, are all ascertained.

Still more deeply placed, and at the extreme limit to which the arm can
be introduced, will be found some or all of the above-mentioned
organs—viz., the small intestine, large intestine, kidney, etc.

=Defæcation: Examination of the fæcal material.= The character of the
fæces is very important in certain diseases; _e.g._, diarrhœa assumes a
varying importance, according as the discharges are of an alimentary,
serous, mucous, or sanguinolent type, and are slight, temporary,
intense, profuse, or continued. In other cases defæcation is slow,
becomes difficult, and various degrees of constipation exist. Defæcation
may be completely suppressed, as in invagination or strangulation of the
intestines; on the other hand, one may observe diarrhœa, dysentery
(microbic or sporozoic diarrhœa), and intestinal hæmorrhage. The last
named may be of varying degrees of acuteness, from the passage of simple
drops or streaks of blood, distributed over almost normal excreta, to
the passage of unchanged blood in liquid jets or in clots.

=Macroscopic examination.= Macroscopic examination takes cognisance,
firstly, of the quantity (40 to 80 lbs.), consistence (firmness or
softness), colour (olive green, blackish green, greyish black, sooty, or
tarry) and odour (normal, fœtid, putrid, etc.) of the fæces.

Sometimes the excreta are moulded and covered with glairy mucus, or
contain such abnormal products as undigested food (a sign of chronic
diarrhœa), false membranes, false membranes due to pseudo-membranous
enteritis, fibrinous clots, or parasites like liver flukes, tæniæ and
strongyles.

=Microscopic examination.= Microscopic and bacteriological examination
is sometimes useful; and even when macroscopic examination has revealed
nothing, it is possible to detect the presence of the eggs of parasites
like flukes, strongyles, hooked worms, etc., the presence of sporozoa
(as in intestinal coccidiosis) and of specific microbes, as in the
diarrhœa of calves, etc.

It is only by the synthesis of methodically collected signs that one
finally succeeds in exactly diagnosing the numerous diseases which may
affect the intestine: intestinal congestion, invagination, volvulus,
intestinal strangulation (mesenteric or diaphragmatic herniæ, etc.),
atresia of the anus, acute or hæmorrhagic enteritis, or intestinal
helminthiasis.

=Liver.= The liver is situated in the right sublumbar region. It is
fixed behind the diaphragm and under the hypochondriac region, and
extends from the ninth to the thirteenth rib. It can be examined by
palpation through the last intercostal spaces and behind the thirteenth
rib. In health it is difficult to pass the fingers sufficiently under
the hypochondriac circle to reach the liver; but in case of morbid
hypertrophy it extends more or less beyond the last rib, and palpation
between the last ribs sometimes reveals abnormal sensibility.

Percussion better than palpation enables one to delimit the space
occupied by the liver, particularly towards the back, where there is no
interposed layer of lung. Percussion is especially useful in detecting
hypertrophy due to cancer, tuberculosis, echinococcosis of the liver,
etc., or hepatic atrophy. In isolated cases icterus may exist,
confirming the conclusions otherwise arrived at.

=Pancreas.= The pancreas is situated rather deeply in the right
sublumbar region, below the kidney, behind the liver, above the floating
colon, and within the duodenal loop. It is therefore very difficult to
examine; moreover, the diseases which affect it are still little
understood.

The point most prominently brought forward by this demonstration of the
topographical anatomy and semiology of the digestive apparatus is the
difficulty of accurately diagnosing digestive diseases in the ox when
one confines oneself to a superficial examination. To have any chance of
arriving at an exact diagnosis, methodical and thorough examination is
indispensable. Given this condition, accurate diagnosis becomes
possible, despite all difficulties.




                               CHAPTER I.
                         DISEASES OF THE MOUTH.


                              STOMATITIS.

=Definition.= By stomatitis we mean inflammation of the buccal mucous
membrane. Stomatitis may be simple—_i.e._, due to accidental causes, to
varying local forms of irritation, or to wounds; or, on the contrary, it
may be specific, of infectious origin, like the stomatitis of
foot-and-mouth disease, gangrenous coryza, cattle plague, etc.; or,
finally, it may be of toxic origin, like the stomatitis of mercurial
poisoning.

Here we shall only study the simple forms of stomatitis, the gangrenous
stomatitis of calves, and mercurial stomatitis. The others will be
noticed in speaking of the diseases of which they form one of the
symptoms.


                           SIMPLE STOMATITIS.

=Causation.= Simple stomatitis of bovine animals is often due to feeding
with rough forage, or forage containing prickly or spiny plants, like
thistles, sea holly, eryngo, etc. Sometimes it follows prolonged
irritation by rough teeth, premolars or stumps, or accompanies the
shedding of the temporary molars. Ingestion of irritant plants like
nettles, certain specimens of the orders _Labiatæ_ and _Umbelliferæ_,
leaves covered with vesicant insects, cabbage and turnip leaves infested
with aphides, oil beetles, etc., or the swallowing of hot liquids, may
also, though more rarely, produce it. Finally, in grave diseases of the
digestive apparatus, the buccal mucous membrane may secondarily become
affected.

=Symptoms.= The primary symptoms are usually represented by ptyalism and
a certain difficulty in grasping food. In other cases the mucous
membrane appears slightly dry for some time before salivation sets in.
On introducing the fingers into the animal’s mouth some elevation of
temperature may be noted, and on direct inspection the non-pigmented
regions are seen to be abnormally vascular, a fact which has earned for
this form of stomatitis the names of “erythematous” and “erysipelatous
stomatitis.”

If the stomatitis is due to local multiple irritation, such as results
from spines and prickles in the food, the abnormal vascular appearance
is confined to the neighbourhood of the abrasions or punctures, and the
affected regions are of very varying size. In some cases, principally as
a consequence of trifling local irritation and of burns of the first and
second degree, blisters of varying size may develop and break, leaving
behind ulcerations, which, however, always heal rapidly. The aphthous
non-contagious stomatitis mentioned by certain authors seems most
probably to pertain to this class.

=Diagnosis.= The diagnosis is usually easy, and a little attention to
the accompanying symptoms is sufficient to avoid confusion with the
various forms of symptomatic stomatitis.

=The prognosis= is favourable.

=Treatment= is based on removal of the determining cause, if this can be
recognised, withdrawal of rough forage, removal of sharp points on the
teeth, extraction of stumps, etc. As a rule, recovery follows rapidly.
It can be hastened by washing out the mouth directly, or by means of a
syringe, with water containing honey, vinegar, decoctions of brier
twigs, oak bark, barley or rice. This treatment is completed by
supplying nourishing gruel and food demanding little mastication.


                     CATARRHAL STOMATITIS IN SHEEP.

“The more delicate buccal mucosa in these animals would render them more
subject to inflammations, but this is more than counterbalanced by the
mode of prehension of aliments, not by the tongue, but by the
delicately-sensitive lips, and further by the daintiness and care with
which these animals select their food. The =treatment= would not differ
materially from that prescribed for the ox.” (Law’s “Veterinary
Medicine,” Vol. II. p. 15.)

[The treatment referred to consists of simple astringent and antiseptic
washes, borax given in the drinking water, or mixed with honey or
treacle and smeared occasionally on the tongue. Washes of sodii
hyposulphis or sulphis, or even weak solution of carbolic acid, may be
used after the irritant cause has been removed. Vinegar or diluted
mineral acids may be used alternately with decoctions of blackberry bark
or other vegetable astringents. When there are symptoms of gastric
disorder a laxative, followed by vegetable bitters and other tonics, may
be prescribed. Foreign bodies—thorns, wire, etc.—fixed in the tongue,
cheek, or palate should be searched for and removed at the first
examination of the patient.]


                    NECROSING STOMATITIS IN CALVES.

=Definition.= This name is applied to a special stomatitis, which in
very young animals produces superficial necrosis of more or less
extensive areas of the buccal mucous membrane, and sometimes of
subjacent parts.

The disease, although somewhat rare in France, has been mentioned by
Lafosse and well studied by Damman and Lenglen.

=Causation.= Its cause is still imperfectly understood. Some regard it
as a consequence of insufficient nourishment, of disturbance resulting
from dentition, of general exhaustion, and of bad hygienic conditions.
These explanations are scarcely sufficient, however, and at the present
time there is a tendency to regard it as a complication of primary
grave, debilitating diseases, like the diarrhœa of calves, omphalitis,
omphalo-phlebitis, etc. Moussu has never seen it apart from omphalitis,
and he considers the lesions due to the action of the bacillus of
necrosis. Infection occurs through the umbilicus becoming soiled by
contact with the litter.

The early symptoms consist in loss of appetite, congestion of the mucous
membranes, and salivation. Early examination of the buccal cavity
reveals the presence everywhere, except on the palate, of whitish-grey
or yellowish patches, whose aspect is markedly in contrast with that of
neighbouring parts. These are fragments of the mucous membrane
undergoing necrosis. They are numerous, are surrounded by a narrow
inflamed zone, and may be from ½ inch to 1 inch in diameter.

Necrosis advances rapidly, and extends throughout the thickness of the
mucous membrane; the slough soon becomes delimited and separates. The
odour of the mouth is then absolutely fœtid, and the saliva appears
streaked with pus and blood.

The ulcerations exhibit a livid base, and show no tendency to heal.
Necrosis extends in depth, and affects the muscles, tendons, and even
the periosteum and the bones. The teeth are frequently loosened.

Grave complications, such as pharyngitis, broncho-pneumonia, infectious
enteritis, and septicæmia soon appear, and the animals are carried off
by septic infection and intoxication in a few days—at the longest in a
week.

=Diagnosis.= The diagnosis is only difficult at first; and, at a later
stage, the only mistake possible is that of confounding the condition
with a very grave attack of aphthous stomatitis. Local sanitary
conditions are sufficient to secure the avoidance of this error.

=Prognosis.= The prognosis is extremely grave; the disease usually
results in death; recovery is exceptional. Very luckily the disease
seems to become rare in direct proportion as the hygienic conditions of
cattle breeding and keeping are improved.

=Treatment.= Curative treatment always appears to be ineffectual when a
grave primary disease has already enfeebled the animal before necrosing
stomatitis appears. In those cases where the stomatitis constitutes the
primary condition, attempts should be made as far as possible to cleanse
the wounds. The buccal cavity should be thoroughly washed out, and the
wounds then cauterised with solution of carbolic acid of 6 per cent.
strength, nitric acid of 10 per cent. strength, hydrochloric acid of 7
to 8 per cent. strength, or chromic acid of 20 per cent. strength.

This local cauterisation is performed with a tampon of cotton wool fixed
to a handle; for necessarily it is impossible to apply any dressing
whatever of a permanent nature. The cauterisations may be repeated twice
a day. The stump of the umbilical cord should never be forgotten, for it
sometimes contains a mass of necrotic tissue the size of a man’s thumb.
It should be thoroughly cleansed and the wound plugged with a mixture of
iodoform and boric acid.

This treatment will not avail unless the functions are stimulated by
rich food that can be easily masticated and digested, and by giving milk
of good quality, or boiled milk, eggs, meat-powder, cooked beans, etc.
Aromatic infusions and hay tea containing coffee and small quantities of
alcohol or tincture of quinine are also of service.


                     MYCOTIC STOMATITIS IN CALVES.

_Thrush. Muguet._

“This is a form of stomatitis manifested by a raised white patch on the
mucous membrane and determined by the presence of the _Oidium albicans_
(_Saccharomyces albicans_), a cryptogam discovered by Berg in 1842 in
thrush in children. It is closely allied to the _mucor_, and attacks
only the young and feeble. The white crust consists of epithelial cells
intermingled with an abundance of the white mycelium and oval spores of
the fungus. Andry in his artificial cultures found that it was pearly
white when grown on gelatine, dirty white on potato, and snow white on
carrot.”

=Symptoms.= “Buccal mucosa, red, congested and tender, shows here and
there white curdy looking elevations, or red erosions caused by the
detachment of such masses. These bear a strong resemblance to the crusts
seen on this mucosa in rinderpest, but are easily distinguished by the
absence of the attendant fever, and by the discovery, under the
microscope, of the specific microphyte. The eruption may extend to the
pharynx and œsophagus and interfere fatally with deglutition, but
usually it merely renders sucking painful and is not serious.”

=Treatment.= Cleanse and disinfect the sheds, “and invigorate the young
animals by sunshine, free air and exercise. Locally ... borax, which
arrests the growth of the parasite, whether in artificial cultures or in
the mouth. The powder may be rubbed into the sores, or it may be mixed
with ... molasses and used as an electuary. As substitutes boric acid,
salol, thymol, potash chlorate, or Condy’s fluid may be used.” (Law’s
“Veterinary Medicine,” Vol. II. p. 36.)


                    ULCERATIVE STOMATITIS IN SHEEP.

The name of ulcerative stomatitis of sheep has been given to a disease
which is characterised by the appearance of a pultaceous deposit on the
surface of the buccal mucous membrane and later by the development of
ulcerations and of vegetative growths.

=Causation.= The cause is imperfectly understood. In certain years the
disease appears to attack lambs at the time of weaning, but it may also
affect flocks of animals as old as fifteen or eighteen months, two
years, or even more. It is contagious, and may extend to one-half or
two-thirds of the entire number in the flock. Full-grown and old animals
appear to be immune.

It was formerly thought, _à priori_, and in consequence of the character
of the buccal deposit, that the disease was identical with thrush, and
that the lesions were produced by _Oidium albicans_. Neumann in 1885
declared, however, that he could not find the fungus in question in
scrapings from the mucous membrane.

Moussu had similar negative results in the experiments he made during
1894, when he examined both young and old animals belonging to flocks in
the departments of Berry and of La Brie.

In addition it has been suggested that the disease affects badly
cared-for and badly fed lambs, and subjects suffering from “watery
cachexia.” This seems correct in many cases, and Moussu has seen
ulcerative stomatitis decimate flocks which had previously been attacked
with intestinal helminthiasis and verminous broncho-pneumonia; but, on
the other hand, in the environs of Melun he saw it in animals which had
previously been quite free of disease and were kept under perfect
hygienic conditions.

The conditions in which animals are reared, the use of common drinking
ponds, and the method of supplying flocks with food, are the chief
causes of the distribution of the disease.

=Symptoms.= The symptoms consist in loss of appetite, or rather in
difficulty in grasping and masticating food, wasting, a certain degree
of dulness, and salivation. Somewhat later one often sees appear on the
free margin of the upper and lower lips an eruption of small
vesico-pustules, which quickly become covered with yellowish-brown
crusts and bleed on the slightest touch. The lips swell, become
sensitive and painful, so that examination of the cavity of the mouth
should be made with care. The mucous membrane is then seen to present a
very varying number of greyish-white or greyish-brown points, each of
which is due to the destruction of the epithelium and to the production
of a pultaceous deposit, which can very readily be removed, leaving
uncovered superficial ulcerations, which bleed if very lightly touched.
These ulcerations are of irregular shape, and are distributed most
freely over the gums, the internal surface of the lips and cheeks. The
palate and tongue are only invaded in the last stages. Still later one
notes, instead of these ulcerations and as a consequence of
abnormalities in the process of repair, reddish-violet turgid
vegetations varying in size from that of a millet seed to that of a
pepper-corn or even of a small mulberry.

The total duration of the disease varies with its degree of intensity.
In favourable cases it may not exceed eight to ten days; in grave cases
it continues for fifteen to twenty days. Recovery is usual when the
subjects are vigorous and well-nourished lambs, or well-kept sheep,
previously free of disease. On the other hand, Moussu has noted a
mortality of 15 to 20 per cent. in thin animals of bad bodily condition
and already depressed by verminous broncho-pneumonia and intestinal
helminthiasis. When the attack is about to prove fatal, complications
such as gastro-enteritis, resulting from septic infection or
intoxication, and accompanied by fœtid diarrhœa, often make their
appearance.

=Diagnosis.= The diagnosis presents no difficulty, the characteristics
of this stomatitis being entirely different from those of the aphthous
form. The claws are never affected, and there is no lameness.

=Prognosis.= In this connection the practitioner will do wisely to avoid
committing himself, and to closely study the conditions under which the
disease has developed. In all cases the appearance of fœtid diarrhœa
must be regarded as of very unfavourable augury.

=Treatment.= The first precaution to take consists in separating all the
healthy animals in the flock, and placing them in a non-contaminated
spot.

The diseased are then treated one by one; each day the buccal cavity is
washed out with boiled water or with a solution of borax or boric acid.
After each washing the ulcerations should be touched with tincture of
iodine or with some other rather active antiseptic solution. Finally it
might be useful, and would be of value, to add to the gruel or water a
small quantity of common salt and of salicylate of soda at the rate of
15 grains to the pint.


                 GENERAL CATARRHAL STOMATITIS IN SWINE.

=Causes.= “Swine suffer from simple stomatitis when exposed to thermal,
mechanical, or chemical irritants. Such irritants comprise food that is
too hot, or is hard and fibrous, or which contains spikes and awns,
capable of entering and irritating gland ducts or sores, or food which
is fermented or putrid, food or medicine of an irritant character. The
habit of catching and holding swine with a running noose over the upper
jaw, and the forcing of the jaws apart with a piece of wood in search of
the _Cysticercus cellulosa_ are further causes. In several specific
infectious diseases inflammation of the mucous membrane, with eruption
or erosion, is not uncommon. This aphthous fever is marked by vesicular
eruption, muguet by epithelial proliferation and desquamation, hog
cholera and swine plague by circumscribed spots of necrosis and erosion.
Patches of false membrane are not unknown, and local anthrax, tubercle,
and actinomycosis are to be met with. Inflammation may start from
decaying teeth.”

“=Symptoms= resemble those in other animals, refusal of food, or a
disposition to eat sparingly, to select soft or liquid aliments, to
swallow hard materials half chewed, or to drop them, to champ the jaws,
and to seek cold water. Accumulation of froth around the lips is often
seen, and the mouth is red, angry, dry, and hot, and exhales a bad
odour.”

“=Treatment= does not differ materially from that adopted in other
animals: Cooling, astringent, antiseptic lotions, honey and vinegar, and
in case of spongy or eroded mucosa, tincture of myrrh daily or oftener.
Soft feeding, gruels, pulped roots, ... and clean water should be
constantly within reach. In case of ... indigestion a laxative, followed
by vegetable tonics, will be in order.” (Law’s “Veterinary Medicine,”
Vol. II. p. 17.)


                    ULCERATIVE STOMATITIS IN SWINE.

“This is the scorbutus of Friedberger and Fröhner, the glossanthrax of
Benion.”

=Causes.= “It has been attributed to insufficient or irritant food, to
damp, close pens, and to chronic debilitating diseases, and all these
act as predisposing causes. In gastritis and in infectious fevers like
hog cholera, swine plague, and rouget (hog erysipelas) the spots of
congestion and petechiæ on the buccal mucous membrane may become the
starting points for ulcerative inflammations. These conditions appear,
however, to be supplemented by infection from bacteria present in the
mouth or introduced in food and water, and, as in the case of other
domestic animals, the most successful treatment partakes largely of
disinfectant applications.”

=Symptoms.= “Loss of appetite, grinding of the teeth, champing of the
jaws, the formation of froth round the lips, fœtor of the breath,
redness of the gums and tongue, and the formation of vesicles, or white
patches, which fall off, leaving red, angry sores. These may extend,
forming deep unhealthy ulcers, with increasing salivation and fœtor. As
the disease advances the initial dulness and prostration become more
profound, and debility and emaciation advance rapidly. Unless there is
early improvement an infective pharyngitis or enteritis sets in,
manifestly determined by the swallowing of virulent matters from the
mouth, and swelling, redness, and tenderness of the throat, or colics
and offensive black diarrhœa, hasten a fatal issue. Rachitis may be a
prominent complication, as it seems in some instances to be a
predisposing cause.”

=Treatment.= “Isolate the healthy from the diseased, and apply
disinfection to all exposed articles and places. Employ local
antiseptics as in other animals. Sulphuric or hydrochloric acids, in
fifty times their volume of water, or tincture of iron, chlorate of
potash, or chloride of ammonia, or borax have been used successfully.
Bitters and aromatics have also been strongly recommended.” (Law’s
“Veterinary Medicine,” Vol. II. p. 29.)


                         MERCURIAL STOMATITIS.

This form of stomatitis possesses certain distinguishing characters, and
develops after severe or trifling mercurial poisoning.

=Causation.= Sheep sometimes suffer from mercurial poisoning as a result
of the use of baths containing corrosive sublimate or mercurial ointment
for acariasis or other cutaneous parasitism. Animals of the bovine
species seem predisposed to the disease as a consequence of their
special sensitiveness to the action of mercury, which is not shared by
other species.

Mercurial poisoning may occur accidentally, but is usually the result of
some attempt at treatment. Any preparation containing mercury or
mercurial salts may produce it. In domesticated animals it most
frequently results from the action of the ordinary mercurial blister or
mercurial ointment of the pharmacopœia, or again of calomel. Sometimes
it follows the use of mercurial salts in uterine douches, or in lotions
used to wash out large abscess cavities or wounds.

The application of blisters or of anti-parasitic dressings, or
infriction with grey ointment over extensive surfaces, favours this
intoxication. It may result from direct local intra-cutaneous
absorption, from vapour given off by mercurial applications obtaining
entrance into the body through the broncho-pulmonary and digestive
tracts, from vapour given off by metallic mercury (as in ships’ holds),
or from ingestion of mercurial compounds licked off the skin, as
certainly occurs. Hitherto in all discussions, even the most recent, on
the mechanism of poisoning, partisans of different views do not appear
to have given sufficient attention to these now clearly proved facts.
The conclusion to be drawn is that in animals of the bovine species
mercurial preparations ought to be used with caution, and that even
under such conditions stomatitis may appear. Finally, it should be
remembered that all lesions of the kidney indicated by albuminuria and
other signs, and all lesions of the liver, favour poisoning by checking
or preventing the elimination of mercury by the kidney, or by
interfering with its transformation in the hepatic cells.

=Nature.= Regarding the essential nature of stomatitis, it would appear
(according to the work carried out in 1890 by Gallipe on mercurial
stomatitis in man), that we should regard it as a septic stomatitis, and
not as a primary toxic stomatitis. The mercury absorbed by the body not
only produces salivation, but a very important change in the chemical
composition of the saliva. The vitality and toxicity of the saprophytic
microbes normally present in the buccal cavity appear greatly to
increase, and although only the most trifling erosions may exist in the
mucous membrane, true intra-mucous inoculation takes place, and forms
the point of origin for septic stomatitis.

It has been found that it is not even necessary to have lesions in the
buccal mucous membrane; in fact, this is the weak point in the theory
emitted. Nor is a modification in the chemical composition of the saliva
sufficient; for when a mixture of iodine and the iodides, for example,
is being given, the saliva is chemically modified, and yet stomatitis,
properly so-called, does not occur.

What seems most probable is that mercurial stomatitis is a
toxi-infectious stomatitis, in the development of which mercury acts
primarily by its toxic effect on the salivary glands, whose secretion it
modifies, and on the buccal epithelium, the renewal of which it checks.
Infection of the mucous membrane is thereby favoured, even in the
absence of any previous lesion, and stomatitis develops.

=Symptoms.= The symptoms consist in abundant salivation with discharge
from the mouth, suggesting the existence of foot-and-mouth disease. In
grave cases the saliva appears streaked with blood, even from the
beginning. The buccal cavity exhales an intense fœtid odour which,
during the following days, becomes more marked; the mucous membrane is
pale in colour, and coated with a greyish exudate. The mouth is hot and
sensitive, the gums are swollen, reddish-violet in colour, and painful.
Alveolar periostitis soon sets in, the teeth become loose, and
mastication is rendered impossible, especially as the inflammation
causes the tongue to swell and lose its mobility. These symptoms are
unaccompanied by fever.

In the last stage ulcerations and local necroses appear on the gums, on
the inner surface of the lips and cheeks, and around the commissures of
the lips. The patients are almost unable to feed, rapidly lose flesh,
become anæmic, and die from septic infection. The temperature is often
below normal.

A toxi-infectious gastro-enteritis, with fœtid, blood-stained diarrhœa,
is grafted on the primary stomatitis. Complications in connection with
the respiratory, circulatory, and urinary apparatus appear, and the
patients die in a condition of absolute exhaustion.

Naturally this termination is not inevitable; trifling cases of
poisoning, and even grave forms, when properly treated, may, and should,
recover.

=Diagnosis.= The diagnosis is mainly based on the history, except in
cases of accidental and unsuspected poisoning.

=Prognosis.= The prognosis is grave, for even when the disease does not
prove fatal the animals remain anæmic and exhausted for long periods.

=Treatment= should principally be directed towards combatting the local
complications. When poisoning is due to external applications of mercury
or its salts the skin should be washed with soap and water, and
afterwards dressed with a soluble sulphide, which renders the mercury
insoluble. The mouth should frequently be rinsed with boiled water, with
decoctions of barley or marsh-mallow, with a 30 per cent. solution of
boric acid or alum, or with a 1 to 2 per cent. solution of salicylic
acid.

Fully grown cattle receive daily doses of 1¼ to 2 drams of chlorate of
potash internally. This drug appears to owe its favourable action to the
fact that it is partly eliminated by the salivary glands. Lastly, with
the idea (which may, perhaps, be illusory) of minimising and checking
the bad effects of the mercury introduced into the body, certain
practitioners have recommended the administration of eggs, flowers of
sulphur (2½ to 5 drams), sulphate of iron (1¼ to 2½ drams), and of
iodide of potassium (1¼ to 2½ drams), drugs which are alleged to form
insoluble compounds with mercury.


                               GLOSSITIS.

The term “glossitis” is applied to all inflammations of the tongue,
whether superficial or deep seated. These inflammations may result from
trifling causes, in which case they are termed “simple, acute, or
chronic glossites”; or, on the other hand, from well-recognised causes,
like tuberculosis or actinomycosis, in which case they receive the name
of “specific glossites.” Here only ordinary glossites are investigated,
the others being more particularly described in chapters specially
reserved for the description of the primary diseases of which these form
symptoms.


                         SUPERFICIAL GLOSSITIS.

This condition is characterised by lesions in the mucous membrane or in
the immediately subjacent tissues, deeper seated structures not being
involved.

The causes are similar to those of simple stomatitis, and as in animals
of the bovine species the tongue is the principal and almost the only
organ of prehension, it is particularly exposed to the chance of injury.

As mechanical injury done by rough fodder first makes its effects felt
on the tongue, superficial glossitis is often due to the action of sharp
or prickly plants like furze, wrestharrow, thistles, sea holly, etc. The
glumes, awns, and spikelets on certain plants play a similar part.

Caustic medicinal draughts, hot drinks, and sharp points on the molar
teeth may also produce the disease without the rest of the buccal mucous
membrane being involved.

=Symptoms.= These are extremely simple. There is, first of all, some
difficulty in grasping the food and some diminution of appetite, which,
however, is more apparent than real, the digestive organs acting well.
The second symptom consists in moderate salivation without special
characters.

The local symptoms alone are characteristic. The mucous membrane
covering the tongue appears red, swollen, locally inflamed, and painful.
The inflamed areas are usually located on the free part near the frænum
or opposite the molar teeth.

Thorns, foreign bodies, awns or spikelets of rough grasses can often be
seen implanted in the tongue, and if the disease has existed for a short
time, little ulcerations may not improbably be discovered.

=Diagnosis.= The characteristics of this superficial glossitis are
sufficiently marked to allow of easy diagnosis, and to prevent it being
confused with the lesions of actinomycosis or tuberculosis or with the
extensive desquamation which accompanies foot-and-mouth disease.

=Prognosis.= The prognosis is never grave. Recovery occurs in six to
eight days, provided the primary cause be removed.

=Treatment= consists in avoiding the use of rough food, in removing
foreign bodies implanted in the mucous membrane or in rasping rough and
irregular teeth. For the rest, as in stomatitis, mere attention to
cleanliness suffices. The mouth is washed out with boiled water, boric
acid solution, mixtures of vinegar and water, or with water containing a
small percentage of alcohol.


                      ACUTE DEEP-SEATED GLOSSITIS.

This disease has also been termed parenchymatous and interstitial
glossitis, because all the deep-seated tissues, including the muscles
and connective tissue layers are involved in the inflammation.

=Causes.= The disease may be due to a neglected attack of superficial
glossitis, to some grave microbic infection, or to excoriation and
ulceration of the mucous membrane. Very often it is of traumatic origin,
and is due to violent traction on the tongue by herdsmen or others when
administering draughts of their own composition. This traction causes
rupture of the muscle and slight interstitial hæmorrhage.

=The symptoms= develop somewhat rapidly. Whilst at first the animal
shows difficulty in grasping food, it is soon totally incapable of doing
so. The tongue loses its mobility, is no longer protruded from the
mouth, and swallowing becomes so painful that salivation sets in. On
direct examination the tongue is found swollen, thickened, immobile,
painful, and occupying the whole of the oral cavity, sometimes
projecting beyond the region of the incisors, and preventing the mouth
being closed. Inflammation may become so intense that the point of the
tongue hangs out of the mouth. It becomes blackish, bleeding, swollen,
and excoriated by contact with foreign bodies or simply with the row of
incisor teeth. The saliva becomes fœtid, blood-stained and purulent, and
contains large quantities of broken down epithelial cells. It is not
uncommon to note more or less extensive necrosis.

=Diagnosis.= The diagnosis of this form of glossitis presents no
difficulty, for if under certain conditions it may resemble, for
example, the glossitis of actinomycosis, it differs essentially from
that disease by its rapidity of development, by its complications, and
also by the absence of the specific ray fungus.

=Prognosis.= The prognosis is grave, not only on account of the possible
complications, but also because the animals are unable to feed and
therefore lose flesh with very great rapidity.

=Treatment.= The first steps in treatment are in the nature of local
disinfection, in order to prevent general infection. The mouth therefore
should be washed out five or six times per day with boiled water,
followed by antiseptic injections until improvement commences. Solutions
of boric acid or borax (3 per cent.), chlorate of potassium (2 to 3 per
cent.), or salicylic acid (3 to 4 per cent.), are useful, but the free
employment of 1, 2, or 3 per cent. solutions of chloral is even
preferable.

With the idea of protecting the organ from external injury, Lafosse
formerly suggested the use of a suspensory bandage for the tongue, fixed
to the base of the horns by small bandages. Guittard recommends
scarification of the free part, and the application of a support
perforated at the bottom to allow the blood, saliva, pus, etc., to
escape. In spite of careful attention the disease may last from two to
three weeks.


                           CHRONIC GLOSSITIS.

This form of disease has also been termed “sclerosing glossitis” and
“non-actinomycotic wooden tongue,” because it is anatomically
characterised by induration of the tissues, and because apparently it
resembles true “wooden tongue,” with which it was confused until within
the last few years. Imminger in 1888 and Pflug in 1891 described two
forms. The first, termed “superficial sclerosing glossitis,” is said to
be the more frequent, and most commonly affects young animals suffering
from irregularities in dentition. It seems due to a superficial acute
glossitis assuming a chronic form. The submucous connective tissue in
time undergoes hyperplastic changes, so that the tongue at first becomes
swollen and afterwards absolutely rigid. One never finds ulcerations or
actinomyces.

=Diagnosis.= A close examination will always enable the case to be
diagnosed at the first visit, or under any circumstances after a short
time.

=The prognosis= is very grave, because the animal has the greatest
difficulty in grasping and masticating food, or may even be unable to do
so. Patients lose flesh very rapidly, and end by dying of hunger.

=Treatment= is of little service. The administration of iodine, the only
drug which appears indicated, has proved of very questionable value.
Economically, it is better to slaughter the animal.

                  *       *       *       *       *

The second variety is rare, and has been termed “deep-seated sclerosing
glossitis.” It is simply a chronic form of ordinary deep-seated
glossitis. The layers of connective tissue separating the muscles are
represented by very hard, inelastic vertical partitions. As a
consequence, the whole tongue becomes indurated and more or less
completely immobile. In this condition, again, there is neither
ulceration nor actinomyces.

=Diagnosis.= The diagnosis necessitates a careful examination. In the
living animal it is very difficult to establish a distinction between
this and the preceding form, though after death the task becomes much
easier.

=The prognosis= is grave, complete restoration of the parts being
impossible.

=The treatment= differs in no respect from that given in the preceding
instance. It is of little value.

                  *       *       *       *       *

Imminger and Pflug have also described a deep-seated nodular sclerosing
glossitis, characterised anatomically by the existence in the depth of
the tongue of fibrous nodules, varying in size between a small nut and a
fowl’s egg. The tongue is only slightly increased in size.

This disease may perhaps be due to actinomycosis.




                              CHAPTER II.
         DISEASES OF THE SALIVARY GLANDS, TONSILS AND PHARYNX.


                        PAROTIDITIS (PAROTITIS).

The term “parotiditis” indicates an inflammatory condition of the
parotid gland. Of this disease several forms exist. The disease is
termed simple when due to accidental causes or infections, specific when
resulting from some special disease germ like the ray fungus.
Anatomically, these diseases consist in inflammation of the glandular
parenchyma and connective tissue stroma which surrounds the acini.


                           ACUTE PAROTIDITIS.

=Causation.= The causes of acute parotiditis are varied. Mechanical
violence or contusions (due to collisions with fixed bodies, horn
thrusts, or blows from the ox-goad) may produce it, the glandular
parenchyma and connective tissue separating the acini or the
peri-glandular tissue being torn, crushed, lacerated, and often also
directly infected in consequence of the injury. Ascending infection
through the medium of the salivary ducts represents a second possible
cause of the disease.

Finally, parotiditis may, in some cases, constitute only a localisation
of a general disease. It seems a fact that in rare circumstances
parotiditis may assume an epizootic character, and attack a large number
of animals in a particular stable or in neighbouring stables; and if,
under these circumstances, we are unable to blame the food (which has
not been done), we are forced to admit the influence of infection and
contagion.

=Symptoms.= Whatever the cause, the symptoms are generally well marked.
In many cases the first indication of the disease is apparent or real
want of appetite, always complicated with difficulty in swallowing, and
often accompanied by trifling fever.

Salivation, resulting from irritation of the gland and inability to
swallow, becomes abundant, and at once draws attention to the buccal
cavity and adjacent parts. Inspection of the patient then reveals the
existence in the parotid region of a diffuse swelling, which on
palpation is found to be hot and painful, and to occupy the whole of the
parotid region between the lower jaw and the upper extremity of the
neck. The lesion is usually unilateral, but occasionally bilateral.

Parotiditis may terminate in resolution, suppuration, or necrosis. The
suppuration may either be simply subcutaneous and extra-glandular, or
may involve a portion of the salivary gland and of the parotid lymphatic
gland in addition.

Necrosis is exceptional, though Moussu saw double and total gangrene of
both parotids, complicated with septicæmia, in the animal, of which a
sketch is given herewith.

[Illustration: $1]

If the disease is due to violent injury by a foreign body, traces of a
wound may be found, but it is often useless to search for these, even
when the parts have been pricked with a sharp goad. When the
inflammation has resulted from ascending infection of the salivary
ducts, exaggerated sensibility may sometimes be detected throughout the
whole length of Stenon’s duct, particularly at the point where the duct
crosses the jaw. There is always marked difficulty in moving the head,
particularly towards the side, and sometimes in a vertical plane. The
head is extended on the neck, and is held stiffly in such a way as to
suggest the possibility of tetanus. Some observers have described as an
important symptom marked swelling of the orifice of Stenon’s duct. It is
certainly difficult to detect, and furthermore is of no great
significance.

=Diagnosis.= Although diagnosis is easy, it is a difficult matter to
detect the point of origin of the disease. The salivation and difficulty
in swallowing might seem to suggest pharyngitis, a condition which
sometimes exists simultaneously. The distinction between this disease
and the forms of chronic parotiditis, or tumour formation in the parotid
(due to actinomycosis, lymphadenoma, melanoma), is also easy, on account
of the slow development of the last-named conditions. The only condition
liable to be confused with that under consideration is abscess of the
subparotid gland.

=Prognosis.= The gravity of the disease varies greatly. When
inflammation is slight, resolution usually occurs in eight to fifteen
days. The onset of suppuration is announced by renewal of the fever, by
more marked swelling, which becomes localised at a given point, and by
the existence of deep or superficial fluctuation. Care, however, is
required to detect the last named.

Necrosis may occur suddenly when the infecting organism is specially
virulent, and may affect one-third, one-half, or the whole of the gland.
The prognosis then becomes extremely grave, and if diagnosis has not
been prompt and treatment energetic, death may follow in a short time
from septic infection.

=Treatment.= Unless some well-marked sign foreshadows a complication,
treatment should be directed to ensuring resolution. Bleeding has been
recommended; its good effects, however, are open to doubt, though one
cannot entirely forbid it. All practitioners agree in recognising the
value of vesicant applications. The affected parts may be freely dressed
with an ointment containing 2 per cent. each of pulverised tartar emetic
and bichromate of potash, with the ordinary cantharides blister, or even
with a weak mercurial blister, provided that the animals can be
prevented from licking the wound.

Some practitioners prefer vesicants prepared with cantharides and croton
oil. Whatever be the vesicant chosen, it is best after three or four
days to apply emollients of slightly antiseptic character, such as
ointments containing camphor, boric acid, salol, etc. When abscess
formation is recognised the abscess should be opened as early as
possible. Some precautions are necessary to avoid injuring important
nerves and vessels; in dealing with a deep-seated abscess it is
necessary to use the knife for dividing the skin alone, to seek the
abscess by blunt dissection with the finger or with round-pointed
scissors, and to open it with a similar instrument. The cavity should
then be freely washed out with a warm antiseptic solution—3 per cent.
carbolic solution, or 1 per cent. iodine solution, etc. If necessary a
drain composed of iodoform gauze can be inserted, or a counter-opening
made.

In the case of partial necrosis, all the necrotic tissue must be
carefully removed, injury to vessels, which would favour septicæmic
infection, being avoided. Afterwards free antiseptic irrigation should
be employed several times per day.

In necrosis of the entire parotid extirpation may seem indicated; but
the greatest prudence is demanded, for the operation is extremely
serious and delicate.


                  CHRONIC PAROTIDITIS—PAROTID FISTULA.

When a case of acute parotiditis is not treated, and does not end in
suppuration, it is usually succeeded by chronic inflammation and fibrous
induration of the gland. Any obstruction of Stenon’s duct, whatever the
originating cause (foreign bodies like wheat awns, oat grains, calculi,
etc.) stops the flow of saliva throughout the excretory apparatus, and
produces over the entire parotid region a doughy swelling, which might
seem to indicate the existence of indolent parotiditis. The collections
of liquid thus produced have improperly been termed “salivary
abscesses.” If ascending infection fails to occur, or if infection is
unimportant and does not lead to suppuration, a relatively painless
chronic parotiditis develops, and in this case movements of the head and
mastication and deglutition alone are impeded.

The salivary ducts, however, may become so distended that the main
superficial collecting duct undergoes softening, and the skin covering
it becomes ulcerated, just as would occur had a true abscess formed.
Under such circumstances the skin soon yields and a salivary fistula is
established.

=The symptoms= consist in swelling or induration of the gland,
interference with movement of the head and with mastication; the whole
developing slowly without pain or fever.

The distinction of this condition from actinomycosis of the parotid may
sometimes present some difficulty until a fistula develops.

=The prognosis= is grave, because there is no hope of normal conditions
being restored.

=Treatment.= Treatment often proves unsuccessful. Should the condition
have resulted from an obstruction, it is first necessary to attempt the
removal of such obstruction, whether it be a foreign body or calculus,
and so to re-establish the normal channel for the saliva. Local
stimulation may be tried, though in cases of fistula without much hope
of success. Smart blistering of the parts surrounding the opening and
firing in points have been recommended; but rather than persist in
prolonged treatment of doubtful value, it is often better to prepare the
animals for slaughter.


            INFLAMMATION OF THE SUBMAXILLARY SALIVARY GLAND.

Inflammation of the submaxillary gland is rare in the ox. As in the
horse, it is usually caused by the penetration of foreign bodies, such
as glumes or awns of grain, fragments of straw, thorns, etc., into
Wharton’s duct.

The difficulty in grasping food and the restricted movement of the
tongue are the first symptoms to attract attention. On examination, the
region of the “barbs,” usually on one side, appears injected, swollen,
inflamed, and sensitive.

The submaxillary space is effaced by the swelling of Wharton’s duct; the
corresponding submaxillary gland is doughy and painful on pressure. The
symptoms rarely become more threatening than this.

=The diagnosis= presents no difficulty.

=The prognosis= is favourable.

=Treatment= consists primarily in removing the obstruction from the
duct. Steady pressure from behind, forwards along the course of the
duct, may sometimes cause the foreign body to be ejected into the mouth,
along with a jet of offensive saliva. The distended and inflamed duct
soon becomes emptied, and all the symptoms rapidly diminish. In other
cases, when the obstructing body is firmly fixed in position, it is
necessary to open the duct within the mouth by a stroke of the bistoury.


                          TONSILITIS IN PIGS.

“Acute and chronic forms are seen. The former has the general causes and
symptoms of pharyngitis—fever, dulness, a disposition to lie with head
extended and buried in litter, drooping ears, watery eyes, indifferent
appetite, painful deglutition, and sometimes vomiting. Mouth red and
hot, breath fœtid, tonsils swollen, their alveoli filled with
muco-purulent matter or with fœtid cheese-like masses. Cough at first
dry and hard, later loose and gurgling.

In chronic form there is general swelling of the tonsils with distension
of follicles by above-mentioned putty-like masses, which are often
calcareous. These are due to the proliferation of microbes, which find
in these alveoli a most favourable field for their propagation. The
affection usually ends in recovery, but may go on to grave local
ulceration and general infection.

=Treatment.= Astringent antiseptics to buccal mucous membrane.
Electuaries of honey or treacle and borax, sal ammoniac, chlorate or
permanganate of potash and externally stimulating embrocations to the
skin of the throat. In some cases solutions of iron chloride or tincture
of iodine may be used with advantage and as a wash for the mouth and
fauces. Attend to general health. If constipated give Glauber’s salt or
jalap, ... and elimination through the kidneys must be sought through
the use of nitrate of potash or other diuretic.” (Law’s “Veterinary
Medicine,” Vol. II. p. 46.)


                              PHARYNGITIS.

Inflammation of the mucous membrane of the pharynx is less frequent in
the ox than in the horse, a fact probably due to its less sensitive
character in the ox and to differences in the methods of working oxen.

=Causation.= The causes are numerous and varied; and although local
microbic infection undoubtedly plays the most effective part in the
development of the disease, it is none the less certain that external
influences are of considerable importance. For this reason chills,
sudden variations in temperature, sudden arrest of perspiration, and
currents of cold air have always been invoked as causes. Cruzel thinks
that the ingestion of ice-cold water in winter is sufficient to produce
acute pharyngitis. The action of rough forage may of itself explain the
development of pharyngitis in animals constantly kept indoors under
excellent hygienic conditions. In such cases the disease may be regarded
as of traumatic origin. Furthermore, it is necessary to mention direct
injuries of the mucous membrane caused by clumsy examination,
awkwardness in passing the probang, and attempts on the animal’s part to
swallow sharp foreign bodies, which scratch, tear, lacerate, or
penetrate the mucous membrane and become fixed in it.

Finally, another series of causes, and not the least important, remains
to be considered—viz., the forced administration of irritant substances
like ammonia, tincture of iodine, oil of turpentine, very hot liquids,
etc.

To sum up, the four great series of causes consist in direct irritation,
intra-pharyngeal wounds, variations in temperature, or primary or
secondary microbic infections.

=The symptoms= are characteristic. They consist in loss of appetite,
difficulty in swallowing, consequent on the condition of the pharynx,
and fever, which is often marked from the first. Pharyngeal dysphagia
can easily be distinguished from that due to injury of the œsophagus,
inasmuch as it occurs on the first attempt to swallow.

Urged on by hunger, the animal grasps food, which it chews and attempts
to swallow, but immediately allows it to fall back into the manger, or
ejects it by a painful coughing effort. In the case of liquids, even of
lukewarm drinks, the same accident occurs, the food or liquid being
returned by the nostrils. Slight salivation results from this difficulty
in swallowing. The animal’s attitude is similar to that in parotiditis.
The head is held stiffly, extended on the neck, in order to avoid
compressing the region of the pharynx, and can only be moved slowly and
with much pain. There is no apparent swelling of the parotid region, but
on manipulating or pressing on the gullet the animal sometimes manifests
the very acute tenderness of the parts by coughing and endeavouring to
thrust away or to kick the examiner. Finally, examination of the mouth
sometimes shows reddening and excessive sensibility of the soft palate
and of the pillars of the fauces.

These symptoms often assume a more alarming character, or are
complicated by others; in fact, the condition very rarely stops at
pharyngitis, but is usually accompanied by inflammation of the larynx,
of the soft palate, and of the naso-pharynx. The whole throat is then
inflamed; the nose and sometimes the eyes discharge, and there is
difficulty in swallowing, interference with respiration or noisy
respiration, and intense fever.

=Diagnosis.= The diagnosis presents no difficulty, the symptoms
mentioned being easy to identify, whether the condition be simply
inflammation of the pharynx or be of a more extensive character.
Nevertheless, cases occur where the symptoms are alarming, but in which
one might hesitate between the diagnosis of ordinary acute sore throat
and the sore throat which ushers in gangrenous coryza. A definite
expression of opinion must then be deferred to a later date; for one
cannot be absolutely certain whether or not the other signs of
gangrenous coryza will appear.

When there is only difficulty in swallowing one might _à priori_ suspect
traumatic injury of the mucous membrane, with or without the presence of
a foreign body. It is also necessary to bear in mind the possibility of
difficulty in swallowing being occasioned by reflex irritation without
local lesions, originating in enlargement of the retro-pharyngeal
lymphatic glands as a consequence of tuberculosis or other disease.

=The prognosis= is favourable; even without treatment acute pharyngitis
usually tends to recovery in eight to twelve days, and rarely becomes
complicated. Nevertheless, some reserve ought to be exhibited in cases
of pharyngitis due to the action of rough forage, the removal of the
cause being here indispensable to any improvement. Similarly in cases of
pharyngitis due to foreign bodies having penetrated the mucous membrane,
which are chiefly characterised by inability to swallow, the disease may
continue for a very much longer time than above indicated, unless the
foreign body is discovered and removed. Inflammation is limited to a
zone surrounding the point of implantation. It extends more deeply with
movements of the foreign body, and may end in the formation of an
abscess. Of this variety is Hopsomer’s remarkable case, in which a
darning-needle finally obtained exit through the submaxillary space, in
which it had caused the formation of an abscess.

=Treatment.= The treatment is the same whether we are dealing with a
simple acute pharyngitis or with a more widely distributed inflammation.
It consists in smartly stimulating the region of the throat with
mustard, cantharides oil, or ointment, or with an ointment containing 2
per cent. of tartar emetic and of bichromate of potash, and then
covering the parts with a flannel hood. This mode of treatment seems
preferable to that recommended by German authors—viz., the application
of cold compresses to the throat, the administration of cold gargles,
etc. Moderate bleeding, to the extent of two or three quarts, has the
great advantage, as in all similar cases, of lowering the temperature.

This treatment may, if necessary, be completed by the internal
administration of 3 to 5 drams of Kerme’s mineral (oxysulphuret of
antimony) in electuary, according to the animal’s size. Medicated
inhalations diminish local irritation, render swelling less painful, and
facilitate the separation of false membranes and the discharge of
adherent mucous secretions.

The ordinary food should be replaced by cooked roots, lukewarm drinks
and gruels, all rough fodder being prohibited.

If difficulty in swallowing alone continues, the operator should examine
the mucous membrane of the pharyngeal cavity with the hand, in order to
discover and remove any foreign body which may have become implanted
there.


                PSEUDO-MEMBRANOUS PHARYNGITIS IN CATTLE.

In addition to the above acute forms of pharyngitis, a
pseudo-membranous, croupal, or pseudo-diphtheritic pharyngitis has been
described in the ox. It is due to polymicrobic infection, and is
characterised by the formation of false membranes on the pharyngeal
mucous membrane. The condition seems to be a pharyngitis of exceptional
intensity, varying markedly from the classic type and being most nearly
related to severe sore throat, laryngitis, gangrenous coryza, etc.

It rarely attacks aged cattle, but is readily transmissible to calves
and young stock. Cadéac failed to inoculate it on guinea-pigs and
rabbits. Damman succeeded with sheep and with rabbits, the latter dying
in twenty-four hours after inoculation with hæmorrhage at the seat of
puncture. Löffler hypodermically infected mice and produced extensive
infiltration of the abdominal walls, and often of the peritoneum,
surface of the liver, kidneys and intestine, on which formed a thick
yellowish exudate containing the organism.

=Causes.= Löffler found filaments of a long delicate bacillus about half
the thickness of the bacillus of malignant œdema. The bacillus did not
grow in nutrient gelatine or in sheep’s blood serum, but readily grew in
blood serum of the calf. Cadéac gives as predisposing causes: sudden
chills, rapid alterations of temperature, inhalation of irritant
vapours, suppression of cutaneous secretion, swallowing irritant
liquids, and injuries.

=Symptoms.= The nasal membrane is reddened, thickened and covered in
patches with false membrane, causing snuffling and wheezing breathing.
The throat is tender and swollen, cough is frequent, gurgling, and
followed by expulsion of false membrane, muco-pus and some blood. Shreds
of false membrane adhere to the nose and lips. Other symptoms are:
fever, accelerated pulse, dark mucous membranes, haggard countenance,
mouth open, hanging tongue, stringy salivation, and constipation or
diarrhœa.

The disease runs a rapid course, and death may occur in twenty-four
hours. Recovery may be equally rapid, but often convalescence is
protracted.

=Lesions.= Intense congestion of mucosæ of nose, mouth, pharynx, larynx,
and bronchi, with here and there patches of false membrane, which may be
soft or tough, according to the duration of the attack. The deep surface
of the false membranes is blood-stained; and, according to Preitsch,
false membranes sometimes occur in the œsophagus, rumen, and omasum,
which in consequence may show patches of ulceration.

=Treatment= (as for the horse). This includes poultices,
counter-irritants, laxatives, febrifuges, alkalies and antiseptics.
Inhalations of medicated vapour, warm water to which has been added some
antiseptic—carbolic, lysol, creolin, camphor, sulphurous acid; or for
calves, iodoform, oil of turpentine, calcium sulphide, silver nitrate,
coal tar. To detach the false membranes ipecacuanha and potash chlorate,
or soda sulphate, or magnesia sulphate may be tried. Papayin and pepsin
have been suggested as appropriate remedies. Anyodnes—digitalis,
belladonna, morphia and aconite—may be useful. Tracheotomy is indicated
as a last resort.


                PSEUDO-MEMBRANOUS PHARYNGITIS IN SHEEP.

Roche-Lubin states that this is common in flocks as a result of moving
the sheep in dusty enclosures. The dust is supposed to excite the
intense croupous inflammation of the mucous membrane. The disease has
been noticed in spring in young lambs shortly after weaning. Damman
states that he transmitted the disease to the sheep from the exudate of
the calf.

=Symptoms.= Frothy salivation with constant movements of the jaws,
viscid nasal discharge, difficult deglutition, panting, snuffling
breathing, throat swollen and very tender, frequent cough, discharge of
exudate. The head and neck are extended, the eyes dull, appetite is
lost, the mucous membranes are red or cyanotic, and the animal appears
weak and listless. As respiration becomes more difficult the mouth is
held open, the tongue is protruded, and with each cough shreds of false
membrane are expelled. Death from suffocation is not uncommon.

=The lesions= are not different from those seen in the calf.

=The treatment= is similar to that for the calf. Tepid drinks containing
hydrochloric acid, or sulphate of soda (1 lb. to 50 sheep) in the
drinking water, has been recommended. Fumigation with sulphurous acid or
chlorine may be tried. Small numbers may be treated by swabbing the
throat with solution of sodii hyposulphis or weak caustics and
antiseptics.

                  *       *       *       *       *

In young and in adult pigs pseudo-membranous pharyngitis is often only a
manifestation of pneumo-enteritis. It therefore calls for no special
description at this point. No exact investigation of the organisms which
produce these forms of pharyngitis with false membrane formation has
been made in veterinary surgery. We only know that these diseases are
not true diphtheria due to “Klebs’ bacillus.” Treatment should be very
energetic from the commencement, but otherwise it differs in no respect
from that ordinarily adopted.

Tonics and stimulants, like alcohol, wine, coffee, etc., are indicated.

[The following account of the disease is summarised from Law’s
“Veterinary Medicine,” Vol. II.]

“Pseudo-membranous pharyngitis has long been recognised as a contagious
disease of swine, attacking especially swine kept in herds or in close,
insanitary pens. Young pigs are more liable to attack than older
animals, perhaps, owing to the older animals having suffered the disease
in early life.

Modern observation shows that pharyngitis with false membranes is common
in swine plague, and the present tendency is to refer all such cases to
that category. It is, however, altogether probable that the occurrence
of local irritation, with the addition of an irritant or septic microbe
altogether distinct from that of swine plague or hog cholera, gives rise
at times to this exudative angina. Certain it is that septic poisoning
with the food is not at all uncommon in the hog, in the absence of these
infectious diseases.

=Symptoms= are those of sore throat, with much prostration, a croaking
cough, yellow discharge from nose and mouth, and marked muscular
weakness. The tongue, tonsils and soft palate are red, swollen, and
studded with patches of false membrane. The identification of swine
plague may be made by the history of the outbreak, the number of animals
affected, the tendency to pulmonary inflammation, the enlarged lymph
glands, the presence of the non-motile bacillus, which does not generate
gas in saccharine media, and which readily kills rabbits and pigs with
pure cultures of the germ.

=Treatment.= Isolation, cleansing and disinfection. Locally antiseptics
and generally a febrifuge regimen will be advisable.”


                           PHARYNGEAL POLYPI.

The term “pharyngeal polypi” includes tumours of varying character,
which affect the polypus form, and occur with considerable frequency in
the bovine species. Many of these polypi are simply actinomycotic
growths springing from the pillars of the fauces, from the upper parts
of the palate or from its posterior surface. Less frequently they arise
from the lateral walls or the free surface of the hard palate.

=Symptoms.= The symptoms are so characteristic that the diagnosis rarely
presents much difficulty. They may shortly be described as indicative of
repeated obstruction in the pharyngeal, œsophageal or laryngeal region.
At the moment of deglutition, the polypus is thrust towards and
obstructs the œsophageal orifice.

Reflex stimuli are thus excited, which prevent deglutition; an attack of
coughing occurs, and food mixed with saliva is ejected from the mouth
and nostrils. The attack of coughing displaces the polypus either in a
forward or lateral direction, and swallowing then again becomes
possible, until by changing its position the growth produces fresh signs
of obstruction.

In other cases the polypus may only be of such small size as to impede
the food passing through the pharynx on its way into the œsophagus or to
cause difficulty in respiration by partially blocking the pharyngeal
portion of the nasal cavities. In such cases deglutition is only checked
and rendered slower.

Or again, the pedicle of the polypus may be sufficiently long to allow
the growth at certain moments to fall in front of the laryngeal opening.
Respiration is then painful, difficult and noisy. Unless the growth is
displaced during the subsequent attack of coughing, asphyxia may appear
imminent, or may even occur unless assistance is afforded.

Guided by these symptoms, the operator will explore the pharynx
manually, and thus discover the position and size of the tumour. Tumours
of the naso-pharynx produce very similar symptoms.

=The prognosis= is based on the information obtained by manually
exploring the pharynx. It is relatively favourable if the polypus has a
well-marked neck, but is very grave if the tumour is largely sessile and
cannot be removed.

=Treatment.= Medical treatment appears useless except in cases of polypi
due to the presence of actinomyces. The administration of iodine and
iodide of potassium, in large doses, may then lead to resorption; but
extirpation is often preferable.

In other cases extirpation is the only rational treatment. The operation
necessitates the performance of provisional tracheotomy in order to
avoid risk of asphyxia. The growth may be directly removed through the
buccal cavity without incision, provided that it prove possible to pass
the chain of an écraseur around the pedicle; or through the buccal
cavity, with incision, after vertically or obliquely dividing the soft
palate; or, lastly, through the larynx, after performing median
laryngotomy, thus obtaining access to the pharynx.

Only the first method of intervention is to be recommended; the last two
are more delicate. They necessitate after-treatment, and when the
patients are in a condition for slaughter it is frequently preferable to
send them to the butcher. The essential point is not to act without a
full knowledge of the causes.




                              CHAPTER III.
                       DISEASES OF THE ŒSOPHAGUS.


[Illustration: $1]

The œsophageal tube is of very simple anatomical construction, and
performs an equally simple physiological function; nevertheless, in the
ox it is liable to a large number of diseased conditions. These
conditions may affect only a circumscribed area of the mucous membrane
or the entire extent of the tube. Again, both the muscular and mucous
tissues may be affected, as in inflammation of the œsophagus accompanied
or followed by contraction, and in the formation of œsophageal abscesses
and tumours; or the muscular tissue alone may be affected, as in cases
of dilatation. Even where no lesion is apparent the normal rhythm of
deglutition may be interfered with, either by the presence of a foreign
body (obstruction) or by spasm of the muscular layers (œsophagismus) or
by compression due to tissues surrounding the œsophagus (false
contractions).

We shall successively study the different forms of œsophagitis,
contraction, and dilatation, together with their complications; then
obstructions, ruptures of the œsophagus, œsophagismus, and false
contractions.


                              ŒSOPHAGITIS.

Inflammation of the œsophagus may be due to many different causes, and
may occur in one of three different degrees of severity. It may be
either superficial, _i.e._, limited to the epithelial layer of the
mucous membrane; or deep, affecting the entire thickness of the mucous
membrane (epithelium, corium, and œsophageal glands); or, finally, it
may attack both the mucous and muscular layers. German authors recognise
various divisions, such as erythematous, catarrhal, follicular, and
phlegmonous œsophagitis. In reality these are not always different
forms, but simply successive stages in the evolution of a single morbid
condition. Here we shall only study the ordinary forms of œsophagitis,
leaving on one side those which occur symptomatically during
foot-and-mouth disease, cattle plague, gangrenous coryza, actinomycosis,
etc.

=Causation.= The causes of œsophagitis may be divided into three groups
of different character:—(_a_) Rough fodder (clover containing
wrestharrow, thistles, thorns, furze, or splinters of wood, etc.) must
be placed in the first rank, for its repeated action abrades and
irritates the mucous membrane to such an extent as finally to produce
inflammation. This inflammation usually remains superficial and of
moderate intensity; its occurrence can be anticipated during years of
scarcity, when the animals feed on rough and irritating material like
fern, broom, heather, furze, etc.

(_b_) Hot drinks, whether in the nature of beverages or medicinal
draughts, are a frequent cause of œsophagitis if administered by
careless or inexperienced persons. The mucous membrane is scalded over a
varying area and with different degrees of severity, or is destroyed by
the chemical action of such drugs as ammonia, dilute acids, iodine
solution, etc.

(_c_) Rough or clumsy manipulation in withdrawing or displacing foreign
bodies, or merely passing the probang, produces that variety of
œsophagitis termed traumatic. In clumsy hands œsophageal sounds or
catheters may abrade or even tear the mucous membrane and subjacent
tissues.

=Symptoms.= These vary to some extent, according to the intensity of the
inflammatory phenomena. If the lesions are superficial and only
implicate the epithelium, as in catarrhal œsophagitis, the symptoms
often pass unnoticed, and only produce difficulty in swallowing. When
inflammation has involved the entire thickness of the mucous membrane
the immediate consequence is loss of appetite due to pain during
swallowing. After the bolus of food has been masticated, and has passed
into the pharynx, the animal stretches out its head and neck and seems
to be making efforts to force it down the œsophageal canal. The progress
of the bolus is slow and clearly difficult.

In œsophagitis due to scalding the blisters are soon broken by the
passage of food, the corium is exposed, and the animal has equal
difficulty in swallowing either solids or liquids. The reflex action
provoked by the passage of the food over these lesions may be so violent
that the ingesta never arrive at the stomach, but are violently rejected
by a sudden and unexpected antiperistaltic contraction. Even saliva is
returned. Moreover, in these cases the history is generally clear, and
the animal is feverish or greatly depressed. These objective symptoms
are very significant, and when, in addition, an abnormal and exceptional
degree of sensibility is detected at some point by palpation, they
unmistakably indicate the existence of œsophagitis.

The irregularity in deglutition, and therefore also in rumination,
sometimes excites moderate tympanites without any very apparent cause.
Should the condition still appear doubtful the œsophageal sound may be
passed, but with great care. It generally aggravates the pain and
produces intense antiperistaltic movements, which the practitioner
should not attempt to overcome.

=Complications.= If œsophagitis is moderate, recovery is the rule. The
symptoms of pain gradually diminish.

When, on the contrary, inflammation is very intense, as in certain cases
of traumatic œsophagitis, the injured spot may become infected and
suppuration follow. The existing fever then persists or becomes more
marked; the animal is extremely depressed; respiration may be difficult
and accelerated, and appetite is entirely lost.

If the œsophageal abscess remains submucous the diagnosis is difficult,
but it is often problematical, even when the abscess develops in the
cervical region. The jugular furrow (usually on the left side) becomes
the seat of a severe diffuse inflammatory swelling, the course of which
clearly indicates the development of the symptoms. In exceptional cases
fluctuation may be detected.

If from the first the abscess develops around the œsophagus or in the
course of suppuration comes to occupy this position, swelling in the
jugular furrows is more apparent and easier to detect, and in this case
fluctuation may be localised. When the lesions are within the thorax no
tangible symptoms can be detected. Death may occur in a few days, when
an abscess in the lower cervical region breaks into the anterior
mediastinum, or when an abscess in the thoracic region opens into the
pleural cavity. In œsophagitis produced by scalding and from swallowing
hot or caustic liquids the mucous membrane, and sometimes the muscular
tissue, is destroyed, and ulcerations and cicatrices result, or the
œsophagus may even be perforated, with rapidly fatal results; even when
recovery occurs, cicatrices form and cause very grave contraction.

=Diagnosis.= The diagnosis is generally easy, provided that the symptoms
noted are methodically analysed and the history of the case is taken
into consideration.

=Prognosis= is favourable in ordinary cases. On the other hand, it may
be very grave when general symptoms become marked, when the vital
functions are disturbed and a deep-seated abscess appears to be forming.

=Lesions.= In the first degree the lesions are confined to inflammation
and desquamation of the epithelium; in the second, to inflammation of
the corium and of the mucous membrane; in the third, to infiltration of
the submucous layers and of the muscular and periœsophageal tissues.
Sloughing and perforation follow the administration of caustic liquids.

=Treatment.= As the direct application of medicines to the inflamed
mucous membrane can only be of a momentary character, treatment is
confined to administering emollient, anodyne, and slightly astringent
drinks, the action of which is assisted by feeding with milk,
farinaceous or mucilaginous foods. Under these circumstances recovery
occurs in ten to fifteen days. The application of stimulant or
blistering ointments along the jugular furrow may have a good effect.

When the general condition of the patient becomes aggravated, and the
formation of an abscess appears certain, it is best to recommend
slaughter. In the case of a submucous abscess the passage of the probang
may, however, predispose or cause the abscess to open into the
œsophagus, and thus lead rapidly to recovery, but this is exceptional.
The “pointing” of the abscess and its opening towards the jugular furrow
may be followed by temporary improvement, but at a later stage is
followed by fistula formation, or by contraction of the œsophagus
itself. From an economic standpoint it is better to slaughter.


                      STRICTURE OF THE ŒSOPHAGUS.

Under normal conditions the cavity or lumen of the œsophageal tube is,
so to speak, imaginary: the walls of the tube lie flatly together, and
the mucous membrane is in folds. During the act of swallowing the tube
becomes dilated to a degree varying with the size of the bolus of food,
and again retracts as soon as deglutition is effected. Whenever the
dilatability of the tube is markedly diminished by changes in its walls,
and, in a much higher degree, when this dilatability has disappeared,
true stricture exists. In the former case small boluses of food and
liquids alone succeed in passing the stricture; in the latter, liquids
alone can pass.

=Causation.= Strictures are never primary. They result from intense
attacks of œsophagitis, ending in sclerosis of the mucous coat,
extensive ulceration consequent on scalding, or interstitial
inflammation affecting the muscular coats, which then become thickened
or sclerosed.

Internal injuries due to attempts to withdraw or propel foreign bodies
along the œsophagus may also cause strictures.

=Lesions.= In simple strictures the lesions are confined to the
development in the depths of the mucous membrane and in the muscular
layers of inflammatory tissue, which becomes denser with lapse of time.
This alters the character of the walls and the structure of the tissues,
and causes them to lose their elasticity. After extensive ulceration the
tissue of the cicatrix contracts and hardens to a very varying degree.

=Symptoms.= The apparent symptoms are very clearly marked; the appetite
is good, and the animal masticates as usual, but in the act of
deglutition is seen to extend the head on the neck, and to make efforts
to swallow, which prove unavailing when the contraction is too marked. A
reflex antiperistaltic movement often causes the substances ingested to
be at once rejected. These violent efforts, however, in time provoke
dilatation above the stricture. A quantity of food accumulates in this
dilatation, and the symptom so characteristic of œsophageal stricture
then appears—viz., regular regurgitation. The second constant symptom
associated with compression or obstruction of the œsophagus is
tympanites after feeding, however trifling may be the amount swallowed.
Rumination is suspended, and even eructation of gas is difficult.
Finally, the characteristic sign of stricture is noted on passing the
probang, which reveals the existence of the condition, indicates its
position, and suggests its degree of development.

[Illustration: $1]

=Diagnosis.= Strictures only develop progressively and slowly, a fact
which enables them to be differentiated from œsophagitis. It is more
difficult to differentiate them from dilatations, because the stricture
always ends by becoming complicated with dilatation; but this
distinction is of little practical importance, the consequences being
identical.

=Prognosis.= The prognosis is very grave, and there is no economic
reason for attempting treatment except in special cases; the indications
are in the direction of slaughter.

From the economic standpoint there is no treatment. Basing their actions
on human practice, the Germans have recommended progressive dilatation
of the lumen of the œsophagus by passing a series of catheters of
gradually increasing size. What, however, is justifiable in human
medicine, where the only object is to keep the patient alive at any
cost, may be highly objectionable in veterinary practice; and in the
present instance this is the case. Except in very rare instances, which
the practitioner alone can appreciate, dilatation is contra-indicated,
and the owner’s interest lies in slaughtering the animal before it has
lost much condition.


                      DILATATION OF THE ŒSOPHAGUS.

Dilatations are more frequent than strictures. Their mode of origin is
easily understood. When the muscular tissue has lost its tonicity and
contractile power at a given point, or when, as a consequence of any
form of inflammation, it has begun to undergo atrophy, the mucous
membrane becomes herniated, because its circumference is not supported
regularly during deglutition. The ectasia, which at first is of small
size, becomes more marked in consequence of the tendency that exists for
the food to accumulate in the dilated region. Dilatation is thus set up.

[Illustration: $1]

Localised attacks of œsophagitis, accidental injuries and fissuring of
the œsophageal muscular tissue, produced by clumsy efforts to displace
foreign bodies with the probang, are the principal causes of dilatation.
When the probang is imprudently or clumsily manipulated, it may press
excessively at any point where the œsophagus makes a slight bend, and
thus split the contracted muscular coat without injuring the lax mucous
membrane.

Œsophageal contractions, as we have seen, may form the point of origin
of dilatations, but in this case the dilatations are more regular in
form, and affect the entire circumference of the tube. The muscular
tissue is still everywhere normal, and becomes dilated in consequence of
equally-applied eccentric pressure.

=Symptoms.= When the dilatation develops slowly and progressively, as a
consequence of muscular atrophy, the symptoms remain unnoticed for a
long time, and the owner only begins to be anxious when the animal loses
condition, or when the driver or cowman detects masses of half-chewed
food mixed with the saliva in the manger.

Certain signs are pathognomonic; others may be regarded as of secondary
importance. By carefully watching an animal which is feeding the
following symptoms may be noted: As a general rule hunger is very
marked, and the animal chews its food and swallows the first few
mouthfuls in a perfectly normal way. Three, five, eight, or even ten
mouthfuls may be swallowed; then the animal suddenly stops, appears a
little anxious, extends its head and neck, an antiperistaltic
contraction occurs, and one or two masses of food are rejected and fall
into the manger. The discomfort being thus momentarily relieved, the
animal, which is dying of hunger, although faced with food which it is
unable to swallow, returns to its meal, swallows one, two, or three
boluses of food, regurgitation again occurs, and the whole process is
repeated.

What is going on under these circumstances is easy to explain.

At the commencement of the meal the dilatation is usually empty, or
nearly empty. A mouthful of food is swallowed. It descends the œsophagus
until it arrives at the diverticulum, into which it partially or wholly
passes, the peristaltic wave of contraction ceasing at this point. The
second mouthful follows with the same result, then a third, a fourth,
etc. The diverticulum soon becomes filled to repletion, and no more food
can enter it. The food therefore accumulates in the upper portion of the
œsophageal tube until the latter becomes nearly filled; but as this
tube, provided its innervation is intact, is intolerant of the presence
of any foreign body, and as efforts to swallow prove fruitless, a sudden
antiperistaltic wave of contraction occurs, with the result that all the
material contained in the tube above the dilatation is ejected into the
mouth, whence it falls into the manger. The same result follows any
further attempts to swallow during a particular feeding time. From this
it will be seen that the animal can ingest at a given time only as much
as the dilatation will contain.

In the intervals between meal times and under the action of the saliva
and warmth, the food collected in the dilatation becomes softened,
breaks down, and slowly moves onward towards the rumen. When the next
feeding time arrives the dilatation is almost empty, and the same set of
symptoms recurs.

If, instead of forage, the animal begins by taking gruel or very fluid
material, deglutition appears normal, or at least fairly easy; but if
drinking is deferred until after taking hard food, it becomes almost
impossible, because the passage is obstructed. These symptoms are, so to
speak, pathognomonic. Under any circumstances they are so significant
that error in diagnosis is unlikely.

By careful examination œsophageal regurgitation can very easily be
distinguished from true vomiting; the character of the rejected material
shows that it has not come from the stomach, while the boluses of food
preserve their cylindrical form, and are still saturated with saliva.

Some secondary signs also deserve to be mentioned, such as the animal’s
anxiety and restlessness whilst its neighbours are feeding, the
existence of trifling and intermittent tympanites due to suppressed
eructation, suppression or irregularity of rumination, constipation,
etc. At a later stage there is rapid wasting and disordered appetite,
and finally the patients die slowly of hunger, whatever efforts are made
to feed them.

When the seat of dilatation is in the cervical portion of the œsophagus,
there are other symptoms which leave no doubt as to the condition. When
empty the pouch cannot be detected; but during a meal the accumulation
of food causes it to assume the appearance of a doughy, diffuse,
indolent swelling, which alters the outline of the jugular furrow,
yields to pressure, and sometimes produces respiratory disturbance by
pressing on the trachea, the pneumo-gastric and inferior laryngeal
nerves, etc.

When the dilatation is intra-thoracic and the above-described symptoms
have been observed, the dilated spot can only be detected and localised
by using the probang. The greatest possible prudence, however, is
required in manipulating the instrument, in order to avoid rupturing the
thin walls of the dilated portion.

=The diagnosis= is not always easy; when food is regurgitated, and one
finds by auscultation that the sound usually produced by the passage of
solids or liquids into the rumen is absent, there need be no hesitation
in diagnosing either a dilatation or a stricture. The clinical
consequences being the same, the possible error would be of little
importance.

=Prognosis.= The animal’s life is rarely in immediate danger, but from
the economic point of view the prognosis is extremely grave, and it is
in the owner’s interest to slaughter the animal as soon as possible in
order to avoid loss. Even in cases of dilatation in the cervical region,
surgical interference is not advisable.

=Treatment.= As foreshadowed by what has been said, there is no rational
economic treatment. When the dilatation is in the cervical region, one
might in exceptional cases attempt to restore the regular calibre of the
œsophagus by removing an elliptical portion of mucous membrane, and
bringing the muscular tissue together with sutures; that is to say, when
the rupture or fissuring of the muscular coat has been accidental. But
as one is usually unable to remove the primary cause, to which the
change in the muscular tissue is essentially due, the dilatation would
recur without the operation having conferred any benefit.

When an exact diagnosis has been made, the only useful indication is to
confine the animal to very fluid food, which will not obstruct the
œsophagus. Ordinary forage should be withheld.


                        ŒSOPHAGEAL OBSTRUCTIONS.

In this chapter we shall only consider such obstructions as occur in
consequence of the animal having attempted to swallow without
sufficiently chewing objects which become arrested in the œsophagus.

Obstruction is termed “total” or “partial,” according as the obstructing
body fills the entire calibre of the œsophagus at the point of
obstruction, or only occupies a part of the space. Partial obstructions
produced by beet and turnip tops, etc., are usually but momentary;
liquids and saliva are still able to pass between the obstruction and
the walls of the tube, and as soon as the arrested food becomes a little
softened it is displaced and the œsophagus again becomes patent.

=Causation.= The circumstances under which this accident occurs are
extremely easy to understand. Obstructions are produced by apples,
potatoes, turnips, carrots, cabbage-stalks, beetroots, etc., which,
whether sliced or not, are swallowed gluttonously. Not having been
sufficiently comminuted, and being of larger size than the œsophagus can
readily accommodate, they become arrested at some point between the
commencement of the œsophagus or a few inches behind the pharynx, or
just in front of the point of entry of the gullet into the stomach. The
latter is the commonest position, though not infrequently the
obstruction occurs in the intra-thoracic portion.

It may occur in the stable, but is commoner in animals which, having
broken loose, have entered orchards, gardens or potato or turnip fields
and attempted to swallow apples, cabbages, potatoes, etc., found there.

In sheep, obstruction of the œsophagus is due to similar causes, but in
their case the above-mentioned objects are replaced by small wild
apples, turnip shells, Jerusalem artichokes, horse-chestnuts, carrots,
etc.

The symptoms may be divided into general and local.

=General symptoms.= As soon as the foreign body becomes fixed in
position, the animal begins to make exceptional efforts to swallow. The
head is extended on the neck, and the œsophagus and the muscles
surrounding the trachea are violently contracted. These efforts proving
fruitless, feeding is necessarily stopped, and the animal at once
appears slightly anxious.

Very soon afterwards salivation sets in, saliva being continuously
secreted. If the obstruction is total, the saliva cannot be swallowed,
and is either returned in quantities by antiperistaltic movements or
escapes in frothy filaments from the mouth.

Tympanites is not long in appearing. It is progressive, and results both
from arrest of eructation and from continued fermentation in the rumen.
It may eventually come to a standstill, or may continue and threaten to
produce asphyxia.

=Local symptoms.= The local symptoms are difficult to appreciate, except
in cases of cervical obstruction. Sometimes the foreign body produces a
local swelling, which changes the outline of the jugular furrow, most
frequently on the left side. In many cases it can only be detected by
manipulating the parts between the trachea and the lower surface of the
cervical vertebræ. When the obstruction is within the thorax, the
probang alone can detect its position.

=Diagnosis.= The diagnosis is usually easy. The history and the observed
symptoms are often very clear, and the suddenness with which the
obstruction has made its appearance prevent the condition from being
confused with dilatation or stricture.

=The prognosis= is very variable. It is often easy to remove the
obstacle; in other cases intervention is difficult, and death may occur
rapidly.

=Treatment= is confined to one essential point—removal of the
obstruction. The chief difficulty lies in choosing the mode of
intervention. Moreover, success depends on several factors, which, in
the order of their importance, are as follows: the size of the
obstructing body; the time which has elapsed since the accident
occurred; the bodily condition of the animal—_i.e._, whether it be fat
or thin—and the extent to which tympanites has developed.

The first thing to do (and in favourable cases all that is required) is
to puncture the rumen and leave the canula for some time in position.
The onward progress of the foreign body, especially when the obstruction
is in the intra-thoracic portion of the tube, is often impeded by the
tympanites, which tends to thrust the object towards the pharynx, or at
least to fix it in position. In consequence of a sudden change in the
conditions of pressure the foreign body may move and pass into the
rumen; all danger is then at an end.

Even though the obstruction does not immediately cease, puncture of the
rumen, by removing the danger of asphyxia, allows one at least to wait
for several hours, sometimes until next day, during which time the
object may pass into the rumen without further extraneous assistance.
The other methods may be grouped into four series:

I. =External taxis.= This is directed towards loosening the foreign body
and thrusting it towards the pharynx and buccal cavity. It can only be
used against obstructions in the cervical region. Two methods, although
very ancient, are still practised.

(_a_) The first is carried out in the following way: the animal is fixed
to a post or tree so that it cannot struggle, its head being drawn up as
high as possible. The operator stands on the left side, with his back
turned towards the patient’s head, his left hand is pressed into the
right jugular furrow, his right hand is placed on the left jugular
furrow immediately below the foreign body. By using the fingers the
foreign body is moved, and is progressively thrust towards the pharynx,
in spite of the animal’s efforts to swallow. In carrying out this
manipulation it is absolutely indispensable not to let slip the
obstructing body for a single instant, otherwise the peristaltic action
will immediately return it to its former place. When it has been raised
as far as the pharynx, an assistant passes his hand into the back of the
mouth, as indicated in a former chapter, seizes the object and withdraws
it; or, instead, the assistant takes over the operator’s duties, while
the latter himself extracts the foreign body.

(_b_) In the second method the animal is fixed in a different position,
the head being held about 10 to 12 inches from the ground, with the neck
lowered and inclined towards the earth. As in this position the
œsophagus is longitudinally relaxed, and can be dilated to its fullest
extent transversely, the difficulty of displacing the obstacle should be
very much less. In this case the operator always stands on the left side
of the neck, but with his back towards the animal’s body. The right arm
is passed around the neck and the right hand pressed into the right
jugular furrow, the left hand being similarly engaged in the left
jugular furrow. The method of employing the fingers is identical, or
instead of the fingers the thumbs may be used.

[Illustration: $1]

When the obstructing object has been lifted as far as the pharynx it has
a tendency to fall out of the mouth, and if it fail to do so it can be
fixed in position and removed as in the preceding case.

II. =Extraction.= These methods are applicable to cases where the
foreign body has become fixed in the cervical region, but more
especially to obstructions in the intra-thoracic part of the œsophagus.
In the majority of cases they are dangerous, and may lead to pinching,
rupture, or perforation of the œsophageal mucous membrane. They should
therefore be regarded as exceptional measures. Theoretically, the
instruments described are perfect, but practically they do not secure
the results anticipated, because one can never prevent displacement,
wrinkling, and involution of the œsophageal mucous membrane.

The forceps probang has the drawback of seldom grasping smooth foreign
bodies with sufficient firmness to permit of their extraction.

The corkscrew sound exposes one to the great danger of completely
piercing the œsophagus, because it has to be managed blindly, and
because one never knows at what depth the corkscrew portion should be
protruded in order to obtain a proper hold of a foreign body.

III. =Passage of the probang.= When taxis fails or is inapplicable, we
are forced to attempt thrusting the foreign body onwards. The method is
much safer than the preceding, but, nevertheless, demands great tact,
prudence, and gentleness. Suitable œsophageal sounds are made with
cupped extremities, though in cases of emergency an instrument can often
be successfully improvised from a cane, whip handle, or flexible stick,
about 4½ to 5 feet in length, securely wrapped at one end with cloth or
tow and freely coated with some greasy material such as lard, vaseline,
or oil.

The end of the sound having arrived in contact with the obstacle, the
operator exercises moderate but permanent pressure. The obstacle may not
move immediately, because of spasm of the œsophagus, which grasps it. It
is therefore necessary to wait and to take advantage of a moment when
the resistance is less, and even then the obstacle may not move.

Rough manipulation with improvised sounds may tear, fissure, or
perforate the muscular and mucous coats, producing the gravest
consequences.

IV. =Crushing.= The crushing of an obstruction in the cervical region
was long ago suggested, and is still greatly commended by empirics and
farriers. It is performed by means of a little mallet and a piece of
board. The method is barbarous, and exposes the animal to such grave
complications as crushing of the œsophageal walls, followed by necrosis,
laceration of the connective tissue, and interstitial hæmorrhage,
injuries of the superficial or deep-seated jugulars, of the carotid
artery, pneumo-gastric nerve, etc. It should never be practised, even
although attempts have been made to improve it by replacing the mallet
and board by specially formed forceps intended for crushing potatoes or
roots. Only in the rare cases where one is certain that the foreign body
consists of a very ripe fruit could crushing be justified, and in this
case there is no need to have recourse to special instruments, for the
hands alone suffice.

=Injection of alkaloids.= The practitioner occasionally finds himself in
the embarrassing position of having vainly tried all the above methods.
Before adopting the last resource, viz., œsophagotomy, it is then worth
while to test the action of certain alkaloids, injected subcutaneously,
after having punctured the rumen.

We know that pilocarpine and eserine stimulate secretion and the action
of the bowels. Injected under the skin they cause frequent swallowing
efforts, and intense peristalsis extending throughout the length of the
digestive tract. Doses of 1½ to 2 grains of pilocarpine and 1 to 1½
grains of eserine, according to the size of the animal, sometimes
produce excellent results, and rapidly remove obstructions.

Apomorphine, the effects of which are, so to speak, inverse, because
they tend to produce anti-peristalsis and vomiting, may be tried in
doses of 2 or 3 grains.

=Œsophagotomy.= The last resource is œsophagotomy, which, however, is
only applicable in cases of obstruction of the cervical portion of the
œsophagus. It should be performed as described in the section hereafter
on operative manipulation. (See also Möller and Dollar’s “Regional
Surgery,” p. 166.)

The point selected is necessarily governed by the position of the
obstacle. There is no need to enter into full details. We may remark
that it is not always necessary to perform the complete operation, and
the third and fourth stages can sometimes be avoided by substituting for
them attempts to break down the foreign body by submucous manipulation.
The œsophagus, having been exposed and isolated, is punctured with a
straight tenotome immediately below the obstacle. A curved tenotome is
then introduced, and the root, potato, or fruit divided. As a rule, a
little pressure from the outside then causes one or other of the
fragments to move onwards and deglutition becomes normal.

Attempts have also been made to divide the obstructing body directly
without previous incision and without isolating the œsophagus. It is
much more difficult, for the least movement of the patient changes the
relationships of the superposed layers and introduces obstacles to the
manipulation of the blunt-pointed tenotome which is employed. More
success often attends attempts to puncture the object with a fine
trocar.


              RUPTURES AND PERFORATIONS OF THE ŒSOPHAGUS.

=Causation.= Wounds of the œsophagus caused by external violence are
rare, or at least secondary; lacerations produced from within, on the
contrary, as a result of clumsy manipulation are relatively frequent.
They may extend throughout the length of the tube, but in a far greater
number of cases are found near the entrance to the stomach at the point
where the œsophagus turns towards the left.

The passage of the œsophageal sound or probang is apt to exaggerate this
curvature, and if pushed violently the instrument may produce first a
flexure, then a partial rupture or even a perforation of the tube.

In other cases a rough, irregular, infected foreign body may when
swallowed penetrate the wall and cause inflammation, necrosis and
perforation of the œsophagus.

=The symptoms= are always very grave, and of rapid development. They
consist in local œdematous swelling, sero-sanguineous infiltration at
the entrance to the chest, in the pretracheal region and along the
jugular furrows.

The pneumo-gastric and inferior laryngeal nerves being compressed,
dyspnœa results. If the œsophagus is perforated in the thoracic cavity
septic pleurisy at once sets in.

=Diagnosis.= The diagnosis is easy, provided the history point to
perforation of the œsophagus.

=The prognosis= is fatal whenever the perforation is within the thorax.
It is sometimes possible to intervene in cases of perforation in the
cervical region, but from the economic standpoint such intervention is
of little value.




                              CHAPTER IV.
               DEPRAVED APPETITE—PICA—THE LICKING HABIT.


Depraved appetite, causing animals to swallow bodies which cannot
properly be described as food, is frequent. The condition is commonest
in adult animals of the bovine species, in calves and in lambs. The
consequences are sometimes very serious, so that although depraved
appetite does not represent a well-defined morbid entity, it is
important to be in a position to remedy it.

Depraved appetite does not appear under the same conditions in young and
in old animals. In adults it often results from faulty feeding, or from
some wasting disease which develops insidiously, or remains
unrecognised; in young animals it is the result of insufficient
nourishment.

Roloff & Röll hold that pica is the first symptom of osteomalacia (which
see).


                      DEPRAVED APPETITE IN THE OX.

=Causation.= In the bovine species depraved appetite occurs in adult,
debilitated animals, which are often, though not always, suffering from
some well-marked digestive disturbance.

The frequency of this symptom, and the peculiarities in its occurrence,
have caused it to be referred to a large number of different causes,
among which may be mentioned bad hygiene, chronic gastro-enteritis,
tuberculosis, osseous cachexia, pasteurellosis, gestation, etc.

It is very certain that the peculiarity in the appetite is, above all,
the result of incomplete and irrational alimentation. The animal has
certain special requirements, to meet which the food must be of suitable
composition. If these alimentary and digestive conditions are not
fulfilled, depraved appetite may occur, even in animals which appear
well nourished. Certain authors refer the appearance of this condition
to want of certain soda salts in the daily ration, and, in support of
this opinion, they point to the frequency of the disease in mountainous
regions where the geological formation is chiefly granite, as in the
Black Forest. Alluvial soils are supposed not to produce it. It
certainly seems more common on soils lacking in certain constituents or
exhausted by repeatedly growing certain crops. Nevertheless, in France
it might be urged that pica occurs equally on all kinds of soil, and a
German author, Lemke, ascribes this perversion of nutrition to the want
of phosphorus. Haubner and Siedamgrotsky attribute it to a nervous
disorder. All causes which exhaust the organism, especially all chronic
diseases of digestive origin, may induce aberration of appetite.

Permanent stabling, confinement, absence of sunlight, want of exercise
and pure air contribute to the general debility which predisposes to
attack. Dry seasons, by reducing the supply of food, have a similar
effect.

In tuberculosis and in pasteurellosis, it is the general organic decline
which produces these puzzling changes in appetite. Similarly the
influence of gestation depends on the superadded demands on the organism
caused by the development of the fœtus.

=Symptoms.= The symptoms may be divided into two phases.

In the first phase, the animals still preserve their appetite, but
whenever they have an opportunity they eat earth, sand, manure, litter
saturated with urine, plaster, etc. They lick the walls, the boarding,
the mangers and the trees, and they chew and swallow linen spread out to
dry.

This phase may continue for a very long time, three to four months or
more, provided no acute complication results from the eating of such
foreign material. There is no fever, but the appetite, although well
preserved, is often capricious, and the ordinary food is eaten slowly.

In the second phase, which frequently marks the development of
complications produced by the passage, contact, or prolonged sojourn of
various materials in the digestive tract, fever appears, little marked
as a rule, but continuous in character.

The appetite is diminished. The animal wastes; the secretion of milk
diminishes, and signs of chronic gastro-enteritis may be noted. The
perversion of appetite still continues; rags, decomposing or filthy
materials, pieces of old shoes, etc., are eaten, and it is not
surprising that such substances should have an unfavourable effect on
the mucous membrane of the digestive tract.

The wasting process slowly leads to marked emaciation, and after an
interval of from six months to a year, or even two years, the patients
die in a state of complete exhaustion. The lesions found on post-mortem
examination are those of various diseases capable of producing depraved
appetite or simply lesions of chronic gastro-enteritis.

=Diagnosis.= The diagnosis presents no difficulty. The important point
is to discover whether or not there exists some previously unrecognised
primary disease.

=Prognosis.= The prognosis of this condition is grave, because depraved
appetite is frequently only a symptom of some incurable disorder, or
because the changes in the digestive mucous membrane are already too far
advanced to permit of much improvement.

=The lesions= comprise: general emaciation, presence of a yellow serum
in the fatty tissue, muscles pale and flabby, catarrh of the mucous
membrane of the stomach and bowel. The blood seems less in quantity and
coagulates feebly or not at all.

=Treatment.= The treatment should be directed against the primary cause,
if such exists (osseous cachexia, pasteurellosis, gestation, etc.).

In other cases a change in management and in feeding, and the
administration of food rich in mineral salts like chlorides, carbonates,
and phosphates of lime, soda or potash, produces the best possible
results. The leguminous foods, sainfoin, clover and lucern, are to be
recommended. The animal, if formerly stabled, should be turned out and
its living conditions entirely altered.

It is often useful to place a block of rock-salt in the manger; when
hyperacidity of the stomach is suspected lime water, chalk, or magnesia
should be given. Where digestion is weak or slow HCl, pepsin and
vegetable bitters are indicated. Nevertheless, one sees cases which
refuse to yield to any of the ordinary methods. In treating these, Lemke
has recommended the subcutaneous injection of chloride of apomorphine, a
drug which may be regarded as a true specific. The doses vary between 1½
and 3 grains, and an injection is given once a week for three weeks in
succession. After this the tendency to pica is said to disappear and the
general condition to improve. The treatment must be repeated every three
months in countries where depraved appetite appears general and
permanent.

It is difficult to understand by what mechanism this drug produces the
effects attributed to it, but those who have employed it speak very
highly of its action.

We may add that in addition to the different modes of treatment, it is
not infrequently necessary to hastily perform gastrotomy in order to
avoid fatal consequences, which would otherwise follow indulgence in
this habit. When an animal has swallowed a considerable quantity of
linen, for example (and Moussu has seen cases in which many pounds
weight had been devoured), immediate intervention is required to avoid
intestinal obstruction. Furthermore, when the history is quite clear
gastrotomy allows the entire mass of foreign bodies, ingested at
different times, to be removed.


                 DEPRAVED APPETITE IN CALVES AND LAMBS.

=Causation.= Depraved appetite is commonest in calves and lambs when the
animals are insufficiently nourished, or when the mothers are suffering
from chronic debilitating diseases and are therefore yielding milk poor
in fat and in mineral constituents. In a few rare cases it is impossible
to discover what causes the young animals to devour these foreign
materials. Even fully-grown sheep, when shut up together in winter,
acquire the habit of chewing each other’s wool, sometimes to the extent
of virtually depilating their fellows and accumulating wool balls in
their stomachs.

=Symptoms.= Calves have a tendency to lick themselves or their
neighbours, and thus little by little collect a varying quantity of hair
which they swallow. When this habit of licking is little marked the
quantity of hair ingested may not be dangerous; but in the contrary case
the hair (which cannot be digested) accumulates and is permanently
retained in the abomasum. It soon becomes converted into masses,
cemented together with mucus, and forms round balls, to which the name
of œgagrophiles has been given. If these œgagrophiles, or hair balls,
are of small size, they prove of trifling importance; but too frequently
they attain considerable dimensions and obstruct the pylorus or the
intestine. The young calves then refuse all nourishment, and die in
twenty-four to forty-eight hours in a state of complete exhaustion or
after a series of epileptiform attacks.

In lambs the complications due to depraved appetite develop in a similar
way, but the wool swallowed is obtained from the mothers. The lambs
first suck the locks of wool, then tear them off and swallow them. So
long as these peculiarities of appetite are little marked no bad results
follow; but if the shepherd is careless, and fails to note the condition
of his young flock sufficiently early, accidents occur.

The wool is not so easily converted into balls as is hair, but it soon
accumulates in the pyloric region or in the intestine, and forms
obstructing masses. The little patients lose appetite and lie down in
corners, where they are found dead after twenty-four to forty-eight
hours. The masses of wool or of hair are rarely passed with the
excrement; more frequently they are vomited, but this again is
exceptional; usually they become arrested at the entrance to the
pylorus. The lambs show colic, tympanites of the abomasum, and attempts
at vomiting, though unfortunately these are often overlooked. The
quantity of wool found in the abomasum and intestine on post-mortem
examination may be considerable, in relation to the size of the
digestive compartments. Death results from intestinal obstruction,
exactly as in the case of calves.

These aberrations of appetite in lambs have been considered as due to
the want of sufficient mineral salts in the mother’s milk; and it has
been stated that the lambs practise this habit because of the laxative
result of the fat contained in the wool swallowed. The explanation seems
very logical, though it is by no means perfectly proved. It is certain
that this habit becomes particularly common after years in which forage
has been scarce and among flocks in bad bodily condition. The force of
example also plays a certain part, and animals probably imitate one
another, and so acquire the disease. This explains the importance of
early segregation.

=Diagnosis.= The diagnosis of depraved appetite, pica, or the licking
habit presents no difficulty; but it can only be arrived at by the
cowman or shepherd, for the symptoms can only be detected by continued
watching.

The diagnosis of pyloric or intestinal obstruction is very difficult in
the absence of information. It becomes easy after the first post-mortem
examination has been made.

=Prognosis.= The prognosis is grave. In calves, obstruction of the bowel
by hair balls inevitably causes death, and in sucking lambs the
mortality may be high: as much as 15 per cent. to 20 per cent. according
to the observations of several observers. The mortality occurs about the
age of six weeks to two months, whilst the licking habit may begin
towards the end of the second week.

=Treatment.= Prophylaxis demands that the mothers (whether cows or ewes)
be well fed. An excellent precaution consists in adding to the food a
sufficient quantity of salt and of phosphate of lime (2 drams to 2½
drams of each). This treatment of the mothers is necessary as soon as
the tendency to licking becomes manifest.

In calves the best method of avoiding fatal results is to prevent the
young animals licking one another; and the method now usually practised
on well-managed farms consists in applying a simple muzzle of wicker
work immediately after each meal.

In lambs treatment is more difficult. As soon as the shepherd sees any
tendency to depraved appetite the lambs should only be left with their
mothers whilst being suckled. The flock should be exercised in the open,
and ordinary salt should be placed at a number of points on the ground
occupied by the animals.


                            COLIC IN THE OX.


        COLIC DUE TO INGESTION OF COLD WATER. CONGESTIVE COLIC.

=Causation.= Congestive colic occurs in the stable, in animals which
have been doing heavy work, and, returning in a heated condition, drink
large quantities of cold water. It is commoner when animals have not
eaten for a considerable time, and when, therefore, the stomach is
nearly empty. Under these circumstances chill of the digestive viscera
is direct and immediate.

=Symptoms.= This form of colic occurs suddenly, soon after the water has
been swallowed, and is characterised by violent pain. At first the
animals show uneasiness, stamp, and continually move about striking
themselves in the flank with the feet or horns, swishing the tail, etc.
They refuse food, lie down and rise frequently, and paw the ground.

As a general rule this form of colic lasts from half an hour to one
hour, and terminates in recovery. In some rare cases where death
occurred Cruzel found on post-mortem examination congestion of the
abomasum, and, in a few, congestion of the small intestine, with or
without rupture.

=The diagnosis= is easy, on account of the suddenness of onset, rapid
development and history of the disease, discovered on questioning the
owner or herdsman.

=The prognosis= is not grave. This form of colic generally cures itself.
Nevertheless precautions are required against possible complications,
such as intestinal hæmorrhage and invagination.

The necessary preventive measures are self-evident. Animals returning
from work should not be allowed to drink freely of cold water, but
should first receive a little food and afterwards water at the
temperature of the atmosphere.

When colic has set in, the patient can be walked about. If pain
persists, the region of the abdomen may be dressed with oil of
turpentine, mustard, or similar counter-irritants. The application of
warm clothing is also useful. Finally, in grave cases, a moderate
quantity (three, four, or five quarts) of blood may be withdrawn from
the jugular. The administration of stimulants like wine, alcohol, etc.,
is also indicated.


                       COLIC DUE TO INVAGINATION.

Invagination consists in the passage of one portion of the intestine
into the next-following portion. When once the condition has been set up
it tends to become aggravated, the invaginated part being drawn further
and further forwards. Invaginations therefore may vary in length between
a few inches and sixteen to twenty inches.

Law states (Vol. II. p. 347) that in cattle and swine invagination of
the large colon is almost impossible owing to the relation of the bowel
with the layers of the mesentery. The anatomical arrangement is opposed
to the formation of invagination, yet this accident is not uncommon in
cattle and swine. The small intestine can be invaginated into the cæcum
or into itself. The cæcum may become invaginated, or it may pass into
the colon or rectum.

Cartwright, _Veterinarian_ (1829), reports a case of invagination in a
bull calf, and Youatt gives particulars of a similar case which was
followed by sloughing and discharge per anum of the intussuscepted
portion of bowel. (See also Möller and Dollar’s “Regional Surgery,” p.
328.)

=Causation.= This variety of colic is due to a number of somewhat
obscure causes. In a general sense we may say that anything which
increases intestinal peristalsis increases the risk of invagination. The
accident may follow intestinal congestion, but is most frequent in
animals suffering from intestinal worms, or in animals used for heavy
work. Under the influence of violent tractive efforts the peristaltic
movements are stimulated, and the intestine being in an oblique position
on a plane inclined backwards, the contracted portion may slip into the
dilated section behind it.

[Illustration: $1]

Invagination may also occur without any apparent cause, even in animals
standing in the stable.

=Symptoms.= The attack always occurs suddenly, develops rapidly, and is
of an extremely grave character.

Colic comes on while the animal is working, moving about, or resting,
according to circumstances, and at first resembles that due to
congestion. It afterwards becomes very violent; the animals paw, stamp,
show great uneasiness, throw themselves violently down, and rise
suddenly, only to again lie down as before. The face expresses anxiety,
suffering and depression; the tail is often kept lifted, and efforts are
continually made to defæcate, mucus being passed. By passing the hand
into the rectum the invagination may occasionally be discovered.

Colic persists with great intensity for ten to twelve hours, interrupted
only by rare periods of calm. At the end of this time, however, it may
suddenly disappear, and the animal may fall into a semi-comatose state.
This indicates the onset of necrosis in the invaginated section, the
painful reflexes no longer being transmitted to the sympathetic system.
The disappearance of colic is sometimes regarded as a sign of
improvement, but this improvement is illusory. From this time onwards
the animals stand stolidly, obstinately refusing both food and drink. If
they lie down, it is with great care. Palpation of the right side of the
abdomen is painful, and the animal actively resents it. One of the most
important and constant signs at this stage is the absence of defæcation,
due to obstruction of the intestine, which is occluded. The animals may
survive for ten, twelve, or even fifteen days (see also Möller and
Dollar’s “Regional Surgery,” _loc. cit._). The invaginated, necrosed
portion may even be passed with the fæces, and recovery may occur, the
continuity of the intestinal tube being secured by the adhesion of the
serous surfaces; but such spontaneous recoveries are exceptional.
Usually after a few days death results from peritonitis.

Occasionally, trifling invaginations may become reduced spontaneously,
Diarrhœa, with the passage of blood-stained material is then seen for a
time, a sign which alone at this stage would justify the diagnosis of
invagination.

=Diagnosis.= The intensity of the colic and the absence of defæcation
for several days afterwards, justifies the diagnosis of invagination.
Purgatives then remain without effect. In addition, rectal exploration
offers a valuable means of diagnosis. The last portions of the intestine
are found absolutely empty, and the arm when withdrawn is found to be
covered with viscous blood-stained mucus, resulting from the
sero-sanguinolent exudate, due to compression of the blood-vessels.

In cases of this kind accompanied by the above-mentioned symptoms
abdominal exploration by the rectum should always be practised, but it
rarely gives exact information. The hand, when passed towards the right
flank, may sometimes reach the invaginated part, which conveys the
impression of a cylindrical swelling. The invagination, however, can
rarely be reached. If the operator is successful, he will find that as
he displaces this cylindrical mass or attempts to grasp it, the animal
shows signs of exaggerated sensitiveness.

=The prognosis= is of exceptional gravity. Apart from the rare cases
where the invaginated portion becomes necrotic and is eliminated, death
is inevitable. Unless an operation is performed, septic peritonitis may
develop about the fifth or sixth day.

=Treatment.= The only treatment consists in surgical intervention. Some
practitioners have recommended giving large doses of purgatives with the
idea of causing changes in the neighbourhood of the invaginated part;
but such treatment presents little chance of success. The same is true
of the administration of large doses of olive oil, either in the form of
draught or of enema.

Siebert attempted reduction by generating CO_{2} from soda bicarbonate
dissolved in water and diluted HCl, injected successively per rectum. In
time fæces and CO_{2} escaped, and the patient recovered. Siebert claims
to have cured by this method a cow with invagination of five days’
duration; but the effect of his treatment may be doubted, as afterwards
a portion of bowel was found in the cow’s dung.

When diagnosis is certain, the only treatment that can be recommended
consists in performing laparotomy followed by enterotomy. One cannot,
however, operate in all cases, nor do all cases offer the same chances
of success. If the invagination is situated in the first portion of the
small intestine, and is hidden beneath the circle of the hypochondrium,
intervention is out of the question, but if it has been detected by
rectal exploration in the last portion of the intestine, operation may
prove successful. Only in cases of the latter description should it be
attempted.

Laparotomy is performed in the right flank according to the usual method
(see Möller and Dollar’s “Regional Surgery,” p. 313). After opening the
peritoneal cavity, the invaginated loop of intestine must be sought. It
is not always easy to discover amongst the mass of intestines present,
but can be recognised by its hardness and by the congestion of
neighbouring parts. After withdrawing it through the abdominal opening,
the operator may then proceed by one of several methods.

(1.) Some authors recommend grasping the two ends, drawing them apart,
and thus reducing the invagination. The actual manœuvre is not
difficult, but even when unattended by accident or tearing of the
intestine it is by no means always followed by recovery. Although the
intestine may not appear gangrenous externally, necrosis often occurs
eventually.

This method should only be practised during the first twenty-four hours
after the appearance of colic, and even then one must always bear in
mind the possible consequences just mentioned, and the chances of
rapidly fatal septic peritonitis.

(2.) The second method consists in removing the invaginated portion of
intestine. It is best to apply bichromatised catgut or silk ligatures to
all the arteries which pass from the mesentery into the loop to be
removed; after which the loop itself may be simply divided an inch or
two above and below the invagination, in order to be quite certain that
one is operating on healthy tissue, the divided ends being held
meanwhile by an assistant. The intestine is afterwards sutured with a
fine needle and bichromatised catgut or boiled silk. The form of suture
will be found described in Dollar’s “Operative Technique.” It may be
valuable to test the efficacy of decalcified bone tubes for uniting the
ends of the intestine.

The operation is long, delicate and difficult, and it is imperative not
to infect the abdominal cavity during its performance. To prevent this
the liquid and solid materials present in the bowel may be thrust
upwards and downwards away from the diseased part before the section is
made; and in this way the wound and the operator’s hands are preserved
from infection. The intestine should be kept closed during the
application of sutures by means of flat clamps cautiously applied. In
their absence the ends may be held by an assistant, whose hands should
previously have been carefully disinfected.

(3.) In cases where the serous coats of the two portions of bowel
constituting the invagination are to some extent adherent, another
operation of a less perilous character may be performed. This consists
in liberating the invaginated part by means of longitudinal incision,
without previously disengaging the parts, and without resection. The
invaginated (external) portion of intestine is divided longitudinally;
the gangrenous part immediately becomes visible, and may be removed. The
operator has then only to suture the longitudinal wound, an operation
which is much easier and demands much less time than any circular
intestinal suture whatever. These operations must not be attempted
except in response to the express wish of the owner, who should be fully
informed of the dangers to which they expose the animal; for after the
second day of invagination local peritonitis has often developed and one
is then operating on injured or infected tissues, in itself a very
unfavourable modifying condition. The current formula that “the
operation was very successful” is not accepted in veterinary practice
when the patient dies three or four days afterwards. From the economic
standpoint it is better to slaughter animals of any value, for unless
secondary peritonitis has occurred, and the animal is not feverish, the
meat is fit for consumption. “Volvulus,” or twist of the intestine, is
said to be almost unknown in cattle, though Reichert records a case of
volvulus of the ileum.


                  COLIC AS A RESULT OF STRANGULATION.

The symptoms of this colic differ very little from those of the
preceding with which they are often confused. But in regard to its
causation the condition is essentially different.

=Causation.= Strangulation of the intestine in the ox may be produced in
several different ways: by the passage of a loop of intestine through a
tear in the epiploon, through the diaphragm, mesentery, broad ligament
of the uterus, the serous layer surrounding the spermatic cord, etc., or
by strangulation of an intestinal loop by fibrous bands resulting from
chronic peritonitis, etc. Of these various causes, the three principal
may here be described:—

(1.) Tearing of the mesentery. As a result of mechanical violence the
epiploon or mesentery becomes fissured, and the peristaltic movements
cause a loop of intestine to pass through and become fixed in the
fissure. If the opening is narrow, as is usually the case, the base of
the intestinal loop, riding on the lower lip of the slit, becomes
constricted by the margins of the opening through which it has passed.

[Illustration: $1]

(2.) In pelvic hernia a loop of intestine passes between the spermatic
cord and the walls of the pelvis. The fissure in this case is in the
serous fold which supports the large testicular arteries and the vas
deferens. The fold is often ruptured during castration, especially
during the practice of “bistournage,” in consequence of traction
exercised on the cord.

(3.) Pseudo-ligaments and fibrous bands due to chronic peritonitis.—In
local, subacute or chronic peritonitis false membranes may become
organised, forming fibrous cords or folds connecting the
parieto-visceral or inter-visceral surfaces. If by accident a loop of
intestine insinuates itself beneath one of these fibrous bands, the
passage of digestive material is first impeded and then stopped. The
intestine becomes engorged, and symptoms of strangulation soon follow.

=The symptoms= appear suddenly, and are similar to those of
invagination. They consist of very acute colic, which disappears after
ten to twelve hours.

The peristaltic movements drive the semi-digested food, whether liquid
or gaseous, towards the lower (strangulated) end, from which it cannot
escape. It therefore distends the herniated loop and sets up intestinal
engorgement. This constitutes the first stage of strangulation, and is
accompanied by severe disturbance in the local circulation. The mucous
membrane of the intestine becomes swollen and infiltrated, so that it
alone soon fills the entire neck of the hernia. Necrosis of the loop of
intestine is then only a matter of time.

=The diagnosis= of colic by strangulation is difficult. The condition
cannot often be recognised at an early stage, and may easily and
excusably be confused with invagination. Only in rare cases will rectal
and abdominal examination enable one to detect a pelvic or mesenteric
hernia.

=The prognosis= is even graver than in cases of invagination. Intestinal
hernia progresses very rapidly, necrosis soon sets in, and is followed
by fatal consequences if the condition be not relieved.

=The treatment= is exclusively surgical. As a general rule, whenever
colic is recognised as resulting from strangulated hernia, it is
immediately necessary to perform laparotomy in the right flank, and
after having discovered the cause of strangulation, to divide the
mesentery, epiploon, serous fold supporting the testicular cord, or
accidental fibrous bands, so as to free the herniated loop and avoid
necrosis. If necrosis already exist, the intestine may be resected,
exactly as in invagination.


                        DISEASES OF THE STOMACH.

In ruminants diseases of the gastric compartments are numerous, and,
although they have been recognised since the earliest times, much
remains to be discovered concerning at least some of them. This fact
results from the imperfect state of our knowledge concerning the
essential phenomena of gastric digestion in ruminants. Digestion really
consists of a number of different acts—some mechanical or neuro-motor,
some chemical; in addition to which must be reckoned the phenomena of
sensation, concerning which patients cannot give any information.

The mechanical phenomena, consisting in the constant movement of
ingested material through the different compartments, rumination,
eructation, evacuation towards the intestine, etc., are well known to
us; and a careful examination of diseased animals enables us to estimate
the importance of changes in them.

On the other hand, the chemical phenomena are little understood. It has
hitherto been considered that the rumen, reticulum, and omasum are only
simple diverticula, with mechanical functions, and that the abomasum is
the reservoir in which the chemical changes take place. Another view,
which is perhaps not altogether justified, presupposes that the chemical
transformation of the food in the abomasum takes place as in other
animals, and in particular as in man, in whom the chemistry of gastric
digestion has been the object of extremely careful research by certain
French and other pathologists. We do not believe (for reasons too long
to be explained here) that the gastric digestion of ruminants, or even
of herbivora in general, can be identified with that of omnivora.

The nature of the food being totally different, the chemical reactions
in the stomach and intestines are also different; in proof of which we
need only cite the single fact that ptyalin is absent from the saliva.
Straw and oats are not digested in the same way as a mutton cutlet.

But even supposing that the broad outlines of physiological action are
the same, nothing has hitherto been discovered in veterinary surgery
respecting possible variations in the chemical processes taking place in
the stomach during different gastric diseases; and it appears not
improbable that in this direction causes might be discovered which
veterinary practitioners have hitherto sought elsewhere. Excess or
insufficiency of hydrochloric acid, and variations in the quantity of
the organic acids, play so important a part in the theory of gastric
pathology in man, that it is scarcely surprising to find similar ideas
recurring in the pathology of domestic animals. The correctness of these
views remains to be proved; and without wishing actually to classify
dyspeptic conditions as in man, we may assert that diseases described
under other names stand in direct relation to variations in the gastric
secretion or to disturbance of gastric movements—_e.g._, simple chronic
tympanites, which, without a doubt, is often a neuro-motor dyspepsia.

The classification we shall adopt in studying the diseases of the
gastric compartments is, therefore, extremely simple. In the first
series we shall consider sudden, accidental, and temporary forms of
indigestion, and in the second series, acute or chronic forms of gastric
inflammation.


                              INDIGESTION.


                          GASEOUS INDIGESTION.

Gaseous indigestion, also described as indigestion of the rumen, is
characterised by the rapid accumulation of gases (chiefly carbon
dioxide, carbon monoxide, and marsh gas), due to fermentation in the
upper part of the rumen. It is common in oxen and sheep, and has
received the names of mephitic indigestion, acute tympanites, meteorism,
etc. It occurs during or immediately after feeding.

=Causation.= Numerous causes have been invoked to explain the sudden
occurrence of gaseous indigestion.

The most important is the particular condition of the animal at the
moment when it has been attacked. For if external influences alone were
responsible, there is no reason why all the animals of a given herd or
flock, or of a particular stable, which are under similar conditions as
regards feeding, etc., should not be affected in the same way.

That the external causes cited (cold, excessive heat, stormy weather,
etc.) may affect different animals differently and unfavourably is
beyond doubt. But the temporary morbid condition of the animal itself is
the essential condition to the development of indigestion.

In all probability the animal has in every case been more or less
unwell, except in those attacks of indigestion resulting from
progressive poisoning during the course of a meal, such as occur when
toxic plants like belladonna, veratrine, colchicum, poppies, tobacco,
hemlock, etc., have been eaten. In such temporary abnormal states
movement of the rumen is partly abolished, or at least is markedly
retarded, and, as a consequence of vaso-motor disturbance, the mucous
membrane is probably not so abundantly covered with mucus nor so freely
irrigated with secretion, as usual. Under these conditions, if the
animal, which may appear perfectly well, is allowed to partake of soft,
wet, fermentescible food, gaseous indigestion is very likely to develop.

Cultivated grasses, like lucern, sainfoin, clover, and especially
grasses grown on artificially manured fields, are regarded as
particularly liable to cause gaseous indigestion. This conclusion seems
justified by experience, particularly by the fact that young shoots or
young, tender after-growths are very liable to fermentation.

This exaggerated tendency to fermentation of tender grasses has even
been held exclusively responsible for indigestion, and the cessation of
peristalsis in the rumen has been considered a secondary phenomenon, due
to distension.

Whether atony of the rumen be the primary condition and abnormal
fermentation secondary or inversely, whether fermentation be primary and
atony secondary, is not of importance; for either view may be adopted
without altering the results, and without the theory being invalidated
by the objection that other animals subjected to similar influences had
not contracted the condition.

We have already drawn attention to the importance of the condition of
the animal’s health for the time being. Digestive peristalsis being
diminished, eructation, admixture of food in the rumen, and its onward
movement being impeded, fermentation proceeds rapidly. As a consequence
the rumen becomes distended, and, cause and effect changing places, the
distension in its turn arrests peristalsis, which had previously only
been checked.

Local chills, produced by ingestion of food covered with rime,
hoarfrost, or simply with dew, may favour gaseous indigestion; such
conditions retard or suspend the peristaltic movements by direct local
action, and probably by producing vaso-motor disturbance of the mucous
membrane. In very rare cases chill has an undeniable influence, either
by provoking general vaso-motor disturbance, which reacts on the
secretions, or neuro-motor trouble. Gaseous indigestion is not uncommon
in animals living on dry winter food, which have been moved from their
ordinary quarters and sent on railway journeys or to fairs, etc. As a
general rule this form of indigestion is commonest in spring, when the
transition from dry winter food to grass, etc., has not been carefully
effected. It is also frequent during stormy weather in full summer.
Marked barometric changes seem to have an influence on the general
health, and particularly on the nervous system, thus favouring organic
fermentations.

=Symptoms.= The earlier symptoms of indigestion escape observation, but
they soon begin to develop rapidly, and are then very easy to follow.
They always exhibit the same characters, developing, however, with more
or less rapidity in different cases. Soon after they commence feeding
animals appear to experience special discomfort, which causes those at
grass to stop grazing; even when stabled they stop feeding. From this
time they show eructation, repeated yawning, restlessness, and some
anxiety.

In a quarter of an hour, or less, the left flank begins to project, both
laterally and vertically, so that eventually the walls of that part of
the abdomen may project above the transverse processes of the lumbar
vertebræ. The right flank also becomes swollen, as a consequence of the
intestine being thrust out of position. The animal very rapidly shows
general disturbance; the nostrils are dilated, the mucous membranes
congested, respiration becomes rapid, and asphyxia threatens. The
respiration soon becomes panting, for the distended rumen paralyses the
diaphragm and compresses the lungs. To ease respiration the animals open
the mouth, extend the neck, and stand with the front limbs spread apart;
but this fails to prevent dyspnœa becoming more intense and asphyxia
imminent.

The heart beats more rapidly, the superficial veins appear swollen, and
the mucous membranes cyanotic. The rhythmic contractions of the rumen
can no longer be detected by manual examination of the left flank; and
on auscultation one neither hears the liquid nor the rolling sound, but
only exaggerated crepitation. Finally, there is marked tympanitic
resonance on percussion.

In cases of very grave tympanites the gaseous pressure in the interior
of the rumen appears to stop the crepitation sound. The animals soon
become unable to walk or even to move, suddenly fall to the ground, and
die rapidly from asphyxia.

The rapidity with which gaseous indigestion develops varies greatly.
Sheep and oxen may die from tympanites, within an hour or even half an
hour of their arrival in the field; but more frequently the symptoms
develop slowly, only becoming alarming after some hours and continuing
for twelve or even twenty-four hours without causing death.

As a rule, the gas is voided by a series of eructations which empty the
rumen, and recovery follows; but when distension is extreme eructation
cannot occur, and gaseous indigestion then ends in asphyxia and death.

=Lesions.= It might be imagined that this form of indigestion would only
appear when the rumen contains a large quantity of food; but, in point
of fact, the rumen often contains very little.

On post-mortem examination the rumen is found to contain an enormous
quantity of gas, which, when collected and submitted to analysis,
reveals approximately the following composition:—Carbonic acid, 74 per
cent.; carburetted hydrogen, 24 per cent.; sulphuretted hydrogen, 2 per
cent.; nitrogen, traces. The composition of this mixture varies within
certain limits, according to its origin; but carbonic acid always
predominates.

Lungwitz, after elaborate experiments with different foods kept in
closed vessels at the body temperature and with similar agents fed for
days as an exclusive aliment to oxen provided with a fistula of the
rumen for purposes of collection, found carbonic dioxide the
predominating gas in all cases, though the proportion varied with the
nature of the food.

Marsh gas varied from 16 to 39 per cent., being especially abundant in
cases of abstinence. Hydrogen sulphide was found only in traces. Oxygen
and nitrogen were present in small amount, and were attributed to air
swallowed with the food. In fermentation the oxygen may be completely
consumed.

The abdominal organs, particularly the intestine, are congested, as a
result of impediment to the venous circulation. The thoracic organs
exhibit the lesions of asphyxia.

=Pathogeny.= Death is due to carbonic acid poisoning, brought about in
two different ways—viz., progressive asphyxia, caused by inability to
inflate the lungs, and absorption of carbonic acid gas from the rumen;
by virtue of the laws of diffusion, part of the gas contained in the
rumen passes into the blood.

=The diagnosis= is always very easy, and even farm servants may
recognise the condition.

=The prognosis= varies, according to the rapidity with which the disease
develops. In rapid cases, where the condition is fully established in
thirty minutes to one hour, asphyxia may be threatened from the
beginning; but in others, _e.g._, when the attack follows consumption of
dry food, tympanites may develop slowly, only attaining its maximum
intensity after a considerable lapse of time. In general one may say
that tympanites is grave in proportion to the rapidity with which the
gas is generated.

=Treatment.= From the prophylactic point of view, it is necessary to
avoid suddenly changing animals from dry to green food; the transition
should be effected by giving mixtures of dry and green food.

Curative treatment comprises a large number of methods.

The latest, and one of the most practical, consists in massage of the
left flank. The open hand is applied to the left flank and sharply
pressed directly downwards, care being taken not to injure the parts.
This manipulation excites reflex action, awakens the dormant
contractility of the rumen, and leads to restoration of peristaltic
movement. The gases pass into the omasum and abomasum, or in many cases
make their way into the œsophagus. The sudden impulses sometimes cause
food to be returned into the mouth, eructation recommences, and the gas
accumulated in the rumen is partially and progressively evacuated. This
manipulation is often practised in breeding districts, particularly in
the case of sheep, in which the disease occurs with the same characters.
The shepherd fixes the animal between his legs, and, thrusting the
extended fingers of either hand into the flanks, makes sudden, sharp
movements, which again set up eructation and get rid of the excess of
gas.

In Germany cold douches are often applied to the flanks. These excite
vaso-motor action and reflex peristaltic movements, which result in
eructations and in the evacuation of the rumen. But this is not a very
practical method, and necessitates arrangements which seldom exist on
sheep farms.

The action of massage may be completed by administering stimulants like
wine, alcohol, or infusions of such aromatic plants as cummin, fennel,
peppermint, camomile, etc. These act first of all mechanically, by
clearing the terminal portion of the œsophagus. Furthermore, they
stimulate the mucous membrane of the rumen, causing reflex peristaltic
contractions, and, as a consequence, circulation of the partly digested
food; finally, the majority of them arrest fermentation.

With the latter object, ether and assafœtida are also given. The use of
these drugs, however, entails disadvantages, and if the animal has
finally to be slaughtered renders the flesh unfit for consumption.

The giving of absorbents is probably most widely practised. The ammonia
which many of them contain absorbs carbonic acid, thereby diminishing
the pressure of gas contained in the rumen, and therefore the distension
of the first gastric reservoirs. Unfortunately this action is only
temporary, and if the drug is given in too concentrated a form, the
mucous membrane of the mouth, of the œsophagus, and sometimes even of
the rumen and reticulum, may be irritated and inflamed, producing
lesions of stomatitis, pharyngitis, œsophagitis, contraction of the
œsophagus, etc., which after recovery from the acute condition may
gravely affect the animal’s general health. A further drawback is that
the flesh rapidly acquires an ammoniacal odour.

Perhaps the best internal treatment consists in administering purgatives
such as hyposulphite or sulphate of soda or sulphate of magnesia, in
doses of 10 to 20 ounces, according to the animal’s size, or, in the
case of pregnant animals, in small frequently repeated doses. These
check fermentation, and so arrest the evolution of gas, whilst by their
purgative properties they excite contraction of the gastric reservoirs
and cause eructation.

None of these methods of treatment, therefore, should be used
exclusively, but all may be utilised as auxiliaries to mechanical or
surgical measures, and all should be preceded by the use of the probang
and puncture of the rumen.

The first of these operations, the technique of which scarcely requires
description, is often of little value; for the solids and liquid
contents of the rumen being permeated with gases, rise as a fermenting
mass into the upper portions of the rumen, and continually obstruct the
open end of the catheter, so that very little gas escapes.

Puncture of the rumen is much more effective and easier to perform. The
owner himself often operates with an ordinary pocket knife, sometimes
introducing a couple of fingers or a short length of elder-wood tube
into the wound thus produced.

The incision should be made at one stroke, for any hesitation may cause
the wall of the abdomen to recede from the rumen, which lies immediately
below. Should gas escape under the skin, emphysema, which often extends
to the loins and along the quarters, may be produced, and may be
followed by diffuse subcutaneous suppuration, resulting from pyogenic
germs entering the subcutaneous tissue.

Large quantities of gas escape from the puncture, sometimes with such
force as to drive out the canula. The flow of gas then ceases. In other
cases the tube becomes blocked; because, as the pressure within the
rumen diminishes, the gases dissolved or mixed with the partially
digested food are freed, and the whole contents of the rumen become
converted into an aerated, bubbling mass. Liquid or semi-liquid
materials may be ejected to some distance, or may pass between the skin
and the muscles, or between the walls of the rumen and the abdomen,
producing various complications, like necrosis, abscess formation, etc.
Such accidents can be avoided by exercising firm pressure with the
fingers on the tissues surrounding the canula.

Even when the rumen has resumed its normal size recovery is not certain,
and may not occur for several hours, or even several days, afterwards.
The patients should therefore be kept under observation for some time,
and it is usually best to leave the canula in place for one or two days,
and to put the animal on low diet.

Necrosis of aponeurotic tissues, fistula formation, and local
peritonitis only occur if the instrument is dirty or is introduced in a
wrong direction.


    IMPACTION OF THE RUMEN. INDIGESTION AS A RESULT OF OVER-EATING.

In this condition the rumen is over-distended with food. The symptoms
are principally due to abnormal fermentation, the peristaltic action of
the rumen being in abeyance, and the food failing to pass towards the
omasum and abomasum. Rumination is generally suppressed.

The disease usually follows change of diet. When the diet has long been
restricted, as occurs during years of bad harvests, and animals are
afterwards set at liberty in rich pastures, they eat greedily, distend
the rumen with large quantities of green fodder, and set up all the
necessary conditions for this form of indigestion. Similar results
follow when gluttonous animals are freely supplied with rich food.
Working oxen also suffer if withdrawn from work and fed with roots,
beetroot refuse, brewers’ grains, or other manufacturing residue for the
purpose of fattening. These materials can only be absorbed in moderate
quantity, and the large amount of water, etc., they contain is apt to
disturb the animal’s digestive powers, while owing to its fine state of
division such food cannot be returned to the mouth for secondary
mastication, and rumination therefore remains incomplete: the food
accumulates in the rumen, distending and eventually paralysing it. This
is a common result of feeding on semi-liquid pulp, which in order to be
ruminated should be mixed with rough forage.

Insufficiency of drinking water is another and more frequent cause,
especially during the winter, because the ox-herd or cowman is often too
lazy to give a regular and sufficient supply unless water is laid on in
the stable itself. The dry food becomes compacted into a mass, which
cannot be returned to the mouth for rumination. Moreover, less saliva is
then secreted, and Colin has shown that rumination is impossible when
the parotid ducts are ligatured.

=Symptoms.= As may readily be imagined, the symptoms vary, according to
the quantity and digestibility of the food swallowed. In the first place
the appetite falls off: animals suffering from commencing indigestion
only take part of their food; later on appetite ceases, and with it
rumination. Trifling colic sets in, resembling that due to congestion,
and is indicated by unrest, switching of the tail, lifting of the hind
legs, slight groaning, moving from side to side, and lying down and
rising at short intervals. The animals seem oblivious of their
surroundings, anxious, and at times semi-comatose.

When the case has been neglected for several days the animal may
masticate without having any food in the mouth, and may attempt to
eructate and to regurgitate food; but such attempts always fail. It then
absolutely refuses food, and animals which have eaten large quantities
of green forage may show tympanites. If called in at this period of the
disease the veterinary surgeon finds nothing positive except signs
referable to the digestive apparatus. By methodically examining the
digestive tract, and in particular the stomachs, one discovers during
palpation of the left flank that the rumen is distended. This is
characteristic. By deep palpation it is even possible to detect marked
resistance and a certain characteristic firmness resulting from
accumulation of food. The percussion sounds over this region are dull,
and pressure causes pain, as though the rumen and peritoneum were
inflamed. When the open hand is laid flat on the rumen and thrust
downwards, no peristaltic movement can be discovered. Finally, on
auscultation the normal sounds, including crepitation, fermentation, and
rolling sounds are all absent.

There are no well-marked general symptoms. Respiration and circulation
are hardly accelerated, nor is the artery particularly tense.

=Course and Termination.= The course of the disease varies, and the
condition may be divided into two forms, acute and chronic. The first
develops in a single day, and may cause death by the same mechanism as
acute tympanites—_i.e._, asphyxia or carbonic acid poisoning; the other
continues for five, ten, or even twenty or thirty days, according to the
promptitude with which treatment is undertaken.

In protracted cases, however, the indigestion itself ceases to be as
important as the complications. Sometimes spontaneous recovery occurs,
the food passing away towards the intestine, or even being vomited,
though the latter conclusion is rare. Recovery may also follow from
treatment. If the disease is neglected it may become complicated with
gastro-enteritis.

=The diagnosis= is not very difficult. Indigestion resulting from
impaction is distinguished from acute tympanites by its less rapid
course and by the less marked distension of the rumen (in this case due
to solid food), and from acute gastro-enteritis by the varying degree of
fever which accompanies the latter condition.

=Prognosis.= The prognosis is always grave, even in cases of acute
indigestion resulting from eating green food.

In this case gaseous indigestion occurs as a complication, and
necessitates immediate intervention. The other forms may rapidly yield
to proper treatment, or, in spite of every care, may give rise to
prolonged complications.

=Lesions.= On post-mortem examination of animals which have died of
complicated forms of the disease, we find certain lesions peculiar to
gaseous indigestion associated with impaction of the rumen.

If death has followed the consumption of root pulps, we see signs of
poisoning. As a consequence of prolonged stagnation of food in the
rumen, there follows an exaggerated organic fermentation, whose products
are absorbed through the stomach or intestine and pass into the
circulation.

These various fermentations, which may be of the lactic, butyric, and
even putrid order, produce changes in the mucous membrane of the rumen;
wide tracts of the epithelium may be shed, exposing the corium, and
producing enormous ulcerations, which in certain cases implicate the
entire inner surface of the rumen.

=The treatment= must be varied, according to the cause, symptoms, and
immediate complications. When the disease is of an acute type, such as
that produced by over-gorging with lucern and green food, it is best to
proceed as in gaseous indigestion, _i.e._, to puncture the rumen and
give frequent large doses of purgatives until the stomach and bowels
have been freely unloaded. The animals should then be kept for some days
on small quantities of easily digested food, and should be allowed
lukewarm, mucilaginous drinks.

When tympanites and impaction occur simultaneously, immediate surgical
intervention becomes necessary, and gastrotomy may then be performed by
a very simple method.

Two loops of cord are passed around the abdomen, one behind the
hypochondriac circle, the other in front of the angle of the haunch.
Assistants placed on the right side draw these loops tight, so as to
immobilise the left flank. A bistoury is then thrust directly through
the walls of the abdomen and rumen. As a consequence of the pressure
exercised by the ropes, if not of the pressure of gas itself, the food
material contained in the rumen is often expelled in a powerful stream.
As the superposed tissues cannot very readily change their mutual
relations, the author of this suggestion claims that there is little
danger either of infectious materials passing into the subcutaneous
connective tissue, or of peritonitis; but this rude treatment can only
be resorted to in cases of extreme urgency, and it appears by no means
without danger.

Injections of 10 to 15 centigrammes of pilocarpine and 5 to 10
centigrammes of eserine are also useful.

When impaction of the rumen assumes a less acute form, moderate doses of
purgatives may be given and repeated daily, or twice a day, until the
peristaltic action of the rumen is restored and resumes its normal
rhythm. In certain cases, however, recovery is only apparent. The food
in contact with the walls of the rumen breaks down, and passes away into
the abomasum and intestine, while appetite returns. The animals then
resume feeding, and some days afterwards show all their former symptoms.
Low diet should therefore always be continued for some time.

In spite of treatment, or in consequence of treatment being too long
delayed, no improvement may follow. The ingested food is not expelled.
Putrid fermentation results, auto-intoxication sets in, and the
temperature rises to 40° or 41° C. Unless gastrotomy is performed death
is then certain.

This operation should be undertaken whenever the fever rises to 40° C.,
and two-thirds of the contents of the rumen removed. The rumen should
not be completely emptied, as there is danger of collapse of its walls.
Complications in the region of the wound can be avoided by drainage.

If the operation succeeds, the patients must be placed on very low diet
or on milk for some days, and should be given lukewarm farinaceous
drinks, and a little hay of good quality to excite rumination. In old
milch cows this operation is seldom followed by a satisfactory recovery.
Apart from the loss of milk, the animal loses condition, refuses to
feed, and gradually succumbs to exhaustion.


                IMPACTION OF THE OMASUM (THIRD STOMACH).

=Definition.= “A form of indigestion, of which the prominent feature is
the drying and impaction of the ingesta between the folds of the third
stomach. It may seem to be a primary disease, but in very many cases it
occurs as a result of some acute febrile or inflammatory affection.”
(Law’s “Veterinary Medicine,” Vol. II. p. 123.)

=Synonyms.= Dry murrain, clew-bound, fardel-bound, stomach staggers,
grass staggers, vertigo, chronic dyspepsia, chronic indigestion.

=Causes.= Torpidity of the omasum, suppression of salivary secretion,
with absence of “waves of liquid floating the finely divided food from
the mouth or rumen to third stomach, are prime conditions of desiccation
of the contents.” The third stomach, like the first and second, has no
provision for liquid secretion, and depends for its supply on constant
flushing by swallowed fluids. Therefore, if feeding and rumination are
arrested and salivary secretion is suppressed, and if movements of the
rumen and resulting overflow into the third stomach are checked, the
ingesta of the third stomach, compressed between its folds, becomes
drained of liquid and converted into a powder or dry mass. All febrile
and inflammatory affections tend to this end, and more or less drying,
with impaction of the contents of the omasum, is a constant feature in
such cases. But in the majority of cases this condition is to be looked
on as a secondary or subsidiary affection, and the real disease must be
sought elsewhere.

The explanation of the susceptibility of the third stomach in
constitutional troubles has been sought in the source of its
innervation. Electric stimulation of the vagus rouses the movements of
the first and second stomachs, but not those of the third. Action of the
third stomach is excited by stimulation of the spinal cord, and of the
sympathetic nervous branches going to the ganglionic cells in the walls
of the omasum (Colin and Ellenberger). Its nerve supply coming from a
different source, derangement of its function may occur independently of
antecedent disorder of the first or second, and its motor supply coming
from a source so closely related to the vaso-motor centres, perhaps
affords some explanation of the connection of disorders of the omasum
with febrile and inflammatory diseases.

Food is an important cause. Impaction of the omasum is a winter
disease—the time of dry feeding. Dry, fibrous, innutritious fodder, and
scarcity of water contribute to its production. It attacks cattle in
spring or autumn on pastures in which fresh grass grows among the dead,
dried, or withered stems of a previous growth. It occurs when stock are
fed on corn or corn stalks (maize stalks) affected with smut or ergot,
or on cereals or grasses similarly damaged, and in both cases especially
when the water supply is deficient or restricted.

Sheep and goats, which habitually drink little, suffer less than do
cattle, which drink freely.

=Other causes.= Fermented foods, microbian ferments and their products,
which tend to induce torpidity of the omasum, fever, and lessened
secretion of saliva, with diminished supply of liquid from mouth or
rumen.

Pericarditis, by causing vascular stasis in the omasum, may induce
torpor and impaction.

Lead poisoning paralyses action and favours impaction. Finely divided
food stuffs—meal and bran—eaten greedily, may pass in quantity directly
into the omasum and induce impaction. “The most acute and fatal forms
occur in connection with a sudden change from dry to rich, luscious,
green food in spring, the unwonted stimulus giving rise to general
irritation of the whole gastric mucosa, with disordered and impaired
function of all four stomachs, but especially of the third. Such cases
are usually congestive and inflammatory, and the suspension of the
gastric movements is a grand cause of impaction. In such cases, too, the
brain or spinal cord, or both, are seriously involved, and the early
death is preceded by torpor, paralysis, violent delirium or convulsions,
following largely the type of acute lead poisoning.” (Law, _loc. cit._)

=The symptoms= depend on the degree of impaction, and vary from simple,
irregular, or suspended rumination to severe gastric and nervous
disorder. The less acute cases are marked by failure to re-establish
regular rumination or partial convalescence from fever or inflammation.
The fever subsides, but the appetite remains capricious, the muzzle dry,
eyes dull, spirits low, and breathing accelerated; the condition is
sometimes accompanied by moaning. Slight tympanites may appear, and the
contents of the rumen may feel solid, the mouth hot, clammy, and fœtid.
The bowels are constipated, the fæces small in quantity, hard, covered
with mucus or blood-streaked, and containing particles of undigested
food; in other cases diarrhœa may set in, to be followed later by
constipation. Alternations of constipation and diarrhœa may be repeated
again and again. Exploration by pressure of the closed hand over the
omasum will give an impression of solid resistance. There may be slight
shivering, the ears and limbs are cold, the hair is erect in patches,
dry and lustreless.

In cases occurring independently of previous disease, diarrhœa may be
the first symptom observed, the malady being preceded by local
irritation and congestion; but this soon gives place to constipation or
diarrhœa and the symptoms above mentioned. The animal is found lying
apart on its left side, with its nose in its right flank, the pulse and
breathing quickened, the eyes congested; expiration is accompanied by a
grunt. The patient walks with its back arched and dragging its limbs.
The appetite may continue, but only in an impaired and irregular form,
and as rumination ceases grinding of the teeth becomes common. The
secretion of milk is diminished or arrested, emaciation advances day by
day. Fœtid eructation may be a marked symptom. This form may last from
ten to fourteen days, and merge finally into paralysis of the hind
limbs, drowsiness and stupor, or delirium and convulsions.

“In more acute cases (from sudden access of green food, change of water,
or ingestion of irritant plants), the affection partakes more or less of
the nature of congestion or inflammation of the viscus (omasitis), and
may run a rapidly fatal course” (Law, _loc. cit._). The animal is seen
apart from the herd in a characteristic recumbent position, the eyes are
red and glassy, the eyelids semi-closed, the patient shows much
drowsiness and stupor, but when raised may still feed in a sleepy,
listless manner. The bowels are loose or confined, the pulse and
breathing accelerated, the right hypochondrium is firm and tender, and
the sound of fermentation absent or subdued over the omasum. Soon
nervous disorder appears, the eyes glare wildly, the animal seeks relief
in motion—sometimes in a straight line, sometimes to one side—and being
blind and unconscious of obstacles, may fall into pits or ditches, knock
against trees, fences, gates, or buildings, and continue pushing against
resisting objects, breaking its horns or teeth; and otherwise sustaining
injury through violent muscular contractions.

=Course.= Chronic cases may continue indefinitely, with symptoms of poor
health, impaired digestion, and gradual loss of condition. After death
the omasum may contain dried food which the animal consumed several
months before the attack.

In cases ending in early recovery there occurs abundant diarrhœa, “the
fæces are mixed with flattened, dark, solid, and polished masses, the
impacted ingesta from the omasum. Tympany subsides; movement in rumen
and omasum and rumbling in bowels can be heard. Appetite returns.”
(Law.)

=Diagnosis.= The condition of the pulse and respiration, and the
grunting with expiration may lead to confusion with pneumonia.

At first there is no fever, tenderness is confined to the right flank;
there is an absence of pulmonary crepitation, of pleural effusion, and
of movement in the rumen and omasum. Signs of gastric and intestinal
disorder can be detected.

=Lesions.= The omasum is gorged—it may be twice its normal size—solid,
resistant, almost stony. The spaces between the leaves are packed with
dried food, which, when removed, carries a layer of epithelium from the
mucous membrane. (This (layer on contents) is not inconsistent with
health.)

The rumen contains ingesta packed in masses, more or less offensive from
putrefaction.

The abomasum is empty of food, but contains much mucus. Its mucous
membrane is congested.

The small intestine is red in places, empty and collapsed.

The larger intestine contains a quantity of dry, glistening pellets, and
much mucus.

=Treatment= follows the lines of impaction of rumen, though the response
is usually less certain, and always slower. Flax-seed tea, several
bucketfuls per day, will often succeed.

Epsom and common salts, with sol. ammoniæ, excite thirst; liquids should
be supplied freely.

In obstinate cases, and in absence of gastric or cerebral congestion, 20
croton beans, or 20 drops of croton oil, may be added to the purgative.
Nux vomica stimulates the nervous supply. Enemata may be given freely.

Other remedies, stimulating contractility and secretion, are: Eserine,
1½ grains; veratrine, 1 grain; barium chloride, 10 to 15 grains; or
pilocarpin, 3 grains, hypodermically.

The patient may be days or even a week without alvine discharge and
recover.

If fever and symptoms of gastric congestion appear, a blister may be
applied to the right side over the omasum.

Nervous symptoms, such as dilated pupils, blindness, congested mucous
membrane, hot horns and ears, drowsiness or excitement, are combated by
applying cold water or ice to poll, etc.

When free action of the bowels is restored, laxative diet, roots
(pulped), green food, plenty of common salt, and free access to drinking
water should be prescribed.

During convalescence a course of tonics, including nux vomica, is
advisable to help in restoring normal gastric functions.


                         ABOMASAL INDIGESTION.

Primary indigestion in the abomasum appears to be rare in adults, for
until the present time no one has given a sufficiently characteristic
description of this disease to enable it readily to be recognised. On
the other hand, it is to be presumed, although final proof has certainly
not been furnished, that in cases of gaseous indigestion, or of
impaction of the rumen, the abomasum, whose physiological action is
predominant, must simultaneously suffer.

Primary abomasal indigestion, on the contrary, is common in young
animals before weaning, so that the condition has been given the name of
“milk indigestion.” It could not very well be otherwise, for the
abomasum is the only one of the gastric divisions which in ruminants is
active during the first few weeks of life. At this period it is larger
than the other gastric reservoirs; and the rumen, the reticulum, and the
omasum do not undergo great development till weaning begins.

=Causation.= Milk indigestion attacks young animals, under varying
conditions.

In animals suckled by the mother the disease rarely occurs, but yet when
the mothers are good milkers, like the Flemish, Norman, Jersey, and
Holland breeds, and when there is too long an interval between the
feeds, calves, which are naturally greedy, and in addition are hungry,
are apt to take too large a quantity of milk—in fact, they often gorge
to the fullest possible extent. Owing to its over-distended state the
abomasum either fails to secrete sufficient of the rennet ferment
necessary for coagulating the milk or secretes an insufficiently active
ferment. The first stage of digestion remains incomplete, giving rise to
so-called “milk indigestion.”

When the cows are employed in ploughing, etc., or in drawing carts, not
only are the calves fed at long intervals, but the milk is not always of
proper chemical composition even in the udder. As a result of work,
fatigue, over-exertion and irregular feeding, the cow’s yield of milk
for the time is less digestible than the normal supply, or may even
prove irritant to the calf’s stomach. Milk indigestion is thus set up.

When the cows are fed on factory waste, like beetroot-pulp or brewers’
grains, toxic or irritant products may even find their way into the
milk, which then irritates the little creature’s abomasum and produces
gastric indigestion. Just as in the production of congenital alcoholism
in man, the young animal is then ingesting, unknown to those responsible
for its well-being, chemical substances which produce various
pathological changes.

But milk indigestion is commonest of all in calves fed by hand. The food
usually given is a mixture of milk from the previous night, and skim
milk or even butter milk. It contains lactic ferments and various
microbes, some capable of producing toxic principles.

When swallowed and brought directly in contact with the mucous membrane
these cause abomasal indigestion.

=Symptoms.= Soon after feeding, the little animal appears dull and
somnolent, and shows moderate abdominal pain, suggesting trifling colic.

This stage is soon followed by nausea; the breathing and the heart’s
action become rapid, vomiting efforts are made, and finally milk, in the
form of firm or partially softened curds, depending on the time which
has elapsed since the last feed was taken, are vomited. The quantity
ejected varies. Pressure over the right side of the abdomen produces
pain, and tympanites of the abomasum may sometimes be detected on
percussion.

The sensitiveness and gaseous inflation are confined to the middle and
lower zone of the hypochondrium. Soon after vomiting the animal begins
to improve. The patient seems brighter, relief is very marked, and in
some cases proves permanent; but more frequently a certain degree of
depression persists, the mouth emits a sourish odour, and for a time the
appetite remains poor. This temporary irritation of the abomasum has a
tendency to become permanent; or even to extend to the intestine, in
which the conditions appear more favourable to the development of
microorganisms than do those in the stomach. Indigestion then becomes
complicated with diarrhœic enteritis.

=The diagnosis= presents no difficulty.

=The prognosis= is not serious, provided that the young animals are
carefully attended to; but such complications as diarrhœic enteritis may
become very grave if neglected.

=The treatment.= To prevent recurrences:

(1) The periods of feeding should be regulated;

(2) The cows should not be worked, or should be worked as little as
possible;

(3) Mixed milk, or milk which has already undergone lactic or other
fermentation, should be avoided.

If the calves must be reared by hand, the mixed milk should at least be
boiled or relatively pasteurised by heating to 70° or 80° C., and the
buckets used for feeding should be kept scrupulously clean. These
precautions become absolutely necessary when diarrhœa exists amongst the
calves. Curative treatment consists in placing the animals on low diet
for two or three days after the attack of indigestion, or in giving them
boiled milk diluted with from one-half to two-thirds of boiled water.

The addition of a mild saline purgative like sulphate of soda, in doses
of one-half to three-quarters of an ounce, usually ensures a cure.
Infusions of lime-tree flowers, peppermint, camomile, etc., may
advantageously be used to replace boiled water in diluting the first
foods.


                  ACUTE GASTRIC INDIGESTION IN SWINE.

=The causes= comprise putrid food, swill, spoilt turnips, potatoes,
apples, succulent vegetables, frozen food, and the admixture of caustic
alkaline powders (used in washing table dishes) with the swill.
Indigestible matters—hoof, horn, hair, bristles, tree bark, etc.—when
not rejected by vomiting, cause gastritis and indigestion. Lastly,
medicinal substances and poisons, paint and lead, sometimes produce the
disease.

Among the symptoms may be mentioned dulness, arching of the back,
standing with the feet brought together, erection of the bristles,
hiding under the litter, grunting, uneasiness, shifting from place to
place, tenseness of the abdominal wall, borborygmus; these may be
followed by diarrhœa and recovery. Speedier relief is afforded by
copious vomiting of irritant matters.

=The treatment= should commence with the free administration of emetics.
To combat alkaline poisoning vinegar may be given, followed by a
laxative. Prophylaxis calls for greater care in feeding.




                               CHAPTER V.
            ACUTE INFLAMMATION OF THE GASTRIC COMPARTMENTS.


                    RUMENITIS—RETICULITIS—GASTRITIS.

=Causation.= Acute primary inflammation of the first gastric reservoirs,
viz., the rumen and reticulum, is not common. It sometimes accompanies
such infectious disorders as foot-and-mouth disease, gangrenous coryza,
etc., but then constitutes an added phenomenon which should be studied
along with the original disease itself. Rumenitis or reticulitis may
however follow the ingestion of irritant foods or plants, of very hot
liquids, and more frequently still of unskilfully compounded medicines.
In such cases the mucous membrane is directly attacked, and pathological
congestion, infiltration, and desquamation may follow, or even vesicles
and ulcerations may rapidly be formed.

=Symptoms.= Inflammation of the rumen or reticulum is announced by loss
of appetite, suspension of rumination or of regular peristalsis, slight
tympanites, and particularly by excessive sensitiveness to palpation.
This sensitiveness is general, but is more specially marked in the left
lower third of the abdominal cavity, and in the retro-ensiform region
which corresponds to the position of the reticulum. Moderate fever is
present.

These symptoms, which indicate the gravity and intensity of the
inflammation, may persist, become aggravated, provoke vomiting from the
rumen, and leave as a legacy motor dyspepsia, or even more serious
consequences. On the other hand, they may progressively diminish and
disappear for good.

=Lesions.= The lesions comprise hyperæmia of the walls of the rumen and
of the mucous membrane, extensive local exfoliation of epithelium, and
sometimes true ulceration of the mucous membrane.

=Diagnosis.= The diagnosis is based on the exceptional sensitiveness of
the gastric compartments on palpation, and also on the history, provided
reliable information can be obtained.

=Prognosis.= The prognosis should be reserved, because it is never
possible to foretell whether acute lesions may not give place to chronic
disease, which, though apparently unimportant, may terminate in grave
consequences.

=Treatment.= Owing to their local action demulcent drinks and teas are
indicated. Cooked food is useful, because it makes little demand on the
digestive powers; steamed hay and farinaceous substances are given, both
on account of their nutritious qualities and of the slight local
irritation they cause when swallowed.

Lukewarm drinks and saline laxatives, such as the sulphate of soda, and
carbonate of soda or Carlsbad salt in small doses of 1½ to 2 ounces,
seem most useful in combatting the reflex atony of the digestive
compartments.

=Inflammation of the omasum=, like that of the rumen and reticulum,
occurs as a secondary phenomenon in conditions like rinderpest, Texas
fever, foot-and-mouth disease, anthrax, and gangrenous coryza (malignant
catarrh); but primary inflammation is much rarer even than that of the
rumen and of the reticulum.

This is accounted for by the deep position of the omasum, which is thus
sheltered from external violence, early contact with irritant foods and
from the effect of chills, etc. It can only become inflamed by the
prolonged action of irritant food and drink, which have already produced
lesions in the rumen and reticulum; or as a consequence of the prolonged
stagnation of dry food in cases where animals have been deprived of
water.

Under these conditions inflammation of the omasum develops slowly, and
from the clinical point of view is identical with what was formerly
known as obstruction of the omasum. Obstruction or impaction is probably
much rarer than has been stated, in so far at least as it constitutes a
primary condition, for in the great majority of cases it is consecutive
to impaction, inflammation of the rumen, or inflammation of the
abomasum. Obstruction of the omasum, which was formerly invoked in all
doubtful and ill-defined cases of digestive disturbance, seldom occurs
as an isolated disease.

It has been suggested that the omasum, being supplied with nerves solely
by the sympathetic system, and provided with a relatively weak muscular
coat, was more susceptible than the other reservoirs to the reaction of
abdominal reflexes, and therefore more subject to inflammation,
indigestion and obstruction. We do not hold that view, because, as a
result of its general situation and the position of its orifices of
communication, this compartment is easily able to expel its contents so
long as they are liquid. Its function appears chiefly to be to complete
the trituration of food after rumination.

We do not consider that inflammation of the omasum never occurs, for we
are well aware of the contrary, and that the inflammation assumes a
subacute course and is accompanied by stasis of the semi-digested food
between the mucous leaves which partly fill the cavity. We simply wish
to emphasise the view that the condition is not a primary and isolated
inflammation.

=Symptoms.= The symptoms are always vague and very difficult clearly to
define.

Inflammation of the omasum is indicated by relative loss of appetite,
marked thirst, general atony, and diffuse and vague sensitiveness in the
inferior half of the right hypochondrium (zone of the asternal ribs).
There are no pathognomonic symptoms.

Obstruction has also been described as accompanied by loss of appetite,
constipation, the passage of black, coated, fœtid and sometimes
blood-streaked fæces, symptoms of chronic tympanites with fœtid
eructations and sometimes vomiting. These sometimes accompany
hydrochloric acid dyspepsia, a form of chronic gastritis, and, from our
standpoint, the stagnation of food in the omasum is only secondary. We
therefore interpret the facts in quite a different manner, and believe
that only by a rational and physiological interpretation of the symptoms
observed can one diagnose the condition.

=Diagnosis.= The diagnosis of inflammation of the omasum can only be
made by a process of exclusion; and although we are admittedly dealing
with a condition secondary to disturbance of the rumen and reticulum, or
on the other hand consecutive to inflammatory states or to modifications
in the secretion of the abomasum (dyspepsia), the diagnosis does not
present insuperable difficulties.

=The prognosis= is only grave when the primary acute or chronic
conditions of the other gastric compartments are serious.

=The lesions= comprise abnormal vascularity of the mucous membrane and
desquamation, and even gangrene, of the leaves. The partially digested
food is not passed on, becomes dry and hard, and in time aggravates the
local condition.

=The treatment= does not essentially differ from that of other gastric
inflammations. The object to be attained is to evacuate as completely as
possible, not only the omasum, but all the gastric reservoirs, for which
purpose one may freely administer demulcent drinks—linseed gruel, bran
mashes and lukewarm liquids containing laxatives. At first such
alkaloids as arecolin and pilocarpine may be subcutaneously injected to
ensure energetic and speedy evacuation.

Later on slightly stimulant aromatic infusions, like infusions of sage,
peppermint, hyssop, thyme, etc., stimulate the functions of the stomach
and hasten the return of normal conditions.


                            ACUTE GASTRITIS.

The term “acute gastritis,” sometimes “gastro-enteritis,” is used in
bovine pathology to indicate inflammation of the abomasum. If this
inflammation is confined to the superficial epithelial layers it is
defined as superficial catarrh of the abomasum; if, on the contrary, it
extends to the deep epithelium of the gastric glands and to the mucous
corium, it is termed deep-seated gastritis.

Clinically it is impossible to make these distinctions. We simply
recognise degrees of gravity, and only in this way can one diagnose
acute gastritis, phlegmonous gastritis, ulcerative gastritis, etc.

=Causation.= The abomasum frequently becomes inflamed as a consequence
of irritant foods, apart altogether from lesions of the rumen or
reticulum, the mucous membrane lining the abomasum being so much more
delicate than that of either of the two first compartments.

Irritant plants, parasites, acid drinks, very cold water, certain acid
or toxic industrial residues like mouldy brewers’ grains, fermented
vegetable pulp, decomposed beet, etc., and mouldy or spoilt forage of
any kind may all produce acute gastritis.

Intense feeding—_i.e._, feeding with farinaceous materials, with large
quantities of beans, roots, peas, given regularly—may also cause
gastritis by overtaxing the functions of the organ. Frozen or fermented
roots and sudden changes in feeding produce similar results. Chills have
also been blamed, but it is probable that they only act as favouring
causes.

=Symptoms.= It is necessary to consider these very carefully in order to
arrive at a correct diagnosis.

Inflammation of the abomasum is attended with moderate fever, diminution
in appetite, irregularity in rumination and some tension of the rumen,
without, however, true tympanites.

At first the bowels are constipated, but in time fœtid diarrhœa sets in.
Examination of the digestive apparatus on the left side and in the right
posterior abdominal region reveals nothing abnormal, but pressure over
the lower portion of the abdomen and along the cartilages of the right
hypochondriac region produces, on the contrary, well-marked pain. This
region corresponds to the position of the abomasum.

The conjunctiva appears reddish yellow, as in most visceral
inflammations.

Some authors have described attacks of extreme excitement, but these are
no more pathognomonic than is grinding of the teeth, which is a constant
symptom, or the metallic sound noted on auscultation of the rumen. This
sound occurs in all cases of inertia of the rumen, and indicates
distension and emptiness of the viscus (acute peritonitis, chronic
adhesive peritonitis, inflammation of the reticulum as a consequence of
the presence of foreign bodies).

Dull colic and groaning are not uncommon. Finally, Thierry and others
have all mentioned an alliaceous smell of the eructations as
pathognomonic.

Acute gastritis develops regularly in ten to fifteen days, after which
the symptoms diminish and disappear, giving place to normal health. In
grave cases, despite proper treatment, acute gastritis more frequently
ends in a chronic condition, finally leading to gastric atrophy, and the
insufficient secretion of hydrochloric acid, with all the consequences
of these conditions. The glands of the stomach degenerate; the secretion
becomes abnormal and dyspepsia is set up.

=Diagnosis.= The diagnosis is rather difficult, for the condition is
very apt to be confused with primary dyspepsia, or with inflammation of
the gastric compartments. It might also be mistaken for acute enteritis
of the first part of the small intestine; but as gastritis is very often
complicated with duodenitis, such a mistake is without serious
consequences.

