TEXT BOOK
                                   OF
                          VETERINARY MEDICINE


                                   BY

                         JAMES LAW, F.R.C.V.S.

 Director of the New York State Veterinary College Cornell University,
                             Ithaca, N. Y.

                                VOL. II

       DISEASES OF THE DIGESTIVE ORGANS—LIVER—PANCREAS—AND SPLEEN


                                 ITHACA
                        PUBLISHED BY THE AUTHOR
                                  1900




                                                            Copyright by
                                                             JAMES LAW
                                                               1900


      PRESS OF
  ANDRUS & CHURCH
    ITHACA, N. Y.




                          VETERINARY MEDICINE.




                   DISEASES OF THE DIGESTIVE ORGANS.

  Second in importance to pulmonary complaints in solipeds; equal in
  ruminants. Extent of digestive organs and character of food, in
  carnivora, herbivora, and omnivora. Ruminant’s stomachs. Gastric
  fermentation. Foreign bodies. Torpor. Unwholesome fodder.


In the horse these maladies are only second in importance to those of
the respiratory organs, while in ruminants they are equally frequent and
important. The varying susceptibility of the digestive organs to disease
in different families and the special proclivity of different parts of
these organs may be, in great part, explained by the great variation in
the food, by the relative extent of the gastro-intestinal surface, and
by the amount of work devolving on the respective viscera.

In =carnivora= the entire gastro-intestinal surface is little more than
half the area of the skin, for their rich animal food does not require a
prolonged retention and an elaborate series of intricate processes to
insure digestion and absorption. This system of organs is accordingly
less liable to disorder in carnivora than in herbivora and omnivora. Add
to this that the carnivorous stomach is very capacious relatively to the
intestine, that the digestion of the great bulk of the food (nitrogenous
elements) is nearly completed in this viscus, and that the contents of
this organ are easily and completely discharged by vomiting whenever
they prove irritating, and we have ample explanation of the comparative
immunity of these animals from digestive disorders.

The =herbivora= stand at the opposite extreme, the gastro-intestinal
surface being over double the area of the skin in the horse, and nearly
three times that extent in the ox. The hard, fibrous and comparatively
innutritious vegetable food of these animals necessitates its prolonged
retention in the alimentary canal in order to the completion of
digestion and the absorption of the nutritive constituents. Hence the
great liability of the herbivora to diseases of the digestive organs.

=Omnivora= occupy a place intermediate between these two classes, as
regards both the nature of the food and the extent of surface of the
alimentary canal, and they are in similar ratio little liable to
digestive disorders. They have besides in common with carnivora a great
facility in the rejection of irritant matters by vomiting, and in thus
protecting themselves against gastric and intestinal disorders.

A fair idea of the area of the intestinal surface may be given by
stating the length of the canal relatively to that of the body:—in the
dog : : 6 : 1, in the rabbit : : 10 : 1, in the ass and mule : : 11 : 1,
in the horse : : 12 : 1, in swine : : 14 : 1, in the ox :: 20 : 1, and
in the sheep : : 27 : 1. The calibre of the intestine varies however and
with it the capacity. Thus in the relatively shorter intestine of the
horse, the capacity is much greater in ratio with the size of the animal
than is the relatively much longer intestine of the pig. The ox’s
intestine though twice the length of that of the horse has little more
than half the capacity.