=Prognosis.= The prognosis is grave, not because death is a frequent
termination, but because the disease very often leads to chronic
incurable lesions.

=The lesions= consist of congestion of the vascular network of the
mucous and sub-epithelial coats, serous infiltration of the corium and
submucous connective layers, desquamation, and later in excessive
proliferation of the epithelium.

When the inflammation is deep seated the epithelium of the gastric
glands becomes swollen and cloudy, and undergoes a kind of atrophic
degeneration. In very grave cases, petechiæ, superficial capillary
hæmorrhages, and slight ulceration may be noted. The mucous folds are
always thickened and infiltrated.

=Treatment.= In cases of gastritis or acute gastro-duodenitis moderate
bleeding (three to four quarts) and local stimulation were formerly
recommended. This practice certainly has its advantages, provided it is
not pushed to excess. Sinapisms give good results, but as they must be
left in position for a considerable time, it is often better to apply
vesicants over the lower right hypochondriac region. At first purgatives
are useful, because they unload the digestive tract, arrest the organic
fermentation which results from stagnation in the movement of food along
the alimentary tract, and diminish the tendency to intoxications or
infections.

At a later stage small doses of laxatives and bicarbonate of soda should
be given daily, the diet being of an emollient character, and consisting
of milk, starchy or farinaceous foods, and small quantities of good hay.

Linseed, bran, cooked grain, decoctions of pellitory, barley and various
cereals may also be administered with advantage.


                     CATARRHAL GASTRITIS IN SWINE.

=Definition.= Inflammation of the gastric mucosa, with muco-purulent
discharge.

=The causes= comprise irritants, fermented or putrid swill, decomposed
food, excess of brine, alkalies (washings from table dishes, hotels,
etc.), gastric parasites.

The condition occurs also in hog cholera, swine plague, rouget, etc.

The chief =symptoms= are: Inappetence, vomiting, uneasiness, colic,
constipation or diarrhœa, fever, stiffness, tense and tender abdomen,
arched back, frequent grunting, limpness of the tail. Sudden vomiting
may bring about a rapid recovery.

=Treatment= calls for a complete change of food, which may include
freshly cooked roots, linseed or meal, butter milk, boiled milk, etc.

As an emetic 30 grains of ipecacuanha may be given. Constipation can be
relieved by a dose of calomel or jalap. If diarrhœa is persistent small
doses of grey powder should be given, and to combat the irritation of
the gastric mucous membrane bismuth subnitrate is also useful.

The piggery should be cleansed and disinfected, and the litter
frequently changed.


                         ULCERATIVE GASTRITIS.

Ulcerative gastritis (ulcer of the abomasum) is recognised after death,
but hitherto it has been impossible to so clearly identify the symptoms
as to permit of diagnosis during the animal’s life. It has been found
after death in adults and in calves (Ostertag).

=Causation and Pathogeny.= The cause of gastric ulceration is decidedly
obscure, though we know that certain forms occur during infectious
diseases like cattle plague, foot-and-mouth disease, gangrenous coryza,
and as a consequence of certain direct local infections; other forms
result from the administration of drugs; and finally some are of
secretory origin.

In human medicine at the present day there is a tendency to refer the
development of round ulcer and ulcerative gastritis to the secretion of
an excess of hydrochloric acid. Probably the same cause may be at work
in domestic animals, but the proof has not yet been given.

With regard to the pathogeny, the theories of embolism or of thrombosis
of capillary vessels find favour with few authorities at the present
day. Yet these explanations are logical enough, for if we prevent
physiological irrigation of any given part, it is possible to conceive
that ulcer formation may follow from auto-digestion, _i.e._, from the
simple action of the gastric juice on a surface which is no longer
protected.

The theory of microbic origin has been advanced; but although it may be
accepted in relation to the intestine, where the most varied organisms
abound, it is scarcely so applicable to the stomach, in which acidity is
always very marked and must exercise a very energetic antiseptic action.
In sucking calves, however, this theory appears the most plausible.

It is quite certain that ulceration may result from the unwise use of
drugs, like tartar emetic or arsenious acid, especially if these be
administered for long periods; but such ulceration always occurs at the
same points, viz., at the deepest portion of the rumen, reticulum, or
abomasum.

On the other hand, ulceration due to secretory disturbance occurs at
different points, and the figure opposite shows that the mucous folds
themselves may be injured and perforated.

=Lesions.= Ulceration of the abomasum varies in severity. The case
referred to showed excavated ulcers from the site of which a portion or
the whole of the epithelium and glandular layer had been shed; true
round ulcers, which had destroyed the entire depth of the mucous
membrane and had produced chronic inflammation and sclerosis of the
muscular layer; and finally perforations resembling cleanly punched-out
holes.

=The Symptoms= are those of a mild form of ordinary acute gastritis,
without marked fever, and without special injection of the conjunctiva.
The appetite is diminished and irregular, but more as a consequence of
excessive reflex sensibility of the injured organ than from absence of
hunger. This excessive reflex sensibility of the abomasum causes
relative or absolute gastric intolerance, so that only a small amount of
the food ingested passes towards the intestine.

Absolute intolerance on the part of the abomasum may even occur, as in a
case described by Moussu in 1895, which produced a very special form of
impaction of the rumen, absolutely different from primary impaction.

Intolerance of the abomasum for food already ingested and ruminated may
extend to the omasum. Peristalsis of the rumen then ceases, and slight
tympanites occurs. The most characteristic condition is the existence of
obstinate constipation. If ulceration takes place without producing any
important vascular lesion, which, however, is rare, the fæces are hard
and coated, but without other peculiarity; if, however (and this appears
to be the rule), local hæmorrhage occurs, the extravasated blood is
modified by the gastric and intestinal juices, and the fæces appear of a
black, tarry colour. This coloration is very significant, and differs
from that produced by the bile. It occurs only in gastric hæmorrhage,
and at intervals.

=Diagnosis.= The diagnosis of gastric ulcer is difficult, and can only
be arrived at with confidence when the above-mentioned coloration of the
fæces can be detected.

=Prognosis.= From an economic standpoint the prognosis is grave. The
patient may recover; the ulcers may heal, but cicatrisation is always
prolonged, and as, on the other hand, the glandular apparatus of the
abomasum is generally more or less injured, complete recovery is
impossible.

[Illustration: $1]

=Treatment= should be directed towards checking hæmorrhage, diminishing
intolerance to food, and assisting the healing of the lesions. These
objects are facilitated by prolonged complete rest in the stable, by
injecting ergotine, or, ·7 per cent. saline solution, at the time when
the hæmorrhage occurs, and, if possible, by placing the animals on milk
diet or on emollient food, like gruels, emollient infusions, barley,
milk, cooked roots, etc.

Stimulation over the region of the abomasum is also of value. At a later
stage, when the acute symptoms have diminished, Carlsbad salts, in doses
of 1 to 2 ounces per day, can be given. Bicarbonate of soda is also of
considerable value.


                          CHRONIC TYMPANITES.

Chronic Indigestion—Obstruction of the Abomasum—Chronic
Gastritis—Dyspepsia.

Among pathological conditions of the stomach in ruminants a certain
number are clinically marked by one constant symptom, viz., chronic
tympanites, a fact which was formerly recognised as indicative of
chronic indigestion.

It is evident that such titles have only the significance accorded them,
and the term chronic indigestion used only to mean that gastric
digestion was badly performed, and that the condition was more or less
permanent. It being granted, on the other hand, that the term
indigestion is used to characterise temporary conditions during which
digestion is suspended, and produces immediate disturbance, it would
appear that the term gastric dyspepsia is more exact and more in
conformity with the present state of our knowledge of general
physiology. In studying this question it is clear a number of facts
still require explanation, for, as has been previously indicated, we
know almost nothing concerning the variations in the chemical phenomena
of gastric digestion under different morbid conditions; nevertheless,
the dominant fact, the imperfect or irregular digestion, is easily
appreciable. Future discoveries will no doubt enable us more exactly to
differentiate several dyspeptic conditions due to chemical or mechanical
causes and with or without anatomical lesions. At present it is
sufficient to indicate the limits of inquiry.

=Causation.= The symptom of chronic tympanites accompanies a great
number of very different conditions—some due to disease of the digestive
tract itself, others to general diseases or lesions of neighbouring
parts. In the latter cases the tympanites is only indicative of
secondary dyspepsia; in the former, on the other hand, the dyspepsia is
primary.

Secondary dyspepsia occurs very commonly during tuberculosis, diseases
of the liver, subacute or chronic peritonitis, gestation, lesions of the
mediastinum, etc., etc.

=(a) Secretory or Chemical Dyspepsia.= In primary dyspepsia it is
impossible to discover any lesion sufficient to explain the disturbance.
Chronic tympanites, for instance, follows prolonged consumption of rough
or bad food (in years when forage has been scarce or winter food has
been lacking), and too short a supply of water for weeks in succession.
It also occurs as a consequence of acute inflammation of one or other of
the gastric compartments—rumenitis, reticulitis, gastritis. Sometimes it
assumes an insidious, slow, progressive form, without any apparent cause
whatever.

In these various conditions, the mucous membrane of the gastric
compartments suffers from the deferred results of the bad feeding or
want of water. Its secretory powers and anatomical structure becoming
modified, it is no longer able regularly to elaborate the juices
necessary for digestion, and chronic indigestion, imperfect digestion,
or dyspepsia result. Similar results follow acute inflammation of the
omasum, reticulum, or rumen. Integral repair becomes impossible.
Anatomical injury is done, disturbance of secretion follows, and
dyspepsia is a necessary consequence.

=(b) Motor Dyspepsia.= Finally, it would appear that general bad health,
abstinence and exhausting work, may produce a form of dyspepsia,
unconnected with secretory disturbance, but resulting from mechanical
disturbance due to general enfeeblement and to atony of the muscular
walls of the gastric compartments. The rumen ceases to perform its work
of mixing the food, the reticulum also acts badly, and the abomasum
receives imperfectly prepared material. The result is what might be
described as motor dyspepsia, in opposition to those forms which are of
chemical origin.

The condition may vary in degree, peristalsis being diminished (one
contraction every two or three minutes instead of two per minute), or
being simply intermittent and occurring only for a few hours during the
day, or finally being altogether suppressed. Suppression is never
absolute, but atony may be so marked that the mixing of the food is very
imperfectly performed.

=Symptoms.= The most constant symptom present in all dyspeptic
conditions is chronic tympanites, indicated by a certain degree of
tension or by permanent dilatation of the rumen.

Rumination is impeded and irregular, the distended rumen loses its power
of contraction, and no longer causes eructation nor passes gas into the
intestine. It becomes progressively inert, whether the inertia be
primary and occur suddenly, as a result of some particular condition of
the sympathetic system (motor dyspepsia), or secondary and of slow
development in consequence of disturbance in the gastric secretions and
of abnormal organic fermentation (secretory dyspepsia).

This symptom of tympanites is always accompanied by irregularity,
diminution, and frequently also by depravity of appetite.

Wasting occurs, but to a very varying degree, according to the nature of
the primary condition and the method of feeding.

These general symptoms are accompanied either by constipation or by
diarrhœa; and as stagnation of food leads to fermentation, which always
forms products differing from those of normal digestion—toxic materials
in fact—a chronic auto-intoxication results, which in its turn, if not
remedied, becomes a cause of irritation, and aggravates the bad general
condition.

In many cases fever is absent, except during the final complications, in
animals in the last stages of wasting; but some signs always exist on
which the diagnosis may be founded.

The most frequent clinical type of these dyspeptic conditions is motor
dyspepsia, consisting in relative atony of the rumen without disturbance
in the secretion of the gastric mucous membranes. Luckily, this is the
most easily curable form, and is only marked by distension, dulness and
constipation.

Dyspeptic diseases of secretory origin are little understood. Their
essential causes have been badly described, and their clinical symptoms
are ill-recognised.

We cannot prove whether the forms said to be due in man to excess of
hydrochloric acid and insufficiency of hydrochloric acid really occur or
are well defined in domestic animals: nor are we better informed as to
the exact part played by the organic acid of fermentation (lactic,
butyric, acetic acid, etc.); but the most complete investigations which
have yet been made justify our supposing there is some parallel.

Moussu described primary ulcerative gastritis in 1895; and as this
form is almost certainly associated with excess of pepsin, the
occurrence of an excess of hydrochloric acid also seems possible, the
more so as the symptoms noted resemble the general symptoms of that
condition—preservation of appetite and of the motor power of the
rumen, accumulation of food in the rumen as a consequence of reflex
intolerance of the abomasum, constipation, and vomiting.

In addition to these two morbid conditions, a third occurs with some
frequency. It is characterised by chronic tympanites, alimentary
diarrhœa (the food being badly digested), and progressive wasting. This
condition seems due to an insufficiency of hydrochloric acid, brought
about by chronic gastritis, the epithelial cells of the mucous membrane
appearing incapable of producing sufficient hydrochloric acid for
digestion.

=Diagnosis.= In the present state of our knowledge regarding digestion
in ruminants the precise diagnosis of these pathological conditions must
always remain difficult; but it is indisputable that with the above
grouping of symptoms we are more likely to succeed than by confining
ourselves to the diagnosis formerly common, viz., that of chronic
tympanites or chronic indigestion.

The difference between primary and secondary dyspepsia should always be
borne in mind, and careful examination will often reveal the special
condition which has served as the point of departure for gastric
disturbance. Thus generalised tuberculosis, or tuberculosis of the liver
or mediastinum, should always be sought for, and the possible existence
of such conditions of the liver as echinococcosis, cancer of the bile
ducts, tumours, etc., and diseases of the kidneys should be borne in
mind. The influence of gestation, which so frequently causes gastric
disturbance complicated with albuminuria, should never be overlooked,
and in these secondary forms of dyspepsia the determining cause, and not
the objective symptoms should receive chief attention.

=Prognosis.= The prognosis of secondary forms of dyspepsia varies with
the gravity of the primary disease. The prognosis of primary dyspeptic
conditions varies greatly, and that state in which hydrochloric acid is
too sparingly secreted is certainly the gravest.

=Lesions.= The lesions have not been carefully studied, but it is
probable that in many cases they might afford a key to the symptoms
noted. Like all mucous lesions, they are difficult to demonstrate
histologically. Infiltration and thickening of the mucous corium and
submucous layers have been described. Such lesions indicate nothing; but
in some cases new growths have been found in the gastric compartments or
contractions about the pyloric orifice, the essential importance of
which cannot be doubted.

=Treatment.= If our knowledge is still insufficient to enable us
precisely to diagnose what we have termed “gastric dyspepsia,” or what
is still currently described as “chronic dyspepsia,” the difficulty is
even greater when attempting to lay down lines of treatment, because of
the lack of known facts and the want of a base for reasoning. Thus we
find, without being able to explain why, that some prescribe tartar
emetic, others rapid and energetic purgatives, others, again, laxatives;
whilst German authors, apparently without any justification, recommend
oil of turpentine. It seems to us, however, that one might do better
than this and attempt to lay down some rational indications for
treatment.

(_a_) In cases characterised only by chronic tympanites, without
diarrhœa, without manifest constipation (motor dyspepsia), and without
any other apparent organic disturbance, drugs calculated to stimulate
peristalsis of the rumen seem indicated. The most promising comprise
ipecacuanha in doses of 1 to 2 drams per day, tincture of nux vomica in
similar doses, powdered nux vomica in doses of 45 to 75 grains, and
laxatives like Carlsbad salts in doses of 8 to 10 drams.

Little by little peristalsis returns, becomes regular, and the chronic
tympanites disappears for good. This is frequently the case during
gestation, when the condition simply consists in motor dyspepsia without
anæmia.

(_b_) If, on the contrary, chronic tympanites is accompanied by
constipation, and the fæces are hard or, as is usually the case, covered
with mucus, suggesting the probability of excess of hydrochloric acid,
salines are indicated—not to the point of producing purgation, which
would not lead to any lasting improvement, but still as laxatives,
continued daily for ten, fifteen, or twenty days, or, if necessary, even
longer.

Carlsbad salts in doses of 8 to 10 drams, or one-ounce doses of sulphate
of sodium associated with 2½ drams of bicarbonate of potash after each
meal, are to be recommended in preference to bicarbonate of soda alone,
because they act on the secretions, on the muscular system, and also on
the liver.

(_c_) Finally, when chronic tympanites is accompanied by diarrhœa, a
condition which usually indicates insufficient secretion of hydrochloric
acid, the administration of that acid tends to arrest or check organic
fermentation and to facilitate digestion in the abomasum by
supplementing the diminished physiological secretion. The dosage is an
important point. At first small quantities should be given, 2½ drams per
day, divided into two doses and freely diluted in the drinking water;
but this amount may, if necessary, afterwards be doubled or trebled. The
drinking water is not rendered irritant by these doses, for it is
admitted, and Moussu has confirmed the fact by analysis, that the
quantity of HCl in the gastric juice may rise as high as ·2 to ·3 per
cent. Chloride of sodium, the excito-secretory action of which on the
gastric mucous membrane is well known, may be given for long periods in
doses of 1 to 1½ ounces per day.

In these various chemico-pathological states the food should receive the
closest attention. The forage, which should be good, may be supplemented
by the addition of cooked roots, demulcent drinks, and, if possible,
milk.


               GASTRIC DISTURBANCE DUE TO FOREIGN BODIES.

These morbid conditions are extremely complex, but the facts that they
are due only to one cause, and that they possess certain symptoms in
common, permit of a certain grouping. It would obviously be illogical to
speak of traumatic indigestion of the rumen, reticulum, and abomasum, as
has been done in more than one book on this subject; for the gastric
disturbances described below should be considered as complications, and
not as diseases.

=Causation.= In young animals foreign bodies may be composed of hairs,
wool, bristles, cotton, and clover hairs.

Hair balls are common in the rumen, and are sometimes met with in the
fourth stomach. They cause irritation, indigestion, sometimes pyloric
obstruction, dilatation, and eventually death.

Wool balls in lambs, bristle balls in young pigs, cause much gastric
irritation. Cotton balls occur in lambs fed on cotton-seed cake; the
fibre constitutes a foreign body. The hairs of clover leaves may form a
ball in the abomasum of lambs.

Under the influence of depraved appetite animals of the bovine species
consume, apart from their regular food, the most varying substances,
such as linen, fragments of wood, nails, stones, gravel, sand, etc.
Moreover, forage, even when of good quality, often contains foreign
bodies like nails and pins (when the fields are near factories), sewing
or knitting needles (when the animals are looked after by women),
fragments of iron wire derived from bales of compressed forage, etc.,
etc. The ingestion of such objects is followed by various consequences,
which may be studied in three divisions, in the first of which the
foreign object is soft in character, in the second is blunt at one
extremity and pointed at the other, and in the third is pointed at both
ends.

(1.) =Soft objects.= The movements of the rumen, the warmth and the
action of the digestive fluids, may cause soft objects to be broken up;
the disturbance they produce is then insignificant.

Of such substances, however, some are quite incapable of digestion
(clothing, sacks, linen, etc.), and may produce obstructions; others are
both indigestible and heavy (gravel and sand), and may fall into the
depressions of the compartments, where they remain, or, if passed into
the reticulum, may become arrested in the deepest lying part. They then
produce atony of the muscular coats, slowing of peristaltic movements,
diminution in the frequency of eructation, and, as an additional
consequence, chronic tympanites, sometimes visible at the flank.

=The symptoms= are vague and common to a number of the digestive
diseases already described. The animals masticate without having
anything in the mouth; rumination becomes irregular or is altogether
suppressed, but this is not characteristic, being a symptom common to
many visceral diseases.

Later, as a result of auto-infection, diarrhœa sets in; under the
influence of abnormal fermentation in the gastric compartments the
eructations become fœtid; the animals fall into a condition of marasmus.
Death usually results after a varying time—when large quantities of
foreign substances have been ingested, in twenty to thirty days.

=The diagnosis= chiefly rests on the history, and can only be of a
confident character when one knows what quantity and what kind of
foreign body has been swallowed.

=The prognosis= is grave, because the animal usually dies of progressive
exhaustion.

=Treatment.= There is only one rational form of treatment—viz.,
gastrotomy, followed by examination of the rumen and reticulum and
removal of the foreign body. Before undertaking operation the surgeon
should be fully informed as to the cause and the probable results to be
expected.

(2.) =Foreign bodies with one pointed extremity.= These usually consist
of large-headed nails, or fragments of iron wire rolled up at one end,
which have been swallowed during primary mastication along with forage.

When ingested, they may become implanted at any point in the gastric
apparatus without necessarily penetrating deeply. When fixed across the
division of the reticulum, they cause slowing of its physiological
action. Should they penetrate the wall either of the reticulum or of the
rumen, they may attack on the right the liver, or on the left the
diaphragm or spleen, producing suppurating hepatitis, splenitis, or
respiratory disturbance. The hypochondriac region then appears
sensitive. The muscular portion of the diaphragm is partly paralysed,
and costal respiration set up, while frequent coughing of reflex origin
is provoked by irritation of the pneumo-gastric and diaphragmatic
nerves, and may give rise to suspicion of some thoracic disease, from
which, however, it is distinguished by the absence of discharge,
expectoration, and pulmonary symptoms.

Finally, if implanted in the lower wall or sides of the rumen or
reticulum, foreign bodies may carry with them infectious agents and set
up localised or generalised peritonitis.

=Early diagnosis= is a matter of great difficulty, as it can only rest
on the diaphragmatic disturbance or on the symptoms of peritonitis.

=Lesions.= Small-sized sharp bodies cause lesions of trifling extent,
which in most cases are only indicated by retardation of movement of the
gastric compartments, between which and the diaphragm, and between the
diaphragm and the posterior portions of the lung, various adhesions are
set up. In such cases the peripheral inflammation ends by producing a
fibrous sleeve, which prevents the pleural cavity becoming infected.
Other cases show patches of adhesive peritonitis or signs of generalised
peritonitis, the real cause of which often evades discovery during life.

=Treatment.= Gastrotomy is the sole means of effecting a cure, but we
are forced to admit that it only gives good results when the operator
knows what he is trying to find. Without this information he acts in the
dark, is obliged to abandon himself to chance, and although luck
sometimes favours him, it more often leaves him in the lurch.

(3.) =Foreign bodies pointed at both ends.= Bodies like needles, pins,
straight fragments of iron wire, knitting needles and broken hairpins,
become implanted in the gastric walls and travel in the most diverse
directions, in obedience to the varied movements of the organ injured.
They produce results similar to those just described. Most frequently
they fall into the lower part of the gastric compartments, pass near the
ensiform cartilage, between the pleura and the triangularis sterni into
the thickness of this muscle, or into the mediastinum, and there produce
either an abscess in the region of the ensiform cartilage, an abscess of
the thoracic wall, or a collection of pus in the subpericardial or
subpleural region (pseudo-pericarditis). They may even reach the
pericardium, causing pericarditis, and sometimes, when adhesions are set
up between the heart and pericardial sac, carditis.

By deviating to the right or left, the foreign body may produce pleurisy
or even pneumonia. If it moves towards the right, it involves the liver
and produces suppurative hepatitis; if to the left, suppurative
splenitis. Travelling in a downward direction, it encounters the
abdominal wall, and after producing an abscess may be eliminated;
passing backwards, it falls into the peritoneum, and may lead to
peritonitis. In those exceptional cases in which foreign bodies reach
the abomasum they generally become implanted towards the greater
curvature, producing in the abdominal wall an abscess which breaks
externally, and through which the foreign body is discharged; gastric
fistula is then a common sequel.

=The symptoms= vary, according to the complications. The earliest
comprise digestive disturbance, which coincides with the passage of the
sharp object through the rumen or reticulum, and depends on whether such
passage produces local peritonitis and pain, rendering movement of these
compartments impossible. Later, when the diaphragm has been penetrated,
respiratory disturbance occurs, and is succeeded by apparent
improvement, which in its turn may be followed by the occurrence of
pericarditis, pleurisy, or abscess formation.

In other cases where suppurative hepatitis or splenitis, or even
peritonitis may be present, the symptoms are extremely vague and very
difficult to refer to their real cause.

=Diagnosis= is difficult, unless the owner is able to supply exact
information that at some previous time the animal had swallowed such and
such an object.

=The prognosis= is grave, though cases occur where a foreign body is
tolerated, and may for a long time be retained without producing
accidents.

=Treatment.= Gastrotomy should not be performed unless the operator is
possessed of very precise information. In such case the rumen and
reticulum should be emptied and the foreign body sought for and removed.

When the symptoms strongly point to the presence of a foreign body
exploratory gastrotomy may be performed, but the operator will do well
to employ the operation only as a last resort.

Many complications, like septic peritonitis, hepatitis, and splenitis,
are practically hopeless; but others show a tendency to recovery. This
is the case when abscesses form in the thoracic or abdominal wall, or
beneath the pleura or pericardium. The entire difficulty consists in
diagnosis, for when once this is clearly defined intervention is fully
justified. As, however, the surgical measures vary in every case, the
exact course to be adopted must be left to the initiative of the
surgeon.


                  TUMOURS OF THE GASTRIC COMPARTMENTS.

=Papillomata= result from hypertrophy of normal papillæ; they resemble
those of the pharynx and œsophagus. The growth may attain the size of a
fist. It often resembles a cauliflower in appearance. When very large,
such growths may cause obstruction. A very striking illustration of a
papilloma of the mucous membrane is given on p. 180 of Möller and
Dollar’s “Regional Surgery.”

=Sarcoma= has been noted by Paule, Kitt, and Schütz as forming in the
subserous tissue of the omasum, and later bulging out as a wounded
swelling of irregular size.

=Actinomycosis of the abomasum= has been reported by Professor Axe.




                              CHAPTER VI.
                               ENTERITIS.


Enteritis consists in inflammation of the intestine, or, more precisely,
in inflammation of the intestinal mucous membrane. All the constituent
portions of the intestinal tube may be affected (duodenum, jejeunum,
ileum, colon, cæcum); but clinical distinctions and localisation of
inflammation in the various parts are very difficult in the domesticated
animals, and at present it is impossible to describe with any accuracy
the differences between duodenitis, enteritis of the jejeunum and ileum,
colitis or typhlitis. Without doubt certain symptoms suggest that some
regions are more affected than others; but clinically we are only able
to distinguish between acute and chronic enteritis. Acute enteritis may
assume different forms, according to its intensity, rapidity of
development, and lesions, so that it is possible to distinguish between
such conditions as simple acute enteritis and hæmorrhagic enteritis.

Chronic enteritis, an abstraction founded on our knowledge of such
specific forms of enteritis as are due to tuberculosis, distomatosis,
helminthiasis, etc., usually assumes the diarrhœic form.


                            ACUTE ENTERITIS.

As acute enteritis, whether localised in one portion of the intestine or
involving the whole intestinal tube, is produced by varying causes, and
assumes very varying degrees of intensity, its clinical symptoms are
equally diverse.

=Causation.= The various forms of enteritis result from two great series
of causes: infections and intoxications. Normally the intestine contains
an extremely large number of different microbes, which may prove of
service so long as circulation, secretion, and peristalsis continue
normal; but as soon as any perturbation occurs, either in the blood
supply or in the movement of the bowel, normal secretion is impeded;
abnormal organic fermentation commences, producing irritant principles
or toxins which at once set up local irritation, or, being absorbed,
produce that complex of symptoms which we recognise as enteritis,
intoxication of intestinal origin, or even infection.

Bearing in mind these facts, we are better able to understand the part
played by cold, by damaged fodder, by intense, stimulating feeding, or
sudden changes in the food, as well as by the action of drastic
purgatives, which modify beyond physiological limits the condition of
the glands, or even cause local desquamation of epithelium.

Toxic substances or plants act similarly by modifying either the
circulatory, secretory, or motor systems.

=Symptoms.= The first appreciable external symptoms appear to result
from fever—loss of appetite, suspension of rumination, dryness of the
muzzle and of the mouth, earthy-red colour of the conjunctival mucous
membrane, etc.

On manipulating the left flank one notes neither tympanites nor
sensitiveness—in a word, there is no indication of functional
disturbance of the rumen.

On the right side, on the contrary, palpation causes the animal to
resist and to show signs of pain. According as this sensitiveness is
more marked in the middle or upper region or towards the hypochondriac
circle, we infer that the inflammation is most acute in the large or
small intestine, either in the middle portions or, again, in the most
anterior portion. The temperature always rises at the commencement,
attaining 103° to 104° Fahr. (39·5° or 40° C.), but rarely a higher
point, a fact which negatives the idea of a rapidly progressive
infectious disease. Slight colic appears, and is accompanied by
constipation; the fæces are covered with mucus, or false membranes, or
are completely enclosed in fibrinous tubes. After four or five days the
fæces change in character. Constipation gives place to a liquid,
blackish, very fœtid diarrhœa. Finally the mouth exhales a stercoraceous
odour, resulting from fœtid eructation.

The passage of flat or tubular false membranes continues for a certain
time.

When false membranes constitute the chief symptom, the condition is
termed “pseudo-membranous, croupal, or diphtheritic enteritis.” This
form is only a variety of acute enteritis, but is grave, because
complications due to hæmorrhage or infection are very liable to occur.

In certain cases movement causes groaning. In the slighter forms the
patient may recover spontaneously. If fed with easily digested
materials, the symptoms diminish in intensity. Towards the eighth day
the fæces become normal, appetite and rumination reappear, and the
secretion of milk which had fallen off rises to its normal amount.
Resolution has occurred.

More frequently, either because the animals have less power of
resistance or because decomposition is taking place more actively in the
intestine, or, again, because intoxication is setting in, the disease
becomes aggravated. Constipation is more marked, and the fæces passed
are in small masses, covered with layers of epithelium, or sometimes
streaked with blood. In other cases the diarrhœa becomes exaggerated and
assumes a mucous or sero-mucous character; the temperature rises, and
death results from exhaustion and infection, microorganisms passing from
the lumen of the intestine through its walls and invading the general
circulation.

=Lesions.= To study the lesions to advantage the autopsy must be
performed as soon as possible after death.

In slight cases they consist of trifling generalised congestion of the
intestinal mucous membrane. The points most affected show infiltration
of the submucous coat, and sometimes of the muscular coat; the wall of
the intestine is double its normal thickness, but the thickening never
equals that seen in cases of rapidly fatal intestinal congestion.

At a more advanced stage the mucous membrane clearly is inflamed, its
surface is covered with a fibrous exudate, and the glandular and
epithelial cells proliferate, assume the embryonic form, and produce the
new tissue which one recognises under the form of false membranes.

The false membranes are generally but slightly adherent, and are readily
expelled.

In other cases, however, they adhere firmly, and when detached by the
friction caused by movement of semi-digested food through the bowel,
produce rupture of capillary vessels; this explains the presence of
blood streaks in the fæces.

=The diagnosis= is relatively easy, especially at the onset, on account
of the special character of the fæces and the sensitiveness of the right
flank.

=The prognosis= is seldom grave. If the enteritis is taken at the
beginning, recovery is usual; but if the animal has been ill for eight
or ten days and is exhausted, and if fever and diarrhœa are intense, the
prognosis should be guarded.

=The treatment= is that of all acute inflammatory diseases. Mustard
plasters may be applied to the chest and abdomen and left in position
for some hours, or may be repeated. Some practitioners prefer hot
blankets or dry friction, or, again, rubbing with essence of turpentine,
but this substance should be spread over large surfaces, in order to
prevent injury to the skin. Bleeding is only justifiable in plethoric
animals, and should never be exhaustive.

To relieve the digestive symptoms purgatives are at first given, even
though diarrhœa is marked from the onset; for purgatives still
constitute the best intestinal antiseptics, because they get rid of the
intestinal contents and microbes. The diet should be carefully selected,
and may consist of gruel, mucilaginous materials, linseed tea, cooked
roots, etc.

Of drugs, sulphate of sodium in doses of 10 to 15 ounces is probably the
best. It can gradually be replaced by 2 to 3 drachm doses of bicarbonate
of soda or of ordinary salt per day. Laudanum, camphor, and bismuth
relieve persistent colic and diarrhœa. Pilocarpine, veratrine and
eserine, though recommended by some authors, present no advantage in our
opinion. The first two of these substances certainly cause purgation,
but the action is quite temporary. The last induces violent contraction
of the striped muscular tissue, and may produce grave lesions or
invagination when the bowel is diseased, thickened or infiltrated.


                         HÆMORRHAGIC ENTERITIS.

This form of enteritis derives its name from the dominant symptom, which
consists in the passage of unaltered or clotted blood in the fæces. In
the former case the blood is bright in colour, as if it came directly
from an open vessel. In the second it is coagulated, and assumes the
form of fibrinous clots, which seem to result from the superposition, in
the intestinal tract of their constituent elements, viz., serum, blood
corpuscles, and fibrin.

=Causation.= Hæmorrhagic enteritis is rarely seen except during the
hottest days of summer, and in young animals which have previously shown
nothing abnormal. The high temperature seems to favour its appearance,
but is always supplemented by another cause, viz., the ingestion of
irritant food, particularly of weeds and toxic plants or herbage of bad
quality; amongst such may be mentioned dog’s mercury, and plants of the
order Papaveraceæ, Euphorbiaceæ, etc. Otherwise the often rapid manner
in which the disease develops indicates toxic enteritis.

In other cases, more benign in appearance, but quite as grave in
reality, blood is passed continually, and the disease assumes a chronic
form. It is then of parasitic origin, and is due to intestinal
psorospermosis.

=Symptoms.= The primary symptoms are similar to those of acute
enteritis, and consist of fever, dryness of the muzzle and of the mouth,
colic and constipation. This is soon followed by loose motions
containing blood or blood clots, according as the hæmorrhage occurs at a
greater or less distance from the rectum. The fæces are then ejected
violently to a considerable distance, on account of the exaggerated
intestinal peristalsis.

The disease may produce death in twenty-four hours, though usually the
end is deferred for several days, or, in cases due to sporozoa, for a
considerably longer time. In these cases there is some chance of
recovery, provided that treatment be prompt.

=The diagnosis= is very easy.

=The prognosis= is in all cases grave.

=The lesions= are ill-recognised. The animals die rapidly, and if not
immediately examined show no characteristic lesions. The changes to be
looked for consist in intense congestion or ulceration of the intestine,
or even in ulceration of arterioles and of arteries of considerable
size.

In parasitic enteritis one finds localised inflammation and, in the
epithelial interstices, sporozoa, which cause the rupture of
blood-vessels.

=Treatment.= It is necessary to act energetically from the outset, and
to arrest hæmorrhage by acting on the intestine, on the vascular system,
and on the skin. Mustard plasters or other external stimulant
applications are therefore indicated. Internally, small doses of
astringents like tannin, preparations of opium, 25 per cent. solution of
sulphuric acid in alcohol, etc., are given to produce constriction of
the vessels, though they seldom arrest the discharge of blood for long.
In most cases it is necessary to have recourse to subcutaneous
injections of ergotine, in doses of 5 to 10 grains in young animals, and
15 to 45 grains in adults. The dose may be given in two parts to prevent
an unduly severe action. The smooth fibres of the small vessels are thus
directly excited, and hæmorrhage ceases in consequence of clotting in
the contracted vessels.

One may give for the same purpose injections of arseniate of strychnine,
which has the advantage of sustaining the tone of the heart and
preventing syncope. The dose should not exceed 1·5 grains in large
animals.

Finally, a stimulating diet containing milk, alcohol, soup, cooked
vegetables, and small quantities of vegetable pulp is useful.

With early treatment animals sometimes recover in a few hours.

Intravenous or subcutaneous injections of physiological salt solution (2
drachms of sodium chloride in one quart of water) may prove of value
when hæmorrhage has been abundant and vascular pressure is low.


                 CHRONIC ENTERITIS (CHRONIC DIARRHŒA).

Chronic diarrhœa is common in byres. It appears suddenly, often fails to
attract attention, and assumes the form of simple diarrhœa, a fact which
accounts for it frequently being described as chronic diarrhœa,
dysentery, etc.

=Causation= and =pathogeny=. This form of diarrhœa occurs sporadically
throughout France, and under exceptional circumstances may permanently
attack a number of animals in a given place.

The immediate cause is not known, but without doubt the disease is of
microbic origin. Like Lignières, Moussu at one time believed that this
disease was very probably identical with that known in Argentina under
the names of diarrhœa, _entéqué_, or bovine pasteurellosis. The
hypothesis has not been verified, and Lignières’ treatment, said by him
to have succeeded in Argentina, always failed in Moussu’s hand.

[Illustration: $1]

The only point which seems admissible is that this disease, which Moussu
considered to have analogies with chronic sporadic dysentery in man, is
due to one or several organisms, which develop in the intestine and
produce toxins, causing diarrhœa, without, however, marked inflammation
of the intestinal mucous membrane.

=Symptoms.= The onset is often overlooked. The diarrhœa gradually
increases without appearing to be very serious; but it persists in
varying degrees of intensity. The patients do not appear to suffer, and
do not lose their appetite or spirits, but in time the diarrhœa becomes
exhausting; they waste, and after some months become excessively thin
and poor.

Intestinal peristalsis becomes exaggerated without the existence of
colic or tympanites. The evacuations are frequent, and little by little
the abdomen retracts, until, in horseman’s parlance, “the belly is up to
the back,” even in cows of four, seven, and eight years’ bearing.

The diarrhœa is serous, always fœtid, and without tenesmus.

The fæces may either be very soft or be passed in veritable jets. They
are always a little discoloured, and frequently contain grain or
undigested forage. They always contain numerous bubbles of gas.

The wasting during later periods of the disease is absolutely
characteristic, and different from that of other wasting diseases, such
as chronic broncho-pneumonia, tuberculosis, etc. The patients finally
become walking skeletons. The red corpuscles of the blood progressively
decrease, until the number may fall as low as 800,000 or even 500,000
red corpuscles instead of six millions, the normal figure. The œdema
common to wasting conditions appears, and the animals die without
suffering, in a condition of absolute exhaustion.

[Illustration: $1]

Complications are rare, though occasionally intestinal hæmorrhage or
broncho-pneumonia occurs. The temperature, which remains normal or shows
very slight changes throughout the course of the disease, may then
oscillate between 101° and 103° Fahr. (38° and 39·5° C.).

[Illustration: $1]

=Lesions.= At the first glance no lesions can be detected on post-mortem
examination except those of generalised wasting, but when the autopsy is
carried out immediately after death all the interior of the intestine
appears affected. The mucous membrane of the abomasum and the mucous
folds appear infiltrated, thickened, and with moderate sub-epithelial
congestion. The intestine seems friable, and tears with the slightest
traction. The sub-epithelial portions of the mucous folds are
infiltrated and congested, while the more prominent parts of the folds,
which are exposed to the friction of semi-digested food, become eroded.

Throughout the length of the jejeunum and ileum the mucous membrane
exhibits multitudes of small ulcerations.

Histologically, the epithelium and the glands seem atrophied, without
any inflammatory change having occurred in the mucous or submucous
coats.

The colon and the cæcum show similar lesions, and in addition brown
deposits of pigment under the mucous membrane and along the course of
the small blood-vessels. This lesion resembles that found in chronic
dysentery in man, and suggested to Moussu a possible connection between
the two diseases.

The liver is less than the normal size. In the heart Moussu has seen one
case of sclerosis of the auricles and calcareous infiltration of the
sub-endothelial lining of the aorta.

In several instances he has noted calcareous infiltration of the
mesenteric lymphatic gland.

=Diagnosis.= It is easy to diagnose this condition, and quite possible
to distinguish it from the diarrhœa of tuberculous enteritis, infectious
hepatitis, and other conditions.

=Prognosis.= The prognosis is very grave, and the disease almost always
proves fatal.

=Treatment.= At the present moment no curative treatment is known.
Lignières’ treatment—viz., the injection of physiological salt solution
and serum from healthy oxen, and saline solution or defibrinated
blood—has never given permanently successful results.

All the drugs usually employed against diarrhœa, the antiseptics,
astringents, etc., fail, or confer merely momentary benefit.
Economically, nothing is to be gained by keeping the patients alive.
With great care existence may be prolonged for months, or even for
several years, but the animals never regain condition, and are never of
any use.

The most rapid and lasting good effects follow the administration of 2½
to 8 fluid drachms of hydrochloric acid per day, given in two portions
and very freely diluted.


                          DYSENTERY IN CALVES.

This disease sometimes appears on the first day after birth, frequently
on the second or third. It may be mistaken for septicæmia of umbilical
origin.

=Symptoms.= The young animal may be born vigorous and in good condition,
though this is exceptional. More frequently it is puny and below normal
weight. The first evacuation (of meconium) may exhibit the diarrhœic
character; in other cases this peculiarity only appears on the second or
third day, when half-digested milk is passed. The fluid is greyish,
extremely fœtid, and rapidly becomes brownish and blood-stained.
Evacuation is frequent and accompanied by tenesmus.

The patients at once become very dull, refuse to suck, and resist
efforts to feed them by hand. The temperature rises, and the diarrhœa,
which at first was of an alimentary character, becomes mucous, serous
and blood-stained. The little patients appear “tucked up,” the flanks
sink in, the strength diminishes, and in twenty-four hours, or two or
three days at most, they die of exhaustion.

Recovery is exceptional, and when the disease assumes this character it
usually attacks a considerable proportion of the other animals in the
byre.

=Causation.= The exact cause of this form of dysentery in new-born
calves has not yet been identified, but the disease is undoubtedly a
microbic enteritis, and may even be a primary septicæmia of puerperal
origin.

For a very long time this dysentery was mistaken for simple diarrhœa,
though it exhibits neither the characteristics, course, nor termination
of the latter disease.

The co-existence of epizootic abortion and dysentery in certain byres
has led some authors to believe that a connection exists between the two
diseases, and that the young are infected with dysentery at birth.
Evidently, intra-uterine infection is not exceptional, and it seems
quite natural that the new-born calf may equally suffer when the fœtal
envelopes and fluids are infected before parturition. Epizootic abortion
is probably not the only disease which may produce this condition.

=The diagnosis= is very simple. The course of the disease and its rapid
development prevent it from being mistaken for ordinary diarrhœa. It is
more difficult to distinguish from septicæmia of umbilical origin,
although this disease also has well-marked characteristics.

=The prognosis= is not hopeful. Statistics show that almost all the
affected animals die, and that those exceptional cases which survive
remain puny and sickly. There is no economic advantage in attempting to
save them.

The mothers of affected calves seldom show any sign of illness, though
the after-birth is often retained.

=Lesions.= The macroscopic lesions are of very trifling importance
compared with the gravity of the disease. The digestive tract appears
congested throughout. The intestinal mucous membrane is moderately
swollen, but without gross lesions. The intestinal contents exhale a
sickly, fœtid odour. The smaller vessels and capillaries forming the
peripheral vascular network appear distended, as in septicæmia. The
carcases putrefy with extreme rapidity.

Curative =treatment= is very uncertain. Varying results have been
obtained with doses of 4 to 5 drams of slight purgatives like
borotartrate of potassium, sodium sulphate, and magnesium sulphate;
small doses of intestinal antiseptics like salicylic acid, 15–grain
doses of salicylate of soda, 45 to 75 grains of carbolic acid, 2 per
cent. carbolic solution in doses of 7 to 12 drams; 1 per cent. Lysol
solution in doses of 2 to 4 ounces; benzo-naphthol, lactic acid 45 to 75
grains, tar water, lime water, etc. Although all these preparations,
when carefully used, generally give good results in the early stages of
simple diarrhœa, they appear to fail in dysentery of new-born calves.

Prophylactic measures are more reliable. They consist:

(1.) In scrupulous disinfection of the byres when the first case of
abortion occurs;

(2.) In successively isolating cows which are about to calve in a small
specially detached stable;

(3.) In carefully disinfecting the genital organs of cows which have
aborted, firstly with boiled water at a temperature of 100° Fahr., and
then with 1 per cent. iodine solution.

Calves which are infected when born cannot be saved, but abortion can be
prevented and dysentery so stamped out.


                     DIARRHŒIC ENTERITIS IN CALVES.

This disease is usually called “simple sporadic diarrhœa.” It may appear
at any time before weaning, and can usually be cured if treated early
before the patients show bodily wasting.

=Causation.= Indigestion from failure of the abomasum to deal with the
milk usually precedes diarrhœic enteritis; it may terminate without
complications, but very often is followed by diarrhœa. Anything which
produces milk indigestion, therefore, favours the occurrence of
enteritis. Such predisposing influences include over-distension of the
abomasum, milk of bad chemical composition, milk tainted by keeping or
by storage in dirty and infected pails, etc. The addition to the milk of
nutritive substances which the abomasum and intestine are not yet
capable of digesting, such as wheat, rye, barley, or maize meals, very
often produces diarrhœa even when the meal is well cooked.

Chills, privations, irregular feeding, and badly-managed weaning may
facilitate its development, but none of these causes, however important
they may be, seem to play any other part than that of favouring the
multiplication of the numerous varieties of microbes to be found in the
intestinal tract. Vascular disturbance occurs, either as a result of
direct irritation of the intestinal mucous membrane or of the action of
toxic products contained in milk which has served as a culture medium
for these microbes; this is followed by secretory disturbance, and the
intestinal contents being modified in character, the microbes normally
present undergo changes in number and quality. Inoffensive organisms
assume pathogenic qualities and secrete toxic principles, normal
digestion is disturbed, the intestinal defence becomes less perfect,
toxic principles which the liver is incapable of destroying are
absorbed, and diarrhœic enteritis is set up.

=Symptoms.= Diarrhœic enteritis appears during the second week of life,
towards the end of the first month, or even later. It is characterised
by the passage of fæces consisting of mucus and containing little clots
of milk.

This is the first stage of alimentary diarrhœa, also termed “white
diarrhœa” or “white scour.” It may prove unimportant; it may last a day
or two and then cease. Most commonly diarrhœa increases and assumes a
mucous and then a serous character, whilst the dejecta exhale a very
characteristic repulsive smell. The excrement becomes greenish brown,
and after several days or a week or more may appear blood-stained. The
number of evacuations varies enormously, depending on the gravity of the
condition. The ejected material is irritant, and the parts soiled by it,
like the perineum, hocks, and back of the cannon bones, become slightly
inflamed as though blistered; later, the hair falls away.

The general health then begins to suffer. Fever remains moderate, but
the mouth is pasty, the tongue coated, and the breath fœtid.

The patients become thin, and lose their appetite and spirits. Palpation
of the abdomen, especially of the right flank, is slightly painful, and
the pulse is accelerated.

The diarrhœa may spontaneously diminish if the animal’s constitution
prove sufficiently strong; but if it follows its course, the little
patient becomes weaker, eats less, the evacuations increase and are
accompanied by tenesmus. In seven to eight days, in rare cases in four
to five, the animal dies from toxi-intoxication of intestinal origin, or
from infection resulting from intestinal germs, particularly the
bacterium _Coli communis_, obtaining entrance into the circulation. On
the other hand, the diarrhœa may continue for weeks.

=The diagnosis= is easy, and there should be no difficulty in
distinguishing this disease from dysentery and from umbilical phlebitis,
which are also accompanied by diarrhœa.

=The prognosis= is grave, unless treatment is early undertaken. In the
latter case there is a good chance of recovery.

=Lesions.= The macroscopic lesions are not of much interest, being
confined to congestion of the intestinal mucous membrane, superficial
desquamation of the epithelium, small vascular erosions, and general
wasting.

The mesenteric lymphatic glands are swollen and œdematous.

After death from general infection, it is not uncommon to find pleural,
peritoneal, and pericardial exudation or even endocarditis.

Even in cases where no post-mortem change has had time to occur cultures
from the blood yield varieties of the bacterium _Coli communis_.

=Treatment.= The meals should be given at fixed hours, and regulated
both as regards quantity and quality. These precautions alone suffice to
prevent the appearance of diarrhœic enteritis.

Curative treatment has every chance of succeeding when undertaken at the
outset. Delafond and Trasbot recommend mild purgatives, which act more
rapidly than intestinal antiseptics. These comprise borotartrate of
potash in doses of 4 to 5 drachms, sodium sulphate in doses of 2½ to 4
drachms, sulphate of magnesia, etc. By evacuating the bowel and removing
a large number of the germs which have multiplied there, they arrest
intoxication and prevent infection. Nevertheless, they should not be
administered for long, and after one or two doses should be followed by
antiseptics like benzo-naphthol, in doses of 15 to 30 grains, salicylic
acid in doses of 5 to 10 grains, or salicylate of soda 45 to 60 grains.
Mucilaginous and sweetened drinks containing lactic acid in doses of 45
to 75 grains per day may be given between the meals, or at intervals if
the calf is sucking.

Laudanum in doses of 6 to 10 drops per day administered in rice water,
extract of opium, weak solutions of tannin, etc., are also of value.
Filliàtre has successfully used tar water in the first stages. The
solution consists of vegetable tar 6 drachms, boiling water 1 quart.
This solution is used tepid in the proportion of 1 part to 3 parts of
warm milk.

Decoctions of spiked purple loosestrife, willow bark, etc., are also of
great value in certain districts.

The drug which appears least dangerous, however, is that so often
successfully used in young children—viz., subnitrate of bismuth. It can
be given in doses of 30 to 45 grains per day, with lactic acid in doses
of 75 to 150 grains, according to the size of the patients. If the
animals are greatly exhausted and have been ill for some time there is
less chance of recovery, and under these circumstances Dr. Lesage’s
anti-colic serum might be used.

It gives excellent results in infants, and it has proved successful in
simple diarrhœa of calves.




                              CHAPTER VII.
                               POISONING.


Accidental poisoning is frequent in domesticated animals. It may present
no visible lesions, and it is therefore very important to recognise the
symptoms which indicate the secret lesion.


                         POISONING DUE TO FOOD.

Under this title are included all forms of poisoning resulting from the
ingestion of bad fodder. Such expressions as “intestinal typhus” and
“typhic gastro-enteritis” only indicate a special stage in the
condition, which is never twice the same.

=Causation.= The most important changes in the food ingested do not
consist in a mere modification in its chemical composition, but in the
presence of various parasites which develop in grain and forage, after
moistening, or after abnormal fermentation in the interior of the
grains. These parasites are chiefly represented by fungi belonging to
the genus Mucor: _Aspergillus_ or _Penicillium_; blight—_Puccinia
graminis_, _Uredo linearis_; smut—_Tilletia caries_, _Ustilago segetum_,
_Ustilago maydis_; yeasts of different kinds resulting from the
fermentation of brewers’ grains; and, finally, unrecognised microbes
which act by means of the poisons they secrete.

=The symptoms= are always very vague. At first the only marked symptom
is loss of appetite, accompanied by dryness of the mouth and muzzle,
depression and constipation. The animals never clearly show signs of
gastro-enteritis; nevertheless, the changes in general health point very
clearly to a digestive origin.

In cases of acute poisoning the symptoms develop rapidly. Torpor becomes
more marked, the movements of the heart tumultuous, and the temperature
rises to 105° Fahr. (40·5° C.), diminishing later until death occurs.

In chronic forms of poisoning constipation is present at first, but is
soon followed by profuse, fœtid, blackish diarrhœa, sometimes containing
streaks of blood and accompanied by abdominal pain.

In exceptional cases these digestive symptoms are amplified by the
presence of broncho-pneumonia, pleuro-pneumonia, nephritis, and
cystitis, as in poisoning by tannin and essential oils. These
complications are of infectious origin.

In young animals, like lambs and young pigs, still with their mothers
alimentary intoxication may also occur though the mothers show no signs
of illness. The passage of poisonous principles into the milk cannot be
disputed. Moussu has seen numerous cases of alimentary intoxication in
lambs whose dams were fed with decomposed beet pulp, and in sucking pigs
whose mothers had received bad maize, turnips, etc.

=Diagnosis.= Careful examination of the substances with which the
animals are fed, and consideration of the history, prevent confusion
with ordinary poisoning. Anthrax as a cause can easily be eliminated.

=The prognosis= is grave, unless the practitioner is summoned early.

=The lesions= are those of acute gastro-enteritis—congestion of the
mucous membrane, abomasum, and intestine, submucous infiltration,
shedding of the epithelium, which sometimes attains the stage of
ulceration, suffusion and intestinal or superficial hæmorrhage,
dilatation of the capillaries, etc.

The symptoms of poisoning are produced by the absorption of toxic
products, which pass from the intestine into the blood current.

Poisoning is frequently complicated by infection produced in a similar
manner.

=Treatment.= The first point is to change the food. This alone is often
sufficient to dispose of the digestive disturbance in a week or two. In
addition, mustard plasters may be applied, and purgatives, stimulants
and mucilaginous drinks may be given. Finally, diuretics are useful in
eliminating the toxic products accumulated in the blood. They comprise
general stimulants like wine, alcohol, tea, coffee, etc. Subcutaneous or
intravenous injection of physiological salt solution is indicated.


                     POISONING BY CAUSTIC ALKALIES.

=The cause= consists in the administration of insufficiently diluted
solutions of ammonia in cases of tympanites, or the ingestion of
quick-lime, used for disinfecting stables, by animals suffering from
depraved appetite.

=The symptoms= indicate injury to the anterior part of the digestive
tract. They consist in salivation, loss of appetite, colic, indigestion,
diarrhœa, and progressive loss of strength.

=Diagnosis= is only possible when the history is clear.

=The prognosis= is grave if the doses swallowed have been so large as to
cause severe burning of the mouth, œsophagus, rumen, etc. The local
lesions are grey and soft.

=Treatment= consists in immediately giving acidulated draughts
containing vinegar or 1, 2 or 3 per cent. of hydrochloric acid, and
emollient, mucilaginous drinks containing opium for the purpose of
calming the irritation.


                      POISONING BY CAUSTIC ACIDS.

Cases of this kind are rare. Gerlach described a case of poisoning by
straw which had been removed from sulphuric acid carboys. Abadie saw a
number of cases which were traced to the unskilful treatment of two
empirics.

=The symptoms= point to the existence of stomatitis, œsophagitis, and
gastro-enteritis. Death occurs rapidly, with a running-down pulse. On
post-mortem examination one discovers more or less deep burning of the
mucous membrane of the digestive tract.

=The diagnosis= is difficult in the absence of information.

=The prognosis= is grave.

=Treatment= comprises administration of alkaline draughts, solutions of
bicarbonate of soda, calcined magnesia, etc., and of mucilaginous drinks
containing opium, chalk, etc. This may produce temporary relief.

Water mixed with whipped whites of eggs is also extremely valuable, but
it is often better to slaughter the animal as soon as the condition is
diagnosed.


                       POISONING BY COMMON SALT.

This form of poisoning is rare in oxen on account of the large quantity
of salt which can be ingested without producing bad effects. It is
commonest in animals to which old brine has been given or which have
received rough salt containing toxic substances (sheep and pigs). Beef,
pork, or fish brine, four or five months old, is especially dangerous
because of the toxins it contains. Half a pint is a fatal dose for a pig
(Reynal). The symptoms include marked thirst, vomiting and diarrhœa; at
a later stage motor and nervous disturbance appears, resulting from
poisoning of the cerebro-spinal system. Paralysis, epileptiform
convulsions, trismus, coma and death characterise extremely acute cases.

To the naked eye, the =lesions= are those of acute gastro-enteritis;
and, in many cases, of marked congestion of the brain and medulla and of
the mucous membrane of the bladder.

=The treatment= is prophylactic and hygienic. Old brine and salt of
doubtful purity should be avoided. The symptoms should be treated by
administering diuretics, preferably soda bicarbonate, which does not
irritate the kidney, and by giving mucilaginous drinks with anodynes.


             POISONING BY THE NITRATES OF POTASH AND SODA.

This form of poisoning has frequently been described as following the
ingestion of water used for washing sacks which have contained chemical
manures. Occasionally it results from the administration of medicines
containing excessive doses of nitrate of potash. The symptoms vary in
severity with the purity of the salt, with its nature, and with the
degree of concentration of the solution: nitrate of potash is more
dangerous than nitrate of soda.

The chief =symptoms= may be grouped as follows:—

Salivation, indigestion and tympanites, nausea, vomiting, diarrhœa, and
(especially) intense polyuria: the kidney may be irritated to such a
degree as to produce albuminuria and hæmaturia. Intense dulness and
general weakness precede death, which sometimes occurs in four to twelve
hours after the poison has been taken.

The =lesions= are to be found in the digestive and urinary apparatus.
The kidneys are congested and hypertrophied, or present changes
indicating epithelial nephritis. The ureters and the bladder may show
similar lesions.

=Treatment= comprises removal of the cause, and the administration of
emollients, narcotics, and diffusible stimulants.


                      POISONING BY TARTAR EMETIC.

Tartar emetic is sometimes given for the purpose of favouring secretion
and restoring rumination; occasionally the proper dose is exceeded and
poisoning occurs. Given repeatedly, tartar emetic is apt to accumulate
in the deeper portions of the gastric compartments and to produce
general symptoms of super-purgation, and such local symptoms as
ulceration and even perforation of the walls of the stomach, which in
turn is followed by abscess formation in the abdominal wall.

=Diagnosis= is easy. =The prognosis= is grave.

=Treatment= is confined to the administration of mucilaginous and
diuretic fluids. Tannin has been recommended.


                         POISONING BY ARSENIC.

Overdoses of Fowler’s solution produce rapidly fatal results, in
twenty-four to forty-eight hours. Lesions are little marked.

Arsenious acid acts like tartar emetic by accumulating and producing
local gastritis; it may also cause acute poisoning, being in that case
characterised by severe colic with tympanites, salivation, and fœtid,
sometimes blood-stained, diarrhœa. The urine becomes albuminous, and
remains scanty. Incomplete paralysis is sometimes produced, and various
forms of hæmorrhage result from changes in the constituents of the
blood.

If the gastric compartments are perforated, an abscess may develop in
the abdominal wall. The =lesions= are those of acute gastro-enteritis.
The contents of the stomach exhales an odour resembling garlic. The
parenchymatous organs—the liver, kidney, and heart—show fatty
degeneration in chronic cases.

In prescribing arsenic, one should begin with small doses, which can
gradually be increased as the animal becomes accustomed to the drug.
Curative =treatment= consists in administering antidotes, such as
hydrated oxide of iron, sulphate of iron, and calcined magnesia.

Haubner described a form of chronic arsenical poisoning produced in the
neighbourhood of blast furnaces near Freiberg. Similar forms of
poisoning may perhaps occur in the neighbourhood of chemical and
smelting works in England.


                         PHOSPHORUS POISONING.

Though the chronic form is common in men, phosphorus poisoning only
occurs accidentally in animals through eating phosphorus paste, used as
a poison for rats, or as a consequence of excessive doses given
medicinally. Some cases have been described by Maury.

=The symptoms= comprise salivation, loss of appetite, alliaceous odour
of the buccal cavity, arrest of intestinal peristalsis, indigestion,
colic, diarrhœa, exhaustion and death in a state of coma. Albuminuria
and icterus also occur.

=The lesions= are the same as those of arsenical poisoning—viz.,
stomatitis, pharyngitis, and gastro-enteritis. The specific changes
consist in fatty degeneration of the liver and kidneys, and the peculiar
odour resembling garlic exhaled by the flesh.

Death is a consequence of deoxygenation of the blood, which appears
black, and when spectroscopically examined reveals only the lines of
reduced hæmoglobin.

=Treatment.= Oil and milk dissolve phosphorus and render it more easily
assimilable; they should never be administered. Large doses (up to six
fluid ounces) of essence of turpentine have been recommended. This
prevents the phosphorus absorbing oxygen at the expense of the blood.
Saline purgatives assist in eliminating the poison.


                          MERCURIAL POISONING.

Mercurial poisoning may result either from the administration of
medicines or from accident. Cases of the former kind follow the internal
use of sublimate or calomel. Doses of 2 to 2½ drams of calomel, if
repeated for a certain time, may prove toxic in the ox. Accidental
poisoning results from the use of mercurial ointment as a parasiticide
over large surfaces. Poisoning, however, rarely occurs unless the animal
is able to lick the parts. Some authors have tested this point by freely
applying mercurial ointment over parts likely to absorb it readily,
without having seen any bad effect.

=Symptoms.= Free salivation, the saliva gradually becoming fœtid and
blood-stained. The slight irritation of the buccal membrane first seen
is soon replaced by congestion of the gums, then by gingivitis and
periostitis, with local ulceration and hæmorrhage. The portion of the
gums surrounding the teeth becomes violet, and suppurative alveolitis
may follow.

As a consequence of disturbance in the digestive secretions digestion
ceases, defæcation becomes irregular, the fæces are often hard and
coated, and can only be passed with difficulty, though sometimes there
is profuse fœtid diarrhœa.

Respiration is difficult, jerky, or even dyspnœic, and is accompanied by
discharge from the nose and by expectoration. The gait is irregular, and
paralysis may follow. Finally the skin shows an eruption resembling that
of impetiginous eczema; vesico-pustules, covered with yellowish crusts,
appear over the entire surface of the body.

=Lesions.= The lesions of hæmorrhagic gastro-enteritis are sometimes
accompanied by catarrhal tracheo-bronchitis, and even intra-pulmonary
hæmorrhage. The muscles are discoloured, appear as though boiled, and
are covered with ecchymoses. Blood effusions occur beneath the
eczematous crusts, but the rest of the skin is anæmic.

=Treatment= includes administration of raw eggs, or, better still, of
white of egg beaten up in water; the albumen in coagulating imprisons
the mercury. Failing these, other bodies, like flowers of sulphur and
iodide of potassium, which with mercurial salts form soluble and
harmless compounds, may be given. Chlorate of potash has also been
recommended.

Complications like stomatitis and gastro-enteritis are treated by the
usual methods.


                       LEAD POISONING: SATURNISM.

Lead poisoning is very rare, and seldom occurs except near camps or
factories. It then results from swallowing lead “spray” mixed with the
grass or from inhalation of lead vapour.

=The symptoms= comprise salivation, nausea, colic, obstinate
constipation, tympanites, and arrest of milk secretion. A peculiar form
of trembling affects the head; epileptiform convulsions, amaurosis, and
paralysis may also occur. General sensibility diminishes, and death
follows.

The disease may assume a chronic form, characterised by a blue line
around the gums, changes in the joints, albuminuria, and bodily wasting.

=The lesions= are those of ulcerative stomatitis, anæmia of the mucous
membranes, and fatty degeneration of the epithelium. In the chronic form
the kidneys are atrophied.

=Treatment= consists in giving substances which form insoluble compounds
with lead. It comprises the administration of dilute sulphuric acid,
solutions of sodium sulphate or magnesia, milk, eggs, and iodide of
potassium.


                           COPPER POISONING.

This is a rare form of poisoning. It may follow ingestion of food stored
in copper vessels, licking of ointments containing copper salts, or
ingestion of vine leaves, or leaves of other plants which have been
sprayed with sulphate or acetate of copper to prevent “mildew.”

=The symptoms= comprise vomiting of green-coloured material, colic,
diarrhœa, muscular weakness, and convulsions. The urine contains
dissolved albumen and hæmoglobin.

=The lesions= are those of acute enteritis and dilatation of the
stomach. The essential lesion consists in decomposition of the blood
with the formation of methæmoglobin. Nephritis and granular degeneration
of the muscles form secondary symptoms.

=Treatment= consists in administering raw eggs, albumen, milk, mucilage,
flowers of sulphur, or calcined magnesia.


                        CARBOLIC ACID POISONING.

Carbolic acid poisoning sometimes follows the use of carbolic acid
solutions in the form of injections, enemas, or baths.

=Symptoms.= Administered in over-doses or for too long a time, carbolic
acid produces stomatitis, œsophagitis and vomiting.

True poisoning is characterised by changes in the kidneys and bladder;
the urine becomes brown and turbid, and possesses a well-marked carbolic
odour, the animals suffer from severe trembling and appear stupid, and
coma and paralysis precede death.

The specific =lesions= consist in parenchymatous nephritis, sometimes
accompanied by renal hæmorrhage, cystitis and hyperæmia of the lung and
brain. The flesh has an odour of carbolic acid, which renders it unfit
for human consumption.

=Treatment= consists in giving stimulants and slight diuretics, such as
ether, alcohol, wine, coffee, saline sulphates, or Glauber’s salt. The
last named forms phenyl-sulphuric acid, which is not toxic. Olive, rape,
or linseed oil has been recommended. All these drugs are useless if the
kidney lesions have become too pronounced.


                          POISONING BY ALOES.

This form of poisoning is caused by administering over-doses of aloes.

Apart from the accidents possible in pregnant female animals, large
doses of aloes produce symptoms of super-purgation—profuse diarrhœa,
running down pulse, and nervous prostration.

=The lesions= are those of gastro-enteritis, the intestine being empty,
and its mucous membrane of red colour.

=Treatment= is confined to administering drugs like camphor, rice,
bismuth, opium, chloral, and emollients, which diminish peristalsis and
lessen secretion.


                          IODOFORM POISONING.

=The causes= are limited to the licking of wounds which have been
dressed with iodoform.

=The symptoms= include gastric disturbance, somnolence, coma, and the
signs of iodism.

The only =lesions= are those of fatty degeneration of the kidneys and
liver.

=Treatment= comprises the exhibition of vomitants, stimulants, and
diuretics.


                       IODINE POISONING: IODISM.

Death by iodine poisoning is absolutely exceptional: the complications
described under the name of iodism are rather to be referred to
saturation of the organism than to true poisoning.

=The cause= of iodism is unduly prolonged administration of iodide of
potassium, or of iodine in solution.

=The symptoms= include discharge from the eyes, coryza, hypersecretion
from all the mucous membranes, and gastric disturbance. The cutaneous
eruption exhibits special peculiarities, including desquamation of the
epidermis in the form of branlike scales, and pruritus.

The first indications in =treatment= are to discontinue the drug and to
administer stimulants and nutrients like milk, cod liver oil, etc.


                         STRYCHNINE POISONING.

Strychnine poisoning is most commonly due to over-doses of the drug
accidentally given during treatment.

=The symptoms= comprise tetanic convulsions, hyperæsthesia and dyspnœa.
As a result of muscular rigidity, the ribs cannot be moved, and death by
asphyxia follows.

=Treatment= comprises the use of anæsthetics, and the administration of
chloral hydrate, as long as the contractions continue. Bromide of
potassium, tobacco, tannin, etc., are also useful.

                  *       *       *       *       *

The chief part of the botanical descriptions in the following list have
been extracted, by permission, from the Annual Report for 1898 of the
United States Bureau of Animal Industry, p. 392. To Dr. D. E. Salmon,
who gave this permission, and who also kindly supplied the blocks, the
writer (Mr. Dollar) desires to express his very sincere thanks.
Considerable modifications have been made, and in the case of the more
important poisonous plants, details of symptoms and treatment have been
added.


                 LIST OF PLANTS POISONOUS TO STOCK.[2]

Footnote 2:

  The names of plants proved beyond doubt to be poisonous to stock are
  marked with an asterisk. The evidence in regard to the toxic
  properties of others is not in every case entirely convincing, though
  there is good ground for strong suspicion.


                    PERISPORACEÆ (ROT-MOULD FAMILY).

=Aspergillus glaucus.=—This is the common flocculent woolly mould which
sometimes develops to a dangerous extent on corn, oats, and other food
grains which have either been harvested before full maturity or been
stored in a damp place. The mouldy growth is pure white at first, but
changes with the ripening of the spores to gray and then green. The
spores are apparently the cause of the so-called enzootic cerebritis, or
“staggers,” of horses, which, during the winter of 1898–99, was reported
as having caused very heavy losses in the southern portion of the United
States. European investigators have shown that the spores of this mould
will grow within the living body if they are introduced into the blood.
Death is probably caused by some poison which is simultaneously produced
with the mould in the body of the animal.


                      HYPOCREACEÆ (ERGOT FAMILY).

* =Claviceps purpurea.=—This, the most common species of ergot, infests
various species of native and cultivated grasses. It sometimes causes
great losses of stock.


                  POISONING BY ERGOT OF RYE: ERGOTISM.

=Causation.= This form of poisoning is due to the presence of ergot in
grain or forage.

=Symptoms.= The symptoms are seldom very marked. In mild cases pregnant
females may abort; grave cases are indicated by local gangrene of the
mucous membrane and gangrene of the extremities, particularly in
poultry, in consequence of the constrictive action of the drug on the
peripheral blood-vessels, on the vaso-motor centres, and on unstriated
muscular fibres.

=Treatment.= The use of chloral and morphine has been suggested in this
condition; but as the lesions when discovered are established and
permanent, this treatment seems illusory. More is to be expected from
preventive measures and the avoidance of ergotised food.


                      USTILAGINACEÆ (SMUT FAMILY).

=Ustilago maydis.=—The black powdery fungus known as corn smut is common
throughout the corn-producing districts of the central United States,
and is occasionally reported as being fatal to stock. Experiments made
in Wisconsin and elsewhere show that it is not a very active poison when
eaten in moderate quantity. When given in gradually increasing amounts
up to 2 lbs., no effect was noted, but 4 lbs. on each of two successive
days caused the sudden death of one cow. Since corn smut has been shown
to be less fatal when wet, it seems probable that its physical and not
its chemical character may be responsible for the death of cattle which
have eaten it in considerable quantity.

[Illustration: $1]


                      POISONING BY SMUT OF BARLEY.

=Causes.= The presence of smut in straw, in millers’ grains, or in
damaged kiln-dried grains which have fraudulently been added to grain
sold for feeding, represents the principal source of this form of
poisoning.

=The symptoms= are very vague. There is indigestion, with a tendency to
nausea, and vomiting. Diarrhœa may be present: At a later stage the
heart and nervous system are affected. The gait becomes hesitating, the
animals show general dulness and spasm of the pharynx; death, when
occurring, is by cardiac or respiratory syncope.

=Treatment= consists in giving an entire change of food, and
administering stimulants and purgatives.


                     AGARICACEÆ (MUSHROOM FAMILY).

=Amanita muscaria.=—The well-known fly amanita (fly fungus; deadly
amanita) may be found from spring to early winter in pine forests
throughout the United States. Cows are supposed to be killed by eating
it, and almost every year the daily papers chronicle the death of
several human beings who were led to eat the fungus through mistake for
some edible species. The fresh cap is frequently rubbed up with milk and
used to poison flies.


                     PHALLACEÆ (STINK-HORN FAMILY).

* =Clathrus columnatus.=—In an article published in the _Botanical
Gazette_ (Vol. XV. p. 45), Dr. Farlow, of Harvard University, gives an
account of an investigation of a case of poisoning in hogs which was
caused by eating this peculiar fungus. It grows in patches in oak woods
and openings, and is quite common throughout the Southern States.


                      POLYPODIACEÆ (FERN FAMILY).

=Pteris aquilina.=—In July, 1895, nineteen cattle died in Maryland,
which were supposed to have been poisoned by eating the common bracken
fern. Very few similar cases are on record, but one European authority
cites one in which five horses were killed by eating hay contaminated
with this fern, and another states that cases are quite frequent among
cattle in England.


                    EQUISETACEÆ (HORSETAIL FAMILY).

=Equisetum arvense.=—The field horsetail was reported from Connecticut
in 1871 as being poisonous to horses. Cases are very rare, and it is
probable that this plant is deleterious only when eaten in considerable
quantity, and then perhaps only on account of its physical character.
Experiments made in Europe show that a similar species (_E. palustre_)
is fatal to horses when fed in considerable quantity with hay.


                         TAXACEÆ (YEW FAMILY).

=Taxus minor.=—The common yew, or ground hemlock, is called poison
hemlock in some places. The leaves of this shrub are probably poisonous
to stock, as are those of the European yew. This species is more
accessible to stock than the western yew (_Taxus brevifolia_), which
grows only in deep cañons.


                     YEW POISONING (TAXUS BACCATA).

The leaves of yew, when eaten in any considerable quantity, are very
poisonous. Two ounces to eight ounces, according to the size of the
animal, slow the heart’s action, produce weakness, staggering, and
apoplectic congestion, which may have a fatal result in less than an
hour. The bark is less injurious, and the fruit is scarcely poisonous at
all.

The early =symptoms=, which are only seen in chronic cases, consist in
excitement, followed by somnolence and muscular weakness, with slowing
of the respiration and circulation.


                         POACEÆ (GRASS FAMILY).

=Lolium temulentum.=—The seed of the darnel, or poison rye grass, an
introduced annual especially abundant on the Pacific Slope, is
considered poisonous to both man and animals.

=Stipa robusta.=—This is a perennial plant which is known in Arizona and
New Mexico as sleepy grass. It produces a narcotic effect on horses and
cattle that feed upon it, but stock bred in that region rarely touch it.

=Zea mays.=—The numerous deaths that are frequently attributed to Indian
corn are mostly due, not to any poison inherent in the plant, but rather
to parasitic or saprophytic fungus growths, as noted under _Aspergillus_
and _Ustilago_. The green fodder is very apt to cause severe and even
fatal tympanites if the animal’s diet is not properly regulated. Death
has also been attributed to the presence of nitre (potassium nitrate) in
the growing stalks. It is supposed that in very rich soil this substance
will sometimes accumulate in the stalks in considerable quantity during
prolonged drought.


                 POISONING BY THE MALE TUFTS OF MAIZE.

The green tufts alone are toxic; the toxicity disappears after drying.
Prolonged administration produces nephritic colic and renal lithiasis.


                   POISONING BY SWEET SORGHUM GRASS.

This form of poisoning is characterised by attacks of trembling,
tympanites, and frequent attempts to urinate. The heart beats feebly,
and the pulse grows progressively weaker, until at last it becomes
imperceptible.


                   MELANTHACEÆ (BUNCH-FLOWER FAMILY).

* =Chrosperma muscætoxicum.=—The bulbous portion of the fly poison, or
crow poison, an eastern plant, is sometimes eaten by cattle with fatal
results. The bulbs, when crushed with molasses, are used to stupefy
flies.

[Illustration: $1]

[Illustration: $1]

* =Veratrum viride.=—The leaves of the common swamp hellebore (American
white hellebore; false hellebore; Indian poke) of the eastern and
northern portions of the United States have proved fatal to man and to
horses. Sheep eat the young leaves and shoots with apparent relish. The
seed is poisonous to chickens.

=Zygadenus venenosus.=—The name death camas has been applied to this
plant in the North-West of America to distinguish it from the true camas
(_Quamasia quamash_), which is highly esteemed for food by the Indians.
In Oregon it is erroneously called “lobelia” by most stockmen and
farmers. Horses, cattle, and sheep, as well as man, are poisoned by
eating the bulb.

=Zygadenus elegans.=—The bulbs, and perhaps the leaves, of the _Glaucous
zygadenus_, or alkali grass, are poisonous to cattle.


              CONVALLARIACEÆ (LILY OF THE VALLEY FAMILY).

_Convallaria majalis._—All parts of the lily of the valley are
powerfully poisonous, and are liable to injure cattle and horses.


                    HÆMODORACEÆ (BLOODWORT FAMILY).

=Gyrotheca capitata.=—This is the red root, or paint root, of the
Atlantic coast and Cuba, so called on account of the red colour of its
sap. White hogs are supposed, throughout the Southern United States, to
be particularly subject to the poison contained in the plant.


                        FAGACEÆ (BEECH FAMILY).

=Quercus sp.=—In Europe the acorns of various species of oak cause
sickness and death in hogs and cattle. This effect may possibly be due
to tympanites, but may also be due in some way to the tannin or the
bitter principle which they contain.


                          POISONING BY ACORNS.

The acorn, or fruit of the oak (_Quercus robur_ and _Quercus
sessiliflora_), is much valued as a food for swine. “A peck of acorns a
day with a little bran will make a hog, ’tis said, increase a pound
weight _per diem_ for two months together.” Though largely consumed by
swine with no apparent ill effects, acorns constitute a dangerous food
for young cattle, especially when eaten before they are ripe and when
herbage or other feeding is scanty or restricted.

=The symptoms= comprise dulness, loss of appetite, constipation,
followed by diarrhœa, with straining and colicky pains, head carried
low, eyes retracted, with mucus about the eyelids and blood-stained
discharge from the nose. Frequently the abdomen is distended.
Temperature normal.

=The lesions= are, abrasions of the buccal membrane on the palate,
cheeks, etc.; impaction and intense congestion of the omasum.

=Treatment.= Change of pasture. Alkalies—potash or soda bicarbonate,
magnesia; tonics and stimulants.


                       URTICACEÆ (NETTLE FAMILY).

* =Urtica gracilis.=—The slender nettle covers thousands of acres of
reclaimed swamp land in Michigan and Wisconsin, which is made nearly
worthless by its dense growth, horses refusing to pass through it to
cultivate the soil.


                   CHENOPODIACEÆ (GOOSEFOOT FAMILY).

[Illustration: $1]

=Sarcobatus vermiculatus.=—Black greasewood, or chico, is a scraggy
shrub which grows in strongly alkaline soil in the south-western and
western portions of the United States. A correspondent in New Mexico
states that on one occasion he counted as many as 1,000 sheep that had
been killed by eating the leaves of this plant. It is claimed that cows
are not affected by eating it at any time, and that sheep can eat it
quite freely in winter. Death is perhaps due more to tympanites rather
than to any poisonous substance which the plant contains.


                    PHYTOLACCACEÆ (POKEWEED FAMILY).

* =Phytolacca decandra.=—The leaves of the common pokeweed (poke;
garget; American nightshade) of the eastern half of the United States is
occasionally eaten by cattle with fatal results.


                        ALSINACEÆ (PINK FAMILY).

* =Agrostemma githago.=—The common corn cockle (cockle; mullein pink) is
a weed common to both the United States and Europe. Poultry and
household animals are occasionally poisoned by eating the seeds or the
bread made from wheat contaminated with the seeds.


                     MAGNOLIACEÆ (MAGNOLIA FAMILY).

=Illicium floridanum.=—The leaves of this species of anisetree are
supposed to be poisonous to stock.


                    RANUNCULACEÆ (CROWFOOT FAMILY).

* =Aconitum napellus.=—Aconite (monkshood; wolfsbane) is very commonly
cultivated in gardens, and is therefore capable of doing great damage to
stock. Horses and cattle have frequently been poisoned by eating the
leaves and flowering tops.

* =Aconitum columbianum.=—The Western aconite, or monkshood, is native
in the north-western portion of America, where it sometimes poisons
sheep.

=Anemone quinquefolia.=—The common wind flower, which grows throughout
most of the United States, is extremely acrid and poisonous. Cattle
seldom touch it. The plant loses most of its poison in drying.

[Illustration: $1]

* =Delphinium tricorne.=—The dwarf larkspur, or stagger weed, of the
north-eastern quarter of the United States has been especially reported
from Ohio as fatal to cattle in April, when the fresh leaves appear.

* =Delphinium consolida.=—The seeds of the commonly introduced field
larkspur are well known to be poisonous; the leaves are known in Europe
to be fatal to cattle.

* =Delphinium menziesii.=—The purple larkspur of the north-western
quarter of the United States is very common throughout Montana. In one
case of poisoning reported by Dr. E. V. Wilcox, of the Montana
Experiment Station, over 600 sheep were affected, 250 of which were
claimed to have been killed by the weed. An experiment made by Dr. S. B.
Nelson, Professor of Veterinary Sciences in the Washington State
Agricultural College, shows that it is possible to feed as much as 24¾
lbs. of the fresh leaves to a sheep within a period of five days without
any apparent ill effect taking place. An experiment made by Dr. Wilcox
shows that the extract from less than an ounce of the dried leaves
killed a yearling lamb in two hours, the dose having been given by way
of the mouth.

[Illustration: $1]

[Illustration: $1]


                    LARKSPUR POISONING IN SHEEP.[3]

Footnote 3:

  The following account is summarised from a bulletin of the Montana
  Experiment Station by Dr. Wilcox.

Severe losses have from time to time been recorded, especially in
America, from larkspur poisoning, the number of animals lost amounting
to thousands. The first signs of poisoning are slight general stiffness
and straddling gait, especially of the hind legs. The stiffness becomes
more and more pronounced, until walking is difficult and evidently
painful. Soon there are manifested various involuntary twitchings of the
muscles of the legs and sides of the body, and loss of control or
co-ordination of the muscles. Ordinarily there is no increase in the
quantity of the saliva, no dribbling of saliva from the mouth, no
champing of the jaws or attempts at swallowing. The sheep manifest none
of the mental disturbances frequently seen in cases of poisoning from
other sources, as for example loco weed and lupine. There is no
impairment of the special senses. The sheep seem to hear and see as well
and as correctly as under normal conditions of health.

No indications of any disturbances of the digestive functions are to be
seen. The appetite remains good, and the sheep eat up to the very last.
They were observed eating industriously during the intervals between the
attacks of spasms which they have during the last stages.

At first the frequency of the pulse and of the respiratory movements is
lessened and the temperature is lowered. The pulse remains very weak,
but in the later stages becomes very rapid, in some cases 130 per
minute. Toward the last also the respiration is very shallow and rapid.
During the final convulsions the respiration is sometimes 120 per
minute, but so shallow that the air is simply pumped up and down the
windpipe. The air in the lungs is therefore not renewed, and the animal
dies by asphyxia or suffocation.

So long as the sheep can stand on its feet, or walk, it keeps up with
the flock as nearly as possible. The exercise, however, excites it,
makes its respiration more rapid, and it has frequently to lie down for
a moment and then get up and hobble along after the flock. The worst
cases can thus easily be detected, since they straggle behind the rest
of the flock.

The later stages follow rather rapidly. The involuntary movements become
more frequent and more severe. All four legs tremble and shake
violently. In fact, all the muscles of the body contract spasmodically
until the animal totters over on its side and dies in the most violent
spasms.

Larkspur has the effect of arresting the heart’s action and respiration
and of paralysing the spinal cord.

=Treatment.= Place the animal by itself in a cool, quiet, shaded place
and avoid all excitement. Of the drugs tested, atropine sulphate
dissolved in camphor water has given the best results. Wilcox (Bull. 15,
Montana Ex. Station) recommends for sheep from ¹⁄₂₀ to ¹⁄₁₅ grain in the
earlier, and ⅙ to ¼ grain in the later convulsive stages. Cattle require
from four to five times these doses. Inhalations of ammonia vapour, and
small doses of alcohol and ether, are also useful.

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In other cases very good results have been obtained from giving
permanganate of potash in the form of a drench: 5 to 10 grains for an
adult sheep or pig, 15 to 20 grains for a horse, and 30 to 50 grains for
an ox, dissolved in a pint or two pints of water.

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* =Delphinium geyeri.=—The Wyoming larkspur is well known throughout
Wyoming, Colorado, and Nebraska under the name of poison weed. It is
reported to be the most troublesome plant to stock in Wyoming, the
dark-green tufts of foliage being especially tempting in spring when the
prairies are otherwise dry and barren.

=Delphinium recurvatum.=—This species of larkspur grows in wet subsaline
soil in the southern half of California. It has been reported from San
Luis Obispo county as fatal to animals.

=Delphinium scopulorum.=—The tall mountain larkspur of the Rocky
Mountains has been reported to the Canadian Department of Agriculture as
poisonous to cattle in the high western prairies of Canada.

=Delphinium trolliifolium.=—This plant is common throughout the coast
region of northern California, Oregon, and Washington. In Humboldt
County, Cal., it is known as cow poison, on account of its fatal effect
on cattle. Its toxic character has been questioned. Perhaps it is not
equally poisonous throughout all stages of its growth.

* =Helleborus viridis.=—The green hellebore is a European plant,
sometimes self-sown from gardens. All parts of the plant are poisonous.
Cattle have been killed by eating the leaves.


                        POISONING BY HELLEBORE.

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This form of poisoning is of slow progress, the plant producing
irritation of the digestive mucous membrane. The =symptoms= consist in
loss of appetite, blackish, glairy diarrhœa, and intermittence of the
pulse.


* =Ranunculus sceleratus.=—The cursed crowfoot, or celery-leafed
crowfoot, is found throughout the eastern half of the United States and
also in Europe. Cattle generally avoid all of the buttercups, but fatal
cases of poisoning from this plant are recorded in European literature.
When dried in hay, the plant appears to be non-poisonous. The bulbous
crowfoot (_R. bulbosus_) and the tall crowfoot (_R. acris_) are
well-known to be very acrid in taste, and it is probable that all of the
species which grow in water or in very marshy land are poisonous.


                       POISONING BY RANUNCULACEÆ.

Poisoning only occurs when the green plants are eaten. Drying causes
certain essences contained in them to disappear, and thus destroys their
toxicity.

This form of poisoning is indicated by yawning, colic, blackish, fœtid
diarrhœa, and rapid loss of strength.

The animals suffer from stertorous breathing, weakness of the pulse, and
aberration of vision. They die in convulsions.


                    BERBERIDACEÆ (BARBERRY FAMILY).

=Podophyllum peltatum.=—The leaves of the common mandrake, or May apple,
of the eastern half of the United States, are sparingly eaten by some
cattle. Cases of poisoning are very rare, but the experience of one
correspondent shows that the milk from a cow that had been feeding on
the plant off and on for about three weeks was so extremely laxative as
to be positively poisonous. The accident occurred to a baby, fed
exclusively on cow’s milk. The physiological effect of the milk was
precisely like that of mandrake. It was shown that the cow ate the
plant, which was abundant in one pasture, and when the animal was
removed to a pasture free from the plant the child’s illness stopped at
once.


                 BUTNERIACEÆ (STRAWBERRY-SHRUB FAMILY).

=Butneria fertilis.=—The large oily seeds of the calycanthus, or
sweet-scented shrub, contain a poisonous alkaloid, and are strongly
reputed to be poisonous to cattle in Tennessee.


                      PAPAVERACEÆ (poppy family).

=Argemone mexicana.=—The Mexican poppy is reputed to be poisonous to
stock both in the United States and in New South Wales. The seeds are
narcotic, like opium.

* =Chelidonium majus.=—The yellow milky sap of the celandine, an
introduced weed common in the eastern United States, contains both an
acrid and a narcotic poison. Both are powerfully active, but cases of
poisoning are rare, as stock refuse to touch the plant. Reeks, of
Spalding, however, describes (_J. Comp. Path. and Therap._, Dec. 1903,
p. 367) an outbreak of poisoning by common celandine in which twenty-one
valuable cows were affected and three died. The symptoms comprised
excessive salivation and thirst, convulsions, unconsciousness and
epileptiform movements.

* =Papaver somniferum=, opium poppy, or garden poppy: =P. rhœas=, field
poppy, red poppy, or corn poppy.—These plants are sometimes self-sown
from gardens. Both contain acrid and narcotic poisons, and European
literature records the death of various animals from eating their leaves
and seed pods.


                         POISONING BY POPPIES.

The consumption of poppies causes arrest of peristalsis, secretion of
foamy saliva, colic, depression, coma, and in severe cases death by
stoppage of respiration.


                        PRUNACEÆ (PLUM FAMILY).

* =Prunus caroliniana.=—The laurel cherry, or mock orange, is native in
the south-eastern quarter of the United States, and is there often
cultivated for hedges. The half-withered leaves and the seeds yield
prussic acid, and are poisonous when eaten by animals.

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* =Prunus serotina.=—The wild black cherry is a valuable forest tree
which ranges throughout the eastern half of the United States. Cattle
are killed by eating the partially withered leaves from branches thrown
carelessly within their reach or ignorantly offered as food. The leaves
of various other wild and cultivated cherries are probably poisonous to
cattle in the same way.


                         VICIACEÆ (PEA FAMILY).

=Aragallus lambertii.=—The Lambert, or stemless loco weed, is, next to
the following species, the best known representative of a large group of
closely related plants which are native to the western half of the
United States, and are known as loco weeds on account of the peculiar
excited condition which they induce in animals that eat of their leaves.
Horses and cattle are both affected, but the chief damage is done to
horses. After being permitted to graze on any of these plants the animal
acquires an unnatural appetite for them, and soon refuses all other
kinds of food. It rapidly becomes unmanageable, shows brain symptoms,
and finally dies from lack of proper nourishment.

=Astragalus mollissimus.=—This, the woolly loco weed, is perhaps the
best known of all the loco weeds. It is the species most abundant in
Colorado, where from 1881 to 1885 nearly $200,000 was paid out in
bounties in an attempt to exterminate it. The plant is still abundant in
that State, and reports of the damage done by it continue frequent.
Specimens of the three following species of _Astragalus_ have been
forwarded to the Division of Botany with the information that they were
causing great financial loss in the districts noted. It is quite
probable that other species are dangerous also.

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           POISONING BY WHITE LOCO WEED (ARAGALLUS SPICATUS).

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This is an erect tufted perennial, 4 to 18 inches high, with pinnately
divided leaves and spikes of white or cream-coloured flowers, shaped
like those of the pea. The pod is one-celled, and when shaken produces a
rattling sound, which gives the plant the name of “rattle weed” in some
localities. The white loco weed is exceedingly common throughout
Montana. It occurs most abundantly on the northern slopes of foothills
up to an altitude of about 8,000 feet. Its preferred habitat is for the
most part in rather dry situations. The habit of the plant varies in
different parts of Montana. In some localities the flowers are pure
white, while in others they are decidedly yellow.

In Colorado the plant which is most ordinarily known as loco weed is
_Astragalus mollissimus_, while in Montana the species already named is
perhaps most important; but there are others which have a rather wide
distribution and are known to produce the same effects. Among these may
be mentioned _A. splendens_, _A. lagopus_, and _A. besseyi_.

The losses caused from the loco disease are very heavy in nearly all the
Rocky Mountain States. The locoed condition is so commonly observed
among sheep and horses that cases are not reported, and it is
practically impossible to learn the exact extent of the disease. In the
Judith Basin one prominent stockman was nearly ruined financially by the
prevalence for a number of years of the loco habit among his sheep. In
another instance the raising of horses was abandoned over a large tract
of country on account of the loco weeds.

The loco disease occurs under two forms—an acute and a chronic. An acute
case of loco disease was observed by Dr. Wilcox in a two-year-old ewe
with a lamb at its side. The ewe was observed eating large quantities of
white loco weed on May 22nd, 1900. During the afternoon of the same day
it became unmanageable, and the lamb was badly affected. An examination
of the ewe at this time showed that it was completely blind and was
affected with dizziness. It walked around in long circles to the right,
and after a short period remained standing for a few moments in a sort
of stupor. At the beginning of each attack the head was elevated and
drawn to the right; eyelids, lips, and jaws were moved rapidly. Each
attack lasted from one to two minutes and the intervals between the
attacks lasted about five minutes. The second day the attacks became
more severe and of longer duration, the head being turned more decidedly
to the right and the animal sometimes falling upon the ground. Similar
symptoms, accompanied by digestive disturbances, were manifested by the
lamb during the second day, and it died during the afternoon. On the
morning of the third day it was found that the ewe was pushing against
the fold, and had apparently been in that position during the greater
portion of the night. The animal then began to whirl round to the right.
Later it became unable to stand, and the spasmodic movements were
largely confined to the legs. On the morning of the fourth day it died.
The pupil of the eye was at no time dilated, and the expression was
nearly normal. The pulse was at first very irregular, but on the second
day became again regular and of normal frequency. The only remedy which
was tried was frequent injections of one-quarter grain doses of
morphine, but this was without effect. Two other ewes ate smaller
quantities of loco weed at the same time and were similarly affected,
but less severely. In these cases morphine was tried with better
success. The lambs, however, died from the poisonous properties
contained in the milk of the mother.

The general =symptoms= of loco disease are quite familiar to all stock
raisers. Perhaps the most characteristic are those of cerebral origin,
and are shown in peculiarities of gait and action, which may be compared
to a drunken condition. The brain disturbances may consist in impairment
of the special senses or in irregular motor impulses, which produce
incoherent muscular action. In some cases the animal becomes blind. More
frequently the animal makes errors in judgment of the size and distance
of objects. These visual disturbances are often quite ludicrous. The
animal often takes fright, apparently at imaginary objects, or at
objects which under ordinary circumstances would cause no alarm. Locoed
horses are somewhat dangerous for driving purposes on account of their
tendency to run away. Such horses are frequently attacked with kicking
fits without any apparent cause. The sense of hearing is often affected,
and the response to sounds is irregular and out of proportion to the
volume and character of the sound. Irregularities in muscular movements
of sheep may assume a variety of forms. The animal may simply carry its
head in an extended or otherwise unnatural condition. In some cases the
back is arched. Trembling is a characteristic symptom. In locoed horses
a great difficulty is sometimes experienced in persuading them to go
backward. Locoed sheep are exceedingly difficult to manage. The
different members of the flock may suddenly take a notion to run away in
different directions, with the result that it is almost impossible for
the shepherd to prevent their becoming separated. In cattle the disease
appears to be rare, although symptoms, so far as observed, are
essentially the same as those in sheep and horses. Occasionally locoed
cattle manifest dangerous symptoms, and attack men and other animals.

In chronic cases of loco the animal gradually becomes more emaciated and
crazy. In sheep the fleece may be shed in patches or as a whole. The
animal becomes unable to care for itself, and is apt to fall into the
water while attempting to drink. Fits of trembling are of frequent
occurrence, and the animal finally dies of inadequate nutrition and
total exhaustion. In chronic cases of loco disease in horses the animal
is usually left to its own resources on the range. During the later
stages it may remain for weeks at a time upon a small area of ground
without taking water. Dr. Wilcox saw a number of such cases in horses
that were almost unable to walk. Under such circumstances the animals
seldom or never lie down. One horse which was seen remained for a period
of two weeks, in 1897, upon a piece of ground about 150 feet square.
During this time the horse had no water.

Numerous autopsies on locoed sheep and horses revealed slight congestion
of the brain membranes in all cases. The lungs and heart were in normal
condition. Fatty tissue was considerably reduced in quantity, and the
muscles were paler in colour than under normal conditions.

The most serious mistake in connection with loco disease is made in
allowing locoed sheep to remain with the rest of the flock. The loco
habit is apparently learned by imitation of locoed animals, and so long
as locoed sheep are allowed to remain with other sheep the loco habit
rapidly spreads. An experienced sheep raiser, after being nearly ruined
financially through the loco disease, adopted the method of immediate
isolation and the feeding of locoed sheep for mutton. His stock was
replaced with sheep that were free from the loco habit, and the trouble
has been entirely eradicated from his range.

No specific remedy for the loco disease has been discovered, and in the
nature of the case no such remedy is likely to be found. In the present
state of knowledge concerning the subject the only rational =treatment=
to be recommended is that of confinement and feeding with a nutritious
diet. By separating the locoed sheep at once from other sheep the
spreading of the habit will be prevented, and the locoed animals may be
fattened and thus prevented from becoming a total loss. Although locoed
animals may readily be fattened and sold for mutton, their recovery from
the loco habit is apparent only, and is due to their inability to obtain
the loco weed. Such animals when allowed to run upon the range again
almost invariably return to their old habit of eating loco weed. Animals
which have once been locoed are, therefore, unsuitable for stocking the
range.

In combatting the loco disease the most rational methods include
providing salt for the sheep, the immediate removal of locoed sheep from
the band, confining them in a fold, and feeding them upon a nutritious
diet. They may thus be fed for market, and their pernicious habit will
not spread to other sheep. In the case of locoed horses, an apparent
recovery takes place if they are confined in a stable and fed on
ordinary cultivated forage or allowed to run in pastures where no loco
weeds are found. Such horses are always somewhat dangerous, and more apt
to run away or become unmanageable than horses which have not become
affected with this disease.


* =Crotalaria sagittalis.=—The rattlebox (rattle weed; wild pea) is an
annual weed which grows on sandy soil throughout most of the eastern
half of the United States. In some years it is especially abundant in
the bottom lands of the Missouri Valley. Horses and sometimes cattle are
killed in this region by eating grass or meadow hay which is
contaminated with the plant.

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=Lupinus leucophyllus.=—This herbaceous shrub is a representative of a
very large genus of plants, many of which are widely and abundantly
distributed throughout the western United States, and are generally
known as lupines. The above species is very abundant in Montana, where
it is said to have caused the death of a very large number of sheep.
There is some question whether the animals are killed by a poisonous
constituent of the plant or merely by tympanites. The seeds of all the
lupines are probably deleterious in the raw state. In Europe, however,
the seeds of _Lupinus albus_, after the bitter taste has been removed by
steeping and boiling, are eaten by human beings as well as by cattle.


 POISONING BY LUPINES (LUPINUS LEUCOPHYLLUS; L. SERICEUS; L. CYANEUS).

These plants are commonly known by the names blue pea, blue bean, and
wild bean. They are coarse, silky-haired perennial herbs, with blue
flowers arranged in conspicuous terminal racemes, which blossom in June
and July, with long-stemmed leaves, which are divided into from seven to
eleven leaflets radiating from a common point. The fruit is a hairy,
several-seeded pod, and the seeds are small and somewhat flattened.

As a rule these plants do not occur in the flat river bottoms. They
occur most abundantly on the foothills and mountain ranges at moderate
elevations.

During the season of 1900 the lupines in Montana began to bloom about
May 20th, and the first full pods were collected on June 5th. Lupines
are not very extensively eaten by sheep during the spring and summer,
except when they are unusually hungry or are being driven from one range
to another. Lupines are more often eaten by sheep in summer on the
mountain sides, and in the fall and early winter after early frosts have
opened the pods and the seeds have fallen out. Lupine hay is greedily
eaten by all kinds of stock during the winter, and large quantities of
this hay have been fed for the past fifteen or twenty years. Lupine hay
is cut in different years at dates ranging from the 1st of July to the
middle of September. When cut during the first half of July the newly
ripe pods, full of seeds, are secured in the hay. When, however, the
harvesting of lupine hay is postponed until September, the pods become
ripe and split open, and the majority of seeds fall out. A striking
variation in the quantity of pods containing seeds is noted during
different years. During seasons in which May and June are wet the
quantity of pods is usually large. When, however, these months are dry
only a few pods are found on each plant, and a vast majority of the
flowers fail to be fertilised.

Dr. Wilcox has observed that sheep are especially fond of the pods of
various leguminous plants before they become mature and while they are
still in a succulent condition.

Dr. Wilcox saw a flock of sheep which while being driven from one range
to another, in a hungry condition, was allowed to feed upon an area of
lupines in a nearly ripe condition. Within two hours the sheep
manifested violent symptoms of poisoning, and ultimately 100 out of the
lot of 200 died. He afterwards saw many hundreds of fatal cases in sheep
and a number in horses, both from eating green lupines and lupine hay.

As an experiment two sheep were given each 150 medium-sized lupine pods
(_L. leucophyllus_) which were entirely full of ripe seeds. The sheep
ate the pods readily. Both sheep became frenzied within about forty-five
minutes after feeding upon the lupine pods, and died about one hour
later. The symptoms in these cases were the same as those observed in
poisoning under natural conditions.

=The symptoms= of lupine poisoning are so well known in Europe that
chronic lupine poisoning has been given the name _lupinosis_. It is
characterised by loss of appetite, fever, dyspnœa, constipation, and
yellowness of the visible mucous membranes. Diarrhœa, sometimes of a
sanguinolent type, appears later. The urine becomes albuminous, tinted
with bile products or stained red by hæmoglobin, and the head shows
œdema. Death occurs in a few days. In America the chronic form has not
been observed. In cases of lupine poisoning in Montana there was noted
acute cerebral congestion, accompanied with mental excitement. The sheep
rushed about in different directions, butting one another and other
objects. The first stage of frenzy was soon followed by a second stage,
characterised by pronounced irregularity of movement, spasms, and
falling fits. In the majority of cases death occurred in from one-half
to one and one-half hours. In extensive cases of lupine poisoning it was
uniformly observed that a number of the sheep lingered on from two to
four days before they died. The muscular convulsions resembled those
caused by strychnine. The excretion of the kidneys was much increased
and frequently was bloody. Post-mortem examinations of sheep poisoned by
lupines revealed conditions similar to those in acute forms of loco
disease, with the addition of a congested condition of the kidneys.

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No remedies have been tried in cases of poisoning from American species
of lupine, but it seems reasonable to suppose that potassium
permanganate would probably destroy the lupine alkaloids in the stomach
if administered promptly after the first signs of poisoning. Experience
and observation indicate that lupine hay is always dangerous for sheep
if cut at a time when the seeds are retained in the hay. The evidence
thus far collected regarding this matter indicates that the seeds are
the most poisonous part of the plant.


          POISONING BY VETCHES (LATHYRUS SATIVUS): LATHYRISM.

In the horse this disease is due to feeding on grain containing the
seeds of vetches, but in the ox to eating the green portions of the
plants. Feeding has to be continued for at least a month to produce
accidents.

The earliest =symptoms= consist in suppression of milk secretion, and
somnolence. Nervous symptoms—from which alone the horse suffers—soon
make their appearance. The neuro-muscular system is attacked.
Interference with the nervous system is followed by inco-ordination of
movement, and later by paraplegia of the hind quarters. Roaring is not
noticeable, probably because the patients rarely move rapidly.

=The lesions= have been little studied, but appear to consist in
congestion and infiltration of the meninges, cord, and roots of the
lumbo-sacral plexus.

=Treatment.= If the animals are paralysed, treatment is rarely of value;
otherwise it is sufficient to remove the cause and to administer
purgatives and diuretics, with the object of eliminating toxic products.
Recovery follows in three to four weeks.


=Robinia pseudacacia.=—The common locust tree is native in the central
and eastern parts of the United States, and is extensively cultivated
for ornamental purposes throughout the Union. The bark and leaves
contain a powerful poison, and persons have been killed by eating these
parts.

* =Sophora secundiflora.=—The beautiful bright-red beans of the
frijo-lillo, or coral bean of southern and western Texas contain a
powerfully poisonous alkaloid. The plant is said to have poisoned stock
in Texas and in northern Mexico.


                         LINACEÆ (FLAX FAMILY).

=Linum rigidum.=—The large-flowered yellow flax is reported from Pecos
Valley, Texas, as poisonous to sheep. An investigation made by the
Bureau of Animal Industry, U.S.A., showed that the plant is poisonous.

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                    MELIACEÆ (UMBRELLA-TREE FAMILY).

* =Melia azedarach.=—The Chinese umbrella-tree is much cultivated for
ornament, and sometimes grows wild in the South. A correspondent from
Arizona stated that three of his hogs were poisoned by eating the seeds,
which were ignorantly offered to them for food.


                     EUPHORBIACEÆ (SPURGE FAMILY).

=Euphorbia.=—There are many species of spurge native to the United
States, nearly all of which contain an acrid milky juice. Stock
generally avoid them, but cattle have been poisoned by drinking water
into which the plants have been thrown. The juice of _E. marginata_ and
_E. bicolour_ is used to some extent in Texas to brand cattle, it being
held to be superior to a red-hot iron for that purpose, because screw
worms will not infect the fresh scar and the spot heals more readily.

* =Jatropha stimulosa.=—The seeds of the spurge nettle of the Southern
States are extremely poisonous. Stock avoid the plant on account of its
stinging hairs.

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* =Ricinus communis.=—The castor oil plant is quite commonly cultivated
in the warmer portions of the United States, and grows wild in the
South. The seeds have been accidentally eaten by horses with fatal
effect, and they have been strewn on pasture lands in the North-West for
the purpose of killing sheep that were trespassing thereon. A Frenchman
has discovered a method of making cattle immune to the effects of the
toxalbumin contained in the seeds, so that they may be fed to stock
without causing any apparent ill effect. A note on poisoning by castor
oil cake will be found hereafter.


                         BUXACEÆ (BOX FAMILY).

* =Buxus sempervirens.=—The leaves of the common box, cultivated for
hedges, are poisonous to all kinds of stock.


                   ÆSCULACÆ (HORSE-CHESTNUT FAMILY).

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=Æsculus californica=, California buckeye: =Æ. glabra=, Ohio buckeye;
fœtid buckeye: =Æ. hippocastanum=, horse-chestnut: =Æ. pavia=, red
buckeye.—The leaves and fruit of these species are generally regarded as
poisonous to stock. The fruit may be easily converted into food by
washing and boiling. It is believed that a small quantity of the
unprepared fruit of the California buckeye will cause cows to slip their
young.


                 HYPERICACEÆ (ST. JOHN’S WORT FAMILY).

* =Hypericum perforatum.=—The common St. John’s wort is commonly
believed to cause disagreeable eruptions on cows’ udders and on the feet
of white haired animals. This species and the spotted St. John’s wort
(_H. maculatum_) were brought into the United States Bureau of
Agriculture by Dr. G. W. Bready, from Norwood, Maryland, who stated that
five horses were poisoned in May, 1898, by eating meadow hay which
contained nearly 50 per cent. of these plants. One horse died from the
effects of the poison, and two were killed to prevent their further
suffering.


                     POISONING BY ST. JOHN’S WORT.

The ingestion of St. John’s wort produces excitement followed by
dulness, interference with vision and hearing, and by visual
hallucinations with a tendency to lean backwards, the front limbs
remaining fixed in position. The patient often sits down on the hind
quarters like a dog.


                        APIACEÆ (CARROT FAMILY).

* =Cicuta maculata.= This is the water hemlock (spotted hemlock; beaver
poison; cowbane), which grows most abundantly throughout the United
States. It is one of the best known poisonous plants. Stock are not
infrequently killed by eating the fleshy roots or hay with which the
plants are mixed.

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* =Cicuta vagans.=—Cattle are frequently killed in Oregon and Washington
by eating the large fleshy rootstocks which have been washed, frozen, or
dug out of the soil, or by drinking water in marshes where the roots
have been trampled upon. The roots of the other species of _Cicuta_ are
undoubtedly poisonous, but cases have been reported against one other
species only, namely, _C. bolanderi_. It grows in marshy land in
California.

* =Conium maculatum.=—The well-known poison hemlock, or spotted hemlock
of Europe, is an introduced weed not uncommon in the north-eastern
section of the United States and in California. The plant is generally
avoided by stock on account of its bad odour, but animals have been
killed by eating it in the fresh state. Since the poisonous constituent
is volatile, the dry plants are not so dangerous.

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     POISONING BY HEMLOCK AND WILD CHERVIL (ANTHRISCUS SYLVESTRIS).

Poisoning only results from ingestion of the green plants. It is
characterised by salivation, nausea, dyspnœa, generalised trembling and
vertigo, paraplegia, and symptoms of gastro-enteritis.


                          POISONING BY FENNEL.

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This disease, seen in Algeria, and recently studied by Bremond and
Bojoly, need only be mentioned. The information at present available is
indefinite, and the symptoms so closely resemble those of Texas fever
that there seems a possibility of confusion having arisen.

=The lesions= are those of hæmorrhagic gastro-enteritis.

=Treatment= consists in giving tannin, opium, and emollients.


=Oxypolis rigidus.=—The cowbane is natural in swamps throughout the
eastern half of the United States. The leaves and roots are reputed to
be poisonous to cattle.

=Sium cicutæfolium.=—The leaves of the hemlock water parsnip, which is
more or less common throughout the United States, are said to be
poisonous to stock.


                        ERICAEÆ (HEATH FAMILY).

=Andromeda polifolia.=—The wild rosemary, or moorwort, is a plant native
to the northern regions of Europe, Asia, and America, entering the
United States only in the extreme north-east. The leaves, which have
been eaten by sheep with fatal effect, contain a narcotic poison known
as andromedotoxin. The plant is not very dangerous in its native
habitat, because it grows in bogs which are inaccessible to stock.

* =Azalea occidentalis.=—The California azalea is very much dreaded by
sheep men who drive their flocks into the southern Sierras for pasture.
Investigation has shown that the leaves contain a poisonous substance.

* =Kalmia angustifolia.=—The narrow-leaf laurel is abundant in the
north-eastern section of the United States, where it is also well known
as sheep laurel and lamb-kill. The leaves contain andromedotoxin, and
sheep and calves are frequently poisoned by eating them.

* =Kalmia latifolia.=—The broad-leaf laurel is native throughout the
greater part of the eastern half of the United States, and is known by a
great variety of common names, the most important of which are laurel
and ivy. The latter name is most commonly used south of Maryland. Scores
of cattle and sheep are poisoned annually by eating the plant. It is
probably the most dangerous of all the shrubs belonging to the heath
family.

[Illustration: $1]

[Illustration: $1]

* =Leucothoë catesbæi.=—This is the branch ivy, hemlock, or calf-kill,
of the Allegheny Mountains. It is well known in that region to be fatal
to all kinds of stock.

* =Leucothoë racemosa.=—The swamp _Leucothoë_ of the Atlantic and Gulf
States has been reported from New Jersey as especially fatal to calves.

* =Pieris mariana.=—The stagger bush of the Atlantic Coast region,
Tennessee, and Arkansas is commonly known to be poisonous to calves and
to sheep. The name stagger bush was applied to the shrub on account of
the peculiar intoxicating effect of the leaves.

* =Rhododendron californicum.=—The California rhododendron is native on
the Pacific Slope from San Francisco to British Columbia. The plant is
reported from Oregon as poisonous to sheep. It is quite probable that
the leaves contain andromedotoxin, but they have not been tested.

[Illustration: $1]

* =Rhododendron maximum.=—The great laurel (rosebay; mountain laurel;
rhododendron) is a large evergreen bush or small tree which is quite
commonly cultivated for ornament, and is found native in the Allegheny
Mountains. The leaves contain andromedotoxin, and they are occasionally
eaten by stock with fatal effect.


                     PRIMULACEÆ (PRIMROSE FAMILY).

=Anagallis arvensis.=—The pimpernel is a European plant which has
obtained a specially strong foothold in California, where it grows
luxuriantly and is sometimes known as poison weed. It is suspected of
having caused the death of a horse at Santa Ana. Chemists have isolated
a powerfully poisonous oil and a strongly active ferment from the plant.


                        OLEACEÆ (OLIVE FAMILY).

=Ligustrum vulgare.=—The privet, or prim, is a garden shrub, introduced
from Europe and Asia, which is much used for hedges, and has escaped
from cultivation in western New York and southward to North Carolina.
Accidents have been occasioned in children both by the fruit and the
leaves. The plant is to be suspected in cases of poisoning in animals.


                      APOCYNACEÆ (DOGBANE FAMILY).

=Apocynum androsæmifolium=, spreading dogbane: =A. cannabinum=, Indian
hemp.—These plants are generally distributed throughout the United
States. Stock generally avoid them in pasture fields on account of their
acrid milky juice. When dry they are not so poisonous as when in the
fresh state.

=Nerium oleander.=—The oleander is a common house plant throughout a
large portion of the United States. It grows freely out of doors in the
Southern and Western States, and has probably escaped from cultivation
in some places. It grows wild in northern Mexico. The leaves are well
known to be most powerfully poisonous, and stock are occasionally killed
by eating them.


                    ASCLEPIADACEÆ (MILKWEED FAMILY).

[Illustration: $1]

* =Asclepias eriocarpa.=—This is the plant with broad mullein-like
leaves which is known as milkweed in California. Several authentic
accounts of the poisoning of sheep have been secured against the plant
in Mendocino County. It is especially feared on very warm days by sheep
men when they are compelled to drive their flocks through dry, barren
valleys. It sometimes grows on cultivated land, and is cut with hay.

* =Asclepias syriaca.=—This is the common milkweed, or silkweed, of the
north-eastern quarter of the United States. Experiments show that the
milky juice so abundant in all parts of the plant is very acrid and
poisonous. It is listed among the poisonous plants of Europe.


                       SOLANACEÆ (POTATO FAMILY).

* =Datura stramonium=: =D. tatula=.—These two species very closely
resemble each other, and are most commonly known in the United States by
the name of jimson weed. They are European plants which have become
weeds in waste grounds and about dwellings throughout the greater
portion of the country. One or two instances are recorded in which
cattle have been poisoned by eating hay containing the young leaves.

* =Hyoscyamus niger.=—The black henbane is an ill-smelling plant, a
native of Europe, now naturalised in Michigan, and from New York
northward. One or two cases are recorded in European literature in which
stock have been poisoned by eating the plant of their own accord, but
there is very little danger from it, on account of its ill odour and
harsh texture.

[Illustration: $1]

[Illustration: $1]

* =Nicotiana tabacum.=—This is the tobacco most commonly cultivated in
the United States. It is native to South America and has escaped from
cultivation to some extent in the Southern States. According to some
authorities stock are not always disposed to shun this plant on account
of its characteristic ill odour and taste, but, on the contrary, will
eat a small amount of the leaves with apparent relish, especially when
they are somewhat fresh. Stock have, however, been poisoned by eating
leaves which were placed within their reach to dry, and also by eating
food contaminated with the juice of the leaves. Considerable precaution
should be used in applying tobacco juice to fresh cuts or bruises in
stock, as the poison is easily absorbed into the system and may prove
fatal. There are several native species of tobacco in the western half
of the United States, all of which are undoubtedly poisonous if eaten
even in moderate quantity.


                           TOBACCO POISONING.

[Illustration: $1]

Tobacco poisoning may be produced by baths or lotions containing tobacco
juice, which is often used as a parasiticide. The ingestion of tobacco
leaves in forage may also produce poisoning. Doses of 1 ounce in the
goat and 10 ounces in the ox are toxic.

=The symptoms= consist in salivation, vomiting, nausea, diarrhœa,
cardiac palpitation and dyspnœa.

=The lesions= are those of gastro-enteritis with cerebral congestion.

=Treatment= consists in giving tannin, black coffee, etc.


=Solanum dulcamara.=—The bittersweet, or climbing nightshade, is a
European weed, now introduced in the north-eastern quarter of the United
States. The leaves are suspected of being poisonous to stock.

* =Solanum nigrum.=—The black nightshade (common nightshade; garden
nightshade) is a common weed in cultivated fields throughout the greater
portion of the United States. Cattle seldom eat the plant, but a few
cases of poisoning are recorded for calves, sheep, goats, and swine.

* =Solanum triflorum.=—The spreading nightshade is a native of the Great
Plains (United States), and also a common garden weed from Arizona and
Texas to British America. Complaints of the poisoning of cattle by this
plant have been sent to the Department of Agriculture from Nebraska.
Experiments show that the berries are poisonous.

=Solanum tuberosum.=—The small, immature tubers of the common cultivated
potato and those that have turned green from exposure to the sun are
slightly poisonous. The green fruit and the white sprouts from mature
potatoes are likewise poisonous. In all of these cases the deleterious
substance may be removed or destroyed by thorough boiling.


                   SCROPHULARIACEÆ (FIGWORT FAMILY).

[Illustration: $1]

=Digitalis purpurea.=—The purple foxglove is a common garden plant which
has sparingly escaped from cultivation and is naturalised to some extent
on Cape Breton Island. Horses are occasionally poisoned in Europe by
nipping the plants from gardens or by eating hay contaminated with it.

=Gerardia tenuifolia.=—The slender gerardia is native to the eastern
half of the United States, and has been specially reported as poisonous
to sheep and to calves in the Southern States.

=Gratiola officinalis.=—The hedge hyssop of the Southern States contains
an acrid poison. The same plant grows in Europe, and is there regarded
as poisonous to stock.

=Pedicularis.=—The plants of this genus are commonly called lousewort.
In Europe several species are suspected of being slightly poisonous to
stock. One of these, _P. palustris_, occurs in Labrador, and there are
over thirty species native to the United States, largely Western. They
should all be suspected of being poisonous.


                   CAMPANULACEÆ (BELL-FLOWER FAMILY).

=Lobelia inflata=, Indian tobacco: =L. kalmii=, brook lobelia: =L.
spicata=, pale-spiked lobelia: =L. syphilitica=, great lobelia.—All of
the species in this genus contain an acrid and usually milky juice, and
are poisonous. None has been specially reported as poisonous to stock,
but the above-named species are to be suspected, because they frequently
occur in grass and are sometimes found in meadow hay.


                     AMBROSIACEÆ (RAGWEED FAMILY).

=Xanthium canadense.=—The young seedlings of the American cocklebur are
reported from Texas as being rapidly fatal to hogs.

=Xanthium spinosum.=—The spiny clotbur is suspected of being poisonous,
but few cases have been definitely recorded against it. The seeds
apparently contain a toxic compound.

=Xanthium strumarium.=—The young seedlings of the broad cocklebur are
reported from Georgia as being fatal to hogs. Experiments seem to show
that the seed is poisonous.


                      CARDUACEÆ (THISTLE FAMILY).

* =Helenium autumnale.=—Sneezeweed (sneezewort; autumn sneezeweed;
stagger weed; false sunflower) is found throughout the greater portion
of the United States, being most abundant in the Southern and Eastern
States. Sheep, cattle and horses that are unfamiliar with the plant are
often poisoned by it when driven to localities where it is abundant.
Stock avoid it, as a rule, but it is claimed that they sometimes develop
a taste for the plant, and are killed quickly by eating it in large
quantity.

=Senecio jacobæa.=—The tansy ragwort, or stagger wort, is a European
plant which grows as a weed in ballast about New York and Philadelphia.
Farther north, in Nova Scotia, it has become extensively naturalised,
and it is there regarded by stock men as poisonous. It is interesting to
note that _S. guadalensis_ of Mexico is also considered fatal to stock.


                          COLCHICUM POISONING.

Fodder of bad quality often contains leaves, flowers, and particularly
seeds of colchicum, which produce nausea, vomiting, colic and diarrhœa.
The colchicine acts particularly on the kidney and heart, producing
specific disturbance, indicated by hæmaturia, polyuria, and cardiac
palpitation, with lowering of the body temperature.

Even when poisoning is not fatal, it is very apt to produce abortion.


                      POISONING BY ANNUAL MERCURY.

Annual mercury given in green fodder is stated to produce indigestion,
diarrhœa, vesical and intestinal hæmorrhage, and early death. Some
authors, however, deny that it has such toxic properties.


                          POISONING BY BRYONY.

In large doses all parts of the bryony plant are toxic—the root, stalk,
and leaves.

Bryony is sometimes used as a purgative. Poisoning is characterised by
nausea, sweating, diuresis, frequent action of the bowels, and, in grave
cases, by tetaniform convulsions followed by death.


                     POISONING BY CASTOR OIL CAKE.

=Causation.= Excessive use of this form of cake is the usual cause of
such poisoning, though bad quality is also an important factor. The
castor oil beans are often insufficiently crushed and compressed, so
that a considerable amount of oil is contained in the cakes as sold; but
the most dangerous constituent is undoubtedly the material known as
ricin, which, in some specimens of cake, may exist in highly dangerous
quantity.

The oil contained in the cake, like every other fatty substance, favours
intestinal peristalsis and the onward movement of the digested food. The
laxative principle excites secretion, and if the cake be given for
considerable periods, the most serious consequences may ensue.

Cakes prepared from mixed rape seed and castor beans act in a similar
way, though in a longer or shorter time, according to their richness in
ricin.

The earliest =symptom= consists in purgation, which gradually develops
into super-purgation, and is followed by direct irritation of the mucous
membrane, indicated by serous, fœtid, and sometimes sanguinolent,
diarrhœa. The symptoms may appear in twenty-four hours. They are usually
accompanied by a rise in temperature of 2° to 3° Fahr. Secretion of milk
ceases, and animals heavy with young sometimes abort. In exceptional
cases death follows.

=The lesions= are those of hæmorrhagic enteritis.

=Treatment= is principally of a preventive character. The cakes should
be examined, and if they contain insufficiently crushed seeds or beans
should be discontinued or given in smaller quantities. The proportion of
ricin in mixed rape and castor cakes should be determined.

Curative treatment consists in removing the cause and treating the
enteritis. The latter is best controlled by giving emollients,
diuretics, and mucilaginous drinks prepared from linseed, marsh-mallow,
barley, etc.


                       POISONING BY COTTON CAKE.

Cotton cake forms a rich food, which fattens animals very rapidly, but
given in excess may produce true poisoning, and if prepared from
undecorticated seed may produce mechanical irritation ending in
obstruction of the bowel.

The latter accident occurs only in the sheep. It consists in obstruction
of the omasum (œsophageal gutter), and particularly of the abomasum, by
the woody seed covering, the fibres of which become agglutinated and
close the pyloric opening, just as do the fragments of wool or the hairs
in animals affected with the licking habit (pica, depraved appetite).
The mass thus formed passes into the intestine, and is apt to become
fixed at some point and to cause death.

In the ox, as in the sheep, true poisoning may result from the action of
an injurious principle which Cornevin discovered in the seed and
particularly in the meal. The relative rarity of such accidents is
explained by the composition of the cakes, which are rich in husks but
poor in meal.

In the first series of accidents the =symptoms= resemble those produced
by the intestinal obstructions peculiar to the licking disease; in the
second they appear about the eighth to the fifteenth day, and are
indicated by sensitiveness of the abdomen and by efforts to pass urine.
The urine is albuminous; at a later stage it becomes darker in colour,
reddish, and stained with hæmoglobin. The mucous membranes exhibit a
sub-icteric tint.

=Lesions.= The liver shows interstitial hepatitis, consequent on changes
in the hepatic cells due to the poisonous principle. The kidney first
shows lesions of interstitial, but afterwards of epithelial, nephritis;
the endothelium of the tubes appears to be undergoing proliferation.

=Treatment= should only be undertaken when the organic lesions seem
trifling, and suggest the possibility of cure without excessive outlay.
Under such circumstances it is sufficient to remove the cause and to
supply proper diet.


                     POISONING BY MOLASSES REFUSE.

Molasses refuse is much used about Paris and in the department of Le
Nord for fattening or simply for feeding animals. Added to rough fodder,
even of poor quality, the refuse renders it palatable, and thus forms an
economic food; it also improves the condition of animals with broken
wind. Its poverty in nitrogenous materials (the refuse consists of 60
per cent. of hydrocarbons; 10 to 12 per cent. of potash and soda salts)
renders it necessary to enrich it in this respect. Moreover, only a
limited quantity should be given. If given in larger amounts than 2 to
2½ parts per 500 parts of body weight it may produce bad effects. In
this case the earlier symptoms point to interference with the urinary
apparatus, the digestive apparatus being affected later; both accidents
are due to the potash and soda salts present in the refuse, and may
become so well marked as to constitute true poisoning.

=The symptoms= consist in abundant diuresis, resulting from the excess
of potash and soda salts, and are followed by albuminuria.
Superpurgation is usually present.

=Lesions.= On post-mortem examination one finds lesions of irritant
gastro-enteritis, and of chronic nephritis.

=Treatment= consists in withdrawing the molasses refuse, and giving
milk, mucilaginous fluids, barley-water, and cereals, which soothe the
kidney.


        DISEASES PRODUCED BY DISTILLERY AND SUGAR FACTORY PULP.

This disease, which is very common in France and Germany, results from
feeding on distillery and sugar factory residues, consisting for the
most part of beet pulp.

In 1860 Guionnet described it under the name of disease of the abomasum,
and more recent work by Butel, Rossignol, and Arloing has thrown a great
deal of light on its exact nature.

=Causation.= Guionnet attributed the injurious action of beet pulp,
etc., to excess of acidity, due to the addition of sulphuric acid during
manipulation in the factory; but it has since been shown that this
acidity, if existing, is specially due to various fermentation products,
the results of lactic, butyric, and acetic fermentation, etc.

Rossignol regarded the symptoms as wholly due to the excessive
proportion of water, viz., 90 per cent.; but this does not explain the
general symptoms of poisoning.

The real cause is to be sought in the manner of preserving the pulp in
simple earth silos or in cemented silos, where it undergoes fermentation
and putrefaction. The contained liquid is then extremely toxic. Filtered
through porcelain and injected under the skin, it produces vaso-motor
and vaso-paralytic disorder, identical with that seen in acute forms of
the disease; in other cases it excites abnormal secretion, and leads to
permanent diarrhœa and chronic gastro-enteritis.

This liquid, if injected intravenously, may prove toxic in doses of 2 to
3 cubic centimètres per kilogram of bodily weight. Its injurious effect
is due to toxins secreted by special bacilli, which were isolated and
studied by Arloing. The toxicity diminishes as the pulp becomes older,
and can be avoided by adding antiseptics like common salt, which prevent
fermentation. These experiments of the Lyons professor are certainly
very interesting, and, although perhaps not identical with what occurs
in practice, sufficiently indicate the way in which poisoning occurs.

Pathological disturbance only follows the use of decomposed pulp.

Animals reared on farms where distillery and sugar factory pulp is
regularly given become accustomed to it, and are rarely affected. The
chief sufferers are those recently imported, or recently placed on such
food; in them the disease may assume either the acute, nervous,
subacute, or chronic form.

=Acute form: Symptoms.= This form is exceptional in the ox, but is more
frequent in the sheep. In oxen the earlier symptoms point to digestive
disturbance, and consist of dulness, loss of appetite, colic,
sensibility of the abdomen, cessation of rumination (without
tympanites), and constipation. The excreta are hard, coated, and
blackish in colour, but not blood-stained.

Diarrhœa follows, is accompanied by aggravation of the general symptoms,
the temperature rises to 104° or 106° Fahr. (40° or 41° C.), and
exhaustion is pronounced. Other, less characteristic, symptoms, such as
grinding of the teeth and mastication without food being present in the
mouth may accompany the above and arouse fears of peritonitis. In sheep
the dulness and prostration shown at first suggest the existence of
anthrax—a view strengthened by the fact that the respiration becomes
very frequent and the fever intense, whilst death may be rapid, and may
sometimes occur with startling suddenness.

=Lesions.= Bacteriological examination, or even a naked-eye examination,
made immediately after death enables one easily to differentiate between
the two conditions. When the animals have died very rapidly—in one
night—lesions of enteritis alone are present. More marked cases exhibit
thickening and intense congestion of the mucous membrane of the
abomasum, which may be of a deep mahogany colour.

The intestine itself is affected, and even though the glandular
epithelium is little changed, the intercellular spaces show ecchymoses
and multiple hæmorrhages, which give the contents of the digestive tract
the appearance of wine lees.

The abdominal viscera scarcely present any characteristic lesions. The
liver has the appearance of having been boiled, as in many forms of
poisoning. The kidney is congested and blackish; the spleen only appears
hypertrophied when post-mortem examination has been delayed and
microorganisms from the intestine have invaded the circulatory system.
After death the kidneys and spleen very rapidly undergo softening.

=Nervous form: Symptoms.= Whilst in the first form the symptoms appear
especially due to diastatic ferments present in the pulp liquid, in the
nervous form they appear rather to result from the convulsing and
paralysing action of ptomaines.

The ox seems more particularly susceptible to the action of the latter.
It shows symptoms resembling those of horses suffering from a severe
abdominal form of influenza: profound depression, mahogany-coloured
conjunctiva, lachrymation, infiltration of the cornea, high temperature
(104° to 106° Fahr.—41° to 41·5° C.), strong action of the heart, but
small pulse. The cerebral symptoms are especially marked. The animal
suffers from vertigo, and when excited, or when attempts are made to
administer medicine, it thrusts its head against the wall, as though
suffering from a cerebral tumour. It also shows hyperæsthesia, slight
colic, and sensitiveness of the abdomen.

In sheep the symptoms consist in alternate extreme depression and
extreme excitability.

In both species the termination is always rapid: death occurs in a few
days.

The abdominal =lesions= are identical with those of the acute form. They
consist in gastro-enteritis, or, rather, intense congestion of the
abomasum and intestine, with extravasation of blood around the acini of
the glands and beneath the mucous membrane, etc., and in more or less
marked desquamation of epithelium.

The annexed organs sometimes present secondary changes: in the nervous
centres the lesions are more marked; the meninges are congested, in some
cases inflamed, and cerebro-spinal fluid is present in increased
quantity.

=Subacute or Chronic form: Symptoms.= This form is equally frequent in
the ox and sheep; it develops insidiously, and for a time may escape
detection.

The symptoms are those of slight gastro-enteritis without tympanites;
but this condition is succeeded by serous, fœtid, uncontrollable
diarrhœa, which weakens the animal and causes death from excessive
wasting and hydræmia.

The sensitiveness of the entire right side of the abdomen, the special
diarrhœa, the cardiac disturbance, and the widely distributed œdema,
usually suffice to prevent confusion with the ordinary forms of
gastro-enteritis. In sheep the diarrhœa is blackish, sometimes
blood-stained, and is accompanied by a sub-icteric or icteric tint of
the mucous membranes, of the skin, and of all the tissues. The intensity
of coloration affords a guide to the rapidity of development of the
disease. The urine is also bile-stained, and there appears to be an
exchange of functions between the two great depurative organs, the liver
and kidney. The urine may become sanguinolent, because it contains
either unchanged blood or simply dissolved hæmoglobin.

=The lesions= are similar to those previously described, but with
modifications of intensity. When diarrhœa has been marked and
persistent, the digestive mucous membrane is hardened, indurated, and
appears as though tanned. This is due to chronic inflammation, probably
to the gastro-enteritis with which the condition begins. The liver
appears as if cooked; the fat, the majority of the tissues, and
especially the conjunctiva, exhibit a light yellow tint, pointing to
hepatic disturbance.

=The diagnosis= is generally easy in all three forms, provided that the
food be examined.

=The prognosis= varies; the acute and nervous forms are usually fatal.
But when the disease develops slowly, recovery may occur.

=Pathogeny.= Practical observation and laboratory researches show that
the above conditions result from poisoning. Histological examination of
livers from sheep which have died rapidly shows complete degeneration of
the hepatic cells, which become incapable of performing their function.
The biliary acids, no longer being withdrawn from the circulating blood,
produce general intoxication, destruction of the blood corpuscles, and
the appearance of hæmaphæic icterus and hæmoglobinuria.

=Treatment.= Being convinced that acidity alone caused this disease, the
older practitioners suggested the administration of salines. In reality
it is necessary to check fermentation. Drainage of the silos in which
beet pulp is stored is often sufficient for this purpose; but if badly
arranged, drainage rather assists the growth of moulds and various
organisms in the mass, which affords a medium favourable to their
multiplication. Complete desiccation would undoubtedly give much better
results, but cannot economically be effected. The best practical measure
consists in storing the pulp in special silos, divided into compartments
by lattice work partitions. The escape of liquid is facilitated by
forming the floors of the silo with a sufficient slope. Preservation,
however, is not perfect, and some compartments are always found damaged.
Excessive fermentation can be checked by adding ordinary salt to the
pulp in the proportion of ·2 per cent.

Curative treatment comprises restricted diet for several days, and the
administration of milk, carbonate of soda, and stimulants, which favour
excretion of the toxins. Some patients may be saved by subcutaneous
injections of large quantities of normal salt solution. When poisoning
is pronounced, and the viscera are clearly injured, it is more
economical to slaughter the animals, provided that the icterus does not
render the flesh useless for sale.




                             CHAPTER VIII.
                 PARASITES OF THE DIGESTIVE APPARATUS.


Parasites of the digestive apparatus are extremely common in ruminants,
some, like the infusoria of the rumen, being of no importance, others,
on the contrary, appearing to play a predominating part in the
development of certain forms of anæmia and serious wasting diseases,
such as the various forms of gastro-intestinal strongylosis, coccidial
enteritis, etc.


                GASTRO-INTESTINAL STRONGYLOSIS IN SHEEP.


           PARASITIC GASTRO-ENTERITIS. OVINE PASTEURELLOSIS.

Verminous diseases of the abomasum are common in the sheep and goat, but
(in France at least) appear rare in the ox.

=Causation.= Gastro-intestinal strongylosis is produced by various
parasites of the genus Strongylus, such as _Strongylus contortus_,
_Strongylus convolutus_, _Strongylus instabilis_, _Strongylus
circumcinctus_, _Strongylus filicolis_, which occur not only in the
abomasum, but also in the small portions of the first intestine,
sometimes in very large numbers.

The first is a threadlike worm, pointed at both extremities, and from ½
to 1 inch in length. It exhibits a red tint, which zoologists refer to
the presence of blood in its digestive apparatus, derived from the
host’s intestinal mucous membrane. Some doubt has been thrown on the
nature of this coloration, however; and certain Italian authors, in
common with Lignières, have declared it due to a certain red pigment
developed in the tissues of the parasite, the spectroscopic reaction of
which differs from that of hæmoglobin.

The strongyles are said not to penetrate the mucous membrane, but simply
live on the intestinal contents. This may be true of certain varieties,
but it is none the less certain that others penetrate the mucous
membrane deeply, even to the extent of becoming half-embedded in it.
Particularly is this the case with _Strongylus circumcinctus_, found in
the epizooty which occurred at Grignon, and also found by Moussu in
grave epizooties which he has from time to time investigated.

According to Lignières this gastro-intestinal strongylosis only plays a
trifling part in the development of the above-mentioned disease, which
he declares to be due to infection with a cocco-bacillus of the
Pasteurella group, the development of which alone, he states, explains
all the symptoms.

In France the disease now under consideration has never extended beyond
limited regions, but in Argentina, where Lignières carried out his
investigations, it is said to be very fatal. Lignières bases his opinion
on the following facts:—

Firstly, that experimental verminous infection of young animals does not
produce either anæmia or cachexia.

Secondly, that animals in excellent condition may prove to be infested
with large numbers of parasites.

Thirdly, that animals which have succumbed to this disease, hitherto
regarded as verminous, sometimes prove to harbour few or no parasites.

Fourthly, that this grave and fatal disease, and the symptoms by which
it is clinically recognised, can be produced with cultures of the
cocco-bacillus, which he has isolated.

These statements are very precise, but Moussu declares that he has never
yet been convinced of the reliability of the last statement referring to
experimental transmission, any more than of the data regarding alleged
protective vaccination.

=The symptoms= of gastro-intestinal strongylosis or ovine pasteurellosis
point to a progressive pernicious anæmia of chronic or subacute form.
Rapidly progressive cases are exceptional.

In France the form seen is almost invariably chronic. The animals appear
dull, sluggish, and feeble; they lose appetite, waste, become anæmic,
then cachectic, and, after several months, die of exhaustion and
wasting, after having shown diarrhœa during the later stages.

The fæces are pasty, and exhale a very marked putrefactive odour. There
is little room to doubt that auto-intoxication from resorption of
intestinal products is continually going on.

The animal’s general appearance is bad, the ears are pendant, the wool
is dry and dull, and can be removed in handfuls by the slightest pull.
There are no other external symptoms, and the diagnosis can only be
arrived at by discovering the eggs of the parasite in the fæces.

=Lesions.= Post-mortem examination reveals all the general lesions of
advanced cachexia and of gastro-enteritis of varying intensity. The
abomasum and first portions of the small intestine usually contain a
considerable number of strongyles; tæniae are often present in the
intestine, and Moussu declares that he has always found a certain number
of hooked worms and œsophagostomes.

The peritoneal, pleuritic, and pericardial exudates common in most
wasting conditions are always present, but the quantity of exudate in
each cavity varies within wide limits. The liquid may even resemble that
due to inflammation or infection; sometimes it is light pink or red in
colour.

Pulmonary lesions usually exist. Moussu has almost always found gastric
strongylosis associated with pulmonary or tracheo-bronchic strongylosis,
but Lignières asserts that the Argentine cases showed nodules of
hepatisation which had nothing to do with the pulmonary strongylosis,
and which appeared to result from areas of pneumonia produced by the
specific cocco-bacillus and other organisms. He has even found abscesses
and cavernous spaces in the lung.

[Illustration: $1]

=Pathogeny.= According to Lignières the specific agent of pernicious
anæmia is a cocco-bacillus which stains well with fuchsin, violet, blue,
safranin, etc., but does not take Gram, and which in cultures assumes
either the strepto-bacillary form or occurs in barrel-shaped masses. It
grows in simple bouillon at 38° C., but better still in peptonised
bouillon, which turns turbid for five or six days, afterwards becoming
limpid in consequence of the organisms falling to the bottom of the
vessel. It does not coagulate milk. On agar the culture is thin, bluish,
shows an iridescent reflection, and when old appears whitish. Grown on
gelatine, the appearances are similar—the gelatine is not liquefied; on
serum the pellicle is scarcely visible.

The organism is said to be pathogenic for guinea-pigs, rabbits, dogs,
and, of course, for sheep. Moussu, however, does not consider that the
reported cases of transmission through the blood stream or by
subcutaneous injection are really convincing or characteristic. He does
not question the fact that Lignières discovered a special pathogenic
agent in all cases and in all his patients; but what appears to him
debatable is the exclusive part which Lignières attributes to that
agent.

The fact that in Argentina, just as in France, strongyles have always
been discovered in epizootics of this nature of itself constitutes
something; and causes the second fact, that it has never yet been proved
that any heavy mortality occurred in the absence of parasitic
infestation, to assume considerable importance. Moussu regards these two
facts as the greatest obstacles to Lignières’ theory. He states that in
his view the verminous affection is the essential, primordial and
primitive affection, and that microbic infection is only secondary, and
an almost inevitable result of grave verminous infestation.

It is quite certainly wrong to think that verminous affections may
continue with scarcely any injury to the animal, especially when such a
belief is based on observation of a few parasites which are not of a
predatory character. In most cases of the kind now under consideration,
the various parasites found (_Strongylus circumcinctus_ and _filicolis_,
_Anchylostomes_, etc.) cause more or less grave lesions.

These intestinal wounds facilitate the infection to which the fatal
course of the disease is due. The disease, then, is not a special
unvarying infection, but consists of multiple superposed infections.

It is wrong to believe and to teach that the parasitic disease is of no
importance, and Moussu declares his belief that the proposed
vaccinations will prove unavailing. He is of opinion, on the other hand,
that when the parasitic invasion can be overcome the mortality will be
checked, and only those animals which are already suffering from severe
infections will succumb. Is not this precisely what has been observed in
human pathology regarding miners’ anæmia or miners’ worm disease
(anchylostomiasis)?

=The diagnosis= presents no difficulty for those who have had a little
practice with the microscope, since the presence of eggs of the parasite
can always be detected in the fæces in cases where external signs have
given rise to suspicion of gastro-entestinal strongylosis.

The macroscopic diagnosis on post-mortem examination is not so easy as
might be supposed, and when very small varieties are in question it is
sometimes necessary to examine the mucous membrane of the abomasum or
intestine very carefully in order to discover the parasite.

=The prognosis= is grave, because before attention has been drawn to
many patients, the entire herd may be more or less infested. It is also
grave because the pastures are infested with eggs or embryos, and the
power of increase of these parasites is enormous.

=Treatment.= The earliest and most energetic means should be adopted in
all cases. Treatment comprises:—

Drainage of swampy pastures.

Dressing of the pastures with chemical manures, preferably with iron
sulphate, at the rate of 40 to 80 lbs. per acre.

Disinfection of manure to destroy the contained eggs or embryos.

The use of chalk, iron sulphate, various acids, etc.

As regards curative treatment, the diseased animals should be grouped
and isolated as far as possible, and should receive doses of the
following vermifuge:—

                     Powdered areca nut  2 ounces.
                     Arsenic            30 grains.

The above is sufficient for ten animals, and a dose should be given
daily for a period of six days in a small quantity of bran. Treatment is
completed by abundant nourishment, and by distributing about the
pastures pieces of rock-salt suitably protected.

Many other vermicides or vermifuges have been suggested, but are less
easy to use. They comprise essence of turpentine, mixtures of oil with
essence of turpentine and benzine, picrate of potash in doses of 7 to 20
grains per day, ethereal extract of male fern, etc.


                         LUMBRICOSIS OF CALVES.

Following the example of human medicine, we apply the term “lumbricosis”
to a disease caused by ascarides in calves, although Neumann separates
the ascarides of calves from the lumbricoid ascarides with which they
are usually confused in current practice.

=Causation.= The disease is exclusively due to infestation with embryos
of the parasite, which in young calves afterwards develop in the first
portions of the intestine and in the abomasum, interfering with
secretion, and producing mechanical disturbance, colic, and digestive
irregularity, eventually followed by marked loss of condition. Death may
even follow, either from rupture of the pylorus or duodenum, or from
secondary septicæmia of intestinal origin, due to the parasites
burrowing into the mucous membrane and facilitating infection. In adults
of all species lumbricosis is rare. It occurs principally in young
animals from the time of weaning up to the age of eighteen months or two
years.

=The diagnosis= cannot usually be formed until the parasites are found
in the fæces, but microscopic examination sometimes reveals the presence
of the eggs, and thus excites suspicion.

Provided the condition is diagnosed early, the =prognosis= is not grave;
but when patients have become exhausted and anæmic they require a long
time to recover, even when freed from parasites.

=Treatment.= Guittard recommends empyreumatic oil as very efficacious,
and gives it in doses of 2½ to 3 drachms diluted with ordinary oil, or
emulsified with any kind of mucilage.

Calomel gives good results, and maybe administered in doses of 15 to 60
grains, according to the animal’s age and size.

Powdered areca nut would probably be easier to administer with the food.
Oil of turpentine is given mixed with ordinary oil, but its action is
less certain.


                STRONGYLOSIS OF THE ABOMASUM IN THE OX.

Although well studied by Stadelmann and Ostertag in Germany, and by
Stiles in America, this disease has not yet been regarded in France as
giving rise to accidents.

It is produced by the _Strongylus convolutus rel Ostertagi_, which
becomes embedded under the epithelium of the mucous membrane and causes
the formation of small nodules, the size of a pin’s head or lentil,
which can be detected on palpation. The cavity thus formed beneath the
epithelium communicates with the gastric cavity by a little orifice,
through which the cephalic end of the parasite passes.


 PARASITIC GASTRO-ENTERITIS, DIARRHŒA, AND ANÆMIA IN CATTLE, SHEEP AND
                                 LAMBS.

A disease characterised by anæmia with wasting and diarrhœa is sometimes
produced in cattle by the presence in the fourth stomach of small
strongyles varying in size between 3 and 9 millimètres in length,
according to the variety encountered. One variety of the smaller size
has been named by McFadyean _Strongylus gracilis_. Penberthy, who
described the disease in the _Jour. of Comp. Path. and Therap._ for
1894, p. 249, states that in certain cases he also found the _Strongylus
ventricosus_, the _Tricocephalus affiinis_, and minute straight worms
about ²⁄₂₅ of an inch long, which he regarded as anguillulæ. Neumann
declares that pernicious anæmia with catarrh of the abomasum in young
animals is due to _Strongylus convolutus_.

=The symptoms= comprise anæmia, wasting, and diarrhœa of varying
severity. In acute cases, which are common between the ages of six
months and two years, husk is sometimes (accidentally) present. The
disease is rarest in summer. Certain animals lose flesh rapidly, though
appetite is retained. Acute fœtid watery diarrhœa follows. The animal
shows tenesmus, appears dejected, and has a temperature of 103° to 105°
Fahr. The mucous membranes become pale, the pulse small and weak, the
appetite capricious, the eyes sunken, belly tucked up, coat harsh and
dry and hide tight. Wasting is rapid. The animals are listless, and
often lie down for long periods. Death occurs from exhaustion.

=The parasite.= Scrapings from the abomasum and intestine when diluted
with water and viewed under a lens show minute bodies resembling short,
fine hairs. When isolated these are easily visible with the naked eye.
_In situ_ they appear to be lying on the mucous membrane, sometimes with
the head fixed in the latter. They vary in length from ³⁄₂₅ to ⁶⁄₂₅ of
an inch, and are brownish in colour. For a detailed description see
Penberthy _loc. cit._ McFadyean (_Jour. of Comp. Path. and Therap._ for
1896, p. 314) also gives a very full description, illustrated by plates,
of the two species of strongyles which he regards as the cause of
gastritis in cattle in England.

[Illustration: $1]

=The lesions= are those of wasting diseases. The first three gastric
compartments may be thin, but usually show no abnormality. The mucous
membrane of the abomasum shows evidences of catarrh, is sometimes
covered with a loose croupous material, or is denuded of its epithelium
and even extensively destroyed. In acute cases it is more or less deeply
reddened over spots or extensive patches. Occasionally it appears
jelly-like, owing to effusion into its substance. Except for the
catarrhal condition the small intestines may be healthy, but the large,
especially the colon and cæcum, show lesions similar to, but more
pronounced than, those of the abomasum.

=The treatment= comprises administration of the usual vermifuges, of
which Penberthy prefers turpentine. The diet should be nutritious and
easily digestible. Among drugs, non-irritant iron salts, cod liver oil,
bitter vegetable tonics and common salt are recommended. The animals
should be housed and kept warm; the litter, containing parasites, should
be destroyed. The pastures may be dressed with salt and lime; those
worst infected should be ploughed. An uninfected water supply is
essential.

=Parasitic Gastro-enteritis in Sheep and Lambs.= A disease in seven to
eight months old lambs, closely resembling the above, was described by
McFadyean in the _Jour. of Comp. Path. and Therap._ for 1897, p. 48.
Sheep over one year old were not affected.

=The symptoms= comprised diarrhœa, rapid wasting, impaired appetite,
thirst, a tendency to lick and swallow sand or earth, dulness, and
continued fever (105° to 108° Fahr.). There was no evidence of acute
pain or of marked cough.

=Duration.= The disease sometimes proved fatal in one or two days, but
sometimes extended over several days or weeks. The mortality varied from
10 to 20 per cent., but in many cases almost all the members of a flock
exhibited diarrhœa and loss of condition.

=The cause= appeared to be the presence of small nematode worms in the
fourth stomach, which generally exhibited gastritis with inflammatory
congestion of the mucous membrane, though in a considerable number of
cases the lining membrane of the stomach was markedly anæmic. In a large
number of cases the irritation of the mucous membrane was continued into
the duodenum, but as a rule the remainder of the small intestine was not
inflamed.

The worms named by McFadyean _Strongylus cervicornis_ are from 10 to 12
mm. in length, so that although not of microscopic dimensions they
cannot be seen when suspended in the stomach contents. They are readily
detected in microscopical preparations under a low power.

[Illustration: $1]

=The treatment= is similar to that of gastro-enteritis in cattle, but
chief attention should be directed to prophylaxis.

                  *       *       *       *       *

A verminous disease, closely simulating the above, and affecting cattle,
sheep, and goats in Texas, is described by Ch. Wardell Stiles in the
Annual Report of the United States Department of Agriculture for 1900,
p. 356. The disease was of mixed character, and consisted in various
degrees of verminous gastritis, verminous enteritis, and verminous
bronchitis. In the stomach were found the common twisted wireworm
(_Strongylus contortus_) and Ostertag’s encysted wireworm (_Strongylus
Ostertagi_). It appeared to be present in every calf, steer and cow
examined (post-mortem), and was undoubtedly the chief agent in causing
death. The sheep and goats were very similarly affected. In the bowel of
cattle were found the hookworm (_Uncinaria radiata_), nodular disease
worm (_Œsophagostoma columbianum_): in that of sheep the hookworm
(_Uncinaria cernua_) and nodular disease worm (_Œsophagostoma
columbianum_), and the fringed tapeworm (_Thysanosoma actinioides_). In
the lungs of the cattle _Strongylus micrurus_ (the small-tailed
lungworm), and of sheep the threadworm strongyle (_Strongylus filaria_)
were detected.

=Treatment.= Sulphate of copper, gasoline and coal-tar creosote were
tried, but the best results were obtained from doses of 30 grains (for a
lamb) up to 100 grains (for a two-year-old sheep) of thymol in 1 per
cent. coal-tar creosote solution.


INTESTINAL COCCIDIOSIS OF CALVES AND LAMBS (PSOROSPERMOSIS, HÆMORRHAGIC
               ENTERITIS, BLOODY FLUX, DYSENTERY, ETC.).

=History.= This disease is very common in the Avalon and surrounding
districts, sometimes assumes the characteristics of a true epizootic,
and affects young bovine animals between the ages of six months and two
years, but is commonest and most contagious in animals of from ten to
eighteen months old.

It attacks animals in good or bad condition, without distinction of
breed or species. It begins towards the end of July, attains its maximum
development towards the end of August and September, and disappears in
October, though occasionally it continues until November. In exceptional
cases Degoix has seen it during January and February in animals which
had returned from the fields to the byres about the end of November. It
develops earlier than verminous bronchitis, in conjunction with which,
however, it often occurs. It is commonest in warm, moist, rainy years,
and amongst animals pastured on swampy ground containing numerous
springs and streams. Year after year it attacks animals occupying
particular pastures in summer. The soil of these pastures is undoubtedly
infested with the germs of the disease, just as in places the soil is
infested with anthrax bacilli. The appearance of symptoms is preceded by
an incubation period of one or two months. The length of this incubation
period is fixed by the observations which Degoix has made during the
past twenty years, and depends on the time which elapses between the
animals being turned into infected pastures and the appearance of the
preliminary symptoms.

=Symptoms.= The disease commences with liquid, serous, fœtid,
greenish-black diarrhœa, the material being voided without special
straining and the animals losing neither their spirits nor appetite.
Fever can scarcely be detected, the temperature ranging between 38° and
39° C. On the second or third day the diarrhœa changes in character.
Though it always remains fœtid, it now becomes mucous, reddish-black, or
sanguinolent, and contains more or less frequent blood clots of varying
size.

The passage of this material causes violent straining, which becomes
more and more common, and is accompanied by very pronounced rectal
tenesmus. The animals stand with their backs arched for one or two
minutes, sometimes longer, and the liquid escapes in large quantities,
soiling the quarters and hocks. The animals are dull, show a certain
degree of colic, and frequently grind the teeth. Appetite is lost,
thirst is severe, and rumination ceases. Wasting makes rapid strides,
the coat stares, the animals have difficulty in standing on account of
their weakness, fever sets in, and the temperature rises to 40° C. This
condition may last from five to ten days and terminate either in
recovery or death. Recovery is frequently rapid in animals which have
continued to eat, and in which the acute period has been of short
duration—five to seven days at most. On the other hand, it is slow if
the appetite has disappeared and the acute period has been prolonged
beyond ten days.

The diarrhœa, which has lost its sanguinolent character towards the
sixth or eighth day, may continue for somewhat longer. The attacks of
straining become rare, and cease between the tenth and fifteenth days.
The appetite remains capricious for a long time.

Convalescence is marked by alternate improvement and retrogression. The
animals are weak, and only recover quickly under energetic treatment and
forced feeding with concentrated digestible foods like milk, soup,
cooked grain, etc., administered for three weeks or more.

Death may occur towards the tenth or fifteenth day from exhaustion. The
patients become very anæmic and thin, the eyes are withdrawn into the
orbits, and the animals appear indifferent to what goes on about them.
They still groan feebly, occasionally grind the teeth, and lie
continually on the chest with the head extended. The body temperature
falls and death follows.

In well-bred animals in good condition the disease sometimes assumes a
much graver and more rapidly progressive form, with peracute symptoms,
and makes as many, if not more, victims than that previously described.

The process is as follows: After suffering for a day from serous
diarrhœa, to which the owners pay little attention, the animals show
sanguinolent diarrhœa and pass blood clots. This is almost immediately
followed by very violent convulsive attacks—true eclampsia. The animals
are then unable to stand, lie on the side with the head outstretched and
resting on the ground, the eyes withdrawn into the sockets and often
showing pirouetting movements (nystagmus), the neck drawn upwards and
backwards (opisthotonos), and the limbs rigidly extended. From time to
time the whole body is shaken by extremely violent convulsive movements.

This condition, which is sometimes preceded by weakness of the hind
quarters and symptoms of locomotor ataxia and inco-ordination, may
continue from six to thirty-six hours; in nine cases out of ten it
terminates in death.

=Causation.= On microscopic examination of the serous dejections one
finds distributed throughout the liquid mass very small numbers of ovoid
corpuscles having a double outline, and contents of varied appearance;
these are the coccidia.

When the diarrhœa has become sanguinolent and muco-fibrinous, the fluid
contains these coccidia in considerable quantities, and large numbers of
them may be found in the mucus, where they are mixed with epithelial
_débris_, blood corpuscles, and lymphatic cells, etc. They are rarer in
the clots. Coccidia cannot be found in the fæces of healthy animals,
even in those occupying the same pastures with the diseased. Should the
clinical symptoms be thought insufficient of themselves clearly to
identify the disease, a simple microscopic examination of the fæces will
remove any doubt.

=Lesions.= Post-mortem examination immediately after death enables one
exactly to identify the habitat of the parasite and the lesions it
produces. These lesions are to be found throughout the large intestine,
from the cæcum to the anus.