Among =herbivora= the monogastric (horse, ass, mule), and polygastric
(ruminants) animals manifest varying pathological susceptibility
according to the relative development of the different digestive viscera
and the habitual character of their food. The horse and other large
solipeds have small stomachs (16 qts.) and capacious intestines (196
qts.). Digestion is restricted in the stomach and largely carried on in
the spacious bowels. The small stomach requires to be frequently
replenished in moderate amount, but, if this is secured, its liability
to disease is slight while that of the intestines is very considerable.
In the ox the stomachs have a total capacity of 252 qts., while that of
the intestines averages 103 qts. In this animal the capacious and hard
working stomach is a frequent seat of disorder, while the comparatively
small intestines are to a large extent exempt. The small stomach of the
horse is easily overloaded and disordered or paralyzed by an unusually
full feed of grain when hungry, or one of some specially appetizing
fodder, and the case is serious, as relief can rarely be obtained by
vomiting. For the same reason fermentation of the gastric contents with
evolution of gas and tympany usually proves fatal to the horse since
relief by eructation is too often impossible. Cattle are fitted to live
in damp localities where the cloven foot prevents sinking and getting
bogged, and where they may draw in with the tongue a full mouthful of
coarse herbage which they swallow with little mastication or admixture
with saliva. This lodges in the first two stomachs, and if, from any
cause, rumination is impaired, or suspended, it finds itself in
conditions especially favorable to fermentation. The food too, as in the
case of frosted roots, wet clover or partially ripened grain, etc., is
often charged with ferments (bacteria) in a state of great vital
activity, and hence the frequent tympanies of the ox. The ruminant is no
less liable than the soliped to overload the stomach, and though the
return of food from the first two stomachs to the mouth is a normal
process, this is promptly arrested by the supervention of paresis in the
overloaded and overdistended organs. This overdistension further tensely
stretches and closes the lips of the œsophagean opening. The rapid
swallowing of the food, with only one or two strokes of the teeth for
each morsel, renders the large ruminant more liable to take in poisons,
pins, nails and other injurious bodies, especially when hunger and the
blunting of the sense of smell have been brought on by traveling on
dusty roads. Again the large ruminants, and especially cows are wont to
while away the tedious hours by chewing and unwittingly swallowing
pieces of leather, cloth, bones, iron, etc. Once more the third stomach
in which the food is compressed and triturated between the multiple
folds, is normally comparatively dry, and is liable under dry, fibrous,
heating or stimulating aliment, or in case of fever, to dry up in part
or in whole, and to derange the whole process of digestion.

All herbivora are liable to disease from unwholesome fodder and the
resulting affection may prove epizootic in connection with unfavorable
seasons, or more local, from faulty cultivation.

The symptoms vary so much in connection with the seat and nature of the
disease that it would be impolitic to attempt to generalize them.




                         DISEASES OF THE MOUTH.

  Relative susceptibility to disease of the mouth: Food; irritants;
  bits; ropes; speculum; sharp metallic bodies; micro-organisms;
  functional; nervous.


These are met with in all domestic animals, but are above all common in
horses, oxen and pigs, partly because of special susceptibilities and of
the nature of the food, but largely by reason of the exposure of this
part to mechanical injuries, especially in horses and cattle. Hard bits
and the harder hands of cruel and ruthless drivers, nooses of rope tied
over the lower jaw and tongue, iron stirrup, clevis, or balling iron
used without cover to force the jaws apart, a large drenching horn
employed as a lever for the same purpose, an extemporized Yankee bridle
rudely applied or used in breaking a colt, the method of curing a
balking or jibbing horse by tying a rope to his lower jaw and to a bar
extending forward from the pole, pins, needles, thorns and other sharp
bodies, and irritants in food or medicine are among the causes of such
disorders. Then there are the many irritating microörganismal ferments
in food, water, mucus, etc., and irritant and hot medicines and food to
account for local inflammations.


                         FUNCTIONAL DISORDERS.

Among these are the convulsive closure of the jaws in _tetanus_, the
flaccid state of the lips, cheek, and tongue in _paralysis_, and the
pendent state of the lower jaw in _paralytic canine madness_. See these
different subjects.




                          STRUCTURAL DISEASES.
                  INFLAMMATION OF THE LIPS, CHEILITIS.

  Causes of Cheilitis: Local injuries; poisoned; envenomed; secondary
  disease. Symptoms: swelling; salivation; difficult prehension; cracks;
  blisters; ulcers; indurations. Treatment: obviate causes; astringents;
  antiseptics; derivatives; gravitation; for venoms antacid; antiseptic,
  Iodine.


_Causes._ Blows, pricks, wounds and bruises with bits or twitch, and
other mechanical and chemical irritants, irritant vegetables, bites of
leeches or snakes, stings of insects, etc. It may be a skin disease
dependent on disorder of some remote organ, or a local engorgement due
to a constitutional state. (See, Urticaria Surfeit, Purpura
hæmorrhagica, Variola, Strangles).

_Symptoms._ Swelling, stiffness, heat and tenderness of the lips, with
or without local abrasion, or incised or punctured wound. Food may be
entirely refused from inability to take it in with the rigid tender
lips, and saliva drivels from the mouth because of their imperfect
apposition. Cracks, blisters and raw sores or ulcers may or may not
supervene. In old standing cases the lips become indurated and
comparatively immobile.

_Treatment._ Remove the cause whether irritants in food, or drugs, sharp
pointed bodies lodged in the tissues, injuries by bit, twitch or
otherwise. Local applications have comparatively little effect, being
promptly removed by the tongue, yet a lotion of vinegar and honey;—of
borax 10 grains and honey or glycerine 1 oz.;—or of alum in a similar
medium will often prove useful. A dose of laxative medicine will favor
resolution, and if there is great tumefaction, feeding thick gruels from
high manger, and tying to a high rack so as to prevent drooping of the
head, will favor recovery. In snake bites and stings the local
application of aqua ammonia and its administration internally (horse and
cow 1 oz., sheep 2 dr. in 20 times its volume of water) should be
practiced; or permanganate of potash may be used.