The large intestine is almost or entirely empty, the mucous membrane is
reddish-brown in colour, lies in folds, is œdematous, and everywhere
covered with a coating of mucus. This coating varies in character at
different points; in places it forms more or less thickened patches of
greyish or yellowish colour, and of a resistant character, as though
mixed with coagulated fibrin. These patches are fairly well defined,
they are irregular in form, and vary in width from some millimètres up
to several centimètres. They are more or less adherent to the mucous
membrane, from which they can easily be stripped away. The mucous
membrane thus exposed is slightly depressed, and of a whitish colour,
thus markedly contrasting with the surrounding red coloration. This
depression represents a slight ulceration, which, though superficial, is
clearly visible to the naked eye.

Microscopic examination of the mucus patches reveals the existence, both
superficially and in the depths, of epithelial cells derived from the
mucous membrane, of vesicular cells derived from the Lieberkuhnian
follicles, of numerous blood and lymphatic corpuscles, and, distributed
irregularly throughout this mass of cells, of coccidia, resembling those
found in the dejections.

In thin sections of the intestine, made through the ulcerated
mucus-covered patches, and in a direction perpendicular to the mucous
membrane, one finds that the epithelial covering of the intestine has
disappeared.

The Lieberkuhn’s follicles are shortened, their orifices are irregular
and partly blocked with epithelial _débris_. In a large number of these
follicles the blind extremity is dilated, and more or less filled with
coccidia, varying in appearance according to their stage of development.
The epithelial cells normally lining these blind ends seem to have
disappeared, and to have been replaced by the parasites. This, however,
is not really the case. It is easy to prove by suitable dissection
(after maceration of the sections in 30 per cent. alcohol) that the
coccidia are lodged in epithelial cells which have become modified in
shape and undergone hypertrophy as the parasite has grown, whilst the
nucleus has been pushed to one end and undergone atrophy.

Alongside the deceased glands may be found others which are quite
healthy. In the parts which are most markedly affected the
interglandular connective tissue is infiltrated and slightly thickened.
Degoix has never discovered coccidia in the cells of the intestinal
mucous membrane itself. The lesions may be met with throughout the large
intestine, but are more numerous and grave as the rectum is approached.

This disease is characterised by extensive inflammation, affecting the
entire mucous membrane of the large intestine, by more or less extensive
ulceration of this bowel, the ulcers being covered with muco-fibrinous
patches rich in coccidia, by localisation of the parasites in the
epithelial cells of the glandular cul-de-sac, by the appearance of the
disease at a special time of year and in special districts, where it
assumes the form of an enzooty, and by the fact that it always appears
in the same pastures. The mortality varies between 12 and 25 per cent.
from year to year.

=Microscopic appearances.= The protozoa which produce this disease
assume the form of ovoid cysts, varying in length from 18 to 25 µ, and
measuring at the widest part about 13 µ. They possess a hyaline envelope
whose existence is proved by its double contour line, and yellowish,
granular, highly refractile contents. This granular material does not
always occupy the whole of the cavity. At a certain stage of development
it collects towards the centre, forming a nucleus and leaving clear
spaces at the poles of the cell. At a later stage this nucleus divides
into four portions which afterwards separate.

=Treatment.= The protozoa, in their cystic condition, are very resistant
to destructive influences. The most common natural cause of their
destruction is drying in the open air. Unfortunately, in the localities
where the patients usually live, that is, filthy byres, wet pasturages,
etc., this destruction only takes place to a very limited extent.

The disease can be attacked by prophylactic and therapeutic measures.

Prophylaxis consists—firstly, in destroying the parasites contained in
the dejections by the free use of 3 per cent. sulphuric acid solution;
and, secondly, in removing the young animals from infected fields during
the months between June and September.

Therapeutic treatment comprises—firstly, stimulant applications to the
abdomen; secondly, disinfection of the intestine by the administration
of salol, benzo-naphthol, very diluted solutions of creolin, etc.;
thirdly, intestinal irrigation by the administration of mucilaginous
drinks containing bicarbonate of soda, supplemented by general tonic
treatment and the supply of concentrated, very nourishing, and easily
digested food (Degoix, _Revue générale de Médecine Vétérinaire_, No. 28,
February 15th, 1904, p. 177).

                  *       *       *       *       *

McFadyean describes a similar disease to the above in two to three
months old lambs (_Jour. of Comp. Path. and Therap._, March, 1896, p.
31). The mortality reached 10 per cent. The lambs at the time the
disease broke out in the flock were closely folded together with the
ewes on growing roots, which, needless to say, were much soiled with
earth and fæces before they were completely consumed.


                 INTESTINAL HELMINTHIASIS IN RUMINANTS
                           (Ox, Sheep, Goat).

[Illustration: $1]

Verminous disease of the intestine is often accompanied by similar
disease of the stomach (gastro-intestinal strongylosis of the sheep,
lumbricosis of the calf), but it also occurs apart from the presence of
gastric parasites. Parasites are more frequent in the intestine than in
the abomasum, because the alkaline intestinal juices prove a much more
favourable medium for their development than do the acid juices of the
stomach.

The actual parasites may include ascarides, strongyles, hooked worms,
œsophagostomes, tricocephales, sclerostomes, and various tæniæ (_Tænia
expansa et alba_). Many of these have already been, or will hereafter
be, referred to.

Helminthiasis due to round worms like strongyles, and the various forms
of hooked worm, is graver than that due to flat worms, but most
extraordinarily varied collections are sometimes met with. Speaking
generally, however, helminthiasis more particularly affects young
animals like calves, lambs, and yearling sheep, is rarer in adults, and
in all cases the complications it produces are of trifling importance in
adults as compared with those caused in the young.

The persistence of verminous diseases in certain infested countries,
districts, farms, or pastures is explained by the enormous number of
eggs or embryos passed with the fæces and disseminated with manure, as
well as by the high degree of resistance of the eggs and embryos to
destructive influences.

=Causation.= The various forms of intestinal helminthiasis are all due
to embryos or eggs of worms obtaining entrance to the stomach or bowels
of susceptible animals. Nevertheless, external conditions largely favour
infestation. The existence of marshes, ponds, and stagnant water on
certain pastures, heavy annual rainfall, the occurrence of wet seasons,
etc., favour the existence and growth of embryos, and, as a consequence,
the infestation of animals.

[Illustration: $1]

=The symptoms= of intestinal helminthiasis are always very vague,
whether the victims be oxen, sheep, or goats. They point to the slow and
progressive development of a pernicious anæmia, characterised primarily
by interference with appetite and digestion, then by anæmia, and finally
by cachexia. The patients are dull, lose condition, suffer from depraved
appetite, and, during the cachectic period, from diarrhœa, and die in a
condition of exhaustion. These forms of helminthiasis are much more
frequent in sheep than in oxen.

=The diagnosis= is only arrived at by discovering parasites in the
fæces, or, in those doubtful cases where one has been led to make a
microscopic examination of the excrement, by the detection of large
numbers of eggs.

From an economic standpoint the =prognosis= is grave, because severely
infected animals recover their condition very slowly, whatever treatment
be adopted.

=Treatment= includes the measures previously indicated regarding the
destruction of germs, eggs, or embryos distributed over the pastures,
and the drainage of wet grounds and stagnant pools. Where such diseases
are common, the pastures should be dressed with iron sulphate, and the
stable manure disinfected or burned.

Curative treatment comprises the administration of such anthelmintics as
can be given with the food. They should not require to be administered
by force, as this proceeding would not only necessitate a great loss of
time, but might result in accidents.

Arsenious acid, in doses of 15 grains per day, and tartar emetic, in
doses of 75 to 150 grains, according to the animal’s size, are among the
best drugs for oxen, and may be given for four or five days running.
Benzine, oil of turpentine, and empyreumatic oil are more difficult to
administer.

In the case of sheep, preference should be given to areca nut, in doses
of 75 to 120 grains, according to the animal’s size, and to tansy, which
are convenient to give, and can be added to bran, oats, or beetroot.

Adult tapeworms of oxen are of relatively minor importance, but one
tapeworm of sheep, viz., the fringed tapeworm (_Thysanosoma
actinioides_), also known as _Tænia fimbriata_; _Moniezia fimbriata_
deserves notice, as at times it forms a veritable scourge to the sheep
industry of North America and South America.

[Illustration: $1]

[Illustration: $1]

=Disease.= The disease in sheep caused by the fringed tapeworm has been
studied in detail by Curtice, who considers that next to scab it is the
most important sheep disease of the western plains of North America. The
financial loss it causes is extensive, and results from the failure of
the lambs to fatten, the small crop of wool, and the weakening of the
animals, so that they cannot withstand cold winter weather. The
parasites develop slowly, and are present in considerable numbers before
their presence is suspected. Toward September the lambs fail to grow as
they should; in November the symptoms are marked. First, the worms
produce local irritation of the intestine, which finally develops into a
chronic catarrhal inflammation; their presence in the gall-ducts
produces similar results, and obstructs the flow of bile; infected lambs
are large-headed, under-sized, and hidebound; their gait is rheumatic,
and they appear more erratic than the other sheep, standing oftener to
stamp at the sheep dogs or herds, and lagging behind the flock when
driven; the general symptoms are those of malnutrition, and Curtice
considers them nearly identical with the symptoms of the “loco” disease;
in fact, he states that it is extremely difficult to distinguish between
the two diseases, and believes that the fact that the worms “may tend to
produce depraved appetites and a morbid craze for a particular food is
also reason for suspecting that the loco disease may depend on the
tapeworm disease.” General systemic disturbances result from
malnutrition; the usual fat is absent; serous effusions are noticed in
the body cavities, serous infiltration in the connective tissue.

=Treatment= is similar to that of parasitic gastro-enteritis of sheep
and lambs (which see).




                              CHAPTER IX.
                         DISEASES OF THE LIVER.


From the physiological standpoint the liver is an organ of such
importance that its pathology should be studied as completely as
possible. Furthermore, it is often the seat of a number of varying
lesions, either of parasitic, toxic, infectious, or cancerous origin.

In animals of the bovine species the liver is placed in the right
retrodiaphragmatic region, so that it is somewhat difficult to examine
by any of the ordinary methods, like palpation and percussion. Under
normal conditions it is entirely concealed beneath the hypochondrium,
except towards the upper margin of the thirteenth rib, where it can be
examined by palpation. When, as in various morbid conditions, it is
considerably increased in size, it extends as far as the margin of the
hypochondriac circle, thus becoming directly accessible to palpation and
percussion. Sometimes it even enters the hypochondriac region, passing
outside the omasum and abomasum, which it then thrusts towards the
middle of the abdominal cavity.

The margin of the liver exhibits a depression lodging the gall bladder
nearly opposite the centre of its vertical depth.

As the liver is so deeply situated, percussion is found to be the method
of examination which gives the best results. Beyond the limits of the
zone of auscultation, percussion gives above a semi-dull sound, then,
proceeding downwards, a dull sound due to the liver, the omasum, and the
collection of liquid in the bowel. When this dulness is well defined,
clear, broad from above downwards, and extends to or beyond the
hypochondrium, it indicates hypertrophy of the liver. By deep palpation
of the posterior margin of the hypochondrium the liver can then be
sounded, and its excessive size detected.

The symptomatology of the liver is still very imperfectly understood,
for in practice the urine is rarely tested for bile pigments, nor
attempts made to ascertain whether the glycogenic function is normal by
the test for alimentary glycosuria.

In this connection nothing has yet been done to assist in diagnosing
certain hepatic conditions. Fortunately, those diseases of the liver
which we have to study are more often of a parasitic nature than true
diseases of the hepatic tissue.

The reported cases of venous or biliary cirrhosis, moreover, are too
ill-defined and too incomplete to be taken as a type for description. We
leave them on one side. In a similar way, apart from parasitic
cholangeitis and cholecystitis, inflammations of the biliary ducts are
little known, and are rare.


                        CONGESTION OF THE LIVER.

In bovine pathology only passive congestion of the liver, often a result
of various primary affections with cardiac lesions, is well recognised.

Active congestions probably occur during infections or intoxications of
various kinds, but have not been made the object of special research.

Among diseases likely to produce passive congestion must be included all
those which interfere with the return circulation through the posterior
vena cava. All cardiac affections with lesions of the valves or orifices
of the right heart, all forms of pericarditis, tumours or lesions of the
mediastinum compressing the posterior vena cava, produce stasis, passive
congestion, and progressive development of what is called “cardiac
liver.”

=Symptoms.= The liver is considerably hypertrophied, as a consequence of
the stasis of blood and progressive dilatation of the portal system. Its
zone of dulness increases in size, whilst on palpation its borders may
sometimes be detected. This condition is always accompanied by digestive
disturbance.

The function of the liver is more or less interfered with; the urine is
scanty in amount and charged with deposit. Ascites of varying intensity
frequently occurs; cardiac disturbance accompanies or usually precedes
the above symptoms.

=The lesions= of passive congestion are represented by progressive
dilatation of the entire portal venous system (nutmeg liver). In time
this dilatation may produce biliary cirrhosis, as a result of chronic
irritation of the blood-vessels and perivenous inflammation. This
condition is known as “cardiac cirrhosis of the liver.”

=The diagnosis= of this pathological condition is generally easy,
provided that the primary disease which causes it be recognised.

=The prognosis= is always grave, and the practitioner is limited to
treating the primary affection, such as endocarditis, pericarditis, etc.


                      NODULAR NECROSING HEPATITIS.

This form of inflammation of the liver is somewhat rare in animals of
the bovine species. The disease is difficult to diagnose, and is often
only recognised on post-mortem examination.

Isolated tracts of the liver become inflamed, between which the rest of
the tissue preserves its normal character; the parts affected appear to
undergo complete degeneration, the cause of which is difficult to
explain. On examining affected animals after death, the liver is found
to be greatly enlarged, and apparently invaded by multiple tumours. On
section, the parenchyma generally is of normal colour, but the diseased
parts are represented by dirty greyish-yellow tissue of a lardaceous
character, somewhat resistant to the knife.

The affected spots vary in size, between that of a lentil or hazel nut
and an egg, and are formed of necrotic tissue.

The periphery is the seat of true chronic fibro-plastic inflammation.

[Illustration: $1]

=Causation.= According to Stubbe, these lesions are produced by
microbes, originating in the intestines, and carried to the liver by the
mesenteric veins. The lesions and blood of the liver yield cultures of a
microbe resembling that of necrosis; nevertheless, such lesions have not
been experimentally reproduced.

According to Berndt, infection from the uterus is possible, and indeed
probable. Moussu has only seen three cases of this particular condition
of the liver in living animals. Two of these were in a working ox and a
bull respectively, so that Berndt’s view would not seem to be
exclusively applicable. Moussu is convinced that infection is of
intestinal origin, and that it takes place through the mesenteric veins;
he claims to have found the proof of this in the existence of multiple
pylephlebitis and complete obliteration of the subhepatic veins in some
cases.

=Symptoms.= The symptoms are so vague as to render diagnosis difficult.
Berndt, on the other hand, regards it as fairly easy. He states that the
disease occurs in old cows, which after parturition show loss of
appetite, polydipsia, fever, dyspnœa, and short, feeble cough,
suggesting pneumonia. After a few days the animals appear extremely
weak, remain lying for long periods, and exhibit icterus. Percussion of
the liver detects abnormal sensibility and hypertrophy.

The three cases seen by Moussu showed only slight yellowness of the
membranes, general weakness and difficulty in walking, which at first
glance appeared to suggest laminitis, marked hypertrophy of the liver,
sensitiveness over the hepatic region, and, as complications,
uncontrollable diarrhœa and peritonitis. But these symptoms are also
noted in suppurating echinococcosis, and even in cancer of the biliary
ducts, so that diagnosis does not appear easy. Nevertheless, there is
always marked fever, and on post-mortem examination it is not unusual to
find, in addition to the hepatic lesions, a certain amount of
perihepatitis, partial peritonitis, and even pleurisy in the region of
the diaphragm. The question is of little practical importance, for the
gravity of the disease just described is such that economically no
treatment is possible. The great point lies in correctly diagnosing
disease of the liver, and that is relatively easy.


                  CANCER OF THE LIVER AND BILE DUCTS.

Cancer of the liver, that is, broadly speaking, the development in the
liver of malignant tumours, capable of becoming generalised throughout
the organism, is comparatively rare when compared with parasitic
diseases of the same organ. It may be primary or secondary in character,
but is much more frequently secondary. In bovines primary cancer assumes
the forms of adenomata, trabecular epitheliomata, or adeno-carcinomata.
Moussu describes a case in which the growths assumed the form of
papillomata or adeno-papillomata extending throughout the biliary ducts,
and partly obstructing the common bile duct, which was greatly dilated.

The real cause of these, as of all other primary tumours, remains
shrouded in mystery.

Secondary cancer is more frequent; it occurs usually in the form of
little isolated tumours (nodular cancer) of varying size and greyish
colour.

=Symptoms.= Clinically the description, or rather the identification, of
cancers of the liver is difficult, and the diagnosis particularly
troublesome in cases of primary cancer.

In secondary cancer (following tumour of the testicle in oxen castrated
by the method of bistournage, for example) the general condition, on the
other hand, is usually so affected that attention is pointedly drawn to
the seat of the secondary growths. The patients lose appetite, the fæces
become fœtid, and diarrhœa sets in without clear signs of enteritis.

Examination of the liver always reveals hypertrophy, and sometimes
sensitiveness. The patients rapidly lose flesh, become cachectic, and
the proportionate number of red blood corpuscles diminishes. From the
normal of six or seven millions the number may fall to one million or
less, while that of the white corpuscles considerably increases. This
leucocytosis, which accompanies all forms of visceral cancer, enables
one to distinguish between cancer and chronic forms of diarrhœic
enteritis; it must not be confused with leucæmia. Moderately developed
ascites is common, in consequence of obstruction in the porto-hepatic
circulation.

[Illustration: $1]

=The diagnosis= of cancer of the liver or biliary ducts is surrounded
with difficulty, and the =prognosis= is extremely grave, because no
treatment is possible.


                      ECHINOCOCCOSIS OF THE LIVER.

This term is applied to the development in the depths of the hepatic
parenchyma of hydatids of _Tænia echinococcus_.

The echinococcus hydatid is found in man, cattle, sheep, swine, etc. It
represents an intermediate stage of development of the echinococcus
tapeworm of dogs. Since this parasite develops its larval stage in man
also, and further, since it is the most dangerous animal parasite found
in man, it is important to thoroughly understand its life history in
order to guard against infection.

=Adult stage= (_Tænia echinococcus_).

=Hosts.= Dog, dingo, jackal, wolf.

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=Life history.= Starting with the adult tapeworm (Fig. 124) in the small
intestine of the dog or wolf, the eggs are scattered over the ground and
are swallowed by the intermediate host with the fodder or water. Upon
arriving in the stomach the egg-shell is destroyed, and the six-hooked
embryo, which is thus freed, bores its way through the intestinal wall,
and wanders, actively or passively (that is, carried along by the
blood), to various organs of the body—liver, lungs, ovaries, bones,
skull, etc.—where it develops first into an _acephalocyst_, which may
develop further, as shown by the accompanying illustrations. The heads
which are formed, upon being devoured by a dog or wolf, then develop
into adult tapeworms.

Young animals are most exposed to this disease; in adults or aged
animals the migration and development of the embryo are more difficult.

[Illustration: $1]

These embryos perforate the tissue of the liver, become fixed in it, and
derive from it the nourishment necessary for their conversion into
cystic bladders of varying size, either sterile or fertile.

The number of vesicles is rarely large, and when only one or two are
present they seldom produce sufficient disturbance to attract attention.
On the other hand, when numerous they deform the liver, produce
glandular atrophy, increase the total size of the organ, and lead to the
appearance of clearly marked symptoms.

[Illustration: $1]

The cystic vesicles contain a clear, limpid, transparent fluid, in which
float secondary, daughter, or granddaughter vesicles.

[Illustration: $1]

=Symptoms.= Echinococcosis of the liver has no well-marked symptoms, and
is therefore difficult to diagnose in animals whose liver is deeply
seated, and therefore beyond palpation. The signs which may characterise
the period of penetration of the embryos through the intestine and into
the depths of the liver, and which are probably represented by slight
colic, vague pain and diarrhœa, usually pass unnoticed. But later, when
the liver is extensively invaded appetite becomes irregular without
apparent cause, animals show intractable diarrhœa, general feebleness,
dulness, and wasting.

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These symptoms do not point with sufficient clearness to a special
visceral lesion, but as they call for a complete examination, the
practitioner is almost forced to a certain conclusion by the fact that
the examination remains negative except in regard to the liver. The
liver seems large and sensitive, and may sometimes be considerably
hypertrophied, for cases have been seen in the ox where the normal
weight of 10 to 12 lbs. has been increased to 60 or even 100 lbs., while
in the pig, whose liver normally weighs 4 lbs., the weight has been as
high as 20 or 40 lbs. In such cases percussion and palpation show that
the liver extends beyond the right hypochondriac region and invades a
large portion of the corresponding flank. But such great enlargement is
exceptional, and when only a dozen vesicles are present, although the
functions of the liver may be seriously disturbed, the information
obtained by physical examination is seldom sufficient to justify an
exact diagnosis. The liver is found to be enlarged and thickened;
otherwise the examination gives negative results.

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The diarrhœa may result from failure of the liver to secrete sufficient
bile to destroy intestinal toxins, or to carry on its glycogenic
function; but it may possibly be the direct result of chronic
intoxication by the contents of the vesicles.

Experience has shown, in fact, that in man, when a superficial vesicle
becomes ruptured, the peritoneal cavity is flooded with the contents of
the cyst; the daughter cysts adhere to the peritoneum, and that almost
invariably vascular disturbance occurs, accompanied by itching of the
skin and an eruption resembling that of urticaria.

The liquid of the vesicles contains an active toxalbumin.

=Diagnosis.= In certain cases, diagnosis is possible, and even easy, but
in others it is extremely difficult and almost impossible.

=Prognosis.= The prognosis is always grave, for if the lesions in the
liver do not produce death, as usually happens, they so profoundly
affect the animals’ general state, that it is no longer worth while to
keep them alive.

No practical treatment exists. In exceptional cases it certainly might
be possible, although in the large herbivora always difficult, to expose
the liver and to puncture and evacuate the contents of some of the
cysts; but the result would be illusory, because some vesicles would
always be inaccessible, and economically intervention would be
incomplete and useless.

[Illustration: $1]

Although there is no useful method of treatment, prophylaxis is possible
and valuable. It consists in preventing the development of tæniæ in farm
and sporting dogs. For this purpose it is sufficient to prevent their
obtaining raw offal containing vesicles of echinococci from sheep, oxen,
or pigs, and also to free them from any helminths which they may
harbour. In this way they no longer spread eggs of tæniæ with their
fæces in the neighbourhood of ponds or drinking places, and the cattle
do not ingest the embryos.


                      SUPPURATIVE ECHINOCOCCOSIS.

=Causation.= Simple echinococcosis may remain undetected for a long
time, and young animals affected with it may grow up without exhibiting
marked general disturbance. The old echinococci end by degenerating, the
wall of the cyst becomes modified, the liquid it contains, turbid,
lactescent, then caseous; the vesicle becomes wrinkled, and finally
nothing resembling the primary vesicle remains. The liquid is soon
absorbed, and the primary cyst is only represented by a caseous magma,
which undergoes calcareous infiltration and progressive atrophy.

Under other circumstances the development of the echinococcus vesicles
is less regular; they may become accidentally infected and transformed
into encysted abscesses, constituting suppurative echinococcosis of the
liver. The membrane of the vesicles usually resists the passage of
microbes, but the fibrous tissue surrounding the cyst is very vascular;
and if, in consequence of vascular disturbance in the liver (which may
result simply from feeding, trifling infection or other visceral
disease), the blood should for a short time be infected, microbes
penetrate through solutions of continuity in the wall of the vesicle,
which becomes a centre of suppuration. The liquid becomes turbid, the
primary cyst is transformed into an abscess, and suppurative
echinococcosis is set up.

=Symptoms.= The general condition resulting from the development of
suppuration in echinococcus cysts is very different from that of true
echinococcosis. If the abscess develops rapidly, acute generalised
peritonitis or localised peritonitis of the right anterior abdominal
region may almost immediately occur, producing all the characteristic
symptoms of ordinary peritonitis. In all cases, even in the absence of
well-marked peritonitis, perihepatitis occurs, and the liver becomes
adherent to the posterior surface of the diaphragm, to the hypochondriac
region, to the abdominal wall, or to one of the gastric compartments.

This perihepatitis is indicated by exceptional sensitiveness in the
right hypochondriac region, and by respiratory disturbance due to
fixation of the diaphragm.

In certain cases these abscesses seem to develop like “cold”
abscesses—_i.e._, without fever, and this without producing very marked
digestive disturbance; but the patients waste rapidly, become weak, show
slight sub-icteric coloration of the membranes, and appear to lose their
strength. Movement is slow and hesitating, as though the animals were
suffering from laminitis, the anæmia becomes more marked from day to
day, and examination of the blood reveals abundant leucocytosis, the
existence of which often assists in the diagnosis of internal
suppuration. In a few months, at least in the cases we have seen, the
animals become cachectic.

In other and still more obscure cases suppuration of the liver is
accompanied by total hypertrophy, excessive sensitiveness in the right
hypochondriac region, progressive loss of appetite, excessive thirst,
and uncontrollable diarrhœa and fever, although in the case mentioned
above there was little fever and no diarrhœa. The course of these cases,
which probably result from intestinal infection, is much more rapid. In
a fortnight or three weeks, sometimes less, the patients are carried off
by intoxication, generalised purulent infection, or septicæmia.

=Diagnosis.= The diagnosis of suppurative echinococcosis and of primary
abscess of the liver is difficult to establish. It is attained chiefly
by a process of exclusion, though the signs furnished by percussion of
the right flank, and by examination of the blood, are of some
assistance.

[Illustration: $1]

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=Prognosis.= The prognosis is extremely grave.

=Treatment= is of little value. Even supposing that the diagnosis has
been exact, surgical intervention is out of the question, and only this
would appear theoretically to offer a chance of success. The abscesses
are multiple, deeply placed, separated from one another, and sometimes
surrounded by enormous tracts of inflamed tissue. In fact, the condition
is of such a character as entirely to prohibit active measures.


                             CYSTICERCOSIS.

[Illustration: $1]

This disease is produced by the thin- or long-necked bladder-worm
(_Cysticercus tenuicollis_) found in cattle, sheep, and swine. The
cysticercus represents an intermediate stage of development of the
marginate tapeworm (_Tænia marginata_) of dogs and wolves.

It is by no means uncommon in Europe and America, and occurs in the body
cavity of cattle, sheep, swine, and other animals, attached to the
diaphragm, omentum, liver, or other organ.

When eaten by dogs or wolves, it develops into the marginate tapeworm,
which was formerly confused with _T. solium_ of man, and gave rise to
the erroneous idea that the pork-measle tapeworm occurs in dogs as well
as in man.

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=Life history.= In tracing the life history it is best to begin with the
egg, produced by the adult tapeworm in the intestine of dogs. These
eggs, containing a six-hooked embryo, escape from the dog with the
excrements, and are scattered on the ground, either singly or confined
in the escaping segments of the tapeworm. Once upon the ground, they are
easily washed along by rain into the drinking water, ponds, or brooks,
or scattered on the grass. Upon being swallowed with fodder or water,
they arrive in the stomach of the intermediate host (cattle, sheep,
etc.), where the eggshells are destroyed and the embryos set free. The
embryos then traverse the intestinal wall, and, according to most
authors, arrive either actively, by crawling, or passively, by being
carried along by the blood, in the liver or lungs, where they undergo
certain transformations in structure. While still in the finer branches
of the blood-vessels of the liver, which they transform into small,
irregularly shaped tubes about 12 to 15 mm. long and 1 to 1·5 mm. broad,
the embryos lose their six hooks, and develop into small, round kernels,
which are generally situated at one end of the tubes. The embryo can
first be seen about four days after infection. The “scars” (Figs. 140
and 141) described in the liver of animals infested with _Cysticercus
tenuicollis_ are nothing more nor less than these tubes, or altered
blood-vessels, caused by the growth and wandering of the parasites.

Curtice takes a somewhat different view—that is, he considers the liver
as a place of destruction for the young parasites, rather than a normal
place for their development; he also claims that the embryos, which may
even travel the entire length of the intestine of the intermediate host,
traverse the intestine and arrive directly in the position where they
complete their larval development without first passing through the
liver.

[Illustration: $1]

After developing into the full-grown bladder-worm, the parasites remain
unchanged until they are devoured by a dog or wolf, or until, after an
undetermined length of time, they become disintegrated and more or less
calcified.

If the hydatid is devoured by a dog or wolf, either when the latter prey
upon the secondary host or when the dog obtains the cyst at a
slaughter-house, the bladder portion is destroyed, the scolex alone
remaining intact in the digestive fluids. The head holds fast to the
intestinal wall with its suckers and hooks; by strobilation (transverse
division) it gives rise to the segments, which as we have already seen,
together with the head, go to make up the adult tapeworm. Reproductive
organs of both sexes develop in the separate segments, and eggs are
produced, within which are developed the six-hooked embryos, the point
from which we started.


              DISTOMATOSIS—LIVER FLUKE DISEASE—LIVER ROT.

In France the name of distomatosis has been given to a disease caused by
the presence of distomata in the bile ducts. It is the “liver rot” of
England, the Eberfäule of Germany, and is produced by the growth in the
biliary ducts of oxen, sheep, and goats of two species of distomata,
viz., the _Distoma hepaticum_ or _Fasciola hepatica_, and the _Distoma
lanceolatum_.

[Illustration: $1]

In 1875 Zundel established the causative relation between the presence
of distomata in the liver and the development of progressive fatal
cachexia in most of the animals affected. This opinion was emphasised by
the works of Leuckart and Thomas on the development of distomata, and at
the present day the parasitic theory is accepted as beyond question.

=Fasciola hepatica= (_Distoma hepaticum_).—The common liver fluke of
cattle, sheep, swine, etc.

=Life history.= The adult parasite, instead of producing young similar
to itself and capable of developing directly into adults in cattle,
produces eggs which develop into organisms totally different from the
adult form, living a parasitic life in other animals. In scientific
language, the parasite is subject to an alternation of generations,
together with a change of hosts. The following summary of the life
history will make this point clear:—

(_a_) _The adult hermaphroditic worm_ (Figs. 144 and 145) fertilises
itself (although a cross fertilisation of two individuals is not
impossible) in the biliary passages of the liver, and produces a large
number of eggs.

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(_b_) _Eggs_ (Figs. 143, 146 and 147).—Each egg is composed of the
following parts: (1) A true germ cell, which originates in the ovary and
is destined to give rise to the future embryo; (2) a number of vitelline
or yolk cells, which are formed in a specialised and independent portion
(vitellogene gland) of the female glands—instead of developing into
embryos the yolk cells form a follicle-like covering for the true germ
cell, and play an important _rôle_ in the nutrition of the latter as it
undergoes further development; (3) a shell surrounding the germ cell and
vitelline cells, and provided at one end with a cap or operculum. The
eggs escape from the uterus of the adult through the vulva, are carried
to the intestine of the host with the bile, then pass through the
intestines with the contents of the latter, and are expelled from the
host with the fæcal matter. Many of them become dried, and then undergo
no further development; but others are naturally dropped in the water in
marshes, or, being dropped on dry ground, they are washed into water by
the rain, or are carried to a more favourable position by the feet of
animals pasturing or passing through the fields. After a longer or
shorter period of incubation, which varies with the temperature, a
ciliated embryo (_miracidium_) is developed. At a temperature of 20° to
26° C. the miracidium may be formed in ten days to three weeks; at a
temperature of 16° C. the development takes two to three months; at 38°
C. it ceases entirely. Experiments have shown that as long as these eggs
remain in the dark the miracidium will not escape from the egg-shell;
accordingly it will not escape during the night. When exposed to the
light, however, or when suddenly brought into contact with cold water,
the organism bursts the cap from the egg-shell, crawls through the
opening, and becomes a—

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(_c_) _Free-swimming ciliated miracidium_ (Fig. 148).—As already stated,
this organism is entirely different from its mother. It measures about
0·15 mm. long; is somewhat broader in its anterior portion than in its
posterior portion; on its anterior extremity we find a small eminence,
known as a boring papilla; the exterior surface of the young worm is
covered with numerous cilia, which by their motion propel the animal
through the water; inside the body we find in the anterior portion a
simple vestigial intestine and a double ganglionic mass provided with a
peculiar pigmented double cup-shaped eye-spot; in the posterior portion
of the body cavity are found a number of germ cells, which develop into
individuals of the next generation.

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Swimming about in the water, the miracidium seeks out certain snails
(_Limnæa truncatula_, _L. oahuensis_, _L. rubella_), which it
immediately attacks (Fig. 148). The miracidium elongates its papilla and
fastens itself to the feelers, head, foot, or other exterior soft
portion of the body of the snail; some of the parasites enter the
pallial (lung) cavity and attach themselves there. After becoming
securely fastened to the snail the miracidium discards its ciliated
covering, and shortens to about half its former length (0·07 mm. to 0·08
mm.). The parasites now bore their way into the body of the snail, and
come to rest in the liver or near the roof of the pallial cavity, etc.;
the movements gradually cease, and we have before us the stage known as
the—

(_d_) _Sporocyst_ (Figs. 149 and 150).—The eye-spots, ganglionic
swellings, and vestigial intestine become more and more indistinct, and
are finally lost. The sporocyst grows slowly at first, then more
rapidly, and at the end of fourteen days or so measures 0·5 mm. The germ
cells mentioned as existing in the posterior portion of the miracidium
now develop into individuals of a third generation, known as—

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(_e_) _Rediæ_ (Figs. 151 and 152).—The rediæ escape from the sporocyst
when the latter are from two weeks (in summer) to four weeks (in late
fall) old. Upon leaving the body of the sporocyst they wander to the
liver of the snail, where they grow to about 2 mm. long by 0·25 mm.
broad. Each redia consists of a cephalic portion, which is extremely
motile, and which is separated from the rest of the young worm by a
ridge; under the latter is situated an opening, through which the next
generation (cercariæ) escape. The posterior portion of the worm is
provided, at about the border of the third and the last fourths of the
body, with two projections. There is a mouth with pharynx situated at
the anterior extremity, the pharynx leading to a simple blind intestinal
sac. The redia, as well as the sporocyst, may be looked upon as a female
organism, and in its body cavity are found a number of germ cells, which
develop into individuals of the next generation, known as—

(_f_) _Cercariæ_ (Figs. 153—155).—These organisms are similar to the
adult parasites into which they later develop. The body is flat, more or
less oval, and provided with a tail inserted at the posterior extremity.
The oral sucker and acetabulum are present as in the adult, but the
intestinal tract is very simple; on the sides of the body are seen two
large glands, but the complicated genital organs of the adult are not
visible. The cercaria leaves the redia through the birth opening,
remains in the snail for a longer or shorter time, or passes out of the
body of the snail and swims about in the water. After a time it attaches
itself to a blade of grass (Fig. 154) or some other object, and forms a
cyst around itself with material from the large glands, at the same time
losing its tail. It now remains quiet until swallowed by some animal.
Then, upon arriving in the stomach—of a steer, for instance—the cyst is
destroyed, and the young parasite wanders through the gall-ducts or, as
some believe, through the portal veins to the liver, where it develops
into the adult hermaphrodite.

[Illustration: $1]

From the above we see that this parasite runs through three generations,
namely:

(1.) Ovum, miracidium, and sporocyst ... first generation.

(2.) Redia ... second generation.

(3.) Cercaria and adult ... third generation.

During this curious development, which lasts about ten to twelve weeks,
there is a constant potential increase in the number of individuals, for
each sporocyst may give rise to several (five to eight) rediæ, each
redia to a larger number (twelve to twenty) cercariæ, and each adult to
an enormous number (37,000 to 45,000) of eggs. This unusual fertility of
the parasite is necessary because of the complicated life history and
the comparatively small chance any one egg has of completing the entire
cycle.

=Hosts.= An interesting and, from an agricultural standpoint, an
important matter connected with this fluke is that it is found in a
large number (about twenty-five) of domesticated and wild animals, and
this fact probably explains to some degree the wide geographical
distribution of the parasite.

[Illustration: $1]

=Symptoms.= The symptomatology of this disease may clinically be divided
into three well-marked periods:

=I. Primary period.= The primary phase commences with the penetration of
the embryos of the parasite into the body, firstly into the intestine,
and then into the liver by ascending the bile ducts. This phase occurs
during the last months of the year, October, November, and December, and
is rarely accompanied by alarming symptoms. At this time the sheep
appear in good health, the summer being over, and the animals, being
well nourished and fat, are able to resist the first attacks of the
parasite, so that even an observant shepherd only notices a little
dulness, want of condition, and muscular weakness. It requires a
carefully trained eye to note these very general symptoms, for the
bodily condition only changes very slowly and progressively, the
appetite remaining good. Experienced butchers, however, in the districts
where distomatosis is common, readily detect this condition. The animals
make little resistance when handled.

[Illustration: $1]

Nevertheless, even in this primary phase, the conditions are not always
as above sketched, and a certain number of deaths may occur. Gerlach has
mentioned the possibility of death by cerebral apoplexy, in consequence
of the young distomata penetrating to the brain. Moussu has certainly
never seen such a complication, but has seen death from hepatitis,
perihepatitis, and secondary pericarditis in animals gravely infested.
The young embryos, whether they penetrate only by the bile ducts, as has
been stated, or are carried to the liver by the blood stream, often
excavate canals in the substance of the gland before establishing
themselves in the bile ducts. They make their way as far as Glisson’s
capsule, and may even penetrate it; and as they carry with them
innumerable intestinal germs, when they arrive _viâ_ the bile ducts,
they set up hepatitis, perihepatitis, with the formation of numerous
false membranes, or even infectious fibrinous peritonitis. Should the
patients die during this phase one finds young distomata at the surface
of the liver, or even in the thickness of the false membranes.

[Illustration: $1]

When infestation is discrete the appearances are quite different.
Careful breeders have even stated that at this period the young sheep
appear to show a greater tendency to fatten.

=II. Second period.= In the primary phase deaths are exceptional; they
only become common towards the end of the winter. During the second or
middle period (December and January) the patients lose flesh, appear
less active, show less regular appetite and greater thirst. The
conjunctiva becomes pale and swollen, the sclerotic has a bluish tint,
and the eyelids are somewhat infiltrated. The wool appears drier and
less curly; locks of wool part readily from the skin, and the individual
fibres become dry and fragile.

[Illustration: $1]

This phase is accompanied by very marked anæmia, rapid exhaustion during
movement, and inability to run for any length of time.

The different methods of examination reveal nothing specially striking,
except that the valvular sounds of the heart are sharper, and that
trifling œdema occurs under the thorax and abdomen.

Microscopic examination of the fæces reveals the presence of eggs of
distomata. The sheep rapidly become thin from about the end of January,
even although the appetite persists and nourishing food is given.

=III. Third, or wasting, period.= The decline, which sets in about
February, appears extremely obstinate, and resists all treatment.

The patients become feeble, eat less, and digest badly. Submaxillary
œdema, common to advanced wasting diseases, then appears. If the sheep
are removed from the fold to pasture, the swelling of the submaxillary
space is very noticeable. It consists in an indolent œdematous
tumefaction, which disappears when the animals are travelled, but
reappears when grazing on account of the low position in which the head
is then held.

The condition then becomes complicated with diarrhœa, and soon grows
alarming. On examination, extensive dropsy may often be found in the
thorax, pericardium, and abdomen.

Death results from exhaustion; the animals do not appear to suffer, but
become extraordinarily anæmic, and perish without a struggle. The blood
is simply rosy in colour, like gooseberry syrup; the clot is soft and
gelatinous; the number of red blood corpuscles has fallen from about
seven millions to a few hundred thousand.

Icterus is rare, though certain cases have been described where it has
appeared during the last and even during the middle stage.

When animals begin to die in a district which has long been infested,
the losses are enormous, the condition sometimes constitutes a perfect
scourge. It should be remarked, however, that all those affected do not
die; animals kept under good conditions may even survive for several
months, although greatly wasted.

Towards March and April the parasites leave their position, and are
conveyed by the current of bile towards the intestine, to be rejected
with the fæces. This is the period of convalescence and recovery; but
recovery is only relative, for the parasites are never entirely
evacuated. The distomata then recommence their life cycle outside the
animal body.

[Illustration: $1]

Unfortunately the mortality caused by distomata is accidentally
aggravated by other diseases, and the scourge then becomes an absolute
disaster for the districts where such complications occur. Thus Besnoit
and Cuillé, of Toulouse have shown that distomatosis may become
complicated with a form of very rapidly fatal hæmorrhagic septicæmia,
produced by an ovoid bacterium.

Distomatosis, already sufficiently grave, then becomes infinitely more
serious, if only from the fact that it may prove the point of origin of
an absolutely fatal complication.

In bovine animals the symptoms develop exactly as in sheep, though the
cachectic period is uncommon and the injury done is often less important
than in sheep. The patients exhibit irregular appetite, wasting without
appreciable cause, anæmia, and even diarrhœa. In spite of excellent
winter feeding they do not regain condition, and relative recovery only
sets in with the approach of spring. Death from simple distomatosis is
exceptional, but in animals so predisposed enteritis develops more
easily, as do all forms of infection of intestinal origin.

The disease is, however, also grave for bovines because successive
reinfection occurs, and the disease may be prolonged for years.

=Causation.= Distomatosis is due to one cause, viz., the entrance of
embryo flukes into the digestive apparatus of herbivora.

The adult distomata in the biliary ducts continually discharge large
quantities of eggs, though the process is most active between February
and June or July. The eggs are carried away with the bile and fæces and
pass on to the pastures, where they continue their life cycle, thanks to
moisture and the presence of stagnant water. The embryos, having escaped
from the egg, enter the bodies of the snails found in or near stagnant
water (_Limnæa truncatula_), become converted into sporocysts, and
afterwards into rediæ and cercariæ. The cercariæ become encysted on the
lower surface of blades of grass in damp pastures, whence they are
transferred to the animals’ stomachs along with the grass itself.

[Illustration: $1]

As the _Limnæa truncatula_ lives not only in marshy regions, but also in
all damp situations, the embryos of distomata are distributed over
enormous areas, and the disease itself is equally widespread. The
embryo, after ingestion, is set at liberty, and passes from the
intestine into the innermost recesses of the liver, being guided up the
bile ducts by the current of bile. At this point it attaches itself to
the wall of the bile duct, passes through its various stages of
evolution, and attains the adult form. It then begins laying eggs, and
thus starts a new evolutionary cycle.

The life cycle of _Distoma lanceolatum_ is not yet known, and this
variety, moreover, is less widely distributed than the _Distoma
hepaticum_.

The bile ducts are more easily penetrated by the distoma in young
animals, a fact which explains why calves and lambs are particularly
affected. Adults present a less favourable nidus, a fact which renders
them less easily infected, but does not entirely prevent the parasites
from attacking them. Old animals, although unable to resist entirely,
seldom harbour many of the parasites.

Wet years appear to favour the extension and propagation of distomatosis
in an extraordinary fashion, a fact which is easily understood, if we
regard the phases of evolution of the parasite. The autumn appears
particularly favourable to the infection of herds. This is explained by
the fact that, during the summer, the dryness of the fields entirely
prevents the development of such eggs as may be distributed over them;
whilst wet periods during the autumn favour this development.

On the other hand, the grass becomes eaten down in autumn, so that the
animals gather it almost level with the ground. As the cercariæ attach
themselves to the lowest leaves they are then ingested in much larger
quantities. The bad effects of wet seasons are not immediately apparent,
but appear during the following spring.

Distomatosis is common throughout almost the whole of Europe, Africa,
and America. In France it is most serious in the moister regions of
Sologne, in Berry, the mountainous and wet districts of the great
central plateau, and particularly in the Pyrenees. It particularly
attacks oxen in the valley of the Meuse, the marshes of Picardy, the
lower regions of Normandy, and in all the mountainous pastures of the
central plateau.

=Lesions.= The lesions of distomatosis vary with the stage of
development of the parasites. During the primary phase of invasion of
the bile ducts by young distomata one finds interstitial diffuse
hepatitis, due to perforation of the gland by young parasites, adhesive
perihepatitis, with the formation of false membranes, and not uncommonly
slight peritonitis.

Zoologists state that the young distomata penetrate the liver by passing
upwards against the current of bile. It does not appear impossible,
however, that they may penetrate by another path, particularly as
so-called “erratic” forms of distomatosis like distomatosis of the lung,
heart, lymphatic glands, and various other tissues are not uncommon. It
has been suggested that the young distomata, arriving in the bile ducts,
perforate the gland, giving rise to these lesions of perihepatitis,
peritonitis or erratic distomatosis; but this view is scarcely in
harmony with the fact that the parasites are usually found in the bile
ducts.

During the second phase, corresponding to the development of almost
adult distomata, the perihepatitis and peritonitis set up either produce
fatal results by secondary infection or diminish and disappear. The
parasites develop in the bile ducts, in which they attain the adult
condition. They steadily ascend towards the origins of the ducts,
dilating them in their passage in an extraordinary way. The number of
parasites varies greatly: sometimes there are but few, and they are only
discovered on post-mortem examination; in other cases the bile ducts are
crammed with them, as many as six or seven hundred or even a thousand
being present. The distended bile ducts always show chronic peripheral
inflammation, which steadily becomes aggravated, producing
pericanalicular atrophying sclerosis. This condition is followed by
change in and disappearance of a certain quantity of hepatic tissue, and
by various forms of vascular and secretory disease.

This is the period of greatest disturbance, not only in consequence of
the actual presence, but also of the mode of living, of the parasites.

Moussu declares that the parasites live principally on blood, at least
during the first and second stage of their sojourn in the liver,
adducing as proof that if one completely injects the vascular system of
the liver (arteries and veins), some of the injected matter will be
found a day afterwards in the digestive apparatus of the parasites.

The disturbances which they produce are therefore due to their actual
presence and its consequences, to their mode of life, and to the
intercurrent infections of which they are sometimes the initial cause.

It is idle to object that the part played by these parasites is less
important than has been suggested, and that the mortality results from
intercurrent infection, and not from the parasites themselves. It is
equally idle to point out that carcases of animals suffering from severe
infection with distomata, particularly the carcases of sheep, are
frequently found in slaughter-houses, in perfectly fat condition, and
with the appearance of not having suffered in any way. These
observations are perfectly correct and well founded. But it matters
little that death results from an infection superadded to the
distomatosis, if the presence of distomata is the determining factor in
causing the superadded infections, and if such infection is, as Moussu
believes, almost inevitable in animals already exhausted by the action
of the parasites.

The fact that animals suffering from distomatosis and slaughtered for
food are well nourished is not a valid objection; for it has long been
known that wasting and anæmia are not immediate consequences, and that
before they are clearly apparent the distomata must have been present in
the liver for several months. Bakewell and the Marquis of Behague have
shown that in moderately infected animals there is a tendency to lay on
flesh during the first and a portion of the second stage of development
of the disease.

If the animals are slaughtered before the period of progressive decline
sets in, it is quite possible to form entirely wrong views regarding the
importance of these parasites.

The wasting process commences towards the end of the second phase of the
disease, and then makes rapid progress. The parasites, which have then
been continuously drawing on the blood for their nourishment for a long
time, produce anæmia, and some infection of the bile ducts, and usually
a certain degree of icterus.

The third phase is accompanied by general signs of cachexia, which need
not again be described. They are similar to those of all progressive
cachexias. In animals which survive this phase and are ultimately
slaughtered the liver always shows very marked sclerosis, commencing
around the biliary ducts. Even after the parasites have been evacuated,
these ducts appear indurated, thickened, fibrous, and sometimes
encrusted with biliary deposits or obstructed with true calculi. These
calculi may or may not contain parasites; sometimes they simply contain
eggs: they are open, tubular, and perforated, but always irregular on
the surface.

When in addition complications have appeared, one usually finds general
lesions of septicæmia and blood infection.

In erratic distomatosis, which is of no importance clinically, distomata
may become encysted in the lung or other viscus, and in time die. The
cysts, which only contain one and rarely two parasites, present a
fibrous shell, enclosing a blackish, pultaceous, grumous magma, which
sometimes has undergone a certain amount of calcareous infiltration. The
parasite may be entirely destroyed.

=Diagnosis.= Early diagnosis is difficult, and can only be established
by microscopic examination of the excreta and the discovery of eggs. On
an average one may find one egg in each preparation when the liver
contains 80 to 100 flukes. When wasting is very marked, and particularly
when there has already been a number of deaths, diagnosis becomes
extremely easy. It is sufficient to find flukes in any form (_Distoma
hepaticum rel lanceolatum_) to be assured as to the cause of disease.

=Prognosis.= In severely infested cases the prognosis is extremely
grave, because no efficient method of treatment exists. Embedded in the
liver, the parasites resist the action of all drugs, and we know of no
anthelmintic eliminated by the bile which in any way affects their
vitality. When the disease is recognised early, the most economical
method is to fatten the animals as rapidly as possible and prepare them
for slaughter.

=Treatment.= There is no reliable curative treatment. The drugs which
one might employ would kill the animal before poisoning the parasites
embedded in the liver. Various mixtures containing sulphate of iron,
juniper leaves, etc., have been recommended; but rich food constitutes
the best of all treatment, both from a curative and a prophylactic
standpoint.

With the view of preventing the disease, however, and protecting flocks
from attack in places where the disease is common, certain precautions
should be adopted. They comprise—(_a_) providing a free supply of
rock-salt, either in masses placed in the mangers or distributed with
the food; the salt increases gastric secretion, and has a slight action
on the parasites: (_b_) adding to the food during the first months of
winter branches of birch, juniper, willow, and broom; the leaves of
these plants contain aromatic or resinous principles which act on the
liver, are eliminated by the bile, and may have valuable results.

But of all preventive measures the most effective consist in draining,
cleansing, and drying low, moist, or marshy lands, because the molluscs
which are essential to the life cycle of the parasites are unable to
develop where the soil is dry. The manure containing the eggs of the
parasites may be disinfected by adding to it lime, sulphate of iron, or
common salt. Common salt and lime spread over the pastures has a double
beneficial influence, acting both as a manure and as a parasiticide.
From May to August is the best time for spreading this dressing.

The fluke embryos are destroyed by 1 to 2 per cent. solutions of common
salt, and by ¾ per cent. solutions of lime.

In over-stocked fields the animals are obliged to graze very close to
the ground, and are thus more exposed to infection. Over-stocking should
therefore be avoided. Animals should not be left too long on the same
ground. If infected they should at once be driven to higher pastures.
Raised water tanks can be placed in the pastures—they are less likely to
become infected. Animals from known infected flocks or herds should not
be purchased. Livers from infected animals should be cooked or
destroyed. If eaten raw by dogs the eggs pass uninjured through the
dog’s intestine and infect fresh pastures.

Sulphate of iron distributed in quantities of 250 to 400 lbs. per acre
is valuable as a manure, and would probably have a greater effect in
destroying the embryos.




                              SECTION III.
                         RESPIRATORY APPARATUS.




                               CHAPTER I.
               EXAMINATION OF THE RESPIRATORY APPARATUS.


From the clinical standpoint a study of the respiratory apparatus
implies the examination of the nostrils, nasal cavities, frontal and
maxillary sinuses, larynx, trachea, and, for the purpose of ascertaining
the condition of the lungs and pleura, of the chest.

=Nasal cavities.= Examination of the external portion of the nasal
cavities is extremely simple. The observer notes the degree to which the
orifices are dilated, the frequency of the respiratory movements and the
condition of the muzzle. He may find various eruptions, crusts due to
discharge, etc., and will remark any peculiarities presented by these.
The depths of the nasal cavities can only be examined through the
nostrils to a very limited extent; but the condition of the pituitary
mucous membrane, its degree of vascularity, and the existence of
ulcerations or of vegetations can be observed.

Digital examination is sometimes useful in discovering the condition of
the lower portions of the turbinated bones. The electric light does not
greatly assist the observer, on account of the narrowness of the air
passages. On the other hand, examination of the face, and palpation and
percussion over the region of the frontal sinuses is of considerable
value. By inspection, one discovers deformity caused by tumours, by
ossific inflammation, or other lesions; and detection is rendered easier
by the fact that deformities are usually asymmetrical, only occurring on
one side.

Palpation reveals the degree of resistance and flexibility of the
external bony wall as well as the condition of the subcutaneous tissues.

Percussion sometimes discloses absolute dulness, due to tumours of the
mucous membrane, of the turbinated bones, or of the bones of the face.

The pharyngeal portion of the nasal cavities is difficult to reach, but
can be examined by passing the hand, palm upwards, into the pharyngeal
cavity, when the fingers may be slipped behind the soft palate and thus
introduced into the posterior nasal chamber. The animals should first be
very carefully secured and a strong gag introduced into the mouth.

=Sinuses.= _Frontal sinus._—The frontal sinus occupies the greater part
of the anterior cranial region and the summit of the head, extending
from the highest point of the poll as far forward as a line drawn
between the two orbits. Above, it directly communicates with the sinus
of the horn core. In this upper region, where it abuts on the sinus of
the opposite side along the median line, it is of greatest size. Below,
on the other hand, it is very narrow, much broken up and incompletely
divided into a series of cells, by thin, bony plates running in all
directions.

[Illustration: $1]

It is in direct communication with the nasal cavity.

The frontal sinus, then, occupies all the supero-lateral portion of the
cranial box, which is thus provided with a double wall. At one point,
however, over a lozenge-shaped area, the cranial cavity is only
protected by a single wall. It is in this region that the slaughterman
strikes the animal when killing it.

The frontal sinus may be examined by inspection and palpation.
Inspection sometimes reveals deformity of the external wall of the
sinus. Such deformity, however, is rare, and Moussu has only observed it
in two cases of tuberculosis of the bones forming the cranial wall.

By percussion one detects abnormal sensibility, and partial or complete
dulness over certain areas.

[Illustration: $1]

_Maxillary sinus._—The maxillary sinus occupies the whole lateral region
of the face, from the inferior extremity of the maxillary spine as far
as the sub-orbito-palatine region. In front its external wall is very
solid, but behind, below the orbit, is extremely thin. Externally the
sinus is largely protected by the anterior insertion of the external
masseter muscle, a fact which explains how rarely it is injured.

=Larynx.= In consequence of its deep situation, the larynx can scarcely
be examined except by inspection, external palpation, internal digital
palpation, and auscultation.

External examination presents no difficulty, and enables one to detect
lesions around or near the larynx.

Palpation reveals the existence of œdematous swellings, enlargements of
the retro-pharyngeal lymphatic glands, inflammatory engorgements, etc.

Internal digital examination, like examination of the pharynx, can only
be performed after very firmly fixing the animal in position, and
inserting a gag in the mouth.

[Illustration: $1]

The hand is introduced, palm downwards, and passed as far as the
pharyngeal cavity. The index finger can then easily be slipped into the
glottis. Exploration must be effected rapidly and without violence. It
reveals the condition of the glottis, the presence, position and form of
growths like myxomata and of new tissues, due to the presence of
actinomyces, as well as tuberculous vegetations or ulcerations.

By auscultation we discover the presence of normal or abnormal laryngeal
sounds—roaring, whistling, or bubbling sounds, etc.

=Trachea.= The trachea may be examined by palpation and auscultation.

Palpation reveals the degree of sensitiveness, abnormalities in position
or form, the presence of peripheral inflammations, fractures of rings,
etc.

Auscultation indicates whether the tracheal sound be normal or
otherwise, or accompanied by abnormal sounds, like mucous _râles_, or by
pathological sounds conveyed from the chest.

=Thorax.= The thorax can be examined by inspection, palpation,
percussion, and auscultation.

By inspection we discover whether the formation of the thorax as a whole
is normal, or whether there exist congenital or acquired deformities,
asymmetry like that produced by pneumo-thorax or deviations of ribs from
the normal line, etc. One also notes the breathing movements, the manner
in which the sides expand and contract, the respiratory rhythm, and any
special peculiarities of inspiration or expiration.

Palpation reveals the degree of sensitiveness of the thoracic wall and
of the intercostal spaces, the existence of more or less extensive local
œdematous infiltration, and the presence or disappearance of thoracic
conditions like hydro-thorax.

Percussion indicates the degree of sonority of the chest in different
parts. It can either be practised directly with the hand or through the
medium of a pleximeter. The latter method is preferable when dealing
with fat animals. Percussion, however, gives slightly different results,
according to the degree of fatness of the subjects. It should be
practised both in a vertical as well as in a horizontal direction.

At all points where the muscles are thick or well developed the results
produced are negative, in the sense that only a dull sound is obtained.
This is the result obtained in auscultating the areas marked =1=, where
one meets with the ileo-spinal and common intercostal muscle, and in
that marked =4=, where the olecranian muscles are encountered (Fig.
166). Over the middle and inferior zones, however, the results are much
more instructive.

On the right side percussion of the middle zone gives, under normal
conditions, a clear sound and perfect resonance from above downwards,
and from in front backwards, between the fourth intercostal space and
the ninth rib. Beyond this point lies the liver, which gives a partial
dull sound, and absolute dulness from the ninth to the twelfth rib, in
consequence of its position, and of the projection of the diaphragm
towards the thoracic cavity.

Percussion of the inferior zone produces less marked resonance, which
diminishes more and more towards the base, in consequence of the
thinness of the pulmonary lobes at this point. This resonance does not
extend as far as the hypochondriac region, because the lower part of the
abomasum insinuates itself beneath the costal cartilages and causes a
region of dulness.

On the left side percussion gives precisely similar results, except in
the upper portion of the middle zone. Beyond the ninth intercostal space
the sound changes, and has a tympanic character; because here the
anterior and upper portions of the rumen are encountered, as they are
lodged beneath the hypochondrium. Below, the sound is dull, on account
of the gastric compartments generally being full of food.

Certain trifling modifications of this normal condition may be noted,
depending on the degree of fatness or thinness of the subjects. The
pathological changes which may occur are as follows:—

A tympanic sound, with or without metallic character, may be found at a
point where normally one would expect a clear sound (pneumo-thorax,
diaphragmatic hernia). A dull sound may be met with in the same regions,
all resonance being lost (pneumonia, broncho-pneumonia, pleural exudate,
etc.). Partial dulness and partial loss of resonance may occur in
regions which ought to give a resonant sound (deep pneumonia,
tuberculous lesions, the presence of echinococcus cysts, etc.).

Auscultation—_i.e._, examination by means of the ear—is the most
valuable method of discovering and localising pulmonary, pleural, or
cardiac lesions.

Various sensations are conveyed to the ear, depending on the method in
which the normal or pathological sounds are produced.

The deductions to be drawn as regards the nature of existing disease are
based on the intensity, character, duration, and special attributes of
the sounds noted.

Direct auscultation is the most certain method, but the ear cannot be
applied with equal facility at all points. Under such circumstances a
simple or binaural stethoscope, or the phonendoscope, may be used with
advantage.

To properly appreciate the sounds heard it is essential to be exactly
acquainted with the relation between the lung and thorax. On the left
side (Fig. 60) the anterior pulmonary lobe occupies the space between
the first and fourth ribs, in front and above the base of the heart. The
middle, or cardiac, lobe covers the left upper and postero-lateral part
of the heart from the fourth to the sixth rib. The posterior lobe
occupies all the region beyond the sixth rib as far as the twelfth.

On the right side the arrangement is similar, but the anterior lobe and
the cardiac lobe are more developed (Fig. 62).

Under ordinary circumstances the extensive movement of the lung which
occurs during inspiration produces a special sound known as the
respiratory or vesicular murmur. Contrary to what has been written, and
said, this sound in animals possessing absolutely sound lungs ends with
inspiration. Expiration is silent, though it is easy to estimate its
duration.

In auscultating the lung, we may distinguish four zones, a superior
zone, a middle zone, an inferior zone, and a scapular zone.

The superior zone is bounded by the vertebro-costal gutter, descends
approximately as far as the inferior line of insertion of the common
intercostal muscle, and extends from the summit of the scapula in front
to the hypochondrium behind.

Auscultation of this region through the ileo-spinal and common
intercostal muscle will always reveal, except in very fat animals, the
vesicular murmur to a point as far back as the eleventh intercostal
space. Nevertheless, this vesicular murmur is relatively feeble, and
becomes imperceptible beyond the eleventh rib.

The middle zone comprises the most convex portion of the ribs, and at
this point the wall of the thorax is thinnest, while the lung below is
thickest.

[Illustration: $1]

For these reasons the vesicular murmur is heard at its maximum intensity
at this point. Towards the upper and lower limits of this zone are found
the great bronchial divisions, so that auscultation should always be
practised with the greatest care at this point. The middle zone occupies
approximately one-third of the total depth of the thorax. The vesicular
murmur becomes weaker as one passes backwards, and finally disappears at
a considerable distance from the angle of the hypochondrium, following a
curved line the convexity of which is directed forwards, and which is
continuous with that limiting the upper zone.

These peculiarities are due to the anatomical arrangement and mode of
insertion of the diaphragm on the internal surface of the hypochondrium.

The inferior zone is very limited, and corresponds externally to the
inferior third of the thorax, and topographically to the cardiac lobe or
middle lobe of the lung and to the inferior portion of the posterior
lobe.

As these pulmonary lobes are of comparatively slight thickness, the
vesicular murmur is feeble. It can be heard over a trapezoidal space,
forming a prolongation of the middle zone, but not below in the region
of the sternum or pectoral muscles.

The fourth zone extends over the mass of the olecranian muscles. It is
of triangular form, in consequence of the inclination of the scapula and
humerus. Except in very fat animals the vesicular murmur is readily
audible through the muscular mass on the right side better than on the
left, on account of the development of the right anterior pulmonary
lobe.

On the left side the beating of the heart is heard above the pulmonary
sounds.

Clinically one may hear an exaggeration of the ordinary respiratory
murmur whenever the lung is actively exercised, as, _e.g._, immediately
after trotting. This exaggeration, however, is often pathological. It is
known as “juvenile or supplementary respiration,” when due to the fact
that some other portion of the lung is not acting.

The respiratory murmur may be lessened in certain morbid conditions,
such as emphysema and congestion of the lung, and may completely
disappear in pneumonia or broncho-pneumonia, a fact which is even of
greater significance.

In various pathological conditions the respiratory murmur may also be
modified. On the other hand, the movement of air in the bronchi also
produces various sounds of importance.

A number of different bronchial sounds may be distinguished; these
include both inspiratory and expiratory sounds, for sometimes an
expiratory sound may become audible and clearly appreciable, or may
acquire characters of the greatest importance.

The inspiratory sound may be strong, rough, rasping, painful, moist or
rattling. The pathological expiratory sounds may vary between audible,
strong, rough, prolonged, or rattling. The varieties of souffle, or
rattle, are the tubal souffle of inspiration or expiration (met with in
pneumonia or broncho-pneumonia); the soft, deep-seated pleuritic souffle
(peripneumonia); the continuous cavernous souffle (met with in
tuberculosis); the broad amphoric souffle, in which the vibrations are
extensive and of metallic character (met with in pneumo-thorax).

As to the varieties of _râles_ which usually accompany these souffles,
they may all be met with in tuberculous animals, and comprise crepitant
and sub-crepitant, mucous, cavernous, snoring and sibilant _râles_.




                              CHAPTER II.
                            NASAL CAVITIES.


                             SIMPLE CORYZA.

Simple acute coryza, or inflammation of the mucous membrane of the nasal
cavities, is of comparatively trifling importance in bovine animals,
and, were it not for the possibility of gangrenous coryza being confused
with it, there would scarcely be any necessity for a special
description.

The onset of coryza is indicated by repeated sneezing and coughing, by
congestion of the pituitary mucous membrane, which soon begins to
secrete abnormally, and by difficulty in respiration, which becomes
snoring or whistling.

The discharge, transparent at first, then mucous and muco-purulent, is
abundant in quantity; the inflammation is arrested at this point or
extends towards the facial sinuses, the pharynx and larynx; the eyes are
swollen and watering, and almost all the characteristic symptoms appear
which mark the onset of gangrenous coryza. Two signs, however, are
wanting. The appetite is fairly well maintained, and the temperature
little above normal. Simple coryza occurs at all times of the year in
consequence of sudden chills, but is commonest in spring and autumn.

At first the distinction between this condition and gangrenous coryza
can only be ascertained after taking the temperature.

=The prognosis= is absolutely favourable, and often in forty-eight hours
every symptom disappears.

=Treatment= is confined to keeping the animals in stables at a suitable
temperature, sheltered from draughts. Emollient fumigations and
inhalations of turpentine, creosote, or eucalyptus oil rapidly check the
more alarming symptoms. Warm drinks and foods and cooked roots are
recommended.

In sheep, acute coryza as a consequence of chills, etc., occurs in
autumn, but is more commonly due to a parasitic cause, viz., invasion of
the nasal cavities by larvæ of certain œstridæ. During the succeeding
winter it continues under the form of chronic coryza, as a result of the
larvæ retaining their position in the sinuses.

Treatment of this parasitic coryza consists in trephining the sinuses
and destroying the larvæ.


                           GANGRENOUS CORYZA.

Gangrenous coryza is a grave disease of diphtheritic character, which at
first seems to be localised in the mucous membrane of the upper
respiratory passages, but which exhibits a tendency to affect all the
mucous membranes of the system.

The term “gangrenous coryza,” adopted in France, has been replaced in
other countries, especially in Germany, by such descriptions as
“contagious disease of the head,” and “malignant catarrhal fever of the
ox.” Old writers describe gangrenous coryza as a disease common in the
Jura, the eastern parts of France generally, and in the valley of the
Saône. In reality this disease occurs everywhere, both in the centre,
west and north of France, as well as in the eastern regions. Serious
outbreaks frequently occur in Germany and Italy.

=Symptoms.= Gangrenous coryza assumes three different forms, which,
however, only represent successive degrees of intensity of the attack.
In the peracute form death occurs in three to five days, even when the
characteristic signs are not all as yet apparent. In the acute, and by
far the most frequent form, the disease lasts from fifteen to twenty
days, and also ends in death in by far the greater number of cases.
Finally, in the form usually termed chronic, the disease lasts from four
to eight weeks, and most frequently ends in recovery.

_Acute and peracute forms._—The onset is marked by very striking
symptoms, which precede the local symptoms by some hours, or by a day or
more.

The temperature rises rapidly from the normal to 103° or 105° Fahr.
(39·5° to 41° C.), or even higher. Appetite and rumination are entirely
suspended; the respiration becomes rapid and difficult, while the heart
beats strongly and tumultuously; the muzzle is dry, the mouth hot, and
salivation so abundant as to suggest an attack of foot-and-mouth
disease. Fæces and urine are only passed at long intervals, and dysuria
is present.

At first everything seems to indicate the development of an acute
infectious disease; but soon afterwards appear local indications
affecting the respiratory, ocular, digestive, urinary, nervous and
cutaneous systems.

The respiratory symptoms are most important, and almost characteristic.
Respiration becomes difficult, rough as in acute coryza, but soon
assumes a snoring character, and is accompanied by a discharge,
containing false membranes, from both nostrils.

The serous and muco-purulent discharge becomes rusty or reddish-brown,
soon acquires a very fœtid smell, and is found to contain epithelial
_débris_ and yellowish-green false membranes. After the least effort to
cough or the slightest touch on the membranes themselves—sometimes
without any visible cause at all—epistaxis sets in, the blood being
mixed with the discharge or simply escaping in the form of reddish
strings, like that occasionally seen in glanders.

The mucous membrane of the nasal cavities is red, turgid, apt to bleed,
and painful to the touch.

Percussion of the nasal cavities, sinuses, and even of the horns reveals
everywhere exceptional sensibility.

Sometimes, but only in certain subjects, the lower portions of the head,
including the muzzle, nostrils, lips and forehead, become infiltrated,
as though the case were one of purpura. Thoracic complications are
rarely absent, unless the disease is treated. Towards the end of the
first week the respiration, still painful and snoring, becomes more
rapid; and auscultation reveals at various points in the lungs areas of
bronchitis and of broncho-pneumonia, indicated by bronchial _râles_,
rattling breathing, and tubal souffles, etc. These complications are
accompanied by attacks of coughing, which increase the discharge, and
may threaten to end in suffocation. This happens when large masses of
false membranes from the bronchi are thrown into the larynx and cannot
readily be ejected through the glottis, which has been reduced in size
by œdematous infiltration and inflammation.

Percussion is generally useless. The appearance of the eyes is also very
significant. These symptoms develop simultaneously with the respiratory
disturbance, and are marked by infiltration of the eyelids, œdematous
conjunctivitis, and ophthalmia. The cornea becomes whitish, infiltrated,
opaque, and sometimes shows ulcerative keratitis; or, on the other hand,
it remains simply semi-transparent, and through it the media of the eye
may be seen to have become opalescent. Ulcerative keratitis may develop
rapidly and end in perforation of the cornea.

In certain rare instances examination with the ophthalmoscope has
revealed the existence of exudative iritis; this condition may be
complicated with syncchia, intra-ocular hæmorrhage, and result in
permanent loss of vision.

These ocular symptoms are accompanied by continuous, abundant and
prolonged discharge of tears, intense photophobia, and exceptional
sensitiveness to manual examination, etc.

Digestive disturbance appears less important, and may be regarded as
consequent on the febrile reaction, the general disturbance, or the
condition of the respiratory apparatus. But complete examination will
show that from the onset of the disease a special form of stomatitis
occurs. From the first the mouth is hot and dry: soon afterwards
abundant reflex salivation occurs, and the discharge, like that from the
nose, becomes excessively fœtid. This stomatitis differs entirely from
ordinary forms of stomatitis and from the stomatitis peculiar to
foot-and-mouth disease, and is characterised by the necrosis of
fragments of epithelium forming false membranes. These on being shed
leave exposed numerous ulcers distributed over the tongue, cheeks, and
lips. Neither vesicles nor pustules are produced, but merely false
membranes of small dimensions.

The false membranes and ulcerations occur on the soft palate and in the
pharynx.

When the patients survive for a certain time, croupal enteritis and
ulcerative enteritis, sometimes accompanied by hæmorrhage, develop. The
administration of enemata is followed by the passage of fæces containing
considerable fragments of epithelium or of streaks of blood. From the
outset these digestive complications are indicated by failure to
ruminate, by cessation of peristalsis and by constipation, which is
usually succeeded by abundant fœtid diarrhœa.

Functional disturbance of the genito-urinary apparatus is rarer, or at
least more difficult to detect. The animals refuse drink; micturition
seems to be suspended or very difficult. The urine may be albuminous or
rose-coloured, in consequence of the presence of hæmatin; more rarely it
is purulent or sanguinolent. There may also be urethritis, cystitis,
pyelitis, and nephritis, with the passage of hyalin cylinders in the
urine, although this is not always the case.

In females the mucous membrane of the vagina and lips of the vulva
usually seem congested and œdematous; but it is rare to find
diphtheritic false membranes, as on the buccal and nasal mucous
membranes, etc. On the other hand, vaginitis and exudative metritis are
common.

Cutaneous outbreaks also constitute important symptoms by which this
disease is recognised. At points where the skin is fine, on the inner
surface of the thighs, around the girth, on the inner surface of the
forearm, and on the mammæ, etc., an exanthematous eruption occurs,
followed later by the development of pustules, which at first sight
might suggest cow-pox.

These pustules are prominently apparent, and can readily be detected on
palpation. They are more or less confluent, hard, and without a
peripheral œdematous zone.

In the case of the mammæ these pustules occur most commonly on the
teats, are round or slightly oval in form, bright red in colour, and
sometimes violet-red. They never become converted into vesico-pustules,
as in cow-pox, or into vesicles; and in no way resemble the skin
eruption peculiar to foot-and-mouth disease.

Certain nervous symptoms have also been described, comprising trembling,
epileptiform convulsions, and paraplegia of the hind quarters.

Moussu has never seen nervous disturbance assume the form of
epileptiform convulsions, and it is possible that the paraplegia
referred to simply marks the last stage of the disease.

=Causation.= The essential cause of gangrenous coryza has not yet been
definitely ascertained. Within recent years teachers of the highest
authority have represented the disease as a general affection belonging
to the hæmorrhagic forms of septicæmia (Nocard and Leclainche). Nocard
has found ovoid bacteria in the false membranes of the larynx, and
Leclainche a paracoli-bacillus in the mesenteric ganglia and the
intestines, but the disease has never been reproduced in a
characteristic and complete form similar to the clinical type.

Other microbes have also been described as occurring in the blood or
discharges; but attempts to transmit the disease by using cultures or
the different morbid products which observers have collected have
invariably failed, and it has therefore been concluded that the disease
is not contagious, but merely infectious.

Moussu does not regard this disease as a hæmorrhagic septicæmia, because
the blood proves sterile unless grave pulmonary, intestinal or renal
complications occur, and because the disease appears capable of being
cured in a short time by simple methods. In the present state of
knowledge he prefers to regard it as an infectious disease of
diphtheritic form, at first localised in the upper respiratory and
digestive tracts, always tending towards a grave toxæmia, and towards
complications due to various other infections.

Even though direct contagion has not been proved, it is impossible to
doubt that stables may become infected. This is sufficiently proved by
the continued appearance of the disease when disinfection is neglected
after the occurrence of the first case.

It is possible that the causes formerly assigned—viz., chills, the
influence of draughts, and a morbid predisposition—may increase
susceptibility in animals otherwise well cared for, but it is quite
certain that infection of the stable is an important factor.

=Lesions.= The lesions vary with the complications, but those shown in
the beginning are always identical. The mucous membrane of the nasal
cavities is congested, inflamed, sphacelated, and ulcerated at different
points. The turbinated bones and the ethmoid cells may become necrotic;
in the larynx the region of the glottis is always most markedly
affected; the mucous membrane becomes ulcerated in the neighbourhood of
the vocal cords, and the tissues may become more deeply attacked.

In the trachea and bronchi the mucous membrane undergoes desquamation,
and may become ulcerated at the points where false membranes have
formed. The mucous membrane of the sinuses is always affected, but is
rarely ulcerated.

Such complications as capillary bronchitis, broncho-pneumonia, and
gangrene of the lung may be noted.

The mucous membrane of the mouth presents a violet-red or blackish-red
colour; the tongue and gums are swollen, and ulcers as large as a lentil
or a halfpenny may occur either singly or in a confluent form.

The genito-urinary apparatus reveals signs of croupal cystitis,
submucous effusions of blood, vaginitis with the formation of false
membranes, acute pyelitis, etc.

=Diagnosis.= When the symptoms are fully developed the diagnosis of
gangrenous coryza is extremely simple, but the absence of some of these
may justify hesitation in forming an opinion. If the examination is
carefully carried out, it is always possible to distinguish this disease
from simple coryza, which is only accompanied by trifling fever, and in
which appetite is preserved; from foot-and-mouth disease, with its very
characteristic buccal eruption and absence of lesions from the upper
portions of the respiratory tract; and from contagious ophthalmia.

=Prognosis.= Up to the present time the prognosis has always been
regarded as extremely grave, the mortality being sometimes as high as
from 90 to 100 per cent., and moreover the cases which recover are
invariably those of what is considered the chronic form. Sudden sinking
of temperature during the disease is an unfavourable sign. From 1894 to
1900 Moussu never cured a single case, whatever his method of treatment;
nevertheless, it now seems possible to regard the condition a little
more hopefully, provided that no incurable complication occurs before
the beginning of treatment.

=Treatment.= Of all the modes of treatment suggested—viz., anti-febrile
agents, general stimulants, purgatives, diuretics, external stimulant
applications, etc.—none have succeeded. Antiseptics injected into the
nasal cavities, antiseptics given internally, milk diet, and all the
methods hitherto suggested are equally useless.

The only treatment which appears to have achieved any degree of success
is that of injecting physiological salt solution in large doses (up to
six quarts per day, divided into three parts). All the animals treated
by this method recovered, provided they presented no broncho-pulmonary
complications.

The sole inconvenience of this treatment is the difficulty in carrying
it out when the animals are at a distance from the practitioner. It is
indispensable that they should be close at hand, in order that he
himself may make the injections at the proper time. There is some reason
for hoping, however, that serum from animals which have recovered will
prove to be more active than saline injections.

This method of treatment should be followed up by the most rigid
hygienic precautions. The mouth, nasal cavities and eyes should
frequently be washed with antiseptic solutions. The stables should be
freely ventilated, and the floors and bed kept in the cleanest possible
condition, etc.

Whenever a case of gangrenous coryza is observed it should be isolated,
and the stables should most carefully be disinfected.


                     TUMOURS OF THE NASAL CAVITIES.

Apart from actinomycosis of the upper jaw, tumours of the nasal cavities
or of the sinuses are not frequent in bovine animals. They are, however,
occasionally met with, and present symptoms which must be carefully
studied in order to avoid errors of diagnosis. Usually they are of the
nature of myxomata, more rarely of fibro-myxomata.

[Illustration: $1]

=Symptoms.= The dominant symptom is difficulty in breathing, both when
moving and eating, a difficulty which is sometimes so considerable as to
cause snoring respiration or roaring. Nevertheless, examination of the
trachea and of the lung, visual examination of the lower portions of the
nasal cavities, and manual examination of the pharynx, larynx and
glottis give only negative results. It may even happen, as occurred in
the case from which the illustration herewith was taken, that percussion
of the maxillary sinus reveals normal resonance.

In the case of tumours of small size the forehead is not deformed. When,
on the other hand, the tumour partly obstructs the nasal cavities it may
thrust on one side the septum nasi and externally cause well-marked
asymmetry of the face. Sero-mucous or muco-purulent discharge then
occurs.

=The diagnosis= is somewhat difficult, for continuous or temporary
roaring (or at any rate difficulty of respiration), being the dominant
symptom, must be distinguished from roaring due to a laryngeal lesion
like paralysis or tumour formation, from perilaryngeal compression due
to enlarged retro-pharyngeal glands, and from tracheal or pulmonary
lesions; and its origin must be located in the nasal cavities.

[Illustration: $1]

=The prognosis= is grave, in consequence of the difficulty of exploring
the depth of these cavities and of the possible nature of the tumour.
Nevertheless, in the case of simple myxomata permanent recovery usually
follows extirpation.

=Treatment= is confined to extirpation, which is quite possible in the
case of pedunculated tumours; in the case of sessile tumours free
trepanation of the roof of the nasal cavities becomes necessary. The
operation is quite safe.


        PURULENT COLLECTIONS IN THE NASAL SINUSES. NASAL GLEET.

From the clinical point of view two varieties of this condition may be
distinguished—inflammation of the mucous membrane of the maxillary sinus
and inflammation of the mucous membrane of the frontal sinus and of the
horn core. These forms of inflammation frequently lead to suppuration.
The pus collects in the depressions and divisions of the frontal or
maxillary sinus.


               PURULENT COLLECTIONS IN THE FRONTAL SINUS.

=Causation.= In the majority of cases inflammation of the mucous
membrane of the frontal sinus is produced by external causes: fractures
of the horns and horn core accompanied by hæmorrhage into the horn core;
fractures of the horn with exposure of the sinus of the horn core;
wounds and violent blows on the occipital region or the frontal bone;
cracks or depressions of the external wall of the sinus, etc.

In all these cases, whether blood is effused or the mucous membrane of
the sinus is merely infiltrated with serum, infection may be produced by
germs being deposited from the air passing through the nasal cavities
and causing suppuration.

Purulent collections in the frontal sinus may result from continued
irritation, like that due to a badly fitting yoke. They also occur as an
accidental complication of general diseases like gangrenous coryza.

=Symptoms.= The catarrh or purulent collection in the sinus may be
unilateral or bilateral, and the symptoms vary, according to the form
which it assumes.

_Unilateral collections._—Nasal hæmorrhage is often the first symptom,
but this is often regarded as of little importance, because the
formation of pus does not occur until very much later. The animal shows
ill-defined pain, loses appetite, remains dull and somnolent, and
carries its head on one side. The horn on the injured side is hot and
sensitive, and at a later stage the eye becomes affected by contiguity
of tissue. It is then swollen, closed, and watery; the conjunctiva is
infiltrated, and somewhat inflamed. Sensibility and partial or complete
dulness of the affected side may be detected by palpation and
percussion. On the animal being made to cough, a yellowish or
greyish-white discharge of very fœtid and sometimes putrid character
escapes.

_Bilateral collections._—Catarrh is rarely bilateral at first; but if
the unilateral lesion is not treated, it affects the median septum
dividing the two cavities, and the inflammation extends to the second
sinus. The animal then shows dull pain, and exhibits marked depression;
sometimes it appears quite prostrate. The head is carried low and
inclined towards the ground, while the above-mentioned ocular symptoms
and the indications furnished by palpation and percussion extend to both
sides. Coughing produces momentarily a double discharge, which the
animal disposes of after the fashion of horned cattle.

=Diagnosis.= The diagnosis only presents difficulty in the early stages.
Later the warmth and sensitiveness of the horns, the partial dulness,
offensive character of the discharge, etc., render diagnosis easy.

The disease is not likely to be mistaken for gangrenous coryza, despite
the condition of the eyes, because it develops slowly, progressively,
and without marked fever.

=Prognosis.= If treated early, unilateral or bilateral collections of
pus in the sinuses are capable of cure, but later when bodily health is
impaired and the local lesions of the mucous membrane very pronounced,
there is less chance of success.

=Lesions.= The initial lesions consist in cracks, fissures, or fractures
of the bones of the face or exostoses of traumatic origin. In other
cases the mucous membrane alone is affected. As a result of chronic
irritation it becomes thickened, inflamed, and ulcerated, and granulates
freely. The depressions in the sinuses contain grumous, fœtid pus, which
irritates the surrounding tissues and produces pain and general symptoms
of cerebral irritation, which are sometimes very disquieting.

=Treatment.= Numerous methods of treatment were formerly recommended,
such as absolute rest, bleeding, cold affusions, perforation of a horn,
section of a horn, etc. None of these is of any value.

At first, provided only a certain degree of sensitiveness and simple
catarrh without suppuration exist, antiseptic fumigations with tar,
carbolic acid, thymol, etc., are useful; but later, when pus has formed,
they are useless. At this period the only rational and efficacious
treatment consists in trepanation. In unilateral collections three
openings are necessary.

The first is an opening into the sinus of the horn core. It is made ⅜ to
¾ of an inch above the horn-secreting band of the horn. It must not be
forgotten, however, in planning such an opening that the sinus of the
horn core only exists in a rudimentary condition in young animals, and
that it is scarcely possible to trephine the horns before the patient is
three years of age.

The second opening is made towards the upper part of the frontal sinus
about ¾ inch below the horn-secreting ring at the base of the horn and
in a line with the axis of the horn core itself. Whatever the animal’s
age and however little the sinuses may be developed, this opening is
certain to expose the cavity of the frontal sinus.

In old animals where the frontal sinus is enormously developed, and
where very large depressions exist in the orbital region, a third
opening should be made just above a transverse line uniting the upper
margins of the two orbits and inside the suborbital suture.

These openings having been made, treatment consists—firstly, in
completely washing out the cavity with boiled water, cooled to 95° or
100° Fahr.; and, secondly, in injecting antiseptic and astringent
solutions so as to check the formation of pus. Among such may be
mentioned 3 per cent. carbolic solution, 5 per cent. carbolic glycerine,
2 per cent. solution of iodine in iodide of potassium, etc.

Whatever the drugs employed, the cavities should be washed out every
day, first with plain sterilised water, and then with antiseptic
solutions at the body temperature, since cold solutions often cause
inflammation of the mucous membrane of the opposite sinus.


              PURULENT COLLECTIONS IN THE MAXILLARY SINUS.

This disease is much rarer than that of the frontal sinus, and only
within the last few years (Ries, 1899) has a really good description
been given of it.

=The causation= is imperfectly understood. Injuries to the suborbital
region and maxillary ridge, caries of the molar teeth, and inflammation
occurring during the development of general diseases represent the
principal causes.

The dominating and characteristic symptom of the presence of pus in the
maxillary sinus consists in incessant snorting, accompanied by violent
movements of the head and the discharge of purulent or muco-purulent
material.

At the beginning of these attacks of snorting, which are produced by the
reflux of pus from the sinus towards the nasal cavities, the respiration
becomes snoring and rapid, and the animal makes sniffing movements as
though the nasal cavities were partially obstructed. After these crises,
the respiration again becomes silent.

Contrary to what has been observed in purulent collections in the
frontal sinus, the discharge is unilateral, reddish yellow in colour,
viscous in consistence, and is accompanied by clots of a gelatinous
material or even of blood.

During the attacks of snorting, the discharge resembles that of croupal
or pseudo-membranous bronchitis, but the material discharged is not
moulded on the internal shape of the bronchi. The masses of discharge
are irregular in form, and appear as though made up of fibrous tissue
matted together. Attention having been attracted by the discharge,
exploration of the trachea and chest reveals nothing; on an examination
of the sinuses, however, palpation and percussion betray a certain
amount of sensitiveness, together with partial or complete dulness, and
the lesion is discovered.

=Diagnosis.= Confusion between pus formation in the maxillary and
frontal sinuses can be avoided by careful examination.

=Prognosis.= The prognosis is not very grave; the animals maintain their
appetite, but become thinner, and the condition shows no tendency to
spontaneous cure.

=Treatment.= The only rational treatment consists in trephining, an
operation practised immediately above the maxillary tuberosity and over
the lowest part of the sinus (Fig. 164). This opening allows the cavity
to be washed out and the sinus drained.

Antiseptic treatment exactly resembles that of purulent collections in
the frontal sinus. Injections of astringents, dilute carbolic acid and
iodine solutions, etc., are recommended.


              ŒSTRUS LARVÆ IN THE FACIAL SINUSES OF SHEEP.

(FALSE STURDY.)

=Causation.= This disease of sheep, which sometimes produces vertigo
resembling that shown in gid or sturdy, is produced by the growth of
larvæ of _Œstrus ovis_ in the frontal sinuses. The œstrus of the sheep
assumes perfect insect form during the fine days of summer from July to
September. The females swarm around the flocks and attempt to alight on
the animal’s head close to the nostrils, where they deposit their eggs
or larvæ. The larvæ crawl into the nostrils, thence into the nasal
cavities, the meatus, and finally the sinuses, where they become fixed.
In these sinuses they undergo complete development, increasing from a
length of about ⅒ inch to from ¾ to 1 inch before their transformation
into the nymph and perfect insect. They remain in the sinus for eight to
ten months. When numerous and well developed they may fill the whole of
the cavity.

=Symptoms.= It is easy for a careful observer to note the time at which
the larvæ penetrate the sinus. During the hottest hours of the day the
adult insects are continually hovering over the flocks, and on watching
carefully one sees sheep suddenly become excited, tap with their feet,
rub their faces against any hard, resisting object in the neighbourhood,
plunge their nostrils into the dust, and snort violently.

When the larvæ have penetrated the nasal cavities they produce frequent
attacks of sneezing by irritating the mucous membrane, and cause an
intense sero-mucous and afterwards a moderate muco-purulent coryza. As
long as the larvæ remain of small size, the apparent results they
produce are insignificant, as during the first months of winter; but
when they are numerous, and have become of considerable size, they cause
symptoms which might suggest an attack of gid or sturdy.

Thus the bodily movements become spasmodic, the gait irregular, and the
animals show attacks of vertigo. They stagger and fall, making
convulsing movements, grinding their teeth and rolling their eyes, while
frothy saliva escapes from the mouth, etc.

Death may occur during such attacks, which, however, are happily very
rare. Most commonly the animals are simply dull and somnolent. They feed
badly, carry their heads low, and sometimes hide themselves under the
mangers or in corners.

In exceptional circumstances they bury their heads in the wool or carry
them high in the air in walking, while they lift their front legs high,
with a stepping movement.

[Illustration: $1]

=Diagnosis.= The diagnosis of parasitic invasion of the sinus in the
sheep is rather difficult, because certain of the symptoms suggest gid.
One never finds the signs of true gid, however, and, on the other hand,
a certain amount of discharge and attacks of snorting always exist.
Finally, gid (cœnurosis) only attacks young animals, whilst the larvæ of
œstridæ are commonest in adults.

To confound the disease with verminous bronchitis is still less likely,
for although a discharge exists in both cases, this is accompanied by
cough in bronchitis, and only by sneezing attacks in infection of the
sinuses.

Finally, in bronchitis, histological examination leads to the discovery
of eggs or embryos of the strongyles. The diagnosis becomes very easy on
post-mortem examination, the identification of the larvæ of œstridæ
being extremely simple.

=Prognosis.= The prognosis is only grave when infestation is very
pronounced. Most commonly the parasites complete their development
without producing disquieting symptoms; as summer approaches they are
expelled and recovery occurs.

=Lesions.= The only lesions consist in very active inflammation of the
mucous membrane of the sinus, which appears excessively hypertrophied,
and in the existence of larvæ. These develop in the midst of a magma of
purulent, fœtid discharge. The number of parasites usually ranges from
two to twenty, although Zürn declares that he has found as many as
eighty in one subject.

=Treatment.= Many precautions have been suggested for preventing
infestation. Many are impossible or difficult to carry out in current
practice, even the soaking of the nostrils in empyreumatic oil, and the
majority are useless. The only suggestion to which we attribute any
importance consists in trying to prevent the perfect insects from
obtaining a lodgment in cavities in the walls or roofs of sheep-sheds.

The really efficacious modes of treatment are also few in number, for
the larvæ are so firmly lodged in the mucous membrane of the sinuses
that they can only be detached after these have been trephined. The use
of nasal injections, embrocations and powders, with the object of making
the animal sneeze, are ineffectual.

Trepanation should not be performed until it is quite clear that the
flock is badly infested, and when serious symptoms appear to threaten
the lives of some of the animals.

The operation, although very simple, requires care on account of the
thinness of the bones.

The anatomical directions are the middle line of the head, and a
transverse line uniting the upper margin of the two orbits. The orifices
are made in the two lower angles produced by the intersection of these
lines (Fig. 169).

It is then easy to remove with the fingers or forceps the larvæ situated
immediately below the point of trepanation, and afterwards to wash out
thoroughly the cavities of the sinuses. If some lie at points which
cannot be directly reached, they can be killed by injecting a little
benzine and water. This proceeding is quite safe.




                              CHAPTER III.
                      LARYNX, TRACHEA AND BRONCHI.


                              LARYNGITIS.

Laryngeal diseases are common, but are usually only the local expression
of some grave general infection, such as foot-and-mouth disease,
gangrenous coryza, or tuberculosis. Pathological conditions such as
these can be disregarded for the moment, as they will receive attention
under special heads.

The two current forms of laryngeal disease are acute laryngitis and
stridulous laryngitis.


                           ACUTE LARYNGITIS.

Acute laryngitis, like simple coryza, of which it is often only an
accompaniment, is caused by chill, by irritant vapours, by smoke, etc.,
or by external traumatic causes.

The cough is dry and painful at first; afterwards it is accompanied by a
discharge or by the swallowing of mucus or muco-purulent products. The
respiration sometimes appears accelerated and difficult, but roaring or
whistling and marked fever are rare. The slightest pressure over the
laryngeal region causes pain and attacks of coughing. The respiration is
normal while the animal is at rest, provided that the laryngitis remains
localised; frequently, however, it is complicated with bronchitis.

The appetite is somewhat diminished, but all these symptoms very rapidly
improve.

=The diagnosis= is based on the frequency of the cough and the
sensitiveness of the throat region.

=The prognosis= is favourable in cases of simple laryngitis.

=Treatment= consists in the administration of steam inhalations, warm
drinks, the application of mustard plasters or blisters around the
laryngeal region, and the administration of expectorants to facilitate
mucous discharge.


                     PSEUDO-MEMBRANOUS LARYNGITIS.

Pseudo-membranous laryngitis, also termed by German authors croupal or
diphtheritic laryngitis, because it bears a certain resemblance to human
croup, is characterised by the formation of false membranes on the vocal
cords, arytenoid cartilages, and subglottal region, etc.

In France it has been described under the name of stridulous laryngitis,
because its dominant symptom consists in attacks of intense dyspnœa,
during which the respiration is accompanied by whistling. Without making
any attempt to prejudge the nature of the disease, which resembles the
pseudo-diphtheritic forms of laryngitis in man, we prefer the term
pseudo-membranous laryngitis. Moreover, this pseudo-membranous
laryngitis very frequently accompanies pseudo-membranous sore throat,
tracheitis and bronchitis, with formation of false membranes.

=Causation.= The causes suggested are similar to those of simple sore
throat: they include chills, the ingestion of ice-cold water, or the
inhalation of irritant gases, during outbreaks of fire, etc., etc.; but
it is quite certain that here, as in many similar cases, a primarily
simple laryngitis is complicated by a well-marked infection.

=Symptoms.= The general symptoms seen during the early stages consist in
loss of appetite, general depression, rigors, and a rise in temperature
of 1° to 2° Fahr.

Then, after twenty-four or forty-eight hours, the respiration becomes
more rapid, difficult, whistling and dyspnœic, with intermittent attacks
of suffocation.

Examination of the chest gives negative results, but, on the throat
being manipulated, the slightest pressure exercised over the larynx
produces attacks of coughing. During the first few days these attacks
are loud, spasmodic, and difficult, but on succeeding days they lead to
the discharge, from the nostrils or mouth, of masses of false membrane
accompanied by whitish and sometimes blood-stained fluid. Secondarily
the mucous membrane of the nasal fossæ appears inflamed to a varying
degree. The conjunctiva is also affected, the eyes are watering. An
important symptom consists in the fact that this watering is accompanied
by internal ophthalmia, as in gangrenous coryza.

In consequence of the respiratory difficulty, the animal takes up a
characteristic attitude, holding its neck stiffly in a horizontal
position and its head completely extended; the nostrils are widely
dilated. When the disease is fully-developed rumination is suppressed,
the bowels are constipated and the fæces are coated as in grave cases of
enteritis, the yield of milk diminishes, the heart beats feebly, the
pulse remains small; death may occur from asphyxia, and probably also
from intoxication.

The disease usually lasts from eight to ten days, but death may occur
earlier. In the majority of cases, however, the animal can be saved. All
the symptoms diminish, the temperature falls, rumination again appears
and with it appetite, and the whole condition becomes normal. Many
animals, however, remain thin and recover slowly; these are principally
cases which have suffered from pseudo-membranous bronchitis.

=Lesions.= The lesions may be confined to the larynx, but may also
invade neighbouring cavities. They consist in the formation of
mucoalbuminous and fibrinous exudates, covering the mucous membrane in
superposed layers, penetrating the epithelial stratum, and adhering so
strongly to the corium that attempts to loosen them cause the deeper
seated structures to bleed.

=Diagnosis.= The symptoms are sufficiently well marked to prevent any
confusion arising except with gangrenous coryza, but in this case there
is no ophthalmia lesion of the nasal cavities, cutaneous eruption, or
eruption over the claws.

=The prognosis= is grave when the disease attacks debilitated or
exhausted animals.

=The treatment= is confined entirely to treating symptoms. As in all
acute inflammatory affections, moderate bleeding, sinapisms over the
region of the larynx, repeated as often as necessary, or applications of
antimonial ointment have been recommended. Applications of moxas or
setons in the neighbourhood of the dewlap might possibly prove of value.

Internally tartar emetic, in doses proportioned to the size of the
animal (2½ to 3 drachms in adults), has been recommended; also iodide of
potassium.

General stimulants, like alcohol, coffee, tea, acetate of ammonia, and
suitable hygienic conditions suggest themselves. Tepid drinks can be
given freely. Nourishing and easily digested food, and a ration of milk
complete the treatment.

Emollient and antiseptic fumigations are also of value, as in ordinary
sore throat or laryngitis, for they favour the separation and discharge
of the false membranes.


                         TUMOURS OF THE LARYNX.

Acute forms of pseudo-membranous laryngitis, or even tuberculous
laryngitis, are not the only diseases which affect the larynx. It is by
no means exceptional to discover intra-laryngeal tumours, mucous polypi,
tuberculomes, and growths due to actinomyces, etc.

The presence of these tumours is indicated by difficulty in respiration,
fits of coughing, and threatened suffocation, accompanied by discharges
of varying character.

When the tumour is largely sessile, the respiration may simply be
snoring or whistling, without any suggestion of suffocation; but if, on
the other hand, it is pedunculated, displacement of the polypus produced
by the currents of air during inspiration and expiration causes spasm of
the glottis, fits of coughing and threatened suffocation.

=The diagnosis= is not always easy, though examination of the nasal
cavities, the sinuses, trachea and chest gives negative results.
Auscultation of the larynx may suggest the existence of the lesion, but
an exact diagnosis can only be attained by digital examination of the
larynx through the pharynx.

[Illustration: $1]

=The prognosis= of these tumours is grave, because death from asphyxia
may occur during an attack of coughing or as a consequence of the fits
of suffocation.

=Treatment.= As it is usually extremely difficult, if not impossible, to
discover the exact nature of the tumour, medical treatment, except for
instance in the case of actinomycosis, is of very uncertain value.

Surgical treatment alone suggests itself. Before attempting an operation
tracheotomy should be performed and a metal canula inserted. The animal
having been cast, and the upper laryngeal region anæsthetised by means
of cocaine, a vertical incision is made in the median line below the
larynx, passing through the skin, the vertical junction between the neck
muscles and the three first circles of the trachea, and access is thus
obtained to the larynx and subglottal region. The operation should only
be performed in exceptional cases, such as that of a valuable stud
animal.

Provided that the new growth has a well-developed pedicle it can be
removed through the mouth by the use of an _écraseur_ or simply by
tearing out.


                              BRONCHITIS.

Diseases of the bronchi in bovine animals reveal very different
characters, according to the nature of the primary cause, for which
reason cases occur of simple acute bronchitis, verminous bronchitis,
simple chronic bronchitis, pseudo-membranous bronchitis, tuberculous
bronchitis, etc.


                        SIMPLE ACUTE BRONCHITIS.

Simple acute bronchitis co-exists with, or is often only the logical and
inevitable complication of, coryza and acute laryngitis. It is commonly
associated with inflammation of the mucous membrane of the trachea.

It accompanies cold and wet seasons, and usually appears with the autumn
frosts, in animals still at grass. In animals under shelter it occurs
after undue exertion followed by chills, and after sudden rain storms.
It also attacks working oxen, which are much exposed to the weather.

=The symptoms= follow very rapidly on the determining cause. They are
ushered in by rigors, trembling attacks, diminution or loss of appetite,
arrest of rumination, acceleration of breathing, and the appearance of a
rough and spasmodic cough.

In ordinary cases these symptoms rapidly diminish, even without
treatment. The appetite again becomes moderate, rumination returns, but
the cough remains more or less rough and spasmodic, ending in the
discharge, or more often in the swallowing, of abundant bronchial mucus.

This is the condition at the period of crisis. Percussion of the thorax
reveals normal resonance. On auscultation of the sides during the period
of onset, rough _râles_ are heard, which at the period of crisis are
replaced by mucous _râles_. The cough diminishes in frequency, and after
a fortnight everything again becomes normal.

=The diagnosis= is very easy, the important point being not to confuse
common bronchitis with tuberculous bronchitis, which very often assumes
a chronic form.

=Prognosis.= The prognosis is not grave, even though the disease may
assume a chronic condition.

=Treatment= does not differ from that of acute bronchitis in the horse.
It consists in antiseptic and steam fumigations, tepid drinks, the
administration of doses of 2 to 3 drachms Kerme’s mineral in adult
animals, and of 1 to 1½ drachms of iodide of potassium, given in a mash
or in honey electuary. During convalescence tar water should be
administered.


                          CHRONIC BRONCHITIS.

Chronic inflammation of the mucous membrane of the large bronchi and
trachea may follow acute bronchitis, but it is also a frequent
termination of verminous bronchitis. It is found in fully developed
animals, adult or old, and particularly in those inhabiting wet, cold
valleys.

It is characterised by frequent paroxysms of coughing, which appear on
the slightest provocation, such as the action of cold air on leaving the
stable or of the air of a confined space on animals returning from the
open; concussion of the chest by the pleximeter, squeezing of the loins,
rapid movement, etc.

This coughing is accompanied by the discharge of mucus, which rarely
arrives at the nostrils, but is swallowed in passing through the
pharynx. Such mucus is always thick, greenish yellow in colour, and
without smell.

The respiration, although regular whilst the animal is at rest, becomes
accelerated on moving, and after attacks of coughing. It is sometimes
rapid and whistling.

Percussion discloses neither partial nor complete dulness, but
everywhere irregularly distributed mucous rattling and sibilant _râles_
are revealed by auscultation.

There is no fever, the appetite is maintained, and, what is an even more
important point, animals in good condition preserve their flesh.
Interlobular pulmonary emphysema and emphysema resulting from dilatation
are inseparable accompaniments of chronic bronchitis, for which reason
the flank respiratory movement is frequently very marked.

=The diagnosis= is of only moderate difficulty, because although in
certain conditions the disease may be mistaken for tuberculosis or
emphysema, it can be distinguished by bacteriological examination of the
discharge, by an injection of tuberculin, by careful auscultation, and
by consideration of the general condition.

=Lesions.= The walls of the bronchi are thickened, the submucous
connective tissue is sclerosed, the muscular fibres are modified in
structure, and have become fibrous, while the epithelial layer is
desquamated and suppurating. The peribronchial tissue also undergoes
sclerosis, and in certain cases the smaller bronchi present marked
dilatations resembling small caverns (bronchi-ecstasis).

=Treatment= can never be more than palliative; the aim should be to
prevent the lesions becoming aggravated, and to check the pathological
secretion from the bronchi, but the lesions already existent can never
be removed. Tar water should be perseveringly administered. Essence of
turpentine in doses of 2 to 2½ drachms per day in electuary (adults),
creosote in doses of 1¼ to 1½ drachms, and terpine in doses of ¾ to 1
drachm give the best results, and produce a marked improvement.


                     PSEUDO-MEMBRANOUS BRONCHITIS.

The pseudo-membranous forms of bronchitis, formerly termed “croupal or
diphtheritic bronchitis,” are rare. They develop suddenly or follow
pseudo-membranous laryngitis. Like the latter, they are due to a
specific infection, possibly aided by accidental causes.

Their =causation= is imperfectly understood, and they cannot be
compared, still less homologated, with diphtheritic disorders in man.
They are characterised by the formation of false membranes, which
develop on the mucous surface, mould themselves over the internal
surface of the large bronchi, and ramify throughout the bronchial
channels like branches of trees. They are of greyish-yellow colour, and
appear to be formed of fibrin, coagulated albumen, and epithelial
_débris_ cemented together with mucus.

=Symptoms.= At the outset these pseudo-membranous forms of bronchitis
have the same characters as acute bronchitis, which at the crisis would
be marked by the expulsion of fragments of false membrane by coughing.
Most frequently it seems that the bronchitis follows its regular course,
and in such case it is only during convalescence or a considerable time
afterwards that the membranes begin to be discharged during paroxysms of
coughing.

The patients are subject to intense dyspnœa, appear about to suffocate,
and during the efforts then made the false membranes are discharged in
the form of half-organised layers, or, on the other hand, in branched
masses, resembling twigs.

The dyspnœa at once ceases. Despite the development of these false
membranes in the bronchi, no alarming symptoms are produced, which is
explained by the fact of the false membranes being adherent only to the
inner surface of the principal conduits, without closing or even
markedly obstructing them or the smaller passages leading to the
pulmonary alveoli. When, however, they are displaced, violent reflex
spasms are produced as soon as the fragments approach the larynx.

=Diagnosis.= The diagnosis rests entirely on examination of the
expectorated material.

So far as the =prognosis= is concerned, it is less grave than might be
supposed from the symptoms. The gravity arises from the fact that this
disease has a certain tendency to become chronic.

=Treatment= scarcely differs from that of ordinary bronchitis. Tar,
creosote in doses of 2½ to 5 drachms given in oil; terpine in doses of ½
to ¾ drachms per day can be recommended. Iodide of potassium also has
certain advantages.


     VERMINOUS BRONCHITIS IN SHEEP AND CATTLE (HUSK, HOOSE, ETC.).

Lambs, young sheep, and calves sometimes suffer severely from
infestation with lung worms, which set up great irritation in the
bronchial passages, leading to chronic bronchitis. The animals show
frequent attacks of paroxysmal coughing, during which some of the
parasites may be expelled. The irritation produced causes serious loss
of condition, and if not alleviated may lead to death. The parasite of
the sheep is known as _Strongylus filaria_ (sheep lungworm), that of the
calf _Strongylus micrurus_. The worms are from 2 to 4 inches long,
whitish in colour, and of the diameter of a hat-pin.

=Treatment.= According to generally accepted views among veterinarians
and zoologists, it is a comparatively simple matter to kill worms in the
bronchial tubes, and a number of cases of the disease are reported in
literature which are alleged to have been cured. These views, however,
are open to very serious doubt.

Neumann (1892b, pp. 590, 591, 593, 594) summarises the subject of
treatment as follows:—

Two different procedures in treatment are pursued. In one, substances
are passed into the digestive canal, which, being diffused in the blood,
are believed to be capable of attacking the worms in the bronchial
tubes. With this view, the picrate of potash (0·20 to 0·40 gram per
head) is given, dissolved in thin gruel or mucilage; creosote; oil of
turpentine; a mixture of equal parts of oil of turpentine and tincture
of camphor—a teaspoonful every day to each lamb in a mucilaginous fluid;
a mixture of creosote 120 grams, spirits of wine 500 grams, and water
700 grams—an ordinary spoonful every day to each animal; or creosote 60
grams, benzine 300 grams, water 2 litres—an ordinary spoonful given
every day for eight days to each sheep. Hall states he has successfully
employed prussic acid in ten-drop doses, morning and evening.

But experience has shown that, while such treatment is troublesome to
carry out, its efficacy cannot be relied upon.

Success is more certain with fumigations, as they penetrate directly to
the worms, stupefy them, and induce fits of coughing that cause
expulsion. They are practised in buildings from which all forage is
previously removed, and which are well closed. Into these the diseased
[animals] are introduced, and on a red-hot shovel are placed rags,
horns, feathers, hair, old pieces of leather, empyreumatic oil, tar,
juniper berries, asafetida, etc. The intensity, duration, and number of
these fumigations are graduated as the sheep become accustomed to them.
At first once a day may suffice, and then the intensity should be
moderate and the duration about ten minutes; afterwards two, and finally
three, may be given during the day, each lasting for twenty minutes.
Kowalewsky says he has obtained very good results from similar
fumigations. Fumigations with chlorine, sulphur, and sulphuret of
mercury or cinnabar have been recommended, but they are dangerous.

(Stephen recommends as follows: Put about forty lambs at a time into an
air-tight house, and place tar, sulphur, and turpentine in a pot of
burning coals, suspended by a chain from the ceiling and brought as near
to the heads of the animals as possible; the fumes are to be allowed to
fill the house, and more ingredients are added as required, the lambs
being kept in the place for twenty-five minutes each time, and the
process to be repeated on three occasions.)

Tracheal injections in the verminous bronchitis of calves are of great
utility; but for a flock of sheep they would be troublesome and
difficult to administer. However, Nieman, has successfully employed them
on 384 sheep belonging to several small owners. He used a solution of 2
parts iodine and 10 parts iodide of potassium in 100 parts of distilled
water. This fluid was mixed, in equal parts, with oil of turpentine, and
made into an emulsion with olive oil; each sheep received 5 to 8 grams
of the mixture, and the number of the injections varied according to the
gravity of the disease—from two to three at two days’ interval. The
worms were killed and expelled during the paroxysms of coughing, and the
bronchitis was modified.

The medical treatment should be assisted by very nourishing food, and by
bitter, stimulating, and ferruginous tonics, which arouse the digestive
functions and allow those animals which are least exhausted to reach the
period of elimination of the parasites.

At the commencement of any kind of treatment it is well to have an
examination of the flock, with the object of sending the worst cases to
the butcher.

The same medicaments have been employed in treating this malady in
calves as in that of sheep, and no better results have been obtained.
Neumann and Janné have, however, been successful with asafetida (30
grams), Chabert’s empyreumatic oil (60 grams), and a mucilaginous
decoction (500 grams)—a spoonful of this mixture being given in a half
litre of milk, and the treatment continued for about a month.

The results are less uncertain if the worms lodged in the bronchial
tubes are directly acted upon, either by means of injections of the same
kind as those employed for sheep, or fluid medicaments introduced
directly into the bronchi.

Read says he has cured calves worn down almost to skeletons by verminous
bronchitis by the following procedure: The head of the calf is slightly
elevated, and about 2 drachms of ether, chloroform, oil of turpentine,
or rectified oil of amber—single or combined—are poured into each
nostril and allowed to vaporize there; it will then, by the respiration,
be carried into the air passages, and thus destroy the filariæ. In some
cases it must be repeated two or three times, but once has frequently
the desired effect.

The method of treatment by intra-tracheal injection, introduced by Levi,
of Pisa, has yielded very satisfactory results. Levi has been completely
successful with a sheep. Éloire has employed it in sixteen calves
affected with the disease, and all were cured. He used the following
mixture: Black poppy oil, 100 parts; oil of turpentine, 100 parts;
carbolic acid, 2 parts; purified cade oil, 2 parts. Each calf received
10 grams of this mixture daily for three days.

The injection, which should be given slowly, is followed by a fit of
coughing, and the expired air has the odour of turpentine. This
treatment has also been successful at Milan. Similar favourable results
have followed Hutton’s treatment of eight calves, some of which were in
the last stage of verminous bronchitis. He employed a mixture of oil of
turpentine, tincture of opium, pure carbolic acid, and water—the oil of
turpentine forming one-half of the mixture. The dose was ½ an ounce, and
in the serious cases this was given every day for three days, and in
other cases every second or third day. Kriwonogow has likewise cured
twenty-two calves by giving each of them two tracheal injections of 8
grams of the following mixture: Essence of cloves and oil of turpentine,
360 parts of each; carbolic acid and olive oil, 30 parts of each.

(Williams speaks highly of the administration of prussic acid. Penhale
gives—by intra-tracheal injection, and slowly—oil of turpentine 2 drams,
carbolic acid 20 minims, and chloroform ½ a dram.)




                              CHAPTER IV.
                           LUNGS AND PLEURÆ.


                         PULMONARY CONGESTION.

Besides passive congestions of the lung, which it is unnecessary to
describe here, and which result from cardiac or pericardiac affections
or the compression of important vessels, there sometimes occur,
particularly among young animals, cases of active congestion of the
lung. Such cases are produced by over-exertion on the part of animals
which have escaped from control or have been chased by dogs.

They are most common in animals usually kept in stables, but which have
accidentally escaped, or in very fat animals.

Dyspnœa and cough are the chief =symptoms=. The animals stop as though
exhausted, extend their neck and head, dilate their nostrils and thrust
their limbs out on either side of the body, while at the same time they
appear in a condition of terrible distress.

The respiration is rapid and short, the patient can scarcely breathe,
and asphyxia seems imminent. On auscultation it seems that the
respiratory murmur has disappeared over almost the entire extent of the
lung.

Death may occur very quickly.

=The diagnosis= is extremely easy, provided that the history is known.

=The prognosis= is grave.

One of the most successful methods of =treatment= consists in free
bleeding. In a great majority of cases this causes the symptoms to abate
as though by enchantment. Cutaneous stimulation by mustard and similar
irritants, as well as ablutions of cold water, are useful. The animal
should be placed in a very airy spot.


                           SIMPLE PNEUMONIA.

=History.= Veterinary surgeons have long been divided in opinion on the
question whether simple pneumonia occurs in animals of the bovine
species. Whilst some affirm it, others think that all lesions of the
lung in the ox, apart from pneumonia due to foreign bodies, should be
regarded as of the nature of peripneumonia.

Some ten years ago two veterinary surgeons of the department of the
Aisne, Coulon and Ollivier, practising in a district where peripneumonia
rages, made some extremely interesting observations on pneumonia in the
ox. Their object was to distinguish between contagious peripneumonia and
simple pneumonia during life, simple pneumonia having formerly been
regarded as a non-contagious peripneumonia. Despite the rather
unfavourable conditions in which ordinary practitioners are frequently
placed, these gentlemen performed a work of great value. The facts which
point to the occurrence of simple pneumonia are as follows:—

=The disease= is not contagious. One may allow affected animals to mix
with normal subjects without the disease being communicated. Pulmonary
exudate from cases of simple pneumonia can be injected into the dewlap
and hind quarters of young and adult animals, without pathological
results.

=The lesions= and =course= of simple pneumonia entirely differ from
those of peripneumonia.

=Causation.= Simple pneumonia is not common, and only occurs quite
exceptionally in fat stock, or in milch cows kept in stables at a
regular temperature, as in the north of France and near Paris.

It occurs most commonly in working animals, which are exposed to
variations in temperature and to chills. By causing vascular
disturbance, chill favours microbic infection and visceral inflammation.
Trasbot has described the case of an ox which, after having worked hard,
and whilst freely sweating, was left exposed to the wind under a shed
for about three hours. This animal contracted unilateral pneumonia the
following day.

Coulon and Ollivier have seen the disease in animals living in damp,
low-lying valleys, or valleys exposed to the north wind, which are
exposed in consequence to great variations in temperature.

=The symptoms= follow almost the same course as in the horse, and one
may distinguish three periods:—

=I. Period of onset.= The symptoms which mark the onset of the disease
are moderate fever, which progressively increases, and acceleration of
respiration and of circulation. The number of the respiratory movements
rises to twenty or twenty-five per minute, those of the pulse to fifty,
sixty, or eighty. The conjunctiva becomes injected, and then of a yellow
tint. At this period the appetite never disappears completely,
rumination is regular, and there is neither tympanites nor colic.

These general symptoms, which are not of special significance, are
supplemented by more precise local symptoms—an abortive, difficult and
painful, cough which is easily induced, and a whitish discharge. The
rusty expectoration which is characteristic of simple pneumonia in the
horse and in man has never been observed.

Percussion discloses partial dulness, usually on one side, in the lower
region of the chest: the respiratory murmur in this region is
ascertained by auscultation to have diminished, whilst in the upper part
and also on the opposite side the respiratory murmur is increased.

=II. Period of exacerbation.= This period is characterised by
accentuation of all the symptoms: the temperature rises, and may attain
104° Fahr.; the submaxillary artery is tense; the dulness becomes more
marked, whilst crepitant and mucous _râles_ are heard. In the portions
still unattacked the function of the lung is exaggerated in order to
make up for the defect of the diseased parts, and the respiration
becomes juvenile.

The appetite, which previously had been maintained, diminishes
considerably, without, however, entirely disappearing, and intense
thirst sets in, as a consequence of the fever.

=III. Period of crisis.= The general symptoms remain stationary for four
or five days; the respiration, which is always affected, sometimes
becomes as rapid as thirty to forty per minute; the tubal souffle which
invariably occurs in pneumonia of the horse is not always clearly
audible.

=Terminations.= (1.) Resolution.—This is indicated by the attenuation of
all the symptoms and the disappearance of fever, which gradually sinks
from 105° to 101° Fahr. The respiratory movements become fuller and
fewer in number, the pulse slower, and the artery softer and more
compressible. The cough changes its character, is stronger, more
sonorous and prolonged, and is accompanied by the free discharge of
muco-pus. The dulness descends, and the tubal souffle, if previously
existing, is replaced by the returning crepitant _râle._ In general the
disease runs its course in eight to ten days in young and in fourteen to
fifteen days in aged subjects.

(2.) Death by asphyxia is almost the only fatal termination of pneumonia
in the ox. It occurs in one-third to one-fourth of the subjects
attacked. Its approach is announced by a deep mahogany-red coloration of
the conjunctiva. The pulse becomes very rapid, 100 to 110 per minute,
thready, small, and almost imperceptible, whilst the beating of the
heart is strong and tumultuous. Respiration is rapid and very laboured
(50 to 70 per minute). The animal’s attitude is typical; it stands with
its limbs thrust out, its head extended, its nostrils dilated, and its
mouth half open, discharging foamy and viscous saliva. Throughout the
greater portion of the lung gurgling sounds and crepitant mucous _râles_
can then be detected.

(3.) Cases ending in gangrene and suppuration are excessively rare, and
others resulting in chronic pneumonia have not been authoritatively
described.

Pneumonia is distinguished from broncho-pneumonia by the existence of
dulness at the period of crisis, whilst in the case of broncho-pneumonia
this period is only marked by partial dulness, which is even then
sometimes slight. Moreover, broncho-pneumonia usually develops much more
slowly.

The disease, then, is distinguished from peripneumonia by the following
points:—

(_a_) By the character of the temperature curve, which is regular in
pneumonia, only attaining its highest point at the period of crisis,
whilst in peripneumonia it ascends suddenly, and presents sudden
oscillations.

(_b_) The appetite remains, although diminished.

(_c_) Sensitiveness in the region of the ribs is but feebly marked, or
is entirely absent, simple pneumonia not being accompanied by pleurisy.

(_d_) The dewlap never shows œdema, a symptom which usually accompanies
the period of crisis in peripneumonia, when the jugular veins and the
anterior vena cava are compressed.

(_e_) These signs alone are almost sufficient on which to base the
=diagnosis=, but they are often supplemented by two others, of some what
less importance (for in exceptional cases they may also be observed in
simple pneumonia), viz.—the absence in most instances of a membranous
sound, and of a well-marked souffle.

=Prognosis.= Two-thirds of the cases recover. This proportion might be
increased if the veterinary surgeon were called in at the beginning.

=Lesions.= Post-mortem examination reveals neither pleural exudate nor
pleural lesions. The lung is large and of increased weight, hepatised
along its lower borders, and congested in its upper part.

The sero-hæmorrhagic infiltration of the interlobular spaces varies,
according to the region examined: the upper regions are engorged and
black, owing to capillary hæmorrhages and blood clots, which completely
surround the pulmonary lobule, the latter being violet or brownish-red
in colour. In the hepatised portions the lobules are of a washed-out
reddish tint, and the interspaces of a whitish colour.

The bronchi are filled with frothy, whitish mucus; the small bronchi
sometimes contain fibrous concretions and the mucous membrane is
injected, and may be destroyed in places. The bronchial lymphatic glands
are enlarged, congested, and contain small hæmorrhages.

It is important in making a post-mortem examination to be able to
distinguish pneumonia from peripneumonia. This is comparatively easy if
one bears in mind that in the latter pleurisy always exists, that the
interlobular connective tissue spaces are always greatly distended with
a citrine-coloured serosity, that on section the peripneumonic lung
resembles a mosaic; and that, finally, the course of hepatisation is
centripetal, the inflammation commencing at the periphery of the lobule,
and progressively extending towards the centre. In pneumonia, on the
contrary, pleurisy is always absent; the interlobular connective spaces
are only distended slightly, if at all, and always contain a
brownish-red serosity: the course of hepatisation is centrifugal; it
commences in the pulmonary alveoli, and extends towards the periphery
and the interlobular divisions. The following table gives a _résumé_ of
the other differences between the two diseases:—

          _Peripneumonia._          │           _Pneumonia._
                                    │
 Œdema of the dewlap.               │No œdema of the dewlap.
 Pleural exudate.                   │No pleural exudate.
 Centripetal lobular hepatisation.  │Ascending centrifugal lobar
                                    │  hepatisation.
 Extreme infiltration of the        │Moderate infiltration of the
   interlobular connective tissue   │  interlobular connective tissue
   spaces (primary yellow           │  spaces (secondary reddish-brown
   infiltration).                   │  infiltration).

=Treatment.= Good hygiene, regular ventilation, moderate warmth, and the
administration of tepid drinks facilitate recovery.

Certain German authors recommend cold compresses to the thorax, douches,
and cold enemata in pneumonia. We do not think that such treatment has
proved very successful, although it has been well tried.

The classic treatment commences with moderate bleeding, the free
application of mustard to the sides, the application of moxas, frictions
with antimonial or blister ointment, and the administration of draughts
containing 2 to 2½ drachms of tartar emetic per day, or considerable
doses of alcohol; and this treatment seems to have given the best
results. Antithermic agents, like acetanilide, phenacetin and quinine
sulphate, are too costly to be greatly used in bovine medicine.
Salicylate of soda is preferable.

In order to assist circulation, support the tone of the heart and avoid
engorgement of the lung and asphyxia; digitalis should be given in doses
of ¾ to 1 drachm per day, or digitalin in subcutaneous injections of 5
to 6 milligrammes, continued for five or six days. Finally, iodide of
potassium may be given in doses of 1 to 1½ drachms, to reduce
inflammation and as an expectorant.


         PNEUMONIA DUE TO FOREIGN BODIES—MECHANICAL PNEUMONIA.

It may happen that in examining a patient pneumonia is diagnosed under
circumstances which seem to forbid its being regarded as simple or
primary. This may be explained by the fact that ruminants are very apt
to suffer from pneumonia produced by foreign bodies. The lung may be
penetrated either by some sharp object making its way forwards from the
rumen or reticulum or by liquid or solid material passing into the
trachea. These are two common methods by which this form of pneumonia is
produced.


  PNEUMONIA DUE TO THE MIGRATION OF FOREIGN BODIES FROM THE RETICULUM.

=Causation.= The conditions under which food is swallowed by ruminants
after preliminary mastication permit indigestible objects, such as
stones, fragments of wood, nails, needles, bits of iron wire, etc., to
enter the rumen, whence they reach the reticulum in consequence of
peristaltic movements. Sharp, perforating objects, like needles or
fragments of iron wire, penetrate the walls of the gastric compartments,
and, impelled by the movements of these organs, pass through the
intervening tissues, usually in the direction of the heart. Under
conditions which cannot precisely be defined, these foreign bodies make
their way towards the pleural cavity (usually the right, in consequence
of the situation of the reticulum), traverse the diaphragm, and directly
penetrate the base of the lung.

As the migrating object is usually infected, its passage through the
diaphragm always produces a localised patch of diaphragmatic pleurisy.
Although possible, it is only rarely that the pleural sac becomes
generally infected, or that rapidly fatal septic pleurisy is set up.
Usually the localised pleurisy causes the base of the lung to become
adherent to the anterior surface of the diaphragm. The foreign body
continuing its movements, passes into the lung, and there sets up
pneumonia.

=Symptoms.= When the practitioner is first consulted he often finds only
indications of the crisis period of a localised pneumonia at the base of
the affected lung. The symptoms include fever, accelerated breathing,
moaning, loss of appetite, cough without discharge, dulness over the
base of the lung on percussion, disappearance of the respiratory murmur
in the dull area, souffle opposite the inferior bronchi, and normal or
juvenile respiration towards the front, _i.e._, in the anterior lobe,
and sometimes in the cardiac lobe.

The temptation under such circumstances is to deliver a diagnosis of
simple pneumonia with prognosis of probable recovery. It should be
remembered, however, that in all cases of basilar pneumonia without
affection of the anterior lobes there is a considerable chance of the
condition being due to the presence of a foreign body. On more careful
examination it is found that the intercostal spaces opposite the
affected region are very sensitive, and that the circle of the
hypochondrium is correspondingly sensitive. The owner, moreover, almost
always informs the practitioner that for several weeks his animal has
coughed, shown tympanites, diminished appetite, etc.

Compression of the roots of the corresponding diaphragmatic nerve at the
base of the neck always produces coughing.

These symptoms rarely accompany the development of simple pneumonia.
Furthermore, the =course= of this accidental pneumonia is entirely
different. Instead of developing regularly according to the
above-described cycle, pneumonia due to foreign bodies develops slowly,
and only becomes well defined after several weeks, whilst its tendency
is to grow more and more aggravated. The zone of dulness extends both in
a forward and upward direction. The souffle extends forwards.
Auscultation and palpation sometimes reveal the formation of an abscess
or local gangrene; while there is slight œdema of the wall of the chest,
as well as a gurgling sound at the moment when the lung is displaced,
high fever, intensely coloured urine, and very marked leucocytosis, etc.
Death is inevitable, and when gangrene exists it sometimes occurs
suddenly.

=Diagnosis.= The diagnosis is based on the information furnished with
regard to the course of the disease, the localisation of the hepatised
zone, and the progressive character of the affection.

The diagnosis, nevertheless, is always a little doubtful, but may be so
far assured as to attain the position of a quasi-certainty.

=Prognosis.= The prognosis is unequivocal.

=Treatment.= No practical treatment, either to extract the foreign body
or to combat the special pneumonia which it has produced, can be
attempted. All the interlobular connective layers and the lobules
themselves are invaded by various microorganisms carried by the foreign
body. Numerous fragments of tissue serve as centres of suppuration and
gangrene, and the only chance would lie in attempting resection of the
lung. Such intervention has no practical interest in veterinary surgery.
It is true that when the existence of an abscess is suspected, an
aseptic exploratory puncture may be made, and, in the event of the
diagnosis being so far confirmed, the abscess might be opened through an
intercostal space. Under such circumstances, however deep the point of
penetration of the foreign body, the development of the resulting
abscess causes local pleurisy and adherence between the pleura and lung,
so that there is no immediate danger of producing purulent pleurisy and
pneumo-thorax. If small the foreign body might possibly be discharged
through the passage thus afforded.

In practice the best plan is to recommend slaughter as soon as the
diagnosis becomes certain, provided that the meat can still be utilised.


                   PNEUMO-MYCOSIS DUE TO ASPERGILLI.

The term pneumo-mycosis, or pulmonary aspergillosis, is used to denote a
condition due to the growth in the respiratory apparatus of a fungus of
the order aspergillus (family, _Perisporiæ_; sub-order, _Perisporiaceæ_;
order, _Ascomycetes_).

In ruminants, as in all other animals, pulmonary aspergillosis occurs
accidentally, and may often pass unperceived, in spite of the
indications given by Lucet and Bournay regarding its development and
symptoms.

It seems most frequently to be caused by _Aspergillus niger_ and
_Aspergillus fumigatus_, particularly by the latter, which, according to
Rénon’s work, also appears to be the most pathogenic. It only develops
in animals whose respiratory apparatus is injured and is the seat of
such lesions as those of chronic bronchitis, bronchi-ectasis, and of
parasitic lesions or those containing cavernous spaces resulting from
abscess formation, etc., etc.

The fungi, or more properly the spores, which have accidentally
penetrated into the respiratory channels germinate and develop in the
pathological dilatations, causing disseminated areas of pneumonia and
some mechanical disturbance, but not producing intoxication by
liberating toxins.

=Causation.= Infection occurs through the air passages, in consequence
of the inspiratory current carrying spores of the fungi into the
ramifications of the bronchi, where they develop if the soil is
favourable. Development is favoured if the animals exposed to
contamination are in bad condition, or if, as sometimes happens, the
walls of the stables are not kept clean, and are covered with various
forms of fungi.

Prolonged feeding on musty fodder may also favour respiratory infection;
but it seems highly improbable that under ordinary conditions infection
can occur through the digestive tract. Infection of the lung must also
be regarded as exceptional, if one bears in mind the frequency with
which oxen are fed on musty or mildewed fodder and the small number of
accidents recorded.

=Symptoms.= The symptoms are obscure, and pulmonary aspergillosis is
often only discovered on post-mortem examination. A cough is the chief
symptom. It is dry at first. Afterwards it becomes spasmodic and
frequent.

Respiration is difficult, dyspnœic, effected only with effort, and
sometimes even discordant. Expiration is sighing.

Percussion reveals zones of partial or complete dulness when the lesions
are near the surface of the lung, which, however, is rare. Bournay has
noted the occurrence of a musical sound resembling that obtained by
tapping a small crystal or glass bell.

Auscultation is said to reveal rough or sibilant _râles_, but as the
lesions occur only in animals whose respiratory apparatus has already
been impaired, it is difficult to offer an opinion on the subject.

These signs are invariably accompanied by a certain amount of general
ill-health, wasting, and irregularity of appetite and of rumination.

On post-mortem examination the lung of the affected animal appears
strewn with nodules, varying in size between a hazel-nut and a walnut.
On section, Bournay claims to have found a wall or fibrous shell
covering a greenish cryptogamic growth, in the centre of which was a
yellowish, sharply defined kernel formed of masses of fungi (_Mycelium_,
_sterigmata_ and spores). In cases of rapid development, the pulmonary
tissue around the parasitic lesion is completely hepatised.

=Diagnosis.= Diagnosis is impossible without recourse to microscopic
examination of the discharge. This examination, which, however, is
somewhat difficult, may, after staining, result in the detection of
_débris_ of the mycelial filaments and of spores, with or without
bacilli of tuberculosis. The diagnosis as regards fungi can only be
assured by preparing cultures.

=Prognosis.= The prognosis is grave, because the disease is always
superadded to lesions, which of themselves would justify a sombre view.

=Treatment.= In consequence of the small number of observations
published and the difficulty in diagnosis, no rational treatment has
hitherto been laid down. From a purely theoretical standpoint,
fumigations with tar and essence of turpentine and the inhalation of
carbolic spray have been recommended. Life in the open air would,
without doubt, be equally or more efficacious. Preventive treatment
consists in withholding musty fodder and keeping the stables clean.


          GANGRENOUS BRONCHO-PNEUMONIA DUE TO FOREIGN BODIES.

Foreign bodies which find their way into the trachea instead of the
œsophagus provoke in most cases broncho-pneumonia, which very rapidly
terminates in gangrene and death.

=Causation.= Forced feeding of sick animals which have lost their
appetite is one of the principal causes of this grave condition. In
order to administer food such as mashes, gruel, hay tea, etc., the
oxherds have a bad habit of lifting the entire head and drawing forward
the tongue whilst they pour the concoctions into the animal’s mouth. The
liquid cannot then be divided into portions, deglutition in the pharynx
is badly effected, and the substances administered find their way partly
into the larynx and partly into the œsophagus. In the case of
astringent, bitter, or highly stimulating drugs, a similar accident may
be caused by spasm of the pharynx or œsophagus, where the tongue has not
been left free and excessive quantities have been given.

Again, during the course of diseases complicated with paralysis of the
pharynx (cow-pox, parturient apoplexy), obstruction of the pharynx and
œsophagus (tympanitic indigestion), intense pharyngeal dysphagia
(foot-and-mouth disease), etc., the risk of broncho-pneumonia due to
foreign bodies is much greater still. It may even occur spontaneously in
animals in the enjoyment of complete freedom (foot-and-mouth disease).

Lastly, cases of broncho-pneumonia have been described as a consequence
of inhaling foreign bodies, when the animals are fed, for example, with
meal made from undecorticated cotton-seed. Under such circumstances the
lesions produced are similar to those of pneumoconiosis in man (the
chronic forms of pneumonia of miners, charcoal-burners, quarrymen,
stonemasons, etc.).

=Symptoms.= The symptoms of gangrenous broncho-pneumonia become apparent
immediately after the foreign body has entered the trachea. They
commence with a violent, spasmodic cough, produced by reflex action,
which in its turn is due to the laryngeal mucous membrane having been
touched. But this cough is now too late to be of use, for the food, drug
or liquid has passed into the depths of the trachea, and cannot be
ejected. The cough soon ceases, and the animals may even return to their
food. These appearances, however, are deceptive, for twelve, twenty-four
or forty-eight hours later the cough reappears, whilst appetite
diminishes. The attacks of coughing are succeeded by the discharge of a
greyish or reddish-grey offensively smelling material; respiration
becomes more rapid, the heart’s action violent, and the temperature
rises to 103° or even 105° Fahr. (39·5 to 40·5° C.).

The patients soon refuse all solid food, and if the chest is then
examined by percussion one finds partial dulness, rarely simple dulness,
over the cardiac lobes opposite the point where the girth passes. The
partial dulness may rise to a varying height on both sides; sometimes it
is confined to one side.

On auscultation the respiratory murmur in the upper two-thirds of the
lung appears exaggerated on both sides, and is found to have greatly
diminished, or disappeared altogether in the inferior zone.

Auscultation through the scapula almost always shows that the anterior
lobes are affected; but, at all events, in the examinations we have
made, checked by post-mortem examination, the cardiac lobes have always
proved to be most affected, a fact attributable to the direction of the
principal bronchi. The lower portion of the posterior lobes may also be
affected, but this is rarer. All the lower zone is irregularly
hepatised, and on auscultation one hears large moist _râles_, whilst
respiration sometimes appears of a blowing character, and divided by a
pause, but there is no tubal souffle. If the patient survive for a
certain time, the sounds heard on auscultation undergo change; gurgling
noises and sometimes true cavernous souffles are heard, as a result of
suppuration in the bronchi and gangrene of one or more areas in the
lung. Diffuse gangrene is rare, and the inferior zone is usually the
only portion affected.

During this phase the expired air has an absolutely characteristic
gangrenous odour.

Death occurs by asphyxia and intoxication, but some animals hold out for
a fortnight and more.

=Lesions.= Post-mortem examination reveals a suppurative but secondary
inflammation of the mucous membrane of the nasal cavities, pharynx,
larynx, and trachea.

In the bronchi, sometimes very deeply placed, remains of foreign bodies
are found in cases where some solid material has been inhaled. The
mucous membrane of the bronchi is violet in colour, in places appears to
be sloughing, and is covered by gangrenous patches immersed in a
reddish-grey putrid fluid of offensive odour. In places the pulmonary
tissue has undergone gangrene; and incision of the diseased centres
discovers irregular cavities, filled with a pultaceous, greyish
material, which often makes its way into the bronchi. These are the
irregular cavities which give rise to the gurgling sounds. The walls of
these cavities are formed of disintegrating pulmonary tissue, which
again is surrounded by a zone of grey hepatisation. The gangrenous areas
may unite, forming vast caverns. If near the surface they cause adhesive
or septic pleurisy.

=Diagnosis.= The diagnosis is not very difficult, provided that an exact
account can be obtained of the circumstances which preceded the
appearance of the disease. The signs furnished by the discharge, the
expired air, percussion and auscultation are sufficiently significant to
remove any doubt.

=Prognosis.= The prognosis is extremely grave, and in the great majority
of cases fatal.

=Treatment.= There is very little chance of recovery, no matter what
treatment may be employed. The most favourable termination consists in
the gangrene remaining limited to the bronchi and to a small fragment of
the lung, so that the damaged tissues, being gradually delimited and
sloughed off, may finally be discharged by coughing.

This is an exceptional termination, but attempts may be made to assist
its evolution by giving alcohol in doses of 8 to 10 ounces per day, and
salicylate of soda in doses of 4 to 5 drachms. When the condition can be
early diagnosed before intense and continued fever has set in, and when
the animal’s condition is good, it is often preferable to slaughter the
patient.


                     INFECTIOUS BRONCHO-PNEUMONIA.

The ox’s lung is liable to so many and such extremely varied diseases
that it seems desirable to add to the above descriptions some remarks on
infectious broncho-pneumonia of external or internal origin.

Anatomically these forms of broncho-pneumonia are characterised by the
occurrence of “islands” of pulmonary hepatisation, more rarely by
extensive (massive) hepatisation; in all cases the hepatisation is
irregular, and in no way resembles that of simple pneumonia.

=Causation.= The internal causes are numerous and varied. They are due
to primary infection of an organ whence arises a general infection,
sometimes even true septicæmia. Some form of broncho-pneumonia, such as
simple broncho-pneumonia, purulent broncho-pneumonia, gangrenous
broncho-pneumonia, etc., then follows as a complication. These
broncho-pneumonias are therefore only manifestations of purulent
infection or septicæmia. They frequently follow post-partum infections,
vaginitis, metritis, and suppurative mammitis.

=Symptoms.= The general symptoms first attract attention, and are
extremely acute. They comprise high fever, loss of appetite, cessation
of rumination and of milk secretion, breathlessness, blowing, etc.—all
signs of grave and rapidly progressive infection.

Sometimes at this period nothing more than the primary lesion, such as
metritis or mammitis, can be detected. It may even happen that the
uterus seems little affected, and, despite the accelerated respiration,
neither partial nor complete dulness of the lung is discovered.

Hepatisation only occurs some days afterwards, and with it irregular
partial dulness localised in the lower zones, disappearance of the
respiratory murmur in the corresponding regions, exaggeration in the
infected regions, an expiratory sound which is barely perceptible or may
be of a blowing character, or, again, after several days may be
transformed into a tubal souffle.

The cough then becomes frequent, generally difficult, paroxysmal,
feeble, and easily provoked. The appetite suffers, the patients seem to
prefer fluid nourishment and lose flesh very rapidly.

If the broncho-pneumonia is about to terminate in suppuration or
gangrene, the respiration becomes sighing, the breath fœtid, and the
cough is accompanied by a greyish muco-purulent or gangrenous discharge.

When the abscesses are deep-seated, the alarming symptoms retain their
primary degree of intensity for weeks, until the animals are completely
exhausted. Abscesses, originating in deep-seated parts, may even extend
towards the surface of the lung, and produce either adhesive pleurisy
that can be detected by palpation, or exudative pleurisy, easily
recognised on percussion.

When the infective microbes are not pyogenic the general condition
appears less grave, the animals exhibit only moderate fever, appetite is
diminished but not lost, wasting is slower, and may continue for months,
but the affected portions of lung become converted into fibrous masses
or a material resembling spleen pulp.

The duration of infectious broncho-pneumonia, therefore, varies with the
nature of the infecting organism. In cases which terminate in gangrene,
the animals may survive for three or four weeks; in those where
suppuration occurs, for several months. In short, recovery is the rule
in simple broncho-pneumonia; but from an economic standpoint there is
little reason for keeping the animals alive.

=Diagnosis.= The diagnosis is not generally very difficult; for if at
first the case may be mistaken for one of simple pneumonia, the
persistence or prolonged aggravation of the symptoms and the
irregularity in position of the lesions revealed by percussion and
auscultation enable the condition to be distinguished at an early period
from simple pneumonia.

Confusion with acute or chronic pleuro-pneumonia may easily be avoided
by noting the absence of pleural effusion, and of the soft pleuritic
souffle of peripneumonia, etc.

Where auscultation is chiefly relied upon it is more difficult to
differentiate between this disease and acute tuberculosis, and between
it and broncho-pneumonia produced by foreign bodies, although the latter
disease develops differently.

=Prognosis.= The prognosis is always extremely grave and, in cases where
there is gangrene or abscess formation, fatal. From the economic
standpoint the chronic form is also very grave.

=Treatment.= As broncho-pneumonia is frequently of a secondary
character, treatment should at first be particularly directed against
the primary condition, whether in the mammary gland, uterus or
elsewhere. Early treatment of suppurative mammitis, metritis, etc., is
therefore necessary.

Broncho-pneumonia is treated by free vesication of the walls of the
chest, the administration of tonics and antiseptics, alcohol in small
doses, acetate of ammonia in doses of 1 to 2 drachms, salicylate of soda
in doses of 5 to 8 drachms per day, salicylic acid in doses of 1 drachm,
and creosote in doses of 1½ to 5 drachms, given in electuary, etc.

Diuretics, farinaceous gruels, etc., may be used freely, and are of
value.

If the symptoms persist or become aggravated, and suggest the
development of an abscess or gangrene, it is better to slaughter the
animal.


                  BRONCHO-PNEUMONIA OF SUCKING CALVES.

Young animals still with the mother, particularly calves during the
first few weeks of life, are liable to broncho-pneumonia of a
specialised character, as regards not only its causes, but its
development and duration.

=Causation.= The causes may be grouped under two principal heads:—

(_a_) In slow or difficult cases of parturition, the fœtus may be
injured whilst being delivered, as a consequence of direct compression
of the great blood-vessels, etc. (particularly of compression of the
umbilical cord, compression of the thorax in the cardiac region, or
partial premature separation of the envelopes), and may thus by reflex
action make automatic inspiratory movements.

Respiration being impossible, inasmuch as the thorax has not yet passed
the posterior passages, such inspiratory efforts made during the passage
through the pelvis may cause amniotic liquid to pass into the bronchi.
This accident is particularly liable to occur during deliveries with
breech presentation. If, as happens frequently, the amniotic liquid has
become infected either prior to or as a consequence of obstetrical
manipulation, the result is fatal; for the passage of infected amniotic
fluid into the bronchi develops a broncho-pneumonia of a degree of
gravity depending on the character of infection.

(_b_) By an entirely different mechanism broncho-pneumonia may occur in
sucking calves during the first few weeks of life, even in the case of
animals born in a vigorous condition, and kept in warm and well-arranged
stables. This form follows diarrhœa, and constitutes a final
complication which is always of very marked gravity, and in most cases
fatal.

Such secondary broncho-pneumonia only occurs when the diarrhœa has
resisted treatment, and it is important to note that the pectoral
lesions appear at a time when the intestinal mischief seems to have
diminished, the diarrhœa having lessened or disappeared. This variety of
broncho-pneumonia of young animals is by far the most frequent. It has
been termed broncho-pneumonia of intestinal origin, and exactly
resembles, so far as its development and gravity are concerned, the
broncho-pneumonia in young infants described by Sevestre and Lesage.

The term broncho-pneumonia, moreover, is not strictly correct, or at
least is not exclusive; for the rapid forms often exhibit lesions other
than those of broncho-pneumonia. Post-mortem examination reveals
pleurisy and pericarditis.

=Pathogeny.= At the outset of these attacks of broncho-pulmonary
disease, a careful bacteriological examination of the organisms to be
found in the discharge of bronchial mucus leads to the discovery of
bacilli which do not stain with Gram, and which resemble varieties of
the colon bacillus; in other cases of streptococci. At a later stage,
when the animal has become weak, microorganisms are present in much
greater variety. Nocard found in lung abscesses the bacillus of
epizootic lymphangitis. It seems that the development of various lesions
in the thoracic cavity may be due to auto-infection, _i.e._, to the
penetration from the intestine of germs which, after passing through the
circulation, establish themselves at some point in the lung. The pleura
is attacked at a later period as a consequence of continuity and
contiguity of tissue.

In a similar way pericarditis and even valvular endocarditis may be
produced.

=Symptoms.= The symptoms are similar to those of all forms of
broncho-pneumonia. Where diarrhœa has been neglected, the conditions may
apparently improve without evident cause, whilst the respiration becomes
more frequent. The patient soon suffers from cough, and in a few hours
the existence of broncho-pneumonia is clearly apparent. Acceleration of
breathing is the dominant symptom. The respirations may rise to fifty to
sixty per minute, at which they continue, while fever sets in. On
percussion the thorax may appear of normal resonance throughout; but
when pleural lesions and exudates exist, resonance gives place to
partial or complete dulness. Should pericarditis or small
cardio-pericardial adhesions exist, they may escape observation, but if
the exudate is abundant or the adhesions multiple or of large size the
usual symptoms of pericarditis develop progressively.

On auscultation the respiratory murmur is always found to be greatly
exaggerated in the healthy parts, usually the upper portions of the
lung. On the contrary, it is attenuated or suppressed in the affected
regions. The other signs vary greatly, according to the extent,
intensity, and more or less advanced condition of the lesions. Crepitant
and bronchial _râles_, blowing respiration and tubal souffles, etc., are
among the symptoms.

The duration of the disease varies; some patients may be carried off in
five or six days, while others survive for one or two months, or even
longer. A few recover, but they remain thin, puny, and atrophied, and
are not worth keeping alive.

=Lesions.= The lesions extend to the bronchi, the pulmonary tissue, and
sometimes the pleura and pericardium. They consist in lesions of diffuse
broncho-pneumonia, pleurisy with false membranes and parietopulmonary
adherences, and pericarditis with partial cardio-pericardial adhesions.

In rare cases abscesses caused by pyogenic streptococci may be found.

The anterior lobes, cardiac lobes, and lower part of the posterior lobes
are those singled out for attack.

=Diagnosis.= The diagnosis is not difficult, provided that the
circumstances preceding the appearance of the pulmonary lesions are
known.

=Prognosis.= The prognosis is very grave.

=Treatment.= Treatment very often proves useless, because the patients
have little resisting power and are exhausted, and also because they are
suffering from a slowly progressive septicæmia. It may, however, be
worth while in the early stages to apply blisters to the chest and
administer general stimulants: alcohol in doses of 8 to 12 drachms per
day, divided into two parts and mixed with milk; acetate of ammonia in
doses of ½ to 1 ounce; and tinctura digitalis 5 to 6 drops.

The primary disease of the intestine is masked by the pulmonary
symptoms, but should not be overlooked. Rice water, subnitrate or
salicylate of bismuth may be added to the milk or albuminous solutions
constituting the diet. When an epizootic of broncho-pneumonia
complicates the diarrhœa it is necessary to take all the preventive
measures which have been suggested in connection with white scour and
umbilical diseases in calves. These comprise disinfection of the
premises and local disinfection of the animals affected.


               SCLERO-CASEOUS BRONCHO-PNEUMONIA OF SHEEP.

The sheep suffers from a special form of broncho-pneumonia, which is
seldom seen except in isolated cases, but which, under exceptional
circumstances, may nevertheless attack a certain number of animals in a
particular flock. It was first noticed and described by Liénaux in 1896,
and has more recently been studied by Sivori (1899). Moussu has only
seen it in flocks in the north of France.

=Causation.= The causes of this disease are still imperfectly
understood.

Sivori’s researches show that the disease may be referred to a
microorganism, but we do not yet know exactly by what path infection
occurs.

The agent of sclero-caseous broncho-pneumonia in the sheep appears
similar to that described by Preisz and Guinard in 1891, and identical
with the microbe of ulcerative lymphangitis of the horse (Nocard, 1897).
It is probable that infection occurs through the respiratory apparatus.

=Symptoms.= The clinical development of the disease is difficult to
describe, because its course is slow and unaccompanied by well-marked
external signs.

The animals lose flesh, pant for breath when moved, drop to the rear of
the flock, cough frequently, feed badly and end by becoming cachectic.
Many suffer from the disease and yet remain in fair bodily condition.

On post-mortem examination the lungs are found not to collapse, having
lost their elasticity, and are of a yellowish-white colour, which is
only seen in this disease. On section the pulmonary tissue appears
dense, hard, and of a fibrous and lardaceous character. At various
points nodules with fibrous envelopes and caseous, yellowish or greenish
contents are found.

When the caseous nodules are near the surface the pleura may be
chronically inflamed and thickened. The liver and kidney frequently
contain caseous lesions.

=Diagnosis.= The diagnosis becomes easy after the first post-mortem
examination, for the lesions discovered cannot be mistaken for those of
parasitic broncho-pneumonia, degenerated pulmonary echinococcosis or
tuberculosis. In the living animal, on the contrary, the diagnosis is
extremely difficult.

=Prognosis.= The prognosis is grave. No special method of treatment is
known.


                          PULMONARY EMPHYSEMA.

Pulmonary emphysema, _i.e._, exaggerated dilatation of the pulmonary
tissue by air, is not uncommon in the bovine species, and occurs under
the two classical forms—(1) alveolar or intra-lobular emphysema limited
to dilatation of the alveoli; and (2) interlobular emphysema, produced
by the entrance and diffusion of air in the interlobular spaces in
consequence of rupture of the lobules.

These two forms are very frequently associated:—

(1.) Emphysema by dilatation usually begins in the right pretracheal
lobe; also in the cardiac and even in the posterior lobes.

(2.) Interlobular emphysema begins in the same regions, but it spreads
readily in a backward direction, remaining interstitial; or, on the
other hand, becoming subpleural at the periphery of the lung.

In both cases the pulmonary tissue is pale, the blood-vessels are
partially obliterated by compression; circulation and aeration of the
blood are impeded—hence the appearance of the disturbance noted.

=Causation.= Emphysema is seen in adult working oxen; also, and to an
even greater degree, in aged cows. It is produced by excessive strains
in draught, or more often by the paroxysms of coughing so common during
simple or parasitic bronchitis, broncho-pneumonia, pneumonia, chronic
broncho-pneumonia, etc. Successive gestations also produce it.

All these pathological conditions also interfere with the nutrition of
the bronchial mucous membrane, particularly of its deep-seated muscular
layer, which is then incapable of regulating the distribution of air in
the bronchial channels. The distribution being no longer regulated by
reflex action, air accumulates at certain points as a result of the
expiratory efforts made during coughing, and dilatation of the vesicles
or lobules occurs.

Diseases of the digestive apparatus, acute or chronic tympanites in
particular, may play a certain part by compressing the diaphragm,
causing expiratory efforts and fits of coughing.

Furthermore, swelling of the lymphatic glands at the entrance to the
chest, by compressing the pneumo-gastrics, provokes reflex cough and
finally emphysema.

=Symptoms.= Pulmonary emphysema is marked by accelerated respiration due
to diminution in the respiratory capacity, which is often very seriously
affected; to insufficient absorption of oxygen in consequence of
diminution in the space available for exchange of gases in the lung, and
to insufficiency of expiration. This acceleration in breathing, though
little marked during repose, becomes very pronounced after exercise, or
during hot weather; and under these circumstances is accompanied by a
paroxysmal, feeble but shrill cough, without discharge. This cough
without discharge is frequently followed by swallowing.

Percussion reveals an important point, viz., increase in the normal
resonance of the thorax.

On auscultation the vesicular murmur is found to be diminished, the
respiration assumes a rough and rasping character, inspiration is
difficult, expiration painful, and often divided into two periods, as
indicated by a slight double movement of the flank. Expiration is
clearly audible. Its duration is generally less than that of
inspiration, although in some cases it is equal or even longer. It is
accompanied by sibilant and snoring _râles_, sometimes even mucous
_râles_, of an intermittent character. In rare cases there may be
difficulty of respiration, as in broken-winded horses.

=Diagnosis.= The diagnosis may suggest a doubt as to whether emphysema
or tuberculosis is present, but in the latter there is fever, the
general condition is poor; on percussion the thorax reveals areas of
partial dulness; and expiration is rough and prolonged, sometimes of a
blowing character, a peculiarity which is exceptional in emphysema.

=Prognosis.= The prognosis is not very grave, except where emphysema is
only an accompanying symptom of another disease, such as chronic
bronchitis, tuberculosis, etc.

=Treatment.= Little can be done to check the development of the above
described pulmonary lesions; but the cough may be relieved, and the
pulmonary circulation improved by assisting the heart.

The most prompt and efficacious assistance is given by digitalis in
doses of ½ to 1 drachm per day for adults, iodide of potassium in doses
of 1 to 1½ drachms, and bromide of potassium in doses of 1 drachm to
guard against reflex excitability of the pneumo-gastric. This treatment,
however, should not be followed for more than five or six days, and
should then be replaced by the administration of arsenious acid in doses
of 15 grains per day, ground horse-chestnuts in doses of 3 ounces per
day, etc., etc.


                        DISEASES OF THE PLEURA.

Primary inflammation of the pleura is very rare in animals of the bovine
species, but secondary diseases of this membrane, on the other hand, are
frequent.


                            ACUTE PLEURISY.

Cruzel, Fabry, and a number of practitioners have described the
occurrence in working animals of acute pleurisy _à frigore_ or
serofibrinous pleurisy in consequence of severe, sudden variations in
temperature, or prolonged chills. At the present day it seems fairly
well established that pneumonia, and not pleurisy, is commonest under
such conditions, and Moussu disclaims ever having seen primary pleurisy.
On the other hand, pleuritic effusions are very common in contagious
pleuro-pneumonia, secondary pleurisy due to pericarditis produced by
foreign bodies, septic broncho-pneumonia or broncho-pneumonia due to
foreign bodies, and the pleurisy which accompanies septicæmia consequent
on parturition, etc. These forms of disease, however, are not simple
serofibrinous pleurisy, but septic or suppurative pleurisy, still little
understood in veterinary surgery.

Tuberculosis of the pleura, although very frequent, is rarely
accompanied by marked exudation. Like secondary disseminated pleural
carcinoma, it usually assumes the vegetative and adhesive form, with
adhesions of greater or less extent between the lung and wall of the
chest.

=Symptoms.= In all these morbid conditions the symptoms vary greatly,
and it would be difficult to give an accurate general description of
them.

In acute pleurisy _à frigore_ shivering attacks, moderate fever,
dulness, loss of appetite, interference with rumination, dryness of the
skin, rapid wasting and intercostal pain, first indicated by dull colic,
constitute the usual symptoms.

The respiration is short and irregular, interrupted when the exudation
is abundant. Pressure over the intercostal spaces produces pain, as does
strong percussion. Percussion reveals an area of dulness bounded above
by a horizontal line.