When the heat and tenderness subside, leaving much thickening and
induration it may be repeatedly painted with a lotion of one part of
tincture of iodine in three parts of glycerine.




                   CANCROID OF THE LIPS. EPITHELIOMA.

  Epithelioma: Animals susceptible; accessory causes; symptoms; lesions.
  Treatment: Warts and polypi. Actinomycosis: Wounds; abrasions;
  infection atria. Symptoms; treatment. Trombidiosis: infected regions;
  not compulsory parasite; European and American trombidia; distinct
  from chigoe. Symptoms. Treatment.


This has been observed in the cat and the horse, commencing at the angle
of the mouth and doubtless partially determined in the latter animal by
the irritation of the bit.

It is characterized by thickening of the tissues of the lips, in the
form of small irregularly rounded masses, and tending to the formation
of a spreading ulcer. The thickened tissues are invaded, pushed aside
and infiltrated by epithelial or epithelioid cells, which, no longer
confined to the surface as in the natural state, grow in the interior of
the tissues and destroy them.

_Treatment._ The disease has little tendency to cause secondary deposits
in other organs and may often be arrested by local measures. In its
earliest stages it may be arrested by the thorough removal of the
diseased structures with the knife, the resulting deformity being
obviated by bringing the raw edges together by suture, so as to secure
their adhesion, or the actual cautery may be used. The tendency to
irritation from putrefaction products escaping from the mouth may be
counteracted by occasional sponging with a weak lotion of carbolic acid
(1 part to 50 of water) or an ointment of one part of very finely
powdered boracic acid to two parts of simple ointment.

Leblanc has repeatedly succeeded in these cases by the use of chlorate
of potash, locally and generally. The local application may be a
solution of two drachms in four ounces of water, while the dose of the
powder for the horse is 2 to 4 drachms daily.

=Warts and Polypi.= These are common on the outer and even the inner
side of the lips, especially in dogs. They are easily removed by the
scissors, after which their roots should be thoroughly cauterized with a
pointed stick of lunar caustic or chloride of zinc.




                       ACTINOMYCOSIS OF THE LIPS.


In the rich river bottom lands of northern Germany and Russia where
actinomyces abound actinomycosis is common in the form of papillæ of
greater or lesser size on the lips and nose of horse and ox. The
abrasion of these parts by thorns, thistles, stubble, dry fibrous
fodders and other irritants, appears to produce a raw surface for the
colonization of the germ, which is not slow to avail of the opportunity.
The resulting lesions take the appearance of warty looking elevations,
more or less indurated, which on section show the sulphur yellow
actinomyces tufts of club-shaped cells converging to a central mycelial
mass.

_Treatment_ is simple as the disease is at first essentially local, and
is easily checked by the local application of iodine. The wartlike
elevations may be shaved off with a razor or cut off with sharp scissors
and the surface painted once or twice daily with tincture of iodine. If
there is suspicion of distant or deepseated actinomycosis the internal
treatment with potassium iodide will be in order.


            TROMBIDIOSIS OF THE NOSE AND LIPS. HARVEST ITCH.

In different parts of Europe and America, and especially in the warmer
regions, or in sheltered gardens, shrubberies, and pastures, different
species of the trombidium abound, and the young hexapod larvæ attack man
and beast, burrowing under the cuticle and giving rise to extreme
itching and persistent and irritating rubbing of the affected part.
These parasites belong to the family of acari or mites, so that the
condition they produce is one of acariasis or mange, only the offender
is not a compulsory parasite, but appears to survive in certain soils
and in the vegetation independently of animal hosts. Their parasitism is
therefore accidental and non-essential to their survival.

The trombidian parasite usually found in Europe is the Trombidium
Holosericeum or silky trombidium, so small (in its larval state) that it
is just visible to the naked eye as a bright scarlet point when moving
on a dark background. It was formerly called Leptus Autumnalis and is
familiarly known as the red beast, _bete rouge_, _harvest bug_, etc. The
common American species is of a dull brick red, so that it is less
easily detected even on a dark background. It is familiarly known as the
_jigger_, though quite distinct from the _chigoe_ or burrowing flea of
the West Indies.

The domestic herbivora get these parasites on the nose and lips while
browsing on the pastures and contract an intolerable itching which may
lead to violent rubbing, abrasions and scabby exudations. The skin
becomes thickened, scabby and rigid, and as new accessions are
constantly received the malady continues until cold weather sets in. The
affection is not in any sense dangerous, and the attacks may be warded
off by a daily application of one of the common parasiticides—decoction
of tobacco, tar water, solution of creolin, naphthalin, etc. The mere
seclusion of the infested animal indoors, without green food, will cure,
as the larvæ pass through their parasitic stage in a few days and drop
off.


           GENERAL CATARRHAL STOMATITIS. BUCCAL INFLAMMATION.

  Mature animals most subject: Causes in horse, mechanical, chemical,
  microbian irritants—alkalies, acids, caustics, hot mashes, ferments,
  fungi, rank grasses, excess of chlorophyll, clover, alfalfa, acrid
  vegetables, bacterial infection secondary, acrid insects in food;
  symptomatic of gastritis, pharyngitis, diseased teeth, specific
  fevers. Symptoms: Congestion and tumefaction of buccal mucosa, lips
  and salivary glands; Epithelial desquamation; fœtor; salivation;
  froth; papules; vesicles. Prognosis. Treatment: Cool soft food;
  antiseptics; wet applications to skin; derivatives.

This is much more common in the adult than in suckling domestic animals.
None of the domestic mammals or birds can be considered immune from it,
but as its causes and manifestations differ somewhat it seems well to
consider it separately in the different genera.




               GENERAL CATARRHAL STOMATITIS IN SOLIPEDS.


_Causes._ These may be classed as mechanical, chemical, microbian and
other irritants. In the horse it is often due to the reckless
administration of irritant liquids as remedies. Owing to the length of
the soft palate the horse can refuse to swallow any liquid as long as he
chooses, and some of the worst cases of stomatitis I have seen resulted
from the retention in the mouth of caustic alkaline liquids given under
the name of “_weak lye_.” Strong acids and caustic salts dissolved in
too little water or other excipient, or suspended in liquids in which
they cannot dissolve, or made into boluses which are crushed between the
teeth are not infrequent conditions. Too hot mashes given to a hungry
horse is another cause of this trouble. Fermented or decomposed food is
often most irritating. Coachmen will sometimes induce it by attaching to
the bit bags of spicy or irritant agents, to cause frothing and make the
animal appear spirited.

Fungi in fodders are among the common causes. The rust of wheat
(puccinia graminis), the caries of wheat (tilletia caries), the blight
(erysiphe communis), ergot (claviceps purpurea), the fungus of rape
(polydesmus excitiosus) and the moulds (penicillium and puccinia) have
all been noticed to coincide with stomatitis, and charged with producing
it. On the other hand, at given times, one or other of these cryptogams
has been present extensively in the fodder without any visible resultant
stomatitis. The apparent paradox may be explained by the fact that these
fungi vary greatly in the irritant or harmless nature of their products
according to the conditions under which they have grown, and the stage
of their development at which they were secured and preserved. Ergot
notoriously differs in strength in different years, on different soils,
under various degrees of sunshine, shade, cloud, fog, etc. In different
States in the Mississippi valley it is not uncommon to find stomatitis
in horses in winter, fed on ergoted hay, while cattle devouring the same
fodder have dry gangrene of feet, tail and ears. Yet in other seasons
the ergot fails to produce these lesions. Rank grown, watery vegetation,
especially if it contains an excess of chlorophyll is liable to cause
stomatitis. Red and white clover, trefoil, hybrid and purple clover, and
alfalfa have all acted more or less in this way, though in many cases,
the food has become musty or attacked by bacterial ferments. Some of the
strongly aromatic plants, and those containing acrid principles (cicuta
virosa, œnanthe crocata, mustard, etc.) cause buccal inflammation and
salivation.

The irritation in many such cases is not due to one agent only, the
vegetable or other irritant may be the starting point, acting but as a
temporary irritant, the action of which is supplemented and aggravated
by the subsequent attacks of bacterial ferments on the inflamed,
weakened or abraded tissues. The bacteria present in the mouth, food or
water would have had no effect whatever upon the healthy mucosa, while
they make serious inroads on the diseased. On the other hand the
vegetable, mechanical or chemical irritant would have had but a
transient effect, but for the supplementary action of the bacteria.

In horses that have the bad habit of retaining masses of half masticated
food in the cheeks the growth of cryptogams is greatly enhanced and such
food often becomes violently irritating.