Auscultation shows the respiratory murmur to have disappeared throughout
the zone of dulness, and reveals the presence of a soft pleuritic
souffle (a soft tubal souffle quite different from that of contagious
pleuro-pneumonia) when pleural exudation is abundant. In septic or
suppurative pleurisy fever is higher, loss of appetite more marked,
wasting more rapid, and depression extreme, with, however, identical
local symptoms.

=Diagnosis.= The diagnosis of pleural exudation presents little
difficulty, because of the peculiar characters of the dulness and the
pathognomonic indications obtained by auscultation. The exudation is
usually unilateral, the mediastinum being very resistant and not
perforated in the ox.

By passing the needle of a Pravaz’s syringe with antiseptic precautions
through the intercostal space a little fluid may be drawn off and the
diagnosis formed, the form and nature of the pleurisy being
simultaneously established. The liquid extracted can be examined
bacteriologically, and can be grown on nutritive media, or inoculated
into experimental animals.

=The prognosis= is grave, because in the ox pleurisy is very often of a
secondary character. The outlook varies, however, with the form of the
pleurisy and the nature and virulence of the infecting organism.

=Treatment.= Treatment consists firstly in applying an energetic
vesicant like antimonial ointment or liquid cantharides blister;
internally diuretics such as soda bicarbonate, nitrate of potash, resin,
and decoctions of pellitory, dogs’ grass, etc., may be given. If thought
desirable the chest may be tapped and the pleural cavity washed out with
an antiseptic solution.


                           CHRONIC PLEURISY.

Chronic pleurisy is frequent in aged animals, but usually assumes the
form of local adhesive pleurisy. The adhesions between the lung and
pleura are more or less extensive; they result from verminous
broncho-pneumonia, echinococcosis, external injuries, etc. Clinically
this form is of no importance, and is almost impossible to diagnose.
During the development of pleural tuberculosis, on the contrary,
adhesive dry pleurisy is frequent, and sometimes becomes so well marked
that almost the whole of the opposing pleural surfaces may become
united.


                             PNEUMO-THORAX.

The name pneumo-thorax is given to the condition produced by the
entrance of air or gas into one of the pleural cavities.

The accident is usually produced by rupture of the parenchyma of the
lung and of the pleura, a rupture which produces a communication between
the alveoli or a bronchus and the corresponding pleural cavity. As soon
as the rupture occurs air passes from the lung into the pleural cavity,
and the lung collapses in consequence of the resilience of its elastic
constituents.

Under other, much rarer, circumstances pneumo-thorax occurs in
consequence of gas generated in the digestive tract passing into the
pleural spaces. The condition then makes rapid progress, and death
occurs in a few days.

[Illustration: $1]

=Symptoms.= The symptoms are well defined. As soon as the accident
occurs the animal exhibits extremely marked and sudden dyspnœa,
accompanied by heaving at the flank or general agitation of all the
muscles of the body. One of the lungs, in fact, has suddenly been called
on to perform the functions of both, and at first it naturally has great
difficulty in meeting this demand.

The heaving at the flank and the general agitation of the body muscles
is due to the fact that the regularity and rhythm of contraction of the
diaphragm are disturbed, and the mechanical conditions have become
different on the two sides. From the first, respiration is moaning and
expiration becomes rapid, stertorous and deep, while the face is
anxious-looking, and the nostrils are dilated as though the animal was
on the point of suffocation. On examining the animal from in front or
behind, the thorax is easily seen to be wanting in symmetry, the side on
which the pneumo-thorax has occurred being immobile as compared with the
sound side. The latter, moreover, is dilated in order to compensate for
the loss of function of the collapsed lung.

Percussion reveals greatly increased resonance on the side of the
pneumo-thorax. On the other hand, the opposite side yields a normal
sound.

Auscultation reveals an increase of the respiratory murmur on the side
which is still acting and, on the contrary, complete and total
suppression of the respiratory murmur on the affected side. On applying
the ear to the chest wall, a large soft, amphoric souffle of well-marked
metallic character is heard. This is particularly clear on respiration,
giving the impression of the existence of a large cavity beneath the
ear. The sighing sound heard on auscultation of the chest wall is louder
than that heard externally or over the region of the nostrils or larynx;
and it seems to be reinforced, as though by the resonance of a large
cavity with thin metallic walls. Once or twice per minute, moreover, a
sound may be heard like that of dropping water. It is of a very special
character, resembling that produced by drops falling to the bottom of a
hollow metallic vase, and setting up prolonged vibration.

As secondary symptoms the heart’s action is accelerated, the number of
beats rising to 80 or even 120 or 130 beats per minute; appetite is
lost; slight tympanites develops as a result of rumination and
eructation being suspended; the peristaltic movements of the rumen are
interrupted, and constipation develops.

=Diagnosis.= The diagnosis of pneumo-thorax is easy, and the condition
can scarcely be mistaken for any other except diaphragmatic hernia; but
the indications derived from percussion and auscultation are so
different in the two cases that they need not be further emphasised.

The task becomes more difficult, however, when an attempt is made to
identify the exact form of pneumo-thorax, for three principal varieties
are recognised.

In open pneumo-thorax, the first and most frequent form, air passes from
the lung into the pleura at each inspiration, and flows back from the
pleural cavity towards the bronchus at each expiration. The
intra-pleural pressure is then approximately equal to the
intra-bronchial pressure, and undergoes similar oscillations. (It should
be noted that the aperture in the lung is seldom sufficiently large to
establish an absolute equality of pressure between the bronchus and the
pleural cavity. Respiration, therefore, though very seriously impeded,
generally continues in a modified form.)

In a second variety, termed “valvular pneumo-thorax,” air passes freely
from the lung into the pleural cavity, but is unable to return from that
cavity towards the lung, because a flap of tissue acts as a valve and
closes the orifice at the commencement of expiration. As soon as
intra-pleural pressure rises above that of the inspiratory effort, the
valve remains permanently closed.

In the third variety, called “closed pneumo-thorax,” the orifice of
communication is obstructed by some mechanism, and the pleural sac only
contains a film of air.

In practice, valvular pneumo-thorax is recognised by the movement of the
thoracic wall (which in open and closed pneumo-thorax remains
depressed), as well as by extreme intensity of the dyspnœa and attacks
of threatened suffocation. Closed pneumo-thorax, which is only a
termination and a stage in the cure of open pneumo-thorax and of
valvular pneumo-thorax, is suggested by progressive improvement in the
symptoms. Scientifically it is very easy to make this diagnosis by
putting a manometric apparatus in communication with the pleural cavity
by means of a simple hollow needle provided with a thick-walled rubber
tube.

In open pneumo-thorax the liquid column in the manometer undergoes
rhythmic oscillations corresponding to the respiratory movements; in
valvular pneumo-thorax the intra-pleural pressure increases
progressively until it becomes higher than the external pressure; and
finally, in closed pneumo-thorax, the column of the manometer assumes a
certain level at which it rests.

=Prognosis.= The prognosis is very variable, according to the primary
cause of the accident. Animals might recover, but economically there is
little advantage in preserving them when the diagnosis is assured,
except in cases of animals of great value, and when the primary disease
admits of it.

=Causation.= Pneumo-thorax may be produced by various causes. The most
frequent cause in large animals is pulmonary echinococcosis, during the
course of which a peripulmonary vesicle, after having injured several
lobules, one of the air passages or even a bronchiole, may break through
the pleura, thereby setting up direct communication between the bronchi
and the pleural cavity.

To pulmonary tuberculosis, with peripheral softened tubercles,
perforating simultaneously into an alveolus or a small bronchus and into
the pleura, must be assigned the second place.

Vesicular and interstitial subpleural pulmonary emphysema is also a
frequent cause of pneumo-thorax, the pleura being ruptured over the
emphysematous points.

Finally, and exceptionally, an abscess of the lung may open into the
pleura and form sinuses, which may establish a communication between the
digestive reservoirs and pleural sacs; but such accidents produce
pyo-pneumo-thorax and septic pleurisy of a rapidly fatal character.

=The diagnosis= of pneumo-thorax, and even of its varieties, does not,
however, enable one to form a prognosis; the important point is to
ascertain the original cause.

=Treatment.= It may be said of pneumo-thorax that no treatment exists,
and that the position is one of expectancy. In fact, we possess no means
of directly dealing with such diseases as echinococcosis, tuberculosis,
or emphysema. For this reason it is best as a rule to advise slaughter.
Nevertheless, when the condition is due simply to pulmonary
echinococcosis of a discrete character, there is some chance that after
several months the animal may recover spontaneously. The communicating
orifice becomes closed by reparative processes (cicatricial contraction,
the formation of a false membrane, limited adhesion between the two
walls of pleura, etc.); the layer of air imprisoned within the pleural
cavity is progressively absorbed, provided that it has not been
accidentally infected; the collapsed and partially splenised lung
progressively regains its function under the inspiratory efforts, and
after some months complete recovery may occur. This termination cannot
always be confidently predicted, because complications may arise at any
moment; under no circumstances can complete recovery be anticipated when
the primary disease is tuberculous.

[Illustration: $1]

In cases of valvular pneumo-thorax with extreme oppression, attacks of
suffocation threatening death as a consequence of excessive
intra-pleural pressure, displacement of the mediastinum towards the
opposite side, compression of the heart, and functional disturbance of
the sound lung, it may be worth considering whether the attacks of
suffocation and threatened asphyxia can be modified or removed by
preventing the excess of intra-pleural pressure. By simply passing a
stout hollow needle through one of the intercostal spaces, the
intra-pleural pressure may be reduced to that of the external
atmosphere, and the effects of compression removed. This, however, is a
last resort, and has no permanent effect.


               HYDRO-PNEUMO-THORAX AND PYO-PNEUMO-THORAX.

When pneumo-thorax is set up, it rarely remains simple. In the great
majority of cases the pleura becomes infected, either directly, by the
lesion which has determined the pneumo-thorax (tubercle, superficial
abscess, actinomycotic lesion, etc.), or secondarily, by the penetration
of germs from the air or from the bronchus (echinococcosis, emphysema).
Simple pneumo-thorax then becomes converted into hydro-pneumo-thorax or
pyo-pneumo-thorax, according to circumstances—that is to say, whether
the exudation into the pleural cavity is of a simple character or is of
the nature of pus.

=Symptoms.= Hydro-pneumo-thorax is characterised by the signs common to
true pneumo-thorax, which constitutes the primary lesion, viz., sudden
difficulty in breathing, exaggerated unilateral resonance, amphoric
souffle accompanied by a sound like that of drops of water falling into
a metallic vessel, and by the signs of secondary exudative pleurisy,
viz., moderate fever, dulness over the lower zones of the chest, limited
above by a horizontal line, slight splashing sound, and a soft distant
pleuritic souffle.

All the secondary symptoms—loss of appetite, suppressed rumination,
sighing, accelerated pulse, etc.—are found in a more or less accentuated
form.

In pyo-pneumo-thorax fever is more marked, while the signs noted on
auscultation and percussion are identical, and are accompanied by
digestive disturbance and marked œdema of the wall of the chest, which
can be seen or detected by palpation.

=Diagnosis.= The diagnosis is relatively easy when the lesion is
secondary; but the difficulty (as in simple pneumo-thorax) is to
identify the exact character of the primary affection.

On the other hand, pyo-pneumo-thorax and hydro-pneumo-thorax are not
always complete; adhesions of very varying character may exist between
the lung and the chest wall; hence it is impossible to group together
all the possible symptoms.

Diagnosis is facilitated by aseptically puncturing the chest with a
Pravaz’s syringe.

=Prognosis.= The prognosis is extremely grave even in cases of
hydro-pneumo-thorax. Treatment is useless, for even allowing that the
primary disease might be cured, this process of cure, after reabsorption
of the transudate, would be extremely tedious, and the animals would
long remain in poor condition.

=Treatment.= In hydro-pneumo-thorax no treatment is advisable. Nothing
is gained by thoracentesis, at least at an early stage, or before the
lesion causing the pneumo-thorax has closed.

In pyo-pneumo-thorax, on the contrary, the theoretical course is to
evacuate the pus and completely wash out the pleural sac with lukewarm
non-irritant solutions of antiseptics.




                               CHAPTER V.
        DISEASES OF STRUCTURES ENCLOSED WITHIN THE MEDIASTINUM.


The mediastinum is a space enclosed in the median plane of the thorax by
the approach of the two opposite layers of pleura. Needless to say, at
those points where the layers are in apposition, the space is
theoretical only. It extends from the suprasternal region to the dorsal
subvertebral region, and encloses all the vessels which pass from or to
the base of the heart, the trachea, the œsophagus, the pneumo-gastric,
diaphragmatic and cardiac nerves, etc., as well as the pericardial sac
and the heart. The organs most frequently affected are the lymphatic
glands lodged in the thickness of the mediastinum, the glands placed at
the entrance to the chest, the bronchial glands, and the glands situated
in the posterior mediastinum.

Inflammation of the mediastinum may coincide with inflammation of the
mediastinal layers of the pleura; but this can only be detected on
post-mortem examination. The lesions which can be recognised during life
are simple inflammation of glands, resulting from pulmonary or pleural
diseases, tuberculous inflammation of glands, and the presence of
cancerous tumours of the mediastinum and hypertrophy of glands due to
lymphadenitis.

Simple inflammation of the lymphatic glands is secondary and consecutive
to broncho-pneumonia, verminous bronchitis, infectious bronchitis, etc.

It produces reflex irritation by compressing the pneumo-gastric and
laryngeal nerves, and is indicated by loud, spasmodic coughing.

=Treatment= consists in administering iodide and bromide of potassium,
terpine, in doses of 1 drachm per day for adults, essence of turpentine
and tar water.

Tuberculous inflammation of glands, inseparable from pulmonary
tuberculosis, has very special characteristics peculiar to tuberculosis.

Inflammation due to lymphadenitis is also very easy to diagnose as a
rule, in consequence of the symmetrical enlargement of lymphatic glands
elsewhere.


                      TUMOURS OF THE MEDIASTINUM.

Sarcomata, carcinomata, lymphomata, and lympho-sarcomata all occur in
the mediastinum. They attack young healthy animals, and sometimes
develop with such rapidity that in a few weeks they become generalised
and invade the heart, lungs, and principal viscera. Their cause is as
yet unknown.

=Symptoms.= At first sight the symptoms are much like those of
pericarditis caused by foreign bodies. They consist in deformity of the
presternal region, swelling of the jugulars, submaxillary œdema,
irregular pretracheal tumefaction, etc.

The tumour, whatever its nature, commences in the mediastinum, develops
towards the entrance to the chest, where it projects, and before long
produces in the pretracheal region clearly marked œdematous swelling.

Between the two first ribs the tumour compresses the carotids, the
jugulars, the nerve trunks, and also the trachea and œsophagus,
producing difficulty in the return circulation, especially in the
jugulars, swelling in the submaxillary space, loss of appetite and
dyspnœa.

Palpation affords indication of a tumour of soft consistence,
bosselated, more or less adherent to the skin, usually painless on
pressure, and of irregular development. Compression of the œsophagus
interferes with the deglutition of rough forage, impedes rumination,
prevents eructation, and thus produces trifling but permanent
tympanites.

The heart is affected reflexly or directly as a result of generalisation
of the tumour, and the pulse may rise to 70 or even 120 per minute.

During the first stages neither auscultation nor percussion points to
any pulmonary lesion. At a later stage the lung itself may be affected.
The other important functions are normal.

Animals suffering from sarcoma, carcinoma, or lympho-sarcoma of the
mediastinum waste very rapidly, lose appetite, become feverish, and soon
develop cachexia.

=Diagnosis.= The diagnosis of tumour of the mediastinum is easy, because
of the well-marked character of the apparent symptoms.

=Prognosis.= The prognosis must be regarded as extremely grave, and in
most cases fatal, for there is no active method of intervention,
extirpation being impossible.

There is no =treatment=. The animal should at once be slaughtered.




                              SECTION IV.
                       THE ORGANS OF CIRCULATION.


                SEMIOLOGY OF THE ORGANS OF CIRCULATION.

The semiology of the circulatory apparatus comprises the clinical
examination of the heart, arteries and veins, and the examination of the
pulse and blood.

=Heart.= In animals of the bovine species, the heart is situated in the
thoracic cavity opposite the third, fourth, fifth and sixth ribs, nearly
in the median plane of the thorax, and inclined from front to back at an
angle of 70 degrees.

The pericardial sac touches the extremity of the sternum where it is in
immediate contact with the lower insertion of the diaphragm. This
peculiar arrangement favours the development of pericarditis due to
foreign bodies.

On the left side the pericardial sac may come in direct contact with the
internal surface of the thoracic cavity opposite the lower extremity of
the third, fourth, and sometimes fifth ribs. At all other points the
pulmonary lobes, as expanded during inspiration, separate it from the
thoracic wall.

Although the pericardium and heart are situated in the median plane,
percussion and auscultation should be performed on the left side, since
the anterior and cardiac lobes of the left lung are less developed than
those of the right; but the heart can be auscultated on the right side,
as is advisable at times.

In the healthy ox there exists an area of the left thoracic wall which
may be called the cardiac zone, on a level with which are heard the
normal heart sounds. In diseased conditions this zone or area may vary
in size, and the sounds may be modified.

The heart can be examined by inspection, palpation, percussion, and
auscultation.

Under ordinary conditions inspection reveals nothing in well-nourished
animals; but in very thin subjects and in those suffering from recent
cardiac lesions or pseudo-pericarditis, a rhythmic movement of the chest
wall is sometimes detected.

Palpation is performed by placing the open hand on the cardiac zone. In
this way the cardiac shock can be felt, its degree of intensity judged,
and, in an imperfect manner, its rhythm.

Percussion by means of the fingers or a pleximeter discloses the extent
of the physiological area of partial dulness, due to the presence of the
heart, as well as its variations in pathological conditions,
particularly in pericarditis with marked exudation.

[Illustration: $1]

In such cases there may even be complete dulness when the distended
pericardium thrusts upwards the corresponding pulmonary lobe, and comes
in contact with the internal surface of the thoracic wall, or, in cases
of pericardial pneumatosis, exaggerated resonance, and a tympanitic
sound.

Auscultation is carried out either directly or by the stethoscope or the
phonendoscope. The normal or pathological sounds of the heart are thus
ascertained, as well as the intensity of the cardiac beats and sounds,
the frequency of the rhythm, etc.

When injuries have occurred which cause murmurs, it is best to use the
stethoscope and to apply it at the points where murmurs are heard at
their maximum intensity, _i.e._, exactly at the spot where the cardiac
shock is noted, and towards the base, in the region where the great
arterial trunks begin.

In the latter case it is often useful to draw the left fore leg forward.

=Arteries.= The arteries are rarely the seat of lesions that can be
detected by examination, and therefore such examination is usually
limited to noting the state of the pulse.

Arteritis and thrombosis of arteries are rare, and although lesions of
atheroma have been discovered in certain chronic diseases, such as
tuberculosis, chronic diarrhœa, etc., they are difficult to detect, even
on examination per rectum of the bifurcation of the aorta.

=Pulse.= The examination of the pulse, on the contrary, is of great
importance. In animals of the bovine species the pulse may be taken at a
number of different points, such as the submaxillary artery, on the side
of the lower jaw: in the case of very thin animals at the radial within
and in front of the elbow joint; at the internal saphenous artery, at
the height of the mamma or scrotum; or at the coccygeal artery, at the
base of the tail.

This examination reveals the frequency (50 to 60 per minute), the
quality, whether strong, feeble, imperceptible, etc., the regularity,
etc., etc.

=Veins.= The veins are more easily examined than the arteries, on
account of their superficial position in most cases.

Inspection and palpation are the only means of examination.

Inspection shows the degree of fulness or collapse, and also the
existence or absence of what has been termed venous pulse.

Venous pulse occurs only at the lower extremity of the jugulars. It is
very frequent in animals of the bovine species, and in thin animals is
not necessarily a pathological symptom. It is due to reflux of blood in
the anterior vena cava, under the influence of the expiratory effort;
sometimes to emphysema, tuberculosis, etc.; in other cases to the return
of blood towards the vena cava and jugulars at the moment of auricular
systole, as a result of lesions of the tricuspid or auriculo-ventricular
orifices.

By palpation of the veins their permeability can be estimated, also the
degree of distension or obstruction, and the condition of their
contents.

=Capillary system.= Among methods of arriving at the state of the
circulatory system must be included an examination of the vascular
condition of the accessible mucous membranes, such as those of the eye,
mouth, nostril, vulva, etc. This examination is easy to carry out, and
is of value in diagnosing congestive states, pneumonia, and local
inflammation.

=Blood.= Examination of the blood is sometimes necessary for the exact
diagnosis of certain diseases, and therefore should be carried out
whenever occasion requires. The physical state, coloration, and rapidity
of coagulation afford valuable data in certain diseased conditions, and
indicate the approximate richness in hæmoglobin, the normal or abnormal
composition of the plasma, and the richness of the blood in white
corpuscles.

Microscopic examination is still more valuable, whether carried out by
the moist method, in which a drop of blood is compressed under a cover
glass, or the dry method with or without staining. In the latter case
the specimen is fixed with a mixture of equal parts of alcohol and ether
or by immersing it in a 1 per cent. solution of osmic acid.

By this means it is possible to detect the condition of the red and
white blood corpuscles and hæmatoblasts; the existence or non-existence
of leucocytosis and its degree, as well as the existence, for instance,
of leucocythæmia.

The blood corpuscles may also be counted.

Histological examination, supplemented by suitable staining, reveals the
presence of normal or abnormal blood corpuscles, parasites such as
piroplasma, or microbes such as bacteria.

Such examination necessarily presupposes a knowledge of what should be
looked for in the normal state.

In normal blood the red blood corpuscles predominate. They are all
similar in form and, with few exceptions, of the same size. They stain
strongly with acid solutions such as eosine. In pathological conditions,
large or giant corpuscles may be found (macrocytes), as well as those of
medium size (normal) and small size (microcytes). Some are vigorous and
stain deeply; others, on the contrary, are degenerating or dead, and
have no greater affinity for one constituent than for another of the
double or triple stains commonly employed.

In pathological conditions the hæmatoblasts occur in very varying
numbers.

The white blood corpuscles found in health may be classified as
follows:—

Large and small lymphocytes, each of which has a round voluminous
nucleus and a narrow border, and contains a non-granular protoplasm;
their proportion varies between 22 per cent. and 25 per cent.:

Polynuclear leucocytes or polymorphous leucocytes with a single nucleus,
which originate in bone marrow, stain best with neutral colours, and are
present in the proportion of 70 per cent. to 72 per cent.:

Mononuclear leucocytes with an ovoid eccentric nucleus stain best with
basic colours, and form about 1 per cent.:

Polynuclear leucocytes stain best with eosine or acid colours, and form
about 1 per cent. to 2 per cent.

When these white blood corpuscles are in larger number the condition is
known as leucocytosis, and when one or other variety is in very great
excess the condition is known as leucæmia.




                               CHAPTER I.
                           CARDIAC ANOMALIES.


                         ECTOPIA OF THE HEART.

Ectopia of the heart, _i.e._, congenital malformation in which the heart
is displaced from its normal position and thrust sometimes completely
beyond the thoracic cavity, is not very rare. The heart may be well
developed, but it is not enclosed by the thoracic walls when the
thoracic cavity closes during the first stages of embryonic life. The
sternum, which is cartilaginous and becomes ossified only at a later
period, remains fissured along the median line, and the fissure, usually
of oval form and with rounded margins, surrounds the auricles and the
vessels at the base of the heart. The ventricles form a hernia
projecting beyond the thorax, which then only contains the two pleural
sacs and a complete mediastinal partition. The pericardium remains
undeveloped.

Despite this malformation, the embryo develops. The fœtus may in due
season be brought forth living, but as a rule death occurs in a few
hours.

=The diagnosis= is easy, but this malformation cannot be treated. All
that can be done is to protect the ectopiated organ against external
violence in cases where the young creature is born alive.




                              CHAPTER II.
                             PERICARDITIS.


Pericarditis consists in inflammation of the pericardial sac. It is
attributable to different causes, varying in importance and in
causation.

=Specific pericarditis= may be produced by the tubercle bacillus, or it
may develop during an attack of contagious peripneumonia. Tuberculous or
peripneumonic forms of pericarditis as a rule form only complications of
chronic pulmonary tuberculosis or peripneumonia. They are very rarely
primary in character, and, like the allied forms of pleurisy, assume a
vegetative and adhesive form in tuberculous cases.

Moussu has never seen the true exudative form either in acute or chronic
tuberculosis, but only vegetative and caseous forms.

=Simple acute pericarditis.= Cases of simple acute exudative
pericarditis have been described, and have been referred to chills,
wounds, or injuries in the region of the heart, and in a few cases to
the rheumatic diathesis.

Such forms of pericarditis may occur, but probably are very rare, for
Moussu has seen but two cases. As the symptoms correspond exactly to
those of exudative pericarditis produced by a foreign body, it is
unnecessary to describe them specially.

The only important detail to bear in mind with this disease is the
possibility of cure by suitable treatment, such as the application of
stimulants or vesicants to the cardiac zone, the administration of
salicylate of soda or diuretics, and complete rest.

=The diagnosis=, moreover, should be confirmed by making an aseptic
exploratory puncture with the capillary trocar. The nature of the liquid
withdrawn will indicate whether the case is one of simple acute
pericarditis or pericarditis due to a foreign body.

=Cancerous pericarditis= is generally secondary, and is caused by
development of tumours on the pericardial serous membrane, and in the
myocardium. Moussu, however, has seen one case of primary cancerous
pericarditis, the tumours being found only on the periphery of the
myocardium. The growth assumes a vegetative form with moderate
exudation. The symptoms, however, so closely approach to those of
exudative pericarditis due to foreign bodies that only the latter
variety, which is by far the most frequent in animals of the bovine
species, need be described.


             EXUDATIVE PERICARDITIS DUE TO FOREIGN BODIES.

[Illustration: $1]

This condition has been erroneously described as traumatic pericarditis,
but the latter term would suggest that the disease was due to an injury
acting from without. It may be defined as a disease produced by the
discharge into the pericardial cavity of some foreign body from the
gastric compartments.

Boizy in 1858 described several cases of this kind of pericarditis.
Hamon in 1866 gave an excellent table of symptoms. Roy in 1875
supplemented this with numerous observations showing clearly the
possibility of recognising the disease by clinical examination.
Pericarditis due to foreign bodies is to-day one of the best
characterised diseases of the ox, and it is easy to diagnose.

Before approaching the etiological side of the question, it is necessary
to recall in a few words the anatomical arrangement of the pericardium
and its relations to neighbouring organs.

In the ox the diaphragm presents a marked concavity directed towards the
abdomen. The pericardium, situated exactly in the median plane, is fixed
by its point to the sternum. A fold of adipose tissue directly connects
it with the anterior surface of the diaphragm. On the abdominal side the
conical right compartment of the rumen is in free communication with the
reticulum, which is closely applied to the posterior surface of the
diaphragm on the median line opposite the spot occupied by the
pericardium on the anterior surface (Fig. 176). As a result of this
arrangement any object passing through the reticulum and diaphragm in
the median plane would enter the pericardial cavity. These particulars
indicate clearly how this form of pericarditis is produced.

=Causation.= One of the chief causes of pericarditis by a foreign body
is connected with the way in which oxen feed. They rapidly swallow their
food and any foreign bodies that may be concealed in it, submitting it
later on to a second mastication in the course of rumination. This
method of feeding results in bolting the food almost without
mastication, hence the possibility of swallowing foreign bodies.

The proximity of the reticulum to the pericardium is also an important
factor, because the foreign bodies fall into the reticulum as soon as
the bolus of food begins to break up. It is important to notice,
moreover, that pericarditis is commonest on farms where the oxen are
attended by women, or in regions where sharp objects are to be found on
roads or pastures frequented by the animals, such as the vicinity of
needle, nail, and rivet factories.

The sole cause is the penetration of a foreign body into the pericardial
sac.

=Pathogeny.= All kinds of foreign bodies are swallowed by oxen, as is
abundantly shown by post-mortem examinations. These indigestible bodies
pass with the food into the rumen, and accumulate in the deepest
portions of that receptacle. Owing to physiological contractions the
lower wall of the rumen rises to the level of the orifice of
communication with the reticulum, and so passes much of the material
accumulated within it into this organ.

Soft foreign bodies fall towards the lower parts of the reticulum, but
sharp objects may lodge in its walls. Very often the bodies penetrate in
this way without causing reticulitis or grave inflammation. The
functions of the reticulum are not impeded. The commonest of such
objects are needles, pins, nails, or fragments of iron wire. On account
of their form, needles are the most dangerous. The sharpness of one
extremity ensures its passing readily through the tissues, and as the
point is the part that offers least resistance, the needle continues
gradually to penetrate.

If the foreign body becomes implanted vertically in the lower wall of
the rumen or reticulum it may be expelled directly through the medium of
an abscess. This is a favourable termination, though it usually results
in permanent gastric fistula.

More often the objects penetrate the anterior wall of the reticulum and
gradually work their way towards the diaphragm, impelled by the
movements of the reticulum and the other digestive compartments. They
perforate the muscle and pass into the thoracic cavity, either in the
direction of the pericardium or of the pleural sacs.

First as to the penetration of the pericardium. The foreign body,
whatever it may be, produces by its presence alone very marked
irritation, and as in addition it is always infected in consequence of
its having passed through the digestive compartments, inflammation is
set up to a degree proportionate to the pathogenic qualities of the
infective agent.

=Symptoms.= The early symptoms are those of indigestion, and not of
pericardial disease, a fact which is easy to understand, because at
first the whole mischief is in the abdominal cavity. The patients are
dull, restless, and seem to be suffering from an obscure ailment. They
remain standing more than usual, show more than ordinary deliberation in
lying down, lose appetite, cease to ruminate regularly, and exhibit
intermittent tympanites.

The cause of these symptoms is as follows: At first the reticulum is
partly immobilised by the local inflammation, and at a later stage
movement of the diaphragm is checked by reflex action when the sharp
body has progressed far enough to touch it. The rhythmic movements of
the reticulum and the diaphragm are interfered with, rumination is
disturbed, eructation ceases, and tympanites appears.

The patient often utters slight groans, particularly when forced to
move; but as this is a sign common to all grave diseases it can only
give rise to a suspicion as to what has occurred. In ten to fifteen days
this primary phase may have terminated; but it is impossible to say how
long it lasts, for it varies with each animal as with each variety of
foreign body, and it may be prolonged for months.

From the moment it reaches the thoracic cavity the foreign object makes
its way towards the channel formed on either side by the ribs and below
by the sternum, and therefore towards the point of the heart. This is
the second phase of development.

The passage of the foreign body through the diaphragm occupies a more or
less considerable time, depending on its length; the beginning of this
second phase is characterised by relative immobility of the circle of
the hypochondrium during respiration. The abnormal sensibility and pain
impede contraction of the diaphragm.

Palpation of the region of the xiphoid cartilage then reveals abnormal
sensibility, and sometimes causes the animal to resent being handled.

From this time the pericardial symptoms proper commence, the foreign
body having come in contact with the pericardium. This phase, unlike
those which precede it, presents well-defined symptoms. The irritation
of the heart and its ganglionic system by a foreign body in the
pericardium is shown by considerable acceleration of the heart beats
even before there is any exudation into the pericardial sac. Instead of
60 to 70 beats, the normal number, the pulse may rise to 80, 90, 100, or
even 110 beats per minute. The heart sounds are tumultuous, dull and
ill-defined, while the pulse appears bounding and strong.

But this period of cardiac excitement while persisting is soon
complicated by other symptoms. As soon as the foreign body penetrates
the pericardial sac, there is infection, which produces an active form
of inflammation and abundant exudation. From this time the pulse becomes
weaker and weaker, until, under the steadily increasing pressure on the
heart, it is almost imperceptible.

There is only moderate fever. As soon as the exudation becomes
considerable, the symptoms of pericarditis grow very marked: they may be
grouped in the following order, according to their importance.

A. =Cardiac symptoms.= On palpation of the cardiac zone on the left the
impulse of the heart is no longer felt. Percussion, which under normal
circumstances reveals only partial dulness, now seems to give pain, and
indicates abnormal dulness distributed in a vertical plane. The
pulmonary lobes between the pericardium and thoracic walls are thrust
upwards. The distended pericardial sac approaches the parietal layer of
the pleura and may adhere to it, hence the dulness. This dulness extends
as far back as the xiphoid appendix of the sternum, and can be detected
on both sides, marginated above by a convex line.

In rare cases the dulness is absent, being partially replaced by
tympanitic resonance, due to the presence of gases in the distended
pericardial cavity, which gases originate in the digestive reservoirs or
result from putrid fermentation of the pericardial exudate.

Simple or double pleurisy, or even pneumonia of the cardiac lobes
resulting from infection by contiguity, may complicate cases of rapid
pericarditis. The dulness then appears modified, as do the signs
observed on auscultation.

Auscultation furnishes valuable indications. From the outset it reveals
acceleration of the heart. At a later stage, but only for a short time,
it permits of the detection of the pericardial rubbing sound which
precedes serous exudation, and which may persist for several days when
large quantities of false membrane are produced.

If exudate is present in considerable quantities a liquid sound is heard
at each heart beat. The heart appears to be beating in water, but the
liquid note varies considerably. It has been termed the “claclaque”
sound (Lecouturier, 1846), in allusion to the sound produced by the
meeting of water ripples; “clapotement” sound (Boizy, 1858), with
reference to the sound produced under the influence of a light breeze on
the borders of a stream; “glou-glou” sound (Roy, 1875), suggested by the
noise of liquid escaping from an inverted bottle into a resonant vessel,
etc. It is important, however, to remember that cases occur (principally
when the pericardium is greatly distended and entirely filled with
liquid) where, with the animal at rest, these sounds are difficult to
detect. To render them noticeable the patient must be walked for a few
yards.

Vernant, again, has described a sound as of dripping water, of quite
special character; he compared it to that resulting from the fall of
drops of liquid on to a marble table or into a half-filled vessel. So
far as can be ascertained this sound of dripping water greatly resembles
that heard in pneumo-thorax, but it is less resonant and less prolonged.

It appears to be characteristic of the presence of air in the
pericardial cavity, and its special quality varies with the quantity
accumulated in the pericardium. Masked by these pericardial sounds the
beating of the heart seems dull, badly defined, distant and stifled.

[Illustration: $1]

B. =Jugular symptoms.= The “jugular” symptoms are secondary, and result
from the accumulation of liquid in the pericardial cavity. No
intra-pericardial exudate can exist without exerting pressure on the
heart, and as the auricles have very thin walls and are more
compressible than the ventricles, this pressure immediately causes
difficulty in the return circulation, whence venous stasis, varying in
intensity, but clearly visible and appreciable on account of the
distension of the jugulars.

The venous stasis is general, for the pulmonary veins are as much
compressed as the posterior and anterior venæ cavæ, but it is only
apparent in the large superficial veins. This stasis is accompanied by
venous pulse, and particularly by peripheral or internal œdema, œdema of
the lung, intestine, mesentery, etc., of the submaxillary space and of
the dewlap and entrance to the chest. Œdema of the submaxillary space is
specially characteristic, for it appears almost first amongst external
signs. That of the dewlap follows at a later stage, and extends
backwards as far as the umbilicus, rising above this point as high even
as the entrance to the chest and the axillary region.

C. =Pulmonary symptoms.= The pulmonary symptoms result from difficulty
in the return circulation and from the venous stasis. They are due to
passive congestion and œdema of the lung or to hydro-thorax. At rest the
respiration may appear fairly regular, but at the least movement it is
accelerated, and may rise to 40 or even 60 per minute.

Percussion reveals lessened resonance of the parts, and in the case of
hydro-thorax dulness marginated by a horizontal line, as in pleurisy.

On auscultation the vesicular murmur may sometimes have diminished or
even disappeared, while the respiration may be blowing, as in active
congestion, and in exceptional cases a tubal souffle may be observed. In
most cases the animal has a paroxysmal, somewhat frequent cough, due to
reflex irritability of the pneumo-gastric.

Cruzel in addition mentions a double respiratory movement like that
produced in the horse by broken wind. This is really the result of
hydro-thorax, and is not a constant symptom.

D. =General symptoms.= When the disease has lasted a certain time the
patients show certain well-marked general symptoms: they remain standing
in one position for long periods, with the head and neck extended, the
front legs thrust outwards from the trunk and the body rigid, as though
the least movement caused them pain. The general attitude expresses
anxiety, the animals lie down with great care and seldom remain long in
this position, which interferes with the functions of the heart and
lung. In the last stages the animals remain constantly standing,
appetite is almost entirely lost, and they waste rapidly.

=The course= of pericarditis due to foreign bodies is very variable.
Sometimes death occurs in eight or ten days. In other cases the animal
may survive for weeks, provided it is well tended. Everything depends on
the rapidity with which the foreign body moves and on the character of
the infectious organisms which it introduces into the pericardium. Death
is the inevitable termination, and occurs as a consequence of cardiac
and respiratory syncope. It may follow suddenly as the result of a
simple forced movement, even when the animal still seems to retain some
amount of strength. When the organisms introduced into the pericardium
are of marked virulence, complications such as septic pleurisy and
pneumonia may be observed, and death soon takes place.

It has been suggested that recovery might follow a return of the foreign
body towards the reticulum. This view can only have been advanced as a
consequence of errors in diagnosis, either as to the existence of
pericarditis or as to its nature. Pericarditis due to cold or rheumatism
sometimes becomes cured spontaneously.

Death, again, may suddenly occur by syncope when the foreign body
penetrates the myocardium, passes through it, and enters the ventricular
cavities.

The return of the foreign body is not conceivable, at all events after
it arrives in the pericardial cavity. Up to that time the only
disturbance is of a digestive character; no pericarditis exists. But
when for example the disturbance is due to long fragments of iron wire
which may extend from the reticulum as far as the pericardium, it is
clear that the pericarditis is of a kind which cannot be cured without
leaving traces. In our opinion, natural recovery is impossible.

=Diagnosis.= The diagnosis of pericarditis cannot be made until such
pericarditis actually exists, _i.e._, until the disease has arrived at
the third stage of development mentioned above.

As long as the symptoms point only to the first or second stage, the
logical diagnosis is reticulitis produced by a foreign body. At this
time the development of pericarditis, although possible, is not
inevitable.

When, on the other hand, one knows how the digestive disturbance has
originated and developed and thereafter notes signs of cardiac
irritation, disappearance of the cardiac impulse, dulness of the heart
sounds, venous stasis, etc., the diagnosis is easy even thus early.

Mistakes are not very likely. Only in some cases are they liable to
occur, as in acute peripneumonia of the anterior pulmonary lobes,
causing compression of the pericardium of the anterior vena cava and
producing secondarily venous stasis and œdema of the dewlap. Cases of
specific pericarditis due to peripneumonia also occur, and under such
circumstances a mistake would be even more excusable. Nevertheless, the
temperature curve in itself is a sure indication, for whilst in
peripneumonia the fever is always very marked, it is scarcely noticeable
in pericarditis due to a foreign body.

When the diagnosis of pericarditis has been arrived at it is desirable
to determine the exact nature of the disease, for whilst cases of
pericarditis due to foreign bodies are incurable and in the interest of
the owner the animals should be slaughtered, pericarditis due to cold or
rheumatism may be successfully treated. Rheumatism generally affects the
synovial membranes even before it produces pericarditis, and this
indication, supplemented by the history of the case usually ensures one
against mistakes regarding the initial cause.

It is much more difficult to distinguish pericarditis due to a foreign
body from pericarditis due to carcinoma and from the forms of
pseudo-pericarditis produced by lesions in the neighbourhood of the
heart. When considering the latter we shall deal with this particular
point.

=Prognosis.= The prognosis is always fatal.

=Lesions.= When the foreign body is very thin and sharp, the reticulum
may not become attached to the diaphragm. In such cases its passage has
been rapid and the tissues have healed.

Usually the reticulum, diaphragm and pericardium are united by a mass of
fibrous tissue as thick as a man’s arm. It resembles a fibrous sleeve
surrounded by an œdematous zone, usually of slight extent. This mass of
new fibrous tissue is traversed by a sinuous tract resulting from the
irritant action of the foreign body on the surrounding tissues. All
writers describe this fibrous sleeve, which, however, only occurs in
cases where a very long foreign body has occupied a considerable time in
passing from the reticulum to the cavity of the chest.

In very exceptional cases the sinuous tract is ramified, possibly as a
result of displacements of the foreign body.

The orifices of the tract are to be found, one in the reticulum, the
other in the pericardium. On the side of the reticulum there is never
more than one opening, and in many instances the tract is already closed
on that side, either by exuberant granulations or by a cicatrix.

On the contrary, the fistula is more frequently open in the pericardial
cavity. Its walls are of very varying appearance, depending on their
age: they may be red, greyish, soft or hard, and when the lesion is of
old standing they may have been converted into a sclerotic tissue.

[Illustration: $1]

The pericardium appears distended with a considerable quantity of liquid
of a special character—sometimes sero-sanguinolent, sometimes almost or
entirely purulent; sometimes yellowish, or greenish-grey; sometimes
frothy, inodorous, or very fœtid.

These characters depend on the nature and number of the germs which have
invaded the pericardial cavity. They also vary with the gravity and
number of the hæmorrhages produced by the action of the foreign body on
the myocardium.

The quantity of liquid also varies within very wide limits. There may be
scarcely any exudation. In that case the pericarditis is of a partially
adhesive character, with abundant false membranes. As a rule the
quantity of fluid exudation varies between seven and eight quarts, but
sometimes the quantity is much greater. Trasbot described an instance in
which the united weights of the heart and pericardium exceeded 36 lbs.
Hamon mentioned a case of pericarditis in which the liquid exudate
exceeded twenty quarts.

“When inflammation is first set up the liquid is serous, yellowish, or
reddish yellow. It contains fibrinous flocculi in suspension. Little by
little this exudate becomes purulent, whilst the internal layers of the
pericardial serous membrane undergo desquamation. These are next covered
with false membranes of varying appearance; the fibro-albuminous
exudation is wrinkled, villous and tufted. The two layers of serous
membrane are connected at certain points by this exudation, the
adhesions being sometimes very extensive. The pericardial sac properly
so called becomes the seat of marked lardaceous thickening, due to
inflammation. The heart appears entirely covered with a layer of greyish
or earthy-coloured granulation tissue, which appears as though baked,
and was compared by Hamon to the back of a toad. It is atrophied as a
consequence of prolonged compression.

Under the influence of the eccentric pressure of the liquid the
pericardial sac is distended and comes in contact with the walls of the
chest, to which it may adhere. The foreign body, especially if small, is
not always easy to find.

The myocardium often displays interesting lesions. At first there is
thickening, or more commonly sclerous degeneration, of the superficial
layers covering the ventricles, and then appears a crop of little
miliary abscesses. Abscesses of considerable size have several times
been detected in the walls of the ventricles and in the interventricular
septum.

The foreign body, moreover, may not only injure the myocardium, but may
even perforate it completely and produce ulcerative endocarditis
(Cadéac). In this case infectious germs very rapidly invade the
circulation and all the tissues, and the animal dies of pyæmia.

These essential lesions are accompanied by others of varying importance.
Thus the lung is congested throughout, and by contiguity of tissue
inflammation may extend from the pericardium to the lower part of the
pulmonary lobes and to the pleura.

Interference with the return circulation induces lesions due to venous
stasis: dropsy of the chief serous membranes, œdema of the connective
tissue, pleural and peritoneal exudations, etc. If the hind limbs never
become swollen it is because the skin covering them is very resistant
and does not readily yield. The liver becomes hypertrophied, congested
and engorged with blood, and when the animals live for some weeks, shows
the appearances known as cardiac or nutmeg liver.

=Treatment.= The treatment of pericarditis due to the presence of
foreign bodies is at present merely palliative. Often the only thing to
be done is to slaughter the animal.

We need not go back to the methods formerly recommended. All are
illusory or mischievous, such as the use of purgatives to arrest or
reverse the progress of the foreign body, removal of the foreign body
after opening the rumen, puncture of the pericardium, etc.

In 1878 Bastin successfully opened the pericardium and extracted the
foreign body through a window produced in the thoracic wall.

This operator recommends that after drawing the left limb forward and
incising the skin and muscles, the operator, with his hand bound round
with a cloth, should perforate the pleura, and then having found the
foreign body, proceed to extract it. By this method it seems difficult
to cause perforation of the pericardium, which would certainly lead to
the production of pneumo-thorax complicated with fatal septic pleurisy.

It must be borne in mind that the two pleural sacs, right and left,
descend as far as the sternum (Fig. 173), and that it is not possible to
touch the pericardium directly without perforating the pleura.

Moussu has drained the pericardium through the pleura in the hope of
relieving the pressure on the heart and facilitating the reabsorption of
the œdema, in order to permit of the subsequent slaughter of the animal,
but has had unsatisfactory results. Lastly, he has practised median
trepanation of the sternum in the infra-pericardiac region. Here again
the operation is difficult, because of the œdematous infiltration of all
the substernal region, while it is so dangerous to the patient, which
must be cast and may suddenly succumb, that it is of no use in ordinary
practice.

There is probably only one condition in which it would be possible to
attempt intervention with a fair chance of success, that is, when there
exists a fibrous connection between the pericardium, lung, and wall of
the chest on the right or left side.

In such cases aspiratory puncture or incision of the pericardium in an
intercostal space might prove of service, because it would not expose
the animal to the danger of pneumo-thorax.

The only difficulty lies in ascertaining beyond all question the
existence of such an adhesion before attempting operation, and this is
really very great, even having regard to the form of the dulness and the
absence of all respiratory sound in the lower third of the thoracic
cavity and cardiac zone. The pulmonary lobe between the heart and chest
wall may be thrust upwards and be partially adherent to the pericardium
and to the parietal pleura, and at the same time it may be impossible to
avoid producing operative pneumo-thorax when the cartilages are resected
to admit of incising the pericardium.

The only logical method seems to be puncture of the pericardium through
the xiphoid cartilage, as described below.

The topographical anatomy of the thoracic viscera shows that the point
of the pericardium extends along the sternum to a point close to the
lower insertion of the diaphragm, and that the pericardial sac is only
separated from the xiphoid region, or rather from the region of the neck
of the xiphoid appendix of the sternum, by the fatty cushion at the
point of the heart.

[Illustration: $1]

A glance at the annexed diagram (Fig. 177) will show this.

The diagram, carefully reproduced from an anatomical preparation of an
animal which succumbed to pericarditis, shows that the distended
pericardium extends close to the neck of the xiphoid cartilage.

=First stage.= Identify the three following anatomical guiding points:—

(1.) Xiphoid appendix and white line. (2.) Point at which the circle of
the hypochondrium becomes attached to the sternum. (3.) Point at which
the external mammary vein penetrates the abdominal wall (Fig. 178).

Lines uniting these three points enclose a right-angled triangle, which
the operator must imagine to be bisected by a third line.

The incision, which should be about 8 inches in length, follows this
bisecting line at an equal distance between the white line and the
circle of the hypochondrium, to a point within about 8 inches of the
anterior margin of the mamma. All these points are readily observable
before the animal is cast.

[Illustration: $1]

The cutaneous incision affords exit to large quantities of fluid, and
the pectoral muscles attached to the neck of the ensiform cartilage can
then be divided with the bistoury. The area of operation is thus
uncovered.

=Second stage.= The second phase comprises incision of the tissues
opposite the neck of the ensiform cartilage, about 8 inches in front of
the base of the triangle and at equal distances from the points Nos. 1
and 2; incision through the skin for a distance of 8 inches, and
dissection of the muscles of the ensiform region exposed at the neck of
the cartilage.

By means of the index finger or the index and middle fingers of the
right hand the mediastinal space is explored, and the fatty masses round
the base of the heart broken through. If the pericardium is greatly
distended, the point of the sac can be felt with the tip of the finger,
or its position can be recognised, even from a little distance, on
account of the fluid contents transmitting the impulse of the heart. The
sensation conveyed to the finger is very clear.

The right index finger is then replaced by the left, and, a trocar about
10 inches long and ¼ inch in diameter being introduced along the index
finger used as a director, the pericardial sac is reached. The exudative
fluid transmits the impulse due to the beating of the heart, and the
pulsations can be clearly distinguished when grasping the handle of the
trocar.

=Third stage.= Digital exploration of the course of the puncture and
fatty cushion at the base of the heart, with the object of discovering
the position of the pericardium.

=Fourth stage.= Puncture with a trocar about 10 to 12 inches in length,
puncture of the pericardium, irrigation and dressing.

[Illustration: $1]

The trocar is inclined in a slightly oblique direction from without
inwards and forwards towards the median plane, in order that the point
may not deviate towards the left pleural sac; the left index finger is
then withdrawn, and by a sharp thrust of the right hand the trocar is
pushed forward about 1 to 1½ inches and the pericardial sac is entered.

The position of the canula should not be altered whilst liquid is
escaping, for if it is thrust in too far a considerable quantity of
fluid may remain in the deepest portion of the sac.

The cavity having been drained, a long strip of iodoform gauze is
introduced into the track and a protective surgical dressing applied
over the incision in order to prevent infection by the litter.

In consequence of the introduction of the fingers into the track caused
by puncture and the escape of pericardial liquid along the canula or
after removal of the canula, the operative wound is necessarily
infected; but this is of little importance, because the opening is
inclined downwards, and also because it is impossible to hope for
aseptic healing.

The dressing is renewed after forty-eight hours, and every three or four
days afterwards.

The œdematous infiltration about the front portion of the body
disappears rapidly in two to three days, and should the animal be
slaughtered the meat is quite sound in appearance.

This operation does not aim at effecting a cure, but is simply for the
purpose of allowing animals which would otherwise be valueless to be
slaughtered and sold.

[Illustration: $1]


                         CHRONIC PERICARDITIS.

Pericarditis when due to tuberculosis may assume the chronic form.
Tuberculous pericarditis, at least in a large number of cases, is only
accompanied by slight exudation, which might remain unnoticed unless the
animals were carefully examined; but it causes the internal surface of
the pericardial sac and the surface of the myocardium to become covered
with exuberant vascular growths, which by setting up adhesions lead to
partial or generalised union of the heart and pericardial sac. Between
these adhesions, which form partitions, are found little cavities filled
with sero-sanguinolent, grumous, or caseous liquid. In time the
adhesions increase in number, pericarditis obliterates the free space,
and the heart becomes wholly adherent to the pericardium.

As in acute pericarditis, the fibrous layer undergoes thickening and
hardening processes. The superficial layers of the myocardium undergo
sclerous transformation, and the tissues forming the adhesions
themselves may assume the characters of fibrous tissue.

In one solitary case Moussu saw another form of chronic pericarditis
with complete adhesion of the heart and pericardial sac, without any
exudation and almost without any false membranes. He was unable to
determine the exact cause, but was strongly inclined to regard the
disease as having followed pericarditis _à frigore_ or pericarditis of a
rheumatic character.

[Illustration: $1]

Adhesions between the heart and pericardial sac are also said to be the
inevitable though delayed result of all punctures of the pericardium
through the ensiform cartilage in cases of pericarditis due to a foreign
body.

=Symptoms.= If the chronic pericarditis is limited to a few partial
adhesions, it remains unnoticed; but when it is more marked it offers
certain signs of acute pericarditis, such as partial dulness of the
cardiac area, which is more extensive than usual, disappearance of the
cardiac shock, weakening of the sounds, feebleness of the pulse, very
marked venous pulse, moderate stasis, extremely rapid and aggravated
dyspnœa when the animal is forced to walk, threatened asphyxia if
exercise is prolonged, and complete asystole.

All these symptoms are due to the existence of adhesions between the
heart and pericardium, which, by destroying the interpericardial space,
interfere with diastole while preventing regular systole.

Sudden death is a frequent consequence.

The =diagnosis= of chronic pericarditis is very difficult. The
=prognosis= is extremely grave, and we do not possess any means of
dealing with the condition.


                          PSEUDO-PERICARDITIS.

Under this title we purpose grouping a certain number of pathological
accidents due to different causes, but manifesting themselves by
identical symptoms, which symptoms offer so marked a resemblance to
those of pericarditis produced by foreign bodies as to suggest the
presence of that disease. This refers to accidents by which the foreign
body closely approaches, without actually touching, the pericardium, the
lung or the pleural sacs, but in which it causes purulent collections
which displace the pericardium, indirectly compress the heart, and
finally cause symptoms of an apparently pericardial character.

=Causation.= During the development of pericarditis the foreign body
perforates the reticulum and diaphragm, passing along the middle line of
the body, without which it would not come in contact with the
pericardium. If the perforation, however, occurs to the right or left of
the median plane, the foreign body moves forward just as easily, but it
misses the pericardium and passes either into the lung, where it causes
fatal pneumonia; or the pleura, where either it sets up septic pleurisy
in the subpleural connective tissue or produces an abscess.

The abscess is generally lateral, situated in the right subpleural
region, or it may develop below the pericardium. These are the two
varieties of pseudo-pericarditis seen by Moussu.

There is, however, a third variety, which might be called “parasitic
pseudo-pericarditis.” It is extremely rare, and Moussu has only seen one
case. It was due to the presence of an enormous hydatid cyst of the
right lung as large as a man’s head, which was situated towards the
mediastinal plane of the lung and pressed on the supero-posterior
surface of the heart and pericardium. In consequence of the permanent
downward pressure which it exercised it interfered seriously with the
heart’s action and caused symptoms of pseudo-pericarditis.

=Symptoms.= The general and external symptoms are those of
pericarditis—viz., dulness, diminution in appetite, irregular
rumination, wasting, œdema of the dewlap, distension of the jugulars,
marked venous pulse, great anxiety and dyspnœa when the patients are
forced to move, etc.

But the cardiac symptoms differ notably, and moreover vary, according to
the nature of the lesions. Speaking generally percussion reveals
complete dulness on one or both sides, and auscultation always indicates
the absence of sounds due to extravasated fluid in the pericardial sac.

When the abscess is situated below the pericardium, a condition
difficult to diagnose, the dulness seldom extends very high on either
side of the chest, and the sounds heard over the cardiac area, while
much weaker than usual, are audible above the normal points.

An abscess developing beneath the pleura on one side displaces the heart
in the opposite direction. The cardiac beat is weakened by the
compression, but, nevertheless, transmits an impulse to the purulent
fluid, which in its turn conveys it outwards through the intercostal
spaces in the form of movements corresponding in rhythm with the beating
of the heart, so that at first glance one might imagine an aneurism
existed at the base of the large arterial trunks. The lower pulmonary
lobe is thrust upwards, and over the area of dulness pulmonary sounds
completely disappear.

When the heart is compressed by a large hydatid cyst or other lesion,
the general and external symptoms are similar to those above described.

Finally, one last symptom, which appears of some importance, may be
mentioned. When animals suffering from pericarditis due to a foreign
body are forced to move, the heating of the heart becomes so tumultuous
that it can no longer be counted, and even in a state of rest it may
rise to 140 or 150 beats per minute. In cases of pseudo-pericarditis it
rarely rises above 90 or 110.

[Illustration: $1]

=Diagnosis.= The attempt to diagnose this condition accurately must not
be regarded merely as a result of scientific curiosity. Under certain
circumstances the diagnosis may be of very great importance. While the
patient affected with pericarditis due to a foreign body is beyond all
hope of recovery, certain cases of pseudo-pericarditis appear amenable
to treatment.

The diagnosis, therefore, is of great importance, and the practitioner
should spare no effort to confirm it, bearing in mind the symptoms
enumerated, and remembering that the normal sounds of the heart never
completely disappear.

An aseptic exploratory puncture with a long, fine needle will sometimes
prove of great assistance.

=Prognosis.= Although grave, the prognosis is less so than in true
pericarditis.

=Treatment.= If clearly recognised, both subpleural and subpericardial
abscesses seem curable. By freely puncturing the pus-filled cavity
through an intercostal space, the liquid may be evacuated and recovery
may occur. Healing is favoured by carefully washing out the cavity with
a non-irritant disinfectant.

The only precaution required in making such punctures is to avoid the
internal thoracic artery and vein, the intercostal artery, and the lower
cul-de-sac of the pleura.




                              CHAPTER III.
                             ENDOCARDITIS.


If the symptoms of pericardial diseases are well defined, we cannot say
the same of diseases of the heart, properly so-called. Such affections
often pass unnoticed, being detected only on post-mortem examination.
Moreover, cardiac diseases are rare. Very frequently they are only of a
secondary nature, accompanying or following better recognised
conditions, such as infectious diseases, post-partum infections, etc.

=Causation.= Endocarditis, _i.e._, inflammation of the endocardium and
valves, is rarely primary, simple and benign. It was formerly thought to
be the result of chills or of the rheumatic diathesis. These simple
forms of endocarditis usually escape observation, though careful
examination in the first instance reveals them.

Much more frequently, however, endocarditis is secondary, malignant,
infectious and infecting. This variety occurs as a complication of
post-partum infection or of very serious general conditions, such as
peripneumonia, gangrenous coryza, aphthous fever, tuberculosis, etc. To
detect it, not only must the original disease be accurately diagnosed,
but all the changes the disease is producing in important organs must be
followed.

While it is generally admitted that all forms of endocarditis, even of
the most benign character, are originally due to infection, it is
certain that in those of the second group the organisms which have
entered the bloodstream through a lesion of the uterus, lung or other
tissue, are endowed with very great virulence. They attack some point on
the endocardium, and produce either ulcerations which become covered
with fibrous clots, or exuberant new growths of a pathological nature,
which generally are papilliform, fragile, and prone to become detached
by rupture of their pedicle and thus to be launched into the general
circulation and to form emboli. The surface of these infected
vegetations, like that of the ulcerations, becomes covered with
fibrinous clots, which are readily loosened, form emboli in their turn,
and infect distant organs.

=Symptoms.= The general symptoms of infectious endocarditis are by far
the most important. They consist of prostration, loss of appetite,
severe thirst, and high temperature. The local symptoms consist
principally of murmurs: soft murmurs due to insufficiency of the
auriculo-ventricular valves, heard during systole, particularly opposite
the point of the heart where the cardiac shock is most clearly felt.
This fact differentiates them from the murmurs of chronic endocarditis,
which are usually due to aortic contraction, and are accompanied by a
systolic sound heard at the base of the heart, more in advance and at a
higher point than those now under consideration.

These murmurs or souffles furthermore vary in intensity and in
character, according to whether the endocarditis results from
post-partum infection, pyæmic disease, or some other cause.

=Diagnosis.= The diagnosis of endocarditis has not yet been the object
of really careful study in bovine pathology, but there is no doubt that
it can often be detected by patient examination.

=Prognosis.= The prognosis is very grave, and patients may die in a few
days.

=Treatment= comprises vigorous local stimulation over the cardiac area,
the administration of antithermic and antiseptic drugs, such as
salicylate of soda, or of digitalis, sparteine or other cardiac tonics.

Pathologists have also described, chiefly as post-mortem curiosities of
interest to pathological anatomists, various diseases and lesions due to
insufficiency or contraction of the auriculo-ventricular, aortic, and
pulmonary openings, lesions due to infectious myocarditis, to the
presence of parasites and to other causes.

The symptoms of these various diseases or lesions in bovine animals are
still too imperfectly understood to permit of more than a very limited
description.

In the present state of our knowledge, diagnosis would always be of an
uncertain character, and for this reason we do not propose to deal with
them at present.




                              CHAPTER IV.
                       DISEASES OF BLOOD-VESSELS.


Diseases of vessels, arteries or veins, in animals of the bovine and
ovine species are frequently nothing more than localisations of grave
general disorders, and rarely admit of treatment. This is specially the
case in regard to arteries, but a study of the diseases of veins has
some practical importance.


                               PHLEBITIS.

Phlebitis, _i.e._, inflammation of a vein, is of interest only in the
case of bovine animals. In them certain conditions may occur which the
practitioner should understand, with a view either to prevention or
treatment. Inflammation of the veins may be due to external causes, such
as surgical or accidental wounds (phlebotomy wounds, accidental wounds,
local inflammations, etc.), or to internal causes of infectious origin
(general infection, puerperal infection, etc.).


                         ACCIDENTAL PHLEBITIS.

The jugular vein may become inflamed as a result of accidental wounds or
of phlebotomy, but the mammary vein in cows is much more frequently
affected. In both cases the disease is due to infection of the clot
which seals the vessel; it may assume the form of either adhesive
phlebitis or suppurative phlebitis. Whether produced directly by the use
of infected instruments or whether it is of a secondary character,
traceable to the clot being infected by germs entering from without
being conveyed to the wounds by the head-stall chains, by litter,
manure, etc., the result is the same. The inflammation, at first
confined to the endothelium, extends to the wall of the vein and causes
fibrin to be precipitated over the inner wall of the inflamed vein for a
distance varying with each case.

If the microorganisms do not produce suppuration, the vein appears
simply thrombosed and inflamed, the phlebitis remains of an adhesive
character, and may disappear spontaneously, provided the animal be kept
quiet. If, on the other hand, suppuration is set up, the clot gradually
breaks down, the internal surface of the vein develops granulations and
undergoes suppuration, and the phlebitis is then said to become
suppurative. The clot may even become entirely detached, transforming
the suppurative phlebitis into a very grave form of hæmorrhagic
phlebitis.

The jugular is the commonest seat of adhesive phlebitis, the mammary
vein of suppurative phlebitis.

=Symptoms.= The symptoms are easy to recognise. The accidental or
instrumental wound is the seat of a painful œdematous swelling. It
discharges a reddish offensive serosity, or exhibits blackish-violet
bleeding granulations surrounding a little central sinus.

The affected vein, whether the jugular or mammary, soon becomes swollen,
is sensitive to the touch and very rapidly becomes indurated in the
direction of its origin for a greater or less distance.

Phlebitis has then set in, and according as one or other complication
predominates, it is described as suppurative or hæmorrhagic.

=Diagnosis and prognosis.= The diagnosis presents no difficulty. In
phlebitis of the jugular the neck is held stiffly, and the jugular
furrow is partly obliterated.

The prognosis is somewhat serious, particularly in phlebitis of the
mammary vein, for obliteration of the vein interferes with the function
of the venous plexus from which it springs, and, although there may be a
limited vicarious circulation, the secretion of milk is indirectly and
secondarily checked owing to difficulty of irrigation.

The extension of phlebitis of the jugular towards the head and the
venous sinuses of the cranial cavity, is quite exceptional.

When the mammary vein is inflamed it appears collapsed in the direction
of the heart and swollen, indurated, and painful in that of its origin
in the mammary gland.

=Treatment.= The first point requiring attention is so to fix the animal
as to prevent the clot from being pressed upon or crushed, though,
unfortunately, this cannot always be properly done. The difficulty is
obviated by applying vesicants, which cause swelling and pain, and so
reduce natural movement of the parts to a minimum.

At first, when the parts surrounding the operative wound are simply
swollen and phlebitis is threatened, repeated application of tincture of
iodine or a liquid vesicant is useful, and may prevent the disease
developing.

In existing cases a blister applied over and around the whole of the
hardened tract may prevent the mischief from proceeding beyond the
adhesive stage. In such case the clot becomes organised, the vein
remains obliterated, and recovery follows.

Similar treatment may also be employed in suppurative phlebitis, but as
the clot gradually breaks down in consequence of the action of bacteria
it is useful and almost indispensable to disinfect the vessel. For this
purpose the opening of the sinus must be enlarged, and, by means of a
sterilised or very clean syringe with a curved nozzle, the parts washed
out daily with warm boiled water, followed by an antiseptic injection
containing 2 per thousand of iodine, 3 per cent. of carbolic acid, or,
better still, glycerine containing 1 per thousand of sublimate.

If in spite of this treatment the phlebitis extends towards the origin
of the jugular or mammary vein, a counter-opening may be made at the
point where the clot still remains adherent, and a strip of iodoform
gauze saturated with tincture of iodine or with blistering ointment
diluted to one-eighth with oil may be passed. Needle firing is also of
value. Finally, as a last resource, a ligature may be applied to the
vein above or beyond the clot.

This operation, which in the horse is confined to hæmorrhagic phlebitis,
is especially applicable to phlebitis of the mammary vein in the cow. As
the vein is subcutaneous, the operation may easily be performed in the
standing position; the successive stages are as follows:—

The patient is firmly secured and its hind limbs hobbled by passing a
rope around the hocks in a figure of eight. It is steadied on one side
by an assistant who presses on the quarter.

One cubic centimètre of a 10 per cent. solution of cocaine is
subcutaneously injected on each side of the vein at the point chosen.
Ten minutes later a button-hole incision is made through the skin and a
loop of thick catgut passed around the vein by means of a curved needle.
The ligature is tied firmly with a surgical knot and the little wound
afterwards covered with a mass of cotton wool secured by collodion.


        INTERNAL INFECTIOUS PHLEBITIS (UTERO-OVARIAN PHLEBITIS).

The internal forms of phlebitis of parasitic or infectious origin are as
yet little understood, but mention may be made of phlebitis of the
utero-ovarian veins which frequently follows parturition and post-partum
infection. This is probably in many instances the real cause of the
post-partum paraplegia without gross or apparent material lesions.

This form of infectious phlebitis may extend to the large internal and
external iliac veins and produce embolism and septicæmia, as is shown by
recorded cases.

The mechanism of the disease is easily understood. The infective agents
penetrate the veins of the uterine mucous membrane and pass from the
lumen into the wall of the vein. Here they cause inflammation of the
vascular endothelium, followed by the deposit of a fibrous clot of
cylindrical form, which sets up partial thrombosis of the vein. This
thrombosis becomes complete by the formation of a central clot due to
venous stasis.

It is not necessary for the germs to penetrate at a number of points.
The thrombosis progresses until it gains a large trunk beyond the
original point of infection.

=Symptoms.= Phlebitis of the veins of the pelvis is frequently
misunderstood or overlooked, because the practitioner is apt to confine
his attention to external signs, the paresis and paraplegia of the hind
quarters.

The symptoms usually appear from five to eight days after normal
parturition or parturition in which there is retention of the
after-birth followed by metritis. The animals show fever and lose
appetite, signs which may be due to metritis, but soon after they
experience difficulty in rising, and some days later remain permanently
recumbent.

The circulation is weak, and the entire intra-pelvic region painful; the
large nervous trunks are affected, exertion becomes difficult, and the
animals refuse to rise. At this stage they should not be forced to do
so.

In two to three weeks improvement may occur and lead to recovery but in
many instances various complications in the nature of purulent infection
or septicæmia set in, or the animals are previously slaughtered.

=Diagnosis.= The diagnosis can only be determined after the symptoms
develop. Confirmation might in some cases be obtained by rectal
exploration made methodically and gently.

=Prognosis.= The prognosis is grave.

=Treatment.= Treatment should be based on disinfection of the uterus by
injections of boiled water or warm iodised solutions and drainage by
means of strips of iodoform gauze. The animals should be placed on a
thick and scrupulously clean bed, and as far as possible be spared any
considerable exertion for a fortnight. By changing their position once
or twice a day complications may be avoided.


                UMBILICAL PHLEBITIS OF NEW-BORN ANIMALS.

One of the most serious conditions met with in practice is that known as
umbilical phlebitis of new-born animals. Whilst in fact it is easy to
deal with phlebitis of the jugular or mammary vein, surgical or medical
assistance becomes extremely difficult in this case, because the
inflamed vein is deeply situated in the abdomen and passes through one
of the most important internal organs, viz., the liver. When it is added
that umbilical phlebitis is in 95 per cent. of cases of a suppurative
character, the reader may form some idea of its gravity.

Unless the condition is early diagnosed and measures are at once taken,
such complications as infectious hepatitis, purulent infection, and
septicæmia cannot be avoided. Death is then inevitable.

In order clearly to understand this phlebitis, however, it is necessary
to recall the anatomical formation of the umbilical region in the
new-born animal.

At birth the umbilical cord is represented by a cylindrical mass,
surrounded by the terminal portion of the amnion. It enters the abdomen
through a circular perforation in the abdominal wall known as the
umbilical ring. This ring may be divided into two parts, one deeply
seated, the fibro-aponeurotic ring, consisting of an aperture in the
white line; the other the superficial or cutaneous ring, formed by the
skin, which is wrinkled all round it, and constitutes a kind of sleeve
about an inch in length. This cutaneous sleeve is continuous with the
amniotic tissues. The entire umbilical cord is therefore enveloped in an
amniotic-cutaneous sheath.

[Illustration: $1]

It is composed of four principal structures—the umbilical arteries, the
umbilical vein, the urachus, and the interstitial mucous tissue.

The umbilical arteries and vein consist of two parts—the extra-fœtal
part, which co-operates in forming the cord, and the intra-fœtal part.

The first is formed of two arteries and two veins, in contra-distinction
to the condition in solipeds, where the cord only contains one vein. In
the second, the arrangement is as follows: The two umbilical allantoid
arteries on entering the abdomen curve backwards towards the entry of
the pelvis, passing over the sides of the bladder enveloped in the
lateral ligaments, and extend upwards towards the bifurcation of the
aorta, finally pouring their contents into the internal iliac arteries.
In the adult they may still be traced as annexes of these latter
vessels. The two umbilical veins on passing through the ring unite to
form one within the abdomen. This vessel passes forwards, rising along
the lower abdominal wall, then becomes lodged in the thickness of the
inferior middle ligament of the liver, and finally penetrates that organ
where it unites with the portal vein. It is also connected with a vessel
known as “the vein of Arantius,” which places it in communication with
the posterior vena cava, a vein not found in solipeds.

The fœtal blood is purified by exchanges between it and that circulating
in the maternal placenta, and when re-arterialised it returns by the
umbilical vein.

The urachus, found in the embryo and fœtus, eventually gives rise to the
bladder. In new-born animals this viscus is therefore open at its base,
and communicates with the allantoid cavity through the urachus. The
urachus starts from the base of the bladder, and, extending along the
median plane of the lower abdominal wall between the two umbilical
arteries as far as the umbilical opening, takes its place in the cord
alongside the vessels. Through it the secretions of the fœtal kidneys
drain into the allantoid cavity. The interstitial mucous tissue, also
called “Wharton’s jelly,” is a gelatinous material which unites these
different vessels and helps to support and protect them in the umbilical
cord. It is particularly abundant opposite the umbilicus.

Immediately after birth the umbilical cord ruptures of itself as a
result of the fall which the young animal experiences or of movements
made by the mother, as for instance when she attempts to rise. In
certain other cases it is divided by the mother biting it, or it may be
ligatured by some person present. However the rupture may be brought
about, it always occurs at a distance of 2 to 4 inches from the
umbilicus. The immediate result is to produce thrombosis of the
umbilical vessels and obstruction of the urachus. The two umbilical
arteries rarely bleed, for hæmostasis is brought about by stretching,
and these arteries, being very elastic, almost immediately retract and
close. The umbilical veins simultaneously become blocked, and the single
intra-abdominal vein having no further _raison d’être_, gradually
becomes obliterated. The urachus should normally be obliterated at the
moment of delivery (Colin and Saint-Cyr), or at any rate soon
afterwards, as a consequence of rupture of the cord (Chauveau and
Zundel).

Immediately after delivery another change sets in. The extra-fœtal
portion of the cord, which remains attached to the umbilicus, dries on
contact with the air, the Wharton’s jelly retracts, the whole undergoes
a kind of necrosis, assumes the appearance of a dry scab, and in eight
or ten days falls away, leaving in its place the umbilicus, which should
be half cicatrised on the fall of the cord. Thus the umbilical cord
presents an extra-fœtal degenerated portion and a persistent portion
about ½ to 1 inch only in length, buried in the cutaneous ring of the
umbilical region.

If all the changes indicated occur normally and physiologically, the
little wound in the region of the umbilicus cicatrises in a perfectly
regular way. But unfortunately this is not always the case. At times the
cicatrix becomes contaminated by manure, urine or dust, suppurates, and
may then become the seat of various complications, such as umbilical
phlebitis, omphalitis or persistence of the canal of the urachus.


               UMBILICAL PHLEBITIS OR OMPHALO-PHLEBITIS.

=History.= Umbilical phlebitis, and in a more general sense all
pathological conditions of the umbilicus, in new-born animals have been
the object of numerous investigations by Lecoq, Bénard, Loiset (1843),
Bollinger (1874); and more recently by Morot (1884), Uffredizzi (1884),
Chassaing (1886), etc.

Omphalo-phlebitis may occur as a primary condition or may appear as a
complication of omphalitis and of persistence of the urachus. It
consists essentially in suppurating inflammation of the umbilical vein,
but is not infrequently accompanied by omphalitis, arteritis,
peritonitis, and cystitis.

=Causation.= The disease results from infection of the (normal) clot and
of the wound resulting from severance of the cord. The infection may
only cause simple phlebitis of the umbilical vein, but if the organisms
are virulent the phlebitis almost inevitably degenerates into
suppurative phlebitis.

Formerly omphalo-phlebitis was thought to be caused by the mother
licking the foal, by irregular tearing of the cord, by crushing and
separation of the obliterating clot, etc. The truth is that all these
causes favour infection of the umbilical wound, which is the primary
cause, suppurative phlebitis being secondary only.

When the cord is ruptured both the veins and arteries become plugged,
and bleeding ceases. This plugging should end in organisation of the
clot and obliteration of the vessels. If, however, the wound is
infected, microorganisms make their way between the clot and walls, and
extend along the inner surface of the vein, infecting first the clot and
then the vein, and thus setting up suppurative phlebitis.

If suppuration does not continue, recovery may occur spontaneously.
Infection may be confined to the clot, producing simple phlebitis, but
it often extends along the umbilical vein to the liver, causes
infectious hepatitis and purulent infection or septicæmia. Similar
results may be produced by infection of the arteries, the organisms
making their way as far as the bifurcation of the aorta, and thus
gaining the general circulation. Moussu believes that this is the
commonest method by which septicæmia is produced in calves.

=Symptoms.= In these cases it is usually the general symptoms which
first attract attention, the local lesion passing unnoticed for a
greater or less time.

The animal shows intense fever, due to either suppurative phlebitis,
infectious hepatitis, or, as often happens, to generalised infection.
Appetite is lost, diarrhœa is abundant, the respiration and circulation
are accelerated, and the temperature rises to 104° Fahr., or even 105°
Fahr.

The local symptoms are those usually associated with omphalitis or
phlebitis. An examination of the umbilical ring reveals an œdematous,
hot, sensitive swelling, the lower part of which exhibits a chronic,
suppurating, fungoid, blackish wound of unhealthy appearance.

This wound is the seat of one or more sinuses which penetrate the vein,
arteries, or urachus. If only one sinus exists, it always passes upward
and forward into the umbilical vein. The utmost precaution should be
employed in examining the parts. Should it be thought desirable to probe
the sinus in order to discover its direction, the probe must be very
cautiously introduced, and only for a short distance, because rough
handling would tear the tissues and carry infective material to deeper
seated points.

=Complications.= These are numerous and very grave. Long ago Lecoq
described a disease suggestive of laminitis, which beyond doubt was only
a form of purulent infection. At a later date Loiset studied a disease
following omphalitis, in which interstitial abscesses developed in the
cord. This also was simply purulent infection.

More recently complications such as pleurisy, pneumonia, infectious
endocarditis, diarrhœic enteritis, and especially suppurative
polyarthritis of young animals have been referred to omphalo-phlebitis.
All these complications result from infection. The microorganisms
themselves or the toxins they secrete appear to have a particularly
injurious action on the serous membranes, a fact which throws light on
the frequency of such complications as pleurisy, peritonitis,
endocarditis and arthritis.

Intoxication also plays a certain part, and microbic toxins are
responsible, at least at first, for the uncontrollable diarrhœa,
arthritis with sterile exudations, etc.

=Diagnosis.= This presents no difficulty. The alarming general symptoms
seen at the outset immediately suggest in the case of young animals the
possibility of disease in the umbilical region.

=Prognosis.= The prognosis is grave, it may be said very grave, because
treatment is difficult to apply, and dangerous complications, which
almost always prove fatal, may already have been set up.

One must always distinguish, however, and take into account in forming
the prognosis, the special characteristics of the phlebitis, and weigh
carefully the signs of complication. The fistula should be cautiously
explored, and its depth, etc., noted, while the temperature,
circulation, respiration, etc., should be carefully studied.

=Treatment.= A very important item of treatment consists in regularly
and scrupulously cleansing the region of the umbilicus after the cord
has separated and until the wound has completely cicatrised. The parts
are washed with boiled water and dusted with boric acid, iodoform, etc.

A still better plan, and one that almost certainly guards against this
disease, is to apply an antiseptic dry dressing as soon as the new-born
animal has become dry. This need only consist of a small sheet of
antiseptic cotton wool fixed to the umbilicus by four pitch bandages or
by two pieces of webbing passed over the back. In this way contamination
of the cord and the risk of infection are avoided.

In cases of fully-developed phlebitis the old generation of
practitioners used to recommend local dressings with adhesive plasters,
astringent and vesicant applications, etc. All such methods are useless,
because they only act on a part of the diseased structures and cannot
reach the blind ends of the sinuses. The classic treatment of
suppurative phlebitis also is out of the question.

All that can be done, therefore, is slightly to open up the sinuses and
wash them out frequently with antiseptic solutions, such as boiled
water, sublimate glycerine, carbolic glycerine, etc., afterwards
applying antiseptic dressings. These methods, however, are scarcely
likely to put an end to infectious complications such as suppurative
polyarthritis.

There is no danger in using strong carbolic solution, 3 per cent.
creolin, 4 per cent. chloride of zinc, sulphate of copper, etc. Should
there be several sinuses and should one of them extend in a backward
direction, it is necessary to make certain that no communication exists
between the urachus and the bladder. For this purpose some boiled water
may be injected into the sinus. If a communication exist, this water
will fill the bladder and distend the urachus. The treatment necessary
in this case is similar to that of persistence of the urachus.

It is well in all cases to be guided by the following principle: never
to resort to treatment unless suppuration has occurred and the sinus is
blind. To check suppuration a blister may be applied around the
umbilical region while means are taken to prevent the animal licking the
parts.

Chassaing in 1886 suggested a rather original method of operation which
deserves description. It is founded on the permanent treatment of
sinuses, and consists in introducing a flexible osier stick, a kind of
bougie, enveloped in tow and moistened with the following mixture:

                           Collodion 3 parts.
                           Sublimate 1 part.

This is introduced for a distance of 3 to 4 inches into the fistula, and
is fixed to the skin with gutta-percha or pitch. The dressing is renewed
every five or six days, and healing takes place, it is said, in one,
two, or at most three weeks.

It is very likely that if the sinuses were previously cleared and simply
plugged with antiseptics or treated by introducing pencils of salol,
nitrate of silver, sulphate of copper, iodoform, etc., at least as good
results might be obtained.




                               CHAPTER V.
                         DISEASES OF THE BLOOD.


                    SEPTICÆMIA OF NEW-BORN ANIMALS.

The above title is given to that exceedingly fatal disease commonly
known as “white scour,” etc., the mortality in which often rises to 95
per cent.

The disease was studied by Poels in Holland in 1889, Dèle in Belgium in
1891, Perroncito in Italy, Galtier in the centre of France in 1891–92,
and quite recently by Nocard in Ireland in 1901.

It occurs throughout all the breeding districts of France, and in some
parts causes enormous losses, the mortality comprising two-thirds or
even three-fourths of all new-born calves. In certain breeding
establishments in Normandy all the new-born animals without exception
die unless special precautions are adopted.

In foals, septicæmia of the new-born is very rare, because
horse-breeding establishments are much better cared for, and breeding
mares are segregated. In byres, on the other hand, the greatest
promiscuity exists. The disease is equally uncommon in lambs, although
it makes numerous victims in folds which have once been attacked. It is,
however, quite common in young pigs.

=Symptoms.= The development and course of the disease are in certain
respects characteristic.

The disease usually appears within two or three days after birth, and
only in rare cases after the second week. Calves which at birth appeared
vigorous and in good health are found dull on the second day; after the
second or third meal they suffer from diarrhœa, and from that time
refuse all nourishment, lie down as though exhausted, and sometimes die
very rapidly.

Some even perish in ten to twelve hours without showing diarrhœa;
although apparently well at night, they are found dead or dying the next
morning. This is the peracute form.

Most frequently the young creatures suffer for two or three days,
sometimes a week. Appetite is partly preserved; at first the diarrhœa
resembles that due to inability to digest milk, but the fæces soon
become greyish or blackish and very fœtid. The hair of the tail,
quarters and hocks is soiled and matted, the skin irritable and reddish;
the patients lose strength, appear unsteady on their limbs, and develop
rapid respiration and tumultuous action of the heart.

They take little food, become weaker by degrees, and die in a condition
of exhaustion.

Fever, well marked at first, frequently diminishes, and the temperature
may remain normal for several days, falling to 97° Fahr., or even 95°
Fahr., twenty-four hours before death.

This is the commonest form of the disease. It lasts three to five days,
and is always grave.

Cattle-men recognise the disease chiefly by the diarrhœa and loss of
appetite.

Lastly, a third and rarer form occurs during which appetite is
maintained in spite of the diarrhœa. The animals remain thin, develop
poorly, but survive for a month, six weeks or two months. The diarrhœa
diminishes or disappears, but its disappearance is followed by
complications such as broncho-pneumonia, pleuro-pneumonia, endocarditis,
acute arthritis, etc., a fact which led Prof. Galtier to give the
disease the name of “septic pleuro-pneumonia in calves.” These
complications, again, are extremely grave, and generally prove fatal
after a period of varying length. They are due to local development of
microorganisms of the kind which produce septicæmia, and similar to
those described under the name of broncho-pneumonia of intestinal origin
in sucking calves.

They differ, however, as regards their cause, from the primary
affection, and may be due to very varied organisms, the commonest being
those of suppuration. These organisms, in fact, are alien to the primary
disease, and obtain entrance from without, very probably by the
tracheobronchial tract.

In young pigs septicæmia assumes the same forms as in the calf. In lambs
the chronic form seems more frequent than the peracute and the ordinary
forms.

=Causation.= The septicæmia of calves, and possibly of all new-born
animals, of whatever species, is produced by a microbe which flourishes
in the manure and litter of stables, and which Nocard included in the
group of Pasteurella. It can be found in the blood from the moment the
first external symptoms appear until the time of death. During the last
hours, however, the bacterium _Coli communis_ also invades the
circulation in many instances, and if cultures are not made until some
hours after death, the colon bacillus and bacteria of putrefaction are
more particularly discovered.

The microbe of calf septicæmia can be readily cultivated in jelly or in
ordinary liquid media. Injected into the veins of experimental animals,
it reproduces the clinical symptoms, and causes death more or less
rapidly, according to the dose injected.

The virulence of cultures grown in defibrinated calf’s blood seems more
intense, and Moussu has been able to reproduce the clinical form of the
disease by applying to the umbilical cord of a new-born animal a pledget
of cotton wool saturated with such a culture, and covering it with a
dressing. The germs of the disease are spread throughout the byres
through the medium of fæces. When the umbilical cord has become dry,
that is, after the third day, the application of virulent cultures to
the stump no longer causes infection.

=Pathogeny.= The pathogeny of this septicæmia of calves and of new-born
animals is easy to explain.

At birth the young animals fall on the litter, and the umbilical cord
becomes contaminated. The infective agent, finding an excellent culture
medium in the tissues of the cord, at once begins to develop, increases
in enormous numbers, steadily ascends along the cord, and sets up
septicæmia. It grows in the gelatinous Wharton’s jelly and in the
fibrinous plug closing the arteries and umbilical vein, and soon enters
the true circulation. Septicæmia is then fully established, general
disturbance sets in, and with it the diarrhœa by which it is externally
indicated.

It is important to remember, however, that infection occurs most readily
through the medium of the cord, and during the first few days after
birth: it may occasionally be brought about towards the eighth or tenth
day, when the shrivelled portion of the cord falls; in this case its
entrance is effected through the little umbilical wound.

=Lesions.= The lesions are sometimes so obscure that the practitioner
may hesitate to deliver an opinion.

In acute cases, where death occurs in two or three days, or even in ten
to twelve hours, post-mortem examination reveals only increased
vascularity of the serous membranes—the peritoneum, pleura, pericardium,
etc.; and it may be almost impossible to discover anything abnormal in
the cord, for although the clots closing the arteries and veins are
infected, they are neither separated from the walls of the vessels nor
broken up.

On the surface of the urachus, at the base of the bladder, and in the
depths of the peritoneal folds supporting the allantoid arteries
(sometimes also the hepatic vein), unequivocal signs of local ascending
infection may, however, almost always be found, together with intense
injection of the capillaries, little hæmorrhagic spots, and commencing
formation of false membranes, etc.

The infection extends also by the lymphatic vessels contained in these
peritoneal folds, and finally attains the sublumbar region.

When the disease develops less rapidly the peritoneal cavity contains a
certain quantity of blood-stained serosity, as do the pleuræ and
pericardium, whilst vascular engorgement of the serous membranes is
extremely marked. The intestine shows traces of congestion and
inflammation throughout its length, and its contents contain the
specific organism in very large numbers.

Finally, in the chronic forms, the serous membranes and the intestine
seem only slightly attacked, possibly because the lesions have undergone
retrogressive changes. The striking features are the secondary lesions,
such as those of pneumonia, broncho-pneumonia, pericarditis, and abscess
formation in the lung.

Nocard gives the following description of the lesions found during his
investigation of “white scour” of calves in Ireland (_Veterinarian_,
April, 1902, p. 171; see also Prof. Mettam’s paper, _Veterinarian_,
June, 1902, p. 307):—“The lesions found on autopsy vary according to
whether the evolution of the disease has been rapid or slow. One lesion,
however, is never absent—that of the navel and the navel vessels. In all
the calves attacked we found a large umbilicus with hardened coats
enclosing a clot easily broken down, sometimes soft and purulent. In
every case, also, we observed blood suffusions, often very extensive,
along the course of the umbilical vessels and of the urachus, invading
often the posterior third of the bladder. In cases where the evolution
had been rapid we found the lesions of true hæmorrhagic septicæmia. All
the viscera were congested to excess; their surface was studded with
petechiæ, ecchymoses, or subserous blood suffusions. The capillary
network of the peritoneum, pleura, and pericardium appeared strongly
injected. This lesion was especially marked on the epiploon. The
intestine was the seat of intense congestion, especially at the level of
the ‘floating colon.’

“The mucous membrane was thickened, gorged with blood, and friable; the
solitary glands, thick and protruding, were sometimes transformed into a
kind of bloody magma, or they were ulcerated, as in anthrax; the
contents of the bowel were mixed with a large quantity of blood. The
mucous membrane of the fourth stomach was altered nearly to the same
degree; it was studded with interstitial hæmorrhages, especially above
the level of the open edge of its folds. The mesenteric
glands—especially those of the colon—were enormous, gorged with blood,
reddish, and often hæmorrhagic. The mucous membrane of the bladder was
often covered with petechiæ, the urine which it contained was clear and
limpid, but always rich in albumen. [In one sample which was analysed,
the urine contained more than 4 grammes of albumen to the litre.] The
lungs were gorged with blood, like the intestines; sometimes they were
manifestly œdematous, but generally their tissue was still supple,
elastic, permeable, and without apparent lesion.

“In the subacute forms the lesions are much less marked. The mucous
membrane of the intestine is less congested; sometimes œdema of the
submucous tissue exists. The mucous membrane of the fourth stomach is
often punctuated with brownish-red patches, traces of the capillary
hæmorrhages which were produced at the onset of the disease. The
mesenteric glands are swollen, gorged with serum, but not hæmorrhagic;
the liver is large and of a yellowish tint; the spleen is little
altered; the urine always contains albumen; the lungs are seldom quite
sound; they usually contain here and there small diffuse centres of
catarrhal pneumonia, of nodular bronchial pneumonia, or simply of
atelectasis.

“These lesions are more constant and more dense if the animals have
resisted the disease for some time; they then constitute the transition
stage between the simple collapse at the beginning of the disease and
the suppurating lesion of lung disease. The joint lesions when they
exist are very interesting. At the beginning all the periarticular
tissues are infiltrated with a yellowish gelatinous serosity. The
synovial membrane is covered with vascular aborisations of an extreme
richness, which extend on to the articular cartilages. The synovial
capsules are distended by a considerable quantity of thick synovia of a
deep yellow or brownish tint, holding in suspension flakes of fibrous
exudate more or less dense and abundant. When the lesion is older the
synovia is replaced by a thick fibrous exudate, which fills
sacculations, and extends between the articular surfaces. In this case
the lesion appears identical with that of the arthritis seen in
pleuro-pneumonia of sucking calves.”

=Diagnosis.= The diagnosis presents no difficulty, for the development
and acute course of the disease (the majority of patients die within a
week of birth) leave little room for doubt.

This disease is easily distinguished from dysentery in new-born animals,
which appears at birth, as also from simple diarrhœic enteritis; in the
latter disease the symptoms are delayed, sometimes occurring only when
the animals are weaned; moreover, the disease is never so grave as that
now under consideration.

Should, however, the post-mortem appearances seem indecisive, the
diagnosis can be based simply on the high mortality.

=Prognosis.= The prognosis is extremely grave. About 95 per cent. of the
animals attacked die, and among those which survive many show thoracic
complications, that render them useless.

=Treatment.= Treatment of animals already affected is useless, and,
moreover, too costly. Drugs administered through the digestive apparatus
to a large extent miss their mark, because the digestive symptoms are
secondary, primary infection having occurred through the circulation.
The administration of purgatives and internal antiseptics can,
therefore, only prove illusory.

On the other hand, prophylactic treatment is of the greatest value; all
that is necessary is to prevent the umbilical cord from becoming
infected.

The great mortality, which causes such severe loss to breeders, is
simply due to want of proper care of new-born animals. Even in carefully
kept byres the mortality may be high, for the specific agent develops in
litter contaminated with fæcal matter, by lying on which young animals
become fatally infected.

[Illustration: $1]

To check or prevent this septicæmia in breeding establishments, it is
merely necessary to take the same precaution as is taken in dealing with
young children, _i.e._, to apply an aseptic or antiseptic dressing to
the stump of the cord after ligation. As soon as the young animal has
been dried by the mother or by artificial means, a carefully boiled
ligature is applied to the cord at a distance of about 1 inch from the
umbilical ring. The portion of the cord below the ligature is snipped
off, the remaining part is carefully washed with boiled water or boric
solution, and is surrounded with a mass of iodoform wool, kept in place
by a bandage passed over the back.

The cord will shrivel a little less rapidly than it would if exposed to
the air, but will be protected from all infection. The young animal
should be separated from the mother to prevent her from displacing the
dressing by licking the parts.

In a few days all danger is at an end. This method is very simple, and
can be carried out even by the breeder and in an infected byre. Nocard
recommends the use of umbilical dressings containing collodion, and the
practitioner can choose whichever method he pleases.

In grave outbreaks involving large establishments, the byres should be
rigorously disinfected, and it is sometimes well to segregate cows about
to calve in a special byre, from which the calves are not allowed to
pass until the umbilicus is cicatrised.


               TAKOSIS: A CONTAGIOUS DISEASE OF GOATS.[4]

Footnote 4:

  Annual Report, U.S.A. Bureau of Animal Industry, 1902, p. 354 (Mohler
  and Washburn).

This disease has been seen in Angora goats brought from Texas into
Pennsylvania, U.S.A.

=Symptoms.= The disease presents many of the symptoms usually
accompanying a parasitic invasion, and is characterised by great
emaciation and weakness, with symptoms of diarrhœa and pneumonia. In the
early stages of the affection there is usually little to indicate that
anything is seriously amiss with the animal. The first observable
symptom manifested is the listless and languid appearance of the animal,
evidenced by its lagging behind the flock, and is usually accompanied by
a drooping of the ears and a drowsy appearance of the eyes. The pulse is
slow and feeble, and the temperature is elevated slightly at first, but
becomes subnormal a few days before death. The highest temperature
observed in the natural disease was 104·1°, and the lowest, in a
prostrated animal a few hours before death, registered 99·7° Fahr.
Snuffling of the nose, as in a case of coryza, with occasional coughing
is sometimes in evidence.

As the disease advances the animal moves about in a desultory manner,
with back arched, neck drawn down toward the sternum, and with a
staggering gait. Rumination is seldom impaired. The appetite, while not
so vigorous, is still present, though capricious, and the affected
animal shows plainly that the ravages of the disease are rapidly
overcoming the restorative elements derived from the food. The fleece is
usually of good growth, and presents a surprisingly thrifty appearance
when the condition of the animal is taken into consideration. All the
exposed mucous membranes appear pale, and the respirations are
accelerated and laboured. The goats finally become so weak that they are
readily knocked down and trampled upon by their fellows. If picked up
they may move off slowly and eat a little, but within a few hours are
down again, and in this way linger for several days, shrinking to about
half their natural weight, and occasionally bleating or groaning, with
head bent around on the side or drawn down to the sternum. A fluid
discharge from the bowels of a very offensive odour is usually observed
in the last few days of life, but this symptom is not constant.

=Course and Susceptibility.= This disease may assume a subacute or
chronic type, usually the latter. The animal dies of inanition in from
eight days to six or eight weeks. Several owners have reported deaths
after only two or three days of illness, but the goats doubtless had
been affected for a longer period, although not noticed on account of
their mingling in the flock. Many of the animals live for weeks, but
gradually become weaker and more debilitated, finally dying in a
comatose condition. In no instance has the natural recovery of an animal
after once the symptoms of takosis were noticed been observed or heard
of.

The younger goats seem to be the most susceptible to the disease,
although the old animals are by no means immune.

=Pathological Anatomy.= As already indicated, the general appearance of
the carcase simulates that produced by a wasting disease. The visible
mucous membranes are pale and anæmic, while the fleece, which appears
somewhat dry and lustreless, furnishes a shroud for the extremely
emaciated condition, that becomes plainly perceptible on skinning. The
same anæmic condition of the subcutaneous and muscular tissues is
observed on eviscerating the carcases. The lungs in most cases are the
seat of a peculiar diversified inflammation, never of a remarkable
extent. The external appearance of these organs is at times mottled,
caused by a few congested areas, several patches of an iron-grey colour
similar to areas of pneumonia during the process of absorption, and
normal tissue. On section through the reddened patches, a frothy mucus
may exude from the bronchioles, and in one case numerous punctiform
hæmorrhages were observed on the sides of the incision. This tissue,
while not so buoyant as a normal portion would be, nevertheless floats
when placed in water.

The heart in all cases is pale and dull, its tissue soft and flabby,
while inflamed areas, more or less penetrating, are present at times on
the epicardium about the auricular appendages, and at other times on the
endocardium, especially that lining the ventricles. These hæmorrhagic
patches consist of either pure extravasated blood or blood mixed with
serum, which gives them a more diffuse appearance and a gelatinous
consistence. The pericardium is slightly thickened, and usually contains
a small increase of fluid tinged with blood. The liver usually appears
normal, although the gall bladder is frequently distended with
pale-yellow watery bile. The kidneys are anæmic and softened. The cortex
appears slightly thicker and paler than normal, and contrasts strongly
with the darker pyramids. The capsule strips off easily from the
parenchyma of the organ. In one instance several pale areas simulating
anæmic infarcts were observed under the capsule extending into the
cortex, which probably resulted from the compression of the capillaries
by the swollen parenchymatous cells. The presence of albumin in the
urine was detected by the nitric-acid test. The spleen appears atrophied
and indurated, and on section the fibrous tissue far exceeds the splenic
pulp. Attachments by fibrous adhesions may fix the spleen to the
diaphragm or the neighbouring organs. The intestines may contain normal
fæcal matter or semi-fluid fæces of a disagreeable odour. The surface of
the mucous membrane is at times covered with a slimy mucus or plastic
exudate, and the appearance is that of a chronic catarrh associated with
necrosis of the mucosa.

=Bacteriology.= Examination of cultures and slides showed the presence
of a micrococcus, usually arranged in the form of a diplococcus, which
was found in pure cultures from the heart’s blood, spleen, kidneys, and
pericardial fluid, and essentially so in the tubes inoculated from the
other organs.

The specific organism of takosis appears in fresh bouillon cultures as a
spherical or oval micrococcus with a diameter of 0·8 to 1 µ. In these
cultures it is single or in chains of two, three, or four elements, but
most frequently in pairs, as diplococci, with a diameter transverse to
the axis of the chain greater than the longitudinal diameter.

=Treatment: Prophylaxis.= Sudden climatic changes should be avoided as
far as possible, and when shipments of goats for breeding purposes are
to be made which necessitate their transportation over considerable
distances the changes should be made during the months of summer or late
spring, and not in the fall or winter, when the contrast of temperature
will be so much greater.

Angora goats should be provided with stables that are thoroughly dry,
erected upon ground that has perfect natural drainage.

As a third measure of prevention may be mentioned careful feeding.

The segregation or isolation of all affected animals as soon as they
evince any symptoms of the disease will be found a most valuable means
of protection for those that remain unaffected, and a strict quarantine
over all of the diseased members of the flock should be maintained so
long as the disease remains upon the premises.

=Medicinal treatment= has proved unsatisfactory in many of the cases of
takosis to which it has been applied. The best results have been derived
from the administration of calomel in 0.1 gram doses twice daily for two
days, followed by arsenic, iron, and quinine, as follows:

                     Arsenious acid    1·40 grams.
                     Iron, reduced    12·00   „
                     Quinine sulphate  6·00   „

Mix and make into twenty powders, giving one to each adult goat morning
and evening at the conclusion of the administration of calomel. After an
interval of two days this treatment is repeated. In case the diarrhœa
persists, the sulphate of iron has been substituted for the reduced
iron, with beneficial effects.

=Conclusions.= After preliminary investigation, the following
conclusions have been reached:—

(1.) The disease described as takosis has appeared in many parts of
America, but particularly in the Northern States, where it has caused
great loss to many breeders of Angora goats.

(2.) It is a progressive, debilitative, contagious disease,
characterised by great emaciation and weakness, with symptoms of
diarrhœa and pneumonia, and causes a mortality of 100 per cent. of those
affected and from 30 to 85 per cent. of the whole flock.

(3.) From the carcases of numerous animals that have succumbed a new
organism, _Micrococcus caprinus_, has been recovered in purity, and is
presumably the etiological factor.

(4.) This micrococcus possesses pathogenic properties for goats,
chickens, rabbits, guinea-pigs, and white mice, but not for sheep, dogs,
or rats.

(5.) Medicinal treatment was attempted with varying success, while the
immunising experiments thus far conducted (although too few to permit of
any conclusive statement or accurate estimate as to their protective
value) have shown highly encouraging results. When accompanied with
measures of isolation and disinfection, the treatment may prove of great
assistance in the suppression and eradication of the disease in an
infected flock.


  BLOOD POISONING (MALIGNANT ŒDEMA) IN SHEEP AND LAMBS IN NEW ZEALAND.

This disease, which occurs during the operations of shearing sheep and
of castrating and docking lambs, is the cause of considerable loss
annually to sheep breeders in several districts of New Zealand. In 1893
J. A. Gilruth, Chief Veterinarian for New Zealand, issued a leaflet
dealing with the disease and the preventive measures to be adopted.
Generally the first thing that draws the owner’s attention seriously to
the condition of his flock is the discovery, in from thirty-six to
forty-eight hours after docking or shearing, of a few dead sheep lying
in various parts of the paddocks. Next morning he finds a few more dead,
and so on for three or four days, when, as a rule, the mortality ceases.

=Symptoms.= In the early stages of this disease the animal seems
listless, disinclined to move about, and, if the sun is shining
strongly, prefers to lie in the shade. If forced to move, the hind legs
are drawn forward with a peculiar stiff, dragging motion, as if there
were no joints. There are slight muscular tremors all over the body,
which become spasmodic as the disease progresses. If the flock be driven
about much, the diseased animal soon shows signs of great fatigue,
ultimately dropping to the ground thoroughly exhausted. The breathing is
fast and painful, being maintained more by a series of spasmodic jerks
than by any regular act. The pulse is quick and weak; the temperature is
very high, registering 106° to 108° Fahr., showing acute fever; the eyes
close, and the whole face is expressive of pain. Gradually the spasms
cease and coma sets in, resulting in death. The scrotum and surrounding
skin right along the floor of the abdomen and between the hind legs
become swollen and black. This gangrenous tissue, when present before
death, can be peeled off without pain to the animal. On post-mortem
examination various conditions are met with. The animals are generally
found to be among the best of the flock and in fairly good condition.
The scrotal and perineal regions in lambs (between hind legs and below
tail) are always, or almost always, gangrenous, this condition extending
along to the floor of the chest, and sometimes implicating the tail.
Many of the muscles, generally those of the shoulders, haunches, and
loins, are dark in colour and infiltrated with a black, watery fluid.
The intestines are generally healthy, though sometimes the peritoneum is
inflamed. The spleen and liver are in the usual condition after death,
due to febrile disturbance. In the chest, either the pleuræ (coverings
of the lungs) or pericardium (covering of the heart) are often inflamed,
with occasionally a fibrinous exudation, causing surfaces to adhere.

=Cause.= In Gilruth’s report for 1900 he demonstrated the cause of blood
poisoning to be a microbe known as the malignant œdema bacillus
(_Vibrion septique_ of Pasteur). This organism, which is found in many
dirty yards, swampy soils, etc., on gaining entrance to the system of
almost any animal by means of a wound, rapidly increases in numbers,
producing gangrene, or death, of the part affected first, and ultimately
the death of the animal.

=Curative treatment= is practically useless.

=Preventive measures.= Destruction of the carcases of animals which have
succumbed to this disease by efficient burial or by fire. Disinfection
of surface soil of yards, etc., by quick-lime. Cleansing of floors and
walls of sheds with strong hot lime wash containing crude carbolic acid
in the proportion of 1 to 50. Disinfection of flesh cuts made by the
shears or the docking or castrating knife. Boiling of docking and
tailing knives before use. Observance of antiseptic applications even
when temporary yards are employed. Sheep and lambs after operation to be
kept in a paddock free from swampy patches.


                             PIROPLASMOSIS.

Under the title piroplasmosis is included a group of diseases caused by
hæmosporidia, and found in animals of the bovine and ovine species.
These affections are far from having the same importance in temperate as
they have in tropical countries; nevertheless, it is very important to
be able to recognise them.


                         BOVINE PIROPLASMOSIS.

Bovine piroplasmosis has been described under different names, such as
hæmoglobinæmia, hæmoglobinuria, Texas fever (U.S.A.), tick fever
(Australia), tristeza (Argentine Republic), African coast fever, East
Coast fever, redwater, Rhodesian fever (Cape), and bovine malaria.

[Illustration: $1]

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It was first described by Babès in 1888, in animals inhabiting the
Danube Valley, and was termed by him bacterial hæmoglobinuria of the ox.
Afterwards it was well described by Smith and Kilborne (in 1889) under
the title of Texas fever. It was rediscovered in Finland by Krogius and
Van Hellens in 1894; in Sardinia by San Felice and Loi; in Australia in
1895 by Pound; and it has been the object of remarkable investigations
by Koch in South Africa (1898–1904).

[Illustration: $1]

Nicolle and Adil-Bey (1899) state that it exists in a latent form in
European Turkey and Asiatic Turkey; and Lignières (1900), after a series
of researches in Argentina, suggests the final solution of the questions
which it raises.

=Symptoms.= Babès describes it as an acute febrile disease, clinically
distinguished by the passage of blood-stained urine. The urine is
coloured by dissolved hæmoglobin; red blood corpuscles are not found.
Smith and Kilborne, and afterwards Stiles, described two forms: an
acute, rapidly fatal form, in which the _Piroplasma bigeminum_ is found
in the blood of the general circulation, in the spleen and kidneys; and
a chronic form, in which, notwithstanding the absence of clinical signs,
the parasites may be discovered in the blood under the form of
diplococci.

Lignières describes a grave and a benignant form. The grave form is
indicated by dulness, loss of appetite, and considerable fever. In
twenty-four hours the temperature rises to 104° or 105° Fahr., and the
pulse to 100 or 120 per minute, while the respiration is greatly
accelerated.

The urine is of a light-red or brownish-red colour, resembling
coffee-grounds, but it contains no blood corpuscles. The animals die in
from three to eight days with symptoms of asphyxia; but this termination
is not inevitable, and recovery may occur spontaneously. Improvement is
indicated by a fall in temperature, disappearance of the blood-stained
urine, and a return of appetite, together with marked thirst.

[Illustration: $1]

Drs. Smith and Kilborne describe the symptoms as follows:—“The beast
when first observed to be amiss appears to be dull and sluggish, with a
disinclination to move, and hence it is generally found apart from the
rest of the herd. The hair stands erect like that of an animal on a cold
day (a staring coat), the ears hang, and the eyes have a dull and
lustreless appearance. In some cases the animals cease to feed, or
ruminate, in others they continue to nibble at the herbage until nearly
the last, but in a languid, indifferent manner, indicating that they
have little relish for their food, and they fall off very rapidly in
condition. There is generally a dribbling of saliva from the mouth, the
muzzle may appear quite moist during the early stages of the disease,
but it invariably becomes dry and crusty as the disease advances. Later
on the animal manifests a strong reluctance to move, and when compelled
to do so, it walks with a dragging, straddling gait, as if weak across
the loins. In severe cases, when the sick beast is left undisturbed, it
will remain almost constantly in one place, standing with its head
depressed and ears hanging in a drowsy semi-comatose condition, looking
the very picture of complete nervous prostration. Other animals will lie
down the greater part of the time and scarcely move, and when dead the
limbs will be found in their natural position, and the head doubled
round on the shoulder as if asleep. On making a post-mortem examination
of some of these cases the carcase was found to be pale and bloodless,
as if the animal had been bled to death.

[Illustration: $1]

“In other acute cases a twitching and quivering of the muscles will be
observed, especially of those situated in the flank and behind the
shoulder. The pulse and breathing are much quickened, and the animal
will stand and grind its teeth and curl up its upper lip, indicating
great uneasiness and pain. The fæces during the early stages of the
disease are very often soft, with a tendency to diarrhœa, more
especially in transport oxen on the road, but they invariably become
hard as the disease advances; but whether hard or soft, they have
generally a brownish tinge, and often mixed more or less with blood and
mucus. In some severe cases which recover, the favourable crisis is
often ushered in by a salutary diarrhœa.”

In the benign form the animal for the space of about a week shows
indifference to its surroundings, loses its appetite, wastes, and, less
frequently, has slight feverish symptoms, without discoloration of the
urine. The only reason for the belief that this trifling disturbance is
due to piroplasmosis is furnished by examination of the blood, in which
the parasites may be found in very small numbers in certain blood
corpuscles.

Calves seldom take the disease except in the benign form.

[Illustration: $1]

=Lesions.= At first glance the lesions appear to resemble those of
anthrax, but may be differentiated from them in many details.

The skin is covered with ticks or shows traces of their punctures.

[Illustration: $1]

The myocardium appears as if boiled, the spleen is invariably
hypertrophied and two or three times as large as in the normal state.

The kidneys are violet in colour and congested, and the adipose layer
surrounding the kidney is infiltrated with a yellowish serosity. The
urine may present a variety of tints, derived from hæmoglobin. The liver
is often engorged with blood and the gall bladder always distended.

When convalescence sets in, icterus appears; but it is a special kind of
icterus, depending on changes in the hæmoglobin—in fact, a hæmaphæic
icterus. Histological examination of the blood furnishes the explanation
of the disease by revealing the presence of the parasite.

[Illustration: $1]

=Pathogeny.= The parasite is the _Piroplasma bigeminum_, which is easily
demonstrated by drying the blood, fixing it and staining with very weak
methylene blue. The blood is light in colour and pale, and the serum is
tinted by the dissolved hæmoglobin. The blood corpuscles diminish in
number with extreme rapidity while the parasites are developing, and in
twenty-four or forty-eight hours may fall from some six millions and a
half, the normal number, to one million or even to two or three hundred
thousand red blood corpuscles per cubic millimètre.

[Illustration: $1]

This destruction is due to the action of the piroplasmata, as may be
shown by staining with a ·5 per cent. methylene blue or carbolised
thionine. These parasites usually assume a simple pyriform shape, and
two or three may be found in one blood corpuscle. The number of
parasites and infected blood corpuscles is generally in direct ratio to
the intensity of the infection. These parasites are found throughout the
blood, but principally in that of the spleen, kidneys, and mesenteric
veins. They are only abundant whilst the temperature is rising or at the
moment when it reaches its highest point, and they often disappear
before death or convalescence.

The pyriform shape is only temporary, and corresponds to the acute phase
of the disease, but the parasite assumes the round form as soon as
convalescence sets in. This round form gives birth to one, two or three
spherical spores, which are set free in the plasma after the destruction
of the maternal protoplasm, and are able after transference to a fresh
red blood corpuscle to again assume the pyriform shape peculiar to the
grave forms of disease.

The parasite can only be cultivated in defibrinated blood from a
hæmoglobinuric subject, and the cultures do not always yield more than
reproductions of the round form, the pear-shaped form only being
produced with red blood corpuscles in the living animal body.

Regarding the method of growth of the piroplasma in the body and in
cultures, Lignières believes that the parasite may produce two forms of
spores differing in their nature. One, the active spore, has little
resisting power. It soon degenerates outside the animal body, forms
rapidly at the expense of one of the pear-shaped parasites, and may
immediately reinfect another red blood corpuscle. The other, called the
passive spore, is very resistant, and retains its vitality for a long
time outside the body, being produced at the expense of spherical
parasites already withdrawn and incapable of producing the disease.

The form of piroplasmosis at present under consideration is peculiar to
the ox, and none of the other domestic animals or experimental subjects
can be inoculated with it.

Subcutaneous or intravenous inoculation of the ox with 5 to 10 cubic
centimètres always gives positive results when made with blood or active
products, such as the pear-shaped parasites or active spores, but is
ineffectual when the parasites have already begun to retract in order to
form passive spores.

Calves seldom contract more than the benign form of the disease, and do
not die.

In the grave form following experimental infection the temperature
begins to rise between the third and sixth day, and corresponds with a
marked increase in the number of parasites to be found within the red
blood corpuscles. The urine at first becomes albuminous, then
hæmoglobinuric, whilst the red blood corpuscles diminish in number to a
very marked extent, falling from about six or seven millions to one
million, or even a few hundred thousands, in the course of a few days.
The temperature, which may previously have risen to above 105° Fahr.,
suddenly falls, indicating the approach of death.

If an immediate autopsy is made, the spleen is always found to be
enlarged, the intestinal mucous membrane reddish in tint or
blood-stained, and the serous membranes, particularly the endocardium,
covered with petechiæ.

Few or no parasites can be discovered except in the blood from the
cardiac muscle and the kidneys.

The grave form may end in recovery. This end is indicated by the
temperature remaining normal after defervescence, the appearance of
hæmaphæic icterus of an obstinate character, and the progressive return
of appetite.

The disease is usually transmitted by adult and larval ticks carrying
the parasite from infected animals. Lignières has proved that this
transmission occurs through the medium of passive spores, which, though
themselves incapable of producing the disease, become active and
infective in consequence of the local irritation produced by the
poisonous saliva of the ticks.

The pathogeny of Texas fever may be shortly summed up as
follows:—Animals suffering from the disease carry in their blood a
protozoan organism called the _Piroplasma bigeminum_, analogous to the
parasite of human malaria; once introduced into the blood, this organism
remains there in an active condition throughout the animal’s life; it is
transferred to susceptible cattle either within or without the infected
district by the Southern (U.S.) cattle tick _Boophilus annulatus_;
Southern cattle, although carrying the protozoa, are harmless unless
infested by this particular tick: the mature ticks and their eggs
contain the protozoa, and the mystery of certain grounds over which
infected animals have passed being first dangerous, then harmless, and
again dangerous depends on—(_a_) the infestation of the ground with
mature infected ticks; (_b_) the destruction or death of the mature
ticks; and (_c_) the hatching out of new (infected) ticks from the eggs
laid on the ground by the mature female ticks.

Dr. Salmon states that in Texas a successful method of protection is in
practice based on the observations that young cattle do not suffer so
severely as adults, and that the disease always assumes a milder form in
winter. Young animals introduced during the winter are inoculated with
virulent blood. They contract a mild form of disease, and afterwards
resist. In this way the losses, which previously amounted to 90 per
cent. of all freshly introduced stock, have been reduced to about 10 per
cent.

A remarkable and very interesting observation (if absolutely reliable)
deserves to be mentioned, viz., that the ticks develop regularly in the
natural prairie, but do not develop in parts artificially sown with
grass such as lucern, and that when contaminated or diseased animals are
transferred to artificial meadows they do not convey the disease to
other animals already there; the latter are proof against it.

=Diagnosis.= The disease is so typical that it cannot be mistaken for
anthrax. In anthrax the urine is never hæmoglobinuric and very rarely
hæmaturic, and the fæces are sometimes blood-stained, a symptom never
present in piroplasmosis. Anthrax can be transmitted to experimental
animals, but piroplasmosis cannot.

=Prognosis.= The prognosis is generally grave.

=Treatment.= Van Hellens recommends the use of quinine in large doses.
He give 5 drachms in one dose, and repeats it for the next two, three,
or four days.

Lignières says that he has never obtained the slightest success with
quinine, though it is true he has never given higher doses than 2½
drachms.

Attempts have been made to confer immunity by injecting animals with
serum from others which have recovered. Vaccination with the blood of
patients arrived at the period of convalescence has also been tried. The
results, however, have not been very satisfactory.

Lignières has formulated an efficient method of vaccination, of which he
has not yet published the full details, but which appeared by reason of
its simplicity likely to render great service. Nevertheless, his most
recent reports seem to show that vaccination is not always efficacious,
and that in the Argentine Republic alone several varieties of the
disease exist, two being caused by allied but different parasites. The
vaccine used against one variety is powerless against the other. The
problem of vaccination would therefore appear to be much more complex
than in the case where one form only occurs in any particular country.

The immunity arising from attacks of piroplasmosis is in direct ratio to
the gravity of the disease, and according to Lignières’ views this
acquired immunity is due to the secretion by the piroplasma of a
substance which is toxic for the red blood corpuscles. This toxic
substance provokes, as in other diseases, an organic antitoxic reaction.


                    BOVINE PIROPLASMOSIS IN FRANCE.

Until recent years it did not seem that piroplasmosis occurred in
France. It had been detected in Algeria, although its existence had not
been conclusively proved. Mathis claims to have met with it in the
department of the Loire in 1896 and in the Ain in consequence of the
importation of Algerian cattle, but its ravages were comparatively
trifling.

Having good reason to suspect that certain morbid conditions, known as
_mal de Brou_, might be due to piroplasmosis, Lignières endeavoured to
verify his theory, and discovered that sometimes, but not often, this
disease was mistaken in France for anthrax and _mal de Brou_.
Piroplasmosis in France appears less grave than in America, and is
rarely fatal.

As regards its =symptoms=, it usually develops suddenly with fever, loss
of appetite, acceleration of the pulse and respiratory movements,
suppression of the milk secretion, and the passage of red hæmoglobinuric
urine. In exceptional cases death may occur in from three to five days.

On post-mortem examination a varying number of ticks (_Ixodes
hexagonus_) are found on the skin, the spleen is always increased in
size, and the kidneys are black and hæmorrhagic.

The disease transmitted by ticks, as in Texas fever, seems due to the
presence of a round parasite, different from the well-known _Piroplasma
bigeminum_.

The elucidation of this disease, which occurs towards the northern
frontier of France in the neighbourhood of Maubeuge, calls for further
investigation. It never appears to be very fatal, and it attacks more
especially animals imported into the infected region. A method of
vaccination identical with that used by Lignières against one of the
forms of the American disease may perhaps in the future prove available
against the disease in France. Until then the best =treatment= would
appear to consist in free subcutaneous injection of saline solution and
the administration of evacuants, sulphate of quinine, and laxatives.


                          OVINE PIROPLASMOSIS.

=Causation.= The existence in France of this disease has not yet been
clearly established, for in the only communication on the subject (by
Leblanc in 1899) the writer seems to have confused the toxic
hæmoglobinuria produced by feeding on decomposed beet pulp with the
parasitic hæmoglobinuria due to piroplasmosis.

In Italy ovine piroplasmosis was described by Bonomo in 1896 under the
title of parasitic icteric hæmaturia of sheep. It is said to be due to a
parasite of the red blood corpuscles (_Amœba sporidium polyphagum_), the
said parasite being of oval form, very refractile, always occupying an
outer position near the free margin of the corpuscle, and sometimes
floating freely in the plasma.

According to Babès, who described it under the name of _gurceac du
mouton_, the same disease appears to occur in the islands and low parts
of the Danube valley.

=Symptoms.= The development of this parasite produces in the patient
loss of appetite and high fever, accompanied by the passage of dark
coloured hæmoglobinuric urine. Icterus is frequently present. The
animals rapidly become exhausted, collapse and die.

On post-mortem examination carried out immediately after death the
spleen is found to be large, the pulp being like wine lees. The liver is
soft and yellowish; the kidneys are soft and black.

The disease is said not to be transmissible by direct transfusion (?).

It would appear that this disease has also been seen in Turkey by
Nicolle and Laveran, near Constantinople, in 1899. The parasites
(_Piroplasma oris_) are round or slightly elongated and occur near the
periphery of the red blood corpuscles. It is to be hoped in the interest
of breeders in localities where this disease rages that Lignières’
method of vaccination against bovine piroplasmosis may prove reliable
and equally applicable in the case of sheep.


                 DISEASES PRODUCED BY TRYPANOSOMATA.[5]

Footnote 5:

  An interesting article and a series of figures on the “Evolution of
  the _Trypanosoma Evansi_” were published in the _Jour. of Comp. Path.
  and Therap._ for September, 1904, p. 210. The same number also
  contained articles on several piroplasmic diseases.

In 1904 Professor Koch delivered an address, from which the following is
a summary, to the Berlin Medical Society regarding his experiences and
observations on diseases produced by trypanosomata in Africa:—

A wide field of study has recently been opened by the discovery of
various pathological protozoa. Three discoveries especially have
directed attention to these special disease organisms—

(1.) Laveran’s discoveries regarding malaria. Ross has shown that the
malaria parasites are carried by mosquitoes (_Anopheles claviger_).

(2.) The discovery of the protozoa of Texas fever by Smith. In this case
ticks (_Rhipicephalus_ (_boophilus_) _annulatus_) convey the disease.

(3.) The discovery of the trypanosoma of the tsetse disease, which is
conveyed by a stinging fly (_Glossina morsitans_).

These discoveries were followed by numerous others indicating protozoa
as causes of disease.

The trypanosomata are morphologically distinguished by the existence of
a flagellum. When fresh blood is examined it is scarcely possible to
overlook the protozoa in the preparation, for attention is at once
attracted by the energetic way in which the red blood corpuscles are
continually being displaced. The peculiar form of the protozoa, however,
can only be detected in stained preparations. Romanowsky’s staining
method is probably the best. Trypanosomata stained by this method show a
fish-shaped body, the front end of which carries a flagellum. The body
of the trypanosoma is coloured blue. At the anterior end may be seen a
red-stained nucleus; at the opposite end a much smaller red spot, which
has been termed the nucleolus, but is more properly described as the
centrosome. From the centrosome a red thread extends along the outer
margin of the body as far as the front extremity, where it becomes
continuous with the flagellum.

The trypanosomata increase by longitudinal fission. The centrosome and
then the nucleus divide, and finally a second flagellum is formed.
Sometimes the young trypanosomata remain connected, producing the
so-called “rosettes.”

The disturbance produced by trypanosomata seldom becomes acute, but
often continues for years. The only sign of disease consists in
ill-defined fever with long intermissions. The destruction of the red
blood corpuscles causes anæmia, the animals or men become weak and waste
away, œdema and sometimes erythema occur at varying points in the body,
and occasionally the lymphatic glands become swollen.

The classical land of the tsetse disease is in the neighbourhood of the
Zambesi. There it was seen and very well described by Livingstone; but,
unfortunately, further investigations have shown that tsetse disease
extends over the whole of Africa.

Whilst the trypanosomata of rats can only be conveyed to the one
species, those of tsetse disease thrive in all mammals, particularly in
the horse, mule, ox, dog, rat, and mouse.

The tsetse organism has been shown to kill both horses and mules, but to
be less dangerous for oxen. A certain relative immunity exists in some
races. As regards the ass, observers are not agreed; Koch failed to
infect it. Sheep and goats are also but slightly susceptible. The
conveyance of trypanosomata from the blood to uninfected animals occurs
through the medium of a stinging fly (the _Glossina morsitans_).

Surra is endemic in the Philippines, Java, and the island of Mauritius.
Koch regards the trypanosomata of surra as strictly analogous with the
parasites of tsetse disease. Horses (and, in India, elephants)
especially suffer from surra. Although the _Glossina morsitans_ does not
occur in India, other stinging flies replace it and convey the disease.

Another variety of trypanosomiasis is _mal de caderas_, seen in South
America, particularly in Argentina and Brazil. It affects horses.
According to Koch, the parasites of _mal de caderas_ exactly resemble
the tsetse and surra parasites. Other observers, however, declare that
the _mal de caderas_ parasites are distinguished from those before
mentioned by their particularly small centrosome. _Mal de caderas_
affects not only horses, but all the other animals which suffer from
tsetse.

Another variety of trypanosoma, the trypanosoma Theileri, is especially
striking on account of its size. It is only found in oxen, and exhibits
a very slight degree of virulence.

Koch divides trypanosomata into two great groups.

The grouping is based on three important peculiarities: firstly, the
morphology of the parasite; secondly, its virulence; and, thirdly, its
relation to the host.

The first group only exists in one species of animal. They have become
so completely accustomed to this method of life that they cannot exist
under other circumstances. Their virulence is slight but constant. This
group comprises the trypanosoma of rats and the trypanosoma Theileri.

The second group (to which all other trypanosomata belong) shows great
variation in virulence and in form. These trypanosomata are not peculiar
to any one species, but may affect dogs, rats, horses, etc. Their
morphological peculiarities also vary according to the animals in which
they are found. Thus, the tsetse parasites when cultivated in the bodies
of dogs and rats become much smaller than usual, and the centrosome
appears near the end; when cultivated in horses the end appears pointed,
and the centrosome lies near the centre; in the pig the parasites lose
their peculiar short flagellum. Their virulence also varies within wide
limits.

It has been found possible, as in the case of bacteria, to modify the
virulence of trypanosomata by successive passages through different
animals. By inoculating dogs with comparatively innocuous trypanosomata
and conveying the disease from dog to dog the virulence is markedly
increased. On the other hand, parasites which prove very virulent for
oxen become much less active for these animals after passages through
rats and dogs. This apparently trifling discovery laid the foundation
for protective inoculation experiments. Parasites of the second group
can also exist in the bodies of almost all mammals.

Koch is of opinion that the parasites of surra in India and of tsetse
disease in Africa are absolutely identical. Laveran, on the other hand,
states that he has protected animals against tsetse, and that they have
nevertheless suffered from surra.

That this in no way disproves the identity of the two parasites is shown
by other experiments.

Koch, whilst in Dar-es-Salaam, made some interesting experiments for the
purpose of discovering a method of protective inoculation. He had found
that the virulence of the ox parasites could be modified. He therefore
inoculated oxen first with these weakened parasites and afterwards with
others of high virulence. All the control animals died while those
treated as above remained alive.

Veterinary Surgeon Schmidt kept these animals under observation, and
reinoculated them from time to time with highly virulent material,
notwithstanding which they were still perfectly well six years after the
first inoculation.

In practising this method, however, the trypanosomata used for the first
inoculation must not be unduly weakened. The method would have appeared
fully successful were it not for the fact that the protected and
apparently quite vigorous animals still suffered from the presence of
parasites in the blood. To extend its use, therefore, meant that one
would not suppress, but would spread the disease. The effect would be to
produce herds harbouring the parasite, which herds, though exhibiting no
signs of illness, would nevertheless in a sense be propagating the
active cause. Further observation has also shown that the protection so
conferred is only relative. Dogs can always be infected with the blood
of such animals. It has long been known in Africa that antelopes and
buffaloes harbour trypanosomata in their blood without showing external
signs of disease.

Another method of protection must therefore be sought, such as
destroying the various stinging flies; but this offers little hope of
success. Koch admits that he sees no method of dealing with them. The
other method is directed against the parasite, and here he seems more
hopeful. The disease can be rooted out by killing all diseased animals
suspected of disease. The line of procedure is indicated by the
experience gained in Mauritius and Java. When surra broke out in
Mauritius almost all the oxen died in two years. In Java the nature of
the disease was early recognised, and all suspected animals were at once
slaughtered or isolated until slaughtered; in this way the disease was
soon stamped out.


                              LOUPING-ILL.

The close analogy between the convulsive form of the disease described
as “trembling” (which disease is well known in France) and the condition
known in Britain as louping-ill lead us to give here a short account of
the latter condition. For a great part of what follows we are indebted
to articles by Meek and Greig Smith, published in the _Veterinarian_,
Vol. LXIX, Nos. 820 and 840.

=Nature and Symptoms of the disease.= The disease known usually as
louping-ill or trembling has long been of annual and sometimes of
biennial recurrence in certain parts of Great Britain. In these places
sheep farmers look for the appearance about the middle of April, to its
continuation during May, and to its gradual disappearance early in June.
Lambs are most liable, but sheep are also quite susceptible to the
disease, and in both the symptoms are the same. The disease under
consideration is rendered quite distinct by certain well-known symptoms.
Though these have been described in various ways, the disease can be
recognised by the more or less complete paralysis of the body and limbs.
Symptoms may succeed one another very rapidly, or may be spread over
some length of time. The animal at first loses control over the muscles,
which are seen to twitch convulsively. It may fall down and struggle on
the ground, sometimes jumping up again, often to some height. Between
the fits it is often seen to stand trembling. These symptoms are
frequently accompanied by frothing at the mouth. Some such appearances
are the usual onset to the disease, and are followed by a paralysis
which usually affects the hind limbs, but may also include more or less
of the body and the head and neck. The fore limbs are often similarly
paralysed. The affected limb or limbs become cold to the touch. The
paralysis necessarily brings the animal to the ground, though it may be
able to crawl about by the aid of the unaffected legs. When the head and
neck are affected the former is usually drawn to one side, and the eyes
often become oblique. Excitement is greatly increased when the animal is
disturbed. The symptoms, then, in a few words are more or less complete
paralysis, preceded as a rule by fits and trembling.

The small number which recover present “a wry neck, stiff joint, high
back, or other deformity.” During recovery swellings occur at the
joints; these may be pierced with good results, giving a large discharge
of pus. According to Fair, in the _Veterinarian_, Vol. VIII., “these
abscesses usually appear in the neighbourhood of the joints, but
sometimes above the arms, the brisket, or any neighbouring part of the
body.”

While the disease is characteristically a sheep ailment, other animals
are also liable. Swine fed with the carcases or blood of sheep which
have succumbed to louping-ill die with every characteristic of the
disease in a short time. If the carcase has been boiled this does not
occur. Swine will also frequently take the malady if allowed access to
the grass of affected fields. Cattle are said to take the disease, and
in the North Tyne district it is said that if a cow takes louping-ill,
the milk will give the illness to a calf or lamb. One or two cases of
horses being attacked are also reported.

Regarding the infectious character of louping-ill, the following is very
well known. Sheep bred on diseased places are not nearly so liable to
the disease as sheep which have been introduced from unaffected places.
Louping-ill may be introduced into a new place, but in such cases,
unless the importation from affected farms be continued, the malady may
disappear.

=Distribution of the disease.= In Great Britain it is confined to the
North Tyne district of Northumberland and to the contiguous border
counties of Scotland, extending into Kirkcudbrightshire and certain
valleys of Dumfriesshire. It is rare in Berwickshire, common in the
north and west of Roxburghshire and the similar hilly districts of
Selkirkshire and Peeblesshire. It occurs in Ayrshire, to a slight extent
in Lanarkshire, and is found in the western parts and islands of
Argyleshire and Inverness-shire.

Not only is the disease very circumscribed in its distribution as a
whole, but locally in the places mentioned infected and non-infected
spots are pointed out. These may be quite contiguous. The flocks in the
North Tyne district feed up and down the hills in limited “cuts,” and it
is one of the features of the illness that certain “cuts” are very
liable to it, while others, even on the same farm, are just as free. In
many cases the nature of the pasture is such as to suggest to an
experienced man the probability of its being subject to the disease. A
dry and foggy pasture seems best suited for harbouring the cause of the
malady. These infected places have remained wonderfully constant, but a
peculiar feature about them is that some may be very bad for louping-ill
one year, and others bad another year. Of two adjoining farms, one may
be badly attacked and the other mildly, while in the following year the
conditions may be reversed. Districts may present the same
peculiarities. Thus, though the disease is essentially endemic, it is
not absolutely constant in its recurrence. There seem to be certain
circumstances capable of favouring or retarding it.

[Illustration: $1]

[Illustration: $1]

=Lesions.= The chief lesions are localised in the membranes of the brain
and spinal cord, which are congested or inflamed, and contain an
increased amount of cerebro-spinal fluid or a jelly-like, sometimes
blood-stained exudation. Softening and hardening of the spinal cord have
both been observed. Inflammation of the pleura and pericardium, with
fluid or jelly-like exudation, are common; lobar congestion of the
lungs, endocarditis, gastritis, and enteritis have all been described;
some observers have mentioned congestion of the kidneys and liver and
swelling of the spleen. Lesions of the nerve-centres are the most
constant and reliable.

=Etiology.= Depressing and weakening influences of all kinds have been
blamed for producing the disease, but the general consensus of opinion
points in the direction of infection with microorganisms carried and
introduced into the sheep’s system by the common sheep tick or “grass
tick” (_Ixodes redurius_). The following remarks on, and illustrations
of, this parasite are from an article by Mr. Wheeler, of Alnwick
(_Veterinarian_, Vol. LXXIII., No. 867, p. 141).

=Life History of the Grass Tick.= Sheep ticks (which must not be
confused with the sheep-ked, or keb, a wingless six-legged fly,
universal on sheep everywhere) are allied to the spiders. They pass
through four stages of existence: the egg—the six-legged larva—the
eight-legged pupa—and, finally, the eight-legged adult male or female.

[Illustration: $1]

[Illustration: $1]

In each of the three stages of larva, pupa, and adult female, all
species of ticks attack some “host” or animal, either beast, bird, or
reptile, to which they attach themselves by the “rostrum” or beak, and
become greatly distended by suction of the host’s blood. When replete
they fall to the ground—if a larva or pupa, in order to undergo its
metamorphosis to the next stage of its existence, and afterwards seek a
fresh host; if an adult female, to lay its eggs amongst herbage. The
adult male is not capable of distension by suction, though it equally
attaches itself to a host.

After undergoing metamorphoses, grass ticks, with the exception of
males, are light in colour, soft and lethargic, and remain concealed for
some time while recovering strength before seeking a fresh host.

Professor Neumann alludes to the fact that a fresh host is sought by
ticks three several times during their existence.

=The Larva.= When first hatched out from the eggs, which are supposed to
be laid at the roots of coarse herbage, the young ticks are white and
soft, but soon gain strength. Provided the weather is favourable, they
climb up the stems, and, holding by their two posterior pairs of legs,
await the passing of a host, employing their two front legs as insects
use their antennæ.

In this, as in other “free living” stages of their existence, the young
larvæ show great activity, attaching themselves and clinging tenaciously
to any moving object. They appear to be more numerous on the rank rushes
growing in damp, undrained places.

[Illustration: $1]

On finding a host, larvæ attach themselves by the rostrum, and remain
there for about two days, by which time they are distended, black and
globular. At this time they are easily detached from the host, and have
lost their activity and clinging habits.

=The Pupa.= The possession of eight legs distinguishes the pupa easily
from the larva. The extra pair are placed behind the others. After the
metamorphosis, the pupa takes up its position on the stalks of herbage,
just as the larva had done, for another chance of attachment to a host.
But whereas adult grass ticks seem to confine themselves mostly to
sheep, cattle, and deer, the larvæ and pupæ attach themselves very
readily to various hosts, such as horses, dogs, and even human beings.
After about four days the pupa is again replete with blood, black and
opaque, and again drops to the ground to undergo its second and final
change.

=Adults.= On reaching the adult age, both males and females again wait
on herbage for a passing host. At this time, as well as after distension
of the female on the host, an action which appears to be sexual
intercourse freely takes place, even in confinement. On the host the
females gradually distend (Fig. 202), and in the course of so doing vary
much in colour and appearance. When fully replete, the female _Ixodes
reduvius_ becomes globular and black. One taken in this condition on
April 15th commenced to lay on May 12th, and a few others taken at the
same time commenced shortly afterwards.

Grass ticks never remain on the host to undergo metamorphosis or to lay
eggs. They must therefore during their cycle of existence contrive to
find a fresh host no fewer than three times.

In an article published in the Transactions of the Highland and Ag. Soc.
for 1902 Mr. Wheeler draws attention to the close points of resemblance
between louping-ill, Texas fever, tsetse fly disease, surra,
heart-water, yellow fever, and malaria.

In the article previously referred to he summarises his conclusions as
follows:—

One species only of tick, _Ixodes reduvius_, commonly known as the grass
tick, has been found to carry the louping-ill bacillus to the sheep. It
is easily recognised by the red body of the young females, the legs,
shield, etc., being dark brown.

It lays its eggs, and undergoes its metamorphoses, in coarse herbage,
and after each change seeks a fresh “host” on which to distend itself to
a large size by suction of blood.

[Illustration: $1]

[Illustration: $1]

In all stages grass ticks abstain from all food except when on a host,
and they are endowed with extraordinary powers of fasting until a host
is found.

Ticks soon die of drought where there is no good harbourage among rank
vegetation.

Judging from analogy, it is probable—

That the bacillus can only be obtained from a diseased sheep, and
inserted by the tick into another sheep.

That ticks convey the bacillus through their eggs to their offspring, as
well as retain it through their metamorphoses.

That there is no danger in removing sheep from foul ground to cultivated
lowlands, but that the disease is easily imported from one hill farm to
another.

Strong and fat animals are nearly as susceptible to attack as weakly
ones.

If the land is once free of disease, it can only be re-imported by
diseased sheep, or ticks taken from them.


                   SUGGESTED MEASURES FOR PREVENTION.

Burning and cutting of long grasses, bracken, rushes, etc.

Salt and sulphur given to the sheep.

Inoculation.

Removal of all diseased sheep to a separate inclosure, where
hand-picking and dipping are carefully attended to, the pasture is kept
short, and damp places are drained. The sheep to be confined to this
inclosure so long as the tick season lasts.

Immediate slaughter and burial of all affected sheep.


                                 BRAXY.

[The following is a very condensed account of a paper published by C. O.
Jensen on the above disease. It first appeared in English in the
_Veterinarian_, Vol. LXIX., No. 825, p. 621, along with the original
illustrations.]

The name Braxy is applied to a disease in some respects resembling
anthrax, which appears as an epizootic, and is best known in Iceland,
the Faroe Islands, and parts of Norway, though it also occurs in
Scotland and Cornwall. Krabbe describes the disease as infectious, very
acute in its course, and as proving fatal within a few hours of the
appearance of certain characteristic swellings about the posterior parts
of the body. Post-mortem reveals extensive dark purplish staining of the
abomasum and distension of the digestive canal with gas, while
decomposition of the cadaver occurs with excessive rapidity, the liver
and kidneys undergoing softening, the skin assuming a bluish tint, the
wool becoming loose, and the entire carcase giving off a most offensive
stench. Krabbe states that the disease was regarded as a form of
anthrax—a view, however, in which he does not coincide. Somewhat later
Messrs. J. Sigurosson, S. Jönsson, and Einarsson, all natives of
Iceland, and the Norwegian State Veterinary Surgeon, Ivar Nielsen,
carefully described the disease, throwing considerable light both on the
conditions in which it appears and on its etiology.

According to them, braxy is an acute, or even exceedingly acute,
infectious disorder, which begins as a hæmorrhagic inflammation of the
mucous membrane of the abomasum, is accompanied by excessive development
of gas in the digestive canal, especially in the stomachs, and proves
fatal in some cases by a kind of general infection, in others by a
specific intoxication, or by dyspnœa due to tympanites.

Braxy commits its chief ravages during the winter months: appearing
first in autumn, the cases increase as winter approaches, to diminish
again in spring; in summer they are exceedingly rare. This fact explains
why the disease was so long regarded as due to climatic influences. Even
at the present day, when it is known to be due to a specific organism,
the action of temperature, etc., must still be regarded as probably
playing an important part in infection. The disease is said not to occur
in mild weather; but whether or not this be true, every one is agreed
that it is principally seen during frost, especially when frost is
unaccompanied by snow.

From experience gained both in Iceland and Norway, the disease appears
to be often localised in certain districts and fields—a fact largely
accounted for when we learn that up to the present little or no attempt
has been made to prevent the spread of infection from the dead bodies.

Braxy chiefly attacks young animals, and is rare in those over three
years of age. Hjaltelin estimates the number of deaths in a single
district during the years 1849–1854 at approximately 6,000, made up as
follows:—

                  Yearling lambs                 2,440
                  Two-year sheep                 2,460
                  Three-year sheep               1,020
                  Animals older than three years    80

The younger animals suffer most, and in Norway Nielsen directs attention
to the heavy fatalities amongst lambs.

=Symptoms.= The sheep suddenly appears ill, is dull, lies about, and
cannot be induced to rise; all movement seems to give pain, and from
time to time the animal groans; the posterior parts of the body become
swollen, and a little froth often escapes from the mouth. The pulse
varies between thirty and thirty-five per minute, and is often
imperceptible in the extremities; the temperature may rise to 105° or
even 108° Fahr. This condition may last some hours, and always ends with
the animal’s death; sheep, which overnight had shown no signs of
illness, are often found dead in the morning. The incubation period is
from forty-eight to sixty hours, but ordinary cases seldom live longer
than from five to eight hours after the symptoms declare themselves.

The striking post-mortem appearances, especially the hæmorrhagic
inflammation of the abomasum, were early the subject of remark. This
appearance is very characteristic.

If the animals are slaughtered, the most important change is found to be
a purplish, dark, somewhat swollen patch in the abomasum; during the
course of the disease this increases in size, and if the animal should
be allowed to die of braxy the entire abomasum shows hæmorrhagic or
sero-hæmorrhagic infiltration; the abomasum and the first part of the
small intestine usually contain no food, but may often show a certain
amount of bloody fluid. This hæmorrhagic inflammation may extend in a
forward direction, implicating the other stomachs, or backward, invading
the small or both small and large intestines. The other parts of the
intestinal canal are congested. The pleural and peritoneal cavities
contain a little serous fluid. The blood is dark in colour, but may be
clotted; the spleen is at times somewhat swollen, at others normal. The
liver is usually light-coloured, soft, and degenerated; occasionally
this degenerative process is extremely marked, but due allowance should
always be made for post-mortem change. The kidneys may appear
degenerated; in many cases they are enlarged and soft, or almost fluid
in consistence. The carcase decomposes very rapidly; within a short time
of death the belly is distended with gas, the rectum protrudes at the
anus; the skin assumes a bluish colour in places, and the wool falls
out; sometimes the skin bursts, revealing the presence in the
subcutaneous tissue of a sero-hæmorrhagic fluid.

[Illustration: $1]

Braxy is, then, a primary violent hæmorrhagic inflammation of the
abomasum, with or without secondary general infection.

From careful study it seems quite certain that the Scottish “braxy” is
identical with the Norwegian and Icelandic “bradsot”; it appears at the
same season, and is intimately connected with climatic influences; it
runs its course so rapidly that animals left healthy at night are found
dead in the morning; and the pathological anatomy of braxy is the same
as that of “bradsot.”

To Ivar Nielsen, of Bergen, must be ascribed the honour of elucidating
the etiology of braxy. During the course of investigations, published in
1888, he found, partly in the local lesions of the intestinal track,
partly in the capillaries of the internal organs, a special bacillus,
easy to distinguish from that of anthrax, of which he gives the
following description:

“The bacilli (_B. gastromycocis-ovis_) are oval, of a length varying
from 2 to 6 micromillimètres, and a thickness of one micromillimètre.
They are often in pairs, arranged in a straight line or meeting at an
angle; in the former case, and especially if deeply stained, the pair
may present the appearance of a single bacillus. Occasionally they form
long chains. Near the centre of the bacillus, but not always centrally
placed, may often be found a zone measuring more than half the total
length of the bacillus, and exhibiting little or no colouration. It
appears as though the stained portions gradually contracted, finally
forming two deeply coloured masses at the poles of the lemon-shaped
bacillus, which then somewhat resembles the bacillus of rabbit
septicæmia, except that the unstained part of the braxy bacillus is
larger and more rounded, appearing to be bulged out laterally. In dry
preparations the bacillus is easily recognised on account of the highly
refractile character of the colourless portion; but in sections careful
search is often required, especially if the section be somewhat thick.
Whether the colourless portion represents a spore cannot at present be
said, though such appears probable. The bacillus is always found in the
mucous membrane of the abomasum, and especially in the submucous and
subserous connective tissue. In the other organs the bacillus may be
present in considerable numbers, or, on the other hand, may be
impossible to detect.”

The same bacillus has been found in the tissues of affected sheep both
in Norway and in Iceland; the bacillus, when subcutaneously injected,
produces a violent hæmorrhagic inflammation of the same character as one
finds in the abomasum in cases of spontaneous braxy, and the local
changes at the point of inoculation may, just as in spontaneous braxy,
be accompanied by a general infection with degeneration of different
organs, and with softening of the kidney substance.

The bacillus of braxy is anaërobic. In cultures it develops considerable
quantities of gas, just as it does when inoculated into the tissues. It
is closely related to the bacillus of symptomatic anthrax, which it
somewhat resembles in general appearance, and of which it reminds one by
its ability to produce hæmorrhagic inflammation in the muscular tissues.
It is distinguished from the last named, however, by being pathogenic to
swine, mice, pigeons, and poultry, which are not killed by the bacillus
of symptomatic anthrax.

The bacilli of braxy, malignant œdema, symptomatic anthrax, together
with Ivar Nielsen’s shortly described bacillus of whale’s septicæmia,
and Thoma’s bacillus of malignant emphysema (found in extensive
subcutaneous inflammation and emphysema in man), and certain others less
well known, form a group of closely allied bacilli resembling one
another in form, in being anaërobic, and in producing a sero-hæmorrhagic
inflammation and emphysema, but differing in the manner of producing
their effects.

Experience and analogy both seem to indicate that young animals
occasionally suffer from mild attacks of braxy from which they recover.
Such animals afterwards exhibit a well-marked immunity against the
disease.

Ivar Nielsen attempted to vaccinate against braxy by a method resembling
that used in black-quarter. He dried the diseased kidney tissue, and
injected subcutaneously small quantities of the material thus obtained
suspended in water. A slight local inflammation followed, which appeared
to protect against later “spontaneous” infection. He has used this
method in his own district, and states that it is also practised to some
extent in Iceland. As far as one can judge—and of course a just opinion
is very difficult to form—these inoculations appear of value.

The result of experiment, considered in conjunction with the good
results of inoculation for black-quarter, would seem to indicate that
Nielsen’s method of vaccination against braxy may yet prove of the
greatest possible value, although the method will doubtless require
modification in its details.

These modifications Jensen enumerates at some length.

(Mr. Dollar has been informed that Professor Hamilton and Dr. McCall
have been engaged in an investigation regarding the possibility of
conferring immunity against braxy, and that a Government report will be
issued on the subject. Up to the present time however—April, 1905—he has
not been able to obtain this report or any advance proof sheets of it.)


                   BILHARZIOSIS IN CATTLE AND SHEEP.

This disease is caused by the bovine blood fluke (_Schistosoma bovis_)
of cattle and sheep. Synonyms: _Bilharzia bovis_; _Bilharzia crassa_;
_Gynæcophorus crassus_; _Gynæcophorus bovis_; _Bilharzia hæmatobia
crassa_; _Schistosomum bovis_.

=Geographical Distribution.= Egypt, Italy, Sicily, India (?).

This parasite was discovered by Sonsino (1876) in Egypt in the portal
veins of the ox, and later he found it in sheep, while Grassi and
Rovelli afterwards found it in about 75 per cent. of the sheep
slaughtered at Catania, Sicily.

=Source of Infection.= Clinical observation and analogy point to
unfiltered drinking water as the source of infection.

=Position of the Parasite.= The worms are found in the veins of the
abdomen, the vena porta, vena linealis, vena renalis, and the venous
plexus of the bladder and of the rectum.

=Symptoms.= The young parasites appear to do no injury; in fact, even
the adult worms seem to be inoffensive in themselves. The eggs, on the
other hand, armed with a sharp point, are the exciting cause of the
disease. The position of the parasite in the venous system, and the
consequent location of the agglomeration of eggs, determine the
particular symptoms. Either the genito-urinary system is attacked, in
which case hæmaturia is one of the first symptoms, or the large
intestine is attacked and blood is noticed in the fæces.

[Illustration: $1]

[Illustration: $1]

If the parasites are lodged in the venous plexus of the genito-urinary
system, the chief symptoms are: hæmaturia, pains in the lumbar region,
the left iliac fossa, the thigh, or in the vulva, which may be
spontaneous or may accompany micturition; cystitis, vesical calculus,
urinary fistulæ, vaginal verminous tumours, nephritis.

The eggs accumulate in the capillaries, which they rupture; they
traverse the mucosa and fall into the bladder, thus causing more or less
hæmorrhage; in this way the _hæmaturia_ is established, which is often
the initial symptom. At first the urine is quite bloody, but it
gradually becomes clearer, and it is only at the end of micturition that
muco-purulent flakes are expelled, in which numerous eggs and even
embryos are found; the urine contains also epithelial cells, more or
less pus, eggs, and occasionally embryos. On micturition sharp pains are
felt at the base of the penis or at the gland, possibly due to the
passage of eggs. The passage of eggs through the walls of the bladder
gives rise to _cystitis_; blood becomes more abundant in the urine after
fatigue or coitus; clots may form and cause retention of urine; chronic
urethritis may develop, evidently due to the presence of the eggs. In
Egypt 80 per cent. of the cases of vesical calculus in man coincide with
bilharziosis; the formation of the calculi evidently results from the
presence of the eggs, for the central nodule always contains one or more
of these structures. Urinary fistulæ, opening on the perineum, more
rarely into the rectum, occasionally form. The mucosa of the vagina,
also of the uterus and bladder, becomes impregnated with calcareous
salts. Nephritis develops in grave cases.

[Illustration: $1]

If the parasites lodge in the veins of the rectum the lesions caused are
analogous to those described for the genito-urinary tract.

The heart, lungs, and liver generally remain normal.

=Pathology.= The bladder is reduced in size, while its wall is greatly
thickened, due chiefly to hypertrophy of the muscularis; the mucosa is
also thickened, and at certain points it is indurated by uric or
calcareous deposits, but the principal lesion consists in ulcerations
covered with sanious pus. Lesions analogous to those of the bladder are
also observed in the lower third of the ureters, and may extend as high
as the kidney; the ureter is enlarged and tortuous; the mucosa
irregular; its lumen may remain nearly normal in size, but its wall
becomes very thick: the flow of urine may be obstructed; in short, a
veritable hydro-nephrosis obtains, which results in atrophic lesions of
the kidney, and may finally end fatally.

The mesenteric lymphatic glands may hypertrophy, their substance
becoming tumefied, presenting small hæmorrhagic centres, and containing
eggs. The liver may contain eggs and become somewhat cirrhotic; the eggs
accumulate in the branches of the portal veins, or after piercing the
walls they lie in the hepatic parenchyma. The lungs may also contain
eggs.

=Diagnosis.= The diagnosis may easily be made by a microscopic
examination of the urine to determine the presence of the egg.

=Prognosis, etc.= The severity of the disease varies directly with the
number of parasites (and hence the number of eggs) in the body.
Fortunately, in the majority of cases, the number of parasites is small,
though it may increase from repeated infections to 500 or more. In cases
of comparatively light infection the disease is reduced to a slight
chronic cystitis, with now and then exacerbations, in course of which a
slight amount of blood and pus is passed in the urine. The disease may
last for years without apparent increase. In the most severe cases death
may occur from various causes, rupture of the bladder, ascending
pyelo-nephritis, uræmia, albuminuria; the patient may die in marasmus,
being exhausted by the dysentery or the anæmia.

Bilharziosis is accordingly not such a fatal disease as has sometimes
been supposed.


                       HEAT STROKE—OVER-EXERTION.

In oxen and sheep heat stroke is rare as a primary accident, but it is
frequently produced by over-exertion resulting from the combined action
of the sun’s rays, heat, and fatigue due to work or travelling.

It is commonest during the hottest months of the year in oxen doing hard
work or in flocks which have been travelled considerable distances. It
may also be seen during cooler seasons as the result of exceptional
fatigue.

The disease results from a general intoxication which reacts most
markedly on the cerebro-spinal centres. It is in fact a complex
intoxication resulting from failure of the natural excretory organs to
perform their function completely, and from excessive central heat
acting on the nervous centres.

Fat animals out of condition are more readily attacked than working
animals or sheep reared in the open air.

=The symptoms= are very characteristic. Oxen when attacked first of all
show extremely rapid respiration and dyspnœa, announcing progressive
asphyxia. They move with the nostrils dilated, the eyes prominent and
injected, the mouth open and the tongue lolling out. Then all of a
sudden they come to a stop beside a wall, or, if at liberty, in a ditch,
and refuse to move. They may die rapidly with symptoms of asphyxia if
they are forced to move until completely exhausted. In others, after a
rest of several hours, the breathing becomes slower, the anxiety less
and normal conditions return.

In sheep the same general signs may be seen: panting respiration,
cyanosed mucous membranes and extreme anxiety, while death follows
rapidly in the same way, with symptoms of asphyxia.

The =diagnosis= is extremely easy. The =prognosis= is grave.

=Treatment= consists in prompt and free bleeding to prevent pulmonary
congestion. The animals should be rested in a shady, sheltered spot.
They should have cool drinks and be sprinkled over the head, neck, or
entire surface of the body with cold water.

To prevent such attacks, fat animals should not be moved for long
distances, or during the hottest hours of the day, while difficult and
prolonged exertion should be avoided.




                              CHAPTER VI.
                   DISEASES OF THE LYMPHATIC SYSTEM.


Diseases of the lymphatics are numerous, highly important, and still
imperfectly understood. They follow various accidents, local
inflammations, certain specific diseases, such as tuberculosis, and may
occur in an isolated form without involving any other part of the body.

[Illustration: $1]

Inflammation, usually of infectious origin, may attack lymphatic vessels
(lymphangitis) or lymphatic glands (adenitis), giving rise either to
simple lymphangitis, suppurative lymphangitis, or again to simple or
suppurative adenitis.

It is unnecessary to emphasise this point in general surgical pathology,
for it is identical with that which is observed in other domestic
animals, but in order properly to detect the glandular symptoms in
certain diseases peculiar to the lymphatic apparatus, and in certain
specific diseases, such as tuberculosis, farcy of the ox, etc., it is
necessary to understand thoroughly the topography of the lymphatic
system.

=Topography of the lymphatic glandular apparatus: Examination.= The
lymphatic glands are in some cases superficial, in others deep seated,
and are arranged symmetrically on either side of the body.

[Illustration: $1]

Beginning with the head and fore quarters, the lymphatic apparatus
comprises a subglossal, a preparotid, a subatloid, a prescapular and
several prepectoral glands (Fig. 209).

None of these glands are very deeply placed, and all are easily
accessible to palpation, provided their exact position is known and the
animals are not too fat.

The subatloid is a little more difficult to detect, but in thin animals
the tips of the fingers can easily be passed under the wing of the atlas
so that the condition of the gland can be examined.

In a normal condition, any gland on being examined conveys a sensation
of softness and elasticity of a special character which never varies.
Palpation is painless.

When, however, the gland is diseased, palpation causes pain in the case
of all acute affections. It may, indeed, be impossible to reach the
glands, as they are buried sometimes in œdematous swellings of varying
size. On the other hand, they may be painless on being touched, but
swollen, hypertrophied, indurated, hardened or caseous.

The deep-seated glands of the fore portion of the body comprise the
retro-pharyngeal and the cervical chain running along the posterior
border of the trachea. Normally these glands cannot be examined (Fig.
210); but when the seat of certain morbid processes, they may be so
enlarged as even to be readily visible. The larynx and pharynx are then
displaced downwards, the depression between the head and upper extremity
of the neck disappears, together with the depression known as the
jugular furrow. Such deformities may be either perfectly symmetrical, as
in lymphadenia, or (as is more commonly the case) asymmetrical, as in
tuberculosis; and if inspection leaves any doubt, the glands may be
further examined by palpation.

[Illustration: $1]

To obtain the fullest information both hands should be used, one arm
being passed over the neck and the fingers engaged behind the trachea.
The operator may also stand in front of the animal, whose head should be
lifted so that the points of the fingers can be thrust deeply inwards on
either side of the trachea in the direction of the vertebral column.

In the posterior portion of the body the number of glands that can be
examined is much smaller. The gland of the stifle, also called “gland of
the flank,” is, so to speak, the only one which can readily be detected
by examination or palpation. Nevertheless, in cases of lymphadenitis,
tuberculosis of the glands, etc., it becomes easy to detect lymphatic
glands in the loose fold of skin known as the flank. These glands are
very small, and three in number. They are arranged in a triangle, one
being much more prominent than the two others. In exceptional cases,
little nodular glands, indistinguishable at ordinary times, may become
hypertrophied. This is particularly true of the small glands in the
neighbourhood of the last rib.

[Illustration: $1]

The retro-mammary glands need only be mentioned, but it is important to
know that a deep-seated popliteal gland also exists above the
semi-tendinosus and semi-membranosus muscle in the thickness of the
muscles of the thigh; as also an ischiatic gland opposite the ischiatic
notch, which can only be examined by internal palpation from the pelvis,
and an anal gland situated deeply on the sides and in front of the
sphincter ani.

With the exception of those of the pelvis and of the sublumbar region,
the glands of the thoracic and abdominal cavity cannot be examined, but
change in them is indicated under certain circumstances by clearly
defined clinical symptoms, and moreover it is necessary to be able to
detect changes in these glands on post-mortem examination.

In the thoracic cavity the lymphatic apparatus comprises the mass of the
prepectoral glands, which extends into the anterior mediastinum between
the first ribs (glands of the entry to the chest), the aortic lymphatic
gland situated beneath the dorsal portion of the spine opposite the
bifurcation of the aorta, and the lymphatic glands of the posterior
mediastinum, one of which is relatively small and is lodged in the
concavity of the posterior aorta, the other large, elongated and
situated immediately above the œsophagus in front of its passage through
the diaphragm.

In the abdominal cavity a sublumbar chain is found situated on the sides
of the lumbo-sacral portion of the vertebral column, the mass of the
subsacral lymphatic glands, and, at the entrance to the pelvis,
extending on either side along the course of the external iliac arteries
and veins and resting on the shafts of the iliac bones, the iliac
glands.

All these glands are partly accessible to examination by the rectum.

Last of all, we may mention the gland situated on the hilum of the
liver, the mesenteric glands, and the little lymphatic glands above the
sternum.

In the front limb the only glands of importance from a clinical
standpoint are those of the internal surface of the shoulder, close to
the divisions of the brachial plexus.

When enlarged or invaded by any specific organism, they may, by
compressing the nerve trunks, cause lameness.


                       THE LYMPHOGENIC DIATHESIS.

(LYMPHADENITIS, LYMPHO-CYTHÆMIA, MYELO-CYTHÆMIA.)

It has been questioned whether the term “lymphogenic diathesis,” which
was employed in human medicine by Jaccoud to describe certain morbid
conditions also found in animals of the bovine species, should continue
in use. At the present moment it is difficult to determine the question.
Under any circumstances it has the advantage of including diseases of
the lymphatic system, indicated by hypertrophy of the lymphatic glands
(adenitis) or by an exaggerated production of white blood corpuscles
(leucæmia), and the passage into the general circulation of products
derived from the lymphatic apparatus. For these reasons it may be
employed here.

Clinical investigation long ago demonstrated that in man certain
pathological conditions were characterised by a peculiar colour of the
blood, due to the presence of white blood corpuscles in excessive
quantities, whence the names “leucæmia” (Virchow) and “leucocythæmia”
(Bennett). In the same way it has been shown that the change in the
blood characterised by a superabundance of white blood corpuscles
generally coincides with engorgement or more or less marked hypertrophy
of the lymphatic system and of the adenoid tissue of the body (lymphatic
glands, spleen, bone marrow, and, in exceptional cases, liver, kidneys,
etc.)—leuco-cythæmic lymphadenitis; but that many cases also occur in
which this hypertrophy of the adenoid tissue or of the lymphatic gland
tissue may exist, without any excessive number of white blood corpuscles
in the blood, whence the name “aleucæmic lymphadenitis or
pseudo-leucæmia.” Cases of true leucæmia without adenitis are much
rarer, the lesions therein being confined to the adenoid tissue of the
bone marrow.

These three morbid conditions—leucæmic lymphadenitis, or leucocythæmia;
aleucæmic or pseudo-leucæmic lymphadenitis, or more simply adenitis; and
true or simple leucæmia—are frequently found in the bovine species.
Whilst stating that these diseases are frequent, we must, however, be
understood to except the numerous cases of tuberculous lesions formerly
included under the same head.

Jaccoud has shown that in reality the causes of these three morbid
conditions are very similar, and that a case which at first appears to
be of the nature of aleucæmic lymphadenitis may later become transformed
into leucæmic lymphadenitis; or, inversely, that a case which at first
appeared to be a simple leucæmia might often become complicated with
lymphadenitis: hence the grouping of these different morbid conditions
under the heading of lymphogenic diathesis.

Investigations have now thrown more light on the subject because of the
more perfect recognition of the varieties of white blood corpuscles, and
the above-mentioned morbid conditions may be defined as follows:—

(1.) The first variety consists of a more or less marked adenitis or
lymphadenitis without leucæmia (aleucæmic lymphadenitis).

(2.) The second variety, consisting of leucæmic lymphadenitis, or
leucocythæmia, is a lymphatic lucæmia or lympho-cythæmia, the anatomical
characteristic of which is enlargement of lymphatic glands, and the
histological characteristic increase in number of the large and small
lymphocytes.

(3.) A third variety, formerly regarded as simple leucæmia without
lymphadenitis, is myelogenic leucæmia or myelo-cythæmia, the
anatomico-pathological characteristic of which is to be found in myeloid
hypertrophy of the bone marrow, giving to the bone marrow on post-mortem
examination a puriform appearance, and in the myeloid condition of the
spleen.

Histologically this variety is characterised by an absolute increase in
numbers of the large mono- and poly-nuclear eosinophile leucocytes.

=Symptoms.= Simple lymphadenitis begins in an insidious manner, and is
characterised by weakness, anæmia, paleness of the mucous membranes, and
wasting without apparent reason, although the appetite is preserved. It
is only at a later stage that the glandular enlargements are discovered
(adenitis), and often this discovery is not made until the veterinary
surgeon is called in.

The existence of the disease is indicated by enlargement of the
superficial glands, and this enlargement, which may commence at any
point, extends along the course of the lymphatic vessels to the
neighbouring glands, until in a shorter or longer time it involves all
the lymphatic glands in the body.

The enlargement of the glands is usually symmetrical, and on clinical
examination it is sometimes easy to detect at the outset an increase in
size of the retro-pharyngeal glands, the glands of the neck, the
prescapular glands, the glands of the flank, etc.

Rectal exploration reveals hypertrophy of the glands of the pelvis and
of the sublumbar region, etc. The animals waste very rapidly, and
sometimes in a few months become incapable of standing. They develop
cachexia, and die in a state of exhaustion, with no other lesions than
those of lymphatic hypertrophy. Neither do they exhibit any marked
increase in the number of white corpuscles in the blood.

In lympho-cythæmia the beginning of the disease is often identical with
that of simple lymphadenitis, the increase in the number of white blood
corpuscles not occurring until later. In other cases, on the contrary,
leucæmia appears first, and the enlargement of the lymphatic gland
follows; but what characterises this form and allows of it being
distinguished from myelo-cythæmia is the great increase in the number of
large or small lymphocytes. The development is identical with, and
sometimes much more rapid than, that of the preceding form. The animals
waste away and become anæmic and cachectic, dying at last in a state of
absolute exhaustion.

Post-mortem examination reveals, as in the previous condition,
symmetrical hypertrophy of all the lymphatic glands; the spleen is very
often enormous, and the liver is sometimes affected, as are also, in
exceptional cases, the kidneys.

It may happen that the spleen alone appears affected, or at least that
it has been first attacked, a fact which explains the existence of
leucæmia before any enlargement of the lymphatic glands.

=Causation.= The causes of lymphadenitis and of lympho-cythæmia are
unknown in veterinary as in human medicine. Apparently these diseases
are more common in adults than in young animals. Some regard them as
infectious in character, but this can hardly be the case, as all
experimental attempts to transmit the diseases have failed. It is more
plausible to compare the development of these morbid conditions with
that of malignant tumours, and although some doubt still exists, simple
lymphadenitis may be described as an aleucæmic lymphoma or
lympho-cytoma, which has gradually become generalised, spreading by way
of the lymphatic channels from the gland first affected through the
surrounding glandular system. Lympho-cythæmia, on the other hand, may be
said to be a leucæmic lympho-cytoma, which spreads both by the blood
circulation and by the lymphatic paths (spleen, hæmatopoietic glands and
organs).

This view of the development of the lesions enables us to class
lympho-sarcomata with lymphomata and lympho-cytomata. The malignant
character and extremely rapid development of lympho-sarcomata appear due
to its extending by contiguity of tissue, and simultaneously by the
lymphatic paths.

This new grouping would consequently place on one side myelogenic
leucæmia, also called myelo-cythæmia, which is perhaps a different
morbid species. This would destroy the unity implied in Jaccoud’s theory
of the lymphogenic diathesis; but for all that this method of grouping
might be justified by reference to specific cellular characteristics. In
myelo-cythæmia the disease appears to commence as a lympho-cythæmia,
_i.e._, it is unaccompanied by enlargement of lymphatic glands or
hypertrophy of the spleen or liver, though the blood appears leucæmic.
The condition is not a leucæmia due to lymphocytes, but rather a
leucæmia produced by mono- and poly-nuclear eosinophile leucocytes,
_i.e._, leucocytes derived from the bone marrow.

The patients are carried off rapidly after persistent wasting, decline
and cachexia, whilst on post-mortem examination the puriform aspect of
the bone marrow is an extremely striking characteristic.

=Diagnosis.= There is rarely much difficulty as regards the diagnosis.
The enlargement of the lymphatic glands, for instance, can readily be
detected, and the only disease with which this can possibly be
confounded is tubercular enlargement.

With the means at present available for diagnosing tuberculosis, such as
microscopic examination of the discharge, inoculation with discharge,
examination of material from the glands, injection of tuberculin, etc.,
the nature of the disease can always be placed beyond doubt.

In lympho-cythæmia and in myelo-cythæmia, the whitish-violet lactescent
appearance of the blood is of unmistakable significance, particularly
when the manifest progressive wasting of the whole system is taken into
account.

Histological examination of the blood after fixation and staining will
in the former cases reveal the presence of very large numbers of
lymphocytes, and in the latter an absolute increase in the number of the
mono- and poly-nuclear lymphocytes. It should be easy, therefore, to
distinguish the two diseases, especially as other symptoms vary.

In the early stages leucæmia may be mistaken for the leucocytosis seen
in infectious diseases. These forms of leucocytosis are very common in
animals of the bovine species. They occur in certain forms of
tuberculosis, in uterine infections, in cases of internal suppuration,
in tumour of the heart, the rumen, etc., and vary in so far as one style
or another of white blood corpuscle predominates. The diagnosis,
therefore, necessitates that the white blood corpuscles should be
counted, and whenever it is found that their variations in number are no
more than between 5,000 and 15,000 per cubic millimètre, the case may be
regarded as one of temporary leucocytosis.

If, on the other hand, those corpuscles number more than from 15,000 to
20,000, or, as may sometimes happen, they attain to from 200,000 to
300,000 per cubic millimètre (one white to two or three red blood
corpuscles), the case is one of leucæmia, and, according to the
predominance of the particular type of cell, it is a lympho-cythæmia or
a myelo-cythæmia.

In leucæmic conditions the red blood corpuscles are also present in
fewer than the normal numbers. They are more irregular, assume giant and
dwarf forms (macrocytes and microcytes), sometimes exhibit lacunæ, and
are always polychromatophile, _i.e._, without special affinity for any
particular constituent of double or triple stains.

=Prognosis.= The prognosis of diseases included in the lymphogenic
diathesis is extremely grave, and in the present state of our knowledge
it may be assumed that sooner or later death is inevitable.

=Treatment.= Treatment can scarcely be considered to exist, for at the
best it can only delay the development of the disease. Nevertheless, and
with this reservation, it is certain that preparations of iron, iodine
and arsenic have a certain effect, probably by acting on the
hæmatopoiesis.


                  CASEOUS LYMPHADENITIS OF THE SHEEP.

In the sheep the lymphatic glands are sometimes the seat of peculiar
changes, which do not appear to have any marked effect on the general
condition. Thus a post-mortem examination or an examination of animals
in the slaughter-house sometimes shows a certain number of isolated or
symmetrical glands, such as the mediastinal, tracheal, inguinal, pelvic
or sublumbar glands, to be greatly enlarged and completely degenerated.
The precrural, prescapular, and popliteal glands are said to be most
frequently affected. Their contents are caseous and yellowish, enveloped
in a fibrous sheath, and show no signs of peripheral inflammation. The
other organs and viscera may either be healthy or exhibit caseous
lesions identical with those found in caseous broncho-pneumonia.

=The causes= of this disease are imperfectly understood, although Cherry
and Bull (1899, the _Veterinarian_, Vol. LXXII., No. 860, p. 523) have
isolated from the lesions an organism identical with Preisz’s bacillus
and with the microbe of ulcerative lymphangitis in the horse.

Norgaard and Mohler (Annual Report, United States Bureau of Agriculture,
1899, p. 638) have studied the disease. In June, 1897, Turski, at
Danzig, found about 150 breeding ewes, from eight to twelve years old,
suffering from nodules or abscesses the size of a child’s fist in the
inguinal and prescapular regions. They had been sold for slaughter, and
many were in very poor condition. The disease occurs in Europe, Western
America, South America, and Australia. Several thousand cases are
annually seen in the slaughter-houses of the United States.

=The symptoms= generally escape notice, and it is only by accident that
one sometimes detects marked enlargement of the lymphatic glands of the
neck or of the superficial inguinal glands. The patients, moreover, may
remain in very good bodily condition, so that the lesions are only
discovered on the meat being inspected.

Having regard to our imperfect knowledge of this disease, it is
impossible to express an opinion as to its importance or treatment.


                      GOITRE IN CALVES AND LAMBS.

Although not strictly relevant to the foregoing matter, a few remarks
may here be made on the subject of goitre.

True goitre consists in hyperplasia of the follicles of the thyroid
gland, with colloid change of their contents, which are chiefly
albuminous. The swelling is mainly due to enlargement of the follicles,
and is termed struma follicularis. It may attack the entire organ or
only one-half; less frequently it is confined to certain sections. Other
varieties of goitre are recognised, such as fibrous, varicose and cystic
goitre. (For fuller details see Möller and Dollar’s “Regional Surgery,”
p. 149.)

[Illustration: $1]

=Treatment= by injection of thyroid juice or by feeding on thyroid
extract has given better results than drugs.

The following account of an outbreak in New Zealand is summarised from
the Annual Report of the Chief Veterinarian of New Zealand, 1901:—

The calves affected were born with enlarged thyroids. The farm is of
rich alluvial deposit, and rather below the level of the river, which it
borders. The land has been in occupation, however, for many years, and
no similar condition had been previously noted. At first, as calves only
were affected, it was thought possibly to be due to the bull, a
two-year-old animal, but when a foal was born suffering from a similar
malformation this theory naturally fell to the ground.

The land had been ploughed with a special plough 20 inches deep, but
this is no uncommon practice in the island.

About the same time, a similar disease was discovered affecting lambs at
a farm near Outram. From 450 ewes, 150 lambs had been lost, the glands
being enlarged to the size of a cricket ball. A few had been born dead,
many only lived a few hours, others lived several days, and a
considerable number recovered. There was no connection, directly or
indirectly, between the two farms, they being at least fifty miles
apart. A few of the calves died or were killed, the remainder recovered,
and the foal grew rapidly better. The land on both farms is very similar
in composition.

Mr. Wilkie states, from observation of previous cases in lambs, that “it
appears to be always associated with malnutrition and a condition of
anæmia in the parent, induced in most cases by feeding with watery,
innutritious foods.”

Specimens were forwarded, from a calf and from a lamb, of enlarged
glands. The gland of the calf was enormously enlarged, being at least
twice the size of an orange, dark in colour, flabby in consistency, and
on section a mucous material exuded copiously from the cut surface.
Micro-examination showed the acini to be larger than normal, filled with
the usual mucous material, and lined with cubical epithelium. The
connective tissue surrounding the alveoli was, however, crowded with
round-cells, so much so that the whole parenchyma seemed to be
practically composed of these cells.

A specimen of an enlarged thyroid from the lamb was about the size of a
sheep’s kidney, and very much the same shape and colour. Sections
microscopically examined showed a different condition to that of the
calf’s thyroid. Here the acini were filled with epithelial cells loosely
arranged as if the lining epithelium had been proliferating rapidly,
while the connective tissue surrounding the acini was fairly normal. The
section had a somewhat adenomatous appearance.




                               SECTION V.
                            NERVOUS SYSTEM.


                          CEREBRAL CONGESTION.

According to Cruzel, cerebral congestion is somewhat frequent in working
oxen subject to continued concussion from the yoke, especially among
animals working on a rocky soil. The condition may also be produced by
prolonged exposure to the sun, as well as by sudden and intense cold.

Passive cerebral congestion by stasis may be produced by any cause
markedly interfering with the return circulation (pericarditis due to
foreign bodies). Clinically it is of no importance.

The animals, previously in good health, suddenly appear comatose. They
are insensible to stimulation of any kind, the head is rested on any
convenient object or is held stationary, the animal looks drowsy, the
gait is hesitating or vacillating, the respiration slow or irregular.
Left at liberty, the animal does not seem to know where it is going;
indeed, sometimes it is absolutely blind and strikes against any
obstacle in its path, or falls and suffers from epileptiform
convulsions. The cranial region is abnormally warm. The =course= of the
attack is rapid, and the animal either dies in a state of coma or
convulsions or else recovers rapidly.

=Diagnosis.= The diagnosis is decidedly difficult; and the =prognosis=
should be reserved.

=Treatment= commences with free bleeding, the amount of blood drawn
being proportioned to the animal’s size. The sides of the body may then
be stimulated and a purgative administered.


                              MENINGITIS.

The generic term “meningitis” includes all inflammations of the
arachnoid, pia mater and internal surface of the dura mater.

These forms of inflammation occur in diseases such as tuberculosis and
in parasitic diseases of the brain. Under other circumstances, they are
rare, and may be produced by very varying causes.

An epizootic cerebro-spinal meningitis of the bovine species has also
been described, principally in Germany. It seems almost unknown in
France, and French literature contains no well-authenticated case.

Furthermore, an epizootic cerebro-spinal meningitis of sheep, or rather
of lambs, has been described in Germany, in Italy, and in France. These
descriptions are all open to many objections. It seems that under the
term “cerebro-spinal meningitis” have been grouped cases of enzootic
tetanus, doubtful cases of poisoning, and particularly cases of
cœnurosis in the first stage of development. We therefore discard these
descriptions, which differ too much among themselves to be of any value.

=Causation.= Meningitis occurs in the ox and sheep as a complication of
wounds in the cranial region, accompanied by fissuring of the bone,
periostitis, abscess formation, etc.

It is also seen as a complication of fractures of the horns, and
old-standing catarrh of the facial sinuses. In the sheep it follows
parasitic catarrh due to the larvæ of œstridæ.

The meningitis appears, according to circumstances, in the forms of
local meningitis, anterior frontal meningitis, basilar meningitis, etc.
Finally, it may develop as a complication of different diseases, such as
gangrenous coryza, purulent infection, subparotid abscess, suppurative
phlebitis, suppuration of the eye or of the orbit, etc.

=Symptoms.= It is difficult to detect and interpret the first symptoms
shown, because these chiefly consist in dulness, want of appetite and
constipation, without any particular fever. At a later stage, excessive
excitability is produced by noises, by changes of light, or by handling.
Careful examination of the patients shows a change in their expression,
rapidly followed by contraction and inequality of the pupils or
deviation of the visual axis (strabismus, squinting). The pulse becomes
irregular, as also the respiration. The appetite is entirely lost, and
it is not uncommon to note a contraction of the muscles of the neck and
jaws, as well as inability to move about and symptoms similar to those
of dropsy of the cerebral ventricles.

The chronic form is rare.

=Lesions.= The lesions comprise local or general hyperæmia and exudative
inflammation of the pia mater and arachnoid, together with the formation
of false membranes or of pus in the subdural space. The meninges are
partially adherent, and the superficial layers of the brain are also
inflamed by contiguity of tissue.

=Diagnosis.= The diagnosis must be based on the disturbance of vision,
movement, and appetite, and on the course of the symptoms, as well as on
the external signs in the case of such diseases as are prone to become
complicated with meningitis.

=Prognosis.= Sooner or later the case is likely to end fatally, and
there is no practical use in treating the patient.

=Treatment.= If in exceptional cases slaughter is objected to, setons
and blisters may be applied to the poll or the parotid region, or the
parts may be enveloped in ice bags or compresses of iced water
frequently renewed.


                             ENCEPHALITIS.

Encephalitis, _i.e._, inflammation of the cerebral substance, is very
closely allied to meningitis; in a great number of cases meningitis and
encephalitis co-exist. In other cases encephalitis may be found apart
from meningitis, and _vice versâ_. Moreover, many of the symptoms of
meningitis are to be found in cases of encephalitis.

Encephalitis may develop as a complication of meningitis. Encephalitis
may also follow abundant parasitic infestation, as in cœnurosis (which
will be particularly studied as it affects sheep), or microbic
infection, the commonest form of which in the ox is tuberculosis. The
encephalitis may be diffuse or circumscribed, according to the cause,
while the symptoms are varied and numerous. Very frequently,
particularly in cases of tuberculosis, encephalitis assumes a chronic
form.

=Symptoms.= The earliest symptoms are extremely difficult to detect,
because they are scarcely characteristic and because it is impossible to
ascertain the sensations of the animal.

It is only when the disturbances in walking, in the eyesight, in
swallowing, etc., are noted that suspicion is aroused.

The symptoms may appear suddenly. Nevertheless it is beyond doubt that
there are certain slightly marked prodromata, indicated by diminution of
appetite, wasting, and changes in vision. Soon afterwards occur other
forms of disturbance, which may be classified under the heading of
“motor, visual, nervous, and impulsive.” The patients appear stunned,
their movements are slow and hesitating, they partially lose control
over their limbs and display lameness, with spasmodic movements of one
or two limbs. Examination of the joints shows no injury. The lameness
may simultaneously affect two diagonal limbs or two fore and two hind
limbs, or even three limbs. This lameness is of central origin.

The ocular disturbance is marked by diminution or loss of vision, by
strabismus, or by frequent unconscious movements of the eyes and
eyelids, and also more particularly by inequality, contraction or
dilatation of the pupils.

Nervous, impulsive disturbance is most readily noted when the animals
are at liberty. Even when the sight remains, they seem quite incapable
of avoiding obstacles or as though absolutely forced to move to the
right or left, etc.

Attacks of giddiness, moreover, are not unusual under the influence of
the slightest excitement. During such attacks the animals thrust the
head against a wall, or they involuntarily recoil or make lateral
movements. In many cases these vertiginous attacks end by the animal
falling and showing epileptiform convulsions, during which it may die.

The symptoms are never the same in two different animals, but they may
easily be classed according to the above indications. The indications
furnished by the condition of the eyes and by the peculiar impulsive
movements are particularly significant.

On the other hand, there are modifications in breathing without apparent
local cause, and difficulty or even impossibility of swallowing, etc.,
although there exists no material obstacle.

=Diagnosis.= The condition is often confused with meningitis, and the
mistake is not serious, because meningitis and encephalitis frequently
accompany one another.

=Prognosis.= The prognosis must be regarded as fatal. The patients very
seldom recover, and there is no reason for keeping them alive.

=Treatment.= Here, again, blisters may be applied to the upper extremity
of the neck, or setons may be passed. Cooling applications to the
cranial region have also been suggested. None of these methods produces
more than a temporary palliative effect.


                           CEREBRAL TUMOURS.

The brain may be injured and compressed by various tumours of other than
parasitic origin. Such tumours may originate in the bones, the meninges
or the choroid plexus, or they may simply be due to generalisation of a
previously existing tumour. Whilst of very varied origin and nature, all
tumours of the cranial cavity have one common effect, viz., to compress
the brain. This continuous compression causes progressive atrophy of the
brain, but its existence is not always suspected, because the lesions
may not give rise to any marked symptoms.

The hind portions of the hemispheres and the white substance are
generally very tolerant. The front portions, on the other hand—the
frontal lobes and the grey substance—resent compression, which provokes
various symptoms in consequence.

=The symptoms= of compression and atrophy of the brain differ greatly, a
fact which is easily understood, inasmuch as the seat of the change may
vary, and therefore it is possible only to trace the chief
manifestations, which suggest the existence of a cerebral tumour.

The general changes are indicated by signs precisely similar to those so
common in horses with dropsy of the ventricles (general depression,
inability to back, long intervals between the prehension of successive
mouthfuls of food, sudden cessation of mastication, etc.), by an
impulsive or automatic gait, and by the assumption of strange attitudes
(kneeling down in front, etc.). When at rest the animals appear to be in
a state of continual torpor.

Special symptoms sometimes occur, which enable the seat of the injury to
be localised in more or less exact fashion. These symptoms affect the
vision (amblyopia, amaurosis, strabismus, nystagmus), general
sensibility (hyperæsthesia, anæsthesia, etc.), and the power of movement
(total, partial or crossed hemiplegia, want of co-ordination of
movements, etc.).

Trifling stimuli almost always lead to marked and even epileptiform
attacks.

=The diagnosis= of cerebral tumours is very difficult, particularly when
attempts are made to indicate their exact seat, but that of other
cerebral lesions is somewhat easier.

=The prognosis= is very grave, and in the case of domestic animals
nothing can be done. In the ox intra-cranial operations are difficult,
by reason of the presence of the sinuses which obstruct the approach to
the brain cavity; economically surgical treatment is seldom advisable.


                              INSOLATION.

Insolation is an exceptional accident in animals of the bovine, ovine,
or porcine species. If at liberty these animals move about, and always
seek shelter when the sun is fierce. If, on the contrary, they are
harnessed and kept standing for long, exposed to the full midday sun
during June, July or August, they may suffer from insolation.

During the International Cattle Show attached to the Exhibition of 1900
in Paris, a considerable number of cases of insolation occurred in
animals of one class, exposed to the full midday sun, in an
ill-ventilated spot. The other classes only received sunlight from the
sides, and in them not a single case occurred.

Death may follow in a few hours; it is difficult to say precisely how it
is brought about, but it is always accompanied by congestion of the
cerebro-spinal centres and general blood stasis.

=The symptoms= of the development of insolation occur very rapidly. In
animals of the bovine species there is accelerated respiration, which
soon amounts to dyspnœa. The mucous membranes then become cyanotic. The
animals attacked seem anxious, although not agitated, and soon
afterwards the eyes water, the mucous membrane and the lips of the vulva
display œdematus infiltration and congestion, and areas of cutaneous
congestion, closely resembling mud fever in the horse, appear over the
mammæ. At this stage the animals move with difficulty, and show all the
symptoms seen at the outset of gangrenous coryza.

All these symptoms develop in one, two, or three hours, and death may
follow if nothing is done. They disappear, however, as rapidly as they
appear. In an hour or less we have seen in some cases a complete return
to the normal condition. Given the facts, the =diagnosis= is extremely
easy.

=Treatment.= Treatment should be commenced by immediately removing the
animal to a cool, airy, shady place. It may then be bled, and the head
and neck should be freely drenched with cold water. The symptoms
generally disappear as though by magic.


      POST-PARTUM PARALYSIS—MILK FEVER—MAMMARY TOXÆMIA—PARTURIENT
                    APOPLEXY—DROPPING AFTER CALVING.

For a great part of the following short account we are indebted to an
excellent report by J. J. Repp, V.M.D., in the _Journal of Comp.
Medicine and Veterinary Archives_, September, 1901:—

The word “fever” in connection with the terminology of this disease is
not very appropriate, because in the majority of cases fever is not
present, but the animal has a subnormal temperature. The term milk fever
is very misleading and indefinite, as it is also used by the laity to
designate other diseases, such as parturient septicæmia and the various
forms of mammitis. Parturient paralysis must be clearly differentiated
from parturient septicæmia, which is a disease of an entirely different
character and which may occur in any of the domestic species, whereas
parturient paralysis occurs only in the cow.

=Distribution.= Parturient paralysis occurs wherever milch cows are
kept. It is more prevalent in dairy districts, because it is the heavy
milking strains of cows that are most subject to the disease.

=Cause.= No definite cause can be assigned for this disease. Schmidt’s
theory is that parturient paralysis is caused by the evolution in the
mammary gland of a poisonous substance through the over-activity of the
epithelial cells of this gland excited by the determination to the udder
after birth of large quantities of blood which was supplied to the
uterus and the fœtus before birth, but which now goes to the udder
because of the natural demand for milk secretion. This poisonous
substance being carried in the circulation to various parts of the body,
brings on the symptoms which characterise the disease. It is well
recognised that living cells may, under certain circumstances, produce
poisonous substances. Schmidt’s theory, therefore, is in accord with an
established principle.

=Pathogenesis, or generation, of the disease.= Parturient paralysis, as
a rule, occurs in cows which give a heavy flow of milk and which are in
a high state of nutrition. It may develop at any age, but is extremely
rare in cows before they have reached adult age and have given birth to
several calves. It is also rare in old cows. It occurs, then, in cows
which are of middle age and in the full height of their activity as milk
producers. The disease attacks the cow after she has given birth to a
calf, usually within twenty-four hours thereafter, but in some cases not
until a week or even a month after parturition. In a few cases the
disease has its inception a short time before parturition. Cows which
are stabled and deprived of exercise are said to be more prone to the
disease than those which are permitted to exercise at will. There are
many exceptions to this statement, although it is the usual teaching.
Further observation may show that it is not correct. In Iowa more cows
take this disease while at pasture than in any other circumstance. This
doubtless arises from the fact that in Iowa cows are given more freedom
than is customary in older dairy States. The disease may arise at any
time in the year, but, on account of the fact that spring-time is
pre-eminently the calving season, most cases originate at this season.

=Morbid anatomy.= The morbid alterations are limited and variable, and
offer nothing characteristic. The blood is irregularly distributed, a
condition which probably indicates marked vaso-motor disturbance
resulting from the profound interference with the nervous functions
which accompanies the disease. The abdominal organs are usually filled
with blood. The brain may be anæmic, œdematous, easily torn, and
yellowish in colour. In other cases it shows hyperæmia of the meninges
and of the brain substance.

=Symptoms.= The disease usually appears within twenty-four to
forty-eight hours after parturition. In extreme cases it may not occur
until two months or even six months after parturition. It may rarely
occur before birth. It usually follows an easy birth. At the onset of
the disease the cow manifests some uneasiness; it moves about in a
restless manner, stamps, strikes the abdomen with its hind legs, perhaps
bellows, grinds the teeth, and may have spasms of groups of muscles or
even a general convulsion. After this period, which may be unnoticed,
the symptoms of paralysis come on. The cow shows weakness, staggers, and
at last falls. As the paralysis advances it stretches on the ground,
lying on its side usually with the neck bent to one side so as to bring
the nose into the flank or the costal region. This is the characteristic
position in parturient paralysis. If the head is brought into the normal
position, it at once returns to the unnatural position in which it was
found. The animal is in a state of partial or complete unconsciousness,
does not respond to blows or calls, and takes no note of its
surroundings. The eye is dull and not sensitive to the finger touch,
sunken, pupil dilated, and the upper lid is drooping; the tongue is
paralysed, saliva runs from the mouth, the pharynx and œsophagus have
lost the power of motion, so that the animal is unable to swallow; the
peristalsis of the stomachs and intestines is in abeyance, and as a
result digestion is arrested, fermentation sets in, and the animal
becomes tympanitic; the contents of the rectum and colon are hard and
dry, and may be covered with mucus or blood, urination is suspended; the
os uteri is almost invariably dilated if the disease occurs within a day
of parturition; pulse small, often imperceptible, 60 to 120 per minute;
temperature, usually normal or below normal, may be as low as 95° Fahr.,
in some cases may be as high as 105° Fahr. Such a high temperature
probably does not occur in a case of pure parturient paralysis, but only
when there is a complication of parturient septicæmia. The extremities
are cold. The after-birth is sometimes retained. There may be
accompanying prolapse of the uterus.

=Course.= Without treatment, and, indeed, with most kinds of treatment
which have been applied in the past, the disease usually runs rapidly to
a fatal issue. It lasts two to three days, and in some cases longer, the
condition gradually becoming more and more aggravated. Death results
from sudden failure of the heart or brain, and is often preceded by
profuse diarrhœa. In milder cases the cow may linger as long as two to
four weeks and then die of pneumonia, which results from the inhalation,
or introduction through attempts at medication, of foreign substances
into the lungs during the period of paralysis of the pharynx and
œsophagus. If recovery occurs, the animal is entirely well in two to
five days. In rare cases paralysis of the hind parts may persist for a
long while.

=Diagnosis.= This is made by a study of the history and symptoms. It is
comparatively easy.

=Differential diagnosis.= It must be distinguished from ante-partum
paralysis, broken-back, parturient septicæmia; but one familiar with the
character of these diseases will find no difficulty in making this
differentiation.

=Treatment.= This may be considered under two distinct subdivisions,
viz., preventive treatment and curative treatment.

(_a_) _Preventive treatment._—By considering what has been said under
the head of “generation of the disease,” one can easily infer what
measures should be adopted to prevent the disease. Cows in the later
stage of gestation should be fed moderately, grain especially being
given sparingly or entirely withheld; the animals should be given an
opportunity to take plenty of exercise; the bowels should be kept in
good condition by the administration of such salines as magnesium
sulphate, sodium chloride, and sodium bicarbonate. The after-birth
should be removed soon after parturition and several uterine douches
administered.

(_b_) _Curative treatment._—The older methods of treatment comprised:
warmth and friction to the mammary gland; the administration of
sedatives, such as opium, chloral and bromide of potassium; stimulants,
including ammonia, ether, turpentine and alcohol; washing out the uterus
with water or disinfectant solutions; the relief of tympany by the use
of the trocar and canula (by which instrument medicines may also be
injected directly into the rumen); the removal of fæces from the rectum;
warm clothing of the body and general attention to the animal’s comfort,
and to the teachings of hygiene. For all these widely diversified
methods good results have been claimed, and, we may add, bad ones at
times recorded. F. T. Harvey (Cornwall) estimates the average mortality
at from 40 to 66 per cent., though he claims for his more recent
practice a lessened mortality of only 20 per cent.

Schmidt does not claim that his method of treatment disposes bodily of
the morbid condition, but that it does measurably assist Nature in her
efforts to restore the animal to the normal physiological state. It is
well known that after the beginning of the attack the animal, if left to
itself, rapidly grows worse until the crisis of the disease is reached,
at which time death occurs or convalescence begins, usually the former.
It has been observed, however, that if the treatment is applied within a
few hours after the inception of the disease its progress is modified in
such a way that convalescence at once begins, as a rule, and the animal
hastily recovers its health, usually within twelve hours, although in
extreme cases it may be as late as forty-eight hours. The following is
an outline of the plan of treatment of parturient paralysis suggested by
Schmidt. The operator should disinfect his hands and the udder and teats
of the cow by washing with a 5 per cent. solution of carbolic acid or
creolin, or a 1½ per cent. solution of lysol or trikresol. The apparatus
needed for the treatment consists of a small glass funnel, a rubber hose
three feet long and one-eighth inch in calibre into which the funnel
fits, and an ordinary milking tube over which the rubber hose fits. This
apparatus should be sterilised immediately before it is used by boiling
or soaking in such a solution as recommended for washing the udder.
Dissolve from 2 to 2½ drachms of potassium iodide—the size of the dose
depending upon the size of the cow and the character of the attack—in
about one quart of clean water previously boiled to sterilise it, and
allow the solution to cool to a little above body temperature, or 40° C.
or 104° Fahr. The temperature may be determined with the clinical
thermometer. Withdraw all the colostrum or milk from the udder. Then
insert the milking tube, with hose and funnel attached, into one of the
teats, elevate the funnel about two feet above the teat and slowly pour
in one-fourth of the solution, allowing the funnel and hose to become
empty several times during the process in order to permit the entrance
of a liberal quantity of air. Repeat this infusion with the other three
quarters of the udder. After all is introduced, knead the udder
carefully so as to cause the solution to permeate the ducts and acini as
much as possible.

As the condition of the cow is usually such as to call for additional
treatment, the veterinarian should not be content with injecting the
potassium iodide solution, but should resort to any and all other
measures which promise assistance.

As the cow is usually unable to urinate, the bladder will be found
filled with urine. This should be removed with the catheter, and its
removal accomplished at intervals until the recovery of the cow renders
this procedure no longer needful.

It may be advisable that catharsis be brought about. As the cow is
usually unable to swallow, it is dangerous to attempt to give medicines
by the mouth. This may be done if assurance that the cow can swallow is
obtained. Some have given medicines successfully through a probang
inserted into the stomach. The plan is feasible. Schmidt says that he
usually resorted to an aloe powder. If this is done 1 ounce to 1½ ounces
of aloes may be given. It would seem preferable to give the aloes in a
bolus, capsule, or drench. Some have given linseed oil or Epsom salts.
If the animal cannot swallow and a probang is not at hand, one may
administer 1½ to 2 grains of physostigmine salicylate subcutaneously,
repeating the dose in about three hours if purgation is not produced.
Rectal injections should be given at short intervals in order to get rid
of the accumulation of hard, dry fæces in the rectum. These injections
may be of linseed oil, cotton-seed oil, or warm soap solution. Schmidt
recommends, also, enemata of sodium chloride solution. Meanwhile the cow
should be kept propped up on the sternum by means of bags of straw or
pieces of wood. If the temperature is below normal, as it usually is,
the cow should be thickly clothed with blankets and straw heaped up
about it. Schmidt used powdered digitalis given by the mouth when the
heart was rapid and weak. It would seem much better in every way to give
the tincture of digitalis subcutaneously. He has also resorted to
subcutaneous injections of camphor and caffeine. This is good treatment.
If the cow does not show marked improvement within eight hours the
potassium iodide infusion may be repeated. Schmidt has found that as
much as 6 drachms may be injected into the udder without harm to the
cow. Schmidt, in his first report, made in 1898, recorded 50 cases
treated for parturient paralysis by this method with but two deaths from
the disease. There were, however, only 46 recoveries, as two cows were
slaughtered for beef during the first day of convalescence. A short time
later a report was made by Jensen showing that in Denmark up to that
time sixty-five veterinarians of that country had treated 412 cases by
the Schmidt method, 90 per cent. of which recovered. Such results seem
to indicate this as the treatment _par excellence_ for parturient
paralysis. It still remained to secure the introduction of this
treatment into the United States and to determine what results could be
obtained. In all 166 cases were reported; of these 166, 119 resulted in
recovery, while 47 were fatal. Of the fatal cases, in eight of the cows
death may be traced to some complication, such as prolapse of the
uterus, foreign-body pneumonia, etc. In these cases the Schmidt
treatment cannot be said to have failed, for it is not in any way
intended that it shall be able to overcome such accidental conditions.
If the cow has recovered from its condition of paralysis as a result of
the Schmidt treatment far enough to be out of danger from that source
and to promise recovery, but later falls a victim to some complication
that is in no measure a part of parturient paralysis, but only a result
of that disease, it may with justice be said that the Schmidt treatment
was a success so far as the malady against which it was directed is
concerned. Looking at the reports from this generous point of view, in
127 cases out of 166, or 76·5 per cent., the Schmidt treatment was
successful so far as the parturient paralysis was concerned.

In a paper published in the _Berliner Thierärztliche Wochenschrift_ in
August, 1902, Schmidt reviews the results of his treatment as evinced by
914 patients treated by thirty-one different practitioners: 884, or 96·7
per cent., recovered, twelve died and six were slaughtered during the
course of the disease. Twelve others were slaughtered at a later period
in consequence of complications. Jensen reported the results of 1,744
cases.

Schmidt also found that the simple injection of air was in many cases
sufficient to produce recovery, and subsequent observation tends to show
that the fluid injected is of less importance than was first
anticipated. A large number of unirritating solutions may be employed.
Schmidt, however, still counsels the use of a quart of 1 per cent.
solution of iodide of potassium, in which can be dissolved 5 grammes of
caffein sodio-salicylate if the heart’s action is weak. About 10 ounces
of this solution are injected into each quarter, and are followed by a
liberal injection of air. The parts should afterwards be freely
massaged.


                  CŒNUROSIS (GID, STURDY, TURN-SICK).

Cœnurosis is a disease due to invasion of the animal body by embryos of
larvæ of the _Tænia cœnurus_ of dogs and wolves. These embryos only
develop freely in the brain substance (_Cœnurus cerebralis_) and medulla
oblongata. The hosts of the larvæ include the calf, sheep, goat,
roedeer, reindeer and horse.

The disease was formerly erroneously called “turn-sick,” for the turning
is only a manifestation, and even a tardy manifestation, of the disease,
while in addition it is not invariably present.

Cœnurosis principally attacks lambs of from three to six months,
although it occurs up to eighteen months, and sometimes even two years.
It is exceptional, however, in adults. Similarly in the bovine species
it usually affects young animals up to the fourth or fifth year.

Cœnurosis with diffuse parasitic encephalitis often remains
unrecognised, the animals being regarded as affected with epizootic
meningitis of unknown cause or septic intoxication, and when they die
the owners are ignorant as to the cause of death. The stage
corresponding to turn-sick, which is an advanced phase of the disease,
is only seen in animals which have been infested to a slight extent, and
in which three or four parasites only, sometimes only one, have attained
the brain and developed there. Such cases exhibit all the classic
symptoms of turn-sick, viz., turning movements, heaviness, vertigo, etc.

=Causation.= Cœnurosis is due solely to one cause, viz., the ingestion
of eggs or embryos in feeding or drinking.

The _Tænia cœnurus_ lives in the dog, and fertilised segments are passed
with the fæces in yards, pastures and fields, and on the margins of
roads, ditches and ponds. Amongst damp grass or in water the eggs, which
contain more or less well-developed embryos, may retain their vitality
for several weeks, and when swallowed the embryos are set at liberty in
the intestine.

The six-hooked embryos perforate the walls of the intestine, pass into
the blood stream or chyle ducts, and from these points are carried in
all directions. Those which gain the nervous centres, the brain or
spinal cord, continue to develop; the others, dispersed through
different tissues, degenerate and disappear.

Experimental infection with these parasites shows that the brain is
invaded after about a week’s time. From the twentieth day the presence
of embryos can easily be detected in the superficial layers of the
convolutions. They make their way through the grey substance, leaving
behind them greenish-yellow sinuous tracts with caseous contents.

The cyst or finn undergoing development can be found at the end of one
of these tracts in the form of a little transparent bladder, of a size
varying between that of a pin’s head and that of a lentil or a small
hazel-nut.

Later the tracts, with their caseous contents, disappear, and the
development of many of the vesicles proves abortive. At the end of a
month the vesicles, continuing to develop regularly, attain to about the
size of a pea. Between the fiftieth and sixtieth days heads or scolices
appear in the interior of the vesicle, which then reaches the dimensions
of a hazel-nut. From this time the vesicles continue to increase in size
until the death of the patient. Usually they become as large as a
walnut, or even larger, and the interior contains hundreds of scolices,
each showing a head.

[Illustration: $1]

The cystic phase only develops completely in animals whose brains
contain a limited number of cysts, and in such the signs of turn-sick
are well developed. In others, where the numbers are large (ten to
fifteen embryos or more), death occurs during the primary stage, usually
towards the end of the first month, in consequence of acute encephalitis
and without any of the symptoms of turn-sick.

[Illustration: $1]

The number of animals attacked is sometimes enormous. Moussu has
recorded cases where fifty, one hundred, and even four hundred lambs of
one flock were affected. The enormous mortality in such cases is very
apt to cause errors in diagnosis. Cœnurosis occurs most frequently
during rainy seasons, moisture favouring the preservation of the eggs.
Young animals become infected, particularly during the spring and
autumn, more rarely in the summer, as prolonged desiccation, say for a
period of twelve to fifteen days, destroys the vitality of the eggs, but
animals may become infested at any time through drinking contaminated
water. Moussu has seen cœnurosis (acute encephalitis) from the
last-named cause in the middle of January.

=Symptoms. First phase.=—_Disseminated encephalitis._—The symptoms vary
with the phases of evolution of the parasite and of the disease which it
causes. After the six-hooked embryos have penetrated to the brain, the
animals affected lose appetite and show a certain degree of dulness,
which is all the more marked inasmuch as the animals usually affected
are young, and therefore should appear bright and alert. Then follow
wasting and depression; the animals remain stationary for whole hours
together, the head being carried low or inclined to one side. At this
stage disturbance in vision and irregularities in movement may appear.

[Illustration: $1]

[Illustration: $1]

The eyesight is almost always affected, but the symptoms may vary
widely. In some cases the patients seem to be absolutely blind, and
strike against any obstacle in their way; in others the power of vision
seems to be lost only on one side. All that can be discerned objectively
is an inequality in the pupils, together with retraction or dilatation,
convergent or divergent strabismus, nystagmus, etc. The humours of the
eye appear infected, but examination with the ophthalmoscope reveals
lesions of more or less extensive neuro-retinitis.

The visual disturbance is of central origin. The powers of movement may
be affected in numerous ways, which at times are extremely difficult to
estimate with accuracy. Sometimes the gait is uncertain, inco-ordinated,
and hesitant; at others the animal shows lameness or loss of control
over a front or hind limb, or over two limbs simultaneously (either the
two front or hind limbs or the diagonal limbs), or it may be absolutely
unable to stand.

It walks obliquely, or the front or hind limbs collapse; or again, it
may persistently lie down, a fact which makes the shepherd think it is
suffering from paralysis. On examination, however, no true indications
of paralysis can be found; sensation and motor power are both preserved
in a modified form.

[Illustration: $1]

Death is very frequent at this stage of the disease; the animals eat
little or nothing, refuse drink, and die of exhaustion.

All this general disturbance is of central origin, and is due to
disseminated parasitic encephalitis, but up to this point the seat of
the disease is not yet clearly apparent.

=Second phase.=—_Turn-sick._—The central symptoms are slow of
development, and are due to the progressive growth of one or two, more
rarely three or four, fertile vesicles. These are the true symptoms of
turn-sick, and it is only after this phase of the disease has developed
that the term becomes appropriate.

Left at liberty, the patient usually walks in a circle towards the right
or left in an impulsive and irresponsible fashion. Sometimes it
describes a circle, always of the same size. In other cases, on the
contrary, it travels along a spiral track, getting further from or
nearer to the centre as the case may be. The turning movement may become
so accentuated that the animal appears to revolve as on a pivot, and if
it is confined in a field or straw-yard its legs become caught in the
litter and it falls to the ground.

Attempts have been made under these circumstances to discover the exact
point of compression, _i.e._, the point at which the cyst exists, by
noting the direction of the turning movement. The diagnosis, however
arrived at in this way is frequently illusory, because it is not
uncommon to find two or three vesicles, and in any case the most
important information in regard to diagnosis is to be derived from the
ocular symptoms.

When only one vesicle exists, the turning movement usually occurs
towards the side on which it is situated, and the eye of the opposite
side is affected with amaurosis.

[Illustration: $1]

If the cyst is situated near the olfactory lobes, the animal marches
with a high-stepping movement and the head drawn back towards the body.
If the cyst is in the cerebellum the animal is incapable of moving,
because it can no longer co-ordinate its movements. Finally, if the cyst
develops in the occipital region, animals turn towards the wind, with
the neck raised and the head extended.

At the moment when they fall to the ground they sometimes have
epileptiform convulsions, grind their teeth, and salivate profusely. In
a severe attack even death may supervene at this point.

=Cœnurosis of the Medulla.= The embryos may develop in the medulla
oblongata as well as on the brain itself. Compression and atrophy of the
medulla then give rise to true paralysis.

The animals exhibit paralysis of the hind quarters, unilateral paralysis
only, or still less marked signs. Everything depends on the degree of
development of the cysts.

=Bovine Animals.= Cœnurosis in oxen is less important than in sheep.
Moreover, it very rarely affects a large number of young animals
belonging to one farm. Loss of appetite, dulness and depression are the
earliest indications, as in sheep. The gaze seems fixed, the neck is
held stiffly and almost rigidly, the animal shows a tendency to vertigo,
pushes its head against a wall, or leans the head or neck on the manger
or trough.

[Illustration: $1]

Inequality in the size of the pupils, amaurosis, hesitating and
inco-ordinated movements may also be seen developed in different
degrees. The animals have the appearance of horses suffering from
“_immobilité_”—that is, the very peculiar general condition produced by
dropsy of the brain ventricles, or from encephalitis. They forget to eat
or do not attempt to chew unless handfuls of food are thrust between the
molars; they plunge the muzzle into a bucketful of water and do not
drink, etc. They take little notice of what passes around them, although
they may become greatly excited if an attempt is made to move them, to
give them medicine from a bottle, or to set them at liberty, etc. Such
attacks of excitement often end in vertigo and in the animals falling to
the ground and showing epileptiform movements. All these symptoms may
occur with extraordinary variations, due in reality to the peculiar
position which the cœnurus occupies.

=Second phase.= If set at liberty during the first phase of the disease,
the animal’s gait appears only slightly disordered, but when a single
vesicle has become well developed in one of the hemispheres (and this is
usually the case with oxen), the symptoms of turn-sick appear as in
sheep, and are equally varied. The patients seem impelled to move in a
given direction, whatever obstacles may be in their way. It is not at
all uncommon to see them thrusting their heads against walls or trees,
falling into ponds or ditches, or attempting to force their way through
blind alleys between hay or straw stacks.

After the cyst develops in the cerebellum, the animals are soon unable
to move. They may be able to stand in one position, but on any attempt
to move they fall.

=Lesions.= The lesions develop successively from the moment the embryos
arrive in the mass of the brain. At first the six-hooked embryos only
excite a slight disseminated encephalitis. Their course through the
brain is marked by short, greyish-green caseous tracts, the thickness of
a needle, which are readily discoverable in the superficial layers.
Later these caseous deposits become absorbed, the lesions of
disseminated encephalitis diminish and disappear, while a certain number
of vesicles after partial development undergo atrophy and disappear.
Before long nothing remains but local atrophic encephalitis caused by
the development of the vesicles, and from this time the central symptoms
begin to appear.

=Diagnosis.= When the turning movement has developed the diagnosis is
generally easy, but it is more difficult during the first period, when
encephalitis alone exists; or at least, it is very difficult at this
period to discover whether the symptoms are attributable to
encephalitis, meningoencephalitis, cœnurosis, tuberculosis, or to some
injury.

[Illustration: $1]

=Prognosis.= The prognosis is grave, and very few animals recover. Zürn
estimated the cases of recovery in flocks at 2 per cent. In these cases
the cysts degenerate and disappear.

=Treatment.= At the present moment there is no really practical curative
treatment.

The best plan appears to be to trephine the skull and remove the cyst,
provided its exact position can previously be determined. That, however,
is the great difficulty. Its solution presupposes a perfect knowledge of
the central nervous system and of the real purport of any apparent
symptoms.

On the other hand, in sheep at least, the position of the cyst must
always remain somewhat uncertain, because there are generally several,
and the symptoms are of a mixed character.

The only treatment, therefore, which would be likely to succeed is
difficult to carry out, and more difficult in the ox than in the sheep
because of the great development of the frontal sinuses.

It has been mentioned that under exceptional circumstances the cœnurus,
if very superficially placed, may cause atrophy of the cranial wall in
the sheep by the outward pressure it exerts, and that the points of
least resistance may be detected by the touch. In such cases
intervention is necessary and is greatly facilitated; but they must be
extremely rare, and Moussu declares he has never seen one.

Hartenstein has suggested continuous cooling of the cranium by
irrigation or by applications of ice, the local lowering of temperature
serving to impede the development of the cœnurus. This method should be
tried in animals of high value, and, if the symptoms have not yet become
too alarming, recovery is possible. On the other hand, when the symptoms
indicate the presence of an old-standing cyst, there is little chance of
success. Moreover, the treatment could not be applied where a large
number of animals are affected.

It is much better to send the animals to the butcher if they are in good
condition. In Scotland, however—particularly in Caithness—operation is
said to be frequently practised with success.

=Prophylaxis.= In well-managed establishments it is easy to avoid the
appearance of cœnurosis.

The development of this condition being due to the _Tænia cœnurus_ of
the dog, which passes ripe segments containing eggs with its fæces in
the pastures, the first indication is to prevent the development of this
tænia in sheep dogs, sporting dogs and house dogs, and the sole
precaution required is to avoid giving them as food sheeps’ heads
containing the bladder-worms. But, as despite these precautions they may
accidentally contract infection with _Tænia cœnurus_ by eating the offal
of slaughtered animals, it is a wise precaution to administer to all
farm dogs, twice a year at least, a dose of some tænicide.

They should be starved and kept in for twenty-four hours, and should
then receive a full dose of some energetic vermifuge, such as areca nut,
kamala, kousso, powdered pomegranate root, extract of male fern, etc.,
followed by a purgative. The material passed and the fæces should be
burned or mixed with quick-lime. By these simple precautions the losses
which formerly proved so heavy may entirely be prevented.


               “TREMBLING,” OR LUMBAR PRURIGO, IN SHEEP.

The above term is applied to a disease peculiar to sheep, and
characterised by neuro-muscular disturbance, which always ends fatally
after a longer or shorter period.

=Symptoms.= Clinically the disease occurs in two forms, one termed the
convulsive form, the other the pruriginous form. In the convulsive form
the patients rapidly lose appetite, soon appear unable to stand, fall on
their sides, and exhibit spasmodic contractions of certain groups of
muscles. After a time the clonic contractions may give place to
persistent rigidity. The patients are carried off rapidly in a week or
two without other important symptoms. This disease appears to exhibit
certain analogies with louping-ill, but these do not seem to be
recognised in France, where it chiefly occurs.

In the pruriginous form the beginning of the attack is obscure, and only
the shepherd is able to note anything unusual. The animals move in a
jerky way, the hind limbs being lifted at times after the manner of a
horse suffering from stringhalt. They are excitable, exhibit trembling
movements when touched, with convulsive movements of the head, and
present an anxious and vacant appearance. The development of these
symptoms, which constitute what may be termed the first phase of the
disease, is sometimes prolonged, and in winter may last from one to two
months. In summer it rarely lasts longer than a week or two.

At this stage a special pathognomonic symptom develops, viz., intense
and permanent pruritus of the hind quarters, which causes the animals to
rub the croup against any projecting objects, walls, mangers, etc. They
thrust themselves backward against the object, and rub with such
violence that the wool is torn away and the skin itself often
excoriated, although the irritability appears to be in no wise
diminished thereby. In the fold the animals sometimes rub against one
another, making their sides raw, and bite themselves on the croup, the
quarters, and the tail.

When the affected parts are touched with the hand, peculiar movements of
the head and the lips are immediately excited, similar in character to
those caused by mange. Up to this time the animals continue to feed, but
they progressively lose condition, become weak in the hind quarters, and
fail to keep up with the other animals in the flock. Their gait becomes
hesitating; they move with a trotting step and appear semi-ataxic.

All these symptoms develop without fever, but become aggravated from day
to day, until they end in paraplegia and death. This second phase lasts
for a period of from two to four months in winter.

=Lesions.= No lesions can be detected on a simple examination of the
dead bodies. Gilbert has mentioned a change in the blood; Trasbot,
chronic inflammation of the pia mater and of the lumbo-sacral portion of
the spinal cord. German writers have described sclerotic changes in the
posterior portions of the cord. Moussu has carried out a large number of
examinations, but has never found these lesions, either on anatomical or
on histological investigation, and he considers that they are not by any
means present in all cases.

Besnoit and Morel, who carried out a very remarkable anatomical and
pathological study of the disease, used Nissl’s staining method, but
only found very discrete changes in the cord (vacuoles in the motor
cells of the anterior horns). They found, however, significant lesions
of neuritis in the peripheral nerves.

=Causation.= The cause is as yet little understood, and it is difficult
to prove how the forms of neuritis described by Besnoit are brought
about.

The disease was not known in France before the introduction of Merinos,
and former investigators referred it to heredity, consanguinity,
precocity, and even to sexual excitement. German writers declare that it
seems more particularly to attack rams and the better-bred varieties. In
reality, the disease occurs in all flocks, and in all kinds of sheep
indiscriminately; it attacks ewe lambs and young castrated lambs as well
as rams. Moussu is absolutely of this opinion, and for want of more
precise information agrees with Trasbot, and, he believes, with Besnoit,
that the symptoms shown may possibly be referred to a chronic
intoxication.

=Diagnosis.= The diagnosis is difficult during the early stages, but
when the pruritus becomes manifest there can no longer be room for
doubt.

Cases of paraplegia might perhaps be mistaken for paraplegia due to
cœnurosis, but in the latter case there is no pruritus.

=Prognosis.= The prognosis is extremely grave, observation having shown
that all the patients die after a longer or shorter time.

=Treatment.= Until now treatment has proved absolutely useless, and it
would seem the best course to slaughter the animals before wasting
becomes marked.




                              SECTION VI.
            DISEASES OF THE PERITONEUM AND ABDOMINAL CAVITY.




                               CHAPTER I.
                              PERITONITIS.


Peritonitis, _i.e._, inflammation of the peritoneum, may attack any of
the domesticated animals. It must, however, be regarded as an almost
accidental and relatively infrequent disease. It is due to infection of
very varying character, and from the clinical standpoint may assume one
of two forms—acute peritonitis or chronic peritonitis.


                           ACUTE PERITONITIS.

The microorganisms which produce peritonitis have not been the subject
of special investigation in the domesticated animals, though the colon
bacillus and streptococci, so frequently found in the female genital
tract after parturition, seem to be the most frequent causative agents.
Certain putrefactive organisms may also bring about the disease.

The peritoneum may become infected, and acute peritonitis ensue under
various circumstances.

All operations in which the peritoneal cavity is opened, such as
castration of the cow and of the sow, laparotomy, gastrotomy,
enterotomy, etc., may be followed by acute peritonitis if performed
without sufficient regard to aseptic precautions. Peritonitis then
usually assumes an acute septic form.

Even simple puncture of the rumen, though usually quite harmless if
carefully performed, may by followed by local or general peritonitis
should food material escape from the rumen and find its way into the
peritoneal cavity.

One of the most frequent causes is infection from the genital tract soon
after parturition. Here the agents of infection are not introduced
directly into the cavity, but find their way there in consequence of a
diseased condition of the mucous membrane and the uterine walls.
Ascending infections of this character and infections by contiguity of
tissue may only give rise to local peritonitis, though in too many
instances they become generalised.

Acute peritonitis may follow infection from the stomach or bowel, should
a foreign body perforate the rumen or reticulum and pass backwards
towards the peritoneal cavity, or a serious intestinal inflammation
(enteritis, invagination, etc.) facilitate the passage of microbes
through the thickness of the intestinal wall.

Abscess of the liver, suppurative echinococcosis, renal infection,
pyelo-nephritis, acute cystitis, rupture of the bladder, etc., may in a
similar way become complicated with acute peritonitis.

Finally, abdominal wounds may cause interstitial ruptures and lesions in
the serous membrane, accompanied by local exudation (kicks,
horn-thrusts, blows from cart-poles, etc.), and if microbic agents are
brought within the region of the lesion by the general circulation or
otherwise, peritonitis may follow.

=Symptoms.= At first the symptoms are vague and imperfectly defined, and
diagnosis is always very difficult during the first few days, except in
cases where there exists a lesion or a condition previously recognised
as likely to become complicated with peritonitis.

The early symptoms comprise fever, loss of appetite, arrest of
rumination, rigors, constipation, etc., but these symptoms only attain
full significance when accompanied by what has been termed “peritonism.”

The patient appears to be suffering from tympanites, as may really be
the case, but the tympanites of the rumen and gaseous distension of the
loops of bowel are not primary, and only result from the arrest of
peristalsis. The primary condition is peritonism, _i.e._, distension of
the peritoneal cavity, this being indicated by a symmetrical fulness of
the right and left flanks.

The patients suffer from dull colic, and from this time always assume an
attitude indicating pain. They remain in one position, with the back
arched, the limbs gathered together, and the lower abdominal wall
shortened. The face expresses suffering, the respiration is short and
rapid and of the costal type, movement is painful and causes groaning,
and the animals do not shrink when the lumbar region is pressed upon.

Palpation of the abdomen causes pain, and if practised at certain points
may be followed by groaning. This method of examination, however, gives
no further information, because the abdominal wall is rigid, tense, and
as though tonically contracted.

Percussion is followed by tympanic resonance in the right and left upper
zones, due to accumulation of gases of fermentation, and to distension
of the peritoneal cavity itself. Towards the lower parts, however,
percussion produces a dull sound. The presence of liquid can here be
detected by the manner in which impulses are transmitted, particularly
at the period of crisis and when much exudation exists.

Abdominal auscultation shows that the digestive movements are arrested.
Peristaltic movement ceases, and the movements peculiar to the rumen and
to the progress of food through the intestine are absent. Fermentation
sounds, however, can be detected.

The heart beats are strong, rapid and violent, and yet the pulse remains
feeble, though the artery is tense.

At a later stage, when the disease becomes aggravated, pain is less
acute, depression is extreme, the animals no longer even drink, the
abdominal wall becomes relaxed, and diarrhœa is succeeded by
constipation. Palpation of the abdomen is less painful and does not
cause groaning, but the pulse becomes feebler, much more frequent,
imperceptible, and at last the animal dies from intoxication and
exhaustion, caused by the fever and pain.

When peritonitis is due to rupture of the intestine or escape of
alimentary material from the rumen into the peritoneal cavity, as may
occur after puncture of the rumen or gastrotomy, etc., fever is not
always very marked. The temperature may even fall below the normal
point. Some cases vary greatly from the type described as regards their
development, but the important features are always present, and the
difference is chiefly found in the course of the disease.

=Diagnosis.= The diagnosis is rather difficult, but when there is colic,
together with persistent peritonism, exaggerated sensitiveness to
palpation and arrest of the functions of the digestive apparatus, there
is little room for doubt.

=Prognosis.= The prognosis of acute peritonitis is very grave.

=Lesions.= The lesions vary with the primary cause (traumatism,
metritis, suppurative echinococcosis, foreign bodies escaping from the
digestive tract into the peritoneal cavity, etc.).

The parietal and visceral layers of the serous membrane are always
inflamed, vascular, roughened, dull, and in places covered by
vegetations. Between the loops of intestine and in the peritoneal
pockets there are discovered more or less numerous and more or less
thickened false membranes, presenting the characteristics of the false
membranes seen in acute pleurisy.

The liquid varies in quantity and in colour, being sometimes
lemon-yellow, sometimes purulent, sanguinolent, or even blackish, and of
putrid odour.

The lesions may appear more marked at a particular point, such as the
uterus, rumen, hypochondrium, etc., and the intestinal loops may become
partly fixed in position by false membranes. In time these false
membranes may solidify and undergo transformation into fibrous tissue.

=Treatment.= Treatment is generally useless in cases where peritonitis
results from rupture of the bladder or intestine or from eventration.
Complete and perfect cleansing of the infected abdominal cavity is
impossible in large animals.

In other cases the animals should be left completely at rest, and
purgatives should be avoided. Movement or the administration of
purgatives provokes peristalsis, and, as a consequence, almost
inevitably leads to generalisation of a lesion which might otherwise
have some chance of remaining localised, as in pelvi-peritonitis and
peritonitis due to foreign bodies issuing from the rumen or reticulum.
If the movements of the intestinal loops disperse the septic liquids
beyond the points originally injured, the whole cavity becomes
inoculated and generalised peritonitis is set up.

Emollient and diuretic drinks containing opium, and oatmeal or linseed
gruels, have the advantage of soothing the colic and preventing
stagnation in the bowel. These should be given from the first and solid
food entirely avoided.

The sides of the abdomen should be mildly stimulated, provided the
operation does not give rise to undue pain and cause the animals to
struggle. Vesicants are preferable to mustard, though mixtures of
mustard and linseed meal may be used, and, if found advantageous, can be
repeated.

Mercurial salts, though much used in earlier times, are now entirely
given up. Diuretics, such as bicarbonate of potash, nitrate of potash,
alcohol, and acetate of ammonia, should be used, according to
circumstances.

Aseptic washing out of the peritoneal cavity would be advantageous, but
in large animals cannot easily be effected.


                          CHRONIC PERITONITIS.

=Causation.= Chronic peritonitis may occur as a termination of the acute
form, but it may also develop gradually as a result of disease of the
kidney (pyelo-nephritis), of the uterus or ovaries (chronic metritis,
tumour of the ovary), of the liver (suppurative echinococcosis), or of
any other lesion in neighbouring parts which is capable of setting up
continued irritation.

It also accompanies tuberculosis of the peritoneum, cancer of the
peritoneum, chronic disease of the bladder, etc. Further, it appears,
but more rarely, in certain chronic diseases, such as chronic dysentery
and lymphadenitis.

=Lesions.= The lesions consist of local thickenings of the peritoneal
layers, and numerous papilliform vegetations scattered very irregularly
over the parietal peritoneum, mesentery, epiploon, etc.

If the disease has existed for a long time, fibrous bands or solid
adhesions may be discovered, connecting various parts of the digestive
apparatus with one another, or with the abdominal walls.

Sometimes the intestinal contents seem almost entirely adherent to the
abdominal walls.

The primary lesions of the liver, spleen, kidneys, or genital organs,
from which the disease originated, are also found.

The quantity of exuded liquid varies greatly; sometimes there is a great
quantity of a transparent or lemon-coloured liquid, resembling that of
ascites. In other cases the liquid is scanty, and may be confined
between layers of bowel, which are connected by an inflamed layer of
epiploon.

These old-standing lesions cause atrophy of the abdominal organs,
contraction of the intestine, and sometimes true obstruction.

In chronic tuberculous peritonitis the adhesions between the intestine
and the abdominal walls may be enormous. The peritoneum is generally
covered with great masses of tuberculous new growth, while the
mesenteric and sublumbar lymphatic glands are attacked.

=Symptoms.= The disease develops without marked fever or grave
interference with the chief functions, and the first approach of the
disease may, therefore, easily be overlooked. Chronic peritonitis,
moreover, may remain strictly localised.

When the disease assumes the ascitic form the dominant sign is readily
detected. Where new membranes form the principal lesions the symptoms
are much less definite, and the existence of disease is chiefly
indicated by digestive disturbance, such as diminished peristalsis, the
occurrence of colic, diarrhœa, etc.

It is well to remember, however, that these troubles often follow an
ascitic stage, which may gradually disappear owing to the fluid becoming
absorbed. Even in the fibrous form, where the intestines appear
completely glued together by adhesions, the volume of the abdomen is
increased and the belly is deformed, as in ascites.

In time patients suffering from primary lesions of an important internal
organ are affected in their digestion, lose flesh and become anæmic, and
finally cachectic.

=Diagnosis.= The diagnosis is by no means easy, particularly in the
fibrous forms, owing to the great difficulty of discovering the primary
lesion.

=Prognosis.= The prognosis is grave, though it must not be regarded as
necessarily fatal. In cases resulting from genital diseases, and in
localised chronic peritonitis resulting from persistent, but not
excessive, mechanical violence, complete and perfect recovery may occur.

On the other hand, in cases of chronic lesions of the liver, kidneys,
heart, etc., and in tuberculosis, carcinoma, etc., recovery cannot be
expected.

=Treatment.= Treatment should be directed towards combatting the chronic
inflammation. With this object resort may be had, when necessary, to
persistent stimulation of the sides of the abdomen, mild blisters and
mustard plasters, or friction with turpentine.

The food should be easy of digestion, and of first-rate quality. The
most useful drugs comprise mild, unirritating diuretics, general
stimulants, and tonics.

Animals affected with incurable lesions should not be treated.


                                ASCITES.

True ascites consists in dropsy of the peritoneum, unaccompanied by
inflammation of that membrane, or by the presence of infectious
microorganisms in the transuded liquid. Properly speaking, it is not a
morbid entity, but only a symptom common to several very complex
diseases.

=Causation.= The diseases which produce it may be set forth under five
principal heads:—

(1.) Cardiac affections in general, particularly chronic lesions of the
heart, interfering with venous circulation, and causing prolonged stasis
of blood in an organ or tissue.

(2.) Pericarditis due to foreign bodies, and the various forms of
pseudo-pericarditis, _i.e._, lesions in the neighbourhood of the heart,
causing compression of that organ and of its vessels.

(3.) Generally speaking, all lesions which interfere with the return
circulation, particularly lesions of the liver (distomatosis,
echinococcosis, and interstitial hepatitis). These produce compression
of the portal vein or other obstacle to circulation, and the
transudation is exclusively localised in the abdominal cavity. The
connective tissue does not become infiltrated.

(4.) Diseases of the kidneys (nephritis, pyelo-nephritis), which
secondarily produce cardiac disturbance.

(5.) Gestation, which causes compression of certain digestive viscera,
and of certain veins of the pelvic cavity.

Ascites was formerly regarded as always forming a complication either of
anæmia or of hydræmia. We now know that the primary cause of these three
collections of symptoms (ascites, anæmia, and hydræmia) is the
development of certain chronic wasting diseases or chronic lesions of
the heart, liver, and kidney, which act and react upon each other.

=Symptoms.= True ascites is unaccompanied by fever. The condition
develops slowly, insidiously, and therefore escapes notice at first.
Only when the exuded liquid is present in considerable quantities is the
condition apparent. The symptoms are similar to those of ascites
following chronic peritonitis.

The transuded liquid progressively accumulates in the peritoneal cavity,
the lower portion of which it distends. When the animal is viewed from
behind the enlargement appears symmetrical, despite the position of the
rumen. The intestinal contents float on the liquid and are thrust
upwards towards the lumbar region. On palpation, the abdominal cavity
seems unusually full, the tension differing in proportion to the
quantity of liquid. The accumulation of liquid may become considerable
and interfere with respiration, circulation, and movement. Very marked
anæmia always exists, the mucous membranes are extremely pale, the
respiration is rapid, the pulse feeble, all these symptoms being
consequent on the primary disease of the heart or liver. Percussion of
the lower part of the belly produces a dull sound. On the left side this
dulness often extends from the linea alba as high as a horizontal line,
uniting the external angle of the ilium and the hypochondriac circle. On
the right it is bounded by a horizontal line. Percussion or, better
still, palpation provokes on one side of the abdomen a wave or impulse
of the liquid, perceptible to the touch or even to the view at the
opposite side.

=Diagnosis.= In general diagnosis is easy, thanks to the slowness with
which the disease develops.

=Prognosis.= The prognosis varies in each case, more especially
according to the more or less marked debility of the animal. Ascites due
to gestation is usually of a very simple character, but if it is the
result of pericarditis produced by a foreign body, or of nephritis, the
outlook is very gloomy; lesions of the kidney in particular showing
little tendency to recovery. Finally, the prognosis varies when the
ascites follows disease of the liver, for certain exceptional cases have
been noted in which an attack of hepatitis has led to the disappearance
of the transudate.

=Lesions.= The lesions peculiar to this disease are very trifling.
Transudation takes place without inflammation of the peritoneum,
although the veins of the abdominal cavity are abnormally dilated. The
abdominal wall is thin and distended, and the tissues are colourless as
though soaked in water. The cavity is distended with a clear
lemon-coloured albuminous liquid free from blood corpuscles.

=Treatment.= The treatment must vary according to circumstances, _i.e._,
having regard to the primary cause. Ascites due to gestation, which is
always slight, calls only for simple hygienic treatment; but when the
disease is attributable to lesions of the heart, pericarditis, or
chronic affections of the kidney or liver, it is generally incurable in
common with the original lesions themselves.

If, finally, no clearly defined cause can be detected, or if the ascites
is due to chronic peritonitis, treatment should be attempted. The first
step may consist in evacuation of the liquid for the purpose of reducing
the excessive pressure on the diaphragm and facilitating respiration.
For this purpose an aseptic puncture is made with a fine trocar on the
right side of the abdomen in the flank region, about equidistant from
the umbilicus and the loose flap of skin in front of the stifle. The
absorption of liquid may afterwards be assisted by administering
diuretics, such as digitalis, bicarbonate of potash or nitrate of
potash, and by giving lukewarm drinks, tonics, etc. In Germany
injections of pilocarpine have been suggested, but it is doubtful
whether they have proved satisfactory.


                       PERITONEAL CYSTICERCOSIS.

The above name has been given to a parasitic disease caused by the
infestation of young animals, such as calves, lambs and young pigs, with
embryos of the _Tænia marginata_ of the dog.

=Symptoms.= Peritoneal cysticercosis is often of so mild a character,
and the number of embryos which penetrate the body so small, that in the
majority of cases there are no visible symptoms. It is not until the
meat comes to be dressed by the butcher that little cysts (_Cysticercus
tenuicollis_) are discovered in the abdominal cavity.

Unfortunately, in exceptional cases it may also happen that the number
of embryos in the abdominal cavity is so great as to produce lesions of
acute hepatitis, acute peritonitis, and sometimes pleurisy. These grave
forms are more common in young pigs and lambs.

The animals appear dull, feeble, exhausted and without appetite, but
exhibit marked thirst, lose flesh and become anæmic in a few days. Soon
afterwards they show symptoms of acute peritonitis, with exudation of
fluid, and death may follow in a week or two.

In cases where infestation is less marked, the animals may exhibit only
progressive anæmia, without well-developed symptoms of peritonitis,
until death occurs.

=Lesions.= On post-mortem examination a sero-sanguinolent exudation is
seen, together with more or less numerous false membranes, and a varying
number of young cysticerci floating freely in the liquid or enclosed in
the folds of the mesentery. The cystic vesicles are spherical, ovoid, or
elongated, and translucid or opalescent. They are some millimètres in
diameter, and in some cases are very numerous, ranging from a few
hundreds up to several thousands, but in others comparatively few.

The liver shows signs of intense hepatitis, caused by embryos burrowing
into its tissue.

=Causation.= The causes are limited to a single fact, viz., ingestion of
the eggs of _Tænia marginata_, which are spread over the fields in the
excrement of dogs suffering from that parasite.

=Diagnosis.= The diagnosis can only be arrived at by a post-mortem
examination, when cysticerci in various stages of development are
discovered.

=Prognosis.= The prognosis is difficult to indicate, because everything
depends on the intensity of the infestation.

=Treatment.= No curative treatment is possible, direct action on the
developing parasites being impracticable. Nevertheless, some patients
survive, and after having shown grave general disturbance may gradually
improve.

The only efficacious treatment is of a prophylactic nature, as in
cœnurosis and echinococcosis. Dogs suffering from tæniæ should
periodically be treated and freed from their parasites.




                              CHAPTER II.
                               HERNIÆ.[6]


Footnote 6:

  For a fuller description of herniæ and their treatment, see Möller and
  Dollar’s “Regional Surgery,” pp. 263–309.


                           CONGENITAL HERNIÆ.


                     PERINEAL HERNIA OF YOUNG PIGS.

This variety is very common in young pigs, on account of their
anatomical peculiarities and of the persistence and enlargement of the
inguinal canal. Loops of intestine, impelled by their own weight,
accumulate at the lowest point and readily pass into the canal.

It is usually when the little pig begins to eat, _i.e._, a fortnight or
three weeks after birth, that the symptoms become plainly apparent.

The hernia is indicated by a swelling which commences in front of the
pubis and extends backwards behind the hind limbs. When the herniated
loop of intestine is examined by palpation, the presence of liquid in it
can be detected, particularly after a meal, while a characteristic
gurgling sound is heard.

=Diagnosis.= To confirm the diagnosis, the animal is placed on its back,
whereupon reduction as a rule is easily effected. As soon as the animal
rises again the hernia returns.

=The prognosis= is not grave.

=The treatment= is exclusively surgical, and the hernia can be reduced
and castration performed at one and the same time. The animal being
placed on its back and firmly held, an incision of about 2 to 3 inches
in length is made in the inguinal region, dividing the skin and
subcutaneous connective tissue only. The vaginal sheath is then
completely isolated, the hernia reduced, and a ligature applied to the
sheath and the spermatic cord close to the abdominal wall. The testicle
is then removed.

If adhesions have been set up, which is quite exceptional, the vaginal
sheath is incised and the loop of adherent intestine liberated, when it
can readily be returned. The vaginal sheath and spermatic cord are then
twisted as high as the level of the inguinal ring and tied with catgut.
To prevent this ligature becoming displaced, it should be fixed by
passing a sterilised thread through it and through the mass of tissue;
the hernial sac should be divided immediately below. In order to ensure
greater security, it may even be desirable to pass a suture through the
margins of the inguinal ring.


                           UMBILICAL HERNIA.

Umbilical hernia is less common in young animals of the bovine, ovine
and porcine species than in the foal, and when existing almost always
disappears at the period of weaning. The rumen then assumes its full
development, the loops of intestine are displaced and thrust towards the
sublumbar region, and the hernia disappears. The same is true of the
young pig, the development of the stomach producing the same favourable
result.

In the rare cases where this hernia is not reduced spontaneously, it may
be necessary to utilise the methods so frequently employed in the foal,
and, despite the number of these, there are only two which can
thoroughly be relied on to give good results.

In the first, irritants are employed.

Subcutaneous injections of concentrated solution of common salt,
_filtered and sterilised_, or 10 per cent. solution of chloride of zinc
produce enormous engorgement of the connective tissue, which thrusts
back the herniated loop of intestine and later causes the development of
very resistant fibrous tissue, which prevents the hernia returning.

To ensure this result, however, it is indispensable that perfect asepsis
should be observed in the injections, for if germs are introduced severe
suppuration occurs at the point of injection. The injections are made at
four opposite spots in the subcutaneous tissue surrounding the hernia, 1
to 2 drachms of saline solution being injected at each spot; of the
chloride of zinc solution half a cubic centimètre is used. This method
is only of value in small herniæ, which may sometimes be cured by the
application of sinapisms alone.

The second method is applicable to larger herniæ, and aims at destroying
the hernial sac.

The application of clams is simplest, and can be recommended. The
patient is placed on its back, reduction is effected, the hernial sac is
drawn upwards vertically, and the clams placed as near the abdominal
wall as possible, after care has been taken that no portion of the
intestine is included in the sac. The clams are kept in place by a
suture passed through the neighbouring tissues.

In other cases where a radical cure is necessary, because of adhesions
within the hernial sac, the patients are similarly placed on their
backs, the hernial sac is opened aseptically, the adherent parts
liberated, the herniated portions of intestine reduced, and the hernial
ring sutured with sterilised strong silk, the skin being afterwards
brought together with silk sutures after removal of the sac itself. A
surgical dressing can then be applied to the umbilicus. The patients
should be carefully dieted.

When the hernial ring is large and its lips widely dilated, the silk
sutures, even when supported by secondary sutures, sometimes cut through
the tissues and do not achieve the desired result.

[Illustration: $1]

Degive’s method (see “Möller and Dollar’s Regional Surgery,” p. 304) can
then be employed. The hernial sac is opened under antiseptic
precautions, in order to break down any existing adhesions, and the skin
and edges of the hernial ring are transfixed with packing needles about
8 inches long. Above these is adjusted a clam, which is closed, by means
of a screw and firmly secured. The packing needles are then replaced
with horse-shoe nails, the points of which are bent round. In about a
week the necrotic tissue falls away, and recovery occurs even in severe
cases in which previous treatment had failed.


                            ACQUIRED HERNIÆ.

Acquired or accidental herniæ are not serious, and only deserve to be
studied in so far as they affect organs contained within the abdominal
cavity. They may result from violence, or may occur without the
intervention of any external cause.

Traumatic herniæ may occur at any point in the abdominal wall. Under the
influence of a violent blow from a waggon pole, a horn thrust, a kick, a
fall, etc., the muscular tunic of the abdominal wall is injured and
becomes fissured in the direction of its fibres. The peritoneum is
rarely affected. Being pushed outwards by the digestive viscera,
however, the peritoneum projects into the muscular layer, distends it,
separates the layers of subcutaneous tissue, and finally forms a
distinct hernia.

The consequent disturbances are more or less marked and the lesions more
or less variable, according to the part affected. In the lower region
fissure of the abdominal wall affects the rectus abdominis, obliquus
abdominis and transversus abdominis, and on the right side gives rise to
hernia of the abomasum or small intestine, on the left of the rumen. In
the lateral regions muscular fissures can be produced only in the
transversus and obliquus abdominis muscles. Hernia of the rumen is rare
on the left side. On the right side hernia of the intestine is more
readily produced.

In all cases where hernia is suspected, the hernial orifice should be
examined. Its situation will at once show which organ is affected.

Spontaneous herniæ are very rare in the domesticated animals. They occur
only in aged animals, and various reasons have been suggested to explain
their appearance. Certain herniæ of this character are only found in old
female animals which have borne a considerable number of young. Repeated
gestation produces elongation and relaxation of the muscular fibres from
the weight of the fœtus and its envelopes. In time, the abdominal walls
become thinner and thinner under the weight of the viscera, and thus
facilitate the slow formation of a hernia. Certain practitioners
consider that some of these spontaneous herniæ are due solely to the
pressure produced by the distended viscera, as for example in
greedy-feeding animals. In such cases the weight of the viscera would
cause, as in the previous case, a certain degree of anæmia and
emaciation of the abdominal muscles.

These spontaneous ventral herniæ are due in reality to changes in the
nutrition of the abdominal wall, the exact cause of which it is
difficult to ascertain. The elastic tunic becomes atrophied, and ceases
to act as an automatic girth; the muscular wall gradually becomes
sclerosed from the white line towards the sides, and having lost its
elasticity becomes distended and thinned.

These changes are not exclusively caused by old age, for they may be
found even in young animals.

Nothing can be done in cases of spontaneous herniæ. The qualities
originally pertaining to the abdominal wall cannot be restored, and
=treatment= is confined to applying suspensory bandages, and, where
possible, preparing the animals for slaughter.


                          HERNIA OF THE RUMEN.

=Causation.= Hernia of the rumen is, as a rule, of traumatic origin, and
always occurs in the left flank, either in the lower or middle regions.
Cases of spontaneous hernia of the rumen have been observed in very old
and anæmic animals, as well as in females which have borne many young
and which have suffered from spontaneous progressive hernia of the
uterus.

=Symptoms.= The symptoms are the same in all herniæ. Immediately after
the injury the abdominal organs show a tendency to escape in the
direction of least resistance. A fold of the rumen passes through the
muscular fissure, and a swelling soon becomes visible externally, which
alters the contour of the abdomen. Most frequently at this time traces
of the injury can be detected on the surface of the skin, either the
linear trace due to a horn thrust, the ill-defined lesion due to a kick,
or what not. There follows rapid swelling, which results from the
inflammatory reaction due to rupture of small vessels within the muscle.
A certain amount of sanguineous exudation and of œdematous swelling
occurs, and may at first suggest the existence of an abscess of the
abdominal wall. At the same time there is more or less fever, which may
continue for a few days, but the swelling seldom lasts very long; in two
or three days even, it becomes reabsorbed, commencing at the upper part
and diminishing progressively downwards.

Henceforth the hernia alone remains.

It is soft, compressible, and sometimes susceptible of reduction. On
palpation, the operator feels a rupture extending through the tunic and
the abdominal wall, sometimes even through the muscular tissue of the
rumen, in cases where the skin is neither perforated nor torn through.
The mucous membrane of the rumen is rarely ruptured.

Whether or not the peritoneum is injured, the rumen presses between the
lips of the wound, thrusts back the skin, and separates the connective
tissue, thus setting up local irritation and œdematous swelling. The
rumen may contract more or less close adhesions with the abdominal wall,
and even with the subcutaneous tissues.

Afterwards, when the exudate has been reabsorbed, palpation reveals a
different condition of things. The mass is uniformly fluctuating or
semi-fluctuating, and is surrounded at the base by an indurated ring of
very varying dimensions. The final indication—which, however, is not
invariably seen—deserves attention, viz., the change in volume of the
hernia at different moments, particularly during meals. This change in
size only occurs if the hernial orifice is large.

In cases of spontaneous hernia of the rumen, the condition is not fully
established at first. It is always progressive, and the lesion is
situated in the lower abdominal region. It increases in size from day to
day, from week to week, whilst the animals lose appetite and flesh.
Spontaneous herniæ are never accompanied either by exudation,
engorgement, fever, or traces of mechanical injury.

When only slightly developed, herniæ do not threaten life, a fact which
often prevents the owners troubling about them. Progressive herniæ may
become of considerable size, and two cases are recorded in one of which
the opening of the hernial sac was 13½ inches in length and 18 inches in
width, and in the other 28 inches in length and 24 inches in width. The
latter is the largest ever recorded.

=Complications.= Complications are not always grave. If the hernia is
little marked the function of the rumen is not greatly affected and its
rhythmic contraction continues. When the original injury has caused
rupture of the muscular tissue of the rumen, and the mucous membrane has
passed into the opening, it may become strangulated and gangrenous.

Finally, if the mucous membrane has been torn at the same time as the
muscular tissue (which is very uncommon), alimentary material may escape
into the subcutaneous connective tissue, setting up either cellulitis
and death by infection, or suppuration; abscess formation and rupture
towards the exterior, followed by a persistent sinus; or again septic
peritonitis, and death.

The same results may occur when the hernia is in a very low portion of
the abdomen; food accumulates in it, becomes stagnant there, sets up
local irritation and inflammation, and sometimes abscess formation with
external discharge, followed by fistula of the rumen.

Gastric fistula without secondary complications is compatible with life,
and even with fattening for slaughter, provided the peritoneum covering
the rumen becomes attached to the opposing surface of peritoneum around
the perforation. The fistula is then surrounded by a circular mass of
fibrous tissue, forming a kind of sleeve.

=Lesions.= The lesions are the same in all herniæ. They consist
primarily in rupture of the abdominal wall, and, later, of
sero-sanguinolent infiltration of the margins of the wound, similar to
that accompanying the formation of an abscess. Hernial swellings are of
very varying size. Apart from cases similar to those above described,
the swelling may be simply an inch or two in diameter, or it may attain
the dimensions of a hen’s egg or even of a man’s fist.

When the abdominal tunic only has been ruptured, as is most frequently
the case, the peritoneum is thrust outwards and forms a cavity, the
hernial sac. This sac is absent when the peritoneum is ruptured. Little
by little the surrounding connective tissue forms a pseudo-serous
hernial sac. But, nevertheless, in some cases there may be found,
immediately under the skin, the mucous membrane of the rumen in a state
of congestion and ready to become gangrenous.

=Diagnosis.= Easy in all cases.

=Prognosis.= Very variable. In the case of small herniæ situated in the
lateral regions of the abdomen the prognosis is not very grave. If,
however, the rupture is wide, and situated in the lower portion of the
abdominal walls in a dependant position, the hernial swelling steadily
grows in size in consequence of the weight of the food which is
constantly thrust in this direction by the contraction of the rest of
the rumen, and recovery is impossible. The only resource is to fatten
the animals as quickly as possible for slaughter.


                        HERNIA OF THE ABOMASUM.

=Causation.= This condition is due to causes similar to those above
mentioned, including mechanical violence. It is rare in adults, but much
commoner in young animals, especially in sucking calves, where the
abomasum is the most highly developed digestive compartment.

Hernia of the abomasum is produced essentially and almost exclusively by
horn thrusts inflicted when calves attempt to suck cows other than their
own mothers.

=Symptoms.= Hernia of the abomasum always occupies a certain position in
the lower part of the right flank, or, rather, in the space comprised
between the white line and the lower part of the circle of the
hypochondrium.

The immediate symptoms are similar to those of hernia of the rumen. They
include: progressive swelling, formation of a peripheral œdematous ring,
interstitial sero-sanguineous exudation, which becomes absorbed after a
few days; finally, the development of a hernia, formed as a rule by the
larger curvature of the viscus, which is in direct contact with the
abdominal wall.

=The lesions= are those common to all hernia, and usually include a
partially healed wound.

=Diagnosis.= The diagnosis is easy, particularly in calves, and the
possible existence of the condition should always be borne in mind when
dealing with injuries of the right pre-umbilical zone. An abscess of the
lower abdominal wall may occur at or near the umbilicus as a result of
omphalitis or umbilical phlebitis, but it is readily distinguished from
a hernia.

=The prognosis= is graver than in the case of hernia of the rumen, for
the displacement of the abomasum interferes with its regular function.
The prognosis varies, however, in accordance with the size of the
hernia. If the rupture is small, there is some chance that the abomasum,
on account of its longitudinal position, many penetrate but slightly
into the fissure.

If, on the other hand, the rupture is large, the prognosis becomes very
serious. It is sometimes best to slaughter the animal, if in good
condition; otherwise an operation is necessary.


                        HERNIA OF THE INTESTINE.

=Causation.= This is due to the same cause as hernia of the rumen—a blow
which, while injuring the skin only to a trifling extent, damages the
abdominal walls, and even the intestine itself.

=Symptoms.= The hernia is situated in the lower or lateral zone of the
right flank.

The symptoms present some peculiarities. The loop of intestine which has
passed through the aperture in the abdominal walls becomes distended by
the accumulation in it of semi-liquid alimentary material, and, acting
by its own weight, produces a hernial sac, which steadily grows in size.
The skin being very mobile, and the subcutaneous connective tissue very
loose, they readily yield and become separated. The inflammatory
symptoms disappear, and are followed by a swelling under the skin, which
is compressible all over, and can readily be reduced, whereupon it gives
forth a gurgling noise, or a sound as of borborygmus. Reduction is
easier when the animal is lying on its left side, or on its back.

=Complications.= Strangulation of the small intestine is the only
serious complication in this form of hernia, but it is very dangerous.
It occurs frequently when the rupture is somewhat highly-placed on the
lateral portion of the abdominal wall, because the loops of intestine
have a tendency to descend, thrusting away the skin owing to the weight
of material which they contain.

The partially digested food is apt to accumulate in the herniated loop,
and hernial engorgement, the first phase of strangulated hernia, rapidly
occurs.

Fermentation is set up in the half-digested food, and putrid gases are
generated. Thus the hernial sac becomes distended, the vessels are
compressed, circulation is arrested, and gangrene supervenes.

At this time gurgling sounds and a certain degree of tympanitic
resonance may be noted. These are followed by all the symptoms of
intestinal strangulation—namely, intense colic, which suddenly
disappears when the intestine becomes mortified, absolute loss of
appetite, stoppage of rumination, constipation, suppression of
defæcation, tympanites, and peritonitis.

=The diagnosis= is comparatively easy at an early stage, owing to the
peculiar character of the soft swelling, which is easily compressible.
At first there may be difficulty in distinguishing it from a collection
of serous fluid, but the facility with which the swelling can be reduced
removes any doubt.

=The prognosis= is always serious, on account of possible complications,
due to strangulation of the herniated loop. When the hernia is chronic,
reduction is much more difficult, there being, as a rule, adhesions
between the intestine and the hernial sac.


                          TREATMENT OF HERNIÆ.

Numerous attempts have been made to treat abdominal hernia in bovine
animals.

Irritant and vesicant applications to the skin have been recommended,
with the object of producing a large swelling, and thus thrusting back
the herniated mass into its proper position.

One of the most popular of these applications is nitric acid of a
strength of 36° Baumé, applied to the skin twice at an interval of ten
days. Skilfully used, it gives good results in umbilical herniæ, but its
effects in ventral herniæ are less certain. It causes slow mortification
of the skin, abundant subcutaneous swelling, and produces an eschar,
which separates in about a fortnight.

An ointment of yellow chromate of potash (1 to 8) has been recommended,
and can be applied two or three times at intervals of eight or ten days.

Bandaging and various forms of local dressing have also been employed
from time to time. Serres employed simple bandages similar to those used
in cases of inguinal or crural hernia in human beings. These bandages
have a pad, which is applied over the hernial opening, but their action
is strictly palliative. They simply allow of the animal being kept a
certain length of time for fattening.

When the hernia has been reduced recourse may be had to bandages
saturated in melted pitch, care being taken to extend the dressing a
considerable distance beyond the limits of the hernial opening.
Successive layers of bandage are superposed across and across, and, to
make the dressing more solid, the pads may be reinforced with a sheet of
solid cardboard. This method only succeeds when the swelling is slight
and is situated elsewhere than in the lowest portions of the abdomen.

Some practitioners prefer a cloth bandage after reduction. The bandage
is ten to fifteen yards in length, and should be considerably wider than
the greatest measurement of the hernial opening. Such bandages can
easily be applied to calves, whose bodies are of regular shape, but in
adults, in which the body is of ovoid formation, they prove faulty, and
tend to slide backwards or forwards.

All these measures are merely more or less palliative and of temporary
effect.

The only rational and radical treatment is surgical. This is clearly
indicated when the hernia is recent and of small size. At a later stage,
when fibrous adhesions have formed between the various organs, and
reduction has become difficult, caution must be observed. Surgical
treatment is always a serious matter, and should only be attempted in
the case of valuable breeding animals, or those which cannot be sold for
slaughter.

Young animals are kept without food for twenty-four hours and are cast
on the side opposite the hernia; they can be placed on the right or left
side, or on the back, as seems most convenient. The site of operation is
disinfected, and the operation carried out with aseptic precautions. The
skin covering the swelling is incised and, the margins of the hernial
orifice having been examined, the sac is isolated. Next, an incision is
carefully made, any adhesions which may exist are broken down and the
herniated parts are reduced. It only remains to suture the wound with
silk or catgut, bringing the lips of the fissure together. Finally the
skin wound is firmly united, and a large suspensory bandage tightly
applied.

If the hernia is of long standing, and is irreducible on account of
numerous adhesions, operation may still be attempted. In that case the
incision must be an inch or two longer, all adhesions should be
destroyed, and the margins of the orifice need to be freshened so as to
insure their uniting.

During the days following operation, the animals should have light food,
principally gruel, mashes and cooked roots. But it must be borne in mind
that this operation is serious, and may possibly be followed by
eventration.


                         DIAPHRAGMATIC HERNIA.

The term diaphragmatic or mediastinal hernia denotes a condition in
which certain of the abdominal viscera penetrate into the thoracic
cavity. This displacement may be congenital, acquired, or accidental.

The accidental herniæ are of traumatic origin, and are often caused by
fractured ribs, which injure the diaphragm. The hernia is then purely
diaphragmatic.

Congenital or acquired herniæ are more frequently mediastinal; they
occur exactly in the median plane as a consequence of fissure of the
diaphragm above the ensiform cartilage, and cause a separation between
the two layers of serous membrane enclosing the posterior mediastinum.

The region immediately behind the diaphragm in the ox being occupied by
the large viscera—namely, the anterior conical portions of the rumen,
the reticulum, the omasum, and the liver—diaphragmatic or mediastinal
hernia is far from being common, though occasionally it may be
discovered or at least suspected.

=Causation.= The causes of diaphragmatic and mediastinal hernia are
closely connected with injuries in the region of the hypochondrium; with
arrest in the development of the diaphragm; or with accidental vertical
fissuring consequent on gestation or acute tympanites.

The fissure seems most commonly to occur between the point where the
œsophagus passes through the diaphragm and the ensiform cartilage of the
sternum, in which case mediastinal herniæ most commonly supervene. As,
on the other hand, the rumen, owing to its size, form and position,
cannot readily be displaced, the reticulum and omasum are the viscera
which most commonly pass into the thorax.

=Symptoms.= In true accidental diaphragmatic hernia visceral
displacement only occurs on the right side, and symptoms of this are
immediately apparent. The passage of the liver, reticulum, or omasum
into the right pleural sac compresses the lung, causes attacks of
dyspnœa and acceleration of the heart’s action.

[Illustration: $1]

Percussion may not reveal any important change, but on auscultation
digestive sounds can plainly be heard within the chest.

The symptoms are far from being well defined. They may be more or less
intense, and colic may or may not be present. Mediastinal hernia (Fig.
223) appears to develop slowly, and it is only by degrees that the
viscera become displaced.

There is then no sudden change, no clearly marked disturbance, but
simply a certain amount of digestive irregularity, together with loss of
appetite, cessation of rumination, slight indigestion, and moderate
tympanites. The disturbance is really due to obstruction in the
alimentary canal and displacement of the reticulum and omasum, so that
rumination and deglutition are affected.

Very often this condition may last for weeks, in either a stationary or
more or less aggravated form, so that there is an appearance of chronic
gastro-enteritis, motor dyspepsia, or chronic indigestion.

Though a diagnosis in this sense would be correct, the atony of the
rumen is not primary, but of mechanical origin.

One indication is constantly present, which might suggest indigestion
due to overloading of the rumen, and which is also seen in ulcerative
gastritis, viz., progressive stasis of food in the cavity of the rumen.
When the patients remain for some time under observation, this stasis
becomes every day more marked, and, being recognised, the diagnosis
becomes easier. Animals suffering from mediastinal hernia lose
condition, waste away, and in the end may die in a state of cachexia.

[Illustration: $1]

=Lesions.= The lesions vary greatly. In accidental diaphragmatic hernia
they are confined to rupture of the diaphragm, sometimes of the liver,
and to changes in the reticulum or omasum.

In intra-mediastinal hernia the layers of the mediastinum form a true
hernial sac, and if the lesion is of old standing the displaced viscera
may become attached to it, compressed, and partially strangulated.

=Diagnosis.= The diagnosis is very difficult, at all events in
mediastinal hernia, and can only be arrived at by a process of
exclusion. The most significant symptom is progressive stasis of food
within the rumen, suggestive of some obstacle in the alimentary canal.

=Prognosis.= The prognosis is extremely grave, because it is impossible
to reduce the hernia.

=Treatment.= No treatment is possible. The essential point is to confirm
the diagnosis as soon as possible and to slaughter the animal while it
is yet in good condition.


                              EVENTRATION.

Eventration belongs to the same group of lesions as herniæ, of which it
is merely a more serious form. It differs from them only in the fact
that the entire abdominal wall is injured. The skin, muscle, and
peritoneum are torn, and the digestive organs pass into direct
communication with the external air.

The name eventration has also been given to enormous subcutaneous
abdominal herniæ, in which the sero-muscular wall is injured over a
large area and the viscera become displaced and separate the
subcutaneous tissue layers while at the same time they alter the whole
shape of the abdomen.

=Causation.= The cause is always the same—some grave mechanical injury
to the abdominal wall, producing an extensive perforation. The injury
may be due to a horn thrust or to the animal falling on some sharp-edged
body.

=The symptoms= are very marked. Through the wound, the rumen, the
abomasum, or the intestine protrudes more or less. Generally it is the
small intestine which becomes displaced, because it is the most mobile
of the abdominal viscera. These organs soon become dried by contact with
the air, and may become infected, soiled, congested, thickened, torn, or
gangrenous. The successive development of these changes causes serious
and violent colic, accompanied by expulsive efforts; the animals throw
themselves on the ground, and may tear the mesentery, the intestines,
etc. At an advanced stage the animal may stand motionless, looking at
its viscera. Death may also be caused in a very short time by the
intense pain.

=Diagnosis= and =Prognosis=. The diagnosis is evident. The prognosis is
always very grave, although, of course, it depends on the condition of
the displaced viscera.

=Treatment.= It is often useless to attempt anything, and if the animal
is in suitable condition it is best, as a rule, to slaughter it.

If the accident is quite recent, and the viscera only slightly injured,
surgical treatment may be attempted. With this object, the displaced
organs are carefully and thoroughly washed with lukewarm boiled water,
or with some unirritating disinfectant, to guard against peritonitis,
and are then reduced.

The abdominal wound must afterwards be carefully sutured. This is
performed in two stages. The musculo-serous layer is first brought
together with catgut, or better still with silk, and the skin joined by
means of deep and closely placed stitches. To prevent these sutures
being torn out, and to support them, the abdomen is swathed in a broad
cloth bandage, tightly applied.


                  FISTULÆ OF THE DIGESTIVE APPARATUS.

Fistulæ of the digestive apparatus are of accidental origin and of
relatively small practical interest. In most cases they necessitate
surgical and other treatment of too delicate a kind and too prolonged a
character to justify the necessary expense. Their nature and origin
sufficiently suggest the course to be adopted.

[Illustration: $1]

These fistulæ are divisible into two varieties, gastric fistulæ and
intestinal fistulæ. Gastric fistulæ comprise fistulæ of the rumen,
reticulum, and abomasum. They may be of external origin, but in the
majority of cases they are produced by foreign objects accidentally
swallowed and eliminated through the medium of an abscess of the
abdominal walls. Their position and direction indicate their point of
origin. (Fistulæ of the rumen appear on the left side of the reticulum,
near the ensiform cartilage and middle line; those of the abomasum on
the right side, near the middle line.) In doubtful cases, chemical
analysis of the liquid which escapes will afford valuable information.
Acidity alone is a sufficient indication in fistula of the abomasum.

Fistulæ of the rumen and reticulum are difficult to close on account of
their low position in the abdominal wall, but, if great care is
exercised, they may be successfully treated. Those of the abomasum, on
the contrary, only tend to increase in size, and any surgical
interference still further favours the destructive action of the gastric
juice. As a rule, therefore, they cannot be treated.

Fistulæ of the second variety comprise all intestinal fistulæ. They may
be either accidental or artificial, and they are less grave than gastric
fistulæ, because they are rarely situated in the lower portions of the
abdomen. With time they may become closed either spontaneously or by
means of simple treatment tending to regulate the passage of food
through the bowel.




                              SECTION VII.
                        GENITO-URINARY REGIONS.


                   DISEASES OF THE URINARY APPARATUS.

=Symptomatology.= The urinary apparatus comprises the organs of
secretion (the kidneys) and those of excretion (the ureters, the
bladder, the urethra).

A thorough examination of the urinary apparatus should include, firstly,
that of the external organs (the sheath, glans penis and urethra) in the
male, and, in the female, the vulva, meatus and urethra; secondly, that
of the internal organs (the bladder, ureters and kidneys) in both sexes.

To carry out the external examination, the head must first be fixed and
the hind limbs hobbled. If necessary, the animal can be attached to the
side of a wall.

External examination comprises inspection and palpation, which is only
possible in males. Inspection will reveal at once the existence of
malformation, deformity, traumatic lesions, or tumours of the organs.

By palpation the sheath and glans penis can be examined, and cellulitis,
abscess formation, calculi in the urethra, obstruction of the extremity
of the canal by very fine gravel, as in the case of sheep, etc., can be
detected.

The inner margin of the right kidney may also be examined by external
palpation, though only in very thin animals. The examination is made
from the flank region, behind the last rib, in an upward direction and
towards the right (Fig. 227). The kidney, attached under the lumbar
region, sometimes extends back beyond the last rib, under the transverse
processes of the lumbar vertebræ. On the left the presence of the rumen
prevents any examination.

In sheep this examination requires special care.

Examination of the internal urinary organs must be made through the
rectum. It should be undertaken slowly and gently. In the male the hand
detects the condition of the organs contained within the pelvic cavity,
the fulness or emptiness of the bladder, or the existence of calculi
within it. More deeply seated can be felt the entire length of the right
ureter; its state of dilatation can be felt, and the existence of
diverticula of inflammation, if any, can be ascertained. The left ureter
cannot readily be examined, on account of the position of the rectum,
except as regards the posterior part, close to the bladder and the
rumen.

[Illustration: $1]

In the abdominal cavity the rectum, or rather the floating colon, turns
to the right, in such a way that, in spite of the shortness of the
meso-rectum and meso-colon, the hand can be passed as far as the right
kidney. It is, then, easy to discover whether this organ is sensitive to
pressure, hypertrophied, atrophied, cystic, etc. The paunch interferes
with examination on the left side.

[Illustration: $1]

In females the ureters and kidneys can be examined in the same way, but
the bladder and the canal of the urethra must be reached through the
vagina. About 2 or 2¼ inches from the vulva on the floor of the vagina
is the entrance to the urethra, covered with a special valve. The meatus
becomes visible by separating the lips of the vulva and the vaginal
walls. For this purpose a speculum _ad hoc_ can advantageously be used.
It is clear that if it is thought desirable to examine the bladder
through the rectum, which is not absolutely impossible, the vagina will
be interposed between the arm and the urinary organs, and the sensations
experienced will, therefore, be much less clearly defined (Fig. 226).

In passing a catheter for the purpose of emptying the bladder the end of
the sound should be introduced under the valve of the meatus. By
slightly lowering the back end of the sound, the front end is lifted
above the cul-de-sac, and the operator at the same time pushes gently
forwards. It is then only necessary to lift the hand, and the sound
passes readily into the urethra and the bladder.

Examination of the urine and even chemical analysis are of great
importance in diagnosing diseases of the urinary tract.

From the clinical point of view very complete analyses are not
necessary, but the tests for albumen, sugar, bile pigments and indican
are absolutely indispensable; and the same is true of microscopic
examination for ascertaining the presence or absence of epithelial
cylinders, blood corpuscles, pus corpuscles, etc. It is important also
to note the colour and odour and the quantity passed.

These examinations are by no means difficult. Albumen is detected by
adding a few drops of acetic acid to the urine, and heating, or by
adding nitric acid and Esbach’s liquid. Esbach’s albumenimeter is
sufficiently exact to discover the approximate amount of albumen
present. Sugar is detected by the use of Fehling’s solution, bile
pigments by nitric acid, and indican by adding a few drops of 10 per
cent. chloride of calcium solution and hydrochloric acid. Should indican
be present a more or less deeply tinted indigo blue circle appears,
resulting from its oxidation.

Hippuric acid is precipitated by pure hydrochloric acid.




                               CHAPTER I.
                 POLYPI OF THE GLANS PENIS AND SHEATH.


In young animals the extremity of the glans penis and the margins of the
sheath are not infrequently studded with polypi, soft swellings of
papillomatous or verrucous appearance, sometimes of considerable size,
which interfere with micturition, and deform the glans. The existence of
these growths is shown by very well marked signs—viz., difficulty in
micturition, deformity of the sheath, deviation of the jet of urine,
obstruction in the passage of the penis, and more or less marked
deformity of the penis itself.

These polypi are of the same nature as those so common in dogs, viz.,
papillomata.

=The diagnosis= is very easy. On digital examination the growths are
almost always found at the base of the sheath.

At an early stage the =prognosis= is benign, provided intervention is
promptly undertaken. If the disease is of old standing, or is not
treated, the animals may become somewhat thin. They suffer pain, caused
by retention of urine and inflammation of the sheath; urethritis may
even be set up.

=The treatment= is fairly easy, and is exclusively surgical; but as it
necessitates casting the animals the bladder should first be examined
per rectum, and operation should never be attempted until the bladder
has been emptied so as to avoid possible rupture. The animal being fixed
on its back, the penis is withdrawn from the sheath, and the polypi can
then be snipped off with scissors, the wounds being slightly cauterised
to arrest hæmorrhage: in the case of the sheath, rather extensive wounds
must sometimes be produced; these may be sutured.

To prevent the wounds afterwards becoming infected and suppurating, the
sheath should be regularly washed out with an antiseptic solution and
the animal kept on a very clean bed.


                      INFLAMMATION OF THE SHEATH.

This condition is much more common in the ox than in the horse on
account of the different anatomical structure of the parts, and the
methods of keeping and using oxen.

=Causation.= Several predisposing causes undoubtedly exist. The sheath
is prolonged beneath the abdomen to a considerable distance beyond the
glans. It is narrow, deeply seated, and, during micturition, not even
the point of the penis passes beyond it. The urine, therefore, soils the
interior, or a certain quantity may be retained, according to whether
the orifice is more or less obstructed by urinary sediment, sebaceous
material, manure, or other material. Moreover, experience shows that of
all the large ruminants, those used for outdoor work are the most
affected.

Of the occasional causes, if we except sebaceous and urinary products,
the most important is mechanical violence, such as the lacerations or
wounds produced by the bed-piece of the trevis when the animal is being
shod. The working ox throws its whole weight on this bed-piece, on which
it lies on one side or the other, according to the foot which is being
lifted. The sheath is compressed, and if the animal is heavy and
struggles, the parts may be abraded and torn, or the sheath and even the
glans may be crushed. In less dangerous cases the connective tissue may
be lacerated by the edge of the bed-piece. Any injury so inflicted is
aggravated by dirt in the neighbourhood.

=Symptoms.= The first signs which attract attention are of a general
character, and seldom very strongly marked. The animal shows slight
fever, dryness of the muzzle, is restless and continually moves about,
as though to get rid of the pain it feels. The hind limbs are frequently
lifted. In this attitude it makes efforts to urinate, but urine is
passed very slowly, and the act seems painful; then, later on, the
appetite diminishes, rumination is suspended, and, as in all intense
forms of cellulitis, complications may occur.

The local symptoms are more suggestive. The slowness and difficulty with
which urine is passed at once attracts attention to the diseased parts.
Examination immediately reveals extreme sensitiveness of the sheath,
although as yet there is only slight engorgement. At a later stage a
large swelling develops and extends along the abdominal wall on either
side, sometimes upwards into the groin. In certain cases the sheath may
be totally obstructed by sebaceous and inflammatory material, and in the
absence of surgical assistance the bladder may become ruptured.

Inflammation most frequently ends in the tardy formation of an abscess,
which shows little tendency to open spontaneously. It is usually
accompanied by gangrene and by mortification of a mass of skin and
subcutaneous tissue, sometimes of portions of the abdominal tunic. Such
grave complications may even lead to the opening of an artery, and to
fatal hæmorrhage.

All these symptoms develop comparatively slowly. Abscesses scarcely ever
appear before the twelfth or fifteenth day, but when the disease is not
treated it may continue as long as five or six months. On the other
hand, resolution is the ordinary termination under suitable treatment.

=Diagnosis.= The diagnosis is easy when the exact facts can be
ascertained. The difficulty in micturition is the chief indication. At a
later stage, local swelling and acute sensitiveness are characteristic.

=Prognosis.= The prognosis is grave, having regard to possible
complications and the chronic character which the inflammation tends to
assume.

=Treatment.= When the sheath is filled with sebaceous material or
foreign substances it may be necessary to cleanse it daily with mild
antiseptic injections. Some practitioners recommend laying open the
external orifice, an operation which may be performed in the standing
position. This, however, is not without danger, and infection may easily
occur.

When the subcutaneous connective tissue surrounding the sheath and the
glans penis is infiltrated and inflamed, the inflammatory swelling must
be examined every day, so as to detect the abscesses as early as
possible, and open them without delay. Under some circumstances deep
firing in points produces very favourable results.

When an abscess has caused partial necrosis of the sheath, it is well to
pass a drain and wash out the parts frequently with antiseptic
solutions. For this purpose a counter-opening is made through the skin
opposite the fluctuating point. The mucous membrane of the sheath is
then cautiously punctured, and a seton or strip of gauze is passed by
means of a seton needle, so as to allow of constant drainage.


                      PERSISTENCE OF THE URACHUS.

This condition is an infirmity or congenital anomaly, rather than a
morbid condition. Persistence of the urachus after birth and after
separation of the cord is due to the fact that the canal which
communicates with the bladder fails to close up. The urine, instead of
escaping through the urethra, passes along the urachus, and the animal
urinates through its umbilicus.

=Causation.= The causes are simple. Certain practitioners have suggested
that sex has some influence, this being an anomaly occurring more
frequently in males than in females. From investigations which have been
carried out, it would appear that, in some cases, persistence of the
urachus is due to an imperforate condition of the urethra; in other
cases, to its obstruction by accumulations of mucus of a caseous
appearance, which enter the urethra and completely block the passage.
Finally, in other cases the urachus simply persists while no lesion
exists on the side of the urethra.

Whatever the original cause, escape of urine by the umbilicus produces
irritation, which may end in complications, infection of the unhealed
umbilical wound, infection of the canal of the urachus itself and the
bladder, or even infection of the peritoneum.

=Symptoms.= At first, persistence of the urachus is shown by permanent
or intermittent discharge of urine through the umbilicus. Usually this
discharge is only seen from five to eight days after birth, when the
necrosed cord is detached; in most cases it is continuous, for the
opening is abnormal and has no sphincter.

Contact with the air and the wound causes the urine to undergo a kind of
ammoniacal fermentation and to irritate neighbouring tissues, such as
the stumps of the umbilical vessels, the interstitial connective tissue,
and even the skin. The wound constitutes an excellent culture medium for
microbes. The umbilicus becomes swollen and œdematous, and soon exhibits
a saccular swelling, 2 to 4 inches in diameter, which, on palpation,
proves to be hot and painful; its centre is occupied by the opening of
the urinary fistula. A probe passed into this fistula travels upwards
and backwards (see Fig. 183).

At a later stage other complications, including omphalitis and
omphalo-phlebitis, may set in. The most frequent of the delayed
complications is purulent cystitis, with the formation of purulent
concretions in the bladder, which may occur even after the fistula of
the urachus has healed. In other cases the canal of the urachus
contracts and becomes obliterated towards the bladder. A blind fistula
then persists, with an opening at the umbilicus, or, the parts having
healed externally, all that remains is a phlegmonous swelling with the
characteristic symptoms.

=Diagnosis.= A thorough examination will invariably allow of urinary
fistulæ being distinguished from other diseases of the umbilicus, the
escape of urine at this point being so suggestive.

=Prognosis.= The prognosis is rather grave, on account of the
complications, which are possible, and, in fact, usual, unless the
disease is promptly diagnosed.

=Treatment.= Formerly as a preventive measure a ligature was applied to
the whole mass of the cord at birth, but this ligature in no way
prevents the canal of the urachus persisting after the atrophied portion
separates. Cauterisation of the urinary fistula with Rabel’s fluid or
tincture of iodine can have no good result, unless the urethra is
permeable.

If the urethra is obstructed it is evidently from that side that
treatment should be attempted, either by displacing the mucoalbuminous
plugs with a catheter or in some other way. Such intervention is very
delicate and difficult in the case of young animals. Sometimes it is
better to allow the discharge of urine from the umbilicus to continue,
and to recommend that the animal should be rapidly fattened for the
butcher.

In practice, pervious urachus may be treated by suturing, by firing
across the fistula, and sometimes by blistering. The first step in all
cases is to see that the urethral passage is free. English veterinary
surgeons claim to have had a fair measure of success from these methods.

If a radical cure were thought desirable, the abdomen would have to be
opened, and the operator would proceed to isolate the urachus, resect
it, and suture the base of the bladder by bringing together its external
surfaces. The operation, though not perhaps impossible, is of no
practical value.




                              CHAPTER II.
                        DISEASES OF THE BLADDER.


                            ACUTE CYSTITIS.

Cystitis, or inflammation of the bladder, may be divided into two
varieties: simple (acute or chronic) cystitis, and chronic cystitis due
to the presence of calculi.

Simple acute cystitis occurs most commonly in the cow, less frequently
in the ox, and rarely in the pig or sheep. Female animals are more
subject to it than males.

It consists of more or less acute inflammation of the vesical mucous
membrane. The inflammation sometimes extends to the muscular coat and
the peri-vesical tissues, setting up local or general peritonitis.

=Causation.= The internal causes to which Cruzel attributes the disease
are rather open to question. Retention of urine in particular is common
in working oxen, which only pass urine when resting, and this would be
more likely to produce distention, paralysis, or rupture of the bladder
than true inflammation; it is doubtful whether inflammation would even
follow the chronic irritation resulting from frequently repeated
over-distention.

The ingestion of irritant plants certainly has a more marked action.
Irritant principles eliminated by the kidneys might not injure them,
although they would bring about changes in the vesical mucous membrane,
with which they would remain in contact for some time.

More frequently cystitis is the result of inflammation due to continuity
of tissue, and forms a complication of urethritis, vaginitis, and the
conditions set up by retention of the after-birth. It may also result
from ascending infection causing pyelo-nephritis, or ascending infection
of any kind which eventually attacks the bladder. It is a very common
consequence of the use of unclean catheters, but only in equines and
females, as the catheter is not passed in the ox or bull until after
urethrotomy.

In by far the majority of cases it is of infectious, and not of toxic,
origin.

=Symptoms.= At first the symptoms are obscure. They commence with slight
colic, and are afterwards characterised by frequent, difficult and
painful micturition and by the small quantity of urine passed on each
occasion.

The urine, moreover, is modified in appearance. At first it contains a
small quantity of blood, and is reddish, or at least of a darker tint
than is usual. Later it becomes thick and whitish, and contains greyish
films of epithelium, and the _débris_ of fibrinous coagula. The
microscope reveals in it the presence of pus corpuscles, flat polygonal
cells with large nuclei, and sometimes red blood corpuscles.

Locally almost all that can be detected in male animals is a little
tenderness of the neck of the bladder on rectal examination, and in
females on examination of the meatus urinarius by means of a speculum.

The vaginal mucous membrane then appears inflamed around the meatus,
which itself is exceedingly sensitive.

In cases of very marked inflammation, accompanied by partial necrosis of
the mucous membrane or the production of false membranes, the
temperature rises as high as 104° Fahr. (40° C.), appetite disappears,
colic is extremely acute, and violent efforts to pass urine are
continually made until the animal is completely exhausted. The patient
then refuses to walk about, but frequently lies down, arches its back,
and constantly makes efforts to urinate, which are abortive or end only
in the passage of little jets of fluid.

The urine passed contains little greyish necrotic fragments or _débris_
of false membranes, suggestive of diphtheria. In female animals the
canal of the urethra may also become obstructed, and rupture of the
bladder, though rare, occasionally occurs.

In the ordinary forms inflammation persists for two to three weeks, then
diminishes in intensity, and either ends in recovery or becomes chronic.

In the grave forms, where inflammation and infection extend to the
peri-vesical tissues and the peritoneum, death by peritonitis is the
rule.

On post-mortem examination, the mucous membrane is seen to be of a
greyish colour, and sloughing or gangrenous over surfaces of varying
size, whilst the surroundings are infiltrated, blackish and greatly
thickened. The whole of the connective tissue layer which supports the
peritoneum near the base of the bladder, and also the adipose tissue
around the bladder, are markedly inflamed. At this stage
pelvi-peritonitis or generalised peritonitis may occur as complications.

In the simple forms the mucous membrane is desquamating, infiltrated,
and covered with granulations of apparent healthy appearance.

=Diagnosis.= The diagnosis is comparatively easy, the external symptoms
being so clearly defined. There is a difficulty, however, in
distinguishing this disease from cystitis caused by a calculus. In male
animals this latter form of cystitis is characterised by frequent
spasmodic contractions of the accelerator urinæ. In acute cystitis, on
the contrary, the contractions are temporary only and of no importance.
Lastly, in female animals cystitis due to calculus formation is quite
exceptional, owing to the large diameter and shortness of the urethra.

When nephritis and cystitis co-exist certain signs indicate the fact.

=Prognosis.= The prognosis varies, according to the acuteness of the
disease and the character of the urine and epithelial _débris_, which
afford valuable information.

=Treatment.= The treatment should be directed towards relieving the
vesical and pelvic pain and modifying the local conditions.

Hot fomentations to the loins and flanks relieve pain. The
administration of bicarbonate of soda and of cold drinks, such as
barley-water, decoctions of couch grass and pellitory, mucilage, etc.,
are of service. These materials are readily taken by the patients, and
have a soothing effect. Camphor also produces good results, but benzoate
of soda is most useful on account of the disinfectant action produced
within the bladder, as a consequence of the benzoic acid being
separately eliminated by the kidney. Repeated washing out of the bladder
with antiseptic solutions has been recommended, but is open to
criticism. Such treatment is difficult in male animals, owing to the
special formation of the glans penis and urethra, and in female animals
it is by no means easy. In all cases of acute cystitis, in fact, the
passage of the catheter is painful, and as a metal, gutta-percha or hard
rubber sound is used, the mere contact of the tip of the instrument
injures the diseased mucous membrane, makes it bleed, and gives rise to
danger of autoinoculation, with the possibility of serious results.

Those who recommend this method of treatment can never have followed
closely the development of a grave case of acute cystitis, and if the
practice is at all permissible, only a soft catheter should be used.

In chronic cystitis, on the other hand, washing out the bladder might be
useful.


                           CHRONIC CYSTITIS.

Chronic inflammation of the bladder is still rarer than acute cystitis.
It usually attacks females as a consequence of acute inflammation,
though the condition may be chronic from the first, in which case the
early stages are commonly overlooked.

=Symptoms.= The chief functions of the body do not appear to be
disturbed, although the urine seems abnormal. Micturition is difficult,
slow, and somewhat painful, and is followed by long-continued tenesmus.

The urine appears whitish, purulent, slimy, or of a deeper tint, rapidly
becoming blackish. It is of ammoniacal or fœtid odour, and decomposes
quickly.

The period of development may be prolonged, and recovery rarely occurs
spontaneously. The condition often leads to ascending infection,
inflammation of the ureters, pyelitis, and nephritis.

On post-mortem examination of animals slaughtered before complete
wasting has occurred the vesical mucous membrane is found to be
thickened, granulating, or suppurating. The muscular tissue shows
infiltration and localised sclerosis, and is very irregularly thickened,
inelastic, and wanting in contractile power. The peri-vesical tissues
may be chronically inflamed.

=Diagnosis.= The diagnosis is easy, provided the peculiar
characteristics of the urine are noted, and an examination is made
through the vagina of the condition of the walls of the bladder, of the
ureters and of the kidneys.

=Prognosis.= The prognosis is grave, because treatment would occupy too
much of the practitioner’s time to allow it to be rigorously carried
out, and therefore animals are usually slaughtered.

=Treatment.= Treatment comprises the use of many of the drugs used in
acute cystitis, particularly benzoate of soda, benzoic acid, and
bicarbonate of soda. The medicines comprised in the balsamic group are
also valuable, viz., turpentine, tar, and terpine.

In this chronic form the bladder should be irrigated, but this must be
done with strict aseptic precautions, the fluids used being cooled
boiled water, boric acid or borax solution of 3 per cent, strength, or
solution of fluoride of soda of a strength of 15 grains to the quart.

We need not point out the difficulties of pursuing this treatment in
ordinary practice. As a rule, treatment is confined to internal
medication whilst the animals are fattened.


                 URINARY LITHIASIS. CALCULUS FORMATION.

Normally the urine contains in solution certain salts, such as urates,
hippurates and phosphates of lime, magnesia or ammonia. Under certain
circumstances, in animals predisposed to the condition, these salts are
precipitated in the kidneys, ureters or bladder, and form powdery or
sandy deposits known as sediments; or, on the other hand, calculi,
produced by the adhesion of the powdery masses. This constitutes urinary
lithiasis.

The sediments are of a greyish-yellow colour.

The calculi are generally rose-coloured, white or somewhat grey. They
contain oxalates and carbonates of lime and magnesia, earthy phosphates,
etc. In appearance and shape they vary greatly. They may resemble coral
or may form growths of a rounded, polyhedric or raspberry appearance.
Some are hard and resistant; others friable. They vary in size between
that of a grain of sand and a hen’s egg or more. A large calculus is
usually solitary; the smaller sizes are often multiple.

Calculi occur in oxen and sheep, but more particularly in the latter
species. They develop slowly without producing any marked external
signs, and often it is only when the urethra becomes obstructed and
urine is retained that the diagnosis is established. Calculi are rare in
females in consequence of the dilatability of the urethra.


                       CALCULI IN BOVINE ANIMALS.

=Causation.= The older writers believed that calculi developed through
winter feeding and a stinted supply of water. Nowadays this would not
apply to well-managed establishments, water being provided regularly,
and winter feeding comprising roots, etc., rich in water. Experience and
observation have shown that the chief cause is excessive feeding,
calculus formation occurring most frequently in animals which are most
richly fed.

Nevertheless, it would be a mistake to overlook the effects of
temperament and constitution. In human medicine the importance of
hereditary predisposition and of the special diathesis is undeniable
(uric or gouty diathesis). In veterinary medicine the same thing
applies, for, apart from rich feeding, it is not uncommon to meet with
cases of gravel in animals living under the most diverse conditions,
although the issue of the same parents.

Certain infections of the urinary passages, though trifling at first, or
at least of slow development, are also capable of causing mineral
deposits in the urinary passages, a fact which Moussu considers to be
proved by his success in experimentally reproducing given forms of
pyelo-nephritis.

=Symptoms.= The symptoms are often overlooked, as long as the calculus
deposits affect only the kidneys, their increase in that part not giving
rise to alarming symptoms. It is certain that the eventual passage of
the calculus through the ureter towards the bladder causes nephritic
colic, but this form of colic is little understood, and has never been
well described. Writers have simply mentioned cases of colic accompanied
by great tenderness in the lumbar region, temporary suspension of the
secretion of urine, and more or less marked dysuria.

Nothing resembling the extremely grave symptoms of nephritic colic in
mankind has been described, though probably there is little difference
in the complaint as it affects the bovine species.

When the sediment or the calculus reaches the bladder there is a
tendency for it to be passed during micturition. The signs then become
more strongly marked, because they point to obstruction of the urethra.
If the deposit is simply of the nature of sediment, there is merely a
little difficulty in urination, accompanied by some moderate amount of
pain, and sediment is afterwards found within the sheath or adhering to
the groups of hair at its extremity.

If, however, the deposit is in the form of small calculi, these are
pushed towards the neck of the bladder and the urethra, which then
appears to be obstructed.

The obstruction may occur at the origin, at the ischial curve, or at the
=S=-shaped curve of the penis (Fig. 226). Henceforth strongly marked and
unmistakable symptoms rapidly develop. Vesical colic appears, owing to
retention of urine, and rapidly acquires extreme intensity, though it
instantly ceases with rupture of the bladder in cases where no treatment
is attempted. This form of vesical colic is accompanied by continual but
unsuccessful efforts to urinate and by spasmodic contractions of the
accelerator urinæ.

Appetite and rumination cease, and the animal shows extreme anxiety.
Palpation along the course of the penis reveals unusual tenderness, and
the calculus can sometimes be felt near the =S= curve, though more
frequently in the ischial arch. The litter is not soiled with urine.

Cautious rectal examination proves the bladder to be extremely
distended, or, in the case of rupture having occurred, entirely
collapsed. In the latter case the spasmodic contraction of the
accelerator urinæ completely ceases soon after rupture, and the animal
appears to be recovering. This deceptive calm is due to the
disappearance of the vesical colic, but the animal’s condition is still
graver in consequence, and it must of necessity die. Rupture of the
bladder is followed by inundation of the peritoneal cavity with urine,
which is partly reabsorbed by the peritoneum, producing a kind of
urinary intoxication, so that despite the elimination of certain
volatile principles through the lungs (the breath has an odour
suggestive of urine), the animal very soon dies.

In many cases, also, the urine is not aseptic, and after rupture of the
bladder acute peritonitis supervenes and carries off the patient in from
six to ten days.

Even when the urine appears to be aseptic, chronic exudative peritonitis
is produced by the irritant action of the urine on the peritoneal
endothelium. The exuded liquid mixes with the urine, and the animal soon
shows marked ascites. Despite this condition, some animals have been
known to survive as long as from three to six weeks without showing very
marked disturbance.

Death is the inevitable sequel after a longer or shorter time. When
large calculi have been arrested, or rather developed, in the bladder
the same symptoms occur should the calculus be thrust towards the neck
of the bladder so as completely to obliterate the passage. This,
however, is a very rare accident. As a rule the obstruction is merely
temporary, and the resulting vesical colic and retention last but a
short time. The displaced calculus falls back again into the lower part
of the bladder, where it is retained, and the urinary passages again
become free.

=Diagnosis.= The diagnosis is sometimes extremely easy, but it may
present serious difficulty.

When the urethra is obstructed, the symptoms are so striking that there
can scarcely be any doubt; but the diagnosis of renal calculus,
nephritic colic, calculus in the bladder, and rupture of the bladder
demands more attention. Examination of the urinary organs through the
rectum then proves of great service.

=Prognosis.= The prognosis is grave in all cases, because of the
possibility of the urinary passages being obstructed, so that surgical
interference is necessary.

=Lesions.= The lesions caused by urinary calculi may vary greatly.
Though insignificant and scarcely apparent in certain cases, they are
often very marked, and comprise simple or suppurative pyelitis,
inflammation of the ureters, hydro-nephrosis, cystitis of varying
intensity, urethritis, and inflammation of the sheath.

=Treatment.= All farmers who fatten their animals know that the use of
alkaline drugs, such as bicarbonate of soda, together with diuretics,
linseed, barley and pellitory diminish the danger of urinary calculus
formation. Bicarbonate of soda is often given with this object, and is
excellent in cases where lithiasis does not extend beyond the production
of sandy or muddy deposits. By rendering the urine more alkaline it
prevents the growth of sabulous deposits, and may even cause slow but
progressive solution of concretions already formed. When, on the other
hand, the urethra is obstructed, and urine is retained, early surgical
treatment (urethrotomy) alone offers any chance of preventing rupture of
the bladder.

Certainly it is possible, as recommended by the older practitioners, to
try massage of the glans penis and urethra opposite the obstruction,
and, after withdrawing the penis, to attempt to loosen and eject the
obstructing matter. But such attempts very frequently fail, because the
material is too firmly fixed, and no time must be lost.

Urethrotomy is usually practised at one of two points, according to
circumstances—firstly, opposite the ischial arch; and, secondly,
opposite the =S=-shaped curve.

=Ischial urethrotomy= is the promptest method of affording relief, and
should always be preferred whenever there is danger of rupture of the
bladder.

It is performed in the standing position, but is only possible when the
animal is not too fat.

In other cases urethrotomy is performed opposite the point where the
calculus is fixed, and aims at removing the obstruction. It can only be
practised after casting the animal; but, in this case also, it is
indispensable that the animal should not be excessively fat, as in such
cases a secondary urinary abscess is almost certain to form.

Should the animal be so fat as to render treatment difficult, it is best
to slaughter it at once.


                       URINARY CALCULI IN SHEEP.

Urinary calculi are commoner in sheep than in oxen, and seem to depend
more on the breed and on conditions of feeding. They are almost
exclusively confined to animals which are richly fed, to show animals,
and to males. In exceptional cases they are seen, under ordinary
conditions of feeding, in aged subjects.

Calculus formation can moreover be induced experimentally, and in a
relatively short time, by giving certain rations—_e.g._, 7 lbs. per day
of maize, lentils and beans for adults, and 3 lbs. for lambs. The other
favouring circumstances, viz., hereditary gouty diathesis and infection,
are less well established than they are in the case of the ox.

In sheep the symptoms are still less characteristic than in oxen, for
which reason gravel in sheep merits special description.

It shows itself in the passage of turbid urine, forming a deposit at the
extremity of the sheath, which becomes somewhat inflamed. The colic
resulting from retention of urine is shown by depression, want of
appetite, dysuria, and generalised convulsive shivering fits.

The patients lie down in the sterno-abdominal or sterno-lateral
position. They constantly suffer from attacks of general violent
shivering, and die after twelve, twenty-four, or forty-eight hours.

On post-mortem examination the bladder is found to be ruptured, or the
urethra obstructed.

=Diagnosis.= The diagnosis involves no difficulty, provided the method
of feeding is understood. In many cases the shepherds themselves
perfectly recognise the cause of the symptoms.

=Prognosis.= The prognosis is very grave, it being impossible to pass
the catheter on account of the perineal valve in the urethra, while it
is difficult to operate, the urethra being very small and deeply
embedded in a thick layer of fat.

=Treatment.= The only resource is massage along the urethra, which may
sometimes break up the mass of sediment or move the obstructing
calculus. One remark may, however, be made, viz., that in the majority
of cases the urethra is obstructed at its extremity by local
accumulations of sediment behind the spiral filiform prolongation of the
penis.

It is then sufficient, and experienced shepherds have no hesitation in
performing the operation, to remove the spiral filament, thus
facilitating the expulsion of the sediment and affording relief. If both
methods, viz., massage and section of the filament, fail, the animal
should be slaughtered, so as to avoid rupture of the bladder, which
would render the flesh useless as food.

From a preventive standpoint, all sheep which are richly fed should
receive an allowance of some slightly alkaline drink.


                       PARALYSIS OF THE BLADDER.

Paralysis of the bladder is somewhat frequent in female, but very rare
in male, animals. In the majority of cases it is the consequence of
difficult parturition, or is a post-partum complication.

It is characterised by incontinence of urine or retention with overflow.
The continuous discharge soils the hind quarters, hocks, shanks,
pasterns, etc., and the urine decomposes and causes irritation; it soon
sets up urinary eczema in all the parts with which it comes in contact,
a condition which can only be successfully treated by removing the
cause.

=The prognosis= is grave, for methods of treatment are few, and of
doubtful efficacy.

=Treatment.= If the condition results from post-partum infection, this
must naturally first receive attention. Should the infection have
disappeared whilst incontinence of urine still continues, the
administration of tonics, _e.g._, tincture of nux vomica in daily doses
of ¾ to 1 drachm for ten days or so in the case of a bovine animal, and
a stimulating application to the lumbo-sacral region, may bring about
recovery.

But if, in spite of such treatment, the incontinence persists, it is
better, from an economic standpoint, to treat the urinary eczema with
astringents, etc., and quickly to fatten the animal.


                        EVERSION OF THE BLADDER.

Eversion of the bladder only occurs in female animals after difficult
parturition. The viscus is turned completely inside out, as occurs in
eversion of the uterus, the base of the bladder becoming invaginated in
the cavity of the bladder itself, and afterwards passing into the
urethra and vagina. The bladder thus becomes totally displaced, and
appears between the lips of the vulva, resting on the inferior
commissure, and forming a mass the size of an orange.

Eversion cannot occur unless the ligaments of the bladder have become
relaxed, stretched or ruptured. Expulsive efforts and the pressure of
the intestinal mass complete the process, the peritoneum and
peri-vasicular layers of connective tissue being torn.

=Diagnosis.= The diagnosis of eversion of the bladder presents no
difficulty. The everted mass appears to have a narrow neck opposite the
meatus, and is seen to form a reddish, unctuous mass. The mucous
membrane now forms the external coat and appears covered with mucus so
long as inflammation does not occur.

The urine continually escapes from the ureters (which open on the
surface of the mucous membrane) as it is formed, and flows away by the
lower commissure of the vulva. The vulva is half open, and the
prominence formed by the bladder projects beyond it.

=Prognosis.= The prognosis is grave, because reduction is difficult, and
may be accompanied by rupture of the organ; also because even in
favourable cases it is invariably followed by acute cystitis.

=Treatment.= Treatment is confined to reduction. Before attempting this,
measures must be adopted to prevent straining, either by passing a rope
round the animal’s body, thus causing it to flex the vertebral column,
or by puncturing the rumen or performing tracheotomy. The open hand is
then applied to the surface of the swelling, which is gently compressed
and thrust in turn through the meatus and urethra. The portions nearest
to the urethra should first be returned. It is sometimes necessary to
use both hands, and even to employ a catheter with a large round head,
to reduce the eversion effectually. After reduction a truss or vulval
clamp should be applied. Subsequent treatment consists in the
administration of sedatives—_e.g._, laudanum, mucilaginous drinks,
barley-water, pellitory, etc.


                               HÆMATURIA.

Hæmaturia, _i.e._, the passage of blood-stained urine, is in itself only
a symptom, which may accompany very varying conditions, such as the
congestion peculiar to the early stages of nephritis, traumatic lesions
of the kidneys, ulceration of the uriniferous tubules, or of the pelvis
of the kidney, lesions of the ureters, bladder, etc., etc. The term,
therefore, does not indicate a disease, but nevertheless in bovine
practice the term hæmaturia has acquired a special significance.

This hæmaturia of bovine animals is clinically indicated by the presence
of blood in the urine; anatomically by lesions of the bladder, sometimes
also of the ureters. It is probable that some forms at least of the
condition will ultimately be proved to be due to the piroplasmata, but
in the present state of our knowledge the disease can only be described
from the clinical standpoint. The reader is recommended to refer to the
article on “Bovine Piroplasmosis,” _ante_.

Pichon in 1863 and Sinoir in 1864 introduced the name “hæmaturia” in the
course of their remarkable investigations concerning the disease. Vigney
in 1845 and Gillet in 1862 had previously described it, and it has since
formed the subject of constant researches.

Detroye in 1891 termed it “essential hæmaturia,” and Galtier in 1892
gave it the name of “hæmorrhagic cystitis.” Boudeaud in 1894 also used
the term “hæmaturia of bovine animals.” In Germany the disease is known
as “stallroth” (stable-red).

=Geographical distribution.= Hæmaturia is a perfect scourge in certain
countries. It seems to have made its appearance in the departments of
the West of France, the Mayenne and the Sarthe, afterwards spreading
into the Maine-et-Loire and the Indre. At the present day, it inflicts
great ravages in the Creuze, the Corrèze, Haut-Vienne, Cantal and
Haute-Loire districts. It has been described in Germany, Belgium, and
Italy. These forms are probably due to _Piroplasma bigeminum_.

=Causation.= The most varying opinions have been advanced regarding its
cause. Pichon believed its appearance was due to changes in cultivation,
which between 1830 and 1860 completely altered the general appearance of
the country and the conditions of breeding in the old province of Maine.
Land reclamations and the use of lime dressings have been mentioned, as
well as the introduction of the Durham breed of cattle. Sinoir
practically adopts the latter view, for he considers that the crossing
with the Durham breed, while increasing the precocity, has diminished
the powers of resistance of the indigenous cattle.

But in course of time these ideas have become modified, and
investigation has taken a new direction. Detroye regarded the disease as
a microbic and easily transmissible disorder, while Galtier in the
following year described it as merely a chronic hæmorrhagic cystitis,
produced by the consumption of irritant plants in animals previously
suffering from distomatosis. In Germany, Arnold attributed “stallroth”
to coccidia developing in the epithelium of the vesical mucous membrane.

Cruzel considered the disease to be due entirely to poor feeding.
Boudeaud thought the same. He says that hæmaturia affected one-tenth of
the whole of the oxen in the south of the Indre and the north of the
Creuze, in parts where the arable soil is thin and poor in phosphoric
acid. Furthermore, he suggests that dressings with lime and phosphates
would result in the disappearance of hæmaturia.

We cannot admit that poor forage and feeding alone are sufficient to
produce hæmaturia, for one frequently sees poorly nourished animals pass
through all the stages of wasting and most profound cachexia without
ever showing signs of this particular ailment. Besides, hæmaturia may
attack animals in good condition.

Detroye’s early opinion as to the infectious or microbic nature of the
disease seems scarcely more acceptable, for it now appears certain that
the organism originally described is incapable of producing the disease.

Galtier’s theory is still less admissible. According to the Lyons
professor, hæmaturia occurs only in animals suffering from distomatosis.
The liver, he says, being affected by the growth of liver flukes, no
longer performs its proper work of destroying toxins, and if under these
conditions the animals eat improper food containing ranunculaceæ,
sedges, rushes, etc., the toxic principles of these plants are absorbed.
Then, he adds, these principles being no longer destroyed, are
eliminated by the kidneys, their stay in the bladder causes irritation,
and hæmorrhagic cystitis is set up, this being afterwards maintained by
microbic agents in the bladder.

This very specious theory, all the points in which may readily be
refuted, in our opinion falls to the ground before the simple fact that
hæmaturia occurs in animals which present no trace of distomatosis on
post-mortem examination, and that, furthermore, it is not seen in the
lower regions of the departments of the Nord, the Pas-de-Calais and the
Somme, where ranunculaceæ and other irritant plants are common and
distomatosis rages.

Moussu states that he has proved that hæmaturia is very rare in young
animals and is exceptional before the age of two and a half years or
three years; that it attacks oxen as often as cows; that it is
particularly common in low regions; and that it is scarcely ever seen
above a height of 800 yards. Careful investigation, moreover, shows that
the passage of blood occurs just as frequently in winter, when the
animals are housed, as in spring, when at pasture.

=Lesions.= The lesions of hæmaturia are to be found in the bladder,
though in exceptional cases they may also affect the ureters and
kidneys. They have been described by Pichon and Sinoir, but as these
observers regarded the condition as a disease of the blood due to poor
feeding, etc., they did not attach much importance to them. Detroye has
described the different appearances very well, though Moussu states that
he has never met with the “blisters” which he mentions.

The first period is accompanied simply by abnormal vascularity of the
bladder, which appears in the form of true varicosities of the submucous
vessels and intra-mucous capillaries. But if this lesion is primary, it
does not correspond to the period during which blood-stained urine is
passed, and is not sufficient to explain it. It always appears in the
form of a more or less abundant hæmorrhagic intra-mucous, sub-epithelial
spotting.

Over the hæmorrhagic area, which may be of very varied dimensions,
ranging from those of a small pin’s head to those of a lentil, the
epithelium is swollen and loosened, and so separated from the
surrounding parts as to have lost its vitality. This patch of separated
epithelium soon falls away, leaving an epithelial ulceration of the
mucous membrane. The subjacent clot rapidly breaks up in contact with
the liquid in the bladder, and is replaced by a small ulceration which
becomes the seat of continual capillary hæmorrhage. Nevertheless, the
neighbouring tissues react, and the process of repair may end either in
true cicatrisation, which appears to be rare, or more frequently in the
formation of exuberant granulations, which are also of the nature of a
soft, bleeding vegetation. This vegetation is either sessile or
pedunculated, and is of very varying size.

The wall of the bladder also reacts, becoming sclerosed and thickened
beneath the granulations, so that, in animals which have long suffered
from hæmaturia, it may entirely have lost its dilatability.

When the disease has existed for a certain time, sub-epithelial
hæmorrhages, ulcerations, vegetations and points of sclerosis may all
co-exist, a fact which shows that the disease does not develop all at
once, but that, on the contrary, every little lesion develops separately
and continuously. This fact also explains the length of time for which
blood may be passed, despite the presence of old or healed lesions.

Finally, in very old standing cases dating from several years back
(Moussu saw an animal aged twenty-eight years which had suffered from
this disease for more than twenty years, but in a very intermittent
fashion), it is not exceptional to find numerous papilliform vegetations
1 or 2 inches in length, either with a fine pedicle or largely sessile,
invading one-half or two-thirds of the internal surface of the bladder.

These vegetations sometimes, though rarely, invade the ureters. When
they occur towards the point where these conduits enter the bladder,
they obstruct the passage of urine, and lead to the development of
hydro-nephrosis or pyelo-nephritis.

=Symptoms.= The early symptoms often escape notice, because general
disturbance is rare. The first appreciable signs are cystitis and
frequent urination.

The urine passed is turbid, particularly towards the end of the act of
urination; then it is of a pink or red colour, and all intermediate
shades between a pale pink and a bright arterial red colour may be
observed.

The patients sometimes seem to pass unaltered blood in the urine, but on
microscopic examination this blood is found to be extremely diluted.
Provided the bladder is not gravely infected by the (secondary)
penetration of germs into its cavity the blood corpuscles remain normal,
or are scarcely changed. As soon as the bladder, however, becomes
secondarily infected an almost immediate change takes place; the red
blood corpuscles become crenated, broken up and dissociated; the
hæmoglobin is also partly dissolved and modified, and at this stage the
urine is red-brown or coffee-coloured, according to the length of time
it has been retained in the bladder.

In other cases, chiefly when hæmaturia has existed for some time, the
extravasated blood coagulates in the bladder, and the urine passed
contains filamentous clots the size of a man’s thumb, a pigeon’s egg, or
more. If the clots formed are too large to be passed, which is often the
case in the ox, they may obstruct the urethra, causing retention of
urine and all the accidents which accompany this condition, even
including rupture of the bladder. This, in the ox, is a frequent
termination. In the cow the dilatability and shortness of the urethra
render retention of urine much rarer. It is certainly possible, however,
and it is not exceptional, to find from 4 to 6 lbs. of clotted matter in
the distended bladder. All these conditions can be detected by rectal
exploration, and by attention to the symptoms of obstruction of the
urethra.

Whenever there is retention of clots dysuria is extremely marked and, so
to speak, permanent, the animals having continual tenesmus.

Hæmaturia observes a slow, progressive course, which, in time, ends in
death by exhaustion, though this is not invariably the case. Hæmaturia
is frequently intermittent, and, after having been very marked for weeks
or months, may suddenly or gradually cease, and only reappear a long
time afterwards. This fact is explained by a study of the development of
the lesions. When ulceration occurs the sub-epithelial vessels of the
mucous membrane, which have contributed to the formation of the
hæmorrhagic spot, are widely open, and a capillary hæmorrhage results;
but as soon as a small clot forms in this position, or local capillary
thrombosis occurs, the hæmorrhage ceases, with the result that the
hæmaturia disappears. Unfortunately, however, the obliterating clots are
not permanent, any more than the local thrombosis—or, in the event of
their proving permanent, another small lesion develops at a different
point, and this lesion may at any time cause the reappearance of the
hæmaturia; the process goes on until the animal succumbs. Should the
lesions heal successively, spontaneous recovery may take place, but such
recovery is exceptional.

The animals may not appear to suffer from the passage of blood for weeks
or even months, but after a time they become less capable of replacing
the loss. They become anæmic, the number of corpuscles falls from the
normal figure of from six to seven millions of red corpuscles per cubic
millimètre to three millions, two millions, one million, and even to
five hundred or eight hundred thousand.

The richness in hæmoglobin simultaneously diminishes; wasting progresses
to the point of cachexia, and the appetite diminishes while diarrhœa
appears; swellings are noticeable about certain parts of the body; and
the animals, continuing to pass blood, die in a state of absolute
exhaustion, without apparent suffering.

This termination is the most common, unless slaughter is determined on,
and is very different from the premature end which follows the formation
of clots and obstruction of the urethra.

Externally the patients only show feebleness, pallor of the visible
mucous membranes, and difficulty in urination. The bunch of hair at the
lower commissure of the vulva is always soiled with blood-stained urine
or little clots.

Hæmaturia may cause death by exhaustion in from six weeks to two months,
but not infrequently it lasts for months or even years.

=Diagnosis.= The diagnosis presents no difficulty when the urine can be
examined; but in the periods of intermittence no opinion can be
advanced. These intermittences are so frequent that in parts of the
country ravaged by this disease it is a usual custom, when selling, to
grant or refuse guarantees for a longer or shorter term.

The condition can be distinguished from parasitic hæmoglobinuria
(piroplasmosis) or from Brou’s disease (a febrile disease of rapid
development) by simply examining the urine or blood.

=Prognosis.= The prognosis is extremely grave, for, up to the present,
no really efficacious treatment has been discovered, and although some
animals may live for years without their lives being in any way
endangered, this cannot possibly be foreseen, and there is no economic
advantage in keeping them.

=Treatment.= No curative treatment is known.

It is true that iron salts, tonics, Rabel’s liquid, decoctions of
certain plants, such as plantain, have been recommended, but apart from
the fact that they are of doubtful efficacy, they cannot be used over
long periods. All these preparations also tend to increase the
coagulability of the blood; but considering that the disease is beyond
question of a parasitic character, good results cannot always be
expected of them.

Preventive treatment appears more hopeful, although even in this
connection, the best informed appear to have considerable doubts. All
those who have studied the question agree in recommending drainage of
the pasturages, and their improvement by the use of various manures,
particularly superphosphates and lime. These improvements alter the
character of the pasture, render the soil healthier, and may perhaps
prove sufficient to diminish or prevent the local growth of the germs.
Under such conditions, Boudeaud declares that he has seen hæmaturia
disappear from farms where it had previously been in permanent
possession. It has also been recommended that the affected cattle should
be sent elsewhere to places where the disease does not exist, and
experience shows that spontaneous recovery is more frequent under such
conditions.

It is probable that, during attacks of hæmaturia in a contaminated
country, successive parasitic infestations occur, which would explain
the persistence with which blood is passed, a symptom which does not
occur in a healthy country. This view, however, is still only an
hypothesis.




                              CHAPTER III.
                        DISEASES OF THE KIDNEYS.


                       CONGESTION OF THE KIDNEYS.

Congestion of the kidneys is not a morbid condition in the strict sense
of the term, for it is merely the forerunner of nephritis caused by
infectious diseases or intoxications (primary active congestions) or the
final consequence of other diseases, such as diseases of the heart or
liver, mechanical compression of the vena cava or renal veins (secondary
passive congestion, cardiac kidney).

Nevertheless, under certain circumstances the development of nephritis
may be arrested at the primary congestive stage, and it is only then
that an opportunity occurs of studying it as a definite complaint.

=Causation.= All infections accompanied by lesions of the kidneys, and
these are numerous (gangrenous coryza, anthrax, parasitic
hæmoglobinuria), produce congestion of the kidneys.

Cold also acts directly under certain conditions, as do large doses of
diuretics, irritant foods the principles of which are eliminated through
the urine (fermenting or putrid sugar-pulp, for example), and foods rich
in resins, essential oils, various glucosides, tannin, etc. (young
shoots of trees during the spring-time).

=Symptoms.= The symptoms are difficult to define accurately, and the
diagnosis can only be arrived at with the aid of the history.

Renal congestion produces pain, indicated by dull colic and repeated and
ineffectual attempts to urinate, suggesting acute cystitis. The patients
lose appetite, and present all the general symptoms of marked visceral
inflammation, viz., fever, acceleration of breathing, somewhat
tumultuous action of the heart, etc.

External or internal examination of the kidneys reveals abnormal
sensitiveness. The urine is of a dark or bright-red tint, owing to the
presence of red blood corpuscles. These blood corpuscles are
precipitated on placing the fluid in a tall glass, and can be detected,
together with renal epithelium, by microscopic examination.

=The diagnosis= is somewhat difficult, and it requires very careful
attention to distinguish between congestion of the kidney and true
nephritis.

=The prognosis= should always be reserved until it is certain that acute
nephritis will not ultimately develop.

=The treatment= consists in removing the cause of the congestion; rich
foods, or foods containing irritant principles, should, therefore, be
avoided, as also the administration of diuretics, etc.

Otherwise, the treatment is similar to that employed in all visceral
inflammations: bleeding to the extent of two to four quarts, according
to the size of the animals, warm poultices to the loins and flanks, dry
friction, mucilaginous drinks and emollient decoctions of barley or
pellitory. The animals should be kept in a warm place.

In cases of passive and secondary congestion, treatment must be directed
towards improving the condition of the organ primarily affected, whether
it be the heart, liver, or lymphatic glands.


                            ACUTE NEPHRITIS.

The term nephritis applies to inflammation of the renal tissues.
Clinically, two forms only can be distinguished, the acute and the
chronic.

As regards its pathological anatomy, the inflammation may principally
affect either the interstitial tissue or the epithelial parenchyma, a
fact which has suggested the division of the condition into epithelial
nephritis, interstitial nephritis, and mixed nephritis. Clinically, such
distinctions are impossible; and in reality all forms of nephritis are
to a varying degree mixed, the lesions predominating in one or other of
the constituent tissues. These lesions depend on the extent, intensity,
and duration of the inflammatory attack, whatever the primary causes.
All the constituent tissues of the kidney may be affected,
simultaneously or individually: the Malpighian corpuscles, the
convoluted tubules, the collecting tubules, or the interstitial
connective tissue.

=Causation.= Cold seems to be an important factor. All acute or chronic
intoxications in which the toxic principles are eliminated by the
kidneys, such as poisoning by cantharides, fermented beet pulp, young
shoots of trees or toxic plants, may cause acute nephritis.

Infectious diseases, such as gangrenous coryza, hæmoglobinuria,
tuberculosis and post-partum infections, also play an important part,
whether the nephritis be direct, that is to say, the result of the
infecting agent itself, or indirect, _i.e._, produced by toxins
generated in the body. In female animals gestation is an often
unsuspected cause. Moussu believes that albuminuria is frequent during
gestation, and although in most cases it is only of moderate degree, he
thinks it is often associated with subacute nephritis, which might be
aggravated by an accidental cause.

Many forms of nephritis are overlooked in consequence of their slight
character.

=Symptoms.= The early symptoms are similar to those of congestion of the
kidney, viz., dull colic, excessive sensitiveness over the region of the
loins, passage of pink urine, loss of appetite, and fever. At a later
stage, in cases of acute nephritis due to cold, the animal stands with
the limbs close together and remains stationary, arching the loins and
back, which are held stiffly. The animal obstinately refuses to move in
consequence of the pain produced by so doing.

The general condition becomes grave, respiration is rapid, the pulse
frequent, the artery tense, the muzzle dry, the accessible mucous
membranes are injected, and appetite is almost entirely lost.

Urine is frequently passed, but the act causes pain, and the quantity is
small. Absolute anuria is rare, and does not last long.

The urine is generally sanguinolent, at least at first, but to a very
varying extent. It is always albuminous, the quantity of albumen varying
enormously, and on microscopic examination, is usually found to contain
red and white blood corpuscles, epithelium from the kidney hyaline or
epithelial cylinders, and, towards the end, pus corpuscles.

Œdema or anasarca, though common in mankind, does not occur in a very
marked form, except in intense acute nephritis. Epistaxis is also rare.

=Diagnosis.= The diagnosis requires some care, because unless the urine
be examined the symptoms might lead to error. Nevertheless, it is always
possible to distinguish between this condition and hæmaturia or
accidental renal hæmorrhage.

=Prognosis.= The prognosis is grave, because absolute recovery is rare,
and because the condition is very apt to become chronic.

The degree of anuria and the respiratory difficulty are of great service
in confirming the prognosis. As soon as urine is freely passed the
prognosis becomes more favourable.

=Treatment.= Among the most effective methods of treatment must be
included bleeding, which always produces some improvement. Dry friction
over the kidneys and flanks, hot moist applications, and the application
of a sheep-skin to the loins are also of service. Internally,
mucilaginous drinks, diuretic decoctions and milk give the best results.
The proportion of albumen rapidly diminishes, dysuria becomes less
marked, urine is passed in greater quantities, and in from eight to ten
days all the alarming symptoms disappear. Bicarbonate of soda may then
be given for a fortnight.

In very grave cases camphor, bromide of camphor, injections of
camphorated oil (1 to 2½ drachms internally, or 1 to 1¼ drachms in
subcutaneous injections) give excellent results in modifying the pain
and moderating the inflammation.

From ½ to 1 drachm of digitalis in powder, or better still an injection
of from 5 milligrammes to 1 centigramme of digitalin may also be given
when dyspnœa is very great and is accompanied by anasarca. Medicines
such as oil of turpentine and considerable doses of nitrate of potash,
however, are contra-indicated.


                           CHRONIC NEPHRITIS

True chronic nephritis, _i.e._, a condition strictly limited to the
renal tissue, and unaccompanied by pyelitis, is still little known among
our domestic animals. The symptoms characterising it have not always
been carefully noted, and the diagnosis is very often uncertain.
Nevertheless, one of the most common forms has been carefully studied by
Seuffert, viz., chronic hypertrophic nephritis.

=Causation.= Chronic nephritis is the common sequel to the acute forms,
whatever their origin, but it may also occur primarily from repeated
chills produced by such conditions as exposure to heavy continued rain
when at grass, chills contracted during cold nights and the great
variations in temperature in spring and autumn. The conditions, however,
thus produced are rather of the nature of subacute nephritis than of
chronic nephritis, properly so called.

These forms of chronic nephritis may also occur primarily in consequence
of chronic hepatic lesions with pressure on the posterior vena cava,
producing blood stasis in the kidneys. Finally, they may represent the
delayed effects of slight lesions which have escaped notice and have
developed during grave diseases or as a consequence of repeated
gestation.

From the anatomico-pathological standpoint, the only conditions hitherto
recognised are the chronic hypertrophic forms of nephritis (large, white
sclerotic kidney with lardaceous degeneration and sometimes marbling).
This is probably because the animals are slaughtered as soon as they
suffer in condition, but if they were kept long enough they would
undoubtedly suffer also from the atrophic chronic forms of nephritis
found in man and in the dog. In the case of man observation has shown
that these two forms only represent different stages in the development
of one disease, the large, hypertrophied kidney of the early stages
afterwards undergoing marked progressive atrophy.

=The symptoms= are at first so vague that diagnosis would be impossible
on a single examination. Seuffert states that the condition develops as
follows:—

The first sign, loss of appetite, is soon followed by constipation and
dull colic, due to congestion of the kidney; the pain is often so great
as to cause intermittent groaning.

The urine passed is always turbid, and sometimes blood-stained, but this
staining rarely lasts longer than a week. The urine then gradually
resumes its normal appearance, is passed in small quantities, and
contains more or less albumen. The yield of milk markedly and
progressively diminishes.

If treatment is resorted to at this stage laxatives and diuretics appear
to effect a real improvement. Unfortunately, however, the apparent
improvement is but temporary; the kidneys become hypertrophied, and the
right soon occupies the whole of the sublumbar space, its margin
extending as far as the extremity of the transverse processes near the
anterior angle of the hollow of the flank.

This hypertrophy and the extreme sensitiveness can be detected by
external palpation. Internal examination confirms the facts so observed
as regards both the kidneys.

The patients eat little and become thin, whatever treatment be adopted.
They progressively waste, and die after some months in a state of
marasmus, exhausted and intoxicated.

It is very probable that the digestive disturbances are complicated by
respiratory and cardiac trouble, as in man and the dog; but neither
cardiac nor uræmic disease of the kidney has been recorded.

=Diagnosis.= When the urine is analysed the diagnosis becomes
comparatively easy. Persistent albuminuria and hypertrophy of the
kidneys during the early stages are significant indications. There can
be little hesitation except in so far as pyelo-nephritis and
hydro-nephrosis are concerned, but the conditions are distinguished by
the character of the urine in the two latter cases, together with the
condition of the pelvis of the kidney, and of the ureters.

=Prognosis.= The prognosis is grave, and Seuffert believes that recovery
never occurs. This is also true, generally speaking, as regards all
forms of chronic nephritis.

=Treatment.= As the disease must be regarded as incurable there is
really no justification for treatment. Nevertheless, if for special
reasons the owner wishes to keep the animals for a certain time, as in
the case of a cow near its time of calving, recourse may be had to the
internal treatment suggested in acute nephritis, viz., mucilaginous
drinks, diuretic infusions, milk, bicarbonate of soda, stimulating
applications to the loins, etc.


                            HYDRO-NEPHROSIS.

Hydro-nephrosis, _i.e._, retention of urine in the pelvis of the kidney
and in the collecting and secreting tubules, is a somewhat common malady
of the bovine species. It is usually confined to one kidney.

[Illustration: $1]

=Causation.= Anything which obstructs the discharge of urine through the
ureters may cause hydro-nephrosis. Thus, vesical tumours pressing on the
orifices of the ureters, calculi which have become fixed in them,
torsion or “kinking” of the ureters, may bring about hydro-nephrosis.
The urine secreted by the kidney being unable to escape, accumulates in
the pelvis of the kidney, in the ureter, and uriniferous tubules,
producing dull colic, which escapes observation, or the exact cause of
which is not discovered, because the second kidney vicariously acts for
the one affected, and urination continues regularly. Secretion
continuing in spite of the obstruction, that portion of the ureter above
the obstructed point, together with the pelvis and the uriniferous
tubules, gradually becomes dilated, until the whole mass of the kidney
is hypertrophied.

The ureter sometimes becomes enlarged to the size of a man’s arm, the
kidney double, treble, or quadruple its normal side: the interlobular
divisions are lost, and each circumscribed lobule soon forms a cystic
cavity varying in size. The pressure due to the accumulated urine causes
the renal tissue, first the medullary substance and afterwards the
peripheral zone, to undergo atrophy.

The kidney is represented by a vast cystic cavity, and the lobules by
culs-de-sac; the cortical layer may become atrophied to such a degree as
to form merely a fibrous sheath, the primary constituent elements of
which are difficult to discover. From 20 to 40 pints of liquid may
sometimes be found in the cystic kidney.

=Diagnosis.= The condition is rarely diagnosed, because, as one of the
kidneys continues to act, no acute disturbance follows. Only in cases
where the cystic kidney projects into the flank are suspicions aroused.
Examination per rectum will then permit of the diagnosis being made.

=Prognosis.= Hydro-nephrosis being, as a rule, unilateral, the prognosis
is not very grave as regards immediate danger. As the condition is
hopeless, however, the lesions being irreparable, the animal should be
prepared for slaughter.

=Treatment.= Practically there is no treatment. Puncture of the cystic
cavity or even the removal of the hydro-nephrotic kidney certainly
suggests itself, but, as such operations are usually opposed to the
interests of the owner, they are rarely or never practised.


                      INFECTIOUS PYELO-NEPHRITIS.

[Illustration: $1]

The term “infectious pyelo-nephritis” describes an inflammation which
may involve any portion of the mucous membrane of the urinary tract, and
which is produced by a special bacillus. As a rule, this inflammation
commences in the mucous membrane of the calices and pelvis (pyelitis).
It afterwards extends into the depths of the uriniferous canaliculi
(nephritis), but in grave and old-standing cases the mucous membrane of
the ureters and the bladder may also be affected. The disease had long
been known in France (Rossignol, 1848). It was afterwards described in
Germany (Siedamgrotsky, 1875; Pflug, 1876), in Switzerland (Hess, 1888),
and also in France (Lucet, 1892; Masselin and Porcher, 1895).

=Causation.= Female animals are more frequently affected than males,
because the lesions are produced by an ascending infection, originating
very frequently in genital infection after delivery. Nevertheless,
calculus formation is also an important factor in producing the disease.

Many different agents are capable of producing pyelo-nephritis. Hofflich
in 1891 described a bacillus about 2 to 8 micromillimètres in length,
which stained readily with aniline colours and with Gram solution. Lucet
in 1892 found a short bacillus which did not stain with Gram, and later
another thin bacillus which did. Kitt has described cocci, but no other
organisms. Masselin and Porcher discovered a cocco-bacillus which
stained with Gram and reproduced the disease in an animal lent by
Moussu, after a single intra-vesical injection of the culture. Cadéac
has met with staphylococci, and Moussu has discovered various bacilli,
some resembling the colon bacillus, and pyogenic streptococci.

There is no doubt that many different organisms may produce
pyelo-nephritis by ascending infection. The most common seem to be forms
of paracoli, such as the _Bacillus ureæ_. Moussu nevertheless believes
that Hofflich’s bacillus, which was rediscovered by Porcher, is that
which produces typical pyelo-nephritis. It grows in the bladder without
producing cystitis, and is succeeded by an ascending infection of the
ureters without causing primary ureteritis, the local inflammation
occurring chiefly, it would seem, in the pelvis and the kidney. All the
other organisms which Moussu has tested have caused lesions of cystitis
and of ureteritis, together with those of pyelo-nephritis.

In these latter cases the pyelo-nephritis assumes the acute form, and is
accompanied not infrequently by cellulitis and abscess formation in the
tissue around the kidney.

=Symptoms.= Pyelo-nephritis develops in one of two principal forms, the
slow chronic form, which is the most frequent, or an acute or subacute
form, much more rapid in its development.

The chronic form for a time escapes notice. There is no doubt that at
first some general disturbance occurs, such as diminution of appetite,
disturbed nutrition, unhealthy general appearance, staring of the coat,
tightness of the hide, wasting, etc., but such symptoms are in no wise
characteristic, being found in all grave diseases.

The signs only become really significant from the clinical standpoint
when the urine appears modified in character, and such modification does
not occur until the pelvis of the kidney and the kidneys themselves are
already gravely diseased.

The urine is then turbid, of a brownish colour, and charged with
sediment, filaments of mucin, pus corpuscles, and earthy phosphates. On
analysis it is found to contain more or less albumen.

At a late stage it may even become glairy, blood-stained, or of the
colour of blood, and when the pelvis or the calices of the kidney are
ulcerated may, on standing, deposit considerable quantities of red blood
corpuscles.

[Illustration: $1]

Exposed to the air, the urine rapidly assumes a brown tint and smells
strongly of ammonia.

Percussion of the loins in the region of the kidneys causes pain, as
does external palpation by the flank. On rectal examination at this
period the ureters are found to be distended and hard, and they give the
impression of rigid or bosselated fibrous cords, sometimes as large as a
child’s arm. The corresponding kidney, often both kidneys, are enlarged,
sometimes to double or treble their normal volume, and are painful on
pressure and fluctuating, at least in the region of the pelvis. On
vaginal examination the meatus urinarius is usually found to be
inflamed, rough and turgid.

In this condition the animals rapidly lose flesh, the appetite becomes
irregular, the general condition gradually gets worse, and they die as a
result of continued uro-septic fever or uræmic troubles.

The acute form takes a much more rapid course, with fever, more marked
general disturbance, acceleration of pulse and breathing, the passage of
turbid and sometimes purulent urine with a strong ammoniacal smell.
Pyo-nephrosis is the most frequent and characteristic end. Ordinary
chronic pyelo-nephritis may also occur in these cases, and the acute
course may be determined simply by accidental ascending infections.

=Diagnosis.= During the early stages diagnosis is extremely difficult,
unless a careful examination of the urine be made. Afterwards it becomes
easy, the appearance of the urine and the indications furnished by
rectal exploration being perfectly characteristic. In very exceptional
cases there may be some doubt, as where the urine remains normal, in
spite of hydro-nephrosis, or where there is old-standing hæmaturia or
renal tuberculosis. In simple hæmaturia the lesions are confined to the
bladder and ureters, the kidneys not being affected, and in renal
tuberculosis the diagnosis can always be confirmed by the use of
tuberculin.

=Prognosis.= The prognosis is extremely grave, for the lesions produced
are irreparable, and, moreover, local intervention is impossible.

=Treatment.= There is no curative treatment. All that is possible is
palliative treatment with the object of facilitating the function of the
kidney and of disinfecting the urinary passages by administering
antiseptic substances which are excreted by the kidney. It is not
possible, however, to administer active drugs of this kind (_e.g._,
combinations of carbolic acid). As the kidney acts badly it soon ceases
to eliminate such substances, and the condition would not be improved,
but aggravated.

Benzoate of soda in doses of 2 to 2½ drachms per day dissolved in
diuretic liquids is the most useful drug, and sometimes holds the
disease in check for a sufficient time to allow of the animals being
fattened.

Treatment also comprises certain prophylactic precautions. As the
infection which produces pyelo-nephritis originates in the genital
tract, it is desirable to protect all animals in a receptive condition
(those about to calve or having recently calved) from infection; hence,
when the disease is detected in a cow-shed, the patients should be
isolated, and the shed thoroughly disinfected.


                SUPPURATIVE NEPHRITIS AND PERINEPHRITIS.

Suppuration of the kidney may occur under two conditions. In the
majority of cases such suppuration occurs as a complication of
pyelo-nephritis; less frequently it is the consequence of infection from
within or infection of adjacent parts, leading to the formation of an
abscess.

When it results from an ascending infection the kidney becomes swollen,
congested and inflamed, and soon displays localised minute hæmorrhages.
Pus then forms within the calices, in the large straight tubes, and
diffuse suppuration invades all the uriniferous tubules. The enlarged
kidney is yellowish, firm under the knife, and when sections are
compressed pus exudes from the openings of the tubular canaliculi.

When suppurative nephritis has resulted from accidental infection of
internal origin, an abscess is found to have produced more or less
extensive atrophy of a portion of the kidney while not affecting the
rest of the organ.

It is only in those favourable cases where the renal abscess opens into
the pelvis that suppuration may invade the whole of the kidney,
producing diffuse suppurative nephritis by secondary infection of the
uriniferous tubules. Such complications are rare. Usually the abscess
empties through the pelvis, and recovery may occur.

More frequently suppurative pyelo-nephritis develops, together with
ureteritis, cystitis, dilatation of the ureters, dilatation of the
pelvis of the kidney, and dilatation of the collecting tubules of the
pyramids, the final stage resembling the lesions of pyo-nephrosis.

Perinephritis and perinephritic cellulitis, _i.e._, inflammation with or
without abscess formation in the connective tissue and adipose layer
surrounding the kidney, always occur in cases of suppurative nephritis
or pyelo-nephritis. Such inflammations may also, in exceptional cases,
follow direct mechanical injury, but they almost invariably represent
complications, the organisms infecting the kidney passing through the
tissues and the layer of fibrous tissue, or extending by the lymphatic
paths, finally attaining the fatty tissue surrounding the kidney and
there undergoing multiplication. The fatty tissue is infiltrated with
reddish serosity, is inflamed, and may become the seat of large
abscesses communicating with or separate from the abscesses of the
kidney itself.

=Symptoms.= Suppurative nephritis is characterised by fever, loss of
appetite, arrest of rumination, and frequent attempts to urinate. These
attempts are painful, are accompanied by groaning, and end in the
passage of an insignificant quantity of blood-stained and purulent
urine.

Palpation, more especially palpation of the right flank, percussion over
the region of the loins, and examination of the kidneys through the
rectum are painful. Wasting is rapid.

If the suppurative nephritis develops rapidly, and particularly if it be
accompanied by perinephritis, the patients refuse to rise and appear to
be suffering from paraplegia, although not really so, both sensation and
motor power persisting in a greater or less degree. Probably the
condition is accompanied by reflex pain and irritation of the nerve
trunks of the lumbo-pubic plexus.

On the other hand, when suppurative nephritis tends to develop slowly
and assume a chronic form, lesions of pyo-nephrosis gradually develop,
and are identical in appearance with those of hydro-nephrosis, except
that the ureters, the pelvis and the dilatations corresponding to the
lobules, are filled with pus.

[Illustration: $1]

=Diagnosis.= The diagnosis is not very difficult. The urinary trouble
and the composition of the urine itself always arouse suspicion. The
diagnosis is confirmed by careful and methodical examination _per
rectum_; the inflammation of the fatty tissue surrounding the kidney can
usually be detected.

=Prognosis.= The prognosis is extremely grave, and almost always fatal,
particularly in cases of diffuse nephritis.

=Treatment.= No curative treatment can be absolutely relied on.
Treatment, if attempted, is limited to the methods suggested for
pyelo-nephritis. Mucilaginous, emollient, and diuretic drinks, and daily
doses of 2 to 3 drachms of benzoate of soda given in the drinking water,
cause some improvement.

[Illustration: $1]

Stimulation of the region of the loins also undoubtedly has a favourable
effect, and should always be practised, particularly where perinephritis
is developing. It may check the course of the disease and prevent the
formation of abscesses. On slaughtering animals suffering as above
described the layer of tissue surrounding the kidney is found to be
lardaceous and fibro-fatty.

Any treatment through the bladder is contra-indicated, for even the
passage of a catheter may cause severe injury of the urethra or the
vesical mucous membrane and produce a fatal aggravation.

If these conditions are diagnosed early, while the function of the
kidney is more or less preserved, and if the animal is still in good
condition, it should be slaughtered.


         THE KIDNEY WORM (SCLEROSTOMA PINGUICOLA) OF SWINE.[7]

Footnote 7:

  From Report of the U.S.A. Bureau of Animal Industry, 1899, p. 612.
  (Louise Taylor.)

In the United States of America a worm is frequently found in the fat
surrounding the kidneys of pigs, and is supposed by farmers to be the
cause of paralysis of the hind limbs.

This so-called kidney worm of hogs (_Sclerostoma pinguicola_) should not
be confounded with the kidney worm (_Dioctophyme viscerale_) of dogs and
man. Both of these parasites belong to the same zoological family
(Strongylidæ), but to different subfamilies and genera. The kidney worm
of dogs grows to a length of 1 to 3 feet. The kidney worm of hogs is
much smaller, attaining at most something less than 2 inches in length.

[Illustration: $1]

The body of the worm is plump, mottled in color—red, yellow, white,
black—according to the organs visible beneath. The average female is
about 37 mm. and the average male 32 mm. in length. The worms seem to
occur in pairs, usually in cysts or canals; thus, upon the examination
of two kidneys with their surrounding fat, fifteen specimens were found,
seven males and eight females. The connective tissue layers between the
fat were found to be the most general seat of infection, and the cysts
were numerous and closely packed together. Although a cyst usually
contained two worms, a male and a female, sometimes three were found
together, two females and one male, or just as often one female and two
males. The cysts contained pus, which bathed the parasites, and in which
were thousands of eggs in the segmentation stage. Still, other cysts,
upon being cut into, were found without parasites and in a necrotic
condition.

It will be noticed that _Sclerostoma pinguicola_ is colloquially known
as the kidney worm. In no case, however, has Miss Taylor found it in the
kidney substance, but only in the tissue surrounding this organ; the
lard appears to be its _normal_ habitat, at least.

Just how the eggs leave the kidney fat or enter the bodies of fresh hogs
has not been demonstrated, but it does not seem unreasonable to suppose
that they eventually find their way out with the urine. Indeed, Dean
reports eggs found in the urine. From analogy one is led to believe that
no intermediate host is required, but that in all probability the
embryos develop for a short time in water, casting several skins, and
they eventually gain access to the hogs either through contaminated
drinking water or food.

Because of the hog’s habits, it is difficult to see any practical
measures which can be adopted to prevent infection. Feeding from troughs
and supplying plenty of pure drinking water will decrease but not
exclude the disease. Leuckart’s advice to the Germans, “Swine should be
kept in a less swine-like manner,” holds good in all countries and in
connection with all diseases. It is equally impossible to suggest
practical methods of treatment. This is all the more true because it
seems probable that a number of distinct complaints are popularly
grouped together by the farmer as kidney-worm disease.




                               CHAPTER IV
                           GENITAL APPARATUS.


=Semiology.= The examination of the genital apparatus properly so called
is easy in animals of large size, whether male or female, but is more
delicate and difficult, and is sometimes partially impossible, in small
creatures.

In male animals it comprises the examination of the testicles by
inspection and palpation, of the vas deferens, and of the intra-pelvic
genital organs (vesiculæ seminales, prostate, etc.).

Inspection and palpation of the scrotum reveals hypertrophy, atrophy,
œdematous or sanguineous infiltrations, inflammation of the tunica
vaginalis, and tumours of the testicle. Intra-pelvic examination partly
covers the same ground as examination of the pelvic portion of the
urethra, and, provided the anatomical relationships of the different
organs encountered are known, there is no difficulty in detecting the
position of possible lesions (Fig. 226).

In small male animals, such as he-goats and rams, rectal exploration is
confined to the use of one or two fingers.

In female animals examination comprises inspection, intra-vaginal
examination, and rectal examination.

Inspection reveals lesions of the vulva and clitoris.

Vaginal examination with the hand establishes the condition of the walls
of the vagina, the neck of the uterus, and the vaginal culs-de-sac.

If a lesion is detected, its character can easily be ascertained by
means of a speculum, which exposes the base of the vagina, the
prominence formed by the uterus, or any particular part of the vagina
itself. Examination with the speculum is the only useful method in young
female animals, heifers in particular, on account of the narrowness of
the genital tract.

In small female animals, such as she-goats, ewes and sows, the fingers
alone can be employed.

As regards examination of the uterus, the direct method gives little
exact information, and examination by the rectum is to be preferred. By
passing the arm into the rectum and gently pressing downwards towards
the base of the pelvis, the hand can be brought in contact with the body
of the uterus, which can be moved and displaced from right to left; the
horns of the uterus can be felt and followed from the body of the uterus
as far as the Fallopian tubes and the ovaries. By this means the state
of the uterus, its degree of sensitiveness and mobility, as well as the
state of the Fallopian tubes and of the ovaries, can all be ascertained.
The examination also reveals the existence or non-existence of
gestation, during which the uterus becomes hypertrophied and is
displaced in a forward direction towards the right flank, at the same
time descending in front from the base of the pelvis over the abdominal
wall and under the mass of the intestinal convolutions.

[Illustration: $1]


                               VAGINITIS.

Inflammation of the vaginal conduit may be primary or secondary. It
usually follows difficult parturition, but may occur under various
circumstances. From the clinical standpoint three varieties are
distinguished: simple or contagious acute vaginitis; croupal vaginitis;
and chronic vaginitis.


                            ACUTE VAGINITIS.

=Causation.= Deep-seated genital injuries leading to metritis, excessive
and prolonged strains due to painful labours, accidental injuries caused
by obstetrical operations, etc., are followed by more or less acute
vaginitis.

Suppurative inflammation of Gartner’s canals, irritant and caustic
injections, and foreign bodies likewise cause local irritation, which
may become complicated by infection and eventually produce vaginitis.
The infective organisms may be numerous and varied.

=Symptoms.= The vagina being closed to external inspection, the symptoms
are not very apparent. At first, acute vaginitis is suggested by
swelling of the vulva, pruritus, and dysuria. The lips of the vulva are
œdematous, injected, sensitive and of a brownish-red or violet-red
colour on the internal surface. Sometimes they are excoriated and torn.

The period of full development is accompanied by the escape from the
vulva of a serous, mucous, muco-purulent or purulent discharge of
varying odour. Urination is painful and defæcation difficult.
Examination of the vagina by means of a speculum shows the mucous
membrane to be excoriated, ultra-sensitive, ulcerating or suppurating at
certain points. The parts are hot.

The general symptoms are little marked, and without importance. The
usual termination consists either in recovery, which may be spontaneous,
or in passage to the chronic form.

The =diagnosis= is easy, and the =prognosis= favourable, provided the
vaginitis has not been caused by severe mechanical injuries, capable of
setting up cellulitis or the formation of deep abscesses of the pelvis.

=Treatment.= One of the principal reasons why vaginitis persists is the
retention of morbid products in the vaginal culs-de-sac. Treatment ought
therefore to aim chiefly at removing these by soothing, astringent, and
antiseptic injections. Soothing injections should first be tried. They
consist of lukewarm water at body temperature, decoctions of
black-cherry bark, poppy-heads, linseed, etc. After a few days, when the
excessive sensibility has disappeared, antiseptic and astringent
solutions may be used, such as crystallised alum, 150 grains to the
pint; sulphate of zinc, 75 grains to the pint; carbolic acid, lysol,
cresyl, etc., 150 grains to the pint.

Injections of permanganate of potash of the strength of 150 grains to
the pint and of solutions of iodine at a strength of 1 in 2,000 are more
active, but require more careful handling. Hydroxyl diluted with from 3
to 5 parts of water is also of great efficacy. Strong solutions should
never be used, because they cause irritation and expulsive efforts.

All these injections may be made without difficulty by passing a simple
perforated drainage tube to the end of the vagina, and connecting it
with a syringe, or, better, with a small cistern hung from the wall,
which allows the required pressure to be obtained.

When there are deep and severe wounds, the parts should be washed out
once or twice daily and the vagina should be packed with surgical wool
and iodoform gauze. The septic liquids are absorbed by the dressing,
which acts continuously. This dressing is renewed until recovery takes
place.


                         CONTAGIOUS VAGINITIS.

During the past few years certain observers have described a disease
which has been termed “contagious vaginitis,” in consequence of the
facility with which it is transmitted.

This vaginitis may be transmitted by copulation, the bulls then serving
as propagators of the disease. The bulls themselves are usually affected
with balanitis.

The causative agent of the disease is unknown.

This contagious vaginitis is characterised by all the symptoms of acute
vaginitis, and it is only from the fact of its appearing in all the
animals served by one bull that its contagious character is established.
A short time after service the vulva appears swollen and extremely
sensitive; at the same time general disturbance appears, viz.,
diminution of appetite and of milk secretion, slackening of rumination,
etc.

Vaginal exploration, which is somewhat difficult, reveals a
papulovesicular eruption, accompanied by a muco-purulent discharge.

This vaginitis is easy to diagnose. It may disappear spontaneously, and
the treatment differs in no respect from that of ordinary acute
vaginitis.


                           CROUPAL VAGINITIS.

Croupal vaginitis is a form of acute vaginitis, from which it is
distinguished by the formation of false membranes resembling those of
diphtheria over the whole of the vaginal mucous membrane.

It was described by Baumeister. Moussu has only seen one case, and that
at a period which rendered recovery out of the question.

=Symptoms.= The external symptoms are those of acute vaginitis, with
greyish, fœtid, purulent or sanguinolent discharge. On examination, the
mucous membrane is found to be covered with yellowish, greyish false
membranes, and with vegetations of a greyish, dirty, verrucous
appearance. The entire extent of the vaginal mucous membrane may be
attacked, together with the neck of the uterus. In Moussu’s case the
uterus itself was entirely invaded.

These false membranes and vegetations are very adherent, and bleed
freely at the slightest touch. They are apt to extend by degrees.

The cause of this infection has not yet been determined. It appears to
obtain access to the parts during parturition, and develops insidiously
for a week or two, when widespread lesions have already formed.

=The diagnosis= is extremely easy.

=The prognosis= is grave, for the lesions have a tendency to extend
towards neighbouring organs. Moreover, the general health is severely
affected; there is rapid wasting, loss of appetite, and continued fever
and death occurs from exhaustion, intoxication, and possibly infection.

=Treatment.= The treatment suggested for the ordinary acute forms
appears to be useless in this condition. The new membranes show too many
folds, depressions, and accidental culs-de-sac for simple injections to
have any real effect. Better results might be expected from packing with
antiseptic gauze or from the use of antiseptic ointments applied after
washing out the cavity with permanganate of potash solution or hydroxyl.

Curettage, followed by the use of gauze dressings, might also be tried;
considerable difficulty must necessarily be anticipated in operating in
a cavity which has become inextensible and partly filled with
vegetations and false membranes.


                           CHRONIC VAGINITIS.

Chronic vaginitis usually represents the last stage of some form of
acute vaginitis, though it occasionally develops in a slow and
progressive fashion as a primary condition in consequence of some
deep-seated genital lesion. There is usually a constant discharge of
irritant material.

The symptoms are not very striking, and are purely local.

Externally all that can be detected is a continuous or, much more
frequently, an intermittent muco-purulent discharge from the vulva,
which occurs only on urination, defæcation, coughing, etc.

Locally, examination with a speculum discloses the fact that the mucous
membrane is of a greyish colour, thickened, less yielding than usual,
and in places sclerosed. The entire thickness of the mucous membrane is
affected, as also at times the muscular tissue, chronic irritation
having caused sclerosis.

The =diagnosis= is very simple, and the =prognosis= of no particular
gravity, because the animals can always be fattened. The condition is
only grave as regards animals intended for breeding.

=Treatment= is often very successful, but, as in all chronic diseases,
it extends over a considerable time. Practically it is not often
attempted. It does not differ greatly from that of ordinary acute
vaginitis, but the best results seem to follow the use of astringents.


                               METRITIS.

Infectious or traumatic diseases of the uterus are of the greatest
importance in bovine pathology, both on account of their frequency and
gravity. They comprise septic metritis, acute metritis, and chronic
metritis.


                            SEPTIC METRITIS.

Septic metritis is also termed “metro-peritonitis” and “parturient
septicæmia.” It may be compared with puerperal fever in woman.

These terms are sufficiently explicit to indicate that if at first the
metritis is typical it frequently becomes complicated with peritonitis,
and too often also with true septicæmia.

=Causation.= The disease only appears after parturition or abortion, and
during the few days immediately succeeding delivery. Parturition may
occur spontaneously in a perfectly regular and easy manner, and
nevertheless be followed by fatal metritis as a consequence of
infection. Usually the labour has been difficult, and the after-birth,
or portions of the fœtal membranes, have been retained. Septic metritis
then develops in consequence of their putrefaction.

Infection with microorganisms is therefore the essential cause, and the
only one of importance. None of the conditions formerly invoked can do
more than favour or check the course of this infection.

Moreover, the subsequent complications are entirely due to the special
character of the infective agent.

These infective agents may be of various descriptions. They have been
the subject of numerous investigations, on account of the gravity of
puerperal fever in woman. Pasteur, Colin, Chauveau and Doléris were the
first to take up this question. In veterinary medicine several inquiries
have been instituted, but a great deal remains to be done. The most
frequent agents are varieties of streptococci, of the colon bacillus,
and of putrefactive bacteria.

Septic metritis may occasionally be purely accidental and only affect
one animal, but infection of stables by a primary case is an obvious
cause of propagation. Moussu has seen six animals successively die of
septic metritis in one year, and in a stable which had not been
disinfected after each death.

=Symptoms.= The first symptoms occur between the first and fourth days
after parturition, when the uterine mucous membrane is still tender,
discharging and bleeding, and the lochial discharge is abundant. The
disease rarely appears after the first week. The earliest symptoms are
dulness, depression, loss of appetite, and general weakness. The animals
appear exhausted, the secretion of milk is diminished or altogether
suspended, and all the chief functions of the body are interfered with.

The temperature varies in a peculiar and significant way. In some forms,
due to infection with streptococci or to mixed infection, it rises to
104° or 105° Fahr.; in others it remains stationary or falls below
normal. It might be thought that in these latter cases, which are
usually due to infection with the colon bacillus, the general condition
was not grave. This, however, would be a very serious error, for in such
cases death follows as rapidly as in the others.

The patients, or some of them at least, have slight colic and peritonism
when the infection extends to the peritoneal pockets at the entrance to
the pelvis. At a later stage they appear prostrate, remain lying, and
seem to be suffering from paralysis of the hind quarters.

None of these general symptoms are in themselves significant, and to
appreciate them at their true value the local signs must be taken into
account.

The external genital organs are moderately swollen, the vagina is
infiltrated and sensitive, and is soiled by exudate of varied character.

The neck of the uterus is sometimes prematurely contracted after the
first or second day, constituting a troublesome complication both in
examining the parts and in treatment. When, however, it is dilated and
the hand can be passed, it is found that the uterus itself is not
contracted or is only half-contracted, and that it is filled with a
reddish-grey liquid of putrid appearance, sometimes without smell, at
others fœtid or even putrid.

The uterine mucous membrane is infiltrated, thickened, and extremely
fragile, partially destroyed, and breaks at the slightest touch. The
cotyledons may become loosened by necrosis, and accumulate in the
depression formed by the gravid horn of the uterus; otherwise they may
be detached without difficulty.

When the neck of the uterus is prematurely contracted direct exploration
gives no result, but rectal examination reveals a much enlarged uterus,
filled with liquid or distended with putrid gas.

If, however, the after-birth has not come away, fragments of fœtal
membranes may be removed from the deeper portions of the uterus or the
surface of the cotyledons.

Death is inevitable unless treatment is early initiated. The animals
succumb to infection produced by germs entering the vascular apparatus.
When the infection extends by contiguity of tissue to the peritoneal
cavity the immediate causes of death are infection and intoxication. In
cases where the infection remains localised within the uterus the animal
is poisoned by the absorption of toxins through the uterine mucous
membrane.

The condition may prove fatal in from four to six days in the cow, but
in a shorter period in the goat, ewe, and bitch.

=Lesions.= The uterus is excessively fragile, and can be torn at will.
The mucous membrane in which the microorganisms more particularly
develop appears necrosed in places. Large areas are sloughing or
ulcerated.

The vessels are thrombosed, and extensive portions of the organ may be
affected by true capillary phlebitis.

The lymphatics are dilated and distended with pus in animals which have
resisted for some days.

If there is peritonitis, the entire floor of the abdominal cavity is
affected, and sometimes the peritonitis is generalised.

The lesions in the other tissues and viscera are similar to those found
in septicæmia and in general intoxication, such as injection of the
capillary system, and interstitial extravasations of blood in the
pleura, pericardium and other tissues.

=Diagnosis.= The diagnosis of septic metritis is not very difficult,
though something more is required than simple observation of external
signs. From the clinical standpoint it is of no great importance to
distinguish between the various forms or to determine the responsibility
of microorganisms for the infection. In every case the practitioner must
utilise all the means at his disposal.

=Prognosis.= The prognosis is extremely grave, and death almost
invariably occurs when treatment is not early undertaken.

=Treatment.= Treatment should be prompt and energetic. Infection of the
genital organs being the cause of the symptoms, it is against this that
remedies should be directed. The parts should first be thoroughly washed
out with boiled water at the body temperature. A stiff drainage tube
about 6 feet in length is passed to the base of the uterus and connected
at its free end with a reservoir of liquid, which can be raised so as to
obtain sufficient pressure. During this operation the animals should be
placed with the front limbs higher than the hind.

When the liquid injected returns perfectly clear, antiseptics may be
employed. Strong solutions containing mercury, carbolic acid, lysol or
creolin should be avoided, partly because of their toxic action, but
principally because they cause irritation and violent expulsive efforts.

A 25 per cent. hydroxyl solution gives surprisingly good results. A 1 in
2,000 iodine solution (iodine 15 grains, potassium iodide 1 drachm, warm
water 4 pints) is also of very great service.

As the first irrigations are difficult to carry out thoroughly, it is
often advisable to cleanse the parts directly by means of a large
disinfected sponge, which should be passed over the whole surface of the
mucous membrane and into the depressions of the uterus, thus directly
removing septic liquids. Thereafter irrigation will be easier and more
efficacious.

This method, however, of cleansing the parts is dangerous for the
operator unless he takes the antiseptic precautions necessary in every
case of delivery.

When the neck of the uterus is prematurely contracted, the difficulties
become much greater, and are sometimes insurmountable on account of the
impossibility of dilating it. It then becomes necessary to use metallic
canulæ or uterine sounds made of aluminium in order to pass through the
neck of the uterus. Liquids can be evacuated by compressing the uterus
through the wall of the rectum, but the method is very troublesome.

This local treatment should be practised twice a day at least until all
danger is over, and may be completed by the administration of diffusible
stimulants, such as alcohol in doses of 6 to 10 ounces, acetate of
ammonia in doses of 2 drachms, wine, coffee, and diuretic decoctions.
These may be given with food or drink to whatever amount is considered
necessary if the animals still retain their appetite. The food should be
light and easily digested.

From 8 to 12 pints of physiological salt solution may be injected
intravenously every day, the temperature at which this fluid is injected
being varied according to the degree of fever. (Physiological salt
solution consists of chloride of sodium 9 parts, sterilised water 1,000
parts.)

=Prophylaxis.= Should a case of septic metritis occur in a byre
containing other cows about to calve the building should be disinfected.


                            ACUTE METRITIS.

The term “acute metritis” is used to indicate a variety of inflammation
of the uterus of a sufficiently grave character, which, however, does
not prove fatal in twenty-four or forty-eight hours.

=Causation.= In domestic animals acute metritis develops exclusively
after difficult parturition and as a consequence of the tearing of
tissues or accidental post-partum infection.

At one time it was the rule to recognise a traumatic form consequent on
wounds by embryotomy hooks, crutches, cords, etc., etc. There is no
reason for maintaining this distinction, because the essential condition
for the development of metritis is the infection of the injuries.

Acute metritis follows non-delivery, incomplete delivery, or accidental
infection.

=Symptoms.= The external signs are very few, and must be carefully
studied, in order that wrong conclusions may be avoided.

Certain of these external signs suggest general disturbance such as one
finds in all acute visceral inflammations, viz., loss of appetite,
progressive wasting, irregular slight fever, diminution or cessation of
the secretion of milk, dulness, etc.

The others are purely local. The discharge from the vagina is mucoid,
muco-purulent, sanguinolent or fœtid, according to circumstances. It is
small in quantity, and occurs only when the animal lies down or makes
expulsive efforts. Examination with the speculum reveals the existence
of slight secondary vaginitis and more intense inflammation of the neck
of the uterus, which remains half open. Rectal examination shows that
the uterus is abnormally large and more difficult than usual to
displace. If acute metritis has existed for some weeks, the uterus is
painful to the touch, and sometimes fixed in position in consequence of
the development of parametritis and of slight pelvi-peritonitis, the
occurrence of which is always indicated by temporary tympanites.

Cases of acute metritis may recover spontaneously, but they rarely do
so. The condition usually tends to become chronic or to be complicated
with peri-uterine diseases which may prove fatal.

=Diagnosis.= The diagnosis can be established without difficulty by
rectal examination and direct examination with a speculum.

=Prognosis.= The prognosis is grave, because the patients are
temporarily or permanently incapable of becoming pregnant, and because
acute metritis may be complicated with pelvi-peritonitis, phlebitis of
the intra-pelvic veins, etc.

=Treatment.= The uterus, and particularly the uterine mucous membrane,
being affected, all our efforts should be concentrated on that organ. A
careful study of the lesions shows that the glandular follicles are
infected, and with them the entire thickness of the mucous membrane. The
object to be attained, therefore, is the perfect disinfection of this
tissue. The parts should repeatedly be washed out with warm water at
blood-heat, followed by antiseptic injections containing 4 drachms of
chloral per pint; a 1 in 2,000 iodine solution or 20 per cent. to 25 per
cent. hydroxyl solution, etc. Despite such injections, the inflammation
disappears slowly and with difficulty, and when the neck is sufficiently
open it might perhaps be possible, as in human medicine, slightly to
curette the mucous membrane of the uterus and plug the cavity with
iodoform gauze.

Where, however, the neck of the uterus is so far contracted as no longer
to admit a sound or canula for irrigation, the difficulties are very
great. Nothing effectual can be done until the neck of the uterus is
dilated, an exceedingly troublesome operation.

In the forms termed “post-partum traumatic metritis” antiseptic
injections must not be made with any considerable pressure, because of
the danger of rupture; plugging the cavity with antiseptic gauze is
preferable.


                           CHRONIC METRITIS.

Chronic metritis is often the termination of acute metritis, though
inflammation of the uterine mucous membrane may assume the chronic form
from the first. All post-partum infections with pathogenic microbes may
give rise to chronic metritis, as may the various forms of cystitis,
vaginitis, rupture of the vulva, etc. Tuberculosis also leads to chronic
metritis, which is easily diagnosed by a simple bacteriogical
examination of the discharge.

=Symptoms.= Chronic metritis is accompanied by bad general health and
persistent local disturbance. The animals show a permanent muco-purulent
discharge varying in amount, or simply an intermittent discharge, which
is then more abundant and only lasts some hours or some days, but
reappears after irregular intervals. On examination the neck of the
uterus is found to be half open, slightly hypertrophied, sometimes
sensitive, and covered with vegetations.

Examination through the rectum may show the organ to be considerably
hypertrophied, sensitive, and comparatively immobile. Cases are
numerous, however, in which the examination reveals nothing very
striking.

In other cases, vaginal examination by means of the speculum reveals
nothing, except that the neck of the uterus is completely closed, and
yet on rectal examination the uterus is found to be of large size,
tense, uniformly fluctuating, and in exactly the position to be expected
were the animal pregnant. This clinical form was formerly termed
“hydrometritis,” but it would be better named “pyo-metritis,” inasmuch
as it depends on chronic metritis. The neck of the uterus remains
contracted, and the morbid products accumulate in the body and uterine
horns, which are gradually dilated. Then suddenly the uterus is seized
with reflex contractions overcoming the resistance of the neck and
expelling the contents in one jet. The discharge may continue for some
days, after which the neck again closes and the disease enters on a new
phase.

=Lesions.= The lesions affect the mucous membrane, more particularly the
glandular tissue and the interstitial tissue. From the anatomical and
pathological point of view different forms are recognised, some with
glandular and mucous atrophy, others with marked hypertrophy, the mucous
membrane being covered in some cases with vegetations and fungus-like
growths.

=Diagnosis.= From a clinical standpoint, it is only necessary to
distinguish the ordinary forms from tuberculous metritis, which latter
is of no clinical importance on account of the impossibility of
treatment.

=Prognosis.= The prognosis is grave, as in all chronic diseases.
Furthermore the animals are, for the time being, sterile and difficult
to fatten.

=Treatment.= One of the fundamental conditions of treatment is to attack
the disease locally, and it is necessary, therefore, that the uterine
neck should be dilated.

If the neck of the uterus is pervious, the parts must be washed out
daily with antiseptic solutions, after having lightly curetted the
mucous membrane with a blunt curette. Boiled water is first used, and is
followed by solutions of chloral, iodine, hydroxyl, or permanganate of
potash.

When the neck of the uterus is contracted, it must first of all be
dilated. In practice such treatment is sometimes considered too costly,
so that the animals are slaughtered or recovery is left to chance.

Moussu has seen several animals suffering from metritis, and even from
salpingitis, recover spontaneously after six to eight months at grass.


                      EPIZOOTIC ABORTION IN COWS.

This disease, which was carefully investigated, first by Professor
Nocard of Alfort, and afterwards by Professor Bang of Copenhagen, may be
regarded as a specific uterine catarrh, determined by a definite species
of bacterium.

It often affects large numbers of animals in one district or on one
farm, and causes very serious loss. It is conveyed from cow to cow
either by the bull or by litter or utensils used in the byre which have
been soiled by the uterine discharges of an infected cow. As in many
other infectious disorders, one attack of the disease seems to confer a
certain immunity, and although some cows become sterile after an attack
and others continue to abort, a certain proportion after aborting two or
three times acquire relative immunity, so that they conceive and carry
their calves the full time. This is probably why epizootic abortion
usually ceases after some years in herds which are kept isolated and do
not receive fresh recruits.

The microbe of epizootic abortion is a very small bacterium which stains
well with Löffler’s methylene blue. When massed together these bacteria
resemble cocci, but isolated specimens are seen to be true bacteria
containing one, two, or occasionally three roundish, elongated
deeply-stained granules. They do not stain with Gram, and are
non-motile.

These bacteria exhibit remarkable vitality. Bang relates cases which
seem to prove that they may exist within the uterus for at least
fourteen months, and in the uterine exudate outside the body for at
least seven months, even at comparatively low temperatures.

On _post-mortem examination_ one finds between the mucous membrane of
the uterus and the fœtal envelopes an abundant odourless exudate,
dirty-yellow in colour, somewhat thin, pultaceous, slimy, or lumpy in
character. Under the chorion is found a thin, clear, gelatinous
substance contained within the fine connective tissue lying between the
chorion and allantois. The umbilical cord is often œdematous. All these
exudates contain the specific minute bacterium.

The above exudate forms the peculiar dirty, reddish yellow, slimy,
flocculent, pus-like _odourless_ fluid which escapes from the vagina
during or immediately after the act of abortion.

The results of infection of the uterus with Bang’s bacterium may be
delayed for a considerable time. In two cases where he injected pure
cultures into the vaginæ of pregnant cows no apparent local results had
been produced at the end of thirty-three and thirty-five days
respectively when the cows were slaughtered; but in the case of two
other pregnant cows, inoculated three months after conception, signs of
abortion became apparent, and one cow in fact aborted in about ten
weeks; post-mortem examination revealed the characteristic local
changes, and microscopical and cultural preparations clearly established
the presence of the specific organism.

Although the sexual organs form the usual channel of infection, it seems
possible that the organism may in some cases enter the body through the
respiratory or digestive tract.

=The treatment= in this condition is chiefly of a prophylactic
character. Bulls which have served cows belonging to herds known to be
infected should not be allowed to cover healthy cows. They should
undergo careful local disinfection, and for a time be withdrawn from the
stud.

Cows which show signs of impending abortion should at once be removed to
a separate shed. The fœtus and its envelopes should be buried or burnt,
and the person who attends the diseased cow should be prohibited from
entering the common cow-shed.

Where space does not admit of this the affected cows should be removed
as far as possible from those still healthy and placed in a separate
row. When they abort the after-birth should be removed by hand, and the
uterus daily washed out with some non-irritant but effectual
disinfectant. Even after apparent recovery a period of probation should
elapse before the cow is again put to the bull.

The genital organs and vaginæ of the still healthy animals may also be
irrigated with a disinfectant solution, in order, if possible, to ward
off infection. For disinfecting the channels and floor of the stable
quick-lime will be found clean, non-odorous, cheap and effective.

In dealing with this disease one must always bear in mind the great
vitality of the bacterium, the relatively long time it may persist
either in the animal’s body or in the infected sheds, and the
considerable period which may elapse before its effects become evident.

The same or a similar organism seems capable of producing abortion in
sheep and mares.


                     SALPINGITIS SALPINGO-OVARITIS.

This section will be brief, because the condition is very far from
having been thoroughly elucidated. Moussu himself has only studied a
single case of simple suppurative salpingo-ovaritis.

Salpingitis and salpingo-ovaritis, _i.e._, inflammation of the Fallopian
tubes and of the ovaries, can only develop as a consequence of ascending
infection, as a complication of acute or chronic metritis, by
auto-infection during the course of tuberculosis, or as an accident
during what is known as tubal gestation.

Tuberculous salpingitis is frequent, and exists in a very large majority
of cases of genital tuberculosis. Accidental salpingitis as a
consequence of tubal gestation is extremely rare, and is usually
overlooked or mistaken for some other condition.

From the clinical standpoint, therefore, we recognise two varieties of
salpingitis—the one suppurative, the other tuberculous.

=Symptoms.= The external symptoms are similar to those of metritis,
because salpingitis develops as a complication of metritis after
parturition, abortion, or retention of the after-birth. The only
external symptom is a discharge of varying quantity from the vulva. This
may be intermittent or permanent, and it is accompanied by frequent
expulsive efforts in no respect characteristic.

The nature of the lesions is ascertained by rectal examination, and as
lesions of the uterus, of the Fallopian tube, and sometimes of the ovary
often co-exist, the examination must be carried out methodically and
gently in order to distinguish between the parts touched. The normal
relationships may be modified by uterine lesions, inflammatory
adhesions, local peritonitis, etc.

=Diagnosis.= The diagnosis requires care.

=Prognosis.= The prognosis is grave. The lesions are too deep-seated to
be directly attacked, and, moreover, salpingitis may terminate in
pyo-salpynx, _i.e._, in encysted abscess of the Fallopian tube.

=Treatment.= The treatment is similar to that of metritis. The natural
opening of the Fallopian tube into the uterus allows pus and morbid
products to escape, and when the metritis disappears the salpingitis may
diminish and recovery may take place.

Treatment therefore is quite indirect, for in veterinary surgery it is
useless to attempt to repeat on large domestic animals the brilliant
operations of human surgery. The relations between uterine diseases and
those of the Fallopian tubes are so close that this method of treatment
gives excellent results. Moussu has seen a case of chronic metritis
complicated with salpingitis recover after simple uterine treatment.


                         TORSION OF THE UTERUS.

Although torsion of the uterus is a condition more particularly
pertaining to the domain of obstetrics, a few remarks on the subject may
not be altogether out of place at this point.

The accident is commonest in the cow, but it has also been described in
the mare, ewe, bitch and cat, and it probably occurs, though less
frequently, in the other domestic animals. In the cow it is commonest
during the last month of pregnancy.

Very little is known as to its cause, though the consensus of opinion—if
any consensus can be said to exist in face of the existing divergent
views—appears rather to indicate that it follows falls in awkward
positions, sudden efforts, severe prolonged exertion, or tympanites.

In pregnant cows the uterus assumes the appearance of a pendulous organ
the body and horns of which constitute the bob of the pendulum, whilst
the ligaments represent the cords by which it is suspended. The fixed
points are formed by the insertions of the two ligaments in the
neighbourhood of the two external iliac angles.

The uterus, however, is also steadied in position by the vagina and by
the cellular tissue surrounding it; in fact, in non-pregnant animals it
can scarcely be regarded as pendulous, but rather as freely floating and
readily yielding to the movements of the surrounding organs.

As soon as the uterus is occupied by a fœtus, however, the conditions
become changed. In consequence of the increased weight of its contents
the uterus exerts a pull on the broad ligaments and sinks lower in the
abdominal cavity. The vagina and the surrounding connective tissue are
rendered tense to a degree depending on the increasing weight of the
calf. The uterus then more closely resembles a pendulum, the bob being
represented by the fœtus and its envelopes. The suspensory apparatus can
be divided into three parts, viz., the two broad ligaments and the
tissue connecting the uterus to the vagina.

The pull on the vagina increases greatly as soon as the gravid uterus is
twisted either to the right or left, for, torsion being attended with
more or less extensive displacement towards the lower abdominal wall,
the tension on the vagina must become more marked.

Considering now how the spiral folds and the constrictions which are of
such importance in diagnosis are formed, we find that both structures,
viz., the wall of the uterus and the ligaments, are implicated, though
to different degrees. Whilst the spiral folds are more particularly
formed by the wall of the uterus, the broad ligaments are chiefly
responsible for the constrictions, though to some extent the spiral
folds also contribute to their production. The spiral folds of the body
of the uterus are formed solely by twisting of its own walls. This can
easily be shown by taking any tubular organ whose walls are not too
rigid, and twisting it round its horizontal axis.

The broad ligaments contribute less to the formation of the spiral
folds, though they play a more important part in producing constrictions
and thus in compressing the wall of the uterus.

=The symptoms= are ill-defined. Sometimes there is difficulty in
micturition, but as a rule little evidence exists of any abnormal
condition until the advent of labour pains. The first pains, which are
usually feeble and separated by rather long intervals, are succeeded by
colic. The succeeding efforts steadily become more violent and frequent,
but the “water-bag” fails to appear, and in a period varying between
twelve and forty-eight hours the pains subside. Rumination is at first
suspended, the pulse and respiration are accelerated, and the surface
temperature is irregular.

If treatment is not undertaken similar symptoms, but of exaggerated
intensity, may again appear in from one to six days. Failing relief
death always follows after a varying interval.

=The diagnosis= is not difficult, provided the maternal passages be
examined. On passing a carefully lubricated hand into the vagina the
operator discovers, at a varying distance from the os uteri, signs of
collapse and twisting of the canal. In cases of quarter twist it is
often possible, by rotating the hand so as to follow the spiral folding
of the vagina, to introduce the fingers as far as the os uteri; but in
half or complete rotation only one or two fingers can be passed so far,
or it may be altogether impossible to reach the os.

In the _Berliner Archiv_ for 1902 Lempen gave a summary of the extensive
literature dealing with this disease and of the varying views held
regarding its origin and treatment, particularly as to the direction in
which the animal should be rolled in order to reduce the torsion.

In common with the majority of authors, Lempen rightly concluded that
the rolling should be in the same direction as the torsion. He also
proposed to describe the torsion as being to right or left, according to
the direction of the spiral folds to be found on the upper wall of the
dilated cervix uteri when the examiner stands behind the animal. This
mode of describing the changes seems least likely to cause
misunderstanding.

In describing the degree of torsion Haase takes as his index the upper
wall of the uterus. Where this has moved through an angle of 90 degrees
he speaks of quarter torsion; when through an angle of 180 degrees (in
which case the upper wall will have become the lower) of half or
semi-complete torsion; when through an angle of 270 degrees as
three-quarter, and when through 360 degrees (the upper wall having then
described an entire circle and returned to its former position) as
complete torsion.

In forming a diagnosis, the extent to which the maternal passages seem
fixed in position, the amount of resistance they offer to the hand, and
the degree of tension in the spiral folds to some extent indicate how
far torsion has proceeded. Where the spiral folds are very tense and the
passages completely immovable, so that the operator cannot reach the
fœtus, torsion is usually complete; in cases of less complete torsion
(one-quarter to three-quarters) the cervix uteri is closed and displaced
to a proportionate extent, and the resistance to the passage of the hand
is in keeping.

=The prognosis= is very grave.

=Treatment= is difficult, and of the numerous methods suggested
(laparotomy and direct abdominal taxis, vaginal hysterotomy followed by
abdominal taxis, vaginal taxis, etc.) most have fallen into desuetude or
are looked on as of so desperate a character as only to be justified in
extreme cases. That which most merits attention and has been attended by
most uniformly favourable results consists in the rotation of the
animal’s whole body. The best results are said to be obtained by casting
the animal, or causing it to lie down, on a sloping surface with the
hind quarters higher than the fore and then to roll it down hill, in the
same direction as the spiral twists discovered in the vagina. It is
possible to follow the course of the manipulation by retaining the hand
in the vagina, but failing this the vagina should be examined after each
attempt. Even, though the first attempts fail hope should not be
abandoned, for Haase has succeeded in effecting delivery after rolling
the animal _twenty_ times. The operation should be performed smartly and
the animal’s body be rolled as a whole, the fore limbs turning along
with the hind.


                         TUMOURS OF THE UTERUS.

The study of tumours of the uterus is still so incomplete that it would
be impossible to give a precise description of them. This is to a great
extent due to the fact that as treatment is difficult the animals are
usually slaughtered as soon as an assured diagnosis can be given.

The general =symptoms= of tumours of the neck, body, or horns of the
uterus resemble those of chronic metritis, viz., permanent or
intermittent discharge from the vulva, wasting, expulsive efforts,
dysuria and sterility. The position of the tumour, its form, point of
insertion, size, consistency, mode of attachment, etc., can be detected
by vaginal or rectal examination.

The diagnosis having been made, the only question is as to =treatment=.
Should the tumour prove mobile, clearly delimited, and with a
well-marked pedicle, it can be removed either by tearing away or by
breaking into fragments, or again simply by dividing the pedicle and
applying antiseptic pads to check bleeding. But if the tumour proves
largely sessile and ill-defined and it extends into neighbouring tissues
the animal should be slaughtered, as such patients can neither be
fattened nor used for reproductive purposes.


                         TUMOURS OF THE OVARY.

We might repeat in regard to tumours of the ovary what has just been
said as regards those of the uterus, though the former are much commoner
than the latter.

Clinically, ovarian tumours may be grouped under two heads, solid
tumours and cystic tumours—the first represented by the fibromata,
fibro-sarcomata and epitheliomata, the second by uni- or multi-locular
cysts.

All these tumours are dangerous; they may develop rapidly, and they
rarely fail to produce disturbance, the animals presenting various
genital troubles, among which may be mentioned sterility and
nympho-mania.

The cystic tumours, which develop at the expense of epithelial
invaginations of the peritoneal covering or at the expense of Pflüger’s
tubes, and not, as was formerly believed, by the morbid development of
the Graafian vesicles, constitute dangerous growths, true
cysto-epitheliomata or cystic epitheliomata, capable of producing fatal
complications (vascular disturbance, local or general peritonitis,
compression of the ureters, etc.).

=The diagnosis= must be arrived at by vaginal and rectal examination. It
is usually possible to distinguish the condition from disease of the
kidney, bladder, or pelvic lymphatic glands.

=Treatment.= The only possible treatment is removal of the diseased
ovary and of the ovarian tumour, but much depends on circumstances. If a
large tumour has formed extensive adhesions, ablation may be
impracticable or so dangerous that under the circumstances in which
veterinary practitioners are forced to operate it cannot be undertaken.
If, on the contrary, the ovarian growth is free and pedunculated, even
though of large size, extirpation is possible.

The method is exactly similar to that of castration of the cow, and
follows the same rules, but the vaginal incision has to be much longer,
so as to allow the entire hand to be passed as far as the tumour. The
pedicle is divided by means of the _écraseur_, which should be worked
very slowly. In removing very large tumours, however, it is possible to
operate from the flank.


                         GENITAL MALFORMATIONS.


                          IMPERFORATE VAGINA.

Many forms of genital malformation occur, but only those which produce
sterility are pathologically important.

One alone causes very marked disturbance, viz., imperforate vagina. This
condition may be accidental or acquired, and may follow either difficult
parturition, with circular lesions of the vagina, or burns or
cauterisation of the vagina, followed by adhesion of its walls.

It is generally of congenital origin, and the obstruction as a rule is
in the region of the hymen, as a consequence of some anomaly in
development, and not of abnormal development of the hymen itself.

This imperforate condition of the vagina is not attended by grave
consequences during early life; but later, when the generative functions
become active, all the products of secretion of the uterine and vaginal
mucous membranes accumulate in the closed cavity, giving rise first to
muco-metritis, then to muco-kolpitis, similar in its development to the
hæmato-kolpitis of young girls. The uterus gradually becomes distended
with liquid, the neck is dilated, and a portion of the vagina may attain
enormous dimensions, so much so as to suggest pregnancy.

=Symptoms.= The symptoms become appreciable only after a time—about one
year or fifteen months in heifers—and they seem to be associated with
the appearance of œstrum. The animals make continued expulsive efforts,
which when the genital canal is much distended may become extremely
violent. There is also dysuria as a consequence of compression, together
with uterine and vesical colic, loss of appetite and wasting.

=Diagnosis.= The diagnosis requires care, and can only be arrived at
after examination of the vagina and examination per rectum. In young
females this examination is extremely difficult, because of the
narrowness of the genital tract and of the rectum. For vaginal
examination we prefer to use a small speculum, which exposes the depths
of the vagina or the transverse septum without necessitating other
manipulation. On rectal examination the uterus and vagina are sometimes
found to be enormously enlarged, and to contain a quantity of fluid, but
no fœtus.

[Illustration: $1]

=Prognosis.= The prognosis is grave. Unless treatment is undertaken the
animals die in consequence of exhaustion or secondary peritonitis.

=The treatment= is simple, and consists in aseptic puncture of the
septum and evacuation of the contents. The operation is carried out with
a long, large-sized trocar, which is passed through the centre of the
most prominent portion of the transverse septum where it projects
towards the vulva. Five, ten, or fifteen quarts of mucous fluid escape,
and the constitutional disturbance disappears almost instantly.

Antiseptic precautions are necessary in order to avoid the development
of secondary pyo-metritis. The artificial orifice can afterwards be
gradually dilated to allow free exit to the discharges, but in practice,
as the animals cannot be used for breeding purposes, they are usually
fattened for slaughter.


                             NYMPHO-MANIA.

The term “nympho-mania” is employed to describe a special condition in
female animals which is manifested by continual sexual excitement. The
animals are almost always sterile. The disease is most frequent in cows.

=Causation.= This general condition may depend on one of many causes,
but is rarely due to a true neurosis, as was once believed. Some morbid
influence of genital origin is always responsible for the appearance of
the symptoms.

Nympho-mania, therefore, often co-exists with lesions of the ovaries
(simple ovaritis, cystic ovaritis, tumours of the ovary), with lesions
of the Fallopian tubes and of the uterus (salpingitis, chronic metritis
and tumours of the uterus), with chronic vaginitis and lesions of the
clitoris (hypertrophy and tumour formation), and even with peri-vaginal
or peri-uterine lesions (cysts or tumours).

In exceptional cases it may be found occurring as a simple nervous
disturbance without genital lesion, and it would then appear to be due
to some temporary genital affection having produced nervous irritation.

In short, nympho-mania may be considered as almost invariably the result
of a genital lesion.

=Symptoms.= The symptoms are very clearly marked. They consist in
persistence of the sexual appetite, which is quite abnormal in female
domestic animals. The patients lose flesh, feed badly and irregularly,
annoy their fellows, cause accidents, and sometimes become dangerous.

=Diagnosis.= The diagnosis of nympho-mania is so simple that the
condition is generally recognised by the owners or cow-herds. The only
difficult point lies in discovering the exact cause. Complete
examination of the genital organs per rectum and per vaginam is
absolutely necessary to settle this question.

=Prognosis.= From an economic standpoint the prognosis is generally
grave.

=Treatment.= The treatment varies considerably, according to the nature
of the lesion.

In mild cases where nympho-mania is due to some lesion of the clitoris
(balanitis, hypertrophy, or tumour formation), the radical treatment
consists in clitoridectomy. The operation is comparatively slight, the
organ being removed with forceps and scissors, or with a bistoury after
the animal has been hobbled or placed in a trevis. The hæmorrhage which
follows removal of the clitoris is of little importance, and
after-treatment simply consists in keeping the parts clean.

Animals so treated can sometimes be preserved for breeding.

[Illustration: $1]

When nympho-mania co-exists with, and is a delayed consequence of,
either chronic vaginitis or metritis localised in the neck of the
uterus, or, again, chronic metritis of the cavity of the uterus, etc.,
the treatment must be directed against these diseases, and the nervous
condition may be sufficiently modified to render the animals useful for
breeding, or at least for slaughter, while fattening is easy.

Similarly, when the nervous condition results from a lesion of the
ovary, improvement will only follow removal of the diseased part. The
operation is similar to that of castration of the female. It presents,
however, certain added difficulties, in consequence of the size of the
organs and of the abnormal adhesions which often occur. Nevertheless,
these difficulties are seldom insurmountable.

In the case of peri-uterine disease operation is difficult, and it is
better to slaughter the animal.

Finally, as may occasionally happen, should there be no congenital
lesion capable of explaining the appearance of nympho-mania, the disease
may be regarded as a neurosis, and may then be treated by such sedatives
as the bromides of potassium, sodium and strontium, in doses of 2 to 3
drachms per day, divided into two or three portions. Bromide of camphor
also gives excellent results by acting simultaneously on the nervous
system and calming excessive genital irritation.

The above method of treatment is much preferable to performing
clitoridectomy, or ovariotomy as a kind of panacea, although certain
writers have suggested these operations without taking into account the
special local conditions.




                               CHAPTER V.
                    DISEASES OF THE MAMMARY GLANDS.


In animals used for the purpose of providing milk, viz., cows, goats,
and milch ewes, diseases of the mammary glands are of daily occurrence,
but are rare in those in which the mammary function is limited to the
nourishment of the young, such as the mare, female ass, sow, etc.

In order clearly to understand the development of these diseases, it is
necessary to bear in mind the anatomical construction of the organs, for
which purpose we may take as a type the mammary gland of the cow, which
is the most complicated.

The udder of the cow is of hemispherical shape. It is situated in the
inguinal region, and is composed of two parts, the right and left, which
are absolutely independent and can easily be isolated from each other
along the median plane throughout their extent. The mass of parenchyma
is enveloped in a fibrous envelope, which is covered with a very loose
layer of subcutaneous connective tissue. Each half is subdivided into
two quarters, an anterior and a posterior quarter. Each quarter again
represents a distinct gland, although anatomical separation between the
anterior and the corresponding posterior quarter would be almost
impossible, the separating fibro-connective partition being common to
both glands.

In very good milkers it sometimes happens that two small supplementary
glands may be found behind the posterior quarters, bringing up the total
number to six.

=Parenchyma.=—Each of these glands is provided with a teat containing a
large sinus. Anatomically the mamma consists of glandular tissue
arranged like a bunch of grapes, in which the active tissues of the
acini deliver their secretion into little excretory canals, which unite,
forming a large collecting plexus. The collecting canals, or
galactophorous canals, open into the galactophorous sinus, which
occupies the entire depth of the teat and communicates with the exterior
by a small pore provided with a sphincter. The interacinous connective
tissue of the udder and the subcutaneous tissue of the teat, which
envelops the galactophorous sinus, is extremely rich in elastic fibres,
enabling the organ to undergo great changes in volume without injury.

=Vessels.=—The mammæ are supplied by two great arteries, the mammary
arteries, which are given off from the prepubic arteries, pass into the
inguinal canal, and penetrate the gland by its upper, deep face. Each
principal lateral artery divides into two trunks, one for the anterior,
the other for the posterior quarter.

[Illustration: $1]

The veins which collect the blood from the mammæ form two systems, the
first accompanying the mammary arteries, the second, more superficial,
giving rise to the anterior subabdominal mammary veins. The
arterio-venous plexus of the udder, which represents the vascular
pedicle of the organ, penetrates the gland, near a line dividing the
posterior and middle thirds of the upper surface, an inch or so in front
of the mammary lymphatic gland.

=Lymphatics.=—On either side of the middle line lies an extremely rich
lymphatic plexus, the origin of which is to be found near the ends of
the teats and in the peri-acinous spaces.

The superficial collecting vessels are dispersed under the skin,
perforate the fibrous sheath towards the base of the teat, and
anastomose with one another on the surface of the gland, the anastomosis
being most intimate between those of the same quarter, finally emptying
separately by two large trunks into the retro-mammary lymphatic gland of
the same side.

The vessels of the anterior quarter enter the lymphatic gland at its
most anterior point; those of the posterior quarter join it a little
below.

The retro-mammary lymphatic glands are two in number, and are situated
very high and towards the back, above the posterior quarters and close
to the perineum, outside the fibrous envelope of the gland. They are
sheltered in a recess excavated within the depths of the gland itself.
The main collecting lymphatics from the anterior and posterior quarters
enter it separately.

The lateral efferent vessels are divided into two groups, one of which
ascends vertically in the perineal region, towards the lymphatic glands
round the anus; the other passes through the inguinal canal towards the
sublumbar region, together with the blood-vessels.

The mammary nerves are two in number. The anterior has a downward course
outside the fibrous envelope and supplies the teat; the posterior nerve
is similarly distributed. In other domestic female animals which have
only two mammæ the general arrangement is precisely the same.


                        PHYSIOLOGICAL ANOMALIES.

=Imperforate condition of the Teat.=—It sometimes happens that although
the udder is otherwise well formed, the teats, or more frequently a
single teat, proves to be imperforate. Between the galactophorous sinus
and the exterior, opposite the sphincter, a little membrane may be found
which closes the teat and entirely prevents the contents of the udder
from escaping. Its existence is only discovered when the animal first
calves and lactation commences. Not a drop of milk can be withdrawn,
although the udder is swollen. Local examination readily reveals the
defect.

=Treatment= is very simple and effective, the membrane being perforated
with the end of a milk catheter.

=Contraction of the Sphincter= (_Atresia of the Extremity of the
Teat_).—Under other circumstances the teat may present a distinct
perforation, and yet milking may be impossible, or at all events may be
extremely difficult. This is sometimes due to contraction of the
sphincter, or possibly to atresia of the orifice.

=The diagnosis= of this condition is easy, but the outlook is not
promising.

=Treatment= is rather difficult. Some operators recommend dividing the
terminal sphincter with a small, specially formed bistouri caché,
provided with two cutting points. The operation has very satisfactory
immediate results, but after the little wounds so produced have healed,
cicatricial contraction takes place around the orifice.

Forcible dilatation is far preferable. It is carried out in the same way
as in human medicine, where the sphincter ani or the orifice of the
uterus has to be dilated. No superficial lesion and no incision is
produced; the result is therefore more permanent (see “Operative
Technique”).


                      WOUNDS OR TRAUMATIC LESIONS.


                           CHAPS AND CRACKS.

These injuries consist in little transverse or oblique wounds of the
teat.

=Causation.= In free milkers the udder appears completely relaxed after
milking. In the intervals between the different milkings, however, the
quarters become swollen, and are sometimes so distended as to overcome
the resistance of the sphincter at the base of the teat. The teats are
then greatly elongated, and, despite the richness of the tissues in
elastic fibres, this distension leads to little superficial epidermic
fissures.

These small lesions are unimportant, but if they become infected by
contact with the litter they granulate and suppurate, so that grave
complications may eventually follow.

The wounds caused by the calves’ teeth when sucking, or simply by the
rough way in which the little animal seizes the teat, may produce
similar accidents.

=Symptoms.= The teat shows one or more little transverse fissures, a few
millimètres to a centimètre or more in length. The base of the fissure
appears of a reddish or brownish-red colour, and has thickened,
indurated, painful, discharging or suppurating margins. Local
sensitiveness may be either slight or very pronounced. In the latter
case, the patients resist being milked, and even refuse to let the calf
suck.

=Diagnosis.= The diagnosis is extremely simple.

In a general sense the =prognosis= is favourable, but nevertheless the
local infection may extend and become generalised, thus giving rise to
interstitial mammitis, sometimes of a very grave character. On the other
hand, the sensitiveness may of itself render milking difficult or
impossible, and thus cause serious distension of the gland with milk.

=Treatment.= As both sucking and milking aggravate the lesions, they
should be prevented by the insertion of a milk catheter.

The surface of the udder and the wounds should be cleansed with an
antiseptic solution and be dressed with a 20 per cent. camphorated
vaseline or with carbolic or iodoform ointment, to favour healing. If
the cracks produce excessive sensitiveness a small quantity of orthoform
may be added to the camphor ointment. Before the milk catheter is
inserted, the teat should be very carefully cleansed with boiled water
and the catheter sterilised by boiling. Neglect of these precautions may
result in infection of the galactophorous sinus and mammitis.


                             MILK FISTULÆ.

=Causation.= Any accidental injury to the udder which establishes
connection between the galactophorous canals or the galactophorous sinus
and the exterior may give rise to milk fistulæ, if the injury occur
during lactation.

Apart from lactation these wounds may be grave, though if carefully
treated they heal without complication. During lactation, on the
contrary, the milk escapes permanently from the injured spot,
cicatrisation cannot occur, and a fistula forms.

[Illustration: $1]

=Symptoms.= The principal symptom is the permanent discharge of milk.
The fistula may be large or small, according to circumstances. In rare
instances it is situated on the udder itself, but it is commonest on the
teat. Milk may escape in mere drops or, on the other hand, in
considerable quantities.

=Diagnosis.= The diagnosis presents no difficulty.

=Prognosis.= The prognosis is grave so far as the loss of milk is
concerned, although the lesion has no effect on the general health. It
is particularly serious, however, because it may cause the interior to
become infected, and an acute parenchymatous mammitis may thus be set
up. It must also be borne in mind that old fistulæ are much more
difficult to obliterate than recent ones.

=Treatment= is much more troublesome than might at first be thought, the
great obstacle to repair being the continual secretion and discharge of
milk.

At first, attempts should be made to re-establish and render permanent
the natural method of discharge. This can be effected by inserting an
aseptic milk catheter and fixing it in position with a little pitch
bandage.

The course of the fistula is then cleansed, curetted, and rendered
aseptic in some way, as for example by washing with boiled salt solution
and dilute hydroxyl.

As there is little hope of obliterating the fistula by merely suturing
the skin, its course should first be closed by passing one or two deep
sutures without touching the external orifice and without passing over
it (Fig. 238). The discharge of fluid being then entirely stopped, the
external portion of the fistula is thoroughly cleansed, powdered with
iodoform, and finally closed with external, closely-applied sutures.
These sutures are protected with a little cotton wool or collodion
dressing, and healing then almost invariably occurs.

The animal should be given a very clean bed, and closely watched to
prevent it tearing out the milk catheter. On the fourth or fifth day the
catheter is removed, and is afterwards only used at intervals.

As all the sutures can be of aseptic catgut or silk, there is no
necessity to trouble about their removal. The dressing can be left until
it falls away of itself.


                         INFLAMMATORY DISEASES.


                        CONGESTION OF THE UDDER.

Congestion—_i.e._, distension of the vascular plexus as a consequence of
momentary stasis, vaso-motor disturbance, or paralysis of the little
vessels in the udder—can only be regarded as pathological in cases when
it precedes mammitis or when it results from prolonged neglect to milk
the animal, external irritation, etc. It was studied long ago by H.
d’Arboval, Gellé, Delafond, Trasbot, Lucet, etc.

It also occurs, but in a form which might almost be termed
physiological, after the first parturition in the large milch breeds,
where the rush of blood which precedes secretion is very great.

=Symptoms.= The udder is swollen, tense, doughy, shining, and œdematous,
not very painful on pressure, but sufficiently so to interfere with
movement. The general condition is little altered, but the temperature
of the udder is abnormally high.

Manipulation reveals the existence of more or less œdema, the parts
preserving the imprint of the finger. Sometimes this œdema extends along
the abdominal wall in front of the udder. The milk may be grumous or
even sanguinolent. The congestive state continues for some days, eight
to ten at the most, and may gradually disappear by resolution. Not
infrequently it terminates in acute mammitis after forty-eight hours.

=Lesions.= In simple mammary congestion the lesions are confined to
excessive dilatation of the peri-acinous capillary vessels, and
extravasation into the connective tissue. On section the tissue has a
dark-red appearance.

=Diagnosis.= The diagnosis is simple.

=Prognosis.= The prognosis is less alarming than might at first sight be
supposed.

=The treatment= consists simply in hygienic precautions, frequent
milking, emollient, sedative applications to the udder, and frequent
washing. As far as possible the use of milk catheters should be avoided.

Boric vaseline and belladonna ointment may be recommended. In very
serious cases blood can be withdrawn from the jugular. This is better
than bleeding from the mammary vein, which always entails the risk of
thrombus formation.


                               MAMMITIS.

Under the heading “mammitis” are included different forms of
inflammation of the mammary tissue, whether such inflammation attack the
parenchyma of the gland or the interstitial tissue. Generally the whole
gland is invaded at the end of a few days, whatever the point of origin,
and the inflammation is therefore of a mixed character.

Mammitis has been recognised from very early times. In his researches on
“contagious mammitis” Nocard in 1884 showed that infection was the
principal factor in its evolution.

Numerous classifications, based on the causes or on the pathological
anatomy of the condition, have been suggested; but most appear too
rigid, and therefore, without discussing them, we confine ourselves to
giving the following _résumé_:—

 Rainard (1845)   │Lacteal engorgement.
         „        │Cellulitis of the udder.
         „        │Mammitis         │Acute.
         „        │        „        │Chronic.

 Lafosse (1856)   │Mammitis         │Acute.
 Trasbot (1883)   │                 │
         „        │        „        │Chronic.

 Saint Cyr (1874) │Mammitis         │Catarrhal.
 Violet (1888)    │                 │
         „        │        „        │Phlegmonous or interstitial.
         „        │        „        │Parenchymatous.

                  │Primary mammitis │                 │
 Lucet (1891)     │  (properly      │Acute            │Galactogenous.
                  │  so-called)     │                 │
         „        │        „        │        „        │Lymphogenous.
         „        │        „        │Chronic          │Galactogenous.
         „        │        „        │        „        │Lymphogenous.
         „        │Symptomatic      │Acute            │Hæmatogenous.
                  │  mammitis       │                 │
         „        │        „        │        „        │Lymphogenous.
         „        │        „        │Chronic          │Hæmatogenous.
         „        │        „        │        „        │Lymphogenous.

All these classifications are justified by the guiding ideas of the
writers, yet, as in every case of attempted systematisation, they have
the disadvantage of not being in entire agreement with clinical
experience.

For instance, the differences between catarrhal and parenchymatous forms
of mammitis are only of degree, and it is difficult, therefore, to see
why they should be divided into two distinct varieties. The difference
is in regard to the prognosis.

Similarly in practice it is difficult and sometimes impossible to
distinguish between an interstitial and a parenchymatous mammitis,
because all the tissues of the gland may be involved at a given moment.
The only factor which allows of differentiation is the discovery of the
point from which infection took place. Finally, it is sometimes so
difficult to distinguish between galactogenous and lymphogenous mammitis
that the attempt has had to be abandoned. In gangrenous mammitis of
milch ewes, for example, the infective organism is found not only in the
sinus and the galactophorous canals, but also in the serosity of the
interstitial tissue and of the perimammary œdema.

Without doubt the causative agent of mammitis may enter the gland by
three principal channels—the galactophorous sinus, the lymphatic plexus
(after some injury), and the blood circulation. But from the clinical
standpoint it is not at all necessary to identify all the causes in
order to establish the classification.

The symptoms allow of a division only into acute and chronic mammitis.
Careful examination of the general condition of the patients will
afterwards allow cases of primary mammitis to be distinguished from
secondary or symptomatic mammitis such as occurs in tuberculosis.
Finally, consideration of the conditions under which a particular case
of mammitis has appeared, and study of the symptoms in detail
(peculiarities of the milk, local temperature, hardness of the tissues,
œdematous infiltration, etc.) will in most cases indicate whether the
mammitis be parenchymatous or interstitial.

This system really differs little from that adopted by Lucet in his work
on Mammitis.

The classification adopted in the following pages is as follows:—

 Mammitis│Acute  │Primary              │Parenchymatous or galactogenous.
    „    │   „   │          „          │Interstitial or lymphogenous.
    „    │   „   │Secondary or         │Hæmatogenous.
         │       │  symptomatic.       │
    „    │   „   │          „          │Galactogenous.
    „    │Chronic│Primary              │Simple.
    „    │   „   │          „          │Parenchymatous.
    „    │   „   │          „          │Interstitial.
    „    │   „   │Secondary            │Parenchymatous.
    „    │   „   │          „          │Interstitial.

We shall leave on one side everything concerning secondary symptomatic
mammitis, the study of which merges into that of the general diseases
from which it arises.


                            ACUTE MAMMITIS.

=Causation.= The general cause of acute mammitis, like that of chronic
mammitis, is infection by pathogenic organisms, whether such organisms
enter by the usual natural path, viz., the galactophorous sinus and
excretory apparatus, by the lymphatic path, owing to some accidental
injury, or, again, by the blood circulation.

Infection of the lymphatics undoubtedly plays a part in superficial and
interstitial inflammations, and it is proved that certain microorganisms
may pass into the milk, as it has been proved that they pass through the
kidney.

But if infection is the determining cause, certain secondary favouring
influences must not be overlooked.

Thus lactation is an almost indispensable condition. It is true that
some cases of mammary inflammation apart from lactation have been
described, but they have been the result of violence, accidental or
mechanical.

Accumulation of milk in the udder (overstocking) has unquestionably a
certain influence in the large milk-yielding animals, not because it
directly produces inflammation, but because milk then escapes
spontaneously; and as the udder cannot be entirely evacuated without
external assistance, the entrance is kept permanently open for the
passage of germs, which are freely transferred to the teat from the
litter and surrounding objects.

Cold, or rather chills, also act in a complex manner, particularly by
disturbing vaso-motor control. Different forms of mechanical violence,
such as blows, crushing strains, wounds, etc., may immediately and
directly set up local or general inflammation.

Bacteriological investigation has proved that numerous and varied
microorganisms can be found in the milk or interstitial exudates in
cases of mammitis, but only a few special forms have been proved to be
specific: streptococcus of contagious mammitis of milch cows, and
micrococcus of contagious gangrenous mammitis of ewes (Nocard).

=Pathology.= The pathogenic results produced by infective organisms
depend on their number and power of reproduction, and on the activity of
their life products.

The most immediate and regular result of acute mammary infection is
coagulation of the milk within the udder by decomposition of the
lactose, and the formation of lactic or even of butyric acid. The acini
and excretory canals are dilated by coagula, and can no longer expel
their products of secretion, so that the colonies of microorganisms
develop there in full security. The active epithelial cells undergo
granular degeneration and disappear, whilst the walls of the glands
become infiltrated and large numbers of leucocytes are poured forth
around the glandular culs-de-sac.

The tissues being thus affected, the virulent organisms penetrate from
the acini into the interstitial tissue, and from this time onwards the
lesions become mixed.

Inversely, should infection originate in the lymphatic spaces, a time
arrives when the organisms make their way from the interstitial tissue
into the acini, with a similar result in the end.

The development of the lesions may be arrested or may pass on to
suppuration, or even gangrene, of the parenchymatous lobules. Cases
happen in which infection is so rapid and severe that the successive
stages cannot even be identified, and gangrene appears without any
preliminary stages at all. Luckily the commonest forms are less serious.

=Symptoms.= Acute mammitis is characterised by its sudden appearance,
more or less acute general symptoms (dulness, fever, and loss of
appetite), and variable local symptoms. When the practitioner is able to
follow the development of the disease throughout, he may sometimes
distinguish well-marked signs, which permit the two clinical varieties
to be distinguished.

A. =Interstitial Mammitis.=—This form, which might perhaps also be
termed peri-mammitis when it primarily affects the subcutaneous
lymphatic spaces, has also received the names of phlegmonous and
lymphogenous mammitis.

It is characterised by alarming general symptoms, and particularly by a
rise in temperature of 2°, 4°, or even 5° Fahr., with all its
consequences, such as loss of appetite, stoppage of rumination,
acceleration of breathing and circulation, slight tympanites,
constipation, and by the thrusting of the hind limb on the affected side
away from the centre line. The animals groan when forced to move.

These symptoms sometimes precede by a considerable interval the
appearance of the local changes, which consist in painful swelling of
one or two quarters, rarely of more.

The perimammary subcutaneous tissue is infiltrated, œdematous, painful
on palpation and preserves the imprint of the finger. The teat is tense,
swollen, very tender, and of reddish colour. In the grave forms the
swelling extends forwards under the abdomen in the direction of the
umbilicus, and backwards towards the perineum. The local temperature is
abnormally high, the secretion of milk in the diseased gland is modified
or checked, and sometimes this phenomenon extends by reflex action to
the neighbouring quarters, although the latter may not themselves be
affected. The inflammation rarely extends from one quarter to another,
because the lymphatic plexuses do not anastomose (Fig. 237).

The animals lose appetite and fall away rapidly.

Resolution may occur after from five to eight days. By degrees all the
symptoms then become less marked. The appetite returns, pain diminishes,
the fever drops, and the lesions gradually disappear, but the yield of
milk rarely regains its former amount.

Suppuration may occur; sometimes a superficial subcutaneous abscess
forms, more rarely, a deep-seated, interstitial abscess, originating in
the connective tissue or lymphatic spaces. With a superficial abscess,
the local symptoms again revive to a slight extent; these are present in
a more marked degree where the abscess is deep-seated. An extremely
sensitive œdematous swelling forms, the skin covering which is at some
point of a deep-red tint, whilst fluctuation gradually appears.

In cases of deep-seated abscess formation the general condition becomes
alarming; the affected quarter is tense throughout, hard and very
sensitive.

Deep-seated suppuration is difficult to detect, and exploratory
punctures with a fine needle may be necessary before the diagnosis can
be made.

Local or diffuse gangrene forms a rare complication. It is due to the
vessels of one or several glandular lobules becoming obliterated or
thrombosed.

Such a termination is indicated by extreme aggravation of the general
symptoms, feebleness of the heart and great weakness of the patients,
who fall into a condition of coma. Locally the udder remains œdematous,
the skin becomes of a blackish-violet colour, whilst the local
temperature falls and the animals die from exhaustion and intoxication.

=Parenchymatous Mammitis.=—Parenchymatous mammitis when mild is also
termed catarrhal mammitis. It is in reality true primary mammitis;
interstitial being primarily and practically perimammary lymphangitis.

In this case infection occurs through the teat, and may be localised in
the sinus or excretory apparatus, giving rise to galactophoritis, but it
usually extends to the acini. Inflammation of the mammary tissue is
therefore direct and primary. It rapidly extends, however, through the
glandular wall into the interstitial tissue, thus setting up (from the
anatomo-pathological standpoint) a mixed mammitis. Clinical distinction
between this form and interstitial mammitis is at first easy.

=The symptoms= usually occur in the following order:—Swelling of the
affected quarter or quarters; appreciable increase in size and
sensitiveness; the presence at first of curdled milk in the
galactophorous sinus, then of clots mixed with slightly red tinged
serosity; complete cessation of the yield of milk, and suppuration in
the secreting portions of the gland.

The general symptoms appear only after the objective signs, and vary
greatly in intensity, according to the case. As in the interstitial
form, there may be marked fever, loss of appetite, cessation of
rumination, groaning, and difficulty in walking.

In some grave forms, where development is peracute, infection spreads
rapidly from the glandular to the interstitial tissue, and subcutaneous,
subabdominal, or perineal interstitial œdema occurs secondarily.

The udder is turgid, tense, shining, and of reddish-violet colour in
places, as if a deep-seated abscess were developing.

Pressure on the galactophorous sinus causes the flow of reddish-grey
milk, sometimes fœtid or of gangrenous odour. The animals seem
exhausted, show signs of profound intoxication, are unable to rise, and
appear paralysed.

But besides these grave forms are others, in which the patients seem
scarcely to suffer: appetite is preserved and all the vital functions
are in full activity. Only the local signs are of importance.

This variability in the clinical symptoms of acute forms of mammitis is
entirely due to differences in the pathogenic infecting organisms.

Parenchymatous mammitis may end in resolution in three to four days,
with progressive but slow return to the physiological condition. This
termination is announced by the gradual disappearance of all the
symptoms and the return of milk secretion. It is, however, quite
exceptional for the former condition to be fully restored, and in many
cases the affected quarter must be regarded as lost from the
physiological standpoint.

It gradually becomes hardened, sclerotic and atrophied.

Suppuration is very common. It attacks the galactophorous sinus, the
excretory canals, and even the acini. If obstructions occur in the
course of the collecting vessels, or if evacuation is not artificially
stimulated by milking, the pus collects in the depths of the gland, and
enormous diffuse abscesses may form at the expense of the mammary
tissue.

Circumscribed or diffuse gangrene, as a primary condition, is rarer.
Infective organisms rapidly invade even the depths of the gland, the
interstitial and subcutaneous tissue, and thrombosis due to infection or
intoxication occurs, followed by gangrene. Death results from infection
or intoxication.

Complications such as necrosis of the abdominal tunic, of the fibrous
tissue enveloping the mamma, and of the muscular layers on the inner
surface of the thighs, may occur in the suppurative forms.

=Diagnosis.= The diagnosis of acute mammitis is easy, and the
interstitial forms (mammary lymphangitis) can be distinguished from the
parenchymatous forms very early in the attack.

Careful examination suffices to differentiate between this condition and
mammary congestion or primary chronic mammitis. The examination,
however, must be much more thorough and searching when a specific
disease (such as tuberculous mammitis) is in question.

=Prognosis.= The prognosis of acute mammitis is always grave, whatever
form the disease may assume, for, if the animal’s life is not invariably
endangered, its economic value is always affected. Moreover, should
superficial or deep-seated abscesses form, prolonged suppuration may
follow, resulting in loss of condition and enormous depreciation.

=Lesions.= The lesions of interstitial mammitis are similar to those of
ordinary lymphangitis, the condition originating near the teat and
gradually extending to the layers of connective tissue between the
acini, mammæ, etc.

In the parenchymatous form the inflammation may remain partial, and be
localised in particular tracts of glandular tissue. The secreting
epithelium, when infected, exhibits cloudy swelling, becomes loosened,
and disappears; the margin of the gland and the interstitial divisions
become infiltrated with enormous numbers of white blood corpuscles, and
are the seat of suppurative processes which end in the production of
small acinous abscesses. By the union of neighbouring abscesses large
branching collections of pus are produced, and lead to partial or total
destruction of tracts of the parenchyma, of the connective tissue
divisions, vessels and aponeuroses.

The abscess tends to break through the skin, which becomes inflamed and
ulcerated, or, when the microorganisms are of slight virulence, the
tissues may react, so that the abscess becomes surrounded with a thick
indurated wall, and finally encysted.

=Treatment.= Very numerous methods of treatment have been proposed, an
admission which, in itself, suggests that no perfect one has been
discovered. No infallible system, in fact, exists of arresting the
disease and restoring the parts to their normal condition.

From a prophylactic standpoint, mammitis can be avoided by placing the
animals under proper hygienic conditions, paying special attention to
cleanliness, avoiding overstocking, and treating excoriations or
injuries to the teat or udder as soon as they appear.

Once acute mammitis has developed, general and local treatment must both
be attempted.

The older practitioners were in the habit of bleeding from the mammary
or jugular vein. Since their time, however, objections have been made to
bleeding because acute mammitis has been proved to be of an infectious
character, and, therefore, it is undesirable to lower the patients’
resisting power.

This reasoning, however, appears to be erroneous. Little by little the
advantages of bleeding, both in intoxications and infections, have been
recognised, and one thing at least is beyond dispute, namely, its action
on fever. Undoubtedly, it must not be resorted to without judgment, nor
should it be freely employed in debilitated animals; but in
well-nourished patients its effect on fever and on the accompanying
respiratory and circulatory disturbance is immediate.

We, therefore, recommend moderate bleeding from the jugular.

Bleeding from the mammary vein entails too great a risk of infection to
be commendable.

Purgatives and diuretics diminish or prevent accidents such as
intoxication and the complications resulting from temporary suspension
of the digestive function.

Local treatment is more or less efficacious in mammary infection. To
relieve pain and check infection it should be of an emollient and
antiseptic character. Ointments containing 10 per cent. of carbolic
acid, boric acid or iodine, or 12½ per cent. of camphor, opium or
belladonna, are of real service during the first stages, particularly of
mammary lymphangitis and interstitial mammitis.

Repeated applications of 10 per cent. carbolic glycerine have similar
advantages.

In the less acute forms originating in the parenchymatous tissue, mild
ointments of plumbic iodide, Goulard’s extract, or mercury may also be
used if precautions are taken to prevent the animals from licking, and
so poisoning themselves.

When the tendency to suppuration is marked, vesicants hasten the
development of the abscess and facilitate puncture. The most commonly
used are the 33 per cent. tartar emetic ointment or the 10 per cent.
biniodide of mercury ointment.

If, on the other hand, the mammitis is of the interstitial type, with
severe subcutaneous œdema, extending over the belly and towards the
perineum, good results often follow deep firing in points over the
swollen region. The points should be widely spaced, venous branches
being avoided. In this way numerous ducts are formed by which the toxic
and septic liquid which causes the œdema is enabled to escape.

This method of treatment can be supplemented by the simultaneous use of
antiseptic ointments.

Finally, in mammitis of the parenchymatous type, where there is no
marked tendency to invade the interstitial tissue, the most important
point is to wash out the interior of the gland, and even the acini as
far as possible, with antiseptic fluids. Practically this is difficult
to effect, because such irrigation must be performed aseptically, and
cannot properly be left to the cowmen.

In current practice, therefore, one often has to be content with
stripping the udder every hour. Milk clots which accumulate in the
sinuses and galactophorous canals are broken down by soft pressure, and
withdrawn with more or less difficulty. By repeated milking they are
prevented from accumulating in the galactophorous sinus and canals, a
very important point. Neglect of this precaution enables the colonies of
microorganisms to develop uninterruptedly in the culs-de-sac, whereupon
the coagula formed of casein obstruct the excretory channels and
complications develop despite all external treatment.

By repeated friction of the udder as in milking the advantages that
would be produced by washing out the gland from the direction of the
acini are secured, and thus the ascending infection is checked.

The diseased udder must always be emptied before making antiseptic
injections, which would otherwise be useless.

Should the practitioner decide to face the practical difficulties of
injections, he must take care that his instruments are aseptic; that the
solutions employed are always at or about bodily temperature; that these
solutions are incapable of irritating even tissues so tender as the
epithelium of the acini or of the galactophorous canals; and, finally,
that the drugs employed will not coagulate the milk within the gland.

Bearing in mind these points, the practitioner will do well to restrict
himself to the use either of boiled water, physiological salt solution
(·9 per cent.); alkaline 3 per cent. solution of borate of soda; or ·05
per cent. of fluoride of sodium. Every precaution having been taken,
from 12 to 20 ounces of liquid can be injected into each quarter,
according to its size. The solutions should be made to penetrate as far
as possible into all portions of the gland by gently manipulating the
parts, and should again be withdrawn in about a quarter of an hour.

It must always be remembered that failure to observe the above
precautions may make matters worse instead of better, and therefore that
intra-mammary injections can only be of value when carried out by a
skilled person.

In otherwise hopeless cases there remains as a last resort total or
partial ablation of the mamma. This operation is advisable in cases of
diffuse gangrene, or of intense massive suppuration, where there is
imminent danger of death from infection.

Directions for its performance will be found in Möller and Dollar’s
“Regional Surgery” (uniform with the present volume), p. 454.


                   CONTAGIOUS MAMMITIS IN MILCH COWS.

Although its cause was unknown before the investigations of Nocard and
Mollereau in 1884, this disease is of very common occurrence in England,
in large dairies in the environs of Paris, and is also seen, though more
rarely, in Normandy, in Brie and the Soissonnais, causing serious losses
on account of its transmissibility.

It had been described in Germany by Gerlach as early as 1854, and Kitt
in 1885 recognised it as common, and proposed for it the title of
“contagious catarrhal agalaxia.” It also occurs in Denmark, Italy, and
England.

Contagious streptococcic mammitis of cows always assumes a chronic form,
during the course of which indurated centres appear, varying in size
between that of a hazel-nut and a walnut.

=Causation.= The cause is always to be found in contagion, the disease
being due to a streptococcus, which has been carefully studied by
Nocard. Its transmission from a diseased to a healthy udder is explained
by the fact that the milkers are careless as to cleanliness, and thus
directly convey the germs to healthy teats and facilitate infection.

=Symptoms.= As in chronic mammitis, general symptoms are not well
marked, though some cases are ushered in with cough, slight nasal
discharge, and offensive diarrhœa. The first appreciable indication is a
change in the milk, which diminishes in quantity, and, although normal
to all appearance, coagulates rapidly if left undisturbed. Infection has
already taken place, although nothing can be detected on examining the
udder.

Next appears a nodule of hardened tissue above the teat. This nodule is
of rounded or ovoid shape, ill-defined towards its periphery, and it
becomes progressively enlarged without any sign of acute inflammation.
The milk becomes watery and of a bluish colour. Microscopical
examination reveals numerous streptococci. The hardening process
proceeds slowly. At the end of several months the sclerosis may only
have extended to one-third of the height of the infected quarter. With
the appearance of these lesions the character of the milk again changes.
It becomes yellowish in colour and fœtid, and contains a fibrous
reticulum, whilst its reaction is distinctly acid. The lesions, which at
first had been confined to one quarter, successively extend to the
others unless precautions are taken.

=Lesions.= The lesions consist in mammary sclerosis, with nodules which
progressively increase in size. This sclerosis originates in the
galactophorous canals, and extends first to the periphery, then to the
interstitial connective tissue; the latter undergoes hyperplasia and
confines within its tracts the true glandular elements, destroying their
secretory power. Locally, catarrhal mammitis exists.

The lesions can easily be recognised on microscopic examination, and,
when the section is suitably stained, numerous streptococci can be
detected in the acini, which are blocked with proliferating epithelial
cells. These lesions are due to the invasion of colonies of
microorganisms, which spread from below upwards.

The streptococcus causing this mammitis colours readily with thionin and
methylene blue. It can be cultivated in liquid and solid media
containing sugar or glycerine, but growth is impeded by the presence of
peptone or common salt. Under ordinary circumstances the culture dies
after some weeks, but if the acidity of the medium is neutralised by the
addition of powdered carbonate of lime, it preserves its vitality for
six or eight months. The culture when injected into the udder of a
healthy cow or she-goat reproduces the disease. The microorganism is not
pathogenic for any of the smaller animals used for purposes of
experiment.

=Diagnosis= and =prognosis=. The diagnosis is easy, the presence of the
sclerotic nodules being characteristic, whilst in doubtful cases a
microscopical examination can always be made.

=The treatment= should be prophylactic and curative.

Prophylactic treatment comprises disinfection of the milkers’ hands,
which are the ordinary vehicles of contagion, and disinfection of the
cow’s udder. Diseased animals in a byre should be milked last of all,
and the milk should be destroyed.

Curative treatment is confined to local antiseptic injections. Warm
concentrated boric solution gives good results. The injections may be
repeated three or four times a day after milking, the liquid being left
for a certain time within the udder. In this way animals suffering only
from a slight attack may be cured, but when the disease is already
somewhat advanced injections lose their effect.

Injections of fluoride of sodium (·1 to ·5 per cent. strength) appear to
be much more effectual. Moussu claims to have cured by this means
several old-standing cases where all four quarters of the gland were
diseased.

These injections necessitate the same precautions as those above
indicated for securing perfect asepsis. In grave cases it is very
difficult to prevent the disease from extending in infected stables,
because the necessary precautions cannot be observed.


                           CHRONIC MAMMITIS.

Chronic inflammation of the udder may form a termination of ordinary
acute mammitis, or it may result from infection with organisms of a less
virulent type.

In cases of acute mammitis, where severe injury of the interstitial
tissue or mammary parenchyma has occurred, its physiological function is
partially destroyed. The circulation is disturbed, the vessels undergo
change, the layers of connective tissue are indurated and sclerotic, the
epithelial tissue is not fully restored, and chronic inflammation of the
udder persists.

Clinically, it is impossible to distinguish all the variations that may
occur, because the constituent tissues are all injured, and the disease
is of a mixed type, with very numerous variations.

=Symptoms.= When chronic mammitis follows the acute form its onset is
only indicated by gradual diminution in the signs of acute inflammation.
The appetite is regained, and all the important vital functions are
properly performed.

Nevertheless, it is possible to distinguish two different clinical
forms. In one, the secretion of milk is almost entirely suspended, the
udder becomes atrophied, shrivelled and sclerotic; the hardening
gradually continues, and the patients, being useless as milch cows, can
only be fattened for slaughter. The induration may be partial, nodular,
or diffused.

In the other form the udder is large, but the milk is replaced by a
purulent secretion which permeates the acini and galactophorous canals.
Although they eat well, the patients remain thin, and are with
difficulty fattened for slaughter.

The suppuration may be diffuse or local. In rarer cases it is localised
in the form of “cold abscess.”

=Treatment.= No treatment can perfectly restore the udder after chronic
mammitis with sclerosis and atrophy.

In the suppurating forms of chronic mammitis the morbid secretion may be
checked by internal irrigation of the udder and antiseptic injections,
but, as this treatment necessitates careful and continued attention, it
is usually out of the question.

If only one quarter is diseased the animal may be kept for milking
purposes, but where two or three quarters are attacked it should be
prepared for the butcher.

In cows suffering from chronic purulent mammitis of all four quarters,
Kroon suggests removing the teats in order to facilitate fattening. The
teats are removed with the bistouri or scissors, by which means a large
opening into the galactophorous sinus is produced, through which the
purulent secretion escapes freely and continuously; the retention of pus
and intoxication in consequence of resorption are prevented and the
animal can be fattened, which would be difficult without the operation.


                   GANGRENOUS MAMMITIS OF MILCH EWES.

This disease occurs in different parts of France, and has also been seen
in Germany.

=Causation.= Lafosse in 1856 attributed it to the dark and dirty
condition of the sheep-folds, a cause which certainly contributes to its
propagation, though it is not the determining cause of the disease
itself. The latter is a specific micrococcus discovered in 1875 by
Rivolta, and thoroughly studied by Nocard in 1886 and 1887.

=Symptoms.= The course of the symptoms offers a certain analogy to that
of septic engorgements and interstitial mammitis or mammary
lymphangitis. As a rule only one gland is infected, but generally
symptoms at once appear, indicating an extremely dangerous condition,
viz., peracute mammitis. The patient suddenly becomes dull and entirely
loses appetite, rumination ceases and respiration is short and jerky,
although the bodily temperature does not always rise to any marked
extent.

Local symptoms soon develop. The udder assumes a violet-red tint and
becomes the seat of an erysipelatous swelling; the local temperature
rises, but as the disease progresses it gradually falls again. Milk
secretion ceases.

All these appearances rapidly become aggravated. The patient lies down;
the œdematous swelling extends to the belly and even to the chest and
thighs; the local temperature falls, indicating the imminence of
gangrene; the teat becomes contracted, and the pulse is very frequent
and almost imperceptible. From time to time the animal grinds its teeth.

The bodily temperature next falls to 98° or even 96° Fahr. (37° or 36°
C.), and the animal shows extreme prostration. The subcutaneous swelling
extends as far as the sternum in one direction and the quarters and
perineum in the other. The udder crackles under the finger. Death occurs
without a struggle.

All these symptoms follow as a rule in barely more than twenty-four
hours. Nevertheless, in certain cases, the disease lasts for three, four
or five days. Cases of spontaneous recovery are exceptional. The
gangrenous part may become delimited and slough away, leaving an
enormous suppurating wound, which slowly cicatrises. Even though the
animals survive, they never recover condition, but remain weakly, so
that, from a monetary standpoint, death would have been preferable.
Moreover, the lambs are starved and require a foster-mother.

=Lesions.= Post-mortem examination reveals œdematous infiltration of the
udder and surrounding connective tissue, and often extensive, diffuse
gangrene. The serosity is of a reddish colour, and sections of the
diseased udder of a violet tint. The tissues of the udder and the serous
liquid contain the specific micrococcus.

It is very small, and stains readily by the Gram-Nicolle method. It
grows rapidly in liquid and solid media, liquefies gelatine, and quickly
renders neutral media alkaline.

The injection of a few drops of culture into the udder of a milch ewe
reproduces the typical disease. In any other species it is without
effect. Infection occurs through the open extremity of the teat, or the
medium of a wound, and the microorganism is so virulent that it rapidly
invades all the tissues.

=Treatment.= No antiseptic treatment appears capable of checking the
course of the disease.

Surgical treatment alone is of any value, and consists in ablation of
the udder, followed by antiseptic dressing. Only a portion of the gland
is removed: an elliptical incision is made, including the diseased teat,
the skin is then dissected free so as to form a flap; the diseased
tissue is isolated; last of all, the vessels are ligatured. The
consequences of operation are less grave than might be expected,
considering the size of the wound, which heals with fair rapidity.

Moussu has frequently practised this radical method of treatment without
losing a single case. The remaining portion of the udder becomes
hypertrophied, and is often quite capable of secreting sufficient milk
for the nourishment of one lamb.


                     GANGRENOUS MAMMITIS IN GOATS.

Goats suffer from a form of mammitis which presents symptoms precisely
similar as regards development and termination to that of ewes. The
disease occurs in a sporadic form in animals giving milk, whatever their
breed or the conditions under which they are kept. It has been seen at
Alfort, as well as at Lyons.

Moussu has seen it in an enzootic form in herds of milch goats near
Bizerta (Tunis), and considers that contagion results from kids sucking
healthy animals after having been suckled by diseased ones. Fifty milch
goats out of a total of three hundred were affected at the time of
Moussu’s visit, and two had already succumbed.

=The diagnosis= presents no difficulty.

=The prognosis= is very grave.

=The treatment= is precisely similar to that of gangrenous mammitis of
milch ewes, viz., ablation of the diseased udder.

Of the above-mentioned herd, twenty animals were operated on, and all
recovered without accident. Among the others treated by less radical
methods, such as scarifications, incisions, antiseptic injections, etc.,
eight died. The only justifiable treatment, therefore, is ablation.


                          CYSTS OF THE UDDER.

Cysts of the udder may assume one of two forms, milk or galactocelous
cysts and serous cysts; possibly the latter are only hydatid cysts.

Both varieties are of the nature of retention cysts, and result from
accidental obliteration of a milk conduit, which has been obstructed by
coagulated casein, or from atresia due to contraction of inflamed
connective tissue. The acini are isolated and become dilated, the milk
undergoes changes in composition, the secretory epithelium degenerates,
and the cyst is produced.

The serous or milk cysts may vary considerably in size, and always show
a rapid tendency to suppuration.

=The diagnosis= is based on the detection of uniform fluctuation without
excessive sensibility, and can be confirmed by an exploratory capillary
puncture.

=The prognosis= is grave, for recovery can only occur after the lining
membrane of the cyst has been destroyed.

=Treatment.= Puncture followed by irrigation is insufficient, whatever
the nature of the cyst.

Free incision, or simple puncture with a bistoury, produces suppuration
within the cystic cavity, which continues until the lining membrane is
completely destroyed; but this takes a very long time.

Removal of the entire cyst, either with the bistoury or by tearing
through the surrounding connective tissue, is the best method of
treatment. The wound thus produced heals regularly and rapidly under an
antiseptic surgical dressing.


                         TUMOURS OF THE UDDER.

Tumours of the udder have been little studied in the larger domestic
animals, the reason being that immediately animals cease to yield milk
they are fattened and despatched to the butcher. Clinically, therefore,
these tumours are not of great practical importance.

Without entering into general considerations of a pathological
anatomical character, by which different varieties of these tumours are
differentiated, we may say that they assume one of three different
forms. The first is sharply circumscribed, of clearly defined shape, and
easily separated from neighbouring tissues, to which it adheres but
slightly. Such tumours are benign, and have no tendency to return after
removal.

The second is ill-defined, very adherent, and appears to infiltrate the
surrounding tissue. It is malignant in character, is often impossible to
completely remove, returns after extirpation, and infects neighbouring
lymphatic glands.

Between these two varieties may be placed a third, occupying an
intermediate position as regards both its characteristics and gravity.

Practically a knowledge of the above facts is a sufficient guide in
dealing with lesions of this character.

=Canalicular Papillomata.=—There exists another variety of tumours which
is of much more frequent occurrence, and which is apt to cause mistakes.
This variety consists of inter-canalicular papillomata.

These show no sign of their existence on external examination of the
diseased udder, and can be diagnosed only by reasoning based on the
signs observed.

They are of very small size, and grow from the internal wall of the
galactophorous sinus or excretory canal. They increase in length,
finally extending for some distance along the sinus, where they remain
unrecognised until some external manifestation arouses suspicion as to
their existence.

Under the mechanical contraction due to milking they easily become
excoriated, and their existence is then suggested almost solely by the
fact that the milk is tinted with blood, for palpation of the udder very
seldom gives more than negative results.

The =diagnosis= is always doubtful. The =prognosis= is grave, because it
is impossible to remove the tumour, which is often deeply placed within
the udder. There is no curative treatment.


                  VERRUCOUS PAPILLOMATA OF THE UDDER.

In cows suffering from cutaneous papillomata the udder is often covered
with a varying number of little sessile warts, which are spread over a
considerable surface, are very sensitive, and bleed at the lightest
touch. Milking is thus rendered extremely painful and difficult; the
animals struggle, kick, and become dangerous.

The condition is extremely troublesome, and in spite of every precaution
the milk is always soiled.

The best method of treatment consists in removing the warts individually
with fine, sharp-bladed curved scissors.

The animals must be firmly secured, if necessary cast, and the operator
should avoid removing more of the skin covering the udder than is
absolutely necessary. The bleeding which follows is trifling, and stops
of itself. After washing the parts with an antiseptic solution, the
little wounds may be powered with a mixture in equal proportions of
tannin and boric acid.




                              CHAPTER VI.
       DISTURBANCE IN THE MILK SECRETION AND CHANGES IN THE MILK.


Changes in the milk are so common and play so important a part in the
milk industry that it is absolutely necessary to mention the more
important, the country veterinary surgeon being frequently consulted on
this point.

The udder acts as a natural emunctory, just like the kidney, by which
are eliminated, in consequence of special selective properties, certain
natural principles (the active principles contained in the forage and
other food, vegetable alkaloids, etc.), drugs (alcohol), and poisons
(nicotine). This physiological peculiarity explains the influence of
changes of diet on the composition of the milk in mothers and on the
condition of their offspring. In the human species it also explains
congenital alcoholism in children, and a number of diseases whose cause
was formerly unknown.

=Agalaxia.=—This term implies a temporary or definite arrest of the milk
secretion. In many instances it represents nothing more than a
disturbance in the physiological function of the gland, but in others it
forms a true diseased condition.

Thus it is beyond dispute that psychical influences may produce
disturbance in this respect. Temporary suspension in the secretion as a
consequence of removal of the offspring from its mother, especially when
the young animal has been sucking for several days or weeks, is a fact
very well known to all breeders.

Under ordinary circumstances, however, the reasons are quite different,
and when the secretion of milk is diminished or suppressed it is due to
the ingestion of plants, substances, or drugs which check the secretion
of milk. All the solanaceæ (belladonna, hyoscyamus, stramonium, woody
nightshade, etc.), certain umbelliferæ (hemlock), colchicum, etc., have
this effect.

As to agalaxia of a true pathological character, it occurs in
debilitating and grave diseases, and sometimes follows certain
contagious forms of mammitis complicated with sclerosis of the udder
(infectious agalaxia of goats).

=Diagnosis.= The diagnosis of agalaxia presents no difficulty.

=Prognosis.= The prognosis varies, according to the determining cause.
In cases of accident and in temporary agalaxia, it is sufficient to
change the food in order to restore the secretion. Cooked food and warm
drinks, with an allowance of roots such as turnips or mangolds, have
excellent results. Where restoration of the secretion is delayed the use
of what are called galactogogues has been recommended, comprising
fennel, carraway, cummin, aniseed, juniper, sulphur, etc., mixed in
equal parts and given in doses of 6 to 8 drachms per day for a cow.

They act principally through the stimulating effects of their aromatic
principles.


                       MICROBIC CHANGES IN MILK.


                            LACTIC FERMENTS.

Microbic changes in milk are much commoner than changes of a chemical
nature. Milch animals differ very markedly one from another, and,
according to circumstances, give milk of ordinary composition, milk of a
very rich character, or watery milk; but the most important changes in
composition are those due to microbic agents.

During the milking, and according to whether this is performed in a low,
dirty byre, in a clean, roomy byre, or in the open air, various numbers
of germs obtain entrance to the milking vessels, and develop there with
extraordinary rapidity. The milk may even become infected by
non-pathogenic germs while still within the udder, in the sinus and
galactophorous canals. The cleanliness of the milking vessels also has a
considerable influence on the number and variety of the microbes which
may eventually germinate in the liquid.

Among the microorganisms usually found in milk there are some, however,
which always preponderate and play the part of organised ferments, viz.,
the lactic ferments and the organisms which cause coagulation of the
casein; these may be regarded as normal constituents. The others are
more or less foreign, and may cause important changes in the milk or
cream.

The lactic ferments are numerous, comprising the lactic bacilli of
Hueppe and Grotenfeld, the micrococci of Hueppe and Marpmann, and the
bacilli and micrococci of Freudenreich. These different agents act on
the lactose of the milk, decomposing it into carbonic and lactic acids,
which coagulate the milk.

Another group of microorganisms which were well studied by Duclaux
comprises those acting on the casein, among others _Tyrothrix tenuis_,
_filiformis_, _turgidus_, _scaber_, _virgula_, etc.

These organisms secrete principles having similar effects to those of
rennet, and are capable of coagulating enormous quantities of milk.
After a certain time, they also secrete a second diastase, viz.,
casease, which acts in the ripening of cheese.

=Clotted Milk.=—This term is used in dairies to indicate milk which
coagulates in lumps immediately after being withdrawn from the udder, or
which coagulates spontaneously a few hours later.

The change may be of a chemical nature, depending on conditions of keep
or feeding. More frequently, however, it is related to a latent
non-pathogenic infection of the udder, or to immediate infection of the
milk after removal by lactic ferments contained in the milk vessels or
the atmosphere.

It is necessary, according to circumstances, either to modify the diet
or disinfect the milk vessels, and immediately pasteurise the milk.

=Milk without Butter.=—Less commonly the diseased condition is indicated
by marked diminution in the quantity of cream.

Churning only produces a poor kind of butter, particles of which do not
readily cohere. This peculiarity is due to the presence of
microorganisms, which have not yet been fully identified. It can be
prevented by disinfection of the milking vessels, as well as of the
dairy itself, and by the use of centrifugal separators.

=Putrid Milk.=—This milk is characterised by its odour. It cannot be
used for making butter. In fact, as soon as the cream separates, little
bubbles of gas form at various points and break, leaving small cavities.
These little separate cavities reunite very rapidly, and the cream
becomes reabsorbed as fast as it is formed. Afterwards oily drops formed
of butyric, capric, and caprylic acids appear in the depressions and
give the milk a repulsive odour (rancidity).

This change is seen during mammitis, but most commonly results from
uncleanliness in byres and dairies. In the latter case putrefaction
occurs about twenty-four hours after milking, and is due to the growth
in the milk of _Bacterium termo_, _lineola_, etc. These organisms are
present in the dust which falls into the milking pails in the byre; when
milk so contaminated is stored in the dairy the changes occur.

Putrid odour may also be due to the presence of ammoniacal gas in the
byre, or to special toxins liberated by microbes which have found their
way into the milk. It is most marked during the warm seasons of the
year.

The occurrence of putrid milk can be prevented by disinfecting the dairy
and the milking pails daily for a certain time.

=Mucous, viscous, or thready Milk.=—These terms are applied to a
condition which usually appears twenty-four or thirty-six hours after
the milk has been withdrawn. The milk seems thick and viscous, and can
be drawn out into threads like mucus. It sticks to neighbouring objects,
and adheres to milk vessels like molasses. It coagulates imperfectly on
standing, gives little cream, and even this cream only furnishes a
mawkish, ill-flavoured butter.

In certain parts of Switzerland the production of mucous milk is
favoured, because it is employed in making cheeses.

The change is due to the presence of various microorganisms. Those which
have been best studied are Schmidt-Mülheim’s micrococci, the
_Actinobacter polymorphus_ of Duclaux, the _Bacillus lactis pituitosi_
of Löffler, the _Bacillus lactis_ of Adametz, the _Streptococcus
hollandicus_, and, finally, three others which are much commoner,
Guillebeau’s bacillus, the _Micrococcus Freudenreichii_, and the
_Bacterium Hessii_. These microorganisms act on the lactose, decomposing
it and causing the formation of a kind of filamentous mucilage, which
can be isolated by the addition of alcohol.

The mucilaginous change in milk can be prevented by ordinary methods of
disinfection.

=Red Milk.=—Milk which becomes red some hours after withdrawal, or
within forty-eight hours after milking, should be distinguished from
milk which on withdrawal from the udder is tinted red in consequence of
hæmorrhage within the udder itself. When the milk is of a hæmorrhagic
tint the blood corpuscles are soon deposited on the bottom of the vessel
if the milk is allowed to remain undisturbed.

The tint which the milk assumes is due to the growth of chromogenic
organisms, the best known of which are as follows:—1. _B. prodigiosus_,
which produces large red patches on the surface. It grows readily on
potato and gelatine, which it liquefies. 2. The _Sarcina rosea_, which
develops first of all in the cream and afterwards invades the milk. It
grows in sterilised milk, on alkaline potato, and on gelatine. 3. The
_Bacterium lactis erythrogenes_, which liquefies gelatine and produces a
reddish coloration. Casein can be precipitated and peptonised by means
of its cultures. It develops in the milk below the cream, the serum
alone becoming red, and only when shaded from the light.

=Blue Milk.=—In this case the milk appears normal when withdrawn, but
some days afterwards shows blue patches, which gradually increase in
size, and by uniting produce a distinct blue tint at the surface.

This change is connected with the presence of the _B. cyanogenus_. The
organism grows in sterilised milk, but in this case merely produces
greyish patches, the blue tint only occurring when a certain quantity of
lactic acid is added or when the ordinary lactic ferments are present.

=Yellow Milk.=—A yellow tint occurs in ordinary milk and cream,
particularly in certain breeding districts—in Normandy, for example,
where the butter produced is greatly valued on account of this
appearance. Pathological yellow milk is the result of the growth of _B.
synxanthus Schröter_, which secretes a substance resembling rennet,
curdles the milk, and finally dissolves the clot, at the same time
producing the yellow colour.

=Bitter Milk.=—Milk which is of a normal character on being withdrawn
from the udder may acquire a bitter taste some hours later. At rest,
this milk produces a small quantity of yellowish, frothy cream. The
organisms which produce the change have been studied in Germany,
Switzerland, and Auvergne. We may mention Weizmann’s bacillus of bitter
milk, Conn’s micrococcus of bitter milk, and Duclaux’s _Tyrothrix
geniculatus_.

=Medicated Milk.=—Medicated milk may be divided into two kinds: Firstly,
medicated milk proper, which differs from normal milk inasmuch as it
contains a certain proportion of drugs, which, when swallowed by milch
cows are partly eliminated through the udder. When taken by a young
animal or child such milk has a distinct therapeutic effect, depending
on the principles employed.

It does not appear, however, that up to the present any very great
success has followed this system. It is possible to increase the
richness of the milk in phosphates, but as regards mercurial or iodine
preparations the failure has been complete.

Secondly, fermented milks, which in addition to their nutritive action
are made more digestible.

Fermented milk is easily digested, and is better borne by the weakest
stomachs.

In human practice the fermented forms of milk are two, viz., kephyr and
koumiss.

_Kephyr_ is prepared in Afghanistan and Persia from camel’s milk, but
for some years past it has been made in England with cow’s milk. A
certain quantity of cow’s milk is placed in a bottle and the ferment,
consisting of kephyr grains, is added. The lactose is converted into
carbonic acid and alcohol in consequence of the action of certain lactic
microbes.

This milk after ingestion does not require to be coagulated and then
digested before absorption, a fact which considerably diminishes peptic
digestion.

_Koumiss_ is a milk preparation resembling kephyr; it is made by the
Kirghizes with mare’s milk according to the same principles, but the
ferment employed gives more alcohol.

=Preservation of Milk.=—On account of the importance of preserving milk
for use in large towns, in hospitals, and in the army during war, the
question of its preservation has long been studied.

_Chemical Processes._—The principle of preserving milk by chemical
action consists in preventing, or at least retarding, the changes which
inevitably follow exposure to the air. For this purpose, chemical
substitutes are added which in themselves have no injurious action.
Those most commonly employed are:—

              Carbonate of soda         45 grs. per quart.
              Bicarbonate of soda       45 grs.     „
              Boric acid          15 to 30 grs.     „
              Salicylic acid            12 grs.     „
              Borax                     60 grs.     „
              Lime                      20 grs.     „

The results obtained are of comparatively little value; the milk only
keeps for a few hours, or at the most for three or four days.

_Cold._—Refrigeration, which is so valuable in preserving all kinds of
animal products for long periods, has also been used for preserving
milk. Unfortunately, although cold impedes the development of bacteria,
it also has the grave inconvenience of causing the cream to separate
from the milk, and it being impossible to mix them again satisfactorily,
milk preserved in this way is more or less unfit for consumption.

_Heat._—The principle of preserving milk by heat is based on the
destruction of the microorganisms at a high temperature. In this respect
again, one meets with obstacles, for, if the heat be applied direct,
some of the principles of the milk are converted into caramel, and if
the temperature rises beyond 157° Fahr. (70° C.) the composition of the
milk is changed.

_Preservation by Oxygen._—Within the last few years the use of oxygen at
a pressure of about two atmospheres has been recommended. When the milk
is to be used it is only necessary slightly to relieve the pressure and
allow the oxygen to escape, the liquor which remains having all the
characters and qualities of fresh milk. The method appears excellent,
but is too costly for every-day use.

_Pasteurisation._—The pasteurisation of milk aims at destroying the
greater proportion of the ferments above mentioned. The milk is heated
at atmospheric pressure, and is kept for a time at a temperature of
between 150° and 157° Fahr. (65° and 70° C.). It preserves its
properties and composition, but sterilisation is not complete, and the
milk cannot be kept indefinitely.

_Concentrated Milk._—Concentrated milk is obtained by prolonged heating
to 157° Fahr. (70° C.) in a vacuum, when it becomes syrupy by
evaporation and its composition is not greatly modified. It is then
drawn off into bottles, which are hermetically sealed and subjected to a
higher temperature to complete the destruction of all the germs.
Condensed milk keeps for a very long time. To prepare it for use it is
mixed with a certain quantity of water, and then yields a liquid similar
to normal milk.

_Sterilisation._—Sterilisation necessitates the use of special apparatus
in which the milk is heated in a water or steam bath sheltered from the
action of the air, the temperature rising to 212° to 240° Fahr. (100° to
115° C.); all the ferments are destroyed, and the milk will keep
indefinitely, but its composition is slightly modified.

=Diseases Transmissible to Man through the Medium of
Milk.=—_Tuberculosis._—The history of tuberculosis contains numerous
facts proving the possibility of contagion by milk from cows suffering
from tuberculous mammitis, though it seems necessary that the milk
should be taken for a certain time to produce these effects.

_Foot-and-Mouth Disease._—Observations recorded by veterinary surgeons
prove that this disease affects the teats. It may be transmitted to man.
The milker may be directly inoculated, but the milk is the ordinary
vehicle of contagion. Chauveau saw an epidemic in a school at Lyons
where milk was obtained from cows suffering from foot-and-mouth disease.
In a similar way 205 persons were inoculated at Dover in 1884, and
suffered from vesicles about the mouth.

Although foot-and-mouth disease is extremely benign in men, it is well
to take every precaution against it.

_Gastro-Intestinal Infections._—Cases have been recorded of
gastro-intestinal infection in young animals and children in consequence
of consuming milk which had undergone abnormal changes. Milk containing
various kinds of microorganisms may at first produce lactic indigestion
and afterwards diarrhœic enteritis.




                              CHAPTER VII.
                          MALE GENITAL ORGANS.


The scrotum, the vaginal sheath, the testicles, the vas deferens, the
vesiculæ seminales, the prostate, and Cowper’s glands may all become the
seat of disease.

The scrotum and testicles seldom reveal more than mechanical injuries of
external origin, producing wounds and cuts and, in the case of severe
contusions, hæmatoma of the scrotum, of the vaginal sheath, and of the
testicles. Inflammation of the testicle, that is to say, traumatic
orchitis, is rare; on the other hand, Moussu has several times seen
tuberculous orchitis, for which he has operated. This, however, was in
the boar. These different lesions, the last named excepted, usually heal
with rest and the application of antiseptic dressings, anodyne and
resolvent lotions.

Breeders seldom retain more entire animals than are strictly necessary
for reproduction. The others are castrated, and this alone explains why
the treatment of genital diseases in male animals of any species is
rare.


                        TUMOURS OF THE TESTICLE.

Of the genital diseases which possess real clinical interest the most
important are tumours of the testicle. These occur not only in male
animals, but also in those which have undergone the operation of
bistournage.

It might _à priori_ be believed that in an animal of the latter class
the testicle had been completely destroyed, not only from the physical,
but from the pathological point of view. This, however, is by no means
the case, and Cruzel has described, under the erroneous designation of
sarcocele, tumours of the testicle which develop in oxen of various
ages.

Moussu has had a similar experience with animals of from four to six
years of age which had been carefully operated on.

These tumours, the origin of which is unknown, develop at the expense of
the rudiments of the atrophied testicle. They vary in character, and
Moussu has only observed tumours of a type different from that of the
testicle itself, containing tracts of carcinomatous, sarcomatous, and
fibrous tissue. They also appear to vary greatly in gravity, for,
although the cases seen by Moussu had become generalised in a few
months, Cruzel states that these tumours may remain stationary for
several years.

[Illustration: $1]

=The symptoms= consist in progressive enlargement of the scrotal region
and the appearance of a tumour surrounded by œdematous or lardaceous
tissue.

The tumour, which is confined to one side, increases in size, is
bosselated and adherent at points to the surface of the skin, while it
is insensitive or only slightly painful to the touch.

In a few months it may increase to the size of a child’s head. The
animals have difficulty in moving or lying down, the hind limb on the
affected side is abducted, and the animal usually lies on its chest and
abdomen. The patient rapidly loses flesh, although the appetite remains
good.

When the growth is removed, it is easy to prove that the tumour has
developed in the atrophied mass of testicular tissue, and that it
remains suspended from the end of the cord.

=The diagnosis= of tumour of the testicle is extremely easy, for the
condition cannot be mistaken for a hæmatoma or for a scrotal abscess.

=The prognosis= necessarily depends on the nature of the tumour, but as
it is impossible to determine this point before extirpation, the
prognosis should always be regarded as very grave.

=Treatment.= Whatever the nature of the tumour, ablation is advisable.
If it is of a benign character, recovery may be complete and permanent,
but if it is malignant, generalisation will rapidly ensue. Before
interfering surgically, however, it is essential to examine the
inguinal, pelvic, and sublumbar lymphatic glands, to make sure that they
are not affected. If they prove to be already invaded, an operation
should be avoided.

[Illustration: $1]

Even despite such precautions and the apparent absence of any glandular
infection, operation may be followed by generalisation in a few months,
although for a short time the condition may seem to have greatly
improved. No special indications need be given beyond those suggested as
necessary in dealing with all kinds of tumours, whatever their nature.

The skin should be freely divided, that the tumour may be thoroughly
dissected out and no fragments be overlooked. The mass of the tumour
having been dissected free, the _écraseur_ is applied to the pedicle or
the cord. Enucleation of the tumour may be very difficult on account of
the presence of numerous ramifications or attachments, but the closest
attention must be given to removing every fragment if a fresh local
growth is to be avoided. In the event of fragments being left, a fresh
growth is certain to occur.

Generalisation, which may extend to all the viscera (lymphatic glands,
liver, spleen, lungs, pleura, peritoneum, heart, etc.), is indicated by
rapid wasting, fever, acceleration of breathing, digestive disturbance,
and sometimes coughing, etc.

Local new growths assume the form of ulcerating swellings. In practice,
if the general condition can be improved for a short time, it is
advisable to slaughter the animal.


               ACCESSORY GLANDS OF THE GENITAL APPARATUS.

(PROSTATE, VESICULAR SEMINALES, COWPER’S GLANDS.)

Inflammatory or other diseases of the above glands are most frequent in
entire animals. As a group they are uncommon, and are still
ill-recognised and ill-described, being seldom identified except on
post-mortem examination.

[Illustration: $1]

The cause of inflammation of the prostate, of the vesiculæ seminales,
and of Cowper’s glands is probably an ascending infection of the urethra
and neighbouring channels, a fact which explains the comparative rarity
of such conditions in castrated animals.

The pathogenic germs penetrate from the urethra into the excretory ducts
of the glands, obtain a lodgment in the culs-de-sac of the glands
themselves, and thus produce simple or suppurative inflammation.

=The symptoms= may easily be mistaken, to some extent at least, for
those of acute cystitis or cystitis due to the presence of a calculus,
and it is only by rectal examination that the diagnosis can be made.

The first symptom is defective micturition, which occurs in jets, is
intermittent and painful, and sometimes causes slight groaning. It is
accompanied by vesical colic, spasmodic lifting of the hind legs, and
more or less unsuccessful expulsive efforts.

These symptoms are of reflex or mechanical origin, and are due either to
direct compression of the urethra by an hypertrophied and inflamed
gland, or to spasm of the vesical sphincter. The urine passed, unlike
that in cases of acute cystitis or in cystitis due to calculus, is of a
normal character. Rectal examination usually reveals distention of the
bladder, and hypertrophy and exceptional sensitiveness at certain
points.

If the painful and hypertrophied area is over the neck of the bladder,
this indicates that the lobes of the prostate are affected. If, however,
the affected parts are situated on the sides of the neck and along the
posterior pointed end of the bladder (Fig. 239), the vesiculæ seminales
are affected; finally, if the painful points are directly above the
ischial arch and below the sphincter ani, Cowper’s glands are the seat
of disease (Fig. 240).

To diagnose these conditions requires very close and careful
examination. They may easily be mistaken for acute cystitis, though the
character of the urine should suggest doubts and lead to rectal
examination.

Although they do not endanger the animal’s life, these conditions give
rise to such serious inconvenience as often to render entire animals
useless for stud purposes.

Local =treatment= is impossible, and the practitioner is restricted to
the use of anodynes, balsamic preparations and diuretics. The treatment,
in fact, differs little from that of cystitis. In cases of suppuration
of Cowper’s glands, the abscess usually forms just below the anus and
close to the median line. Thus the diagnosis may be confirmed by
capillary puncture, the part being laid open if necessary.




                             SECTION VIII.
        DISEASES OF THE SKIN AND SUBCUTANEOUS CONNECTIVE TISSUE.




                               CHAPTER I.
                                ECZEMA.


Under the name of eczema may be grouped a series of cutaneous diseases
characterised by pruritus, by a discharge from the skin, or simply by
epidermic proliferation, without any apparent parasitic or accidental
cause.

These diseases have been referred to a special constitutional condition
termed a diathesis, although during the last few years we have come to
recognise certain microbic and toxic influences in their production. In
the ox eczema assumes different appearances. Accordingly, the disease
has been divided into the acute, chronic, sebaceous, and toxic forms.


                             ACUTE ECZEMA.

=Causation.= In the ox, as in all other species, the determining cause
is to be found in bad hygienic conditions, improper feeding, and in a
special individual condition of the animal affected, that is to say, a
diathesis.

=Symptoms.= During a preliminary period, which might be termed a
prodromic period, only general symptoms can be detected, such as fever,
loss of appetite, digestive disturbance, constipation, etc. Local signs
are still absent, or at least are not noticeable, and are only
represented by congestion of the skin.

The second phase is characterised by a papulous eruption which is
difficult to detect, inasmuch as it occurs in the depths of the coat.
Nevertheless, the skin is distinctly sensitive, and at numerous small
points the hairs appear to stand upright.

The third phase consists in the development of more or less confluent
vesicles, with exudation and discharge. The disease is not really
visible externally until after the hair has become agglutinated by the
discharge. This discharge is seldom as abundant as in eczema in the dog
or horse. It is produced slowly and dries rapidly.

As the crusts fall, carrying with them a portion of the hair, the
general symptoms disappear, but the sites of these vesicular patches now
show cracks extending as deep as the dermis and often complicated by
secondary infection involving suppuration, adenitis, abscess formation,
or diffuse subcutaneous suppuration.

Acute eczema is generally confined to the limbs. It may develop fully in
from twenty-four to forty-eight hours. The acute stage is attained in a
few days, and the condition disappears in two to three weeks provided it
does not assume the chronic form as the result of complications.

=Diagnosis.= The absence of parasites enables the condition to be
distinguished from phthiriasis and acariasis, whilst the history
prevents its being confounded with toxic eczema.

=Prognosis.= The condition is troublesome rather than grave. Suppuration
is often persistent, and despite careful attention the discharge may
only diminish slowly, while the disease is always liable to return.

=The treatment= is local and general. Local treatment consists in
emollient and antiseptic washes and the application of drying powders.
The former comprise glycerole of starch, bran water, boric ointments,
camphorated vaseline, iodine and glycerine. At a later stage the skin
can be washed with decoction of oak bark or a weak iodine solution,
followed by the application of talc or starch powder. As far as possible
this external treatment should be supplemented by the frequent use of
mild purgatives and various diuretics, which seem to have a special
action on the arthritic diathesis.


                            CHRONIC ECZEMA.

Comparatively few cases of chronic eczema have hitherto been described
in oxen, and the details given are extremely meagre. Chronic eczema may
assume that form from the first or may succeed acute eczema. The causes
are probably the same in both conditions.

=The symptoms= appear to be those of the acute form, but are much less
severe. They consist in papulation, a miliary vesicular eruption,
pruritus, and the formation of crusts and epidermic scales.

In a case seen by Mégnin the crusts separated and fell away, leaving
bare spots. The disease re-appeared for several years in succession. The
spots finally remained bare, but showed no thickening of the skin and no
microscopic changes.

=Diagnosis.= Microscopical examination is necessary to distinguish this
disease from scabies or ringworm.

=The prognosis= is grave, because large areas of the skin may be invaded
in succession.

=Treatment.= As in acute eczema, the condition is improved by the
prolonged administration of small doses of salines and diuretics.
Arsenical preparations are also valuable, but should only be employed
for two or three weeks together, with intervals of equal duration. The
dangerous complications which sometimes result from accumulations of
this drug in the system are thus avoided.


                    SEBACEOUS OR SEBORRHŒIC ECZEMA.

Whilst the two preceding forms of eczema result from vascular
disturbance of the skin or dermis that now under consideration seems due
to vascular and secretory troubles in the accessory structures of the
skin, and more particularly in the sebaceous glands.

[Illustration: $1]

=Symptoms.= The disease develops slowly. At first circular or elliptical
patches of skin, distributed regularly over the body, more especially
round the natural orifices, become deprived of hair. The surface of
these patches is covered either with thick crusts of a peculiar
greyish-brown tint which display numerous superficial cracks, or parts
normally free from hair exhibit shining epidermic crusts arranged in
layers, which are shed on the slightest touch.

This depilation has a strong tendency to spread, and so at first it
often resembles ringworm. It results from changes in the hair follicles,
with atrophy of the papillæ and complete loss of hair. The changes in
the skin, however, are little marked. The skin itself is but slightly
thickened and preserves its usual suppleness, while the subcutaneous
tissue is not œdematous.

[Illustration: $1]

[Illustration: $1]

The hairs, however, when examined microscopically are found to be
thickened at their roots, though otherwise throughout their whole length
they remain normal. The condition is a consequence of disturbance in the
circulation and nutrition of the papilla and the root of the hair.

Finally, the congestive process extends to the sebaceous glands, the
secretion of which it modifies, and sets up seborrhœa, which is
responsible for the formation of the crusts and epidermic scales
above-mentioned.

The pathogeny of the disease is difficult to explain, but the stages in
the clinical development are as follows: the skin undergoes repeated
attacks of congestion, followed by seborrhœic folliculitis, epidermitis
and loss of hair.

=The diagnosis= is easy, the absence of ringworm being proved by the
absence of the spores of trichophyton and by the non-contagious
character of the discharge.

=The prognosis= is not grave from the point of view of general health,
the chief functions being perfectly regular, but it is otherwise as
regards possible terminations, viz., partial or total loss of the coat,
which may be irremediable.

=Treatment.= It is difficult to lay down a really satisfactory method of
treatment, because the exact cause of seborrhœa is still unknown. As it
is probably to be sought in some individual constitutional peculiarity,
the feeding and method of life should be changed and the skin stimulated
by washing with lukewarm water and soap and by dry friction. Locally, if
the alopecia threatens to be permanent stimulating applications may be
tried. These comprise lotions containing alcohol, solutions of chloral,
salicylate of soda, etc., and they should be applied with smart
friction.

The sufferers should not be used for breeding purposes.


                ECZEMA DUE TO FEEDING WITH POTATO PULP.

Among the forms of eczema due to toxins, several varieties may be
recognised. Some result from the administration of drugs such as iodine,
others from special forms of food. The only one of clinical importance
is that following the consumption of excessive quantities of potato
pulp.

=Causation.= The disease is seen in all districts in which potatoes are
employed for the manufacture of alcohol and starch, more especially in
Germany. The disease seems to be a direct consequence of feeding with
residual products of distilleries and starch manufactories.

Spinola states that 160 lbs. of potato refuse per day to 1,000 lbs. of
body weight would certainly produce eczema: 60 to 80 lbs. only produce
it in rare cases and 20 to 40 lbs. are harmless.

There is a further point to consider as regards the variation of potato
pulp in toxicity. Potatoes yield a more or less active residue,
according to the year in which they are grown, their state of
germination, and the variety to which they belong. Raw or cooked
potatoes may produce eczema if given in large quantities or for long
periods.

Numerous theories have been advanced as to the nature of the morbid
disturbance producing eczema. Some authorities declare the appearance of
the disease to be due to the presence of a toxic principle contained in
potatoes, viz., solanin. It might be objected that this chemical
principle only exists during germination while potatoes that have not
undergone germination produce the disease. Further, the symptoms of
poisoning by solanin differ from those of this form of eczema, among
which loss of appetite, for instance, or stupefaction, or narcosis is
never observable.

According to other writers eczema is due to the action of the lower
alcohols contained in the refuse pulp, but again these properties exist
in brewers’ and distillers’ grains, the consumption of which produces no
bad results. Similar objections might be made regarding the suggested
action of the acids of fermentation (lactic, butyric, and acetic acids,
etc.).

Johne blames the salts of potassium, which, however, can only act as
digestive irritants, and Zürn suggests mycosic inflammation.

Whatever the toxic principle, its effects are most marked in animals
undergoing fattening, and are rarely found in working oxen, still more
rarely in milch cows. In the last named the injurious principle appears
to be eliminated in the milk, and this theory is supported by the fact
that the liquid has purgative properties; the calves which consume it
suffer from diarrhœa, which ceases when the feeding is altered.

Finally, it has been proved that different animals show different
degrees of susceptibility to the action of potato pulp.

=The symptoms= do not appear until after two or three weeks’ feeding on
the potato pulp. Then the animals walk stiffly, rise with difficulty,
and display redness, swelling and sensitiveness of the limbs. When the
œdematous infiltration and reddening have become distinctly marked there
appear, not only between the claws, as in foot-and-mouth disease, but
over the entire limb and principally near the folds of skin about the
joints, numerous closely-packed small papules, which in one or two days
become transformed into vesicles through exudation below the epidermis.

This marks the eczematous phase properly so called. The vesicles then
become ruptured, the exuded matter glues the hairs together, dries, and
forms crusts, which have a peculiar and distinctive odour.

The disease may extend towards the hocks, the knees, the stifle, the
armpit, etc. In the folds of skin surrounding the joints deep cracks
form, and sometimes become secondarily infected, thus leading to the
development of lymphangitis.

General symptoms, such as fever, loss of appetite and constipation,
always follow; they are afterwards succeeded by diarrhœa and progressive
weakness, ending in death.

The disease is easily curable if seen in its earlier stages, but after
all signs of the first attack have disappeared, the condition may return
five or six times in a year if potato pulp is again given. Recovery is
always very difficult in aged or enfeebled patients.

The mortality varies greatly; formerly it was as high as 20 per cent.,
but at the present time it is much lower.

=Diagnosis.= Provided the history of the case is borne in mind, the
diagnosis is always easy.

=The prognosis= is not grave if the disease is treated early.

=Treatment.= This consists first of all in altering the diet and
reducing the quantity of potato pulp, or, better still, in discontinuing
it entirely. The food should consist of good hay, bran, oatmeal gruel,
pollard, etc. Internally, diuretics are given to assist in the
elimination of the toxic products.

This treatment arrests the course of the disease. Suitable local
treatment will remove the existing lesions. It is precisely similar in
character to that of acute eczema, but it must be borne in mind that it
can only prove effective if the primary cause be removed.


                          IMPETIGO IN THE PIG.

The term impetigo is used to describe a disease characterised by an
eruption of papules, the discharge from which forms yellowish crusts,
which when dry are of a grey or brown colour. The point of origin of the
eruption is unknown, but the crusts rapidly become infected on contact
with the air, and the bodily lesions may end in suppuration. The disease
is not frequent nowadays except in sucking pigs and in large or
badly-kept piggeries.

=Symptoms.= The eruption usually appears between the ages of two and
three months, and is accompanied from the first by moderate pruritus.
The papules rupture after two or three days and discharge a
lemon-coloured liquid, which is distributed over the surface, dries
rapidly, and causes the bristles to stick together at the roots. The
crusts formed in this way remain adherent to the skin, though their
surface becomes cracked. They increase in thickness, cover the head and
part of the body, particularly the belly and the inner surface of the
thighs, and if removed, an operation of some difficulty, leave exposed a
bleeding, sanious, or purulent wound. The animals lose condition and
appetite, cease to grow, seem as though attacked with rachitis, and may
die if the general conditions of their maintenance are not improved.

The =diagnosis= is not difficult, but the =prognosis= depends on how
long the disease has existed and the bodily condition of the patients.

=The treatment= consists entirely in improving the hygienic conditions
and the feeding. The patients must be repeatedly washed or bathed and
carefully disinfected, and they must have better food.

The crusts should be softened before the animals are washed, so that
bleeding may be avoided and the affected areas not be transformed into
suppurating wounds. By applying oil or some fatty matter to the crusts
it is possible to cleanse the parts with bran water. If considered
necessary, this cleansing can be followed by dressing with boric or weak
creolin solution. Open-air life and good food soon relieve the principal
symptoms.


                             ACNE IN SHEEP.

Acne, that is to say, localised inflammation of the sebaceous glands and
hair follicles, sometimes occurs in sheep apart from any parasitic
invasion. The eruption is particularly seen after shearing, and it is
probable that, as in the horse, irritation produced by the machine, and
possibly by accidental infection, constitute the principal determining
causes.

=Symptoms.= The disease is indicated by the appearance of cutaneous
pustules, which are only slightly painful on pressure and which involve
the entire thickness of the skin. The dermis is hardly congested, and no
constitutional disturbance occurs.

Acne lesions may be more or less confluent, and may attain the size of a
small hazel-nut.

=The diagnosis= presents no difficulty. Puncture or incision reveals the
fact that the abscesses are filled with white sebaceous material and are
quite free from parasites.

=The prognosis= is not grave. Recovery occurs spontaneously in a few
weeks.

=Treatment.= Liquid emollient applications and the opening of the small
follicular abscesses appear to represent the only means of hastening
recovery.


                   FAGOPYRISM (BUCKWHEAT POISONING).

Fagopyrism is a disease of toxic origin in sheep, and is due to eating
buckwheat (_Polygonum fagopyrum_).

The disease has also been entitled erysipelatous or gangrenous
dermatitis, according to its form and gravity.

=Causation.= The cause is extremely simple, viz., the consumption of
buckwheat and other food pertaining to a like species, such as
_Polygonum persicaria_. The green plant and the straw give the same
results, but the action of light and air are also necessary for the
production of the disease, a fact which is somewhat difficult to
explain.

According to German writers the disease occurs more frequently in white
sheep and lambs than in those in which the skin is of a very dark
colour.

=Symptoms.= When the sheep are fed in folds, with the green plant in
summer or with the straw in winter, nothing unusual is seen, the herds
being, to all appearance, in perfect health. On their being set at
liberty, however, the first symptoms appear, perhaps in less than an
hour. Some animals become restless, make peculiar movements of the head,
and soon display intense congestion of the parts free of wool, together
with redness and swelling of the ears, eyelids, face, throat, etc. The
condition develops with extreme rapidity, the animals being immediately
afflicted with pruritus over the affected regions. If they are not
removed to the quiet and warmth of the fold the symptoms increase and
papules appear, which may be transformed into vesicles and bullæ. In the
fold, on the other hand, all the symptoms rapidly disappear.

The disease rarely assumes an erysipelatous form, but respiratory and
cerebral symptoms, together with fever and vertigo, are not exceptional.

=Treatment.= The feeding on buckwheat should at once be discontinued,
and the patients should be kept in the fold until the toxic principles
have been eliminated, that is, for a month or more.

Bicarbonate of soda may be added to the drinking water. The local
lesions about the head must be kept clean and dressed with antiseptic
astringent lotions.




                              CHAPTER II.
                              PHTHIRIASIS.


The term phthiriasis is applied to infestation of the skin with lice.

=Causation.= These diseases are due to the presence of various parasites
which live by destroying the epidermic scales, or by piercing the
superficial layers of the skin. They are of a greyish-yellow colour, and
belong to the genera _Hæmatopinus_ and _Trichodectes_.

The _Hæmatopinus_ forms have pointed heads, and are equipped for
penetrating the skin by suction. The _Trichodectes_ have a large flat
head constructed for masticating.

[Illustration: $1]

[Illustration: $1]

The ox harbours two forms of _Hæmatopinus_ and one of _Trichodectes_,
the _Hæmatopinus eurysternus_ and _tenuirostrus_, and the _Trichodectes
scalaris_.

The sheep suffers from _Trichodectes sphærocephalus_ and a _Melophagus_,
the goat from the _Hæmatopinus stenops_ and the _Trichodectes climax_,
and the pig from the _Hæmatopinus urius_.

=The symptoms= are, with trifling variations, the same in all domestic
animals, the principal being rubbing and itching. The animals scratch,
bite and attempt to rub against hard objects, even abrading the skin
when this is thin and the irritation is severe.

The parasites may, however, remain localised, and it rarely happens that
they are present in any considerable number in all parts of the body.

[Illustration: $1]

In the ox they are principally found in the depression at the back of
the base of the horns, and in the upper margin of the neck and the back.
In the absence of treatment phthiriasis may become generalised over the
entire surface of the body.

The trichodectes and the melophagus of the sheep choose similar points,
but when the wool is long they may be found nearly all over the body.

In the pig the hæmatopinus is found on the neck, in the region of the
poll, about the armpits, and round the eyes and ears.

These parasites, whose powers of increase are astonishing, keep the
patients in a continual state of irritation, causing them to lose
condition and, in the absence of treatment, to die of exhaustion.

=The diagnosis= is very easy, the parasites being visible to the naked
eye.

=The prognosis= is not grave unless the condition affects a large number
of animals in herds. In young animals the prognosis is much graver, for
the little creatures rapidly become anæmic and die in a state of
exhaustion.

=Treatment.= When the byre, fold, or piggery is infested the first point
is to remove the animals and thoroughly disinfect and cleanse all parts.

[Illustration: $1]

After the manure has been cleared out, the walls, mangers, racks, etc.,
are washed with boiling water, or, better still, potash solution, and
disinfected first with vaporised sulphurous acid, then, if necessary,
with a washing of caustic lime.

The patients are afterwards clipped, washed with soft soap and dressed
with anti-parasitic solutions, such as 1 per cent. tobacco juice, or a
mixture of equal parts of benzine and oil or benzine and petroleum,
etc., which give excellent results.

A 3 per cent. creolin solution is also a very active anti-parasitic and
very easy to use.

All these solutions, however, are more or less poisonous and need to be
used with caution, weak solutions only being used at first, particularly
in the case of animals, such as oxen, which are given to licking
themselves.

[Illustration: $1]

[Illustration: $1]


                          SCABIES—SCAB—MANGE.

The term scabies is given to a group of diseases affecting man and all
domestic animals. These diseases are produced by two classes of
parasites, viz., sarcoptinæ, which live within the epidermis or on the
surface of the skin, and demodectes (_sing._ demodex), which penetrate
into the sebaceous glands and hair follicles.

Scabies, though known from the earliest times, has long been confounded
with constitutional diseases characterised by cutaneous eruptions. The
symptoms shown were formerly regarded as due to the elimination of
“humours” which the organism was casting off, for which reason scabies
was even treated with internal medicines.

At the present time the cause of the disease is perfectly well
understood, as well as the mode of development of the different
parasites. The rate at which these parasites develop is almost
incredible, a fact which explains the highly contagious character of the
disease.

Each species of animal may present several varieties of scabies, caused
by different parasites, such as sarcoptes, psoroptes, chorioptes,
demodectes, etc.


                           SCABIES IN SHEEP.

Scabies in sheep usually assumes one of three forms—sarcoptic,
psoroptic, or chorioptic scabies. Follicular, or demodectic, mange
affects the eyelids, and is very rare. It is produced by the _Demodex
folliculorum_ var. _ovis_.


                           SARCOPTIC SCABIES

This scabies has long been recognised as affecting more especially the
head, muzzle, etc. It was mentioned as long ago as the fourteenth
century by Jehan de Brie, but, until Delafond’s time, no one recognised
that it was caused by an acarus. In 1858 Delafond discovered the
parasite in Piedmont sheep.

[Illustration: $1]

=Causation.= Formerly, writers on the subject and shepherds attributed
this disease to the wounds and excoriations which sheep receive in
passing through brambles, holly, etc., or in rubbing against their
racks. The true cause of the disease is the presence under the skin of
the _Sarcoptes scabiei_ var. _ovis_, which passes from sheep to sheep by
direct contact. The animals attempt to rub against everything about
them, even against their neighbours. These parasites can be transferred
from the goat to the sheep, and _vice versâ_.

Walraff, Roloff, Delafond, Gerlach and Railliet have described cases of
infection in man, but the disease is rarely more than of a temporary
character.

=Symptoms.= This form of scabies affects the head and the parts free
from wool.

At first the parasites invade the upper lip and the tissues about the
nostrils, sometimes, but more rarely, the eyes and ears. They cause the
formation of vesicular papules, accompanied by violent itching. The
animal, in rubbing itself, excoriates these papules, which discharge a
fluid and soon become covered with yellowish-brown crusts.

The disease afterwards invades the face, forehead, jaws, and entire
head. The skin becomes wrinkled and the brownish crusts thicker and more
abundant. These are fissured and bleeding, and they give the face the
appearance of one vast sore.

The parasite rarely attacks the region of the elbow, the belly, or the
inside of the thigh. The disease never advances in parts covered by
wool, although in breeds of sheep with thick wool, such as are found in
Algeria and Tunis, the sarcoptic form of scabies may become generalised
and attack the entire body. The extremities of the limbs, however, are
usually attacked after all the head has become involved.

Throughout the course of the disease the patients scratch and rub
themselves, thus tearing off the crusts and causing bleeding and the
formation of new crusts of a blackish hue. This form of scabies about
the head may become complicated with conjunctivitis, the inflammation
extending from the extremity of the eyelids to the conjunctiva. This
arises from the fact that the membrane is frequently injured by the
animal rubbing the parts. Conjunctivitis may be so intense as to lead to
purulent ophthalmia and the loss of the eye.

[Illustration: $1]

=Diagnosis.= Sarcoptic mange in sheep cannot be mistaken for any other
disease on account of its localisation.

=Prognosis.= The disease is not very dangerous, for it is easy to treat,
though if left to itself it might in time become fatal.

=Treatment.= Preventive treatment consists in isolating diseased
animals, cleansing and disinfecting the folds, and preventing the
introduction of diseased animals into healthy flocks.

=Curative treatment.= When the disease is detected at an early stage
anti-psoroptic remedies may be directly employed.

If, however, it is of old standing, the crusts must first be softened
and removed by the use of fatty substances, such as vaseline or oil,
before any curative treatment can be undertaken.

The crusts can be removed in from twenty-four to forty-eight hours by
vigorous washing with soft soap and the application of anti-parasitic
solutions. The omission to wash the parts causes drugs to lose much of
their efficacy.

Helmerich’s ointment, oil of cade, mixtures of oil, benzine and
petroleum, and 3 per cent. to 4 per cent. of tobacco juice, are the
commonest and most efficacious applications.

A non-poisonous ointment may be made by taking 4 ounces of oil of
turpentine, 6 ounces of flowers of sulphur, and 1 lb. of lard. Mix the
ingredients at a gentle heat, and rub in well with the hands or with a
brush, at the same time breaking the crusts. The simple sulphur ointment
may be made of one part of sulphur and four parts of lard; one fourth
part of mercurial ointment may be added. Few remedies are so useful as
sulphur iodide, and it may well be given a trial on head scab.

In most countries this disease has been made the subject of special
legislation.


                      PSOROPTIC MANGE—SHEEP SCAB.

This is probably the gravest form of mange. It was described by Cato the
Censor in 160 B.C., by Virgil, Juvenal, Celsius, Columella, Pliny,
Vegetius, etc. In 1787 Abildgaard first showed that psoroptic mange in
sheep could be cured by simple external remedies, without internal
medications. In 1809 Walz described the causes, nature, seat, and
treatment of the disease.

Since then, the parasitic, contagious nature of mange or scabies has
been more and more clearly recognised.

=Causation.= Experience and observation have long shown that the only
cause is the presence of the _Psoroptes communis_ (_ovis_). This disease
is much more contagious than that just described. Psoroptic mange or
scabies exclusively affects those portions of the body covered by the
wool, and may for a long time remain unrecognised.

The parasite is visible to the naked eye, though most inspectors employ
the microscope. The adult female is about ¹⁄₄₀ of an inch long and ¹⁄₆₀
of an inch broad; the male is ¹⁄₅₀ of an inch long and ¹⁄₈₀ of an inch
broad. The mites are discovered more easily on a dark background, and if
a portion of the wool and crusts is placed on black paper and exposed to
the sun for a few minutes the parasites will generally be seen crawling
about on the paper.

The disease is transmitted directly or indirectly by contact from
diseased to healthy animals in the folds, fields, or sheep runs. One
diseased sheep may contaminate an entire flock. The disease is extremely
contagious, and may appear even within a week after exposure.

The parasites have exceptional vitality. It is generally stated that,
kept at a moderate temperature on portions of scab, the adults may live
from four to twenty days, but they will occasionally live much longer;
cases are on record where they have lived three, four, or even six weeks
when separated from sheep; if the atmosphere is dry they will generally
die in about fifteen days; but death is often only apparent, for the
mites may sometimes be revived by warmth and moisture even after six or
eight weeks; the fecundated females are especially tenacious of life.

[Illustration: $1]

Experience has shown that in some cases apparently healthy sheep have
become infected in places where no sheep have been kept for four, eight,
twelve, or even twenty-four months. The conditions underlying this
infection are not thoroughly understood. Possibly some of the eggs have
retained their vitality a long time and then hatched out; possibly the
vitality of the fecundated female has also played a _rôle_; while it is
not at all improbable that an entirely new infection has accidentally
been introduced by birds or other animals. Certain authors of high
standing scout the idea that birds can introduce an infection of scab,
but there is no reason why birds should not do this, and there are some
reasons for believing that they do. It has been noticed on the
Experiment Station of the United States Bureau of Agriculture, for
instance, that crows delight in perching on the backs of scabby sheep
and picking at the scab; while so doing it is only natural that small
tags of wool would adhere to their feet, and thus scatter scab.

Delafond’s experiments show that psoroptic mange is most troublesome
amongst thin, ill-nourished, weakly animals, whilst robust sheep in good
condition may be cured simply by attention to cleanliness and abundant
feeding.

In America this disease causes extremely heavy pecuniary loss, second
only in importance to that produced by hog cholera. It has also
interfered very seriously with the export of American sheep.

=The course= of the disease is affected by the time of year and
surrounding conditions. In autumn and winter, when sheep are in
continual contact in a moist, warm atmosphere within the folds, the
disease makes rapid progress. Young, weak, closely-inbred animals, and
those with long, coarse wool, most quickly succumb. Unhealthy
surroundings, damp, and bad ventilation favour the disease. Pure or
mixed bred merino sheep suffer severely. In summer the animals are
generally shorn and live in the open, and the disease then usually
diminishes or may even be arrested.

A study of the life history of the scab parasite is necessary in order
to determine several important points of practical value, such as the
proper time for the second dipping, etc.

The female mite lays about fifteen to twenty-four eggs on the skin, or
fastened to the wool near the skin; a six-legged larva is hatched; these
larvæ cast their skin and become mature; the mites pair and the females
lay their eggs, after which they die. The exact number of days required
for each stage varies somewhat, according to the writings of different
authors, a fact which is probably to be explained by individual
variation, and by the conditions under which the observations and
experiments were made. Thus Gerlach, in his well-known work (1857)
estimates about fourteen to fifteen days as the period required for a
generation of mites from the time of pairing to the maturity of the next
generation. He divides this time as follows: Under ordinary conditions
the eggs hatch in three to four days, although two authors allow ten to
eleven days for the egg stage; three or four days after birth the
six-legged larvæ moult and the fourth pair of legs appears; this fourth
pair is always present when the mites are two-thirds the size of the
adults; when seven to eight days old the mites are mature and ready to
pair; several (three or four) days are allowed for pairing; another
generation of eggs may be laid fourteen to fifteen days after the laying
of the first generation of eggs. Without going into all of the other
observations on these points, it may be remarked that the eggs may not
hatch for six or seven days; the six-legged larvæ may moult when three
to four days old, and become mature; after pairing, a second moult takes
place, lasting four to five days; a third moult follows immediately,
then eggs are laid and the adults die; in some cases there is a fourth
moult, but apparently without any further production of eggs. Accepting
Gerlach’s estimate of fifteen days as an average for each generation of
ten females and five males, in three months time the sixth generation
would appear and consist of about 1,000,000 females and 500,000 males.

[Illustration: $1]

Several practical lessons are to be drawn from these figures: Firstly,
it is seen that the parasites increase very rapidly, so that if scab is
discovered in a flock, the diseased sheep should immediately be
isolated; secondly, if new sheep are placed in a flock, they should
either first be dipped, as a precautionary measure, or they should at
least be kept separate for several weeks to see whether scab develops;
thirdly, since the chances for infection are very great, the entire
flock should be treated, even in case scab is found only in one or two
animals; fourthly, as dipping is not certain to kill the eggs, the sheep
should be dipped a second time, the time being selected between the
moment of the hatching of eggs and the moment the next generation of
eggs is laid. As eggs may hatch between three and seven, possibly ten or
eleven days, and as fourteen to fifteen days are required for the entire
cycle, the second dipping should take place after the seventh day, but
before the fourteenth day; allowing for individual variation and
variation of conditions, the tenth, eleventh, or twelfth day will be the
best time to repeat the dipping.

=Symptoms.= Psoroptic mange attacks the parts covered with wool, so that
attention is only drawn to the disease by some slight injury to the
fleece, which becomes rough, matted, brittle, and liable to fall.

Scabies commences with intense pruritus. The animals scratch and bite
themselves, and tear away the fleece. These symptoms become aggravated
when the animals are hot, as, for instance, when travelling. If the
sheep have travelled through mud, the fleece becomes matted on the neck,
behind the shoulders, and at all points where they are able to scratch
themselves with the hind limbs.

When a scabby sheep is touched at a diseased point, the animal shows
pleasure by nibbling and moving the head up and down.

At an early stage, if the fleece is divided and the skin examined,
little papules may be discovered somewhat less in size than a lentil.
They are of a yellowish colour, and are distinctly visible against the
reddish colour of the skin. These papules are due to the attacks of the
psoroptes.

[Illustration: $1]

They soon become more numerous and even confluent, break and discharge,
become converted into pustules, and cause the formation of crusts. In a
few days the diseased points are covered with a squamous, yellowish,
sticky covering, under which the psoroptes lie hidden and which affords
them nourishment.

The crusts steadily grow thicker and lift the individual fibres of wool,
tearing them from their follicles, so that patches of skin become bare.
The patches thus formed increase in diameter, for the acari leave the
centre, where crust-formation is replaced by abundant desquamation of
the epidermis. The skin is thickened, assumes the character of
parchment, and in old-standing cases becomes wrinkled.

The disease always commences along the back, withers, loins, and the
upper part of the quarters. Thence it spreads to the flanks and sides of
the chest. The psoroptes are almost exclusively confined to recently
affected points on the edges of the scabby patches. They are visible to
the naked eye, and appear as little whitish-brown points.

Scab is specially liable to attack a flock containing lambs and yearling
sheep, whose skin is thin, fine and supple, and therefore more
susceptible to their attacks. If a portion of a scabby flock be shorn,
the shorn animals will probably recover on account of the psoroptes
transferring themselves to the animals with long fleeces.

=The diagnosis= is easy. Psoroptic mange cannot be mistaken for
sarcoptic mange, on account of the different points affected.

Psoroptic mange only attacks regions covered by wool, and sarcoptic
mange those free of wool. A microscopical examination of acari removed
from the diseased animals will, however, immediately remove all doubt.

Nor can the disease be confounded with phthiriasis, the trichodectes
being immediately distinguished from the psoroptes by their greater size
and the shape of their head. Moreover, they are usually to be found on
the front portions of the shoulders.

It is more likely to be mistaken for another disease, termed by some
writers seborrhœa and studied and described by Delafond under the name
of sebaceous folliculitis. This disease appears mostly in autumn, and
attacks animals much exposed to the weather and on moist, cold soils. It
begins with very violent pruritus, followed by biting and loss of
portions of the fleece. The skin is red, inflamed and painful, and the
wounds are covered with large quantities of yellowish acid discharge of
a sticky and offensive nature. The treatment of this disease consists in
placing the sheep in clean, dry, well-ventilated sheds. Recovery is
assisted by clipping and the application of some emollient dressing to
the diseased parts.

The ease with which the disease can be cured and the absence of
parasites enable one to readily distinguish it from psoroptic mange
(scab).

=Prognosis.= The disease is not specially grave, so long as only a few
animals are affected, for it is not difficult to cure by isolation, good
feeding, and proper external treatment; but if scab appears in a flock,
the freedom with which the animals intermingle is such that all are
rapidly attacked, and the irritation produced at once checks their
growth and causes loss in condition. Many ewes give birth to small,
feeble lambs, which are almost certain to die, and in any case the wool
is considerably diminished in value.

Delafond estimated that psoroptic mange formerly attacked one
thirty-fifth of all the sheep in France every year, causing damage to
the extent of five francs per head. At the present time, and since
proper sanitary laws have been instituted, it has become much less
common.

During the bad season of the year the mortality is greater, and may
reach as much as from 40 to 50 per cent. In cases where scab is
accompanied by some other disease, such as distomatosis, it may even
rise to 80 per cent.

The treatment is preventive and curative. =Preventive treatment=
consists in separating the healthy from the diseased animals and in
disinfecting the folds, sheds, etc.

=Curative treatment.= The first point in this treatment consists in
improving the diseased animal’s food both as to quality and quantity.

It is to be observed that the parasite has more difficulty in living on
robust and well-nourished animals. Moreover, observation shows that
transference from poor land to rich pastures is sometimes in itself
sufficient to bring about a spontaneous cure. Such, at least, is the
belief of the Spanish sheep farmers in Estramadura and of the French
shepherds.

The shepherd can do a great deal to arrest the course of the disease. If
he is careful, zealous, intelligent and observant he will quickly note
the first indications of the disease and, by isolating the animals,
check its spread.

The second point consists in shearing the diseased animals, and this
must be carried out at any season of the year. The money loss is
sometimes important, but must be met, for otherwise treatment is
impossible. In cases of localised scab, empyreumatic oil, oil of cade,
solutions of sulphuret of potassium, decoctions of black hellebore
(water 1 quart, fresh rhizome 4 ounces or dry rhizome 2 ounces),
decoction of tobacco and diluted tobacco juice (6 ounces in 1 quart of
water) have been recommended. Such local treatment, however, is often
useless, because incomplete.

When scab is generalised and it is impossible to define the parts
attacked, general treatment is indispensable and the diseased sheep
should be dipped.

As a preliminary, however, and in order to make sure that the
application will produce its effect, the animals after shearing should
be passed, twenty-four hours before the medicinal bath, through a warm
bath containing soap in order to soften and remove the scabs.
Applications of oil or some fatty substance will also soften the scabs,
which may afterwards be removed with a scraper without producing
bleeding. One pound of soft soap may be dissolved in fifty quarts of
water and each sheep plunged into this and scrubbed with a brush for a
few minutes. Washing alone removes a large number of the parasites.

Whatever bath be used it should not be given until four or five hours
after the last feeding. The dips most popular in France are as follows:—


                        _Tessier’s Bath_ (1810).

            For 100 sheep Arsenious acid    1½ parts or lbs.
                  „       Sulphate of iron  10       „
                  „       Water            100       „

The above materials should be boiled for ten minutes, and, as a
consequence of the chemical fusion which occurs in the process, the
proportion of arsenious acid dissolved amounts to about 2 drachms per
quart instead of 3¾ drachms.

In this bath the arsenious acid acts as a parasiticide and the sulphate
of iron as an astringent, the latter checking the absorption of toxic
principles by the skin and sores, and preventing the sheep from licking
themselves.

Absorption by the skin is not so dangerous as has been believed.
Rossignol has shown that poisoning need not be feared in chemical baths
unless the proportion of dissolved arsenic is above 150 grains per
quart, especially if the period of immersion does not exceed five
minutes. Even pure solutions of arsenic, free from any astringent, may
be used, provided the quantity in the bath does not exceed 120 grains
per quart.

The bath should, if possible, be kept warm—85° to 95° Fahr. (30° to 35°
C.).

Four men are generally employed for the operation. One drives in the
sheep, two others hold and brush them in the bath, and the fourth holds
the head of the animal above the liquid. Tessier recommended gloves for
the use of the operators, but experience has shown that such a
precaution is unnecessary. The udder, and particularly the teats, of
ewes with young may, if necessary, be smeared with some fatty substance,
such as vaseline or oil, in order to guard against the astringent action
of the liquid.

Each sheep is plunged in the bath for one or two minutes, or five
minutes at the most. All the diseased spots must be brushed, rubbed and
cleansed; but care must be taken not to make them bleed.

Tessier suggested leaving the animals for twenty-four hours in some
disinfected place, without straw or food, to prevent these materials
from being wetted by the liquid which runs from the fleece, and which,
if afterwards eaten, might have a poisonous effect. Here, again, the
danger has been exaggerated. Delafond has shown that sheep may be given
a fluid ounce of Tessier’s bath for eight days running without producing
the slightest unfavourable symptom.

Tessier’s bath is excellent from the therapeutic standpoint, but it
imparts a yellow tint to the fleece, which is thus rendered less
valuable. The mixture has therefore been modified in various ways.


                        _Clément’s Bath_ (1846).

            For 100 sheep   Arsenious acid 1·5 parts or lbs.
                  „       Sulphate of zinc   5       „
                  „                  Water 100       „

In this bath every quart contains about 2½ drachms of arsenious acid.
Its toxic power, therefore, is considerably greater than that of
Tessier’s bath.

Clément’s formula has one drawback. The sulphate of zinc may be mistaken
for a non-astringent alkaline sulphate (sulphate of soda), and as a
consequence poisoning may occur, as experience has shown.

Mathieu of Sèvres replaced the sulphate of iron by an equal quantity of
alum. In this case, each quart of the bath contains 2½ drachms of
arsenious acid.

Clément’s and Mathieu’s formulæ have given just as good results as
Tessier’s.

A last formula is that of Professor Trasbot. The aloes is of very little
use, however, because it is almost insoluble.

               For 100 sheep Arsenious acid    2 lbs.
                     „       Sulphate of zinc 10    „
                     „       Aloes             1    „
                     „       Water            25 gallons.

_Condition of the animals after the bath._—On leaving the bath the
abraded parts are slightly cauterised. During the five or six following
days the skin is stiff, and covered with adherent crusts over the points
attacked by the parasites. The animals no longer scratch or bite
themselves.

Towards the eighth day the crusts fall, the skin appears supple and of a
pink colour, and the wounds cicatrise. In animals which have suffered
for a long time recovery is much slower, and may extend over from thirty
to fifty days. The wool again grows soft and bright, while the sheep
rapidly regain their spirits and condition. The cicatrisation of the
wounds is often accompanied by intense itching, which must not be taken
as a sign of the persistence of the disease. It is well, however, to
keep the animals under observation at this period.

Under any circumstances, six weeks or two months should always be
allowed to elapse before giving a second bath. Should a few spots appear
to be attacked secondarily, they may be moistened with a little of one
of the bath liquids.

In Germany the creolin bath is generally employed:

             For 100 sheep { Water   250 gallons or parts.
                   „       { Creolin 6·5         „

Each sheep is bathed a second time after an interval of one week, the
animal being immersed for three minutes in the bath and thoroughly
scrubbed with a brush. The efficacy of this method, however, is less
certain.

In America, where the flocks are large and scabies is frequent, sulphur
baths are employed, the baths themselves being of great size. The
animals are forced to pass through them and remain there for some
minutes.

The size and value of American, Australian, and New Zealand flocks
demand that the modes of treatment practised and the experience gained
in these countries should receive something more than passing notice. We
therefore purpose giving a short _résumé_ of some parts of the very
valuable monograph on sheep scab issued in 1897 by Dr. Salmon and Mr.
Stiles, for the American Bureau of Animal Industry.

In selecting a dip the question of expense will naturally arise; next,
the question as to whether or not scab actually exists in the flock to
be dipped. The facilities at hand, the set-back to the sheep, and the
length of the wool are also matters for consideration, as well as the
pastures into which the dipped sheep are to be placed.

_Expense._—In estimating the expense one should consider not only the
actual outlay for the ingredients of the ooze, but the cost of fuel and
labour, the injury, if any, to the sheep, and the liability of not
curing the disease. It is much more economical to use an expensive dip
and cure scab, than it is to use a cheap dip and fail to cure it.

_Does scab exist in the flock?_—If scab does not actually exist and the
wool is long, the dipping in this case simply being a matter of
precaution, it is best not to select a dip containing lime.

_The facilities at hand for preparing dip._—If fuel is very scarce, so
that it is impracticable to boil the mixture for at least two hours, the
lime-and-sulphur dips should not be selected.

[Illustration: $1]

_The pastures._—In case it is necessary to place the dipped sheep on the
same pastures they occupied before being dipped, it is always best to
use a dip containing sulphur. If a proprietary dip is selected under
those circumstances, it is suggested that sulphur be added, about 1 lb.
of flowers of sulphur to every 6 gallons of dip. The object in using
sulphur is to place in the wool a material which will not evaporate
quickly, but will remain there for a longer period of time than the scab
parasites ordinarily remain alive away from their hosts. By doing this
the sheep are protected against reinfection.

Sulphur is one of the oldest known remedies for scab; its use is best
known in the tobacco-and-sulphur dip and in the lime-and-sulphur dip.
These home-made mixtures are the two dips which have played the most
important _rôles_ in the eradication of scab from certain English
colonies, and their use is extensive in America.


                     _The Tobacco-and-Sulphur Dip._

[Illustration: $1]

The formula as given here, and as adopted by the New South Wales
sanitary authorities, appears to have first been proposed in 1854 by Mr.
John Rutherford. “On the Hopkins Hill Station Mr. Rutherford, with two
dressings of these ingredients, then cured over 52,000 sheep which had
been infected for eighteen months. Since then millions of scabby sheep
have been permanently cured in Victoria in the same way, and in South
Australia and New South Wales hundreds of thousands of scabby sheep have
also been cleansed with tobacco and sulphur. Judging, therefore, from
the experience of the three colonies, there is no medicament or specific
yet known that can be compared with tobacco and sulphur as a thorough
and lasting cure for scab in sheep.” (Dr. Bruce, Chief Inspector of
Sheep for New South Wales.)

The proportions adopted by Rutherford, and afterwards made official by
the scab sanitary authorities, are—

                     Tobacco leaves     1 lb.
                     Flowers of sulphur 1    „
                     Water              5 gallons.

The advantage of this dip lies in the fact that two of the best scab
remedies, namely, tobacco (nicotine) and sulphur, are used together,
each of which kills the parasites, while the sulphur remains in the wool
and protects for some time against reinfection. As no caustic is used to
soften the scab, heat must be relied on to penetrate the crusts.

_Directions for preparing the dip._—Infusing the tobacco:—Place 1 lb. of
gold-leaf or manufactured tobacco for every 6 gallons of dip desired in
a covered boiler of cold or lukewarm water, and allow to stand for about
twenty-four hours; on the evening before dipping bring the water to near
the boiling point (212° Fahr.) for an instant, then remove the fire and
allow the infusion to stand overnight.

Thoroughly mix the sulphur (1 lb. to every 6 gallons of dip desired)
with the hand in a bucket of water to the consistency of gruel.

When ready to dip, thoroughly strain the tobacco infusion from the
leaves by pressure, mix the liquid with the sulphur gruel, add enough
water to make the required amount of dip, and thoroughly stir the entire
mixture.


                        _Lime-and-Sulphur Dips._

Under the term “lime-and-sulphur dips” is included a large number, of
different formulæ requiring lime and sulphur in different proportions.

To give an idea of the variety of the lime-and-sulphur dips, the
following list is quoted, the ingredients being reduced in all cases to
avoirdupois pounds and United States gallons:

(1.) The original “Victorian lime-and-sulphur dip,” proposed by Dr.
Rowe, adopted as official in Australia:

                   Flowers of sulphur    20⅚ lbs.
                   Fresh slaked lime  10⁵⁄₁₂    „
                   Water                 100 gallons.

(2.) South African (Cape Town) official lime-and-sulphur dip, February
4th, 1897:

                    Flowers of sulphur 20⅚ lbs.
                    Unslaked lime      16⅔    „
                    Water              100 gallons.

(3.) Fort Collins lime-and-sulphur dip:

                    Flowers of sulphur  33 lbs.
                    Unslaked lime       11    „
                    Water              100 gallons.

(4.) A mixture which, used to some extent by the Bureau of Animal
Industry, contains the same proportions of lime and sulphur (namely, 1
to 3) as the Fort Collins dip, but the quantities are reduced to—

                    Flowers of sulphur  24 lbs.
                    Unslaked lime        8    „
                    Water              100 gallons.

In case of fresh scab Formula No. 4 will act as efficaciously as the
dips with a greater amount of lime, but in cases of very hard scab a
stronger dip, as the Fort Collins dip, should be preferred; or, in
unusually severe cases, an ooze with more lime in proportion to the
amount of sulphur, such as the Victorian (No. 1) or the South African
(No. 2) dip might be used.


               _Prejudice against Lime-and-Sulphur Dips._

There is at present great prejudice (a certain amount of it justified,
no doubt) against the use of lime and sulphur, emanating chiefly from
the agents of patent or proprietary dips and from the wool
manufacturers.

In the first place, it is frequently asserted that lime and sulphur does
not cure scab. Experience in Australia and South Africa, as well as in
America, has shown beyond any doubt that a lime-and-sulphur dip, when
properly proportioned, properly prepared, and properly used, is one of
the best scab eradicators known.

It is claimed by some that it produces “blood poisoning.” But the cases
of death following the use of lime-and-sulphur dips have been
infinitesimally few when compared with the number of sheep dipped in
these solutions, and when compared with the deaths which have been known
to follow the use of certain proprietary dips. The details of such
accidents, so far as they have been reported, have not shown that death
was due to any property prepared and properly used lime-and-sulphur dip.
It is highly probable that the cases of so-called “blood poisoning” of
shear-cut sheep are generally due to an infection with bacteria in stale
dip containing putrefying material.

The greatest objection raised against the use of lime-and-sulphur dip is
that it injures the wool. This objection is raised by many wool
manufacturers and echoed with ever-increasing emphasis by the
manufacturers of prepared dips; while, after years of extensive
experience with properly prepared dip, its injury to the wool is
strongly and steadfastly denied by the Agricultural Department of Cape
Colony.

It is believed that a certain amount of justice is attached to this
objection to lime and sulphur as generally used; unless, therefore, lime
and sulphur can be used in a way which will not injure the wool to an
appreciable extent, we should advise against its use in certain cases;
in certain other cases the good accomplished far outweighs the injury it
does. Let us, therefore, examine into this damage and its causes.

[Illustration: $1]

The usual time for dipping sheep is shortly after shearing, when the
wool is very short; whatever the damage at this time, then, it can be
only slight, and the small amount of lime left in the wool will surely
do but little harm.

In full fleece lime and sulphur will cause more injury. In Australia the
deterioration was computed by wool buyers at 17 per cent., although in
Cape Colony the Department of Agriculture maintains that if properly
prepared, and if only the clear liquid is used, the sediment being
thrown away, the official lime-and-sulphur formula will not injure the
long wool. The United States Bureau of Agriculture have found some
samples of wool injured by dipping, while on other samples no
appreciable effect was noticeable.

If a lime-and-sulphur dip is used, care must be taken to give the
solution ample time to settle; then only the clear liquid should be
used, while the sediment should be discarded. In some of the above tests
on samples of wool it was found that the dip with sediment had produced
very serious effects, even when no appreciable effects were noticed on
samples dipped in the corresponding clear liquid.

Experience has amply demonstrated that a properly made and properly used
lime-and-sulphur dip is one of the cheapest and most efficient scab
eradicators known, but its use should be confined to flocks in which
scab is known to exist, and to shorn sheep, with the exception of very
severe cases of scab in unshorn sheep. It should only be used when it
can be properly boiled and settled. The use of lime-and-sulphur dips in
flocks not known to have scab, especially if the sheep are full fleeced,
cannot be recommended; in such cases tobacco, or sulphur and tobacco, is
safer and equally good.

All things considered, where it is a choice between sacrificing the
weight of sheep and to some extent the colour of the wool by using
tobacco and sulphur, and sacrificing the staple of the wool by using
lime and sulphur, the owner should not hesitate an instant in selecting
tobacco in preference to lime. The loss in weight by using tobacco and
sulphur is not much greater than the loss in using lime and sulphur,
while the loss in staple is of more importance than a slight
discoloration.

_Preparation of the mixture._—Take 8 to 11 lbs. of unslaked lime, place
it in a mortar-box or a kettle or pail of some kind, and add enough
water to slake the lime and form a “lime paste” or “lime putty.”[8]

Footnote 8:

  Many persons prefer to slake the lime to a powder, which is to be
  sifted and mixed with sifted sulphur. One pint of water will slake 3
  lbs. of lime if the slaking is performed slowly and carefully. As a
  rule, however, it is necessary to use more water. This method takes
  more time and requires more work than the one given above, and does
  not give any better results. If the boiled solution is allowed to
  settle the ooze will be equally safe.

Sift into this lime paste three times as many pounds of flowers of
sulphur as of lime, and stir the mixture well.

Be sure to weigh both the lime and the sulphur. Do not trust to
measuring them in a bucket or to guessing at the weight.

Place the sulphur-lime paste in a kettle or boiler with about
twenty-five to thirty gallons of boiling water, and boil the mixture for
two hours at least, stirring the liquid and sediment. The boiling should
be continued until the sulphur disappears, or almost disappears, from
the surface; the solution is then of a chocolate or liver colour. The
longer the solution boils the more the sulphur is dissolved and the less
caustic the ooze becomes.

Pour the mixture and sediment into a tub or barrel placed near the
dipping vat and provided with a bung-hole about 4 inches from the
bottom, and allow ample time (two to three hours, or more if necessary)
to settle.

When fully settled draw off the clear liquid into the dipping vat, and
add enough water to make a hundred gallons. _Under no circumstances
should the sediment be used for dipping purposes._

[Illustration: $1]

To summarise the position of the United States Department of Agriculture
on the lime-and-sulphur dips:—When properly made and properly used these
dips are second to none and equalled by few as scab eradicators. There
is always some injury to the wool resulting from the use of these dips,
but when properly made and properly used upon shorn sheep, it is
believed that this injury is so slight that it need not be considered;
on long wool the injury is greater and seems to vary with different
wools, being greater on a fine than on a coarse wool. This injury
consists chiefly in a change in the microscopic structure of the fibre,
caused by the caustic action of the ooze. When improperly made and
improperly used the lime and sulphur dips are both injurious and
dangerous, and in these cases the cheapness of the ingredients does not
justify their use. In case scab exists in a flock and the farmer wishes
to eradicate it, he cannot choose a dip which will bring about a more
thorough cure than will lime and sulphur (properly made and properly
used), although it will be perfectly possible for the farmer to find
several other dips which will, when properly used, be nearly or equally
as effectual as any lime-and-sulphur dip. There is no dip to which
objections cannot be raised.


                           _Arsenical Dips._

There are both home-made arsenical dips and secret proprietary arsenical
dips. It is well to use special precautions with both, because of the
danger connected with them. One of the prominent manufacturers of dips,
a firm which places on the market both a powder arsenical dip and a
liquid non-poisonous dip, recently summarised the evils of arsenical
dips in the following remarkable manner:

“The drawbacks to the use of arsenic may be summed up somewhat as
follows: (_a_) Its danger as a deadly poison. (_b_) Its drying effect on
the wool. (_c_) Its weakening of the fibre of the wool in one particular
part near the skin, where it comes in contact with the tender wool roots
at the time of dipping. (_d_) Its not feeding the wool or stimulating
the growth, or increasing the weight of the fleece, as good oleaginous
dips do. (_e_) The danger arising from the sheep pasturing, after coming
out of the bath, where the wash may possibly have dripped from the
fleece, or where showers of rain, after the dipping, have washed the dip
out of the fleece upon the pasture. (_f_) Its occasionally throwing
sheep off their feed for a few days after dipping, and so prejudicing
the condition of the sheep. (_g_) Its frequent effect upon the skin of
the sheep, causing excoriation, blistering, and hardness, which stiffen
and injure the animal, sometimes resulting in death.”

Although this manufacturer has gone further in his attack upon arsenic
than the United States Bureau of Agriculture would have been inclined to
do, it must be remarked that when a manufacturer of such a dip cannot
speak more highly of the chief ingredient of his compound than this one
has done in the above quotations, his remarks tend to discredit dips
based upon that ingredient. Bruce, the Chief Inspector of Live Stock for
New South Wales, speaking of arsenical dips, says: “Arsenic and arsenic
and tobacco (with fresh runs) cured 9,284 and failed with 9,271.”

It may be said, on the other hand, that arsenic really has excellent
scab-curing qualities; it enters into the composition of a number of the
secret dipping powders, and forms the chief ingredient in one of the
oldest secret dips used. This particular dip has been given second place
(with some qualifications) among the officially recognised dips in South
Africa.

_Formulæ for arsenical dips._—Finlay Dun recommends the following:—Take
3 lbs. each of arsenic, soda ash (impure sodium carbonate) or pearl ash
(impure potassium carbonate), soft soap, and sulphur. A pint or two of
naphtha may be added if desired. The ingredients are best dissolved in
10 to 20 gallons of boiling water, and cold water is added to make up
100 gallons. The head of the sheep must, of course, be kept out of the
bath.

A mixture highly endorsed by certain parties consists of the following
ingredients:

         Commercially pure arsenite of soda  14 lbs.
         Ground roll sulphur                34½       „
         Water                              432 gallons (U.S.)

The arsenite of soda is thoroughly mixed with the sulphur before being
added to the water.

_Precautions in use of arsenical mixtures._—Any person using an
arsenical dip should bear in mind that he is dealing with a deadly
poison. The following precautions should be observed:

(1) Yards into which newly-dipped sheep are to be turned should first be
cleared of all green food, hay, and even fresh litter; if perfectly
empty they are still safer. (2) When the dipping is finished, the yard
should be cleaned, washed, and swept, and any unused ooze should at once
be poured down a drain which will not contaminate food or premises used
by any animals. (3) Dipped sheep should remain in an open, exposed
place, as on dry ground. (4) Overcrowding should be avoided, and every
facility given for rapid drying, which is greatly facilitated by
selecting fine, clear, dry weather for dipping. (5) On no account should
sheep be returned to their grazings until they are dry and all risk of
dripping is passed.

The feeling of the United States Bureau of Agriculture towards arsenical
dips is shown by the following:

_Suggestion as to danger._—The formulæ given above are copied from the
writings of men who have had wide experience in dipping, but this Bureau
assumes no responsibility for the efficacy of the dips given, or for
their correct proportions. Furthermore, as long as efficacious
non-poisonous dips are to be had, we see no necessity for running the
risks attendant upon the use of poisonous dips.


                            _Carbolic Dips._

This class of dips kills the scab mites very quickly, but unfortunately
the wash soon leaves the sheep, which is consequently not protected from
reinfection in the pastures. If, therefore, a carbolic dip is selected,
it is well to add flowers of sulphur (1 lb. to every 6 gallons) as a
protection against reinfection.

The advantages of carbolic dips are that they act more rapidly than the
tobacco or sulphur dips, and that the prepared carbolic dips are very
easily mixed in the bath. They also seem, according to Gillette, to have
a greater effect on the eggs of the parasites than either the sulphur or
the tobacco dips. The great disadvantages of this class of dips
are—first, in some of the proprietary dips, that the farmer is uncertain
regarding the strength of material he is using; second, the sheep
receive a greater set-back than they do with either lime and sulphur or
tobacco.

[Illustration: $1]

The United States Bureau of Agriculture is inclined to be extremely
conservative in regard to them, and to advise their manufacturers to
prepare them in a guaranteed strength with more explicit directions for
use than are to be found in the present circulars.

One of the prominent proprietary carbolic dips was formerly recognised
as one of the three official dips in New South Wales, but it has now
been erased from the list. In Cape Town carbolic dips are not much used,
and in the official reports little is said concerning them.

The United States Bureau of Animal Industry gives the following advice
as regards dipping:

(1.) Select a dip containing sulphur. If a prepared “dip” is used which
does not contain sulphur, it is always safer to add about 16½ lbs. of
sifted flowers of sulphur to every 100 gallons of water, especially if,
after dipping, the sheep have to be returned to the old pastures.

[Illustration: $1]

(2.) Shear all the sheep at one time, and immediately after shearing
confine them to one-half the farm for two to four weeks. Many persons
prefer to dip immediately after shearing.

(3.) At the end of this time dip every sheep (and every goat also, if
there are any on the farm).

(4.) Ten days later dip the entire flock a second time.

(5.) After the second dipping, place the flock on the portion of the
farm from which they have been excluded during the previous four or five
weeks.

(6.) Use the dip at a temperature of 100° to 110° Fahr.

(7.) Keep each sheep in the dip for two minutes by the watch—do not
guess at the time—and duck its head at least once.

(8.) Be careful in dipping rams, as they are more likely to be overcome
in the dip than are the ewes.

(9.) Injury may, however, result to pregnant ewes, which must on this
account be carefully handled. Some farmers arrange a stage, with sides,
to hold the pregnant ewes, which is lowered carefully into the vat, and
raised after the proper time.

(10.) In case a patent or proprietary dip, especially an arsenical dip,
is used, the directions given on the package should be carried out to
the letter.


             CHORIOPTIC MANGE, SYMBIOTIC MANGE, FOOT SCAB.

This disease was studied in Germany by Zürn in 1874, and by Schleg in
1877. It has not yet been seen in France.

=Causation.= The sole cause is the presence of _Chorioptes scabiei_ (_v.
ovis_). Contagion is favoured by the animals being in poor condition.
The disease extends very slowly. Only 2 to 3 per cent. of the animals
are affected, and the sufferers are usually those with fine skins.

German shepherds consider this disease to be due to an excessive
allowance of salt, because it is most common during the winter, when the
sheep are housed. Needless to say, this theory is incorrect.

=Symptoms.= Sometimes this form of mange attacks the limbs and develops
very slowly. It commences about the pasterns, and gradually extends
upwards towards the knee or hock. It really advances beyond these
points. The parasites are much smaller than those of common scab, and
are often overlooked. The sheep stamp their feet and scratch and bite
the infected parts, sometimes transferring the disease to the lips and
face, where it may persist for a time.

[Illustration: $1]

In very old standing cases which have been entirely neglected, it may be
met with in the region of the armpit and thigh, the limbs becoming
swollen so as to suggest lymphangitis. In the folds of the hock and
pastern the thickening of the skin may lead to the formation of
yellowish or brownish crusts, according to whether the exudation is
merely of a serous character or accompanied by bleeding.

=The diagnosis= is easy. The parasites are found in the thickness of the
crusts, and are readily recognised under the microscope.

=The prognosis= is not grave, because of the comparative rarity of the
disease and its mildly contagious character. This disease, moreover,
never attacks the head or body, but remains localised in the lower
portions of the limbs.

=Treatment.= The crusts should be removed by washing or by standing the
animals for a time in warm water. Simple cleanliness often suffices,
but, to save time, some anti-parasitic may be used. The condition is
easily cured even without disinfecting the folds.


                            MANGE IN THE OX.

Bovine animals may be attacked by three varieties of mange, all of which
have long been known.


                            SARCOPTIC MANGE.

This is not of any great clinical importance, as it is purely
accidental, and only results from the conveyance of sarcoptes from other
animals, such as the horse, sheep, dog, goat or cat, to an animal of the
bovine species. That the disease does occur, however, is shown by the
following excerpt from a report by Professor McFadyean: The animal
showed no symptom of skin disease at the time of purchase, but soon
after it was brought home it was noticed to be rubbing, and the skin
began to assume an unhealthy appearance. When seen in January (four
months after purchase) it was rather poor, although it had been in very
good condition when sold. Almost the entire skin had become affected,
including that of the legs down to the top of the hoofs. There had been
extensive loss of hair, and the skin was thick, grey, wrinkled, and dry.
At some places it had become thrown into thick folds. Only a few scabs
or crusts had formed where the animal had recently rubbed itself. In
some scurf scraped from what seemed to be the parts most recently
invaded, numbers of acari were without much difficulty found with the
microscope.

A good many cases of mange of undetermined character have been reported
as occurring among cattle in various parts of England during the last
year or two, and in a number of instances the disease was believed to
have been contracted during exhibition at a show. It is not improbable
that some or all of these were cases of this sarcoptic mange, and in
view of its very contagious character it is desirable that care should
be taken to exclude from shows animals exhibiting any symptom of the
disease.


                            PSOROPTIC MANGE.

This condition has also been termed dermatodectic mange. This is very
rare, and, like the former, of trifling clinical importance.

=Causation.= It is due to infection with _Psoroptes communis_ (_v.
bovis_). Poor condition, want of grooming, bad hygienic surroundings and
general neglect, facilitate its spread.

=Symptoms.= It commences at the base of the neck, in rarer cases at the
sides of the neck, along the withers, and at the root of the tail;
thence it gradually attacks the croup, loins, back, shoulders, sides of
the chest, and finally all the body with the exception of the limbs.

It produces violent itching, the animal continually scratching itself,
even causing raw sores. At first the epidermis is elevated in little
miliary points, which may be isolated or confluent, and are filled with
serosity. This fluid discharges, gluing together the hairs; it then
hardens and produces adherent crusts, which increase in number and size.
The skin exhibits large numbers of bare, mangy points; these have
irregular margins, and are covered with thick, grey, scaly crusts. The
psoroptes are found under these crusts.

The skin becomes hard, dry, fissured and cracked, and sometimes forms
large folds on the sides of the neck, shoulders and chest.

The influence of the seasons on the development of this disease has been
well shown by Gerlach and Muller. The disease commences about the end of
autumn, when the animals are stabled. It continues to extend until
February, but diminishes as soon as the animals return to the fields in
spring. The crusts fall, the hair again grows, and the animal appears to
be cured, but the disease again revives during the autumn. The psoroptes
lie hidden during the summer round the poll and the horns. The disease
seldom attacks animals at grass and in good condition, or those over
three years old. Calves, yearlings, and two-year-olds in poor condition
suffer most.

When the disease is very extensive, the animals lose condition and may
even die.

=Diagnosis.= Psoroptic mange in the ox may be mistaken for several
cutaneous diseases, to which it has a certain resemblance, as for
instance phthiriasis and the first stage of ringworm.

These different diseases, however, show their own distinctive symptoms
on a careful examination.

=The prognosis= only becomes grave when the disease has been neglected
and the animals are greatly reduced in condition. When recent, this form
of mange can readily be cured by the application of parasiticides.

=Treatment.= As in dealing with all transmissible diseases, the animals
must be isolated and washed with soap, and the diseased parts must be
dressed with some parasiticide, such as sulphur ointment. The best
preparations are: Benzine and petroleum in equal quantities;
concentrated solution of sulphuret of potassium (8 ounces to the quart);
Helmerich’s ointment; diluted creolin solution; decoctions of tobacco;
ointment of pentasulphuret of potassium, and oil of cevadilla.

One or two applications are generally sufficient to effect a cure, and
relapses are not likely to take place if the stable is disinfected. In
America the disease is common in the West and North-West, where it is
treated by the lime-and-sulphur bath recommended for sheep scab (which
see). Large vats are constructed, and the oxen are lowered into these by
means of a wooden cage controlled by machinery, which is operated either
by a small engine or more frequently by a horse.

The food should be of good quality, for good general health plays a
great part in resisting parasitic invasions.


                           CHORIOPTIC MANGE.

This disease has also been termed dermatophagic and symbiotic mange.

It was first described in 1835 by Kégélaar, and has been the subject of
investigation by Hering, Gerlach, Delafond, and Mégnin.

=Causation.= It is produced by the _Chorioptes bovis_, and is
transferred with difficulty, even by cohabitation.

=Symptoms.= This form of mange in the ox does not affect the same parts
as in other animals. In the horse, etc., it attacks the limbs, whilst in
the bovine species it is usually found at the base of the tail. It
causes slight itching. The diseased region becomes covered with numerous
little pellicles, the hairs gradually fall, crusts form, and the skin
shows deep cracks. When the disease is completely neglected, it may
extend to the loins, back, sides of the body and shoulders. It may also
affect the perineal region, the inner surface of the thighs, and in fact
the whole of the body if the animals are young and in poor condition.

=Diagnosis.= At the outset it is difficult to distinguish between
chorioptic and psoroptic mange, and the use of the microscope is
necessary. On a superficial examination chorioptic mange may be mistaken
for phthiriasis when the latter attacks the posterior portions of the
body, particularly the base of the tail, and when it is accompanied by
eruptions, loss of hair, and intense itching.

The distinction between the two conditions, however, is extremely easy
after an examination of the two parasites.

=Prognosis.= The disease is of slight gravity, and does not threaten the
animal’s health unless neglected for so long a time that the parasites
invade all parts of the body. In that case the disease may cause anæmia
and loss of condition.

=The treatment= of this form of mange comprises nothing special, it
being sufficient to proceed as directed in the previous article.

The stables ought always to be thoroughly disinfected.


                           MANGE IN THE GOAT.

The goat suffers from the attacks of sarcoptes, psoroptes, and
chorioptes, but up to the present time only two forms of mange have been
described, sarcoptic and chorioptic mange.

Psoroptes have only been found about the eye, where the disturbance they
produce is comparatively trifling.


                            SARCOPTIC MANGE.

This disease was noticed in 1818 in goats imported into France from
Thibet.

Henderson published the history of a Persian goat which conveyed
sarcoptic mange to men and horses. In 1851 Walraff noticed an epizootic
mange which attacked the goats in the Prattigau valley of Switzerland,
which was transmitted to men and sheep and which exhibited the clinical
characters of sarcoptic mange.

=Causation.= This disease is due to the presence of _Sarcoptes scabiei_
(_v. capræ_).

It sometimes occurs in an epizootic form, as Walraff’s observations
show, but it seems specially to attack goats in Asia and Africa.

This mange may be transmitted by the goat to sheep, in which animals it
attacks the head and muzzle; it is particularly contagious in sheep
having coarse, dry fleeces.

Similarly sarcoptic mange of sheep may be conveyed to the goat, in which
animal it extends all over the body.

=Symptoms.= This mange causes intense itching. It first attacks the head
and ears, then the trunk, belly, udder, and limbs. If the disease is
neglected it becomes generalised very rapidly, and the animals waste
away and die in a very short time.

At the commencement little crusts, which discharge a viscous liquid, are
found about the head. The goats rub themselves raw, and, as in facial
mange of sheep, there appear dry, scaly, branlike patches. After a time
the diseased area extends, the wool falls, and the skin becomes dry,
thick and wrinkled. The appearance is exactly like that of sarcoptic
mange in sheep, the lower part of the head being seldom invaded. The
animals lose condition, waste and die of exhaustion.

=Diagnosis.= The parasite is readily recognised, and the practitioner,
moreover, is often put on his guard by the epizootic character assumed
by the disease.

=The prognosis= is grave. Walraff declared the mortality in Grisons
(Switzerland) to be as high as 20 per cent.

=The treatment= is identical with that of psoroptic mange in sheep.
After the animals have been sheared and washed with soap, they should be
completely immersed in a bath of the character mentioned in connection
with sheep scab. If only one animal is infected, it may be sufficient to
dress it repeatedly with an ointment containing some parasiticide.


                           CHORIOPTIC MANGE.

This form of mange was noted by Delafond in 1854 at the Jardin des
Plantes (Paris) in some angora goats, and by Mollereau in 1889. The
disease studied by Delafond had invaded both sides of the neck, the
eyes, withers, back, loins, and base of the tail. It was characterised
by partial loss of hair, the finer hair falling and the coarser
remaining in position.

In Mollereau’s case the disease was located in one of the hind pasterns,
and assumed the form of a thickened band, which produced an œdematous
swelling. The chorioptes were discovered in a thick crust formed by the
drying on the hair of the discharge due to their punctures.

=Diagnosis.= The parasites can easily be found under the crusts, and,
once recognised, distinguish the disease from any other infection.

=Treatment.= Ointments containing some parasiticide and solutions of
sulphuret of potassium generally suffice, the disease having little
tendency to become generalised.


                           MANGE IN THE PIG.

The pig suffers from one variety only of mange. It was described by
Viborg, Gürlt and Spinola, who found a sarcopt in the mange of wild
boars in 1847. Hertwig and Gerlach made a similar observation some years
later. Delafond in 1857 discovered the sarcopt of mange in the pig.

=Causation.= Sarcoptic mange in the pig is due to the presence of
_Sarcoptes scabiei_ (_v. suis_), although the pig may contract
(temporarily) the sarcoptic mange of goats.

Contagion is favoured by poor condition, over-crowding, dirt and bad
hygienic surroundings.

The primitive races of pigs resist the disease better than the improved
races. This mange can be conveyed to man and to other animals.

=Symptoms.= It usually commences about the head, ears, and eyes, and
extends to the quarters, internal surface of the thighs, etc. In the
early phases it is impossible to discover the little galleries under the
epidermis, but closely placed reddish papules may be seen. The active
proliferation of the epidermis, together with discharge, causes the
formation of dry crusts of a greyish-white, silvery tint, adherent while
still thin, easy to detach at a later stage, and sometimes ⅜ of an inch
in thickness. The skin becomes wrinkled, the bristles are shed or
loosened in their follicles, and are glued together in little bunches
before falling. As these patches extend over the whole surface of the
body, the animal appears to be bespattered with dry guano (Muller).

Under the crusts the skin is rough, excoriated, and, about the thorax
and abdomen, is indurated, and sometimes measures 1 to 1½ inches in
thickness. In other parts, particularly at the base of the ears, the
papillæ are hypertrophied; they become as large as a pea, or even a
bean, and, lifting the crusts which cover them, assume the appearance of
the warts sometimes found on the cheeks of dogs or the teats of cows.
Sarcoptes may be found under these epidermic growths, though in order to
obtain them the skin must be scraped until it almost bleeds.

The dimensions of these parasites render them visible to the naked eye.
They are the largest variety of the sarcoptinæ, the egg-bearing female
being half a millimètre in length. Guzzoni has found in the ears
specimens of smaller size.

Mange in pigs develops slowly. When it affects the whole body, it
prevents fattening and causes loss of condition.

=Diagnosis.= This is the only parasitic disease which affects the entire
surface of the body and presents these peculiar powdery crusts.

=Treatment.= All the styes should first be carefully disinfected.
Treatment is commenced by vigorously scrubbing the animal with a brush
dipped in soap and water, and thus getting rid of the crusts as far as
possible.

The animals are afterwards dressed with decoctions of tobacco, with
Helmerich’s ointment, or the other mixtures above mentioned.


                            DEMODECIC MANGE.

This mange is produced by parasites of the family Demodecidæ (_Demodex
folliculorum_), which live in the hair follicles and sebaceous glands of
several species of mammals.


                       DEMODECIC MANGE IN THE OX.

This was described in 1845 by Gros, and in 1878 was found by Faxon in
Illinois in the skins of cows prepared for tanning. It has not been met
with in France. The skins examined by Faxon showed numerous rounded
enlargements, resulting from dilatation of the hair follicles in the
regions of the neck and shoulders.

By pressing on these enlargements a whitish, greasy, sebaceous material
was ejected, very rich in demodectes.


                      DEMODECIC MANGE IN THE GOAT.

[Illustration: $1]

This was first noticed by Niederhaüsern, at the Bern Veterinary College,
in a goat which showed little nodosities over different parts of the
trunk, varying in size between that of a pea and that of a hazel-nut. By
forcibly compressing these enlargements a yellowish-grey semi-solid
material, containing a considerable number of demodectes, was caused to
exude.

In 1885 Nocard and Railliet found the same parasite in a young he-goat;
the pustules were spread over the sides and flank. =Treatment= consists
in opening the pustules and dressing them a few times with an
anti-parasitic lotion.


                      DEMODECIC MANGE IN THE PIG.

This was well described for the first time by Csokor. It was afterwards
seen by Neumann and Lindqvist.

The isolated pustules are of the size of a grain of sand, but when
confluent may reach the size of a hazel-nut. They are sometimes dark in
colour, often deep-seated, are surrounded by a zone of inflammation, and
appear in places where the skin is fine (the groin, neck, belly, etc.).
The demodex becomes lodged and multiplies, not in the hair follicles,
but in the sebaceous glands. Csokor regarded this disease as contagious;
in a herd of one hundred he found twenty-two pigs affected with it.
Lindqvist, however, found but one case in a herd of two hundred.


                   NON-PSOROPTIC FORMS OF ACARIASIS.

These are produced in farm animals by arachnide belonging to the
families of Trombidiidæ and Ixodidæ.

(1.) =The Leptus autumnalis= is considered to be the larva of the
_Trombidium Holoscriceum_, or silky trombidion. It lives in late summer
and autumn, in the grass.

=Symptoms.= The animals show intense itching, and cannot sleep owing to
burning sensations. They continually rub themselves, and thus,
secondarily, produce excoriated papules and patches resembling those of
eczema. When the papules are very numerous, particularly if the animals
are thin-skinned, more or less extensive erythema may be produced.

At the points attacked the skin swells, becomes red, and sometimes even
violet, and exhibits irregular, isolated or confluent swellings, ¼ to ⅜
of an inch in diameter.

The parasite most commonly becomes fixed round the lips, the forehead,
the cheeks, the sides of the neck, and the extremities.

=The diagnosis= is easy, the discovery of the parasite removing all
doubt.

The condition is of slight importance. The parasites do not live for
more than a few days on the animal’s skin, so that they only produce
temporary disturbance.

=Treatment= consists in bathing the parts with some lotion, such as 2 to
3 per cent. creolin or 2 per cent. chloral, or in applying mixtures of
oil and petroleum, etc.

(2.) =Ixodes hexagonus=, =I. ricinus=, and other species of the tick
family (Ixodidæ) attack sheep, goats, and oxen in France.

=Symptoms.= In sheep the ixodidæ usually affix themselves at points
where the skin is tender and unprotected by wool, as for instance the
thighs, armpit, and upper part of the neck. Their bites produce
irritation, followed by an intense burning sensation, and the formation
of a red blush round the point bitten.

In the ox the ticks fasten on the neck, behind and within the ears, and
also wherever the skin is tender. Until the last few years little
importance was attached to their development, but since it has been
proved that _Rhipicephalus annulatus_ is the active factor in
desseminating Texas fever, ticks have attracted much attention.

It seems, moreover, to be proved by the researches of Lignières that a
form of piroplasmosis exists in France, and it seems possible that the
_Ixodes ricinus_ may be a means of propagation.

=The diagnosis= of acariasis produced by ticks is easy, for the
parasites attain large dimensions.

=Prognosis.= It is difficult at present to say what importance should be
attached to this form of acariasis, but its existence and possible
consequences should be noted.

=Treatment.= Some authors have recommended killing the ticks by touching
them with benzine, petroleum, essence of turpentine, etc., but these
methods do not always succeed. Applications of concentrated solution of
chloral are more effective. When the parasites are so large as to render
this possible it is better to remove them by hand, taking care at the
same time to remove the rostrum, which, if left in place, might cause
more or less suppuration. In countries where ticks are numerous and
large numbers of cattle are infested, the parasites are destroyed by
smearing and dipping.

[Illustration: $1]

(The cattle ticks of America are of especial importance in relation to
the disease known as Texas fever. Those who wish to study the entomology
of this subject are referred to the masterly account and fine coloured
illustrations of Salmon and Stiles, “Cattle Ticks of the United States,”
Ann. Rep. U.S.A. Bureau of Agriculture, 1900, p. 380.)


                   HYPODERMOSIS IN THE OX (WARBLES).

=Causation.= This is a parasitic disease characterised by subcutaneous
swellings due to the presence of larvæ of the _Hypoderma bovis_. The
larva is met with throughout Europe. It attains the perfect stage during
the summer, from the middle of June to the commencement of September.

The female deposits her eggs on animals with fine skins. These eggs are
elliptical, and provided with a kind of tail of a brownish colour. They
soon become converted into larvæ, provided with rows of little spines.

The manner in which the eggs are laid is not exactly understood, nor are
we better informed regarding the hatching of the young larvæ. Until
recently it was believed that the larva perforated the skin as soon as
it quitted the egg, and then penetrated as far as the subcutaneous
connective tissue. Recent observations, however, have upset this view.
It is probable that this larva, like other gastrophili, is swallowed by
animals of the bovine species, and passes through the intestine into the
surrounding tissues by a path which is yet unknown, possibly by the
blood-vessels, whence it makes its way after a longer or shorter
interval into the subcutaneous connective tissue.

[Illustration: $1]

Certain recent observations seem to support the latter view, which is
also corroborated by known facts regarding hypodermic myiosis in man.
The eggs are laid in summer, and the swellings indicating the presence
of the larvæ only appear during the winter. Henrichsen found young larvæ
in the fatty tissue situated between the periosteum and spinal dura
mater, between the period from December to March.

=Symptoms.= Whatever the mode of development of the larvæ, cutaneous
swellings appear between the months of February and March on the back,
lumbar region, quarters, shoulders and ribs, and, less frequently, over
the chest, belly and thighs.

They vary in number. Commonly there are from ten to twenty, and it is
only in rare cases that less than four or five are found. As soon as
they attain the subcutaneous connective tissue they act as foreign
bodies, causing a circumscribed inflammation, and finally suppuration.
In this way the so-called “warbles” are produced.

Each larva is surrounded by a thick wall, forming a cavity, which
communicates with the outer air by a minute aperture.

When the swelling is sufficiently advanced the larva may be extricated
by pressing with the fingers around the base of the warble. A few days
before it leaves its shelter the larva enlarges the little opening by
thrusting its last rings into it. Soon after the larva has escaped the
discharge of pus ceases, and the skin wound heals.

=Diagnosis.= The times at which the swellings appear and the larvæ are
present render the diagnosis easy.

=Prognosis.= This is seldom grave, for the larvæ rarely cause death. In
cases where they are present in very large numbers, however, they may
set up purulent infection.

=Treatment.= No really effective treatment against warbles is known.
Curative treatment consists in squeezing out or killing the larvæ when
in the subcutaneous tissue, but this is practically useless, as the dead
larvæ then set up prolonged suppuration.




                              CHAPTER III.
                               RINGWORM.


The old term “ringworm” is still used to indicate a well-marked skin
disease due to parasitic fungi which grow at the expense of the
epidermis. Other names, such as dermatophytis and epidermophytis, have
been suggested, to indicate the mode in which the parasite grows. The
term dermatomycosis suggests a cutaneous vegetable parasite.

The dermatomycoses of the domestic animals are caused by fungi belonging
to six distinct genera:—

_Trichophyton_ (horse, ass, ox, dog, pig); _Eidamella_ (dog);
_Microsporum_ (horse, dog); _Achorion_ (dog); _Lophophyton_ (fowl);
_Oospora_ (dog).

Ringworm is common in animals of the bovine species, but very rare in
other domesticated animals, except, perhaps, the horse. It is caused by
the growth of a parasite, _Trichophyton mentagrophytes_ (Robin), of the
genus Trichophyton, family Gymnoascea, order Ascomycetes.

The ascosporaceous form of reproduction is still unknown, but the mode
of reproduction by conidia is characteristic. In cultures the mycelium
is represented by growing filaments branching off at right angles, and
by separate superficial aerial reproductive filaments of the conidian
form. There is some reason for believing that these fungi may lead a
saprophytic as well as a parasitic existence, _i.e._, that they can
exist and multiply apart from the animal body.

Their vitality is marked. Various experimenters have transmitted the
disease with crusts kept for eighteen months. Thin declares that in two
and a half years the spores had lost all power of germination. They
resisted immersion in water for two days, but were dead after eight
days. Soft soap and 1 per cent. acetic acid kill them in an hour.

=Symptoms.= The disease most frequently attacks young animals and milch
cows—very rarely adults or old animals. This peculiarity is very
difficult to explain.

In calves, ringworm seems specially to attack the head, the
neighbourhood of the lips, the nostrils and submaxillary region, as well
as the throat and neck. It assumes the form of circular patches, over
which the hair stands erect.

Gruby in 1842 discovered the parasite of tinea tonsurans, or herpes, and
thus proved that the cutaneous lesions were not due to any
constitutional condition, as was long thought, although dirt, bad
hygienic conditions, and crowded stables favoured the spread of
ringworm.

[Illustration: $1]

Direct contact between healthy and diseased animals and the transport of
spores, by combs, brushes, etc., favour contagion. The disease may not
only be conveyed from one animal to another of the same species, but
from the ox to man, and, with somewhat greater difficulty, from the ox
to the horse. Cases of transmission from the ox to the sheep, pig, and
dog have also been recorded.

Mégnin in 1890 attempted to prove that all the trichophytons producing
ringworm in animals do not belong to the same species, and gave the name
of _Trichophyton epilans_ to that usually found in the ox, because it
causes absolute loss of the hair by growing in the follicle, whilst he
named the parasite found in the horse _Trichophyton tonsurans_, because
it only grows on the surface of the skin and in the thickness of the
hair, without causing inflammation of the hair follicle and without
invading it.

The epidermis soon undergoes proliferation, and becomes covered with
crusts, which adhere to the hairs, gluing them together, and finally
causing them to be shed, leaving bare patches the size of a shilling or
a florin. The lesion extends in an ever-widening circle, until it
attains, perhaps, the dimensions of a five-shilling piece or more.

The affected hairs break off level with the free surface of the skin,
rendering the patches more apparent. White hairs are less affected, and
some always remain projecting above the crusts, causing the patches,
when on a white skin, to retain a certain amount of covering.

At first the crust is closely adherent to the skin, and, if forcibly
detached, exposes the dermis, which is swollen and bleeding. Gradually
the centre becomes detached, whilst the periphery, representing a more
recent lesion, continues to adhere. The crusts then rest on a thin layer
of pus, and the dermis, whilst still inflamed, is punctuated with
numerous minute apertures, representing the roots of the detached hairs.
The pus lifts the crust; gradually it dries up and forms superposed
layers, which may or may not prove adherent to the parasitic products,
and which form a new crust. The latter is purely inflammatory in
character, and is left after the fall of the first. It no longer
contains any parasites, at least within its deeper layers.

This second crust dries up in its turn, falls away or breaks up, leaving
a smooth spot, over which the hairs again appear, either at once, or at
least after a short period of desquamation.

The disease is accompanied by well-marked pruritus, more marked at the
commencement and towards the end than during the intermediate period,
but, nevertheless, much less acute than in scabies.

Ringworm may undergo spontaneous cure in from six weeks to three months.
It is more obstinate in calves than in adults, and the want of grooming
tends to increase its duration. If it extends over a large part of the
body the disease may seriously affect the animal’s health, and the cases
described by Macorps prove that where pruritus is violent it seriously
affects the animal’s general condition.

The patches may finally become confluent and the disease extend over the
whole of the neck, shoulder and back, or it may attack the entire body,
leaving it practically hairless.

When the hair has been shed, the crusts and discharge seen at the outset
disappear, and the bare spots are covered with a scaly coating, due to
excessive production of epidermic cells.

According to Gerlach, such crusts are thicker where the skin is black,
and often exhibit a greyish-white, fibrous, starchy appearance. On
unpigmented portions of the skin, which are usually thinner, the crust
is less dense, and is slightly yellowish. Gerlach failed to reinoculate
the bare patches of skin left after a primary eruption of ringworm.
Where the hair had again grown an eruption could again be produced,
though it was usually of a feeble character.

In a second form of the disease, the spots may be of very small
dimensions. The hair falls away, but there is no exudative inflammation,
and no formation of crusts. In this second form the animals simply show
characteristic circular bare spots about the head, neck, or shoulders.

=Causation.= The disease is due to the growth of germs on the skin of
animals which are in a receptive condition. The parasite thereafter
develops in the hairs, the hair follicles and the epidermis, causing
lesions which vary according to the species.

At the present time three groups of ringworm are recognised as occurring
on animals, Trichophytic, Microsporous, and Favus.

Clinically the trichophytons are divided into the _T. ectothrix_, which
lives outside the hair, and both outside and inside the hair follicles;
_T. endothrix_, which penetrates the thickness of the hair itself,
rendering it brittle and easily destroyed; and _T. endo-ectothrix_,
which both surrounds and invades the hair.

The study of artificial growths of these fungi will probably afford
valuable information on the above points. In the ox the particular
parasite is invariably the _Trichophyton mentagrophytes_, whatever may
be the characteristics of the clinical lesion.

In France ringworm is particularly common in Auvergne and Normandy,
where hygienic precautions are neglected, but cases may also be found
throughout the country.

After affecting cows throughout the winter, the disease often disappears
in the spring. Throughout the winter cows are kept in dark and often
filthy sheds, where the parasite propagates rapidly, whilst in spring
they are sent to grass, where the conditions are inimical to contagion.

=Diagnosis.= The diagnosis of ringworm seldom presents any difficulty.
The appearance of the lesions (Fig. 266), their particular tendency to
spread and contagious character, facilitate the diagnosis. They entirely
differ from those of eczema or mange, and should any doubt exist, the
slightest microscopic examination is sufficient to dissipate it. In
ringworm in the ox the base of the hairs is covered with enormous
numbers of spore chains, which do not extend into the depths.

To detect the parasites it is best to shave off a thin fragment of skin
from the periphery of the patch, place it on a slide with a drop or two
of 30 per cent. caustic potash solution, and heat it for a few seconds
almost to boiling point. By applying a cover glass with firm pressure
the epidermal cells are spread out and the parasites can be seen,
especially around the roots of the hairs. Sometimes they form little
dirty-yellow masses, consisting almost exclusively of spores.

When ringworm has attacked the entire surface of the body, it is much
more difficult to distinguish from sebaceous eczema, and a microscopic
examination or experimental inoculation may become necessary.
Inoculation with ringworm material always succeeds with calves.

=Prognosis.= Ringworm is not dangerous in itself. In time it may
disappear spontaneously, but when it extends over the whole body it may
be dangerous. Owing to their bare condition the animals easily catch
cold, while the epidermic proliferation is very great, and makes great
demands on the animal’s bodily powers. Under such circumstances it is
better to slaughter early.

Spontaneous recovery from small lesions may occur in two or three
months.

=Treatment.= The patients should be isolated, and any brushes, combs,
etc., with which they have been in contact must be disinfected.

The diseased areas should then be dressed with some fatty substance, to
soften the crusts and enable them to be removed without injury.

Dressings are useless unless these crusts have been removed, for the
spores are always in the deepest recesses and in the follicles, so that
the drugs employed never come in contact with them.

Once the skin is cleansed, numerous chemical substances may be utilised,
the solutions being applied for several days in succession. Amongst them
may be mentioned tincture of iodine, oil of cade, 10 per cent. solution
of sulphate of iron, and solution of perchloride of iron. Such drugs,
however, must not be used for a long time, as they all attack the skin
to some extent.

When the patches are small and well defined the following mixture proves
very efficacious:—

               Crystallised carbolic acid } Equal parts.
               Tincture of iodine         }      „
               Chloral hydrate            }      „

Two or three applications generally prove successful.

Despite the natural activity of the spores, which are capable of
germination after three months’ desiccation, some medicines are useful,
although it is necessary, in order to judge of their effects, to wait
for the renewal of the skin, hair follicles, and hair.

Where the disease is generalised this form of treatment is scarcely
practicable, or at least it becomes more difficult.

Nevertheless, by dressing with soft soap the disease may be cured in a
few months. The soap should remain on the skin for some hours and then
be washed off, after which dressings of creolin, lysol, or chloral
solution, etc., should be employed.


                 RINGWORM IN THE SHEEP, GOAT, AND PIG.

Little information regarding the dermatomycoses of the sheep, goat, and
pig is available. Allowing for modifications due to the nature of the
coat, the =symptoms= of recorded cases seem to indicate a close
relationship with ringworm in the horse and ox.

In sheep suffering from ringworm, the wool is at first matted into small
irregular tufts, which grow larger and more numerous. The coat appears
felted together at various points. The neck, chest, shoulders and back
exhibit crustaceous patches covered with branlike epidermal scales, and
the animals suffer from marked pruritus, which causes them to rub and
injure the coat.

Ringworm is very obstinate in the goat.

Two pigs described by Siedamgrotsky showed irregular, rounded patches,
due to trichophyton, from 1 inch to 2 inches in diameter, reddish in
tint, without exudation, but covered with abundant scales.

In the pig ringworm attacks the croup, sides of the chest, flanks and
sides of the abdomen, but is commonest on the back and outside of the
quarters. It forms red isolated patches, from 1 to 2 inches in diameter,
covered with miliary vesicles, which in turn are replaced by brown
crusts. The bristles remain unchanged, and are not shed or broken. There
is no pruritus. Contagion from pig to pig occurs readily. The disease
may be conveyed from oxen to pigs through the medium of litter removed
from the cowsheds to the piggery.

Gerlach was unable to inoculate sheep or pigs with ringworm from the ox.
Perroncito mentions a case of contagion from the ox to a lamb.
Schindelka has seen sheep contract ringworm as a result of confinement
to sheds previously occupied by oxen suffering from the disease.

Siedamgrotsky successfully inoculated two pigs and two sheep with
ringworm from the horse and a goat with the bovine form of the disease.
The two pigs inoculated two others by contact. Contagion from the goat
to the ox was noted in the canton of Zürich in 1852.

Fuller particulars on these heads will be found in a series of articles
by Neumann in the _Revue Vétérinaire_, January to June, 1905.

In 1876 Laillier communicated to a French medical society a letter
written by Lespiau describing an endemic of trichophyton disease in the
cantons of Céret and Arles-sur-Tech. Thirty-four persons, including
twenty-eight children, were affected. A dog was first attacked and seems
to have inoculated a pig, which in these districts often lives with the
human family. The pig inoculated the human beings. A moist season
appears to have favoured the development of the disease. The parts
principally attacked were the head, eyebrows, cheeks, and neighbourhood
of the genital organs. The subjects showed considerable pruritus.




                              CHAPTER IV.
                             WARTS IN OXEN.


Warts are cutaneous tumours, real papillomata, which most commonly
attack young animals such as heifers. As a rule they are pedunculated,
smooth, wrinkled or deeply cracked on the surface, but in some cases
they are sessile.

=Causation.= The cause is difficult to ascertain. It has been referred
to the growth of bacteria (_Bacterium porri_) in the superficial layers
of the skin. It is at least certain that warts can be transmitted by
inoculation or through the medium of cutaneous injuries.

=Symptoms.= On their first appearance warts consist in hypertrophy of
the cutaneous papillæ, which become covered with layers of actively
growing epidermis and end by projecting above the general surface. The
lesions may remain isolated, or they may become confluent or unite at
their base. This form is fairly common, the warts attaining the size of
a man’s fist or more.

The disease attacks the most tender portions of the skin, such as that
covering the udder, internal surface of the thighs, lower abdominal
wall, region of the elbow, posterior surface of the ears, etc. In rarer
cases warts may be seen on the limbs.

When they extend over a considerable surface they become infected,
suppurate and give rise to various complications, the most serious being
pyæmia. The patients lose condition and value.

=Diagnosis.= The diagnosis is easy. It has been proved that warts are
contagious, not only as between animal and animal, but as between animal
and man.

=Prognosis.= Warts are not dangerous to life, but they diminish the
value of the animals, particularly that of milch cows when the teats are
affected.

=Treatment.= Leaving out of account internal medication with calcined
magnesia, many medicines that are still recommended are of comparatively
little value.

Peuch and Cruzel recommend friction with oil of cade. Repeated
cauterisation with nitric acid is declared to give good results by
destroying the new tissue.

These modes of treatment, however, are impracticable in dealing with
large multiple lesions, nor does the elastic ligature give much better
results.

Total removal with the scissors or bistoury, or simply tearing out by
hand, is preferable to any other course. Troublesome bleeding may
follow, but is rarely of great importance. It usually stops in a few
minutes, even where small arteries of the size of several millimètres in
diameter have been divided. As a measure of precaution, however, the
little wounds may be touched with the red-hot blade of the
thermo-cautery.

The _écraseur_ is rarely required. The smaller warts are generally
sessile, and can be removed with a bistoury or a sharp curette. The
removal of those about the udder requires considerable precaution to
avoid injuring the teats.

[Illustration: $1]

All the growths are usually removed at one operation; Moussu has thus
taken away 30 lbs. weight without the slightest ill effect. After the
wounds have been washed with an antiseptic, the raw surfaces are
powdered with a mixture of equal parts of boric acid, tannin, and
calcined alum; cicatrisation occurs in a few days.


                         URTICARIA IN THE PIG.

This disease usually attacks pigs during the spring or summer, producing
characteristic cutaneous lesions, which, however, are of a benign
character. It seems to arise from some form of alimentary intoxication.

=Symptoms.= At first the dominant symptoms point to disturbance of
digestion. The appetite is lost, and the bowels may be confined or there
may be diarrhœa. This is sometimes accompanied by vomiting, and by
fever.

The symptoms may develop fully in from six to twelve hours; sometimes
the skin is covered with slightly prominent reddish patches, varying in
size from ⅓ of an inch to 1¼ inches in diameter.

The patches may also become confluent and form large, irregular red or
violet flattened swellings, sensitive to the touch and spread over the
upper and lateral portions of the body. Only in exceptional cases is
there any oozing of blood.

In favourable cases recovery takes place in forty-eight hours, and even
in grave cases in from five to six days.

=Diagnosis.= It is sometimes very difficult to distinguish this
condition from swine erysipelas, particularly in the first few cases,
although the congested or hæmorrhagic patches occupy different
positions.

=The prognosis= is usually favourable.

=Treatment.= The disease being unquestionably of digestive origin, the
animals should be kept without food and receive repeated doses of mild
purgatives according to their age and condition, sulphate of soda, 4 to
12 drachms, or calomel, 1½ to ·8 grains. Recovery is rapid.


                              SCLERODERMA.

This term is applied to a disease characterised by thickening and
hardening of the skin. Up to now it has been described only in the pig,
and principally in male animals or old animals of either sex.

=The symptoms= are difficult to detect, and in many cases are only
discovered after slaughter. Without any change in external appearance,
the skin becomes thick, hard and sclerosed over limited or extensive
areas, and is thus transformed into hard, rigid, inextensible and
inelastic plates, sometimes as much as 1 to 2 inches in thickness. The
change usually commences about the dorsal region, and extends
irregularly towards the chest and sometimes towards the limbs.

The patient thus becomes imprisoned in a kind of cuirass, which
interferes with its movements and causes unaccountable stiffness.
Palpation of the skin gives the impression of a piece of wood, for it is
hard and resistant over the affected regions, whilst over the belly,
inner surface of the thighs, and region of the elbow, it retains its
usual pliability.

The patient exhibits no other symptoms, the principal functions of the
body appearing to be properly performed. There is no fever, but in time
the animals lose condition and waste away.

=Causation.= This disease is also well known in man, but no general
agreement exists regarding its nature. Some refer it to disturbance of
the thyroideal function, though scleroderma is quite different to
myxœdema. Others attribute it to changes in the cutaneous blood-vessels,
others, again, to peripheral neuritis accompanied by atrophic
disturbance. Nothing, however, is proved.

The apparent =lesions= are limited to hypertrophic sclerosis of the
dermis, with progressive atrophy of the layers of subcutaneous adipose
tissue.

=The diagnosis= is comparatively easy.

=The prognosis= is grave, because it is never known how rapidly the
disease may develop.

No method of treatment being known, the animals should at once be
slaughtered.




                               CHAPTER V.
                        SUBCUTANEOUS EMPHYSEMA.


By subcutaneous emphysema is meant the condition produced by the
entrance of air or gas into the subcutaneous and interstitial connective
tissue. Emphysema may remain localised or it may become generalised,
according to the nature and extent of the lesion which causes it, and
the points where emphysema is developed. Subcutaneous emphysema is
common in the sheep and ox.

=Symptoms.= Sometimes the symptoms of subcutaneous emphysema are
extremely well defined. They consist in the presence of diffuse or
limited crepitant swellings which may appear at various points—in the
flank or the entrance to the chest; more rarely in the region of the
elbow, etc.

The limits of crepitation may be ascertained by palpation, while
percussion produces a peculiar abnormal sound. The subcutaneous tissue
and very often the interstitial tissue appear as though blown out.

Emphysema may be generalised. Such an accident is rare, but may occur in
the ox as well as in the sheep and goat.

Provided the emphysema remains confined to the subcutaneous tissue, the
animals are not necessarily in danger. Where, however, it also extends
to the interstitial tissue, and particularly if the cause to which it is
due continues, death may result in a very short time. This occurs, for
example, when the emphysema extends into the mediastinum, and thus gains
the pleura and lung.

The symptoms of emphysema are then complicated with respiratory and
circulatory disturbance and with signs of asphyxia.

=Causation.= Subcutaneous emphysema may be produced in many different
ways.

If, for example, in puncturing the rumen the canula be carelessly
withdrawn so that the skin is slightly separated from the subjacent
tissues, gas may pass from the rumen into the channel produced by the
instrument. It then becomes distributed throughout the subcutaneous
tissue, and if the cutaneous opening is displaced its escape is confined
to the connective and interstitial tissues in the region of the flank.
Diffuse suppuration may then be set up in these parts, and may extend
far beyond them.

In the ox emphysema rarely becomes generalised, but in the sheep and
goat extension is more common; the patients perish of intoxication,
caused by reabsorption of septic gases.

Under other circumstances emphysema may be due to an injury in some
region where the connective tissue is loose and pliable, as for instance
the region of the elbow, the internal surface of the shoulder, or the
fold of the flank. Every time the animals move the tissues are
displaced, and air being drawn in, it is imprisoned by the valve-like
action of the injured part and gradually finds its way into the
subcutaneous tissue.

Accidental injuries to the trachea, particularly injuries produced by
dogs biting sheep or goats, are always accompanied by local emphysema,
unless the wounds in the skin and trachea correspond, which rarely
happens. At every respiration a portion of the air expelled passes into
the peritracheal tissue, from which it gradually invades neighbouring
parts, and may attain the mediastinum, etc. The injured animal thus
inflates its own tissues and dies from asphyxia.

The open =lesions= due to pulmonary echinococcosis, and the accidents
associated with pneumo-thorax, tuberculous caverns and abscesses, or
pulmonary emphysema may become points of departure for local, general,
interstitial or subcutaneous emphysema.

=The diagnosis= of accidental emphysema presents no difficulty, for the
local swellings can only be mistaken for those of black-quarter. In the
latter disease, however, fever is a constant accompaniment, whilst in
simple emphysema it is absent.

Nevertheless, it is well to remember the possibility of complications
due to compression, asphyxia, and even intoxication.

=The prognosis= may be very hopeful or very grave. Everything depends on
the primary lesion, and it is therefore important that the practitioner
should know how to interpret the course of affairs.

=Treatment.= In slight cases the best method is to immobilise the parts
and await developments, but in grave cases, for instance where the
trachea is much injured, the animal should at once be slaughtered.

Scarification, cutaneous incisions, and massage were formerly
recommended as a means of aiding the escape of gas accumulated in the
tissues. Such methods, however, are useless, and have the disadvantage
of causing numerous suppurating wounds.

Provided the initial wounds are not seriously infected and the animals
are kept quiet, in a well-ventilated place, the gas gradually becomes
reabsorbed, and healing may take place in a fortnight or three weeks.




                              SECTION IX.
                         DISEASES OF THE EYES.


In domesticated animals, apart from parasitic diseases, the diseases of
the eye which particularly deserve description and offer a special
clinical interest are very few. These are the diseases that affect the
globe of the eye or the organs annexed to it.


                            FOREIGN BODIES.

Foreign bodies become lodged on the internal surface of the eyelids, in
the folds of the conjunctiva, in the thickness of the cornea, and
sometimes, though rarely, in the anterior chamber, the lens, or the
vitreous humour. They include particles of grit or dust, the awns and
glumes of grain, etc.

The eyes are half closed and the conjunctiva is swollen, whilst the eye
weeps and the animals dread the light.

=Diagnosis.= This is somewhat difficult, for the parts rapidly become
very sensitive, and the animals violently resist examination. When the
foreign body penetrates the anterior chamber or the lens, it produces
suppuration or traumatic cataract.

Before anything can be done it is often necessary to render the parts
anæsthetic by instilling a few drops of cocaine solution into the eye.

The foreign body may then be discovered by close observation. If the
pain is very intense, and great resistance is offered to opening the
eye, the practitioner may confine himself to passing a soft camel-hair
brush saturated with cocaine solution over the surface of the eye and
into the conjunctival sacs. The brush loosens, and often removes, the
offending body. In the absence of a camel-hair brush, the little finger,
covered with a piece of fine linen, may be used.

Where the parts cannot be touched owing to the resistance of the animal,
lukewarm solutions of antiseptics such as boric acid may be occasionally
injected into the eye by means of a syringe, but care must be taken to
prevent the animal injuring itself against the syringe by sudden
movements.


                     CONJUNCTIVITIS AND KERATITIS.

Inflammation of the conjunctiva and inflammation of the cornea almost
always occur together, and reciprocally induce one another when of a
certain degree of intensity. They may be simple, that is to say,
produced by simple causes, or they may be specific, and of a contagious
character.

Simple inflammation is caused by the action of cold, draughts, dust, or
mechanical injuries. Specific inflammations, the nature of which is
still little understood, occur in the ox and goat. They are very
contagious, and may successively attack all the animals of a herd.

=The symptoms= of acute and specific inflammation differ very little.
They comprise congestion, lachrymation, chemosis, a certain amount of
suppuration, and sometimes superficial ulceration of the cornea. The
patients suffer very acute pain, avoid the light, present all the
symptoms of photophobia, and are affected with spasm of the orbicularis
muscle.

In simple cases these symptoms frequently disappear, provided the byres
are kept clean and astringent eye-washes are applied.

In contagious keratitis, however, the cornea may suppurate and even
become perforated after a few weeks.

=Treatment.= The chief object of treatment under any circumstances must
be to insure the most perfect cleanliness both of the globe of the eye
and the conjunctival sacs.

The eye must, therefore, be irrigated with lukewarm water, the stream
being injected beneath the lids. Each irrigation is followed by the use
of an anodyne and astringent eye-wash containing borate of soda or
sulphate of zinc, combined if necessary with cocaine.

                  Distilled water          100 parts.
                  Borate of soda             4   „
                  Hydrochlorate of cocaine   1   „

But saturated solution of boric acid is simple, and no less effective.

In contagious keratitis the eye lotion may contain 2 to 3 per cent. of
nitrate of silver, the excess of silver being neutralised by washing out
with a weak solution of common salt. After three or four applications
this should be changed for a saturated solution of boric acid.


                       VERMINOUS CONJUNCTIVITIS.

This form of conjunctivitis, described by Rodes in 1819, is due to the
presence of the _Filaria lachrymalis_, which varies in length between ⅜
of an inch and 1 inch.

Like ophthalmia, the disease attacks cattle reared in wet localities.

=Symptoms.= The symptoms are those of acute conjunctivitis, and consist
first of lachrymation, then of injection of the blood-vessels of the
conjunctiva, together with swelling of the eyelids and photophobia. The
animals keep the eye closed, and display extreme sensitiveness. Here
again cocaine proves of value.

Examination is rather difficult, the worms being sometimes displaced
towards the cornea or membrana nictitans, although more commonly they
remain hidden in the folds of the mucous membrane towards the point
where the membrana nictitans is inserted. It is, therefore, necessary to
thoroughly expose the folds of the mucous membrane in order to discover
them.

In time conjunctivitis becomes complicated with diffuse ulceration,
keratitis, and sometimes with ophthalmia and suppuration of the eye.

=Diagnosis.= The diagnosis is rather troublesome, and cocaine is of
great assistance.

=Prognosis.= This is rather grave.

=Treatment.= The object of treatment is the complete removal of the
parasites. This can sometimes be attained by means of the finger, a pair
of forceps, or a very clean feather.

Treatment is completed by injecting an antiseptic and anti-parasitic eye
lotion for several days, lest some of the worms should remain hidden in
the folds of the mucous membrane. One per cent. creolin or 1 in 2,000
sublimate solution may be used.

If in some exceptional case it is difficult to remove the parasites,
they may be got rid of by injections or free irrigation. The stream of
liquid, pointed in different directions, distends the mucous membrane
and washes away the foreign bodies on its surface.


                    VERMINOUS OPHTHALMIA OF THE OX.

This ophthalmia is due to the presence of a small worm, ⅔ of an inch to
1¼ inches in length, which has been regarded as the larval form of the
_Filaria cervina_ of the serous cavities.

It is very common in animals which are kept permanently in low-lying
meadows particularly in some parts of France, as for instance in
Normandy, in the departments of the Sarthe and the Mayenne. Not
infrequently it occurs as an epizootic, and is then regarded as a
contagious ophthalmia. Verminous ophthalmia occurs chiefly during the
spring and autumn.

=Symptoms.= The disease is accompanied by lachrymation, signs of
conjunctivitis, and fear of light. Very soon the media of the eye become
turbid, the sclerotic and cornea are injected, and finally exhibit
marked opalescence.

On examination the eye appears extremely sensitive; in fact, it can
scarcely be touched unless cocaine solution is previously applied.

The parasites, two or three as a rule, but in exceptional cases from
five to seven in number, are seen rolled up within the anterior chamber
of the eye. A week after the beginning of the attack, however, they
begin to move about, and are then found close behind the cornea, upon
the lens, or suspended in the aqueous humour.

The irritation produced sets up inflammation of Descemet’s membrane and
the cornea, together with iritis, and, secondly, keratitis and changes
in the lens.

Unless treatment is adopted verminous ophthalmia inevitably ends in
cataract.

=Diagnosis.= Diagnosis is always uncertain on account of the difficulty
of examination. When the cornea is very opaque examination necessarily
gives a negative result.

=The prognosis= is grave.

=Treatment.= Eye lotions containing tincture of aloes, creolin,
corrosive sublimate, etc., have been suggested, but are practically
useless, because they can have no action on a parasite enclosed within
the globe of the eye. The most logical treatment consists in aseptic
puncture of the anterior chamber of the eye towards its lower border
with a cataract needle.

The escaping liquid carries with it the parasites, and recovery is then
only a matter of time, provided the wound does not become inflamed. The
great danger consists in inflammation and suppuration of the eye. This,
however, can be avoided by antisepsis and by applying a surgical wool
dressing, which can be left in place for a few days.




                               SECTION X.
                          INFECTIOUS DISEASES.


                           COW-POX—VACCINIA.

The name cow-pox, or vaccinia, is employed to describe a special disease
which in animals of the bovine species is characterised by the
development of pustules at points where the skin is fine, and more
particularly the mammary region.

It can be conveyed both to man and the domestic animals.

This disease has been known from time immemorial, and it would appear
that first of all in the East and later in England it was a general
belief that its attacks rendered human beings proof against small-pox.
Medical men, it must be admitted, long regarded this belief as a popular
delusion, as is proved by their continuing to practise inoculation with
true small-pox material.

Jenner in 1770 was the first to declare the truth of this popular
opinion, and by his wise foresight to confer on humanity one of the most
beneficent discoveries ever made, although the weight of modern opinion
is in favour of the identity of cow-pox and human variola. Having
observed that milkmaids who happened to have small cuts or sores about
the hands sometimes contracted the disease in a mild form, and that they
did not afterwards suffer from small-pox, he was struck with the
advantages consequent on such a discovery, and having proved the
possibility of inoculating human beings artificially, he immediately
formulated the principles of vaccination. A child eight years of age was
vaccinated with cow-pox, and afterwards inoculated with pus from a
small-pox patient. It contracted vaccinia in consequence of the first
inoculation, but entirely resisted the attempt to inoculate it with
small-pox. Vaccination had been discovered.

Jenner furthermore proved that cow-pox was transmissible from cow to cow
and from man to man, but it seemed to him that the original disease was
to be sought elsewhere, and that the pustular affection originated
primarily with the horse. The horse is sometimes the subject of a
pustular disease called horse-pox; this disease when inoculated in man
confers immunity against small-pox, just as does cow-pox, and Jenner
believed that the disease did not attack cows unless they had been
accidentally inoculated through the medium of the people about the farm.
Unfortunately, he named the pustular disease of the horse which he had
studied “sore heels,” and for a long time all those who busied
themselves with the question of vaccine confounded “sore heels” with a
number of different diseases, although as early as 1802 Loy had
experimentally proved that so-called “grease” (in reality horse-pox) was
transmissible by inoculation to the cow, in which it produced cow-pox.

Loy’s “grease” and Jenner’s “sore heels” only represent forms of
horse-pox, but for more than fifty years the origin of vaccine was
sought in grease, lymphangitis, and other diseases which attack the
extremities of horses’ limbs. Pételard (1845–1868) rediscovered and
redescribed horse-pox and proved its transmissibility to man; Lafosse
and U. Leblanc discovered it in an epizooty which broke out at Rieumes;
and Bouley in 1862 furnished a synthetical description of it under the
designation of horse-pox. He shows that horse-pox is always a pustular
disease, but that it may sometimes appear in the form of a discrete
eruption around the lips and nostrils, sometimes of an eruption limited
to the pasterns or extremities of the limbs when inoculation has been
effected in this region, sometimes of lymphangitis, and sometimes of a
more or less confluent and generalised eruption.

=Symptoms.= The disease as discovered and described by Jenner was soon
rediscovered and redescribed on all sides—by Sacco in Italy, Hering in
Germany, etc.

The pustular eruption usually appears on the udder in the case of cows,
and on the muzzle, nose, and lips in that of calves. In exceptional
cases the eruption may become generalised.

The pustules are round or slightly elliptical, and are preceded by the
appearance of red congested patches, followed by infiltration and
thickening of the skin.

The pustule is moderately prominent, and after some days there is
exudation at its centre, transforming it into a vesico-pustule. The
exuded liquid collects under the thickened layer of epidermis, which it
raises, and on examination it appears as a white or transparent little
central patch, with a thin grey periphery surrounded by a reddish
inflammatory zone. This liquid becomes thicker and the pustule is
flattened at its centre, then, towards the eighth or ninth day, the
pustule is ruptured, owing to tearing of the epidermic patch. The
vaccine thus escapes.

In what is termed spontaneous vaccinia the udder is covered with a
varying number of pustules, usually in different stages of development.
Some are very small, whilst others have attained the size of sixpence
and are already in course of cicatrisation.

When cow-pox is accidental or the result of inoculation, the eruption
occurs exactly at the point of inoculation, whether the latter has been
through an abrasion, a puncture, an incision, or any other skin injury,
and the eruption may assume the most varied appearances, according to
the nature of the primary lesion, although the mode in which the
pustules themselves form never varies. Pustules experimentally produced
by puncturing the parts may be taken as a type of inoculation. On the
day following the operation nothing abnormal appears. On the third day
there is a slight swelling around the point punctured, and this
increases until the fifth day, when there is exudation, which converts
the primary lesion into a vesico-pustule. On the sixth day the
vesico-pustule becomes umbilicated at its centre, the exudation is
abundant, and already vaccine might be collected.

This may be termed the period of crisis; the appearances are most
characteristic. During the following days the vesicle is ruptured; the
discharge continues from the ninth to the twelfth day, when the pustule
diminishes in size and dries up. After the fifteenth day crusts of a
brownish colour form; these separate between the twentieth and
twenty-fifth days, leaving hard whitish-looking cicatrices, which
permanently remain.

Moderate itching accompanies the development of the eruption, the
principal functions are not disturbed, and fever only appears in the
event of the eruption becoming confluent or extending over a large area.
When the eruption is generalised the pustules or vesico-pustules are
found mostly in the region of the elbow, the lower border of the neck,
the flank and the inner surface of the limbs. They present exactly the
same appearance as the pustules on the surface of the udder, but, being
covered with hair, are less open to inspection.

In certain rare cases the eruption extends to the perineum and lips of
the vulva. Signs of inflammation then develop on one or both sides, the
tissues display œdematous infiltration and disseminated or confluent
pustules. The lymphatic glands and vessels in the neighbourhood of the
pustules are always swollen.

=Causation.= Cow-pox, or vaccinia, is a virulent disease transmissible
by accidental or intentional inoculation. The discharge from the
vesico-pustules and the crusts which afterwards cover them are virulent,
and inoculation can be performed by simply scratching the skin. A first
attack confers prolonged and sometimes perfect immunity, the operation
being successful if only one pustule develops.

The disease is transmitted to healthy animals by milkers, by calves in
sucking, or by the conveyance in whatsoever form of virulent material to
sores or cuts.

The nature of the parasitic or microbic agent which produces the disease
is still unknown. Some investigators have described intracellular
parasites, others extra-cellular parasites, others, again, blood
parasites, etc., but the exact cause has always eluded research.

It is, however, known that filtration of vaccine, pure or diluted,
through porcelain removes the active material, which remains in the
residue arrested by the filter.

Prolonged exposure to a temperature above 104° Fahr. (40° C.) greatly
diminishes the activity of the vaccine. Simple desiccation has no
action. Warming to 140° Fahr. (60° C.) for fifteen minutes also destroys
its action completely.

These facts explain why it has always been so difficult to preserve and
cultivate vaccine in tropical regions.

Mixed with equal parts of neutral glycerine, the virulent material
preserves its activity unimpaired for from six to eight months.

The disease develops equally in man, the horse, the ox, the buffalo, the
goat, and the camel. Its development is less typical in the pig, sheep,
dog, and rabbit. Young animals are best adapted for its cultivation.

The blood and serum of animals suffering from cow-pox possess immunising
properties, but only when administered in very large doses, say from 6
to 12 lbs. of blood, or ½ to 1 lb. of serum.

The curative action of this serum against small-pox is comparatively
trifling.

=The diagnosis= of cow-pox is not very difficult.

At first the disease might be mistaken for false cow-pox, the eruptions
of foot-and-mouth disease, or gangrenous coryza.

In false cow-pox, the nature of which is also little understood,
although it is known to be contagious and is regarded by some as true
vaccinia, the pustules are smaller and thinner, while the vesicle is
more developed, and the disease runs a more rapid course.

In foot-and-mouth disease the eruptions are of the nature of vesicles or
bullæ, not pustules. The eruption occurs in twenty-four hours or less,
and can only be mistaken for vaccinia during the period of desiccation
and the formation of crusts.

Finally, as regards gangrenous coryza, the hardened pustules do not
produce vesicles.

=The prognosis= is generally favourable. The disease runs its course
within relatively fixed periods, according to the development of the
pustules, and recovery occurs without complications.

=Treatment.= No curative treatment can be laid down, the development of
the disease being perfectly regular and tending to recovery. Simple
hygienic precautions and cleanliness are sufficient to avoid
complications due to suppuration.


           COW-POX AND HUMAN VARIOLA—PREPARATION OF VACCINE.

Time and experience having proved that inoculation with cow-pox or
vaccinia protected human beings against small-pox, the question arose as
to the connection between the two diseases, whether or not they were
identical and whether vaccinia in the bovine animal might not merely
represent an alternative form of small-pox. The importance of the
question will at once be understood by bearing in mind the danger to
which human beings would be exposed by vaccination with small-pox virus
unmodified by passage through the calf.

Nevertheless, at the present time the opinion of the early writers
appears to prevail, and the theory of identity is accepted by the great
majority of scientific men. The reason why experimenters in the second
group came to believe in duality is that the method of inoculation
chosen (by puncture) was not entirely reliable. The inoculations proved
too slight, and it is only after inoculation by scarification or
incision that typical eruptions can be reproduced in series.

=Preparation of vaccine.= Whether cow-pox and small-pox are or are not
identical, the benefits resulting from vaccination are none the less
real, and it is to be hoped that vaccination and revaccination will soon
be made obligatory in all countries. We should then no longer have to
deplore those epidemics of small-pox which periodically cause
consternation in large cities and colonies.

The preparation of vaccine has been the subject of such minute care in
every country that neglect of vaccination is astonishing. The material
is obtained from calves or cows. In France the vaccine is prepared from
animals of five to eight months old, free from disease. The old system
of inoculation by puncture has been completely abandoned, the yield
being insufficient, scarifications or incisions being now employed.

The animal is secured or, better still, laid down on a suitable table,
and is shaven over a sufficient surface. The inoculations are made on
the sides of the chest, over the thorax or elsewhere, but preferably
over the flank and thorax, as being most readily accessible. The region
of operation is rendered aseptic as far as possible, and scarified in
lines about 1 to 2 inches in length, the lines of one horizontal row
alternating with those in the next. It is imperative that the slight
bleeding which may result should entirely cease before inoculation is
attempted.

The scratches are inoculated with the purest vaccine obtainable,
preferably with glycerinated pulp which has been kept for six weeks or
two months. From the third day the lines of inoculation become
prominent, and an indurated longitudinal swelling, with all the
characteristics of a pustule, soon projects above the neighbouring
portions of skin. On the fifth day exudation commences, and from the
sixth to the seventh day a large quantity of vaccine lymph may be
collected. The line of inoculation appears slightly umbilicated and
surrounded by a greyish-white zone and a hard peripheral swelling.

Vaccine may be collected from the fifth day in summer to the eighth day
in winter.

The inoculated area having been cleansed with boiled water and carefully
dried, the little crusts covering the inoculation wounds are loosened
and the wounds themselves gently scraped with a special curette of small
size. The exuded liquid is very active.

The base of each swelling is then grasped in a little special clamp,
which acts like a pressure forceps and causes the discharge of a further
large quantity of active vaccine lymph. All the material thus obtained
is mixed; an equal quantity of neutral glycerine is added, the whole is
finely triturated, passed through a cloth, and stored in little
sterilised glass tubes, which are hermetically sealed.

The vaccine thus prepared retains its activity for from five to eight
months, if kept from the action of heat and light. Accidental germs
which may have developed in the wounds and thus gained entrance to the
vaccine gradually lose their activity. After from forty to sixty days
the vaccine may be regarded as absolutely pure and incapable of
producing accidental suppuration, as sometimes occurs when fresh vaccine
is employed.

The old electuaries, dried vaccines, vaccine pastes, etc., have been
almost entirely given up, the above method always yielding a pure and
active vaccine. Vaccination with calf lymph should always be preferred
to vaccination from arm to arm, in view of possible transmission of
grave disease, such as syphilis.


                                TETANUS.

Tetanus is a disease characterised by tonic contraction of the muscles
of one or more limbs or of all the muscles of the body.

=Causation.= It is due to the growth of Nicolaïer’s bacillus in some
part of the body (in accidental wounds, in the uterine cavity after
parturition, etc.), and the contraction of muscles is due to toxins
(elaborated by the microbe), which have a selective affinity for the
nervous centres.

These toxins, secreted by bacilli localised in wounds, are absorbed and
carried away by the lymphatic and vascular channels and distributed
throughout the body. They seem chiefly to affect the cells of the
central nervous system. Infection is due to microbes capable of living
as saprophytes outside the animal body.

Nicolaïer’s bacillus assumes the form of a straight rod, one end of
which is swollen by the presence of a spore. It is anerobic, grows in a
number of different media, most rapidly at a temperature of 100° to 102°
Fahr. (38° to 39° C.), and stains well by Gram’s method.

Though quite common in the horse, tetanus is rare in other domestic
animals.

In the ox it may result either from mechanical injuries, suppurating
sores, or surgical operations. In the cow, goat, and sheep it sometimes
assumes the form of a true enzooty after parturition if the byres, etc.,
are not disinfected. In male animals it principally follows castration
by one of the cutting methods, and in lambs is seen after amputation of
the tail. A large number of animals belonging to one flock may be
affected, and Moussu has known two-thirds of a given number of castrated
lambs to die of tetanus.

Despite the sensitiveness of domesticated animals to tetanic infection
they may all be protected, either by injections of cultures, or by
gradually increasing injections of specific toxin. The latter, however,
are more efficacious when modified by the addition of terchloride of
iodine or of iodine water. The blood of immunised subjects rapidly
acquires antitoxic powers, which may be greatly increased for the
purpose of obtaining anti-tetanic serum.

=The symptoms= of tetanus are the same in all species.

In the first stage the animal appears stiff, walks in a jerky way and
holds the head high, with the ears pricked. The eyes are slightly
withdrawn into the orbits, and the animal shows marked general
excitability.

In the second stage there are muscular contractions, together with
trismus, stiffness of the neck, limbs and vertebral column, spasm of the
spinal muscles and muscles of the limbs (tonic contraction), and the
animal has a peculiar, staring look.

In the third stage mastication becomes difficult or impossible,
respiration is impeded, and the animal suffers from spontaneous attacks
of muscular contraction or from attacks due to external stimulation
(noises, sudden movements, changes from darkness to light, etc.).

In the fourth stage the animal is liable to fall, asphyxia threatens,
and death occurs from respiratory syncope.

Recovery is quite exceptional in the sheep, goat, and ox; death usually
occurs between the second and sixth days.

=Diagnosis.= Tetanus being less common in the ox, sheep, and goat than
in the horse, the diagnosis is not so easy in these animals, but as it
develops under different conditions, and as it usually attacks several
animals in one byre or fold, the diagnosis is rarely very difficult. At
the worst some hesitation may be felt at first, the condition being
mistaken for disease of the brain.

=The prognosis= is extremely grave.

=The treatment= is, above all, of a preventive nature, investigation
having proved that injections of anti-tetanic serum, before the first
appearance of tetanus, are invariably effectual.

If, therefore, one case of tetanus appears in a byre at calving time or
in a flock at the season when the lambs are castrated, no hesitation
should be felt in preventively inoculating all the castrated animals and
the cows which have calved. The quantities required are, for a cow 10
cc. (about 3 fluid drachms) and for a sheep 5 cc. of anti-tetanic serum.

This treatment, however, should be supplemented by general hygienic
precautions and internal treatment, such as irrigation and disinfection
of the parts affected.

Curative treatment has little chance of success. Experiments have also
proved that when the first symptoms of tetanus appear, anti-tetanic
serum is powerless to prevent the development of the disease.
Nevertheless, as its gravity is in direct ratio to the quantity of toxin
absorbed, and as the degree of this absorption depends on the length of
time that the place remains infected, the first thing to be done is to
disinfect and, in certain cases, curette the wounds which are believed
to be the source of mischief. Although antiseptics have little action on
Nicolaïer’s bacillus, they may be used. Solutions of iodine appear most
active, both as regards ordinary wounds and infection of the uterus.

General tonics, diuretics, and lukewarm gruels can be given.
Unfortunately the patients are often unable to swallow them. In such
cases both liquids and medicines may be directly introduced into the
rumen by puncturing the parts with a trocar and canula, the latter being
left in position.

Intravenous injections of large quantities of normal salt solution are
also of considerable value, 4 to 6 quarts per day for an ox and 20 to 40
fluid ounces per day for a sheep.


                             ACTINOMYCOSIS.

Actinomycosis is a disease produced by a fungus belonging to the group
of oomycetes (_Actinomyces bovis_) which develops in the depths of
living tissues in man and the ox, producing grave and sometimes
incurable lesions, most commonly in and about the jaws.

Actinomycosis is very common in America, and is also met with in all
parts of Europe.

=Symptoms.= The disease assumes many different clinical forms, but it
more frequently attacks some parts of the body than others, and by far
the greater number of cases occur in the ox.


                     ACTINOMYCOSIS OF THE MAXILLA.

Actinomycosis of the maxilla attacks young animals, and its usual seat
is in the molar region, although occasionally it affects the incisors.

[Illustration: $1]

The earliest =symptoms= consist in swelling of the bone, which may be
overlooked if within the mouth, but the outline of the jaw soon becomes
deformed, generally in the middle region of the row of molars. Somewhat
tender and firm to the touch at first, the tumour gradually increases in
size, invades the deeper regions of the skin, and displays fluctuation
at one or two points, followed by abscess formation. The pus discharged
may be white, creamy, and inoffensive, but the cavity of the abscess
shows no tendency to cicatrise, and the opening through which the pus
has escaped is transformed into a fistula. From this moment the pus
discharge is of a greyish, sanious nature, and contains a greater or
less number of little yellowish grains. It soon acquires an offensive
odour, and the fistulous opening is surrounded by exuberant
granulations, forming a fungoid mass.

The neighbouring tissues become hardened and lose their sensitiveness,
the jaw becomes completely deformed, and a condition is set up which the
old writers considered as true cancer of the jaw or maxillary
osteosarcoma (Fig. 268).

A probe passed into the fistula penetrates deeply, usually into the
thickness of the jaw itself, and however carefully manipulated injures
the diseased tissues and causes free bleeding.

If neglected, these lesions become steadily worse, mastication is more
difficult, being possible only on the healthy side, and the animals lose
condition and eventually die of exhaustion. The external lesion,
represented by the fungoid mass, increases in size, assumes a blackish
colour, and discharges an offensive liquid. Portions of it undergo
mortification and give off a characteristic and extremely fœtid odour.
The molars become loose and in some cases fall out, but development is
usually slow, and some weeks or months elapse before this stage is
reached.

When the disease attacks the region of the incisors the symptoms are
much sooner apparent, and treatment is much easier. The parasitic
invasion results from an injury to the jaw caused by shedding of the
milk teeth. Swelling of the body of the jaw thrusts the lower lip
downwards, interferes with the prehension of food, and calls for prompt
treatment. The disease is rarely allowed to attain the degree of
development shown in Figs. 269 and 270.

As in the preceding instance, the animals die of exhaustion unless
relieved.

[Illustration: $1]

[Illustration: $1]

For reasons difficult to explain, but probably because inoculation is
less easy, actinomycosis is much rarer in the upper than in the lower
jaw. The disease develops exactly as above described, but shows much
less tendency to external ulceration. It invades the maxillary sinus and
the region of the palate, and fistulæ are found opening into the buccal
cavity, while at the same time the region of the forehead is often
deformed.


                      ACTINOMYCOSIS OF THE TONGUE.

Actinomycosis attacks the tongue apart from any lesion of the jaws, and
produces what is commonly called “wooden tongue.”

The disease develops in the tongue itself, generally in the submucous
zone, and causes chronic interstitial inflammation, infiltration of the
connective tissue, and, in time, changes in the muscular structures
themselves.

The tongue shows progressive hypertrophy, and becomes hard, sensitive,
rigid, and incapable of free movement. As a result the patients first
have difficulty in grasping food, then in swallowing their saliva, which
dribbles from the mouth, and finally are quite unable to feed
themselves.

[Illustration: $1]

The tongue is enlarged and indurated, and fills the entire cavity of the
mouth. Sometimes it projects beyond the incisors, excoriated and
bleeding. On passing the hand into the mouth it is found that the
surface is covered with little yellowish or red ulcerated nodules,
varying in size from that of a large pin’s head to that of a lentil.

In eating, the animals seize food between the lips and lift the head
high, so as to allow the food to fall between the rows of molars. The
motion is very similar to that of a fowl drinking.


         ACTINOMYCOSIS OF THE PHARYNX, PAROTID GLANDS AND NECK.

Actinomycosis may sometimes leave the mouth and tongue unaffected and
attack the pharynx, from which it extends in the direction of the
parotid glands and external surface of the neck. In these cases,
however, the inoculations are more localised than when the surface of
the tongue is attacked, and the lesions consist of vegetations, polypi,
or actinomycomata.

The growths develop on the posterior pillars of the fauces, on the sides
of the pharynx, or near the entrance to the œsophagus. They interfere
with swallowing, and produce symptoms which are easy to detect and
interpret.

The lesions may also affect deeper seated tissues and produce growths in
the parotid or subparotid region, or lead to the development of fistulæ
in the region of the neck. Most fistulæ, however, in this region are due
to specific inoculation of external injuries. Fistulæ originating in the
parotid region and in the upper part of the neck usually resemble in
appearance the maxillary fistulæ. The external fungoid growth, however,
is less exuberant, suppuration is less abundant, and the surrounding
induration less extensive.

=Various localisations.= Although the disease generally attacks the
mouth, tongue or pharynx, it may invade the œsophagus, rumen, reticulum,
liver and intestine, larynx, trachea, lung, peritoneum, epiploon, and
even the udder.

[Illustration: $1]

Localisations in the udder and peritoneum are commonest in pigs, and it
is believed that inoculation occurs either through the galactophorous
sinuses or through the abdominal wounds made for purposes of castration.

=Causation.= The cause of actinomycosis is to be sought in the
development of _Actinomyces bovis_ within living tissues. It seems
problematical whether the germs to be found in the pus or saliva of
affected animals ever directly infect new hosts, and it is difficult to
carry out infection in this manner even in very sensitive experimental
animals. Nevertheless, the persistence of the disease in certain byres
would seem to support the view of direct infection.

On the other hand, it is proved that the actinomyces is a parasite
affecting vegetables, principally the graminaceæ, and that domestic
animals are most commonly infected through injuries caused by vegetable
substances. This is suggested by the discovery of the _débris_ of grain
at the point where the lesions have originated.

[Illustration: $1]

Inoculation is commonest in the mouth and on the surface of the tongue,
parts which are, so to speak, permanently excoriated. The shedding of
the temporary molars favours such accidents, and this is why
actinomycosis of the jaw is, relatively, so common. The incisor region
may also be inoculated during the shedding of the milk teeth, but as the
infected food comes more closely and for much longer periods in contact
with the molars, it is easy to understand why actinomycosis is rarer in
the incisor region.

The conditions are less favourable for inoculation of the pharynx,
because food does not remain in position there for more than a second or
two, but when the epithelium has been shed as a consequence of
laryngitis or pharyngitis, infection may occur.

As regards cutaneous inoculation, the parasite only seems dangerous when
the skin is excoriated or injured either accidentally or as the result
of surgical interference.

[Illustration: $1]

Actinomycosis of the lung is probably caused by the germs being inhaled
along with the inspired air.

=Lesions.= The lesions are very peculiar in character, and end in
completely destroying the tissues invaded.

Once lodged within an organ, the disease shows a tendency to extend in
all directions, and, despite the defensive reaction of the tissues, it
soon forms numerous parasitic centres.

In bones, for example, actinomycosis invades the spongy tissue with the
greatest ease. It causes subacute ostitis, which leads to diffuse
suppuration and local hypertrophy of the bone, destruction of the
compact layers, and the development of an abscess with fungoid,
exuberant, granulating walls which show no reparative tendency whatever.

The pus of the abscess and the liquid from the fistula contain varying
quantities of yellowish grains, representing clusters of actinomyces.
The surrounding tissues, muscles, tendons, skin, etc., are all involved
before long in the inflammatory process, and the granulating masses
themselves are invaded by the yellowish parasitic tufts. All the fistulæ
are surrounded by enormous zones of infiltration, which on incision
exhibit a lardaceous appearance. On section it may appear that the
lesion is confined entirely to the bone, though this is exceptional
(Fig. 274). Ordinarily the neighbouring tissues are also destroyed, and
not infrequently there is communication with the external air. Sections
then display a fungoid tissue, interspersed with perforated lamellæ of
bone and lardaceous tissue containing cavities crammed with actinomyces.

[Illustration: $1]

The lesions in the parotid regions, the neck or other parts attacked
always present the same appearance, viz., wide, tortuous, bifurcated
fistulæ, with exuberant granulations both in the direction of the
cavities and of the exterior, together with lardaceous induration of the
tissues and abundant fœtid liquid pus.

When it affects the tongue the parasite is to be found in the submucous
region, where it causes little swellings, which, when superficial,
rapidly undergo ulceration. The subjacent regions, the interstitial
connective tissue, and the muscular tissue become infiltrated, hardened
and progressively sclerosed. The tongue is gradually hypertrophied, and
soon it becomes as hard as wood, whence the term “wooden tongue.”

Actinomycosis of the lung may easily be mistaken for tuberculosis, for
the centres, although usually confined to one lobe, may also be
disseminated. The lesions, however, are surrounded by an abundant
fibro-sclerous inflammatory tissue.

In the abdominal cavity, particularly in sows, actinomycotic lesions
occur as little masses varying in size between that of a pea and that of
a haricot bean, attached to the epiploon and peritoneum and filled with
pus containing mycosic grains.

=Diagnosis.= Actinomycosis is usually easy to recognise, both on account
of the special character of the lesions and the presence of the little
grains formed by the parasite. The practitioner will rarely fail to
recognise at once the signs of actinomycosis of the jaw, but
actinomycosis of the tongue is more apt to be mistaken for deep-seated
sclerosing glossitis, although a careful examination will always enable
the different symptoms to be distinguished.

It is otherwise with regard to growths in the pharynx and œsophagus,
for, until after removal, simple polypi cannot be distinguished from
actinomycotic growths. In such cases the administration of iodide of
potassium affords valuable indications.

=The prognosis= is grave, whatever the clinical form of the disease.
Important advances, it is true, have lately been made, and the iodide of
potassium treatment is of great value, but too much must not be expected
of it, and its benefits have certainly been exaggerated. Clinical
experience suffices to prove that only actinomycosis of soft tissues can
be cured by drugs, bony lesions being amenable only to medical and
surgical treatment combined. Even combined treatment is often
unsuccessful.

=Treatment.= Thomassen in 1885 first explained the favourable action of
iodide of potassium on actinomycotic growths, and Nocard in 1892 again
directed public attention to the advantages attending the use of this
drug both in man and the lower animals. As too frequently happens,
however, the benefits of this treatment have been exaggerated, and
iodide of potassium has been held out as a specific even against lesions
in bone. With very few exceptions this is incorrect, and, as Moussu has
shown, when the disease affects bone tissue it only yields to mixed
treatment.

The treatment of actinomycosis may therefore be considered under two
heads.

Firstly, the treatment of actinomycosis of soft tissues; and, secondly,
that of bone.

Actinomycosis of soft tissues, muscle, skin, lymphatics, serous
membranes, etc., comprises the most common forms of actinomycosis, viz.,
those of the tongue, pharynx, parotid glands, neck, etc.

The second form comprises actinomycosis of the lower jaw (molar region),
the upper jaw, region of the incisors, etc.

Iodide of potassium in daily doses of from 2 to 3 drachms is almost a
specific in dealing with the first form of disease.

In lingual actinomycosis, for example, the effects may be seen a few
days after treatment is begun. The tongue becomes softer and more
mobile, can be protruded beyond the mouth and retracted into it, and day
by day tends progressively to resume its normal appearance.

The patients, which were previously slowly dying of inanition because
they were unable to feed themselves, again take to their food and begin
to put on flesh. To ensure the treatment being efficacious it should, as
a rule, be continued for three or four weeks.

During the course of this treatment the system becomes saturated with
the drug, but no bad effects follow. The patients suffer from
lachrymation, coryza, bronchorrhæa, and especially iodic eczema, but all
these symptoms diminish and disappear soon after the administration of
the drug is discontinued.

Recovery, however, is not always permanent, and even when the tongue has
resumed its normal appearance a relapse may occur. We have seen several
such cases after treatment extending over more than six weeks, and it is
therefore often advisable to fatten the animals as rapidly as possible
and prepare them for slaughter.

If no relapse occurs, and recovery is regarded as permanent, another
complication may make its appearance, viz., sclerous atrophy of the
tongue. This is almost as dangerous as the primary lesion, because it
prevents the animals from feeding, and constitutes an additional reason
for following the course above suggested.

Other lesions of soft tissues, such as disease of the parotid or
cervical glands, etc., yield to the same treatment, but it is advisable
first of all to clean out the fistulæ, scrape off exuberant
granulations, cleanse the irregular culs-de-sac, and thoroughly curette
all accessible parts.

Treatment is much longer than in the case of actinomycosis of the
tongue, but it is not always necessary to push the remedy to extreme
limits. As soon as symptoms of iodism appear only a drachm or two of the
drug need be given daily.

=Actinomycosis of Bone.=—As a general rule, actinomycosis of bone
resists the administration of iodide of potassium, a fact probably
explained by the much less abundant blood supply in bone as compared
with very vascular tissues, such as the tongue.

To have any chance of success the iodide treatment must be supplemented
by surgical interference. As regards the surgical aspect of the case,
the affected bone should be removed as far as possible, together with
all broken down tissue. Should this be neglected, the disease returns in
a little while.

In actinomycosis of the region of the incisors the method is radical
when adopted in time. The body of the maxilla can be partially removed
with a fine saw, two cuts being made disposed thus: =<= (the letter =V=
sideways). The upper and lower layers of compact tissue should be spared
as much as possible, so that the body of the bone may not afterwards
break. Recovery is only a matter of time.

A very small local iodoform dressing is applied, and, when healthy
granulations appear, cicatrisation can be left to natural means.

Cases of actinomycosis of the jaw are much more troublesome. If, as
usually happens, the lesion is ulcerated before the practitioner is
called in, the external fungoid growth should be removed by means of an
elliptical incision through the skin, the axis of the ellipse being
parallel with the branch of the maxilla. The bony fistula is then
exposed.

In following up this fistula care must be taken not to injure the facial
artery, the facial vein, or Stenon’s duct. Once the bone is exposed the
disease can be attacked in the depths. The diseased interior is cut away
by means of a special curette, all affected portions being removed, and
an iodine or iodoform dressing is then applied.

The operation is extremely troublesome, owing to the enormous bleeding,
and sometimes it is impossible to carry out successfully, as in the case
of old-standing and extensive lesions. To ensure recovery under such
circumstances, it is necessary to remove a portion of the branch of the
jaw, and this, though quite possible from the scientific standpoint,
would not be worth while in an animal, the value of which is usually
small.

Curettage of the bone is only of value in dealing with recent lesions,
and even then should not be practised except in the case of animals
which the owners particularly desire to keep.

In cases of actinomycosis of the upper jaw surgical treatment is just as
difficult as in the lower jaw, and calls for similar precautions.

The diseased portions of bone having been removed, the cavity is plugged
with iodoform or cotton wool, or a dressing saturated with boric acid
and iodoform.

In all surgical operations it is important not to injure the dental
arteries or nerves, or the alveolo-dental periosteum.


                             TUBERCULOSIS.

Tuberculosis is a contagious disease produced by the action of Koch’s
bacillus. It is common to man and all domesticated animals, but it
specially affects animals of the bovine species. Its existence has long
been recognised, although in oxen it was formerly confounded with the
lesions of peripneumonia and echinococcosis.

It was not until the beginning of the nineteenth century that Laënnec
(1811) described the tuberculous lesion from the anatomical and
pathological standpoint. Gürlt pointed out for the first time in 1831
the similarity, the identity in fact, of tuberculous lesions in man and
the ox.

In 1865 Villemin showed that tuberculosis could be conveyed from animal
to animal, always producing similar lesions, and in 1868 Chauveau proved
that, in the calf, infection might arise simply from the eating of
tuberculous material.

At a somewhat later date doubts were entertained regarding the identity
of human and bovine tuberculosis. Virchow denied the identity of the two
diseases on the basis of a comparative study of the lesions. His
opinion, however, has not prevailed, and the doctrine of the identity of
tuberculosis in mammals still appears probable, in spite of the recent
declarations of Koch (1901).

=Causation.= Tuberculosis is due solely to the activity of the tubercle
bacillus. In 1884 Koch isolated and cultivated this bacillus in living
animals, and always reproduced typical tuberculous lesions by injecting
cultures. In 1887 Nocard and Roux described a rapid method of
cultivating the bacillus, and in 1890 Koch announced the discovery of
tuberculin.

The tubercle bacillus assumes the form of a little rod, five or six
micromillimètres in length, and ·03 to ·05µ in thickness. It has a
special staining reaction when treated with Ehrlich’s or Ziehl’s
solution. It grows between 98° and 104° Fahr. (37° and 40° C.) in
various artificial media containing glycerine.

Healthy subjects become infected by the accidental entrance of germs
into their bodies, either by the respiratory and digestive tracts, or
through solutions of continuity in the skin.

The material from tuberculous centres is virulent, whether consisting of
sputum or discharge, saliva, fæces, urine, milk, etc., or tuberculous
tissues derived from the different viscera.

The blood and muscular tissues are not always virulent, even in cases of
generalised tuberculosis.

The virulent organisms usually enter the body through the lymphatic
system; invasion proceeds from the point inoculated towards the nearest
lymphatic glands and thence along the chain of lymphatic vessels, and
the lesions extend, attacking the internal organs more or less rapidly.
The body does not necessarily become fatally infected as a consequence
of accidental or even experimental infection, for the bacillus may
itself be destroyed by the phagocytes, or the lesion may remain purely
local.

Although tuberculosis is the gravest and most widespread disease on the
surface of the globe, its contagious character is relatively little
marked, a fact which has unfortunately led to its receiving little
attention in ordinary life.

Contagion is usually the result of cohabitation, although contact
between diseased and healthy subjects for a period of some days or even
weeks does not seem sufficient to produce the disease. Nocard has fixed
a mean period of five to six months as necessary for the contraction of
the disease by bovine animals, and Moussu has arrived at almost
identical results by placing tuberculous and healthy cows together in a
byre reserved for such researches. In this connection, however, very
great differences of individual susceptibility exist, and these are
difficult to appreciate in the present state of our knowledge. It thus
happens that an animal of vigorous appearance and in good condition may
easily contract tuberculosis, whilst a thinner and less vigorous one
will resist it for a comparatively long time.

Speaking generally, it may be said that young animals contract
tuberculosis by cohabitation in infected places more easily than adult
or aged ones, and the fact that old animals contribute the larger number
of cases is to some extent due to their having in the course of their
lives been more exposed to continued or successive infection.

Contagion does not occur in byres unless as the result of the presence
of animals with open tuberculous lesions, such as caverns in the lungs,
tuberculous bronchitis with ulceration of the mucous membrane,
tuberculous metritis, enteritis, etc. The virulent germs are expelled in
the saliva, nasal discharge, excrement, etc., and are distributed over
the forage, manure, litter, and in the drinking water; after desiccation
they may be spread by currents of air.

The mangers, racks, drinking pails, and various stable utensils become
permanently contaminated, the air of the cowsheds contains virulent
dust, and the animals there confined are continually exposed to
infection either through the respiratory or digestive passages.

Contamination through the respiratory tract is by far the most frequent
cause of the evil, and recent experiments at Pouilly-le-Fort (1900) have
shown how easy it is to convey the disease experimentally by inhalation.

Patients suffering from closed tuberculous lesions of the pleura,
pericardium, spleen, peritoneum, etc., do not spread the bacilli.
Healthy animals may remain in contact with them without danger, but it
is well to remember that such cases are quite exceptional. As a rule the
lesions are of a mixed character, and the general principle may be laid
down that cohabitation of any duration with tuberculous subjects is
dangerous.

Contagion spreads more easily, in proportion to the number of
tuberculous subjects in a given byre, to the total number of animals in
a herd, and to the neglect of cleanliness, good feeding, ventilation,
etc.

Life in the open air and at grass greatly diminishes the chances of
contagion. The virulent products are then disseminated in all directions
and are soon destroyed by the general atmospheric conditions. Close
confinement in ill-ventilated stables, on the contrary, strongly tends
to the propagation and development of tuberculosis.

In calves infection may occur through the alimentary tract by means of
tuberculous milk, whether such milk is obtained directly from the udder
or out of a pail. The same may be true of young pigs fed with skimmed
milk.

Goats contract tuberculosis somewhat readily by confinement in byres
with tuberculous cows, and Moussu declares that contagion afterwards
spreads just as rapidly among goats as among cows. The vaunted great
resistance of goats to tuberculosis, formerly so often spoken of, and by
some wrongly considered as a condition of immunity, is deceptive, and if
tuberculosis is less frequently seen in goats, this is solely because
goats enjoy the greatest liberty at all seasons.

On the other hand, the disease is very rarely conveyed to sheep, even
when they are kept for long periods with tuberculous cows. Moussu found
that two years of close cohabitation were necessary for its development
under these conditions.

Heredity is a factor of the highest importance in determining the
causation of tuberculosis. At the present time a tendency exists to deny
this, but such a view is erroneous.

Observation has clearly shown that tuberculosis is rarely conveyed from
the mother to the fœtus, and that practically none of the calves borne
by tuberculous mothers react to tuberculin (95 per cent.: Nocard and
Bang); but even if this is absolutely correct, it only shows that great
benefits might be derived if proper sanitary organisation and
intelligent hygienic conditions in byres were found everywhere in the
country. Unfortunately in practice this is far from being the case.
These non-tuberculous calves are left in common contaminated byres,
where they rapidly become infected and perpetuate the disease.

Physiologically these facts are easily explained. The placenta resists
the passage of microbes, or at least only allows them to pass under
quite exceptional conditions, and practically only when the
blood-vessels are affected. As, on the other hand, tuberculosis of the
ovaries, Fallopian tubes or uterus generally prevents pregnancy and
causes sterility, there is nothing extraordinary in the fact that
tuberculosis is not hereditary in the strict sense of the term. The
influence of the sire has been invoked, but it has been proved that
direct paternal infection is only possible where ulcerating tuberculous
lesions of the testicle, prostate, or vesiculæ seminales exist. Such
conditions seldom or never occur in the sires of domestic animals.

As a general rule, therefore, it may be said that tuberculosis is not
hereditary. New-born animals become infected during the months following
birth, either directly through the alimentary tract when the mothers are
suffering from mammary tuberculosis, or, perhaps more frequently,
through the respiratory and digestive tracts.

But although microbic infection is not hereditary, it by no means
follows that the offspring of tuberculous subjects are as well prepared
for the struggle of life as the descendants of healthy subjects. What is
transmitted is a greater tendency to contract the disease.

This aptitude or predisposition is of such importance that in Moussu’s
opinion it should be regarded as one of the essential factors in the
development of tuberculosis. The cause of tuberculosis is Koch’s
bacillus. It does not always produce its full effects in animals born of
healthy parents; but in one that suffers from a tuberculous hereditary
taint tuberculosis appears.

Physiological and pathological researches cast considerable light on
this question. In tuberculous mothers the organism not only suffers from
the infection, but from a permanent intoxication which interferes with
normal metabolism in the vital organs and the exchanges between mother
and fœtus. If the microbes remain confined to the system of the mother,
their poisons are conveyed by the blood and pass through the placental
barrier. In a greater or less degree they saturate the tissues of the
little creature in process of development, and communicate to it a
peculiar hereditary taint. The effects of this taint are often
noticeable from the moment of birth, for comparative physiological and
pathological investigations have shown that the tissues of tuberculous
animals assimilate given foods less perfectly and are the seat of
greater losses of all kinds than those of healthy subjects.

Although the disease itself, therefore, is not hereditary, it is
otherwise with the organic taint which plays so important a part in its
development. This organic taint consists in a special condition of the
tissues or cells of the parents, which show a diminished power of
resistance to the action of the germs of tuberculosis; it is therefore
easy to understand how important a part these influences may play under
certain conditions.

Without doubt, in the case of bovine animals, the predisposition could
be neutralised in carefully managed studs by the immediate isolation of
the new-born under conditions which shield them from tuberculous
infection, and experiment has shown the benefits derived from such
precautions; but it must not be forgotten that intelligently managed
studs are the exception, and that for a long time to come we must in
practice take cognisance of the actual conditions under which the
disease develops.

=The lesions= of tuberculosis vary greatly in appearance, according to
the organs affected, though the method of development is always
identical.

The primary lesion corresponds to what has been termed tuberculous
granulation, or anatomical tubercle properly so called; this, the
macroscopical, pathological entity, assumes the form of a small
prominent centre, semi-transparent, greyish, opaque or yellowish,
according to its age.

These tubercles, produced by the presence of colonies of bacilli, are
due to the defensive reaction of the invaded tissues, which gradually
undergo change and are destroyed in a direction radiating from the
centre towards the periphery. The tubercle in itself has no very
specific character—only the bacillus.

The elementary lesion may remain isolated, but very frequently it is
closely surrounded by other similar tubercles, and becomes enveloped in
a common inflammatory area. A large portion of an organ may appear as if
riddled with tubercles of different age and size, while the interstitial
connective tissue reacts and forms fibrous separating partitions. The
general appearance is that described under the term “diffuse tuberculous
infiltration.”

At a still more advanced stage in the development of the disease
conglomerations are produced, consisting of tuberculous masses the size
of a hazel-nut, a walnut, an egg, a man’s fist, or even larger. These
lesions, irrespective of size, undergo caseous degeneration from the
centre towards the periphery.

In exceptional cases the tubercles remain fibrous. More frequently,
particularly in animals of the bovine species, they become infiltrated
with lime salts. Caseous degeneration not only invades the centre of the
tubercles but also the peripheral layers, and sometimes the whole of a
conglomerated mass.

Steadily pursuing their course of pathological development, the
tuberculous masses become softened and are transformed into tuberculous
abscesses, which open towards any free passage, leaving behind sometimes
ulcerations, sometimes caverns of varying sizes, or blind simple or
bifurcated fistulæ.

Recent experiments by Nocard and Rossignol (1900) prove conclusively
that a certain time (always more than a fortnight) elapses between the
moment of entry of the contagion into the organism and that at which its
effects become manifest by furnishing a reaction to tuberculin.
Calcification or softening of the lesions, moreover, never occurs in
less than fifty days.

According to the organs studied, these tuberculous lesions assume
certain appearances, which in each locality seem almost always to be
identical.

Thus, as regards the larynx, trachea, and bronchi, the tubercles develop
in the depths of the mucous membrane, rapidly undergoing caseous
transformation, softening and purulent degeneration, and producing
numerous isolated or confluent ulcerations in the air passages.

According to the case and the kind of animal affected, the lung presents
either disseminated tuberculous formation, tuberculous infiltration,
tuberculous conglomeration, or cavern formation.

The lung may be affected to such a degree that it appears incredible
that the blood can have been sufficiently aerated to support life.

The lungs may be transformed into yellowish, caseous, calcareous, or
softened masses enveloped in thick, fibrous, resistant walls. The
intervening pulmonary tissue may be healthy in appearance, or reddened,
congested, and sometimes hepatised.

The pleural, pericardial, and peritoneal membranes may be covered with
exuberant tuberculous lesions, like ripe mulberries, in consequence of
fusion and massing of the tuberculous growths. The primary tubercles are
surrounded with fibrous walls, which granulate when on the surface of a
serous membrane, and impart to the membrane a vegetative, sometimes
villous appearance, and a colour varying from pink to light or dark red.

The collective lesions lining the cavities are described by butchers
under the significant term of “grapes.” In the interior of these
exuberant masses, which sometimes form layers an inch or more in
thickness, the tuberculous lesions undergo the usual developmental
changes, that is to say, they become caseated or infiltrated with lime
salts, but they do not so readily undergo softening as those of the
lung. The parietal and visceral serous membranes readily become adherent
at numerous points, setting up union between the lung and the walls of
the chest, or the intestine and the walls of the abdomen, etc.

In the pericardium the vegetations are frequently of a fungoid
character.

Tuberculosis of lymphatic glands sometimes assumes a disseminated,
discrete form or that of a diffuse infiltration, or, again, in
old-standing cases it constitutes a massive tuberculous conglomeration.
In point of fact, the lymphatic glands as such no longer exist, their
tissue having undergone total degeneration; they are represented only by
an enlarged, thick, fibrous shell, forming the envelope which encloses
caseated and calcareous masses of a more or less soft nature.

Tuberculous infiltration of the submaxillary and sub-parotideal
lymphatic glands interferes with swallowing and breathing, compresses
the pharynx, œsophagus and larynx, and deforms the head.

Compression of the arteries, veins, nerves, etc., at the entrance to the
chest may cause various symptoms which are not difficult to interpret.
The glands at the entrance to the chest and the whole of the anterior
mediastinum may form a single mass. Lesions in the posterior
mediastinum, however, are of even greater importance and explain certain
symptoms, such as difficulty in swallowing, spasm of the œsophagus,
mechanical contraction of the œsophagus, permanent tympanites, etc., for
which the state of the lungs alone would not account.

Even when the lungs are unaffected it may happen that the lymphatic
glands of the mediastinum (superior or inferior œsophageal lymphatic
glands) and the bronchial lymphatic glands may be so diseased that the
œsophagus is completely surrounded and compressed by them, and its
function thus seriously impaired (Fig. 276).

In the abdomen the mesenteric glands are most exposed to disease, and
when infected through the intestinal tract they assume the form of large
flattened masses arranged along the mesentery.

In the digestive tract, as in the trachea and bronchi, tuberculosis has
a marked tendency to assume the ulcerative form. Disseminated or
aggregated tubercles develop in the thickness of the mucous membrane,
and, after rapidly softening, become ulcerated. The nature of these
lesions can only be determined by noting their character and examining
the discharge.

[Illustration: $1]

The ulcerations are localised in the mouth and pharynx, in the second
half of the small intestine towards the ileum, and in Peyer’s patches.

Tuberculous lesions develop in the vaginal sheath of the male genital
organs exactly in the same way as in an ordinary closed serous cavity;
tubercles may also develop on the surface or in the substance of the
testicle. They become aggregated, undergo softening, spread towards the
interior, and may break down, thus forming abscesses. In the female
genital passages the disease invades the thickness of the walls, but
shows a marked tendency to ulceration, as in the intestine or trachea.

In the udder tuberculosis is generally diffuse, shows a tendency to
hypertrophy and the free formation of fibrous or sclerous tissue; only
tubercles in the glandular layer of the acini become ulcerated. In time
the whole of the secreting structure undergoes diffuse tuberculous
suppuration, fibro-caseous masses form in the depths of the tissue and
may soften, producing deep-seated tuberculous “cold abscesses.” The
mammary lymphatic glands are affected in the same way as other lymphatic
glands.

In the joints tubercles appear either on the synovial membrane or in the
thickness of the bony epiphyses, very often at both points
simultaneously. The synovial membrane is covered with vegetations and
villous growths, the ends of the bones are attacked by a destructive
ostitis, tubercles or tuberculous centres form in the thickness of the
spongy tissue, the articular cartilages are destroyed, the ends of the
bones become deformed, and in the last stages fungoid arthritis in
various forms may be produced.

In bones the tubercles originate in the depths of the spongy tissue.
They produce destructive hypertrophic ostitis, in which the bony tissue
is replaced by tuberculous centres or masses divided by fibrous
partitions. On section, these lesions exhibit the same yellowish
caseated or calcified appearance as the lesions of other affected
organs. The compact layer may sometimes be perforated at several points
before being destroyed.

In tuberculosis of the brain the primary lesions develop at the expense
of the serous layers of the arachnoid and on the pia mater, towards the
base of the brain and the fissure of Sylvius, or at the expense of the
small vessels which penetrate the depths of the nerve substance itself.
Some tubercles remain isolated, become confluent or are collected in
masses of different sizes, and provoke symptoms which vary with the
locality attacked.

=Symptoms.= Tuberculosis is the most protean of all diseases, and at
first sight it often seems impossible to assign to one group, clinical
conditions presenting such essentially different appearances. All the
tissues may be attacked, from the bones to the most delicate of the
viscera, a fact which explains why all aspects of tuberculosis cannot be
described. Certain forms, however, occur very frequently, and may be
regarded as classic; these will be considered in the order of their
frequency.


               TUBERCULOSIS OF THE RESPIRATORY APPARATUS.

Without doubt this form of tuberculosis is by far the most frequent. It
assumes the form either of bronchitis, laryngo-bronchitis, or pulmonary
tuberculosis.

=Tuberculous Bronchitis.=—The symptoms of tuberculous bronchitis do not
essentially differ from those of ordinary bronchitis, though the disease
develops more insidiously and slowly, and is seldom accompanied by
fever. At first the cough is dry and suppressed; later it becomes
paroxysmal, and at a still more advanced period liquid and rough. The
least irritation brings on these attacks of coughing; changes from the
warmth of the stable to the coldness of the outer air or _vice versâ_,
the presence of dust or the action of liquids when drinking, etc., etc.
During the first stage coughing is not followed by expectoration, but
later yellowish-grey, glairy mucus may be discharged: more frequently it
is coughed into the pharynx and swallowed.

These symptoms continue for weeks or months without showing any tendency
to abate. If the larynx is attacked inspiration becomes rattling and
difficult, while the neck and head are held extended, and the least
pressure over the larynx produces coughing.

Tuberculosis of the larynx, trachea, and bronchi is usually accompanied
by disease of the lung, but may occur by itself.

When there is a discharge it consists of thick, viscous, sticky mucus of
a peculiar greyish-yellow colour. Microscopical examination shows it to
contain tuberculous bacilli.

=Pulmonary Tuberculosis= usually assumes the chronic form, and is almost
always preceded by specific bronchitis. The patients retain their
appearance and condition for a longer or shorter time, and, without the
experience resulting from continued observation, it would be difficult
to believe them to be suffering from the slow development of a serious
disease.

Frequent coughing without any apparent reason is the only symptom likely
to arouse suspicion.

At a later stage these animals lose condition, feed less eagerly or
exhibit capricious appetite, and sometimes well-marked and repeated
digestive disturbance, such as slight tympanites with constipation or
diarrhœa, moderate impaction of the rumen, relative atony and slackening
of peristaltic movements. The wasting gradually becomes more marked or,
in the case of pregnant or milch cows, makes intermittent progress,
until the animals become anæmic and finally cachectic. The cough is more
frequent and more severe, and is followed by discharge from the nose or
by swallowing movements. From this time phthisis, properly so called,
exists.

The course of the disease is not invariable. Certain animals may appear
ill for years without clinically showing the least apparent aggravation;
others on the contrary, though living under similar conditions, are
rapidly attacked, and in six to twelve months exhibit all the signs of
advanced phthisis. Pregnancy, suckling, and prolonged lactation favour
the development of the disease by taxing the physical resources of the
animal.

Animals suffering from phthisis exhibit a peculiar appearance. They are
extremely thin, all their soft tissues are wasted, the limbs are dragged
in moving, respiration is rapid and sometimes jerky, the mucous
membranes are pale and discoloured, and the skin is tight and adherent
to the subjacent tissues.

These general signs, however, would not warrant a diagnosis, for, apart
from the cough, certain other diseases present all the external
appearances of the last period of tuberculosis (chronic diarrhœa,
chronic forms of poisoning—bacterial or otherwise—dyspepsia, etc.).

In cases of doubt it is essential to discover by percussion and
auscultation that the external signs are really the result of lesions of
the lung, and that the lung disease has developed gradually in
accordance with the signs shown by simple external inspection.

The symptoms presented during the development of the pulmonary lesions
may be divided into three phases.

In the =first phase= percussion gives no information, though
auscultation reveals rough respiration, inspiration and expiration being
also unequal. Expiration, which, in the healthy subject, is silent,
becomes clearly perceptible, not over the whole lung, but usually over
the anterior lobes, particularly the cardiac lobes. This sign is the
result of tuberculous infiltration and of the neighbouring pulmonary
tissue having lost its elasticity.

Inspiration is rough and rasping, and sometimes occurs in several
stages, the act being interrupted or jerky; expiration lasts longer than
inspiration, is rough and prolonged, but never blowing in character.
These peculiarities are only found in one other condition of the lung,
viz., emphysema.

The patients appear little affected in this, the first, stage of
tuberculosis. But for the cough they may seem perfectly healthy.

In the =second phase= the tuberculous infiltration extends and ends in
the massing, by fusion or centrifugal growth, of the tuberculous masses.

Percussion may now indicate localised dulness, but this is not
invariable, because the diseased anterior and middle lobes of the lung
are concealed beneath the muscles of the shoulder. When dulness is
noted, it is usually over the lower part of the posterior lobes, very
rarely at any higher point on the side of the chest. Frequently the
dulness is only partial.

On auscultation the signs met with during the first stage become much
more marked. Inspiration is always rough, rasping, painful and difficult
at certain points, particularly in the anterior zones. In this region
expiration is rough, prolonged and sometimes of a clearly marked blowing
character. This is particularly the case in the subscapular zone and the
auscultation zones 2 and 3 (Fig. 166). In the dorsal region and in zone
No. 1, respiration may appear normal. Nevertheless, the sounds are
propagated to a distance, the infiltrated lung steadily loses its
elastic qualities, the vesicular murmur entirely disappears from the
affected regions, and the sounds noted are of bronchial origin.

Like the first, the second phase may vary in intensity, extent, and in
the diffusion or localisation of the tuberculous lesions. Blowing
respiration may be noted over different areas, accompanied by sibilant,
snoring and migratory mucous _râles_. The vesicular murmur is
exaggerated in the healthy parts, coughing, accompanied by expectoration
or followed by swallowing movements, is frequent, the appetite becomes
capricious, and the general condition suffers. In this second phase
almost the whole of one lung may be diseased and exhibit the signs
described.

The =third phase= corresponds to the softening of the tuberculous
masses, and the formation of ulcers and caverns. The zones of dulness or
partial dulness may be more extensive, though cavern formation is
usually confined to the anterior or middle lobes. Percussion still
affords no precise information.

As the tuberculous masses undergo softening and ulceration, their
contents are gradually passed into the bronchi, and auscultation reveals
signs indicative of the existence of caverns, which signs vary with the
dimensions of the caverns themselves. On auscultation the respiration is
always found to have at certain points a blowing character, and it may
even develop into a true tubal souffle. In other areas, where the
caverns are merely in course of formation, gurgling sounds are all that
are heard, but where true caverns exist there is an incessant cavernous
souffle.

The lesions peculiar to the third phase are seldom seen in practice;
because the animals become anæmic, exhausted and cachectic, they are
usually slaughtered early. Nevertheless, the third stage occasionally
develops in an astonishingly short time, six to eight months at most.

Very frequently the patients, although cachectic and even phthisical, do
not yield on auscultation the sounds described as peculiar to the third
stage, because the tendency to softening is not very marked in bovine
animals. The lungs exhibit massive infiltration, and, whilst pulmonary
consumption is not uncommon, the development of caverns is comparatively
rare.

The expectoration or discharge in this third form is puriform, glairy,
viscous, and of a dirty-yellow or even greenish-yellow colour.
Bacteriological examination reveals the presence of tubercle bacilli and
adventitious organisms.

These conditions are always associated with various complications, and
the second and third stages of chronic tuberculosis are frequently
accompanied by lesions of the pleura, of the mediastinal lymphatic
glands, of the liver, etc.

Digestive disturbances often occur; the appetite is capricious or in
abeyance, there is atony of the rumen and chronic dyspeptic tympanites.
These disturbances are easily understood where there are lesions of the
liver, intestine, and mesenteric lymphatic glands, but not when the lung
alone appears the seat of the disease. In this condition the patients
probably suffer from permanent complex intoxication, due to toxins
elaborated by the tubercle bacillus and other microbes which multiply on
or in the lesions, and this chronic intoxication reacts on the vital
functions (innervation, secretion, digestion and nutrition). Nor are the
effects limited to these appearances; the heart’s action is also
accelerated, and the temperature rises. During the first and part of the
second phase there is comparatively little fever, but afterwards this is
continuous or of a peculiar intermittent character. In the morning the
patient’s temperature may be normal; in the evening it has risen from
1·5 to as much as 9° Fahr. (1·1 to 5·2° C.) above normal, and this
recurs day by day. These attacks coincide with softening of the lesions,
and when suppurating caverns exist they are more marked and more nearly
continuous, assuming the characters of the hectic fever shown in
consumption.

Often during the febrile periods the urine is albuminous.

In chronic tuberculosis of bovine animals bleeding from the lung is rare
even when caverns exist, and Moussu, in spite of extensive experience,
has seen only two cases. This is in striking contrast with the condition
in human sufferers from pulmonary tuberculosis, two-thirds of whom bleed
at the lungs.


                   TUBERCULOSIS OF SEROUS MEMBRANES.

After pulmonary tuberculosis, tuberculosis of the pleural and peritoneal
serous membranes is the most frequent clinical form of this disease.
Sometimes both forms exist, and although the pleural and peritoneal
lesions predominate or alone attract attention, there are also lesions
in the lung or mediastinal lymphatic glands.

It is difficult to explain how the pleural and peritoneal serous
membranes can be seriously invaded without the lung becoming affected,
though in point of fact such a state of things frequently exists.

Tuberculosis of the pleura without pulmonary lesions is suggested by
very obscure symptoms. The general signs consist in diminution of
appetite, loss of condition, tachycardia, elevation of temperature, and
progressive organic wasting. These are always present, though in
themselves they have no specific significance.

The local symptoms are still more vague. Percussion causes pain, and the
practitioner might at first suspect peripneumonia. The patient edges
away, and tries to avoid the application of the pleximeter hammer. Firm
pressure over the intercostal spaces sometimes causes struggling, and
produces indications of abnormal sensitiveness. There is generally
extensive partial dulness, sometimes complete dulness towards the lower
regions of the chest.

On auscultation the lung may reveal the different indications of chronic
pulmonary tuberculosis, or simply diminution of the respiratory murmur
at points, accompanied by crepitant, sibilant râles, and moist,
crackling sounds. As the anterior portions of the pleural sacs are most
commonly invaded, the anterior vena cava is compressed, causing some
difficulty in the return circulation, and producing venous pulse, which
may extend as high as the parotid gland; there is, however, no swelling
of the dewlap.

Respiration is frequent and difficult in consequence of adhesions
between the pleura and lungs, which are connected by bands of fibrous
tissue of varying extent. Coughing is rarely absent, and if the lung is
diseased may be followed by discharge containing numerous bacilli.
Otherwise the cough exhibits the pleuritic character, that is, it
remains slight, dry, paroxysmal, and painful. The pericardium may be
affected as well as the pleura; if the conditions occur simultaneously
the venous pulse in the jugulars will be particularly apparent.

The symptoms of tuberculous pericarditis are similar to those of
ordinary pericarditis, except that the exudation is less abundant; in a
word, the symptoms are those of rather trifling exudative pericarditis.

Tuberculosis of the peritoneum is frequently accompanied by that of the
pleura or the abdominal viscera. The lesions are localised on the
parietal peritoneum and epiploon, producing in time adhesions between
the viscera and walls of the peritoneal cavity, which affect the action
of the digestive organs, gradually causing interference with the
peristaltic movement both of the rumen and the intestines. The
stagnation of alimentary matter favours fermentation, so that the rumen
becomes permanently distended. The right flank also is swollen, and the
abdomen exhibits a change in shape similar to that in peritonism, which
is a constant symptom of tuberculous peritonitis.

As in the thorax, the tuberculous lesions seldom produce extensive
liquid exudation, so that ascites does not occur, but on palpation the
abdominal walls appear to have entirely lost their pliability and to be
unyielding and greatly thickened, a point which is the more remarkable
as the animals are thinner.

The wall of the abdomen is stiff, incapable of being depressed as in
ordinary subjects, and gives to the fingers the sensation of a thick
hard covering, through which the subjacent organs and their contents,
that is, the rumen, intestine and alimentary material, can no longer be
felt. This rigidity is always most marked in the lower abdominal region.
The digestive peristaltic movement can no longer be detected, and on
auscultation the normal sounds are manifestly much slower than usual.


                   TUBERCULOSIS OF LYMPHATIC GLANDS.

It might perhaps have seemed more logical to place tuberculosis of the
lymphatic glands at the commencement of these clinical divisions of
tuberculosis, as when tuberculous lesions, of whatever kind, occur in
the lung, pleura, abdomen, etc., the lymphatic glands in the
neighbourhood are invariably invaded. In such cases, however, the
lesions in question are not the dominant features.

Under this heading must be classed tuberculous lesions which, on the
contrary, affect the lymphatic glands in so marked a manner that lesions
in other organs may be regarded as secondary. This occurs somewhat
frequently, because at the present day there is a tendency to believe
that inoculation takes place mainly through the mucous membrane of the
pharynx, and thence extends towards the neighbouring lymphatic glands.
At any rate, it is unquestionable that tuberculosis of the lymphatic
glands may exist quite apart from any other lesion visible to the naked
eye.

Two forms are very common, tuberculosis of the retro-pharyngeal region
and of the neck, and tuberculosis of the mediastinal lymphatic glands.

=Tuberculosis of the Retro-pharyngeal Glands.=—In addition to the
retro-pharyngeal glands the cervical chain of lymphatic glands, the
subglossal, subatloid, preparotid, and even the prescapular lymphatic
glands and those at the entrance to the chest, may also be invaded more
or less.

This form of tuberculosis may remain latent for a long time, attention
being attracted to it only when deglutition is impeded and local
deformity becomes apparent.

Swelling of lymphatic glands resulting from tuberculous infection is
slow and progressive, differing entirely from that which accompanies
suppurative adenitis. The neighbouring connective tissue is certainly
somewhat thickened or infiltrated, but the glands themselves can always
be detected. The region of the gullet is enlarged, the depression
marginating the lower jaw is filled up, the subatloid space disappears,
the subglossal glands occupy the space beneath the tongue, and in cases
where the lesions are very pronounced the œsophagus and larynx may even
be pushed downwards.

[Illustration: $1]

Swallowing is difficult, in consequence of compression of the upper part
of the œsophagus, and, as the laryngeal nerves may be included in the
swelling, dyspnœa or roaring not uncommonly results.

By palpation with one or both hands it is easy to identify the glands
and detect enlargement, hardness and sensitiveness. In exceptional
instances the caseous masses they contain undergo softening and
conversion into purulent material.

When the cervical lymphatic glands are attacked the jugular furrows
disappear, and the whole of the pretracheal and lateral regions of the
neck exhibit doughy swellings.

These swellings are rarely symmetrical, a fact which admits of this
condition being distinguished from lesions due to lymphadenitis, without
examining the blood.

The prescapular glands are rarely attacked, but those at the entrance to
the chest, which may be found on either side of the trachea by passing
the fingers between the two first ribs, are frequently enlarged to the
size of a fowl’s egg.

=Tuberculosis of the Mediastinum.=—Whenever the lungs are much involved,
the bronchial glands are also invaded, though the glands of the anterior
and posterior mediastina may escape. On the other hand, the mediastinal
glands are sometimes much involved, whilst the lung remains intact.

The lymphatic glands, particularly those of the mediastinum, may be
enormously enlarged, and the various accidents which result are due as
much to mechanical interference with the functions of adjacent organs as
to the lesions themselves.

When the glands of the anterior mediastinum are affected, they cause
compression of the anterior vena cava, with stasis of blood in the
jugular vein and venous pulse, then compression of the œsophagus and
trachea, and of the nerves at the entrance to the chest, producing
difficulty in swallowing, respiration and circulation.

[Illustration: $1]

If, as often happens, the glands of the posterior mediastinum are
affected and greatly enlarged, they may involve the œsophagus and the
œsophageal nerves, interfere with deglutition and rumination, and thus
produce marked disturbance. The animals only swallow with difficulty,
and later rumination becomes impossible, the antiperistaltic movement
not being powerful enough to overcome the resistance. Soon after eating,
the patients exhibit tympanites, certainly only to a moderate extent,
but the swelling is long in disappearing. This tympanites is due to the
difficulty in eructation and to the impossibility of rumination. The
contents of the rumen pass slowly towards the intestine until the onset
of a fresh attack.

On account of digestive difficulties, the animals rapidly lose flesh,
just as though they were suffering from extensive visceral lesions.


                  TUBERCULOSIS OF THE DIGESTIVE TRACT.

Tuberculosis of the digestive tract is rarer than tuberculosis of the
lungs or lymphatic glands, and occurs in two well-differentiated
clinical forms, that is to say, tuberculosis of the buccal and
pharyngeal membrane and tuberculosis of the intestines. Tuberculosis of
the liver, which is less easily recognised, is indicated by signs of
dyspepsia.

=Bucco-Pharyngeal Tuberculosis.=—This may be primary or secondary, and
occurs in the form of local or general glossitis or superficial
ulcerative stomatitis.

In the former case the glossitis may be regarded as due to
actinomycosis; in the latter it can only be mistaken for simple
ulcerative stomatitis.

It is accompanied by difficulty in mastication, and still more, where
the pharynx is invaded, in deglutition; abundant frothy salivation in
feeding; sometimes by true spasm of the pharynx and rejection of
masticated balls of food.

Locally the buccal mucous membrane (cheeks, tongue, pillars of the
fauces, etc.) exhibit ulcerations, with festooned borders, in size
something between a florin and a five-shilling piece, covered with a
greyish-yellow, earthy-coloured exudation adhering firmly to the
subjacent parts. The margin of the ulceration is but slightly indurated,
and the tongue preserves its mobility, except in cases of general
deep-seated glossitis.

The condition may continue for weeks and months without improvement.

=Intestinal Tuberculosis.=—Tuberculous enteritis is always accompanied
by tuberculosis of the mesenteric glands and of the sublumbar lymphatic
chain. It is indicated at first by chronic tympanites and peritonism,
unaccompanied, however, by atony of the rumen; at a later period by
intermittent diarrhœa, which attains a maximum and is followed by
constipation. Finally, when there exist numerous intestinal ulcers, the
diarrhœa is profuse and intractable, the animals rapidly grow exhausted,
and the disease spreads to other organs with startling rapidity.

The food is ill-digested and the fæces have a repulsive odour, as has
also the gas which escapes from the rumen when it is punctured.


                  TUBERCULOSIS OF THE GENITAL ORGANS.

In males, tuberculosis may attack the testicle and neighbouring organs
and tissues; in females, the ovary, uterus, vagina, or udder.

Tuberculosis of the testicle is rare. Moussu appears only to have seen
one case, namely, in the boar. The disease produces specific vaginitis
and specific orchitis, the serous surfaces of the vaginal tunic becoming
adherent, and tubercles forming in the depths of the testicle, whilst in
time the testicle becomes the seat of fungoid growths.

Tuberculosis of neighbouring glands has only been observed in the case
of the prostate. Clinically it is distinguished by symptoms which
suggest difficulty in urination, and comprise frequent straining,
efforts to micturate, dysuria, etc. Examination by the rectum reveals
changes in the prostate, but affords no exact information as to their
nature.

Tuberculosis of the genital tract in the female is usually a delayed
complication of a preceding visceral tuberculosis, though it may occur
as a primary disease, in which case the lesions are localised about the
vulva or the vagina. Tuberculosis of the ovaries, Fallopian tubes, and
uterus is much more common than that of the two organs just mentioned.
It seems certain that the disease may be transmitted directly from the
male to the female by copulation, in cases where the male animal has a
lesion on the penis.

Tuberculosis of the vulva is rarer, and is indicated by swelling,
sclerotic changes, and the presence of tuberculous nodules, varying in
size between a lentil and a hazel-nut; after ulceration of these
growths, a thick yellowish pus containing the specific bacilli is
discharged.

Tuberculosis of the vagina is also indicated by hardening of the walls,
sclerous infiltration, and the presence of deep-seated tuberculous
nodules, which may or may not become ulcerated. It may follow uterine
tuberculosis, the discharge from the uterus continually soiling and at
length infecting the floor of the vagina. In such cases the lower wall
of the vagina is thickened and infiltrated to a greater extent than the
roof, and is sometimes intersected by transverse ulcerated suppurating
folds. Bacteriological examination reveals the presence of bacilli.

Tuberculous invasion of the ovaries, Fallopian tubes, and uterus is
externally indicated by signs of chronic metritis accompanied by a
purulent discharge, which may or may not be fœtid, but always possesses
special characteristics. The neck of the uterus is half open, and the
discharge is continuous. The pus is of a greyish-yellow colour,
ill-formed, grumous, or more frequently granular, and it sometimes
accumulates in large quantities in the depressions of the vagina.
Examination by means of the speculum is of great value in diagnosing
such lesions. On examining the parts through the rectum, the walls of
the uterus are found to be greatly thickened, sometimes indurated,
bosselated or totally deformed.

The Fallopian tubes and ovaries may have attained enormous dimensions,
and the normal anatomy of the parts is greatly altered both as regards
dimensions and relations.

[Illustration: $1]

The almost inevitable consequences of tuberculosis of the genital organs
are hypertrophy, induration or caseation of the subsacral and sublumbar
lymphatic glands.

=Udder.=—Tuberculosis of the udder may be primary or secondary. When the
infection is slight the results may escape notice for weeks or even
months, the patients appearing to suffer only from subacute or chronic
mammitis, while at the same time the milk preserves its ordinary
appearance. In time, however, the mammitis becomes aggravated, the
infected regions are enlarged, and the secretion becomes grumous,
serous, curdled, and of a yellowish colour, afterwards ceasing
altogether. In some cases one quarter only is attacked, though total
mammitis is more common.

These forms of tuberculous mammitis tend towards hypertrophy, local
hardening, and the formation of deeply-seated cavities containing pus,
the gland itself sometimes acquiring enormous dimensions. The
retro-mammary lymphatic glands are invaded even before the gland itself
is seriously attacked. For a longer or shorter time the udder may
externally appear healthy, although on manual examination these
lymphatic glands are found to be indurated and bosselated.


                TUBERCULOSIS OF BONES AND ARTICULATIONS.

Tuberculosis of the bones is seen only in young animals, and chiefly
affects the vertebral column and the bones of the head. The limb bones
are attacked as a rule only in the vicinity of diseased articulations.

The vertebral lesions corresponding to those in Pott’s disease in human
beings are very difficult to discover before they produce complications,
such as depression of the spine, compression of the spinal cord,
paralysis, etc.

Lesions of the bones of the head or of the limbs are characterised by
local deformity, destruction of osseous tissue, invasion of surrounding
tissues, and by local symptoms peculiar to tumours originating in the
periosteum.

[Illustration: $1]

Tuberculosis of joints produces special symptoms resembling those seen
in the “white swellings” of man, that is, diffuse, œdematous, warm and
moderately painful swelling of adjacent parts, accompanied by lameness
of varying intensity. According to Guillebeau and Hess, many conditions
described as strain or rheumatic arthritis are really tuberculous in
character. They may remain stationary for a long time, or even recede
under treatment. As a rule, however, these forms of tuberculous
arthritis assume the fungoid type and prove incurable.

They are clinically distinguished from ordinary arthritis by the
enormous swelling, which involves the extremities and a portion of the
shafts of the bones. The adjacent muscles are chronically contracted,
and the diseased joint is held semi-flexed. In course of time, if the
patients are kept alive, abscess formation may occur, but this is seldom
seen in practice, because the animals are slaughtered.


                       TUBERCULOSIS OF THE BRAIN.

Tuberculosis of the nervous centres, localised either in the meninges or
the brain proper, may attack both young and old animals, not as a
primary condition, but as a sequel to visceral disease, which, however,
may have produced no outward indications, a fact that renders the
diagnosis extremely difficult.

When localised in the meninges, the disease produces the symptoms of
ordinary meningitis, general weakness, vacillating, staggering or
irregular gait, disturbed vision, variation in the size of the pupils,
difficulty in swallowing, muscular twitching, cramp of the muscles along
the upper margin of the neck, etc.

Tuberculosis of the brain proper seems more commonly to affect the
anterior convolutions and the depths of the frontal and temporal lobes.
It produces some of the symptoms of meningitis or symptoms suggestive of
the existence of cœnurosis, as, for instance, walking in circles,
lameness of central origin, without appreciable lesions of the limbs,
prolonged kneeling, disturbed vision, generalised attacks of epilepsy or
of Jackson’s epilepsy, spasm of the pharynx, general signs of
compression of the brain or cerebral dropsy, dulness, coma, etc.

[Illustration: $1]

In the absence of pulmonary lesions it is extremely difficult to arrive
at an exact diagnosis except after injection of tuberculin, for the
above symptoms very closely resemble those of cœnurosis, brain tumours,
and even tumours in the frontal sinuses.


                       TUBERCULOSIS OF THE SKIN.

Cutaneous tuberculosis is one of the rarest forms of the disease. It is
distinguished by the formation beneath the skin of little hardened
swellings varying in size between a hazel-nut and a walnut, and
containing caseous or calcareous material. These swellings have no
connection with the superficial lymphatic glands. They may be found
grouped together within certain areas, or distributed irregularly over
the whole body, particularly towards the base of the tail.

The condition may be mistaken for generalised sarcomatosis, from which,
however, it is readily distinguished by microscopic examination of the
contents of the swellings.


               ACUTE TUBERCULOSIS—TUBERCULOUS SEPTICÆMIA.

However rapidly the above-described forms of tuberculosis may develop,
the disease as a whole is always of long duration, and continues for
months, or even for years. The development of these chronic forms may,
however, be interrupted by various influences which cause it to assume
an acute character, either for a time or continuously. Each intermittent
attack aggravates the condition of the patient, but gradually subsides,
with or without treatment. Continued attacks, however, rapidly lead to
death; they may be seen in animals previously unsuspected of any grave
disorder.

[Illustration: $1]

The dominant symptom is continuous fever, accompanied by signs of
disturbance of any or all of the chief bodily functions.

The temperature rises to 102° Fahr. (39° C.), or even to 104° or 105°
Fahr. (40° or 41° C.), with morning and evening remissions of some
hours. The respiration is accelerated. On auscultation it is often
difficult to discover signs of chronic tuberculosis. The lung is the
site of repeated congestive changes, resembling those of
broncho-pneumonia or contagious pleuro-pneumonia. The pleura and walls
of the chest become extremely sensitive, as in the last-named disease,
and the abdomen may exhibit signs of peritonism, as at the beginning of
acute peritonitis. The pulse rises to 80, 90, 100, or even 120 beats per
minute, and the urine contains albumen in notable quantities. This
condition continues for weeks without apparent diminution, the patients
refuse food, lose flesh with startling rapidity, and finally die of
exhaustion.

It would be impossible from these peculiarities alone to identify the
nature of the disease which causes such progressive organic wasting, as
the continued presence of fever prevents the use of tuberculin, but
fortunately the preliminary changes in the lungs, lymphatic glands,
genital tract, etc., are sufficient in most cases for the purposes of
diagnosis.

=Sheep, Goats, and Pigs.=—In the other domestic animals tuberculosis is
only of secondary importance to the practitioner.

It has been seen in the sheep and goat, but almost exclusively as the
result of experiment. It must be understood, however, that prolonged
cohabitation with diseased oxen or lengthened sojourn in contaminated
places may easily produce tuberculosis in the goat, though the sheep
continues to resist for a somewhat longer period.

Clinically such tuberculosis presents little interest on account of its
rarity.

The same remark applies to pigs; nevertheless, an entire herd may become
infected, and it may be necessary, after making a preliminary
post-mortem, to examine the other patients. All forms of the disease
occur in pigs, the lung being most frequently affected, but tuberculosis
also attacks the intestine, udder, lymphatic glands, joints, etc. The
pig, in fact, is extremely susceptible to this disease, whilst the sheep
is only subject to it in a comparatively trifling degree.

=Diagnosis.= The clinical manifestations of tuberculosis are so numerous
and so various that it is often an extremely hard task to form a
diagnosis. Without doubt detection is relatively easy in well-marked
forms, such as tuberculosis of the lungs, lymphatic glands and genital
apparatus, but even in such cases the symptoms must be reasonably
well-marked.

At first, unless the lesions produce externally visible signs, diagnosis
is impossible, and in the case of hidden forms, such as tuberculosis of
the serous membranes, mediastinum, intestine, testicle, etc., all that
can be done is to take into account the probabilities.

Clinical diagnosis is therefore possible, but only in exceptional cases
can it be absolutely relied upon. Fortunately, methods of investigation
increase and become more exact every day, so that the points which
clinical examination is incapable of deciding are often cleared up in
the laboratory. Bacteriological examination of morbid products, such as
the nasal discharge, the products of suppuration, the milk or the
diseased tissues, is a valuable means in many cases of determining the
presence of the organism which causes the disturbance. In all cases, in
fact, the tubercle bacillus should be sought for in order to confirm the
diagnosis.

[Illustration: $1]

If this method cannot be employed, as for example in tuberculosis of the
liver, brain, etc., and the diagnosis is uncertain, the use of
tuberculin constitutes the surest and easiest method of coming to a
conclusion. Nocard’s researches have shown the precautions to be
observed. A minimum febrile reaction of 2° Fahr. (1·5° C.) is, however,
necessary before the existence of the disease can be affirmed.

Lastly, there remains a less rapid method, which aims at transmitting
the disease to specially susceptible animals by inoculating with
suspected materials, such as the nasal discharge, pus, milk or pulp of
internal organs. This method is most valuable when bacteriological
examination has failed and tuberculin has produced only doubtful
results. The guinea-pig is the subject usually chosen, but some weeks,
or even months, may elapse before definite results are obtained.

In those forms where ordinary methods of investigation prove sufficient
it is well to bear in mind the symptoms which differentiate this disease
from others closely resembling it.

Pulmonary tuberculosis, for example, should always be suspected whenever
there exists frequent coughing, nasal discharge and poor bodily
condition; if in addition to this respiration is found on auscultation
to be rough, inspiration interrupted or rasping, expiration prolonged or
blowing and the vesicular murmur non-existent, suspicion becomes almost
a certainty. The diagnosis is even more assured if the respiration is of
a blowing character at certain points, accompanied by snoring and
sibilant _râles_ and gurgling or cavernous souffles.

The distinction between pulmonary tuberculosis and chronic bronchitis or
simple pulmonary emphysema is based on the increased resonance revealed
by percussion in the latter case; the different character of expiration;
the existence of a double breathing movement; the external appearance of
the animal; the absence of bacilli from the nasal discharge, and the
failure to react to tuberculin.

The condition cannot be mistaken for verminous broncho-pneumonia if the
information furnished by auscultation and the results of microscopical
examination of the discharge are taken into account, the eggs or embryos
of strongyles being extremely easy to detect.

Tuberculosis of the pleura may be mistaken for peripneumonia if the
observer trusts to percussion alone, but the auscultation sounds are
then different, and an injection of tuberculin will remove any doubt.

Tuberculosis of the peritoneum is often suggested by the indications
afforded by careful palpation (thickening of the walls of the abdomen,
rigidity and sensitiveness), and is distinguished from ordinary acute
peritonitis by the difference in the appearance of the animals and the
absence of much fluid. Chronic exudative peritonitis and ascites also
exhibit sufficiently well-marked characteristics to enable them to be
differentiated from tuberculosis of the peritoneum, but this is
certainly not true of adhesive peritonitis, and in cases of the latter
kind tuberculin is the only means of confirming the diagnosis.

External tuberculosis of the retro-pharyngeal and cervical lymphatic
glands resembles, at a first glance, simple inflammation of lymphatic
glands, but in the last-mentioned disease the lesions are symmetrical
and the glands still retain a certain amount of elasticity, whilst in
tuberculosis they are bosselated, hard, and sometimes fluctuating.

Tuberculosis of the mediastinum is suggested by difficulty in
swallowing, especially if tympanites follows soon after eating,
eructation is absent, and rumination is arrested.

A careful study of the development of the ulcerations will also in most
instances make clear the difference between tuberculous stomatitis and
simple stomatitis or stomatitis due to actinomycosis. Intestinal
tuberculosis and tuberculous enteritis are sufficiently characterised by
persistent intractable diarrhœa accompanied by tympanites, by the fœtid
character of the fæces, and by moderate but continued fever. Chronic
diarrhœa, which alone presents some analogy with this condition, is
never accompanied by permanent tympanites.

Tuberculosis of the genital organs in male animals is always liable to
be mistaken for simple orchitis and the development of tumours in the
testicle; an injection of tuberculin will, however, indicate the nature
of the lesion.

When the symptoms of genital disease or chronic mammitis in female
animals suggest that the disease is of a specific character, the
diagnosis can frequently be confirmed by a microscopical examination of
the pus or milk.

Finally, should the practitioner hesitate as to the nature of the
lesions which are the cause of arthritis, deformity of bones, cerebral
symptoms, etc., tuberculin again will in most cases settle the question.

=The prognosis= in cases of tuberculosis is extremely unfavourable,
whatever the form of the disease or its manifestations. Clinically the
disease should be regarded as incurable in the strict sense of the word,
however limited may be the lesions. The affected animals are not all
doomed to immediate death: some may be kept alive, and may even serve an
economic purpose without necessarily endangering others; it is sometimes
possible to fatten them, though the risks probably far outweigh the
advantages, but one can never rely on recovery in any particular case.

The gravity of this disease is the greater inasmuch as it assumes so
many forms, any one of which may result in the infection of other
animals.

All those forms of the disease, such as tuberculosis of the respiratory,
digestive and genital tracts, in which virulent material containing
bacilli is discharged realise these conditions. The patient becomes a
source of infection to others of its kind, a fact which more than
anything else renders the disease so dangerous to the farmer and
breeder.

Only in cases where the lesions are closed (as in tuberculosis of the
lymphatic glands, serous membranes, joints, etc.) can the sufferers be
regarded as innocuous, and—as these lesions are exceptional or at least,
as animals suffering from them are very frequently afflicted with open
lesions from which bacilli are continually being discharged—every
tuberculous animal must be regarded from a clinical standpoint as a
constant danger to its neighbours.

This, however, must not be understood to mean that there are not
different degrees of danger. It is quite certain that a patient with
pulmonary caverns which are constantly throwing off enormous quantities
of material full of bacilli is much more dangerous than another
suffering only from slight bronchial or tracheal lesions, though the
danger in the latter case is none the less always present.

=Treatment.= There is no really curative treatment of tuberculosis.

It must not be thought, however, that we are completely helpless and
that the present condition of affairs must be allowed to continue
indefinitely. Nocard and Leclainche have minutely laid down the lines to
be followed as regards prophylaxis, though unfortunately the measures
recommended cannot always be carried out.

Tuberculin having been proved an exact means of detecting tuberculous
lesions in animals even where none were suspected, it is desirable,
firstly, to test all the animals in a given establishment with
tuberculin; and, secondly, to separate into classes (1) all animals
which have reacted, and (2) those which have resisted.

The stables, etc., should then be completely disinfected by sweeping,
washing first with hot water, then with strong antiseptic solutions,
brushing over the walls with quick-lime solution and fumigating with
sulphurous acid or formic aldehyde. The healthy animals should then be
placed in one shed and the diseased animals in another. In order to
render this system of isolation really efficacious the isolated animals
and the healthy animals should have nothing in common, and the persons
tending the two classes of animals, the buckets and other utensils, the
watering places, etc., should be kept rigorously apart.

The animals known to be tuberculous should as rapidly as possible be
prepared for slaughter, and if pregnant cows are included in the number
the calves should be removed to the healthy stable immediately after
birth and brought up either on boiled milk or by a healthy mother,
experience having shown that congenital tuberculosis is of rare
occurrence.

After the tuberculous animals have left the shed, this should again be
thoroughly disinfected, in order to make it fit for the reception of
healthy subjects.

Unfortunately such precautions can only be observed in model
establishments. They necessitate expenses and immediate sacrifices of a
very serious character, and breeders too often view only the sacrifice
without regard to the after benefits. For this reason the above system
has only been practised in certain of the best known and best managed
farms.

To ensure the full benefit of these precautions, and to prevent a fresh
introduction of tuberculosis into the herd, every new animal introduced
should be subjected to the tuberculin test. Unless this precaution is
taken, there is always a risk of introducing a tuberculous subject, thus
nullifying all the precautions previously taken.

The problem is therefore still very complex, and the system can only
give good results when rigorously observed and followed out.

As, however, in spite of all precautions, animals regarded as healthy
are always, under normal conditions of existence, more or less exposed
to accidental infection, it is desirable to subject the entire herd to
the tuberculin test annually. This would cause the immediate detection
of any animals with latent infection, so that they could be removed from
the herd.

These wise precautions might, if understood and observed, eliminate the
disease from the country, but they depend on individual initiative, and
have not as yet been grasped by the mass of small breeders, farmers,
etc. This class only see the difficulties in the way of realising the
idea, without appreciating the constant benefit which they would derive
from it.


      SWINE FEVER—VERRUCOUS ENDOCARDITIS AND PNEUMONIA OF THE PIG.

Although it is not contemplated in this work to deal with those
disorders which, on account of their highly contagious or infectious
character, can only be dealt with by legislative action and by processes
of “stamping-out,” it may be permissible to make certain exceptions.
While we have made no reference to contagious pleuro-pneumonia of
cattle, foot-and-mouth disease, rinderpest, anthrax and black-quarter we
have devoted some space to Texas fever and tuberculosis, and give
herewith a summary of the present state of knowledge regarding swine
fever or hog cholera and a hæmorrhagic septicæmia of cattle known under
various names in different countries and of very wide distribution.


                            SWINE FEVER.[9]

Footnote 9:

  Report of the Departmental Committee _re_ Swine Fever. (Annual Report
  of Board of Agriculture, 1896.)

Swine fever may assume two distinct forms, viz., the acute and fatal and
the non-acute or slowly progressive.

=Symptoms.= In the acute form all those symptoms which are indicative of
a severe febrile affection are present. The animals are disinclined to
feed; they present evidence of great prostration and lie about their
dwellings in a listless manner sheltering themselves from cold; their
skins are hot, their eyes partially closed, and they are obviously
suffering from some severe constitutional disturbance. Within a very few
hours after these premonitory symptoms have set in the pigs become
rapidly worse; they may or may not have a deep-red blush on the skin,
which is more particularly noticeable on those parts of the body where
there is an absence of hair, such as the inside of the thighs, the point
of the axilla, and over the abdomen. Choleraic evacuations, having a
most offensive odour, succeeding upon constipation, follow later on, and
the animals die perhaps as early as the third or fourth day after the
symptoms have first been observed.

In some instances the disease proceeds with great rapidity through a
herd, the symptoms being of a most aggravated and pronounced character,
and the outbreak attended with great fatality.

Generally speaking, the above description depicts the symptoms of swine
fever in the acute form, more especially when it breaks out in a herd of
young pigs.

In the non-acute form the disease progresses slowly, the clinical
evidence is extremely obscure, the reddening of the skin, formerly
regarded as being invariably present in swine fever, is absent, and
beyond the fact that the animal is unthrifty, develops slowly, and
perhaps has a constantly relaxed condition of the bowels, it may be
asserted that there are no symptoms which could be regarded as
absolutely indicative of swine fever, and nothing short of a post-mortem
examination will enable even an expert to satisfy himself that the
animal was affected with the disease.

As a general rule swine fever assumes this non-acute and slowly
progressive form in pigs which have arrived at an age when their powers
of resistance to disease are materially increased, _i.e._, in animals of
eight or more months old; on post-mortem examination they are found to
have been extensively diseased, more particularly in the large
intestine, a portion of the digestive apparatus which does not appear to
perform any very important function in connection with the nutrition of
the animal, and so long as the stomach and small intestines remain
healthy, pigs with a considerable amount of disease in the large
intestine may still keep up their condition for a considerable time.

=Etiology.= As regards the etiology of the form of swine fever prevalent
in England no question now exists. It has been proved to demonstration
by the bacteriological inquiry conducted by Professor McFadyean that it
is due to a special pathogenic organism, a bacillus, which, after
cultivation in artificial media, will produce in the healthy pig fed
with the pure cultures the typical ulcerations which are found in the
intestines of pigs affected with swine fever contracted in the ordinary
way.

The observations made by the veterinary officers of the Board of
Agriculture caused them to doubt whether there was any disease of the
lungs of pigs which, in the absence of lesions in the intestinal tract,
could be accepted as evidence of swine fever.

The bacillus which produced swine fever when introduced in the healthy
pig did not induce any special disease of the lungs.

=Pathology and morbid anatomy.= Swine fever, like typhoid fever in man,
is essentially a disease of the digestive system, its chief
characteristic being certain morbid changes of a well-marked nature
which are found upon the surface of the mucous membrane in some part of
the alimentary canal.

The changes referred to consist of what have been commonly described as
the formation of a series of ulcers, single or confluent, distributed
upon some part of the intestinal tract, varying in size and shape, of a
yellowish-grey to black colour, and assuming as a rule a circular form.
In some instances the lesions consist of diphtheritic exudations with
necrosis of the lining membrane of the bowels.

These ulcers or necrotic patches may be found upon the tongue, tonsils,
epiglottis, stomach, and small intestines, but they are more constant in
the large intestines, especially the cæcum and colon. The lesions may
involve the whole thickness of the mucous membrane, but seldom penetrate
the other coats of the intestine; in fact, perforation of the peritoneal
covering of the bowel is very rare in even prolonged cases of swine
fever.

In cases where swine fever assumes the more acute form and death
supervenes rapidly, it is usual to find that the small intestines are
largely involved.

In the non-acute or slowly progressing form the lesions are more
abundant in the large intestines, and in some instances the walls of the
intestines become so thick as a result of infiltration into their
structure and the excessively thick deposits upon the lining membrane,
that it becomes a matter of surprise that the passage of the ingesta has
been possible and that the animal has lived so long.

Next to the intestinal lesions the congested condition of the lymphatic
glands, especially those of the mesentery, may be considered as most
prominent among the pathological changes which occur in swine fever.
Occasionally centres of necrosis are observed in the liver, and some
writers refer to changes in or upon the spleen and kidneys.

The only lesions which can be characterised as absolutely typical of
swine fever are those present in the bowels, the absence of which will
justify any observer in declining to accept the case as one of swine
fever without some further evidence or inquiry. It must, however, be
distinctly understood that in the case of very young pigs which have
died shortly after infection, there is often an entire absence of the
lesions described, the only changes present being inflammation of the
stomach or some part of the intestines.

Further, there are instances where older pigs have been slaughtered in
the early stage of the disease in which no definite lesions have been
found, and in such cases inquiry into the condition of the rest of the
herd becomes necessary.

One most important feature in connection with the morbid anatomy of
swine fever is the disposition which many animals have to recover from
the disease; evidence of the reparatory process having often been
detected in the intestines after they had been carefully washed.

Dr. Klein also maintained that many pigs took the disease in the mild
form, and recovered without presenting any of the marked symptoms of
swine fever.

It was found that, whether infected in the ordinary way or by direct
inoculation, in some pigs killed only a few days after being infected
the ulcers were occasionally seen gradually detaching from the surface
of the intestines, and cicatrisation had already commenced.


                   VERRUCOUS ENDOCARDITIS OF THE PIG.

In the report of the Board of Agriculture for 1894 reference was made to
the numerous instances in which the heart of the pig had been found
affected with verrucous endocarditis.

This form of disease of the heart was known to veterinarians in Great
Britain as far back as the year 1847. For reasons given in that report
it became obvious that this diseased condition of the valves of the
heart was not produced by swine fever. The question arose whether in
addition to swine fever another disease existed, known on the Continent
under the name of swine erysipelas. The importance of this question will
be appreciated when it is explained that on the Continent swine
erysipelas is classed among the contagious diseases of the pig.

The clinical evidence of the disease called swine erysipelas on the
Continent appears to be more or less discoloration of the skin, similar
to that which is frequently observed in swine fever, together with the
occasional presence within the warty growths upon the valves of the
heart of a bacillus which is regarded by Continental authorities as the
cause of the disease.

Early in the inquiry it was ascertained that a bacillus identical with
that found in swine erysipelas was also present in the diseased portion
of the valves of the heart of the pigs in this country.

But the inquiries made did not corroborate or favour the suggestion that
the disease which produced these morbid growths was in any way
infectious or contagious. Such inquiries as could be made led to the
opposite conclusion, since in every instance where the cases could be
followed up it was ascertained that the deaths had been quite sudden,
were limited to a single animal, and that those in contact remained in
perfect health.

At this stage the all-important point to determine was whether the
disease which existed in this country, “verrucous endocarditis,” was
communicable from pig to pig, and with this object numerous experiments
have been conducted to discover whether the bacilli found within the
hearts of diseased pigs were pathogenic to healthy swine.

A large number of healthy pigs have been fed or inoculated with the
blood, the diseased portions taken from the valves of the heart, and
with artificial cultures of the bacilli obtained from the heart, but in
no instance has the attempt to produce this disease been successful.


                         PNEUMONIA OF THE PIG.

The occasional association of pneumonia with or without pleurisy in
cases of swine fever has led many veterinarians in England to regard
lung complications as one of the lesions produced by that disease.

In the Board of Agriculture’s report for the year 1894 a description was
given of the various diseases in the lungs of swine which had come under
notice, and it was therein stated that the Board had been unable to
discover any special lesion of the lung which would warrant them in
stating that it was indicative of swine fever or due to contagion.

It is an indisputable fact that pigs are extremely liable to pneumonia
and pleurisy. But as the clinical appearances present in the lungs
examined in no wise differed from those which take place in the lungs of
other animals which have been exposed to cold or septicæmia and other
causes, the Board’s officers have never accepted these lesions as being
specific.

It is well known that both in Germany and the United States outbreaks of
pneumonia of a contagious nature attributed to the presence of a
bacillus pathogenic to the pigs of those countries are reported to
occur. Indeed, contagious pneumonia of swine under the names of
schweineseuche in Germany and swine plague in America are regarded as
one and the same disease.

In view of the fact that in a large number of cases pneumonia, more or
less extensive, sometimes associated with pleurisy, was found among the
specimens forwarded to London, it was considered desirable that the
departmental committee should institute a series of experiments to
decide whether we had in this country a form of pneumonia in the pig
which was communicable from one pig to another.

Accordingly a series of bacteriological experiments were conducted by
Professor McFadyean with a view to isolate, if possible, a microorganism
which would be capable of inducing pneumonia in healthy pigs. A number
of diseased lungs, some of which were taken from pigs affected with
swine fever, were examined microscopically by him, and, as was to be
expected, several organisms were isolated, but they proved to be
morphologically and culturally different from the bacillus of swine
fever. Inoculations were carried out with these organisms not only
subcutaneously but directly into the lung through the walls of the
chest, and feeding experiments were also conducted. The results of these
experiments were entirely negative; a certain amount of local injury was
caused to the lungs at the seat where they had been punctured, but in no
case was either pneumonia or swine fever induced.

The experiments have therefore demonstrated that the pneumonia found in
the lungs of pigs affected with swine fever is not due to the swine
fever bacillus.

The departmental committee arrived at the conclusion that the pneumonia
which is occasionally encountered as an independent disease of the pig
or in association with swine fever is not ascribable to contagion, but
to the presence of organisms which are generally saprophytic in their
mode of life, and which only in particular circumstances (such as
lowered vitality and diminished resistance on the part of the pig) are
able to multiply in the air passages and lung tissue and thus induce
pneumonia; and it appeared to the departmental committee that in this
country pneumonia of the pig is sporadic and not contagious or
epizootic.


                              CONCLUSIONS.

There is now no reason whatever to believe that there exists at the
present time in Great Britain any disease of a contagious nature
affecting pigs other than swine fever. The disease of the heart,
“verrucous endocarditis,” and the pneumonia which are so frequently met
with in pigs cannot be regarded as lesions indicative of an attack of
swine fever.

As regards verrucous endocarditis and pneumonia, it may safely be said
that they do not exist in England in a contagious form.

Considering all the evidence, it may reasonably be concluded that the
departmental committee were correct in their views when they stated that
“the evidence obtained during the whole inquiry justifies the conclusion
at which they have arrived, viz., that there is no epizootic of swine
except swine fever in any part of the United Kingdom which requires to
be dealt with under the provisions of the Act of 1894.”

Finally, it may be said that the great factors in perpetuating swine
fever will always be pigs which are affected with that disease in the
less fatal and unrecognisable form. These animals are constantly
distributing the germs of swine fever through their highly infective
evacuations wherever they may be taken during the whole period of their
illness, and the final extinction of the malady must depend upon the
possibility of enforcing measures which will have the effect of
preventing the movement of pigs affected with swine fever in this
particular form.


                   HÆMORRHAGIC SEPTICÆMIA IN CATTLE.

In 1902 Drs. Wilson and Brimhall, of the State Board of Health of
Minnesota, U.S.A., described under the title of “hæmorrhagic septicæmia
of cattle” a widespread infectious disease of bovines which has the
following general characteristics:—The disease is distributed the world
over, but is apparently most common in low-lying regions, and most
general in wet seasons. The animals attacked are of all ages. The onset
of the disease is sudden, its course rapid, and its termination usually
(90 to 98 per cent.) fatal. Thirty to 90 per cent. of all animals in an
infected herd die. The clinical symptoms are refusal of food, cessation
of rumination and lactation, initially increased temperature (107° to
109° F.: 42° to 43° C.), rapid, laboured breathing, sometimes bloody
discharge from nostrils, bladder, and bowels, and non-crepitant
swellings in the throat region, back of shoulders, or about the
fetlocks. The most striking pathological lesions are hæmorrhages from 1
millimètre to 20 centimètres in diameter, throughout the subcutaneous,
submucous, subserous and intermuscular connective tissue, infiltrating
the lymphatic glands, and involving several or all of the internal
organs. The spleen is neither enlarged nor darkened. The causative
bacteria, which may be isolated from the larger hæmorrhagic areas, lymph
glands, heart’s blood, lung, spleen, etc., have the following
distinguishing characteristics:

Ovoidal bacilli, with rounded ends of 0·5 to 0·8 microns in transverse
diameter, and 1·0 to 1·5 microns in length; sometimes paired and
sometimes in chains of three to six individuals. The bacilli in the
tissues exhibit polar staining with an unstained “belt” or “middle
piece.” They are non-capsulated, non-spore-forming, non-Gramstaining,
and non-motile. They grow best aërobically at 98·5° F. (37° C.), though
capable of developing anaërobically and at room temperature; prefer the
depths rather than the surfaces of media; grow feebly, if at all, on
potato; fail to liquefy gelatine; produce acid, but no gas in glucose
media, neither acid nor gas in lactose media; and develop varying
amounts of indol and phenol in peptone solution. The organisms have been
named _Bacillus bovisepticus_. The lesions of the disease are reproduced
in cattle and other animals by inoculation of pure cultures of the
organism.

It should be insisted upon that the identification of the disease in a
locality in which it has not been previously described, or by
veterinarians not having had previous experience therewith, shall take
into consideration—(_a_) _the essential clinical symptoms_; (_b_) _the
pathological lesions as observed before the onset of decomposition; and_
(_c_) _the morphological and biological identification of the specific
bacilli_.

The following is a tabulated list of the principal epidemics so studied
and reported to January 1st, 1901:

   _Table showing the Principal Epidemics of Hæmorrhagic Septicæmia in
                 Bovines due to_ Bacillus bovisepticus.
 ┌─────────────────┬─────┬──────────────┬──────────────────────────────┐
 │Name of observer.│Year.│  Locality.   │ Local or reporter’s name of  │
 │                 │     │              │           disease.           │
 ├─────────────────┼─────┼──────────────┼──────────────────────────────┤
 │Bollinger        │1878 │   Germany    │Wild und Rinderseuche.        │
 │Kitt             │1885 │      „       │Rinderseuche.                 │
 │Kitt             │1887 │      „       │Septikæmia hæmorrhagica.      │
 │Poels            │1886 │   Holland    │Septic pleuro-pneumonia of    │
 │                 │     │              │  calves.                     │
 │Oreste et Armanni│1886 │    Italy     │Barbone.                      │
 │Jensen           │1889 │   Jutland    │Rinderseuche.                 │
 │Piot             │1889 │    Egypt     │Kounnaq.                      │
 │Van Eecke        │1890 │     Java     │Septichæmia hæmorrhagica.     │
 │                 │1895 │              │                              │
 │Hubenet          │1895 │      „       │        „           „         │
 │                 │     │   France,    │                              │
 │Galtier          │1891 │imported from │Infectious pneumo-enteritis.  │
 │                 │     │   Algiers    │                              │
 │Reischig         │1891 │   Hungary    │Maladie des buffles ou Angine │
 │                 │     │              │  Charbonneuse.               │
 │Bongartz         │1892 │   Germany    │Wild und Rinderseuche.        │
 │Jakobi           │1892 │      „       │Wildseuche.                   │
 │Buch             │1892 │      „       │Hæmorrhagische septikæmia.    │
 │Güllebeau and    │1894 │      „       │Septikæmia hæmorrhagica.      │
 │  Hess           │     │              │  Charbon Blanc.              │
 │Fischer          │1894 │ Dutch Indies │Septichæmia hæmorrhagica.     │
 │Leclainche       │1895 │    France    │Pneumo-enteritis.             │
 │Von Ratz         │1896 │   Hungary    │Barbonekrankheit.             │
 │Sanfelice, Loi,  │1897 │   Sardinia   │              „               │
 │  and Malato     │     │              │                              │
 │Bosso            │1898 │    Italy     │Septicæmia hæmorrhagica.      │
 │Pease            │1898 │British India │Ghotwa or Ghotu.              │
 │Lignières        │1898 │  Argentina   │Pasteurellosis bovina.        │
 │                 │     │              │  “Diarrhœa” and “Enteque.”   │
 │Fenimore         │1898 │  Tennessee   │Wild and cattle disease.      │
 └─────────────────┴─────┴──────────────┴──────────────────────────────┘

It may not be out of place to give at this point a short list of the
principal infective diseases of definitely known ætiology, with which
hæmorrhagic septicæmia in cattle has been, and may readily be, confused:

   _Name of disease._                 _Diagnostic points._

 Anthrax                 Altered condition of blood, enlarged spleen,
                           presence of _B. anthracis_, etc.
 Black-quarter           Usually localised lesion, crepitant tumour,
                           presence of _B. anthracis symptomatici_.
 Septicpneumo-enteritis  Due to a spore-bearing
   of calves (Galtier)     bacillus—“_Pneumobacillus septicus_”—which
                           grows rapidly on potato.
 Septicæmia of calves    Due to typhoid-like bacilli.


                              CONCLUSIONS.

(1.) Eight outbreaks of hæmorrhagic septicæmia in cattle due to _B.
bovisepticus_ occurred in Minnesota from August to December, 1900.

(2.) So far as can be determined, the only other outbreak of this
disease hitherto published as occurring in America was one near
Knoxville, Tenn., in 1898. The foci of the disease have also apparently
been present in Texas and the district of Colombia. No relation can be
traced between the disease elsewhere and the present outbreaks, nor
between any two of the present ones.

(3.) Of 160 animals in the eight herds, sixty-four showed symptoms of
the disease, and all such died—a mortality of 40 per cent. of all the
animals in the herds, and of 100 per cent. of those showing symptoms.

(4.) The chief symptoms were loss of appetite, fever, stiffness,
swelling of the legs and throat, and a black, tarry, or bloody discharge
from the bowels. Bloody urine and bloody nasal discharge were present in
some cases. Death occurred usually in from six to twenty-four hours
after the first appearance of symptoms.

(5.) The chief lesions discovered at autopsy were ecchymoses, and small
and large hæmorrhagic areas in the subcutaneous connective tissues,
muscles, lymph glands, and throughout the internal organs. The cervical
lymph glands, heart muscle, and alimentary canal were most affected. The
spleen was not enlarged nor darkened (except after onset of
decomposition).

(6.) From the twenty-two animals on which autopsies were made the same
bacillus was obtained from all the tissues examined. Where the
examination was made immediately after death—nine cases—it was unmixed
with any other organism.

(7.) The bacillus was identified as belonging to the hæmorrhagic
septicæmia group of Hüppe, best specifically designated as _B.
bovisepticus_; and besides causing hæmorrhagic septicæmia in cattle
(synonyms—rinderseuche, buffleseuche, barbone, khounnaq, charbon blanc,
ghotwa, pasteurellosis bovina, etc.), closely resembles, if, indeed, it
is not identical with, the bacilli causing wildseuche, swine plague,
schweineseuche, rabbit septicæmia, chicken cholera, grouse disease, duck
cholera, etc. The organism was studied in direct coverglass
preparations, parallel cultures in and on various media, and by
inoculation of animals in which the characteristic lesions were
reproduced, and from the tissues of which the inoculated bacilli were
recovered in pure culture.

(8.) An attempt was made to immunise cattle by the injection of
filtered, and later of the killed, cultures of the bacillus. The chief
difficulties met with were in maintaining the virulence of the bacillus
on artificial media, and in determining the proper dosage. The
experiments were too few, and the results not sufficiently tested to
warrant conclusive statements as to the protective value of the
inoculations, but it would appear that a fairly high degree of immunity
was produced.

(9.) The prompt removal of the dead animals and isolation of sick ones,
accompanied by thorough disinfection by fire, carbolic acid, corrosive
sublimate, and freshly-slaked lime, apparently served to check each
outbreak within a short time after the measures were instituted.




                              SECTION XI.
                              OPERATIONS.




                               CHAPTER I:
                          CONTROL OF ANIMALS.


                            CONTROL OF OXEN.

The safe and efficient performance of surgical operations renders it
necessary that the animal should first of all be placed under complete
control. This precaution, therefore, is the first to merit attention.
Animals are either secured completely or to a more or less limited
extent, according to circumstances. The ox, for example, may be secured
by the head, one or more limbs may be fastened, or, by being placed in a
trevis, the whole of the animal may be secured.


                            PARTIAL CONTROL.

(1.) The simplest method of securing the ox is to grasp the nostrils or
lower extremity of the septum nasi between the thumb and index finger of
the right or left hand (Fig. 57).

(2.) This method may be rendered more complete by the assistant passing
his arm from behind forward over the animal’s head between its horns,
and then grasping the nostrils as above described, whilst one of the
horns is firmly held with the other hand (Fig. 58).

(3.) A third method consists in fixing the head to a post, tree, fence,
or other solid body, by passing a rope round the base of the horns and
tying it to the object selected.


                         CONTROL OF THE LIMBS.

To prevent the animal kicking or moving about during an operation it is
sometimes necessary to fix the limbs. A front leg may be lifted as for
shoeing, or may be kept lifted by means of a rope passed around the
fetlock, over the withers, downward between the front legs, outside the
forearm, in front of the chest and inside the pastern, after which one
or more turns may be made around the pastern to prevent the rope
slipping.

A hind limb may be secured in a simple way by passing the end of the
tail round it in front of the hock (Fig. 284); any violent and extensive
movement of the limb is then necessarily painful to the animal owing to
the tension of the tail.

[Illustration: $1]

Greater security, however, is given by passing a rope backward and
forward around the hind legs, above the hocks, in the form of a figure
of eight (Fig. 285). This does not prevent all movements of the hind
limbs, but it limits them and secures both animal and operator from
danger.

[Illustration: $1]

Should it become necessary to examine the hind foot or interdigital
space, it is useful at times to pass a loop of cord round the leg in the
region of the tendo-Achillis, and to twist and tighten this loop by a
short, stout stick passed through it; this is the leg twitch described
in Dollar’s “Operative Technique,” p. 7.

For such examinations, however, the animal is usually placed in the
trevis, or is secured to the side of a long waggon (Fig. 286).

To secure the limbs beneath the abdomen a strip of webbing or a rope is
fastened round the pastern, passed between the fore limbs, then in front
of the shoulder of the opposite side, over the withers and beneath the
elbow of the same side, being secured with a slip-knot.

For castration in the standing position a hind and a fore limb may be
fastened together, as shown in Fig. 287.

In examining the sole of the hind claws, the animal’s head may be
secured to a tree, and the hind limb lifted by a strip of webbing or
rope fixed to the body of a waggon (Fig. 288).


                            GENERAL CONTROL.

General control in the standing position can only be made really
effective by using the trevis, in which both the head and the fore and
hind limbs are secured.

[Illustration: $1]

[Illustration: $1]

The practitioner, however, is often content with much less perfect
methods, using either the so-called “bulldogs” or the nose ring, which
may usually be so manipulated as to control all but the most dangerous
animals. The nose ring is seldom employed except for bulls, which are
usually ringed at an early age; the “bulldogs” can be employed and
removed at will.

In inserting a nose ring the head is securely fixed, the centre line of
the muzzle is grasped with the left hand, and the septum nasi is pierced
with a straight bistoury, the cutting edge being turned in a backward
direction; the aperture being thus prepared, the ring is introduced and
fixed. Some operators prefer to use a trocar, slightly exceeding in
diameter the ring to be worn; in that case the manual technique is the
same. The puncture is made, the trocar alone is withdrawn, and the
canula remains _in situ_; one extremity of the ring is then inserted
into the canula, and both are drawn through the septum together. There
is no difficulty in thus inserting the ring, though puncture with the
trocar is perhaps rather less convenient than with the bistoury.

[Illustration: $1]

Relative control without casting may also be effected by attaching the
end of the tail to the base of the horns or the head to the cannon bone
of a front or hind limb. These methods, however, are of little value
except to prevent animals at grass from escaping entirely during
operation.


                          CONTROL BY CASTING.

Oxen should always be cast on a thick straw bed to avoid fracturing the
horns.

The simplest method consists in using hobbles and ropes, as for the
horse.

[Illustration: $1]

Another, though less practical, method consists in using two long ropes,
each fixed to the base of the horns and passed first between the front,
then the hind limbs, round the hind pasterns from within outwards and
then brought forward (Fig. 292). When the ropes are drawn tight by
assistants standing in front of the animal, the latter usually falls on
its hocks and rolls over to the right or left, according to the
direction given to it.

A third method is particularly useful in young or feeble animals. It
consists in fixing around the horns a rope about eight to ten yards in
length, the free end of which is carried along the upper margin of the
neck and back. A loop is formed embracing the base of the neck, a second
behind the shoulders in the region occupied by the girth, and a third
around the flanks (Fig. 293). By pulling in a backward direction the
rope is drawn tight, and the animal first backs and afterwards falls on
its hocks, subsiding either to the right or left, as in the case
previously mentioned.

[Illustration: $1]

[Illustration: $1]

In using either of these two methods it is very important, as soon as
the animal falls, to secure the limbs in a certain way, according to the
nature of the operation to be performed. This can be effected with
hobbles and ropes passed round the hocks, above the knee, etc.


                      CONTROL OF SHEEP AND GOATS.

The above animals may be secured, whilst standing, by grasping the head
and neck or, when cast by crossing the front and hind limbs in the form
of an =X= and tying a soft rope or piece of webbing round the crossing
of the limbs.

[Illustration: $1]

[Illustration: $1]


                            CONTROL OF PIGS.

No difficulty is usually experienced in controlling young pigs, either
when standing or cast, only one or two assistants being required, but
aged animals are more difficult and more dangerous to deal with, and by
their tusks sometimes inflict severe wounds.

In the standing position they can be partially fixed by passing a
running loop behind the canine teeth of the upper jaw, but should the
examination to be carried out prove to be of a difficult character it is
best to cast the animal.

A strong assistant grasps one of the hind limbs by means of a running
loop, fixed, for example, above the right hock. He rapidly slides his
left knee towards the front of the left side of the chest, passes his
left hand over the withers, and by the combined use of his knees and
arms throws the animal on its left side, controlling as far as possible
the struggles of the right front and hind limbs, which he grasps with
his hands.

The animal is then further secured by rapidly passing a thin rope in
figures of eight around the front and hind limbs. If necessary all four
legs may be brought together and fastened by a rope passed round the
region of the pastern; a muzzle can afterwards be applied to prevent
biting.


                              ANÆSTHESIA.

Oxen rarely receive general anæsthetics, though in certain obstetrical
cases they may be necessary. Ether and chloroform are given by
inhalation, and chloral of 10 to 20 per cent. strength by intravenous
injection. In utilising the latter method the injection should be made
slowly, the pulse and heart being closely scanned to prevent cardiac
syncope. The dose of chloroform varies with the size of the animal, 2
ounces often sufficing for a full-grown ox. The same methods may be used
for sheep, goats, and pigs, the doses being suitably altered. (For
fuller particulars see Dollar’s “Operative Technique,” pp. 44 to 70.)

Most frequently, however, the surgeon contents himself with producing
local anæsthesia by the injection of a 4 to 10 per cent. solution of
cocaine.




                              CHAPTER II.
                         CIRCULATORY APPARATUS.


                               BLEEDING.

Bovine animals are usually bled from the superficial jugular, or the
mammary vein.

=Bleeding from the Jugular.=—The animal having been suitably fixed, the
jugular is raised by means of a cord drawn tightly round the base of the
neck, and the vessel is opened with a fleam about the middle of the
neck.

The skin of the ox being thick, a long-bladed instrument is necessary.
When the bleeding ceases, the cord is removed: some practitioners take
no precautions as regards the wound; it is better to insert a pin
suture.

Bleeding from the jugular may also be performed with the trocar,
particularly in animals with fine, thin skin.

=Bleeding from the Mammary Vein.=—The mammary vein may be opened with
the fleam, the straight bistoury, or the lancet. The head is firmly
fixed and the hind limbs controlled by a rope passed in a figure of
eight above the hocks.

In bleeding on the left the operator places himself at an angle to the
animal’s side, opposite the hypochondriac region, with his back towards
the animal’s head, and holds the fleam in his right hand. To operate on
the right-hand side the fleam is held in the left hand.

This method of bleeding always causes thrombus formation, on account of
the low position of the opening in the vein. The animal’s bed should be
kept very clean, in order to prevent any local infection which might
cause hæmorrhagic or suppurative phlebitis. The lancet or bistoury can
only be used in animals with very fine skin.

In bovine animals small quantities of blood are sometimes taken from the
facial vein or the veins of the ear or tail.


                           BLEEDING IN SHEEP.

On account of the quantity of fatty tissue and wool covering the jugular
furrow in the sheep, bleeding is scarcely practicable at that point. The
operation is usually performed on the angular vein of the eye, the
external saphenous vein, or the subcutaneous vein of the forearm.

In operating on the facial vein the animal’s head is firmly held, the
operator compresses with the fingers of his left hand the facial vein at
the point where it passes into the maxillary fissure, and with a lancet
opens the angular vein of the eye or one of the other branches of origin
which project prominently beneath the skin. Bleeding ceases as soon as
the pressure is relaxed.

In the case of the external saphenous vein, the vein is raised by
compressing the middle region of the limb and the vessel is opened with
a lancet, a little above and towards the outside of the hock.

[Illustration: $1]

The subcutaneous vein of the forearm can be raised by compressing the
fore limb below the elbow. The vein is visible throughout the length of
the inner surface of the radius, and can easily be opened with a lancet.

It is also possible to withdraw small quantities of blood by opening the
marginal veins of the ear.


                          BLEEDING IN THE PIG.

Breeders sometimes bleed by slitting one of the animal’s ears or cutting
the tail. It is preferable to bleed with a lancet from the marginal
veins of the ear, the external saphenous vein a little above the hock,
or the subcutaneous vein of the forearm.


                   SETONS, ROWELS, PLUGS, OR ISSUES.

Although the application of setons is still practised in horses, that of
“issues” has largely been given up in bovine animals, although some
practitioners still regard issues as of considerable value and as
producing effects similar to, or better than, those of sinapisms.

They are usually inserted in the region of the dewlap; the materials
employed comprise black and white hellebore, veratrine and stems of
clematis.

Two methods are practised.

In the first, a transverse fold is raised in the skin of the dewlap,
which is divided with a stroke of the bistoury, leaving a little
aperture in the skin. By introducing the rounded ends of a pair of
curved scissors the subcutaneous connective tissue is broken down,
leaving a little space beneath the skin, into which the plug is
introduced. Swelling takes places very rapidly—in twenty-four to
forty-eight hours it is very considerable—and if the substance employed
is violent in its action, like hellebore, it must be withdrawn, as
otherwise considerable sloughing takes place. To facilitate this object
a thread or piece of string is usually attached to the plug before it is
inserted.

In the second method, the irritant material is attached to, or smeared
on, a strip of broad linen tape which is passed in precisely the same
manner as in the horse (see Dollar’s “Operative Technique,” pp.
107–111).




                              CHAPTER III.
                        APPARATUS OF LOCOMOTION.


[Illustration: $1]

The customary operations on the apparatus of locomotion are almost
entirely confined to the feet. They consist in operations for sand
crack, picked-up nail, stabs by nails and bruising of the sole,
elsewhere mentioned. As they call for no special precautions they need
not be further mentioned here.


                     SURGICAL DRESSING FOR A CLAW.

The surgical dressing necessitated by the operation for sand crack,
picked-up nail, or injury to the heels is often very difficult to fix in
the ox, and necessitates a support round the pastern. It can, however,
be secured in the following way:

The seat of operation is covered with small antiseptic pads, which are
also applied round the pastern and in the interdigital space. A bandage
is then passed twice round the pastern and over the posterior two-thirds
of the claw, as in fixing the dressing used after removal of the lateral
cartilage in the horse. The bandage is then passed repeatedly round the
pastern in an upward direction and tied above the interdigital space.


          AMPUTATION OF THE CLAW OR OF THE TWO LAST PHALANGES.

It sometimes happens that certain grave diseases in the foot or pastern
(stabs or picked-up nails, panaritium of the interdigital space,
necrosis of the ends of the flexor tendons, etc.) are accompanied by
necrosis of the bones, suppurative synovitis, and even suppurative
arthritis of the second and first inter-phalangeal joints.

If carefully treated these forms of arthritis may disappear, leaving the
joints anchylosed, but unfortunately the application of the necessary
antiseptic injections (free injection with warm boiled water, injection
of 10 per cent. iodised glycerine, 3 per cent. carbolic glycerine or ·1
per cent. sublimate) is difficult and costly.

[Illustration: $1]

[Illustration: $1]

It is better, in such cases, to remove the claw or the two last
phalanges. With antiseptic precautions the stump heals, and recovery
takes place without the interminable suppuration and pain which
otherwise cause such grave loss of condition.

(1.) =Disarticulation of the Claw and Third Phalanx.=—The patient is
cast and suitably fixed. The horn-secreting coronary band of the claw
must be preserved.

=First stage.= The horny wall immediately beneath the coronary band is
thoroughly thinned and the tissues are divided as far as the bone.

=Second stage.= Disarticulation: The tendon of the extensor pedis is
divided and the joint opened. The claw is pressed backwards, and first
the external and internal ligaments, then the flexor tendons of the
phalanges, are divided.

[Illustration: $1]

[Illustration: $1]

This operation is of no great use, because, on account of the position
of the joint and the arrangement of the articular surfaces, the end of
the second phalanx extends beyond the line of section. To avoid
complications, therefore, it is better to remove the lower extremity of
the second phalanx, which, moreover, is always injured to a greater or
less extent in cases of pedal arthritis. To effect this it is only
necessary to draw back the flap of skin a little and rapidly divide the
second phalange at its upper third with a fine saw. The points of
section of the tendons and ligaments must be carefully examined, and if
they exhibit necrosis should be further shortened.

The stump is enveloped in a surgical dressing fixed to the pastern.

=Amputation of the two First Phalanges.=—When necrosis is very serious
and has extended a long way upwards, it is often better immediately to
resort to amputation of the two last phalanges.

The region is first shaved and thoroughly cleansed. The coronary band of
the claw is also preserved in this case.

=First stage.= The horn below the coronary band is thoroughly thinned
and the tissues are divided as far as the bone.

=Second stage.= The skin covering the front of the limb is vertically
incised from the lower third of the first phalanx (Fig. 298) to the
coronary band; the skin is separated and external and internal flaps are
formed.

=Third stage.= The extensor pedis tendon is divided, the first
inter-phalangeal joint opened, the internal and external lateral
ligaments are divided, the claw is pressed backwards, and the flexor
tendons are also divided.

To facilitate disarticulation, and particularly to facilitate section of
the lateral ligaments, the claw is rotated successively outwards and
inwards.

According to circumstances, the lower extremity of the first phalange is
either scraped or divided and the stumps of the tendons are carefully
trimmed to a regular shape.

A surgical antiseptic dressing is applied over the whole of the seat of
operation.

Several other methods of performing this operation will be found in
Möller and Dollar’s “Regional Surgery,” pp. 831–835.




                              CHAPTER IV.
                          DIGESTIVE APPARATUS.


                             RINGING PIGS.

[Illustration: $1]

This operation is customary in countries where pigs are allowed to roam
more or less at liberty, and it is necessary to adopt some precaution to
prevent them from uprooting the soil and thus causing damage, but the
practice tends nowadays to disappear. It simply consists in passing
through the nose some object which on being rubbed against anything
causes pain and thus checks the animal’s natural proclivity.

Numerous methods have been suggested. One of the simplest is as follows:
The animal having been cast, suitably secured and muzzled, two thick
iron wires sharpened at the ends are passed through the snout, and the
two ends are then twisted together in the form of two rings. These can,
if necessary, be united.

Another method, perhaps even more efficacious, consists in bending a
thick wire into the shape of the letter =U=, and preparing a small metal
plate with two holes corresponding in position to the distance between
the two nostrils. The ends of the wire, being sharpened, are passed
through the nostrils and securely united to the metal plate by being
bent into a spiral or simply at right angles.


                               ŒSOPHAGUS.

The operations practised on the œsophagus comprise passage of the
œsophageal sound or probang, taxis, crushing of foreign bodies within
the œsophagus, and œsophagotomy.


                          PASSING THE PROBANG.

Passage of the probang is called for in cases of marked tympanites,
suspected dilatation or contraction of the œsophagus, and accidental
obstruction. Special or improvised instruments may be used, according to
circumstances.

The animal is secured in a standing position with the head extended on
the neck and in a straight line with the body. A gag is placed in the
mouth and the tongue is grasped and withdrawn by an assistant, whilst
the operator, having carefully oiled the probang, passes it through the
gag towards the back of the pharynx. Violence should be avoided, the
probang being gently slid along the centre of the vault of the palate.
When the animal makes swallowing movements, the apparatus is slowly
pushed onwards.

This manipulation, though simple, requires some dexterity, because at
the moment when the instrument enters the pharynx the animal often
thrusts it to one side or the other with the base of its tongue,
bringing it between the molar teeth, and so crushing, or at least
injuring it.

The passage of hollow probangs gives comparatively little relief in
cases of tympanites, because the probang is almost always obstructed by
semi-digested material from the rumen, or plunges into the semi-solid
masses of food contained therein.

When the œsophagus is dilated at a point within the thorax, the progress
of the probang is checked by the accumulated food material, and it
becomes possible to determine approximately the place where the
dilatation occurs. In the same way, should a slender probang be arrested
at a given point in the œsophagus, this indicates that there is
contraction of the tube at that point.

In cases of obstruction the cupped probang is always arrested by the
foreign body. Efforts to thrust the latter onwards should always be made
with great caution, otherwise the œsophagus may be greatly distended or
its walls even ruptured.


                       CRUSHING THE FOREIGN BODY.

No attempt should be made to crush a foreign body within the cervical
portion of the œsophagus unless it is quite certain that that body is of
comparatively soft character. Crushing may be performed by lateral
pressure with the fingers within the region between the two jugular
furrows, or mechanical means may be adopted.

In the latter case a small piece of board is applied to one side of the
neck behind the foreign body, whilst gentle blows are given from the
opposite side with a little wooden mallet. Whatever precautions may be
taken, however, this method cannot be recommended.

The same remark applies to the use of forceps, the jaws of which are so
fashioned as to escape pressing on the trachea whilst they grasp
directly the foreign body through the walls of the œsophagus.


                             ŒSOPHAGOTOMY.

Œsophagotomy, or incision of the œsophagus, is an operation which,
though sometimes necessary, should only be regarded as a last resort
after all other methods have failed. Unfortunately it can be performed
only in the region of the neck, and even then the most favourable point
(viz., the lower third of the jugular furrow) cannot always be selected,
the operation having to be performed directly over the foreign body.

The animal may be either standing or lying down. The seat of operation
should be thoroughly cleansed and disinfected.

=First stage.= Incision through the skin and subcutaneous connective
tissue above the level of the jugular vein and opposite the foreign
body.

=Second stage.= Isolation of the œsophagus by dissection and tearing
through of the connective and fibro-aponeurotic tissue at the base of
the jugular furrow.

=Third stage.= Incision through the œsophagus for a distance just
sufficient to enable the foreign body to be extracted.

=Fourth stage.= Suturing of the mucous membrane, suturing of the
muscular walls of the œsophagus, suturing of the skin, precautions being
taken to allow of drainage at the lower part of the operative wound.


               SUB-MUCOUS DISSECTION OF THE FOREIGN BODY.

As œsophagotomy, despite every precaution, often leads to fistula
formation, Nocard has recommended submucous dissection of the
obstructive body, such body being usually semi-solid. This method has
considerable advantages.

The first and second stages of the operation are exactly the same as
those above mentioned.

The third stage consists in puncturing the walls of the œsophagus with a
straight tenotome immediately behind the foreign body, as in tenotomy. A
curved, button-pointed tenotome having next been introduced and passed
with the blade flat between the foreign body and the mucous membrane of
the œsophagus, it is turned on its axis, and attempts are made to divide
the obstruction. A few moments are often sufficient to effect this,
after which the substance may be further broken up by the fingers.

These various methods may lead to delayed complications, such as
dilatation or contraction of the mucous membrane of the œsophagus,
muscular atrophy of the œsophageal walls, œsophageal fistula, and,
sometimes, abscess formation.


                                 RUMEN.

Two operations are currently performed on the rumen, puncture and
gastrotomy.

[Illustration: $1]


                         PUNCTURE OF THE RUMEN.

Puncture of the rumen is essentially an urgent operation for the relief
of acute and rapidly progressive tympanites. It is performed in the left
flank, at an equal distance between the last rib and the angle of the
haunch, and an inch or two beyond the transverse processes of the lumbar
region.

=First stage.= Incision of the skin to the extent of about one inch (not
absolutely necessary).

=Second stage.= Puncture with a sharp trocar directed forwards,
downwards, and inwards. In making this puncture the point of the trocar
is passed through the incision, and a sharp push is given. The sensation
of resistance overcome indicates that the trocar has penetrated the
cavity of the rumen. Gas then escapes. When the operation is completed,
and the canula is being withdrawn, care should be taken to press down
the skin on either side with the fingers of the left hand, to prevent
accidental lifting and laceration of the connective tissue. Even so
slight an accident as this might cause serious complications at a later
stage.

In the absence of a trocar, and in cases of extreme urgency, the rumen
may be directly punctured with a straight bistoury, and after the
punctured wound is slightly enlarged, but before the blade of the
bistoury is withdrawn, an improvised canula, consisting of a hollow
elder twig, may be introduced. Were the blade of the bistoury withdrawn
before the introduction of the canula, the rumen would be displaced, and
the points punctured would no longer correspond.

=Complications=, such as respiratory or circulatory syncope, attacks of
vertigo, etc., have been noted, but these in reality are very rare.

=Subcutaneous Emphysema.=—When the canula is carelessly removed, and the
subcutaneous connective tissue is torn, local emphysema may occur if the
pressure of gas in the rumen is very great. This gas enters the
puncture, proceeds along the connective tissue, particularly the
subcutaneous connective tissue, and causes crepitant subcutaneous
emphysema, very easy to recognise. This emphysema may remain localised
in the neighbourhood of the puncture and gradually become absorbed. It
may, however, extend to the whole of the flank or even beyond, and in
exceptional cases bring about generalised subcutaneous emphysema. Such
very extensive emphysema as this rarely becomes reabsorbed without
complications.

=The suppuration= which follows puncture of the rumen may assume one of
two forms:—

(_a_) That of a little local abscess at the point of puncture, when
foreign matter or the microbes of suppuration have been left in the path
made by the withdrawal of the canula. Such abscesses are of little
importance. They rapidly heal if opened and treated with antiseptic
injections.

(_b_) That of diffuse subcutaneous or interstitial suppuration following
accidental emphysema.

The pressure of gas forces fragments of food material between the layers
of tissue, and suppuration is set up, the pus escaping by a fistula at
the point of puncture. Such suppuration is decidedly dangerous, because
it may result in necrosis of the aponeurotic layers of the small oblique
muscle, in which case recovery is tedious and uncertain.

=Treatment= consists in laying open the orifice and fistula, and making
a counter-opening at the lowest point of the swelling. Free drainage and
abundant irrigation with boiled water at the body temperature, followed
by antiseptic injections, complete the treatment.

=Peritonitis= is not altogether exceptional as a sequel to puncture of
the rumen, if ordinary precautions are neglected or if infective
material or fragments of food pass into the peritoneal cavity.

At first the condition is usually local, but it may extend and assume
the form of general peritonitis two or three weeks later. The symptoms
are those of acute peritonitis.

Speaking generally, however, puncture of the rumen in cattle and sheep
is seldom followed by any complication.


                              GASTROTOMY.

Gastrotomy is performed for the relief of impaction of the rumen and to
remove foreign bodies, such as linen, nails, bits of leather, etc.,
which have been swallowed.

[Illustration: $1]

A vertical or slightly oblique incision is made in the left flank,
extending from the fourth transverse process of the lumbar vertebræ
towards the last rib. The operation comprises the following stages:—

[Illustration: $1]

=First stage.= Incision through the skin for a distance of from 6 to 10
inches, according to the size of the animal.

=Second stage.= Incision through the muscles and peritoneum and torsion
of any small muscular arterioles, which may be divided.

=Third stage.= Fixation and immobilisation of the rumen with from four
to six sutures (Fig. 303).

=Fourth stage.= Vertical incision into the rumen; manual examination of
the cavity and its contents.

Formerly the operation was confined to these stages. In such cases
localised adhesive peritonitis follows, causing the rumen to adhere to
the internal surface of the abdominal wall, and the fistula continues in
existence for months before complete cicatrisation. It is better,
therefore, to insert sutures in the rumen, in order to secure more rapid
and complete closure.

=Fifth stage.= Suture of the rumen with carbolised silk. The lips of the
wound should be brought together face to face, or they can be slightly
inverted, but the sutures should only pass through the peritoneum and
muscular coats, avoiding the mucous coat. If the silk threads pass
through the mucous membrane and come in contact with the gas in the
upper zone of the rumen they are rapidly macerated, and the sutures tear
out before the wounds can heal. The rumen should always be kept fixed to
the abdominal wall towards the upper and lower extremities of the
operative wound, in order to avoid displacement and occurrence of
peritonitis. For a similar reason the passing of the silk sutures should
be preceded by careful disinfection of the operative wound, and free
washing of the parts with boiled water.

[Illustration: $1]

The operation is concluded by bringing the skin together with a few silk
sutures and inserting a strip of iodoform gauze into the lower portion
of the wound, to serve as a drain.


                              LAPAROTOMY.

Laparotomy is comparatively seldom performed on animals of the bovine
species, though it may become necessary in dealing with cases of hernia,
uterine torsion (where direct taxis is called for), Cæsarean section,
invagination or strangulation of the intestine, and under a few other
exceptional circumstances.

If simple exploration is aimed at, the operation is most conveniently
performed from the right flank with the animal in a standing position,
but should a prolonged operation be contemplated the animal should be
cast. The incision varies in length, according to circumstances, from 8
to 16 inches, and, like that in gastrotomy, should correspond in
direction with the fibres of the small oblique abdominal muscle; the
seat of operation should previously be washed, shaved, and disinfected.

The operation comprises the following stages:—

=First stage.= Incision of the skin.

=Second stage.= Incision through the muscles and peritoneum.

=Third stage.= Exploration, inspection, palpation, extraction or
ablation, etc.

=Fourth stage.= Suture of the peritoneal opening, the lips being brought
together face to face.

=Fifth stage.= Suture of the muscles and the skin. It is sometimes
advisable to insert a drain of iodoform gauze under the skin.

In small animals, such as the sheep, goat, and pig, laparotomy is more
easily practicable, and can be performed either in the right flank or
towards the white line. The stages of operation are exactly the same,
but after operating near the white line it is extremely important to use
numerous and strong sutures, and afterwards to apply a suspensory
bandage around the abdomen, securing it above the loins.


                                HERNIÆ.

The situation and nature of the hernia determine whether or not a
radical cure should be attempted.

[Illustration: $1]

When a decision has been arrived at the seat of operation must first of
all be thoroughly cleansed and disinfected. The animal is cast in a
convenient position, and a general anæsthetic is given or a subcutaneous
injection of 1 per cent. cocaine solution administered.

The operation comprises:—

=First stage.= Incision through the skin covering the hernial sac,
opposite the orifice of the hernia.

=Second stage.= Isolation of the hernial sac.

=Third stage.= Reduction of the hernia and breaking down of any
adhesions that may exist.

=Fourth stage.= Resection of the sac and obliteration of the peritoneal
orifice by suture and ligature.

=Fifth stage.= Suturing of the muscles and skin, and application of a
surgical dressing.

In practice, the deep sutures should be of bichromatised catgut or silk,
and the skin sutures of catgut ligature or aseptic silk.


                     INGUINAL HERNIA IN YOUNG PIGS.

One of the most frequent forms of hernia which the practitioner is
called on to treat is inguinal hernia in young pigs. Although this
allows little tendency towards strangulation it is always desirable to
operate, as otherwise the patients develop badly. There is no difficulty
in this, though the animals must be cast and placed on their backs, the
hind quarters being raised (Fig. 305).

=First stage.= A longer or shorter cutaneous incision over the neck of
the hernia and along its greater curvature.

=Second stage.= Isolation of the hernial sac, consisting of the dilated
internal sheath.

=Third stage.= Direct reduction of the hernia without opening the sac,
provided no adhesions occur, or, in the event of adhesions, after
incision of the sac.

=Fourth stage.= Torsion of the hernial sac and of the testicular cord up
to the inguinal ring. Application of a catgut or silk ligature around
the sac and cord at the level of the inguinal ring.

=Fifth stage.= Fixation of the ligature to the lips of the ring. Suture
of the skin wound, and drainage of the wound with a strip of iodoform
gauze.


                           IMPERFORATE ANUS.

This anomaly of development, which is not uncommon, presents two
different degrees of development.

In the first degree the rectum is well formed, and extends as far as the
skin below the base of the tail.

In the second the rectum is incomplete or non-existent, the floating
colon terminating in a blind end at the entrance to the pelvis.

In calves, lambs, and young pigs very often imperforate anus is not
diagnosed until the second or third day after birth. Defæcation cannot
occur, and death is inevitable unless an artificial anus be established.

FIRST DEGREE.—The patient loses appetite, the abdomen remains distended,
and on examination of the anal region a doughy swelling is felt, which
projects backwards when the animal strains. The operation is quite
elementary, and always proves successful.

=First stage.= The skin beneath the tail is incised vertically; the
rectal cul-de-sac projects towards the incision.

=Second stage.= The rectal cul-de-sac is punctured, the contents are
removed, and the rectum and skin united by a few sutures. An anus is
thus established, though there is no sphincter.

SECOND DEGREE.—The general symptoms are similar, though very often the
little patient shows symptoms of atrophy or arrest in development. The
operation is somewhat complicated.

=First stage.= Vertical incision through the skin at the base of the
tail.

[Illustration: $1]

=Second stage.= Digital exploration of the cavity of the pelvis after
breaking down of the layers of connective tissue, and search for the
blind end of the floating colon. When discovered, the colon is grasped
between the jaws of a clamp or large forceps with smooth jaws, and
gently drawn towards the opening.

=Third stage.= Puncture of the blind end of the colon, and suture of the
latter to the cutaneous wound, as in the former case.

A third condition may exist, where the extremity of the colon remains
within the abdomen. Operation by way of the pelvis then proves
unsuccessful. If considered advisable, an opening may be made through
the right flank, so that the floating colon may be brought to the
surface and an artificial anus produced in this region.

An incision 1 or 2 inches in length is made below the haunch, to allow
of the introduction of the index finger, with which the loop is sought.
The colon is withdrawn, and the operation thenceforth is as above
described.


                 PROLAPSUS AND INVERSION OF THE RECTUM.

This condition occurs in young pigs in various degrees. The necessity
for reduction depends on the extent to which tearing or gangrene of the
mucous membrane has progressed. The inverted portion is carefully
washed, freely dressed with some non-irritant fatty substance such as
vaseline, and progressively pushed back with the thumbs and index
fingers of both hands applied flat on either side of the anus. To
facilitate reduction it is best to check the animal’s expulsive efforts
by placing a gag in the mouth.

In more aggravated cases, when prolapsus of the rectum has returned
several times and the mucous membrane is gangrenous in places so that
such a complication as peritonitis of the pelvic cavity is to be feared,
it is better to amputate the prolapsed portion.

The animal is secured either standing or lying down, and a large enema
is administered to remove the contents of the rectum. The herniated
portion of bowel is carefully examined, for it sometimes happens that
loops of intestine have become lodged in the dilated peritoneal sac,
produced by displacement of the rectum. In such cases reduction should
be effected before anything more is done, and for this purpose the
patient’s hind quarters should be lifted or even suspended.

The operation for removal comprises two stages:

(1.) Fixation of the two layers of bowel by the passage of either two or
four sutures about ½ an inch behind the anus.

(2.) Circular amputation of the sutured tissues; insertion of
interrupted silk sutures through the lips of the wound; reduction. The
patient is restricted to milk diet for a week. Laxative gruels, etc.,
may then be given.

The complication to be feared is peritonitis of the pelvic cavity owing
to the sutures tearing out and allowing infective material to pass from
the bowel into the cavity.

Slight cases of prolapsus might possibly be treated by the injection in
lines of melted paraffin wax beneath the mucous membrane of the last
part of the bowel. The injection is made by means of a large syringe
provided with a long needle, the needle being gradually withdrawn as the
melted wax is expressed. Four “pillars” of wax are usually injected at
equidistant points. As they solidify they support the bowel and prevent
the recurrence of the prolapse. The operation, however, is delicate, and
scarcely to be recommended in pigs. Moreover, in man, in whom it has
chiefly been practised, the deferred results have not always proved
satisfactory.




                               CHAPTER V.
                         RESPIRATORY APPARATUS.


                     TREPHINING THE FACIAL SINUSES.

This operation is necessary when pus, tumours, or parasites exist within
the sinuses, and in some cases where tumours form within the nasal
cavities, etc.


                       TREPHINING THE HORN CORE.

This cavity is opened in front, at the base of the horn, about ¾ of an
inch above the keratogenous band.


                             FRONTAL SINUS.

The frontal sinus may be trephined at one of two points, that is, either
towards its highest or lowest extremity.

In the former case the point selected is in the direction of the axis of
the horn core, about ¾ of an inch nearer the middle line than the base
of the horn itself.

The animal should be cast.

=First stage.= A =V=-shaped incision ¾ of an inch long on each side is
made through the skin and subjacent tissues, exposing the bone.

=Second stage.= The skin and periosteum are dissected away and reflected
upwards.

=Third stage.= Trepanation.

The lower portion of the cavity is trephined within the angle formed by
a transverse line uniting the upper margin of the orbits and the inner
margin of the super-orbital foramen.

The stages are precisely the same as those above described.


                            MAXILLARY SINUS.

In adult animals the maxillary sinus is opened immediately above the
maxillary tuberosity. In the young the point selected is ¾ of an inch
higher.


                              TRACHEOTOMY.

In bovine animals tracheotomy is only performed in urgent cases, in
order to ward off asphyxia or to facilitate some other operation on the
upper air passages. It is performed exactly as in the horse, the animal
either standing or lying down. In the former case, the animal may be
placed in the trevis, but two strong assistants holding the animal’s
head and nose by means of “bulldogs” are often sufficient.

To prevent the animal from striking out with the front legs, a rope is
passed above and around the knees in the form of the figure =8=; the
animal is backed into a corner, and operation is then quite safe.

Large animals must be cast or placed in the trevis.

The seat of operation should be washed, shaved, and disinfected.

The operation may be divided into four stages.

=First stage.= Vertical median incision about 2 inches long through the
skin at the height of the upper third of the trachea.

=Second stage.= Separation with a blunt director of the muscles covering
the trachea. Incision through the pretracheal connective tissue.

=Third stage.= Circular or elliptical opening through the trachea of a
size corresponding to that of the tracheotomy tube.

=Fourth stage.= Insertion of the tracheotomy tube.




                              CHAPTER VI.
                         GENITO-URINARY ORGANS.


In the domestic ruminants the penis exhibits a peculiar =S=-shaped
curve, situated in the subpubic region (Fig. 226), so that when
operation on the urethra, or even on the extremity of the penis, becomes
necessary the organ must first of all be withdrawn.

The manipulation is as follows:—

The animal having been fixed by the head and front legs in a standing
position, and if possible thrust against a wall, the operator stands on
its left side. With his right hand he seizes the penis and the skin
immediately in front of the scrotum and pushes them forward in the
direction of the opening of the sheath.

The extremity is nipped between the first fingers of the left hand, and
to prevent the glans slipping or escaping when the right hand is removed
(for the purpose of taking a fresh hold of the body of the penis further
back) the operator may reverse the free extremity of the penis so that
it forms a loop, and thus secure a firmer hold. With the right hand the
skin is thrust backward, a new portion of the sheath fixed, and the
organ again pushed forward. In this way the penis is gradually extended.
When the animal is cast, this manipulation is much easier.


                         URETHROTOMY IN THE OX.

Urethrotomy consists in incising the urethra, usually for the purpose of
extracting a foreign body or calculus which impedes micturition. In the
ox, calculi may become fixed either in the intra-pelvic portion of the
urethra, though this is very rare; in the ischial curvature, or more
commonly at some point in the =S=-shaped curve of the penis; or
sometimes even within the sheath itself.

Urethrotomy is performed in the ischial or scrotal region, according to
the point where the obstruction exists.


                          ISCHIAL URETHROTOMY.

Urethrotomy is performed in the ischial region either to displace or
indirectly to abstract a foreign body fixed in the membranous portion of
the urethra, or directly to remove one from the spongy portion opposite
the ischial curve.

Calculi fixed in the intra-pelvic region are detected by rectal
exploration.

The exact position of the foreign body is determined by inspection and
palpation, whilst distension of the urethra by urine may be noted even
before more striking symptoms appear.

The urethra can be incised by one of three methods.

The animal should be secured, if possible, in the standing position.

The =first method=, which dates back to very early times, consists in
puncturing the urethra at one stroke with the fleam or lancet, and
opening it more freely, after introducing a grooved director. This
method is very useful where rupture of the bladder is imminent.

The extraction of a calculus fixed in the ischial region, or the
manipulation of an obstruction at any other point, can afterwards be
undertaken.

=Second method.= A second method consists in incising the subcutaneous
tissues, layer by layer, until the urethra is reached at the ischial
arch.

The operation is terminated by puncturing the urethra and enlarging the
incision in an upward direction after passing a grooved director. This
method minimises hæmorrhage and urinary infiltration. By previously
injecting cocaine, the operation may be made practically painless.

=Third method.= Puncture of the urethra by a single stroke with a
straight bistoury at the ischial arch.

The opening is enlarged in an upward direction with the same instrument.


                          SCROTAL URETHROTOMY.

Scrotal urethrotomy is necessary when the calculus is situated in one of
the =S=-shaped curves of the penis or nearer the glans.

The operation is facilitated by casting the animal and withdrawing the
penis from the sheath, but as there is considerable danger of rupturing
the bladder when casting an animal with marked distension of that organ,
the more serious operation should be preceded by puncturing the urethra
with a fleam at the ischial arch.

By repeated moderate traction on the extremity of the glans, the
=S=-shaped curve can be obliterated and the anterior portion of the
penis withdrawn beyond the sheath.

One of two conditions may exist.

=First case.= Where the calculus is in the anterior, extra-prepubic
portion, it is removed through an incision made directly over it. After
extraction and disinfection, one or two sutures are inserted.

=Second case.= Should the calculus be situated in that portion of the
penis which remains within the sheath after the fullest withdrawal of
the organ, it is necessary to proceed as follows:—

(1.) The skin covering the sheath, the subcutaneous tissue, and the
mucous membrane are first incised for a length of from 1¼ to 1¾ inches.

(2.) The penis is drawn through this opening; an incision is made
directly over the calculus, dividing the fibrous layer, erectile tissue
and mucous membrane of the urethra; the parts are disinfected and the
wounds closed with sutures.

With ordinary antiseptic precautions little danger is to be feared.

Even should infiltration of urine occur, the operator need not be unduly
anxious, for, provided the parts are punctured or scarified early,
recovery usually follows.


          PASSAGE OF THE CATHETER AND URETHROTOMY IN THE RAM.

Obstruction of the urethra in rams is more commonly caused by deposits
of gravel than by single large calculi. It is generally found in
highly-fed animals, in which gravel accumulates and becomes massed
together at some point in the canal, often near the free extremity,
where it forms a plug, causing complete retention of urine. In other
cases this retention is due to a mass of sediment formed by vesical
mucus and fine gravel which collects about the neck of the bladder.

Three operations have been advised for the removal of this condition:—

(1.) =Section of the Appendix of the Penis.=—When the disease is just
appearing the sedimentary material may be collected at the anterior
extremity of the penis behind the appendix. The shepherds in such cases
remove the extremity of the penis. The resistance disappears, the plug
formed of gravel yields to the pressure of urine, and micturition occurs
as usual. Excision of the appendix, however, incapacitates the ram for
service.

(2.) =Passage of the Catheter.=—Passage of the catheter has been
recommended for the removal of deposits of gravel in the urethra, but it
seems a very questionable method.

Should it be determined on, the animal must be placed on its back. The
penis is then withdrawn and the double =S=-shaped curve is obliterated.
An incision is made over the canal behind the appendix and a soft
gutta-percha sound is passed. The sabulous accumulation is thus
dispersed.

(3.) =Urethrotomy.=—Scrotal urethrotomy may be performed as in the ox.

[Illustration: $1]

Ischial urethrotomy is impracticable in very fat animals, but when the
obstruction is about the neck of the bladder, and the animal’s condition
admits of it, this operation may be performed.

The patient is fixed on its back, and a metallic or gutta-percha sound
is passed into the urethra. The tissues are incised layer by layer in
the direction of the sound. Once the urethra has been opened the soft
magma may be washed out of the bladder by a free injection of boiled
water or similar aseptic liquid.

[Illustration: $1]


                  PASSAGE OF THE CATHETER IN THE COW.

It sometimes becomes necessary to examine the bladder of the cow.

There is an obstacle, however, to the introduction of the sound into the
urethral canal. The meatus urinarius is covered by a little valve which
springs from the lower wall and forms behind the real opening of the
urethra a cul-de-sac, into which the point of the catheter is apt to
pass. The instrument usually employed is of gutta-percha, glass, or,
better still, of metal, as more easily sterilised (Fig. 308). It is held
like a pen, and is directed along the floor of the vagina as far as the
opening of the meatus, being guided by the index finger of the left
hand, which has previously been introduced. The point being very
slightly depressed, it enters the cul-de-sac. It is then only necessary
to reverse the movement, that is to say, raise the point, whilst gently
pressing forward; a slight resistance is felt and the sound enters the
bladder. If necessary the little valve may be held down by gently
pressing on it with the point of the left index finger.

It is sometimes an advantage to expose the seat of operation. In such
cases the lips of the vulva and the walls of the vagina may be separated
by retractors or by the use of a speculum.


                              CASTRATION.

Castration is performed for the purpose of removing the reproductive
power, either by obliterating the testicle or ovary or by suppressing
their functions.

In ruminants, the testicles are elongated and placed in a vertical
position, the upper portion of the scrotum presenting a constriction and
the whole scrotal mass resembling in shape a cone with its base
downwards.


                    CASTRATION OF THE BULL AND RAM.

These two animals, when destined for slaughter, are usually castrated
either at birth or at latest two or three months afterwards. In
Normandy, in Franche-Comté, and in England breeders castrate young bulls
by torsion of the cord.

Two incisions about 1¼ to 1¾ inches in length are made on the lower
extremity of the scrotum. The testicles are enucleated and the
testicular cords seized with two pressure clamps, with which torsion is
effected. In the South of France, in Auvergne, and in the Limousin,
bulls intended for working are not castrated until after the lapse of
some months, on account of the influence which the testicles have on the
development of the bones and muscles. Such animals are only operated on
at the age of from six months to a year, and as a rule the method
employed is that of bistournage.


                              BISTOURNAGE.

This method of castration has been practised from time immemorial. It
consists essentially of torsion of the testicular cord, and aims at
obliterating the vessels which it contains, and thus bringing about
atrophy of the organs served by them.

=The Bull.=—The animal is operated on in the standing position. The head
is fixed to a post or ring somewhat high up, in order to check movement
of the hind legs. The hind legs are also partially secured by means of
ropes or two pieces of webbing passed in a running noose about the hocks
and fixed above the knee. No preliminary disinfection is practised,
because no wound is made.

[Illustration: $1]

=Manual Technique.= The operation comprises four stages:

[Illustration: $1]

=First stage.= The operator, standing behind the animal’s hocks, grasps
the testicular cords with the hands, immediately above the testicles,
and by exercising strong pressure, thrusts the latter to the extreme
base of the scrotum. The movement is next reversed; seizing the base of
the scrotum with the right hand, he draws it smartly downwards, whilst
he places the left hand above the right, and thrusts the testicles
towards the abdomen. If the testicles do not rise sufficiently high, the
right hand is slipped between these and the left hand, and the testicles
are thus thrust upwards towards the lower inguinal rings, slightly
dilating the latter.

After this manipulation has been repeated two or three times, the
scrotum, etc., become more pliable and the testicles more easily
displaced. The second stage of the operation is thus facilitated.

=Second stage.= The second stage of operation may be effected by one of
two methods.

[Illustration: $1]

_Old method_: The oldest method consists in allowing one of the
testicles to rise towards the inguinal ring and to turn the other in a
vertical plane. If, for instance, it is desired to turn the right
testicle, the cord is grasped between the thumb and index finger of the
left hand (Fig. 311), the lower part of the scrotum is seized with the
right hand, and the object then is to slide the point of the testicle
along the dorsal surface of the fingers (Fig. 311). Simultaneously the
operator presses on the base of the testicle with the thumb of the left
hand, thus causing a rotary movement in a vertical plane; the tail of
the epididymis becomes uppermost. A certain empty space separates the
testicle from the base of the scrotum.

=Third stage.= Torsion of the cord. The testicle having been rotated,
the cord must be twisted so that the vessels may be obliterated. The
left hand continues grasping the cord, which is then brought in front of
the testicle, whilst with the right hand the testicle is pushed
backwards and is made to describe a semi-circle. The cord was previously
on the left side; it is now on the right, and simultaneously the
testicle passes from right to left.

[Illustration: $1]

In completing the turn the hands must not be changed, and, above all,
must not let go their hold; and the cord is pushed forwards and towards
the right with the right hand, whilst the testicle is pushed backwards
and to the left with the left hand. The cord and the testicle resume
their original position; one complete turn has been effected. These
manipulations are repeated several times, and the cord soon assumes the
appearance of a large, hard, tense string. To ensure obliteration seven
or eight turns should be made in the case of the bull and four or five
in that of the ram.

Torsion of the right testicle being complete, the gland is thrust
towards the upper part of the scrotum and the left testicle is submitted
to the same manipulation, the position of the hands, however, being
reversed.

=Fourth stage.= Fixation of the testicles in the inguinal region. Both
testicles having been thrust upwards as far as possible into the
inguinal region, the scrotum is ligatured below them. Tape or thick cord
should be used, to guard against gangrene of the lower portions of the
scrotum. A considerable œdematous swelling soon occurs, and when at the
end of twenty-four or forty-eight hours infiltration is well developed,
the ligature should be removed.

Dubourdieu has described a different method, in which the testicle is
rotated in a horizontal plane. The position of the hands is then
different. The left testicle, for instance, being at the base of the
scrotum, the cord is grasped with the right hand opposite the base of
the testicle, and the tail of the epididymis and the testicle are held
with the whole hand whilst being rotated. If care is taken to fix the
cord with the right hand, rotation is more rapid and easier than in the
preceding method.

[Illustration: $1]

[Illustration: $1]

=Difficulties in Operation.=—Bistournage is highly commended in France
on account of its avoiding all the complications resulting from
sanguinary operations. Nevertheless it presents great difficulties,
particularly in bulls of from two to three years of age, in which the
testicles are hard to manipulate on account of their size, the thickness
of the connective tissue, and sometimes because of abnormal adhesions.
In such cases the preliminary manipulation alone sometimes extends over
half an hour.

Bistournage is of doubtful efficacy when the testicles are small and
round, because after the ligature has been applied the testicular cord
tends to untwist, and the shape of the testicles readily lends itself to
such movements. If untwisting occurs, the operation fails.

=Consequences of the Operation.=—The operation is often followed by more
or less violent attacks of colic; the animal may suffer for five or six
hours, after which it recovers.

If torsion has been clumsily performed, or if the ligature becomes
displaced, the testicle may descend and the cords untwist; the latter
then appear to have lost the firm, tense consistence which they
presented after operation. To prevent slipping of the ligature and
untwisting of the cord, Guittard suggests the use of an iron needle,
with which the scrotum is pierced through the median line, just beneath
the testicles when at their highest position; above this is placed the
ligature, which then cannot possibly slip.

The Basque operators, in order to avoid untwisting, exercise vigorous
traction from above downwards after rotating the testicle. In this way
ruptures occur which diminish the elasticity of the cord and the
epididymis, and tend to check the untwisting of the former.

When the operation has succeeded the testicles gradually atrophy. They
do not disappear completely, and may sometimes be found several years
later of the size of a hazel-nut or a chestnut and of fibrous
consistence. It need scarcely be said that in the event of bistournage
failing, cutting operations can always be resorted to.


                               MARTELAGE.

The process of martelage consists in mutilating with a mallet the
testicular cord whilst still covered by all its envelopes. This
mutilation injures the walls of the arteries, causing the formation of a
clot, which cuts off the supply of blood to the testicle and causes the
gland to atrophy.

The practice is very ancient.

The animal is fixed by the horns as if for bistournage, and the limbs
are secured by two strips of webbing or two ropes, as in the former
case, though some practitioners neglect the latter precaution.

Two cylindrical rods the size of broomsticks and a wooden mallet or
farrier’s hammer are the instruments employed.

The method, however, is barbarous, cruel, and of doubtful value. It
would never be countenanced in England.


                          CASTRATION BY CLAMS.

Castration of bulls by means of clams has been practised in many
different forms.

[Illustration: $1]

=Castration by the Exposed Method.=—The operation is the same as in the
horse, the scrotum being incised on either side, and the dartos,
connective tissue, tunica vaginalis scroti, and tunica vaginalis testis
being divided. Short clams are applied to the cord, and the lumen of the
arteries is completely obliterated in five to six days, when the clams
can be removed.

Instead of an incision being made for the removal of each testicle, the
scrotum and dartos may be divided in the middle line, after which
incisions may be made to the right and left respectively, exposing the
fibrous tissue and enabling the testicles to be enucleated. A clam may
then be applied to each cord, or the two cords may be included in one
pair of clams.

This method has the advantage of inflicting less injury on the scrotum,
a point which is of some importance in animals destined for slaughter.

=Castration by the Covered Method.=—This operation is identical with the
preceding, except that the incision of the scrotum does not involve the
cremaster and fibrous tunic, or the tunica vaginalis scroti.


                         CASTRATION BY TORSION.

The cord may be twisted throughout its entire length or torsion may be
limited to a part of the cord, hence the two methods hereafter
described.

(_a_) =Limited Torsion.=—The testicles are exposed as in castration by
the open method. The cord is then drawn forward and fixed by means of
forceps applied just outside the scrotum; ¾ to 1 inch below this point
the torsion forceps are applied. The cord is slowly twisted, and usually
ruptures about the centre of the fragment included between the two pairs
of forceps.

[Illustration: $1]

(_b_) =Direct or Unlimited Torsion.=—=First stage.= The testicle is
exposed, as in castration by the covered method.

=Second stage.= The cord and vaginal tunic are twisted by grasping the
testicle, which is protected with a piece of clean linen.


                  CASTRATION WITH THE ACTUAL CAUTERY.

The testicles are exposed, the cords are seized with clams and divided
separately or together with a sharp-bladed cautery at a white heat. The
eschar so produced is sufficiently dense to obliterate the vessels.


                  CASTRATION BY THE ELASTIC LIGATURE.

This method has been largely employed during the last ten or fifteen
years. It consists in applying to the upper part of the scrotum several
turns of a tensely stretched round or square rubber thread. The two ends
of the rubber thread are crossed and tied with string. About the seventh
or eighth day the testicles may be removed with a knife close to the
ligature, provided the process of delimitation is well advanced.

The chief objection to this method lies in the fact that the scrotum is
destroyed, which lowers the value of the animal from a commercial point
of view.


                         CASTRATION OF THE RAM.

Most of the preceding methods may be used in castrating rams, but
certain special methods are more generally employed. These we shall
shortly mention.

=Castration by Bistournage.=—The method is exactly similar to that in
the bull. The animals are placed in the position shown in the figure,
except that the hind limbs are extended and held in that position by the
operator’s knees or feet. The process is only applicable to animals of
four or five months old.

=Castration by Tearing.=—This method is only practised by shepherds, and
on animals a few days or at most a month old. The base of the scrotum is
snipped off with scissors, the testicles are enucleated, and each in
turn is seized and torn away with a sudden snatch. Even though a
considerable length of cord is removed with the testicle, bad results
seldom follow, provided the subject is not of greater age than that
mentioned.

[Illustration: $1]

=Castration by Ligature.=—This method consists in passing a stout
ligature in the form of a running knot over the neck of the scrotum and,
by means of two short pieces of wood, drawing it tight. The method,
however, is not to be recommended, as it not infrequently leads to
tetanus.


                  CASTRATION OF BOARS AND YOUNG PIGS.

For castration boars should be cast on the left side, and three legs at
least firmly secured together (Fig. 317). The best method is that of
limited torsion. Care should be taken to avoid dragging the cord
downwards during the operation, for the testicular artery ruptures
readily, and fatal abdominal hæmorrhage may follow.

As the subjects are apt to wallow in the litter after the operation a
strip of iodoform gauze should be applied and secured by one or two
sutures. This is removed on the third or fourth day.

On young pigs the operation is simpler. The animal is cast on the left
side and firmly held, the left hind limb being extended and the right
drawn towards the right shoulder.

The testicles are grasped each in turn with the left hand, whilst with
the right they are exposed by a single sweep of the bistoury. The
testicles are removed by torsion with artery forceps. Many laymen simply
use the hands, the cord being grasped between the left thumb and index
finger, whilst torsion is effected by the right index finger thrust
between the vas deferens and the body of the testicle.


                      CASTRATION OF CRYPTORCHIDS.

Cryptorchids are very rare amongst cattle and sheep, as the testicles
enter the scrotum during intra-uterine life. The internal inguinal ring
in the pig being of very small size, the condition is more common in
that animal.

The same process is employed in castrating cryptorchid bulls, rams, or
boars. The animal is thrown on one side and securely fixed. A vertical
incision is made in the region of the flank, varying in length from 4 to
5 inches in the bull, 2 to 2½ inches in the ram, and 4 to 5 inches in
the pig. The abdominal cavity is examined, the testicle found, and a
ligature applied to the cord, after which the testicle is removed.

Another method consists in employing the _écraseur_ for division of the
cord.

To avoid subsequent complications antiseptic precautions should be
taken.

=Complications after Castration.=—Whatever the method employed, swelling
of a more or less abundant character always develops during the few days
immediately succeeding the operation. It is, however, of little
importance.

Should antiseptic precautions be neglected, suppuration, septicæmia,
tetanus, and sometimes scirrhous cord may follow.


                         FEMALE GENITAL ORGANS.

=Examination with the Speculum.=—In the cow certain diseases of the
vagina, bladder, neck of the uterus, and even of the uterus itself, may
necessitate visual examination in addition to the manual examination
commonly employed. Under such circumstances a special speculum is
introduced in a closed condition, being afterwards opened and dilated to
the required extent.

Before inserting the speculum, however, the genital passages should be
cleaned, and the speculum itself smeared with vaseline. It penetrates
readily with moderate pressure.

Heifers and similar animals require a special (small) instrument (Fig.
318).

[Illustration: $1]

In certain circumstances, moreover, it is preferable to use retractors,
with which local examination is easier. These can be applied at either
side of the vagina and drawn apart, thus exposing the depths of the
genital tract.


                         CASTRATION OF THE COW.

The operation of castrating the cow is very old, and was mentioned by
both Aristotle and Pliny. Many other descriptions of it have since been
given. But more recently the manual technique has been considerably
simplified and very fully described.

=Utility.=—The operation is practised for the cure of nympho-mania; also
to prolong the period of milk-yielding and to facilitate fattening.

As regards nympho-mania, it is only of value where the excessive
excitement is due to disease of the ovaries.

Under ordinary conditions the secretion of milk diminishes more or less,
and becomes very slight after eight or nine months from calving. If,
however, the cow is castrated under favourable circumstances, lactation
continues for several months, sometimes for several years, beyond this
period. It is said that castrated cows yield milk of a more constant
composition and richer in butter fat, casein, and mineral salts than
those which are not castrated, although the point cannot be said to have
been fully established.

To obtain the best results the subjects should have attained their
maximum yield of milk and be from five to seven years old. The best
period is six weeks to two and a half months after calving. Neglect of
these considerations is liable to be followed by inappreciable,
doubtful, or bad results.

The influence of castration on fattening is explained by the suppression
of œstrum.

=Manual Technique.=—An ovariotome with a hidden blade and an _écraseur_
with an extra long stem are the only instruments required. The animals
should be prepared for some days by diminishing their food supply and
administering gentle laxatives.

Acute or chronic lesions of the genital tract should be held to
contra-indicate operation, and it should be noted that tuberculous
animals are particularly liable to awkward complications.

On the day of operation an abundant enema is given, to empty the rectum,
after which the vagina is washed out freely with a lukewarm solution of
some non-irritant antiseptic. The hind quarters, and particularly the
neighbourhood of the anus, vulva, base of the tail, etc., should be
carefully washed and disinfected with a solution of lysol, cresyl or
carbolic acid.

[Illustration: $1]

The patients are secured in a standing position, a rope being passed in
the form of the figure =8= around the hind limbs above the hocks, and
the animal is then firmly thrust against a wall by several strong
assistants.

The operator’s hands and instruments must be rigorously disinfected.

The operation comprises three stages:

=First stage.= Puncture of the vagina.

=Second stage.= Finding and securing the ovaries.

=Third stage.= Ablation.

The hand is smeared with sterilised oil, and, grasping the ovariotome,
is passed into the vagina, which contracts on it and on the forearm.
Within a short time, however, which may vary between two or three
minutes and a quarter of an hour, the vagina becomes distended and its
walls rigid, so that the operator is able to continue his manipulations
more easily. This is the moment for effecting puncture, after an
examination of the pelvic organs through the vaginal walls.

The blade of the ovariotome is advanced until fully exposed, and the
point is brought directly above the neck of the uterus, about ¾ to 1¼
inches from it. By a sharp movement the instrument is then thrust
directly forward, dividing the wall of the vagina in the median line.

The blade is next retracted into its sheath and the instrument dropped
on to the floor of the vagina. The right index finger is at once passed
through the orifice so made into the peritoneal cavity, in order to make
certain that all the membranes have been divided. By pressing on and
slightly tearing the tissues the middle finger is then introduced
alongside the index. Only these two fingers should be passed into the
peritoneal cavity.

In order to secure the ovaries it then suffices (Fig. 321) to thrust
forward the base of the vagina, allowing the two fingers to glide over
the body of the uterus and thence downward over its side to the point
where the horns of the uterus originate. Here the fingers meet the
ovary, which is readily recognisable on account of its size and shape
(those of a walnut). The gland is nipped between the index and middle
fingers, and is drawn into the vagina through the operative opening.

[Illustration: $1]

In order to remove the ovary the operator seizes the _écraseur_ with the
left hand, a loop of chain about an inch long projecting, and slides the
instrument along his right forearm. The arm must be retained in the
vagina, the fingers grasping the ovary. The organ is slipped into the
loop of the _écraseur_, which is then manipulated with the left hand
until the pedicle is divided. To prevent hæmorrhage the screw of the
_écraseur_ should only be turned at the rate of about twice a minute.
The ovary when separated is left on the floor of the vagina, the fingers
being again introduced into the abdominal cavity to secure the second
one. This is removed in precisely the same way.

The pedicles of the ovaries are released, and at once return to the
peritoneal cavity, while the operator, in withdrawing his hand, brings
with it the knife and the ovaries themselves. The lips of the operative
incision come together again spontaneously as the vagina contracts.

This operation is followed by slight colic, which, however, need not
cause alarm.

[Illustration: $1]

=Complications: Hæmorrhage.=—If the incision is unskilfully performed,
it may in exceptional cases result in injury of the terminal portion of
the aorta or the iliac arteries. The blood then streams past the
operator’s hand, and the animal dies of internal hæmorrhage in a few
minutes; nothing can be done.

If there is undue haste in manipulating the _écraseur_, the pedicle of
the ovary is cut rather than crushed, the vessels close imperfectly, and
grave hæmorrhage may occur.

In cases where hæmorrhage is slight the peritoneal clot is readily
reabsorbed; but should the animal happen to be tuberculous or its
vessels in any other way diseased, free hæmorrhage may occur and may
eventually be followed by fatal peritonitis. Hernia of the intestine
through the vagina is a rare complication nowadays, on account of the
small dimensions of the perforations. In former times, when larger
incisions were made, it occurred rather frequently.

=Abscess Formation.=—Suppuration of the wound and peritonitis or
vaginitis are caused solely by the neglect of antiseptic precautions.

Pelvic peritonitis following an operation is indicated, like ordinary
acute peritonitis, by loss of appetite, peritonism, colic, etc.

Even where peritonitis is avoided a local abscess often forms in the
vaginal wall owing to infection of the operation wound. The symptoms are
delayed for several days, sometimes for a fortnight after operation, and
consist in straining efforts, moderate peritonism, diminution in
appetite, etc. Vaginal or rectal examination reveals the character and
extent of the disease. The abscess should be punctured through the
vagina.

Finally, it may happen that castration does not prevent the recurrence
of œstrum. The ovarian pedicle may have been divided too close to the
glandular tissue, a fragment of which has remained adherent to the
pedicle.

Certain other operative complications are also possible in dealing with
cows suffering from nympho-mania which have developed cysts, tumours, or
abscesses of the ovaries. It is then necessary to enlarge the incision
in the vagina and take particular precautions not to rupture the cysts
or abscesses in the peritoneal cavity. The operator must proceed
cautiously and modify his technique according to circumstances.


                         CASTRATION OF THE SOW.

Castration of the sow has been practised since very ancient times. The
operation is performed on animals intended for fattening, and at all
ages between six weeks and maturity.

=Anatomical Arrangement of the Genital Organs.=—Before performing
ovariotomy in the sow it is indispensable to understand the special
arrangement of the genital organs. The uterine horns are very long and
folded on themselves, forming convolutions which give them somewhat the
appearance of small loops of intestine. Nevertheless they can readily be
distinguished by the touch, for they are much smaller in size than the
latter.

In young sows, two to three months old, they are of about the thickness
of a small pencil. Differentiation is more difficult in sows that have
borne litters, but as the ovaries alone are withdrawn, leaving the horns
of the uterus uninjured, this distinction is unimportant.

The horns of the uterus are suspended in the peritoneal cavity by means
of very extensive, well-developed, and very lax ligaments, and, as the
horns of the uterus lie at a very acute angle one to the other, the
ovaries are very close to the median line of the abdomen. The length and
yielding character of the parts and the close apposition of the ovaries
explain why the latter can be found and extracted through a single
incision in the flank, either on the right or left side.

An ordinary convex bistoury or a special knife and two artery forceps
are the instruments employed.

=Manual Technique.=—The animal is cast on the right or left side,
preferably on the right, so that the right index finger can be employed.
Full-grown sows should always be muzzled. In the case of young animals,
the limbs should be grasped by assistants, the hind limbs being crossed
one over the other and drawn backwards.

Antiseptic applications are highly desirable, although they are usually
neglected when a layman directs the operation.

The operator places himself close to the animal’s back. The incision may
be made in one of three different places.

[Illustration: $1]

Certain practitioners recommend a vertical incision about 2 to 2¼ inches
in length, commencing at the external angle of the ilium, or ⅓ of an
inch in front of it, and prolonged downwards; others make a horizontal
incision parallel with the vertebral axis; and, lastly, some believe
that an oblique incision following the direction of the “cord of the
flank” is just as advantageous. A vertical or oblique incision is
probably the best.

The operation comprises four stages:

=First stage.= Incision of the skin and subjacent muscles.

=Second stage.= Perforation of the peritoneum and discovery of the
ovaries.

=Third stage.= Ablation of the ovaries or of the ovaries and horns of
the uterus.

=Fourth stage.= Suture of the wound.

The tissues are divided layer by layer. The skin is formed into a
longitudinal fold and divided in a vertical direction, and the subjacent
muscular layers are then divided with the bistoury. The tissues are next
broken through layer by layer with the index finger until the parietal
peritoneum is reached. This membrane is then fissured, or at least
scraped with the nail, and perforated with a sudden sharp thrust of the
index finger.

[Illustration: $1]

This practice, however, has the disadvantage of sometimes causing the
parietal peritoneum to strip away from the wall of the abdomen, which
greatly increases the difficulties of operation. It is better,
therefore, to grasp the peritoneum with a small pair of forceps, draw it
outwards, and secure it so as to puncture it with more certainty. When
experience has been acquired this precaution will be unnecessary.

The incision being made and the finger introduced into the abdomen, the
operator, who kneels against the animal’s back, searches for the ovaries
with his index finger. The upper ovary of the side in which the incision
has been made will be found immediately in contact with the parietal
peritoneum, and the operator must take care not to displace it by
untimely or careless manipulation, which may thrust it away among the
loops of intestine. The finger being doubled up in the form of a hook,
the ovary is seized and drawn out. Sometimes it may be easier to
withdraw the uterine horn, leaving the search for the ovary until a
little later.

The first ovary having been discovered, its pedicle is seized between
the left thumb and index finger or the jaws of pressure forceps, and
then the search is continued for that of the opposite side. In young
sows the horn of the uterus may be followed up from its extremity
(ovarian extremity) towards its origin (bifurcation of the body of the
uterus) and the search continued along the horn of the uterus of the
opposite side, which is followed in the reverse direction from its base
towards its extremity until the second ovary is found.

The most difficult stage is that at which the change is made from one
horn to the other, for this is the moment when the contraction of the
parts is most violent, the animal’s struggles most energetic and the
pain most acute, so that great care must be taken not to let go the horn
which has already been secured.

When the second ovary appears at the external orifice, it is secured
like the preceding, and both are removed by torsion. The horns of the
uterus are then freed and returned to the abdominal cavity, the wound is
thoroughly disinfected and united with from one to three interrupted
sutures passed through the skin. The animal is then allowed to rise.
Complications are rare.

In small females the uterine horns are often removed by torsion along
with the ovaries. In adults, only the ovaries are removed.

=Subsequent Precautions: Operative Accidents.=—The patients are kept on
low diet for some days after operation. Accidental stripping away of the
peritoneum at the seat of operation may sometimes result in the
formation of a little abscess when the wound has been infected. This is
diagnosed by direct examination or palpation. The lips of the wound are
then opened in order to permit the pus to escape and avoid peritonitis.
Should the horns of the uterus or the broad ligaments be roughly
manipulated, they may be torn to some extent, but this rarely causes
grave complications.

Bleeding from the incision in the abdominal wall is of little
importance.

Hernia rarely occurs, for the opening in the peritoneum is of very small
size.

In rare cases, and when care is not used, a portion of the intestine may
be sutured to the margin of the wound. The intestine then becomes
adherent to the abdominal wall, but grave results seldom follow.


                          SUTURE OF THE VULVA

In cases of recurrence after reduction of an inversion of the uterus or
the vagina it may become necessary to suture the vulva in order to
control the effects of straining.

Several forms of suture are employed; the best are probably those of
Rainard and Strebel.

=Simple Suture.=—Simple suture may be formed of very flexible copper
wires. Three are usually inserted, one at the base, one about the
middle, and one near the upper third of the vulval opening. The ends of
each suture are knotted and drawn moderately tight over the opening,
then one of the ends of the highest knot is united vertically to an end
of the middle knot, and the latter in its turn is similarly secured to
the lowest knot.

To be reliable, sutures should embrace the entire thickness of the lips
of the vulva.

=Rainard’s Suture.=—Rainard’s suture consists only of two oblique
stitches, crossed in the form of the letter “=X=,” starting from the
upper third of one of the lips of the vulva and terminating in the lower
third of the opposite lip. The ends are tied opposite the centre of the
vulval opening.

=Strebel’s Suture.=—Strebel’s suture consists of three stitches inserted
transversely. The material employed is galvanised wire, sharpened at one
end and rolled into a flat spiral at the other. Each wire, which plays
the part of a needle, is inserted separately, and is afterwards twisted
into a spiral by means of special forceps, the excess of length being
thus taken up until the lips of the vulva are brought closely in
contact.

[Illustration: $1]

In practice, in order to avoid the cutting and irritant effect of such
sutures and to increase their efficiency, two rectangular pieces of
leather are applied on either side through holes in which the actual
metallic sutures are passed. West’s vulval clamp is better than sutures.
It is very popular in England.


                                TRUSSES.

Trusses applied for the purpose of preventing prolapsus of the genital
organs are now almost entirely given up, as they very imperfectly
achieve their object.

Lund’s truss, shown in the illustration (Fig. 325), is perhaps the most
efficient of those which survive. The essential portion of this is of
metal, and is approximately of the shape of the letter “=V=.” The two
ends may be separated and drawn together at will by means of a cord.
This apparatus is held in contact with the vulva by means of strings
which pass through eyes in the metallic triangle and are secured to a
collar placed on the neck or to a girth secured round the chest.

[Illustration: $1]


                 SECTION OF THE SPHINCTER OF THE TEAT.

This operation is performed to render easily pervious the ends of teats
which have undergone contraction as a consequence of changes in the
sphincter or from some other cause.

The animals are secured, and the teat to be operated on having been
grasped between the index finger and thumb of the left hand, the point
of the little cutting instrument shown in Fig. 326 is introduced into
the opening of the teat, and it is then thrust in as far as the shoulder
on the cutting edges.


                 DILATATION OF THE ORIFICE OF THE TEAT.

The results of the above operation not always proving permanent, and
cicatricial contraction often following after a few weeks’ time, forced
dilatation by means of the conical tubes shown (Fig. 327) has been
generally substituted for it. Three instruments of varying thickness are
usually sufficient. Forced dilatation may be effected at a single
operation, and has not the drawback of causing cicatrices.

[Illustration: $1]

[Illustration: $1]


                         ABLATION OF THE MAMMÆ.

Ablation of the mammæ is rather frequently necessary, principally in
cases of gangrenous mammitis, of prolonged, continuous suppuration, or
of grave mammitis, where death would otherwise follow.

Provided the anatomical structure of the parts is known (Fig. 327)
ablation does not present any insuperable difficulty.

In the cow, either two lateral quarters or the entire udder must be
removed. The lines of incision through the skin should first of all be
traced.

One half of the udder may be removed by the following method:

=First stage.= Elliptical incision through the skin, including the two
teats of one side.

The lines of incision should extend backwards sufficiently high to
enable the vessels at the base of the gland to be easily ligatured.

=Second stage.= Dissection and breaking down of the subcutaneous and
intermammary connective tissue. The anterior mammary vein must be
ligatured.

=Third stage.= Isolation of the mamma from the front backwards, and
ligature of the vessels of supply. Extirpation.

=Fourth stage.= Suture and drainage of the operative wound with iodoform
gauze.

[Illustration: $1]

[Illustration: $1]

This operation appears to cause formidable injuries, the abdominal tunic
and the muscles of the flat portion of the thigh being largely exposed,
but in reality the wound is less grave than might be supposed, and
healing occurs in a comparatively short time, provided none of the
diseased tissue is left.

The dressing is renewed at intervals of two or three days, and when
cicatrisation proceeds regularly it may be omitted and replaced by
antiseptic irrigation.

In the ewe and she-goat the operative technique is identical:

=First stage.= Elliptical incision, including the teat.

=Second stage.= Breaking through of the intermammary connective tissue
partition and the subcutaneous tissue. Ligature of the anterior mammary
vein.

=Third stage.= Isolation of the mamma from the front backwards. Ligature
of the vessels of supply. Extirpation.

=Fourth stage.= Suture and drainage.




                                 INDEX.


                                   A.

 PAGE

 Abdominal cavity, diseases of, 478

 Ablation of the mammæ, 771

 Abomasal indigestion, 182

 Abomasum, 114
   „ hernia of the, 493
   „ obstruction of the, 194
   „ strongylosis of, in the ox, 268

 Abortion, epizootic, in cows, 553

 Acariasis, non-psoroptic forms of, 645

 Accessory glands of the genital apparatus, 597

 Accidental phlebitis, 396

 Acid theory in diseases of bones, 3

 Acids, caustic, poisoning by, 217

 Acne in the sheep, 606

 Acorns, poisoning by, 228

 Acquired herniæ, 489

 Actinomycosis, 672

 Actual cautery, castration with the, 758

 Acute cystitis, 511
   „ deep-seated glossitis, 131
   „ eczema, 599
   „ enteritis, 203
   „ gastric indigestion in swine, 185
   „ gastritis, 188
   „ inflammation of the gastric compartments, 186
   „ laryngitis, 333
   „ mammitis, 573
   „ metritis, 550
   „ nephritis, 528
   „ parotiditis, 134
   „ peritonitis, 478
   „ pleurisy, 361
   „ tuberculosis, 704
   „ vaginitis, 544

 Æsculaceæ, 246

 Agalaxia, 587

 Agaricaceæ, 225

 Alkalies, caustic, poisoning by, 217

 Aloes, poisoning by, 221

 Alsinaceæ, 229

 Ambrosiaceæ, 256

 Amputation of the claw, 730

 Anæmia in cattle, 268
   „ lambs, 268
   „ sheep, 268

 Anæsthesia, 726

 Annual mercury, poisoning by, 256

 Anomalies, physiological, 567

 Anus, 116
   „ imperforate, 742

 Apiaceæ, 247

 Apocynaceæ, 251

 Apparatus of locomotion, 730

 _Aragallus spicatus_, poisoning by, 237

 Arsenic, poisoning by, 218

 Arsenical dips, 632

 Arteries, examination of, 371

 “Arthritis of milch cows”, 99

 Articular rheumatism, 89
   „ causes, 89
   „ complications, 91

 Articulations, diseases of, 45

 Ascites, 483

 Asclepiadaceæ, 252

 Aspergilli, pneumo-mycosis due to, 350


                                   B.

 Barberry family, 235

 Beech family, 228

 Beef measles, 79
   „ cause, 79
   „ symptoms, 81
   „ where prevalent, 79

 Bell-flower family, 255

 Berberidaceæ, 235

 Biceps femoris, 70

 Bile ducts, cancer of, 282

 Bilharziosis in cattle and sheep, 439

 Bistournage, 751

 Bitter milk, 591

 Bladder, diseases of the, 511
   „ eversion of the, 519
   „ paralysis of the, 519

 Bleeding, 727
   „ in the pig, 728
   „ in sheep, 727

 Blood, diseases of the, 406
   „ examination of, 372
   „ poisoning in sheep and lambs in New Zealand, 415
   „ -vessels, diseases of, 396

 Blood-wort family, 228

 Bloody flux in calves and lambs, 271

 Blue milk, 590

 Boars, castration of, 759

 Bog spavin in the ox, 46

 Bone, actinomycosis of, 681
   „ tumours, 30

 Bones and articulations, tuberculosis of the, 701

 Bones, diseases of, 3
   „ „ acid theory, 3
   „ „ inflammation theory, 4
   „ „ theory of insufficiency, 3

 Bovine animals, calculi in, 515
   „ piroplasmosis, 416

 Box family, 246

 Brain, tuberculosis of the, 702

 Braxy, 435

 Bronchi, 333

 Bronchitis, 336
   „ chronic, 337
   „ pseudo-membranous, 339
   „ simple acute, 337
   „ verminous, in sheep and cattle, 340

 Broncho-pneumonia, gangrenous, due to foreign bodies, 351
   „ infectious, 354
   „ of sucking calves, 356
   „ sclero-caseous, of sheep, 358

 Bryony, poisoning by, 256

 Buckwheat poisoning, 606

 Bull, castration of the, 751

 Bunch-flower family, 227

 Bursal sheath of the flexor tendons, distension of, 49

 Butneriaceæ, 235

 Butter, milk without, 589

 Buxaceæ, 246


                                   C.

 Calculi in bovine animals, 515
   „ urinary, in sheep, 518

 Calculus formation, 514

 Calves, depraved appetite in, 160
   „ diarrhœic enteritis in, 212
   „ dysentery in, 210
   „ goitre in, 453
   „ intestinal coccidiosis of, 271
   „ lumbricosis of, 267
   „ mycotic stomatitis in, 124
   „ necrosing stomatitis in, 123

 Calving, dropping after, 461

 Campanulaceæ, 255

 Cancer of the bile ducts, 282
   „ liver, 282

 Cancerous pericarditis, 375

 Canker, 40
   „ treatment, 41

 Capillary system, examination of, 372

 Carbolic acid poisoning, 221
   „ dips, 633

 Cardiac anomalies, 374

 Carduaceæ, 256

 Carrot family, 247

 Caseous lymphadenitis of the sheep, 453

 Casting, control of oxen by, 723

 Castor oil cake, poisoning by, 257

 Castration, 751
   „ complications after, 760
   „ by clams, 756
   „ the covered method, 757
   „ „ elastic ligature, 758
   „ „ exposed method, 757
   „ torsion, 757
   „ of boars and young pigs, 759
   „ „ the bull and ram, 751
   „ „ „ cow, 761
   „ „ cryptorchids, 760
   „ „ the ram, 759
   „ „ „ „ by bistournage, 759
   „ „ „ „ „ ligature, 759
   „ „ „ „ „ tearing, 759
   „ „ „ sow, 765
   with the actual cautery, 758

 Catarrhal gastritis in swine, 190
   „ stomatitis in sheep, 122
   „ „ general, in swine, 126

 Catheter, passage of the, in the cow, 750
   „ „ „ „ ram, 749

 Cattle, anæmia in, 268
   „ bilharziosis in, 439
   „ diarrhœa in, 268
   „ hæmorrhagic septicæmia in, 716
   „ parasitic gastro-enteritis in, 268
   „ pseudo-membranous pharyngitis in, 141
   „ verminous bronchitis in, 340

 Caustic acids, poisoning by, 217
   „ alkalies, poisoning by, 216

 Cerebral congestion, 456
   „ tumours, 459

 Changes in the milk, 587

 Chaps, 568

 Chemical dyspepsia, 195

 Chenopodiaceæ, 229

 Chorioptic mange, 636, 640, 642

 Chronic bronchitis, 337
   „ cystitis, 513
   „ diarrhœa, 207
   „ eczema, 600
   „ enteritis, 207
   „ gastritis, 194
   „ glossitis, 132
   „ indigestion, 194
   „ mammitis, 581
   „ metritis, 552
   „ nephritis, 530
   „ parotiditis, 136
   „ pericarditis, 389
   „ peritonitis, 481
   „ pleurisy, 362
   „ simple synovitis, forms of, 45
   „ tympanites, 194
   „ vaginitis, 546

 Circulation, organs of the, 370

 Circulatory apparatus, 727

 Clams, castration by, 756

 Claw and third phalanx, disarticulation of the, 731
   „ amputation of the, 730
   „ surgical dressing for a, 730

 Claws, congestion of the, 31

 Clément’s bath, 623

 Clotted milk, 589

 Cœnurosis, 467

 Colchicum poisoning, 256

 Cold water, colic due to ingestion of, 162

 Colic, 116
   „ as a result of strangulation, 167

 Colic due to invagination, 163
   „ in the ox, 162

 Common salt, poisoning by, 217

 Complications after castration, 760

 Condylomata, 38

 Congenital herniæ, 487

 Congestion, pulmonary, 343
   „ of the claws, 31
   „ „ kidneys, 527
   „ „ liver, 280
   „ „ udder, 570

 Congestive colic, 162

 Conjunctivitis, 662

 Contagious disease (takosis) of goats, 412
   „ mammitis in milch cows, 580
   „ vaginitis, 545

 “Contagious foot disease”, 41

 Contraction of the sphincter, 567

 Control of pigs, 725
   „ sheep and goats, 725
   „ oxen, 720
   „ „ by casting, 723
   „ general, of oxen, 722

 Contusions of the sole, 31

 Convallariaceæ, 228

 Copper poisoning, 221

 Coryza, gangrenous, 320
   „ simple, 319

 Cotton cake, poisoning by, 257

 Covered method, castration by the, 757

 Cow, castration of the, 761
   „ „ „ complications in, 764
   „ passage of the catheter in the, 750

 Cows, epizootic abortion in, 553

 Cowper’s glands, 597

 Cow-pox, 665
   „ and human variola, 669

 Cracks, 568

 Creolin bath, 324

 Croupal vaginitis, 545

 Crowfoot family, 230

 Crushing a foreign body in the œsophagus, 735

 Cryptorchids, castration of, 760

 Cysticerci, infection with, 73

 Cysticercosis, 290
   „ peritoneal, 485

 Cysticercus disease of the pig, 73

 Cystic parasites of animals, table of, 73

 Cystitis, acute, 511
   „ chronic, 513

 Cysts of the udder, 585


                                   D.

 Defæcation: examination of fæcal material, 118

 Demodecic mange, 643

 Depraved appetite, 158
   „ „ in calves and lambs, 160
   „ „ „ the ox, 158

 Diaphragmatic herniæ, 496

 Diarrhœa, chronic, 207
   „ in cattle, 268
   „ „ lambs, 268
   „ „ sheep, 268

 Diarrhœic enteritis in calves, 212

 Digestive apparatus, 734
   „ „ diseases of, 106
   „ „ fistulæ of, 500
   „ „ parasites of, 263
   „ „ semiology of, 106

 Digestive tract, tuberculosis of the, 699

 Dilatation of the œsophagus, 149
   „ „ orifice of the teat, 770

 Disarticulation of the claw and third phalanx, 731
   „ „ two first phalanges, 732

 Diseases of the bladder, 511
   „ „ blood, 406
   „ „ kidneys, 527
   „ „ liver, 279
   „ „ lymphatic system, 444
   „ „ mouth, 106
   „ „ œsophagus, 109
   „ „ pharynx, 108
   „ „ salivary glands, 108
   „ „ stomach, 110, 169
   „ „ rumen, 110
   „ „ peritoneum and abdominal cavity, 478
   „ „ urinary apparatus, 502
   „ produced by distillery and sugar factory pulp, 259
   „ transmissible to man through the medium of milk, 593

 Distillery and sugar factory pulp, diseases produced by, 259

 Distomatosis, 293

 Disturbance in the milk secretion, 587

 Dogbane family, 251

 Dropping after calving, 461

 Dysentery in calves, 210
   „ „ and lambs, 271

 Dyspepsia, 194
   „ motor, 195
   „ secretory or chemical, 195


                                   E.

 Echinococcosis of the liver, 283
   „ suppurative, 288

 Ectopia of the heart, 374

 Eczema, 599
   „ acute, 599
   „ chronic, 600
   „ due to feeding with potato pulp, 603
   „ sebaceous or seborrhœic, 601

 Elastic ligature, castration by the, 758

 Emphysema, pulmonary, 359
   „ subcutaneous, 659

 Encephalitis, 458

 Endocarditis, 394

 Enteritis, 203
   „ acute, 203
   „ chronic, 207
   „ diarrhœic, in calves, 212
   „ hæmorrhagic, 206

 Epizootic abortion in cows, 553

 Equisetaceæ, 225

 Ergot family, 223

 Ergot of rye, poisoning by, 223

 Ergotism, 223

 Ericaeæ, 249

 Euphorbiaceæ, 244

 Eventration, 499

 Eversion of the bladder, 519

 Exostoses, 27

 Exposed method, castration by the, 757

 External ischio-tibial muscle, rupture of the, 70

 Exudative pericarditis due to foreign bodies, 376

 Eyes, diseases of the, 661


                                   F.

 Facial sinuses of sheep, œstrus larvæ in the, 330
   „ „ trephining the, 745

 Fæcal material, examination of, 118

 Fagaceæ, 228

 Fagopyrism, 606

 False sturdy, 330

 _Fasciola hepatica_, 294

 Felon, 41

 Female genital organs, examination of, with the speculum, 760

 Femoro-tibial articulation, luxation of the, 61
   „ „ symptoms, 62
   „ „ treatment, 63

 Femur, luxation of, 56
   „ „ „ symptoms, 57
   „ „ „ treatment, 58

 Fennel, poisoning by, 249

 Ferments, lactic, 588

 Fern family, 225

 Fetlock joint, distension of the synovial capsule of the, 48
   „ strain of, 54

 Figwort family, 255

 Fistula, parotid, 136

 Fistulæ, milk, 569
   „ of the digestive apparatus, 500

 Flax family, 244

 Flexor metatarsi, rupture of the, 72
   „ tendons, distension of the bursal sheath of, 49

 Food, poisoning due to, 215

 Foot, diseases of the, 31
   „ rot, 43
   „ „ symptoms, 43
   „ „ treatment, 44
   „ scab, 636

 Foreign bodies causing diseases of the eyes, 661
   „ „ exudative pericarditis due to, 376
   „ „ gangrenous broncho-pneumonia due to, 351
   „ „ gastric disturbance due to, 198
   „ „ migration of, from the reticulum, pneumonia due to, 348

 Foreign bodies, pneumonia due to, 347

 Foreign body in the œsophagus, crushing a, 735
   „ „ „ „ submucous dissection of, 736

 Fractures, 20

 France, bovine piroplasmosis in, 424

 Frontal sinus, trephining the, 745
   „ „ purulent collections in, 327


                                   G.

 Gangrenous broncho-pneumonia due to foreign bodies, 351
   „ coryza, 320
   „ mammitis in goats, 584
   „ „ of milch ewes, 583

 Gaseous indigestion, 170

 Gastric compartments, acute inflammation of, 186
   „ „ tumours of the, 202
   „ disturbance due to foreign bodies, 198
   „ indigestion, acute, in swine, 185

 Gastritis, 186, 188–194

 Gastro-intestinal strongylosis in sheep, 263

 Gastrotomy, 739

 “Gathered Nail”, 37

 General diseases, 4

 Genital apparatus, 542
   „ „ accessory glands of the, 597
   „ malformations, 560
   „ organs, male, 594
   „ „ tuberculosis of the, 700

 Genito-urinary organs, 747
   „ regions, 502

 Gid, 467

 Glands, mammary, diseases of, 565

 Glans penis and sheath, polypi of, 506

 Glossitis, 130
   „ acute, deep-seated, 131
   „ chronic, 132
   „ nodular sclerosing, 133
   „ superficial, 130

 Goat, demodecic mange in the, 644
   „ mange in the, 641
   „ ringworm in the, 653

 Goats, control of, 725
   „ gangrenous mammitis in, 584

 Goitre in calves, 453
   „ lambs, 453

 Goosefoot family, 229

 Grass family, 226
   „ tick, life history of, 432

 Grease, 41


                                   H.

 Hæmaturia, 520

 Hæmodoraceæ, 228

 Hæmorrhagic enteritis, 206
   „ „ in calves and lambs, 271
   „ septicæmia in cattle, 716

 Hæmorrhagic septicæmia, infective diseases confused with, 718

 Haunch, hygroma of, 67

 Heart, ectopia of the, 374

 Heat stroke, 442

 Heath family, 249

 Hellebore, poisoning by, 234

 Helminthiasis, intestinal, in ruminants, 275

 Hemlock, poisoning by, 248

 Hepatitis, nodular necrosing, 280

 Hernia, inguinal, in young pigs, 741
   „ of the abomasum, 493
   „ „ intestine, 494
   „ „ rumen, 490
   „ perineal, of young pigs, 487

 Herniæ, 487, 741
   „ acquired, 489
   „ congenital, 487
   „ diaphragmatic, 496
   „ treatment of, 495

 Hock, hygroma of the point of the, 68
   „ joint, distension of the synovial capsule of the, 46
   „ „ strain of, 55
   „ region, distension of the tendon sheaths in, 46

 Hoose, 340

 Horn core, trephining the, 745

 Horns, anatomy of, 21
   „ detachment of, 23
   „ fissuring of, 24
   „ fractures of, 21, 25
   „ splints for, 26
   „ treatment of, 25

 Horse-chestnut family, 246

 Horsetail family, 225

 Human variola and cow-pox, 669

 Husk, 340

 Hydro-nephrosis, 531

 Hydro-pneumo-thorax, 366

 Hygroma of the haunch, 67
   „ „ knee, 65
   „ „ point of the hock, 68
   „ „ point of the sternum, 69
   „ „ stifle, 67
   „ „ trochanter of the femur, 67

 Hygromas, 64

 Hypericaceæ, 246

 Hypocreceæ, 223

 Hypodermosis in the ox, 646


                                   I.

 Impaction of the omasum, 179
   „ „ rumen, 175

 Imperforate anus, 742
   „ condition of the teat, 567
   „ vagina, 560

 Impetigo in the pig, 605

 Indigestion, 170
   „ abomasal, 182
   „ acute gastric, in swine, 185
   „ as a result of over-eating, 175
   „ chronic, 194

 Infectious broncho-pneumonia, 354

 Infectious diseases, 665
   „ pyelo-nephritis, 533
   „ pseudo-rheumatism in adults, 99
   „ „ „ symptoms, 100
   „ „ „ treatment, 103
   „ rheumatism in young animals, 94
   „ „ „ causes, 94
   „ „ „ symptoms, 95

 Infective diseases, confused with hæmorrhagic septicæmia, 718

 Inflammation of the sheath, 506
   „ „ submaxillary salivary gland, 137

 Inflammatory diseases, 570

 Inguinal hernia in young pigs, 741

 Insolation, 460

 Interdigital space, inflammation of the, 38

 Internal infectious phlebitis, 398

 Interstitial mammitis, 574

 Intestinal helminthiasis in ruminants, 275
   „ tuberculosis, 699

 Intestine, 116
   „ hernia of the, 494

 Invagination, colic due to, 163

 Inversion and prolapsus of the rectum, 743

 Iodine poisoning, 22

 Iodism, 222

 Iodoform poisoning, 222

 Ischial urethrotomy, 747

 Ischio-tibial muscle, external, rupture of the, 70

 Issues, 728


                                   J.

 Joints, luxation of, 56


                                   K.

 Keratitis, 662

 Kidney worm of swine, 539

 Kidneys, congestion of the, 527
   „ diseases of the, 527

 Knee, distension of tendon sheaths in the region of, 49
   „ hygroma of, 65
   „ joint, distension of the synovial capsule of the, 47
   „ strain of, 53


                                   L.

 Lactic ferments, 588

 Lambs, anæmia in, 268
   „ blood poisoning in, in New Zealand, 415
   „ depraved appetite in, 160
   „ diarrhœa in, 268
   „ goitre in, 453
   „ intestinal coccidiosis of, 271
   „ parasitic gastro-enteritis in, 268

 Laminitis, 32
   „ symptoms, 33
   „ treatment, 34

 Laparotomy, 740

 Larkspur poisoning in sheep, 231

 Laryngitis, 333
   „ acute, 333
   „ pseudo-membranous, 333

 Larynx, 333
   „ examination of, 313
   „ tumours of, 335

 Lathyrism, 243

 Lead poisoning, 220

 Licking habit, 158

 Lily of the valley family, 228

 Lime and sulphur dips, 627
   „ „ prejudice against, 628

 Linaceæ, 244

 Liver, 119
   „ cancer of, 282
   „ congestion of, 280
   „ diseases of, 279
   „ echinococcosis of, 283
   „ rot, 293

 Liver fluke (_Fasciola hepatica_), 294
   „ disease, 293

 Local affections, 20

 Locomotion, apparatus of, 730
   „ organs of, diseases of, 1
   „ gait in, 1
   „ inspection for, 1
   „ palpation and pressure to detect, 1
   „ percussion in, 1

 Louping-ill, 429

 Lumbar prurigo, or “trembling,” in sheep, 475

 Lumbricosis of calves, 267

 Lund’s truss, 770

 Lungs, 343

 Lupines, poisoning by, 241

 Luxation of the femoro-tibial articulation, 61
   „ „ femur, 56
   „ „ patella, 58
   „ „ scapulo-humeral joint, 63

 Lymphadenitis, 448

 Lymphatic glands, tuberculosis of, 696
   „ glandular apparatus, topography of, 445
   „ system, diseases of, 444

 Lympho-cythæmia, 448

 Lymphogenic diathesis, 448


                                   M.

 Magnoliaceæ, 229

 Magnolia family, 229

 Maize, poisoning by the male tufts of, 226

 Male genital organs, 594

 Malformations, genital, 560

 Malignant œdema, 415

 Mammæ, ablation of the, 771

 Mammary glands, diseases of, 565
   „ toxæmia, 461

 Mammitis, 571
   „ acute, 573
   „ chronic, 581
   „ contagious, in milch cows, 580


                                   Mammitis, gangrenous in goats, 584
   „ „ of milch ewes, 583
   „ interstitial, 574
   „ parenchymatous, 575

 Mange, 611
   „ chorioptic, 636, 640, 642
   „ demodecic, 643
   „ in the goat, 641
   „ „ ox, 638
   „ „ pig, 642
   „ psoroptic, 614, 639
   „ sarcoptic, 638, 641
   „ symbiotic, 636

 Manual technique in bistournage, 752
   „ „ castration of the cow, 762
   „ „ „ „ sow, 766

 Martelage, 756

 Maxilla, actinomycosis of the, 673

 Maxillary sinus, purulent collections in, 329
   „ „ trephining the, 745

 Measles, beef, 79
   „ pork, 78

 Mechanical pneumonia, 347

 Mediastinum, diseases of structures enclosed within the, 368
   „ tuberculosis of the, 697
   „ tumours of, 369

 Medicated milk, 591

 Melanthaceæ, 227

 Meliaceæ, 244

 Meningitis, 456

 Mercurial poisoning, 219
   „ stomatitis, 128
   „ „ nature of, 129

 Metritis, 547
   „ acute, 550
   „ chronic, 552
   „ septic, 547

 Microbic changes in milk, 588

 Migration of foreign bodies from the reticulum, pneumonia due to, 348

 Milch cows, contagious mammitis in, 580
   „ ewes, gangrenous mammitis of, 583

 Milk, bitter, 591
   „ blue, 590
   „ changes in the, 587
   „ clotted, 589
   „ diseases transmissible to man through the medium of, 593
   „ fever, 461
   „ fistulæ, 569
   „ medicated, 591
   „ microbic changes in, 588
   „ mucous, viscous, or thready, 589
   „ preservation of, 591
   „ putrid, 589
   „ red, 590
   „ secretion, disturbance in the, 587
   „ thready, 589
   „ viscous, 589
   „ without butter, 589
   „ yellow, 590

 Milkweed family, 252

 Molasses refuse, poisoning by, 258

 Motor dyspepsia, 195

 Mouth, diseases of, 106, 121

 Mucous milk, 589

 Muguet, 124

 Muscles and tendons, diseases of, 70
   „ parasitic diseases of, 73

 Muscular rheumatism, 92

 Mushroom family, 225

 Mycotic stomatitis in calves, 124

 Myelo-cythæmia, 448


                                   N.

 Nails, picked-up, 37

 Nasal cavities, 319
   „ „ examination of, 311
   „ „ tumours of, 325
   „ gleet, 326
   „ sinuses, purulent collections in, 326

 Neck, actinomycosis of the, 675

 Necrosing stomatitis in calves, 123

 Nephritis, acute, 528
   „ chronic, 530
   „ suppurative, 537

 Nervous system, 456

 Nettle family, 229

 New-born animals, septicæmia of, 406
   „ „ umbilical phlebitis of, 399

 New Zealand, blood poisoning in sheep and lambs in, 415

 Nitrates of potash and soda, poisoning by, 217

 Nodular necrosing hepatitis, 280
   „ sclerosing glossitis, 133

 Non-psoroptic forms of acariasis, 645

 Nympho-mania, 562


                                   O.

 Obstruction of the abomasum, 194

 Œsophageal obstructions, 152
   „ „ treatment, 154
   „ sounds, 155

 Œsophagitis, 145

 Œsophagotomy, 156, 736

 Œsophagus, 734
   „ dilatation of, 149
   „ diseases of, 109, 145
   „ ruptures and perforations of, 157
   „ stricture of, 148

 Œstrus larvæ in the facial sinuses of sheep, 330

 Oleaceæ, 251

 Olive family, 251

 Omasum, 113
   „ impaction of the, 179

 Omphalo-phlebitis, 402

 “Open arthritis”, 51

 “Open Synovitis, 49

 Operations, 720

 Ophthalmia, verminous, of the ox, 663

 Organs of circulation, semiology of, 370
   „ locomotion, diseases of, 1
   „ „ „ methods of examination in, 1

 Orifice of the teat, dilatation of the, 770

 Osseous cachexia, 7
   „ „ causes of, 14
   „ „ history of, 8

 Osseous cachexia, phases of, 9–11
   „ „ symptoms of, 8, 11
   „ „ treatment of, 18

 Ostitis, suppurating, 29

 Ovary, tumours of the, 559

 Over-eating, indigestion as a result of, 175

 Over-exertion, 442

 Ovine pasteurellosis, 263
   „ piroplasmosis, 425

 Ox, colic in the, 162
   „ demodecic mange in the, 644
   „ depraved appetite in the, 158
   „ hypodermosis in the, 646
   „ mange in the, 638
   „ strongylosis of the abomasum in the, 268
   „ urethrotomy in the, 747
   „ verminous ophthalmia of the, 663

 Oxen, canker in, 40
   „ control of, 720
   „ „ by casting, 723
   „ „ the limbs, 720
   „ warts in, 655


                                   P.

 Panaritium, 41

 Pancreas, 119

 Papaveraceæ, 235

 Papillomata, verrucous, of the udder, 586

 Paralysis of the bladder, 519

 Parasites, cystic, of animals, table of, 73
   „ of the digestive apparatus, 263

 Parasitic diseases of muscles, 73
   „ gastro-enteritis, 268
   „ „ in cattle, 268
   „ „ in lambs, 268
   „ „ in sheep, 268

 Parenchymatous mammitis, 575

 Parotid fistula, 136
   „ glands, actinomycosis of the, 675

 Parotiditis (Parotitis), 134, 136

 Parturient apoplexy, 461

 Passage of the catheter in the cow, 750
   „ „ „ ram, 749

 Passing the probang, 735

 Patella, luxation of, 58
   „ „ bandage for, 60
   „ „ symptoms, 59
   „ „ treatment, 60

 Patellar synovial capsule, inflammation of, 45

 Pea family, 236

 Pelvis, fractures of, 20

 Pericarditis, 375
   „ cancerous, 375
   „ chronic, 389
   „ exudative, due to foreign bodies, 376
   „ simple acute, 375
   „ specific, 375

 Perineal hernia of young pigs, 487

 Perinephritis, 537

 Peripneumonia and pneumonia, differences between, 347

 Perisporaceæ, 223

 Peritoneal cysticercosis, 485

 Peritoneum, diseases of, 478

 Peritonitis, 478
   „ acute, 478
   „ chronic, 481

 Persistence of the urachus, 508

 Phallaceæ, 225

 Pharyngeal polypi, 143

 Pharyngitis, 138

 Pharynx, actinomycosis of the, 675
   „ diseases of, 108, 134

 Phlebitis, 396
   „ accidental, 396
   „ internal infectious, 398
   „ umbilical, 402
   „ „ of new-born animals, 399
   „ utero-ovarian, 398

 Phosphorus poisoning, 219

 Phthiriasis, 608

 Physiological anomalies, 567

 Phytolaccaceæ, 229

 Pica, 158

 Picked-up nails, 37

 Pig, cysticercus disease of the, 73
   „ „ „ „ cause of, 74
   „ „ „ „ examination fo, 77
   „ „ „ „ symptoms of, 75
   „ „ „ „ treatment, 78
   „ demodecic mange in the, 644
   „ impetigo in the, 605
   „ mange in the, 642
   „ pneumonia of the, 710, 714
   „ ringworm in the, 653
   „ urticaria in the, 656
   „ verrucous endocarditis of the, 710, 713

 Pigs, control of, 725
   „ ringing, 734
   „ tonsilitis in, 138
   „ young, castration of, 759
   „ „ inguinal hernia in, 741
   „ „ perineal hernia of, 487

 Pink family, 229

 Piroplasmosis, 416

 Plantar aponeurosis, injury to, 38

 Plants poisonous to stock, 223

 Pleura, diseases of, 361

 Pleuræ, 343

 Pleurisy, acute, 361
   „ chronic, 362

 Plugs, 728

 Plum family, 236

 Pneumonia due to foreign bodies, 347
   „ „ migration of foreign bodies from the reticulum, 348
   „ mechanical, 347
   „ mycosis due to aspergilli, 350
   „ of the pig, 710
   „ simple, 343

 Pneumo-thorax, 362

 Poaceæ, 226

 Poisoning, 213
   „ by acorns, 228
   „ „ aloes, 221
   „ „ annual mercury, 256
   „ „ _Aragallus spicatus_, 237
   „ „ arsenic, 218
   „ „ bryony, 256
   „ „ castor oil cake, 257
   „ „ caustic acids, 217
   „ „ „ alkalies, 216
   „ „ common salt, 217
   „ „ cotton cake, 257
   „ „ ergot of rye, 223
   „ „ fennel, 249
   „ „ hellebore, 234
   „ „ hemlock, 248
   „ „ lupines, 241
   „ „ male tufts of maize, 226
   „ „ molasses refuse, 258
   „ „ nitrates of potash and soda, 217
   „ „ poppies, 235
   „ „ ranunculaceæ, 234
   „ „ smut of barley, 224
   „ „ St. John’s wort, 246
   „ „ sweet sorghum grass, 226
   „ „ tartar emetic, 218
   „ „ vetches, 243
   „ „ white loco weed, 237
   „ „ wild chervil, 248
   „ carbolic acid, 221
   „ colchicum, 256
   „ copper, 221
   „ due to food, 215
   „ iodine, 222
   „ iodoform, 222
   „ larkspur, in sheep, 231
   „ lead, 220
   „ mercurial, 219
   „ phosphorus, 219
   „ strychnine, 222
   „ tobacco, 254

 Pokeweed family, 229

 Polypi of the glans penis and sheath, 506
   „ pharyngeal, 143

 Polypodiaceæ, 225

 Poppies, poisoning by, 235

 Poppy family, 235

 Post-partum paralysis, 461

 Potato family, 252
   „ pulp, eczema due to feeding with, 603

 Preservation of milk, 591

 Pricks and stabs in shoeing, 36

 Primrose family, 251

 Primulaceæ, 251

 Probang, passing the, 735

 Probangs, 155

 Prolapsus and inversion of the rectum, 743

 Prostate, 597

 Prunaceæ, 236

 Pseudo-membranous bronchitis, 339
   „ laryngitis, 333
   „ pharyngitis in cattle, 141
   „ pharyngitis in sheep, 142

 Pseudo-pericarditis, 390

 Pseudo-rheumatism, 94
   „ „ infectious, in adults, 99

 Psoroptic mange, 614, 639

 Psorospermosis in calves and lambs, 271

 Pulmonary congestion, 343

 Pulmonary emphysema, 359

 Pulse, examination of, 371

 Puncture, in exploration of the rumen, 112
   „ of the rumen, 737

 Purulent collections in the frontal sinus, 327
   „ „ „ maxillary sinus, 329
   „ „ „ nasal sinuses, 326

 Putrid milk, 589

 Pyelo-nephritis, infectious, 533

 Pyo-pneumo-thorax, 366


                                   R.

 Rachitis, 4
   „ symptoms of, 5
   „ treatment of, 7

 Ragweed family, 256

 Ram, castration of the, 751, 759
   „ passage of the catheter in the, 749
   „ urethrotomy in the, 749

 Ranunculaceæ, 230
   „ poisoning by, 234

 Rectal exploration, 116

 Rectum, prolapsus and inversion of the, 743

 Red milk, 590

 Respiratory apparatus, 311, 745
   „ „ examination of, 311
   „ „ tuberculosis of the, 690

 Reticulitis, 186

 Reticulum, 113

 Retro-pharyngeal glands, tuberculosis of, 696

 Rheumatism, 89
   „ articular, 89
   „ infectious forms of, 94
   „ muscular, 92

 Ring-bone, 28

 Ringing pigs, 734

 Ringworm, 649
   „ in the sheep, goat, and pig, 653

 Rot-mould family, 223

 Rowels, 728

 Rumen, 737
   „ examination of the, 110
   „ hernia of the, 490
   „ impaction of the, 175
   „ puncture of the, 737

 Rumenitis, 186

 Ruminants, intestinal helminthiasis in, 275

 Rupture of the external ischio-tibial muscle, 70
   „ „ flexor metatarsi, 72

 Ruptures and perforations of the œsophagus, 157


                                   S.

 “Salivary abscesses”, 137

 Salivary glands, diseases of, 108, 134

 Salpingitis, 555

 Salpingo-ovaritis, 555

 Salt common, poisoning by, 217

 Sand crack, 34
   „ symptoms, 35
   „ treatment, 35

 Sarcoptic scabies, 612
   „ mange, 638, 641

 Saturnism, 220

 Scab, 611, 614
   „ dips, arsenical, 632
   „ „ carbolic, 633
   „ „ Clément’s bath, 623
   „ „ creolin bath, 624
   „ „ lime and sulphur, 627
   „ „ Tessier’s bath, 622
   „ „ tobacco and sulphur, 626
   „ „ Trasbot’s bath, 623
   „ foot, 636

 Scabies, 611
   „ in sheep, 611

 Scapulo-humeral joint, luxation of the, 63

 Sclero-caseous broncho-pneumonia of sheep, 358

 Scleroderma, 657

 _Sclerostoma pinguicola_ (kidney worm), 539

 Scorbutus, 104

 Scrophulariaceæ, 255

 Scrotal urethrotomy, 748

 Scurvy, 104

 Sebaceous or seborrhœic eczema, 601

 Secretory dyspepsia, 195

 Section of the sphincter of the teat, 770

 Semiology of the digestive apparatus, 106
   „ „ organs of circulation, 370

 Septic metritis, 547

 Septicæmia of new-born animals, 406

 Serous membranes, tuberculosis of, 694

 Setons, 728

 Sheath, inflammation of, 506

 Sheep, acne in the, 606
   „ anæmia in, 268
   „ bilharziosis in, 439
   „ blood poisoning in, in New Zealand, 415
   „ caseous lymphadenitis of the, 453
   „ catarrhal stomatitis in, 122
   „ control of, 725
   „ diarrhœa in, 268
   „ gastro-intestinal strongylosis in, 263
   „ larkspur poisoning in, 231
   „ œstrus larvæ in the facial sinuses of, 330
   „ parasitic gastro-enteritis in, 268
   „ pseudo-membranous pharyngitis in, 142
   „ ringworm in the, 653
   „ scab, 614
   „ scabies in, 611
   „ sclero-caseous broncho-pneumonia of, 358
   „ “trembling,” or lumbar prurigo, in, 475
   „ ulcerative stomatitis in, 125
   „ urinary calculi in, 518
   „ verminous bronchitis in, 340

 Shoeing, stabs and pricks in, 36

 Shoulder, strain of, 52

 Simple acute bronchitis, 337

 Simple acute pericarditis, 375
   „ coryza, 319
   „ pneumonia, 343
   „ stomatitis, 121

 Sinuses, examination of, 312

 Skin, diseases of, 599
   „ tuberculosis of the, 703

 Smut of barley, poisoning by, 224
   „ family, 224

 Solanaceæ, 252

 Sole, contusions of the, 31

 Sow, anatomical arrangements of the genital organs in the, 765
   „ castration of the, 765
   „ operative accidents in, 768

 Spavin in the ox, 27

 Specific pericarditis, 375

 Speculum, examination of female genital organs with the, 760

 Sphincter of the teat, contraction of the, 567
   „ „ section of, 770

 Spurge family, 244

 Stabs and pricks in shoeing, 36

 Sternum, hygroma of the point of the, 69

 Stifle, hygroma of the, 67
   „ joint, strain of, 54

 Stink-horn family, 225

 St. John’s wort family, 246
   „ poisoning by, 246

 Stock, plants poisonous to, 223

 Stomach, diseases of the, 110, 169

 Stomatitis, 121
   „ catarrhal, in sheep, 122
   „ general catarrhal, in swine, 126
   „ mercurial, 128
   „ mycotic, in calves, 124
   „ necrosing, in calves, 123
   „ ulcerative, in swine, 127
   „ in sheep, 125

 Strain of the fetlock, 54
   „ „ hock joint, 55
   „ „ knee, 53
   „ „ shoulder, 52
   „ „ stifle joint, 54

 Strains of joints, 52

 Strangulation, colic as a result of, 167

 Strawberry-shrub family, 235

 Stricture of the œsophagus, 148

 Strongylosis of the abomasum in the ox, 268

 Strychnine poisoning, 222

 Sturdy, 467

 Subcutaneous connective tissue, diseases of the, 599
   „ emphysema, 659, 738

 Submaxillary salivary gland, inflammation of, 137

 Sucking calves, broncho-pneumonia of, 356

 Sugar factory pulp, diseases produced by, 259

 Superficial glossitis, 130

 Suppurating ostitis, 29

 Suppurative echinococcosis, 288
   „ nephritis and perinephritis, 537

 Surgical dressing for a claw, 730

 Suture of the vulva, 768
   „ „ „ Rainard’s suture, 769
   „ „ „ simple suture, 768
   „ „ „ Strebel’s suture, 769

 Sweet sorghum grass, poisoning by, 226

 Swine, acute gastric indigestion in, 185
   „ catarrhal gastritis in, 190
   „ fever, 710
   „ general catarrhal stomatitis in, 126
   „ ulcerative stomatitis in, 127
   „ kidney worm of, 539

 Symbiotic (chorioptic) mange, 636

 Synovial capsule of the hock joint, distension of, 46
   „ „ „ fetlock joint, distension of, 48
   „ „ „ knee joint, distension of, 47
   „ membranes, diseases of, 45

 Synovitis, 45


                                   T.

 Takosis, 412

 Tartar emetic, poisoning by, 218

 Taxaceæ, 226

 Taxus baccata, 226

 Teat, dilatation of the orifice of the, 770
   „ imperforate condition of the, 567
   „ section of the sphincter of the, 770

 Tendon sheaths, distension of, 48
   „ „ „ in the hock region, 46
   „ „ „ in the region of the knee, 49

 Tendons and muscles, diseases of, 70

 Tessier’s scab dip, 622

 Testicle, tumours of the, 594

 Tetanus, 670

 Thorax, examination of, 315

 Thistle family, 256

 Third stomach, impaction of the, 179

 Thready milk, 589

 Thrush, 124

 Tobacco and sulphur dip, 626

 Tobacco poisoning, 254

 Tongue, actinomycosis of the, 674

 Tonsilitis in pigs, 138

 Tonsils, diseases of, 134

 Torsion, castration by, 757
   „ of the uterus, 556

 Trachea, 333
   „ examination of, 314

 Tracheotomy, 746

 Trasbot’s scab dip, 623

 Traumatic arthritis, 51
   „ articular synovitis, 51
   „ lesions, 568
   „ synovitis, 49
   „ tendinous synovitis, 50

 “Trembling,” or lumbar prurigo, in sheep, 475

 Trephining the facial sinuses, 745
   „ frontal sinus, 745
   „ horn core, 744
   „ maxillary sinus, 745

 Trichiniasis-trichinosis, 84

 Trochanter of the femur, hygroma of the, 67

 Truss, Lund’s, 770

 Trusses, 769

 Trypanosomata, diseases produced by, 426

 Tuberculosis, 682

 Tuberculosis, acute, 704
   „ in sheep, goats, and pigs, 705
   „ of serous membranes, 694
   „ „ bones and articulations, 701
   „ „ lymphatic glands, 696
   „ „ the brain, 702
   „ „ „ digestive tract, 699
   „ „ „ genital organs, 700
   „ „ „ respiratory apparatus, 690
   „ „ „ skin, 703

 Tuberculous septicæmia, 704

 Tumours, bone, 30
   „ cerebral, 459
   „ of the gastric compartments, 202
   „ „ larynx, 335
   „ „ mediastinum, 369
   „ „ nasal cavities, 325
   „ „ ovary, 559
   „ „ testicle, 594
   „ „ udder, 585
   „ „ uterus, 559

 Turn-sick, 467

 Tympanites, chronic, 194


                                   U.

 Udder, congestion of the, 570
   „ cysts of the, 585
   „ tuberculosis of the, 701
   „ tumours of the, 585
   „ verrucous papillomata of the, 586

 Ulcerative gastritis, 191
   „ stomatitis in sheep, 125
   „ „ swine, 127

 Umbilical phlebitis, 402
   „ „ of new-born animals, 399

 Umbrella-tree family, 244

 Urachus, persistence of the, 508

 Urethrotomy in the ox, 747
   „ „ ram, 749

 Urinary apparatus, diseases of the, 502
   „ calculi in sheep, 518
   „ lithiasis, 514

 Urticaceæ, 229

 Urticaria in the pig, 656

 Ustilaginaceæ, 224

 Utero-ovarian phlebitis, 398

 Uterus, torsion of the, 556
   „ tumours of the, 559


                                   V.

 Vaccine, preparation of, 669

 Vaccinia, 665

 Vagina, imperforate, 560

 Vaginitis, 543
   „ acute, 544
   „ chronic, 546
   „ contagious, 545
   „ croupal, 545

 Veins, examination of, 372

 Verminous bronchitis in sheep and cattle, 340
   „ conjunctivitis, 662
   „ ophthalmia of the ox, 663

 Verrucous endocarditis of the pig, 710, 713

 Verrucous papillomata of the udder, 586

 Vesiculæ seminales, 597

 Vetches, poisoning by, 243

 Viciaceæ, 236

 Viscous milk, 589

 Vulva, suture of the, 768


                                   W.

 Warbles, 646

 Warts in oxen, 655

 Whitlow, 41

 White loco weed, poisoning by, 237

 Wild chervil, poisoning by, 248

 Wounds or traumatic lesions, 568


                                   Y.

 Yellow milk, 590

 Yew family, 226
   „ poisoning, 226


       BRADBURY, AGNEW & CO. LD., PRINTERS, LONDON AND TONBRIDGE

------------------------------------------------------------------------




                          BY THE SAME AUTHOR.


               _Royal 8vo, 438 pages, 406 illustrations._

A Handbook of Horse-shoeing.

  With Introductory Chapters on the Anatomy and Physiology of the
  Horse’s Foot. The section on the “Practice of Shoeing” contains 54
  full-page plates and descriptive notes supplied by ALBERT WHEATLEY,
  F.R.C.V.S.


         _60 large pages (14½ × 10 inches), 315 illustrations._

An Atlas of Veterinary Surgical Operations.


               _Demy 8vo, 42 pages, 16 full-page plates._

A Surgical Operating Table for the Horse.


               _Royal 8vo, 618 pages, 95 illustrations._

Studies in Clinical Veterinary Medicine and Surgery.

  By P. J. CADIOT and JNO. A. W. DOLLAR.


               _Royal 8vo, 269 pages, 272 illustrations._

The Practice of Veterinary Surgery.

                      VOL. I.—OPERATIVE TECHNIQUE.


               _Royal 8vo, 853 pages, 315 illustrations._

The Practice of Veterinary Surgery.

  By H. MÖLLER and JNO. A. W. DOLLAR.

                      VOL. III.—REGIONAL SURGERY.

------------------------------------------------------------------------




                          TRANSCRIBER’S NOTES


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 2. Retained archaic, non-standard, and uncertain spellings as printed.
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