Among other mechanical causes may be named pointed or barbed hairs or
spines (barley awns, spikes, thorns, etc.) which, lodging in a gland
orifice, or in a wound of the gum or mucosa, form a source of irritation
or a centre for bacterial growth and abscess.

Again, irritants of animal origin must be named. These are not taken by
choice, but when lodged in fodder, or in the pastures they are taken in
inadvertently with the food. In this way poisonous insects, and
especially hairy caterpillars, cantharides, potato bugs, etc., gain
access to the mouth.

It must not be overlooked that stomatitis occurs as an extension,
sympathetic affection or sequel of diseases of other organs. Gastritis
is usually attended by redness and congestive tenderness of the tongue,
especially of the tip and margins, and other parts of the buccal mucosa,
notably the palate just back of the incisors, are often involved. In
other cases it appears as a complication of pharyngitis, laryngitis, of
affections of the lower air passages, of the teeth and periodontal
membrane or of the salivary glands.

It appears also in a specific form in certain fevers, as in horsepox,
pustulous stomatitis, aphthous fever and even in strangles. Mercurial
stomatitis, rarely seen at the present time, is one of the worst forms
of the disease, and like the infectious forms will be treated
separately.

_Lesions and Symptoms._ At the outset and in the slighter forms of
congestion there is merely heat and dryness of the buccal mucosa.
Redness may show on the thinner and more delicate portions of the
membrane, as under the tongue, on the frænum, and on the sublingual
crest. But elsewhere it is hidden by the thickness of the epithelium,
and the manifestations are merely those of suppressed secretion with
local hyperthermia.

As the congestion is increased there is seen, even at this early stage,
a slight thickening or tumefaction of the mucosa, especially on the
gums, lips, the sublingual area, the orifices of the salivary glands,
and the palate back of the upper incisors. On the dorsum of the tongue,
the cheeks and lips, generally the lack of loose connective tissue tends
to prevent the swelling.

With the advance of the inflammation the redness of the mucosa extends,
at first in points and circumscribed patches, and later over the entire
surface. The epithelium drying and degenerating in its surface layers
forms with the mucus a sticky gummy film on the surface, which, mingling
with decomposing alimentary matters gives out a heavy, offensive or even
fœtid odor.

The different parts of the mouth are now tender to the touch, and this,
with the fœtor and even bitterness of the bacterial products combine
with the general systemic disturbance in impairing or abolishing
appetite. In any case mastication becomes slow and infrequent, and
morsels of food are the more likely to be retained, to aggravate the
local condition by their decomposition.

The dry stage is followed by the period of hypersecretion, and in this
the salivary glands take a prominent part, so that ptyalism (slobbering)
becomes the most marked feature of the disease. The saliva mixed with
the increasing secretion of mucus and the abundance of proliferating and
shedding epithelium, escapes from the lips and falls in stringy masses
in the manger and front of the stall. When there is much motion of the
jaws and tongue it accumulates as a froth around the lips.

A careful examination of the mucosa will sometimes detect slight conical
elevations with red areolæ, representing the tumefied orifices of the
obstructed mucous follicles, and later these may show as minute
erosions. Even vesicles have been noticed (Weber, Dieckerhoff, Kosters),
but when these are present one should carefully exclude the specific
stomatites such as horsepox, contagious pustular stomatitis, aphthous
fever, etc.

Erosions of the mucosa and desquamation of the epithelium have been
noticed in horses fed on purple (hybrid) clover, buckwheat or ergot, and
in some of these cases the inflammation has extended (in white faces
especially) to the skin of the face, the mucosa of the nose, and the
adjacent glands, and as complications icterus, constipation, colics,
polyuria, albuminuria and paresis of the hind limbs have been observed.
These latter are common symptoms of cryptogamic poisoning.

_Prognosis._ In uncomplicated cases the disease is not a grave one,
lasting only during the continued application of the local irritant, and
recovering more or less speedily when that has been removed.
Complications are dangerous only when due to some specific disease
poison (glanders, actinomycosis, strangles, etc.), and even poisoning by
the usual cryptogams of leafy or musty plants is rarely persistent in
its effects.

_Treatment._ This resolves itself into the removal of the irritant cause
and the soothing of the irritation. When the cause has been definitely
ascertained the first step is easy.

In the direction of soothing treatment, a careful selection of diet
stands first. Fibrous hay and even hard oats, barley or corn may have to
be withheld, and green food, or better still, bran mashes, gruels,
pulped roots or fruits allowed. Scalded hay or oats, ensilage, sliced
roots, or ground feed may often be taken readily when the same aliments
in their natural condition would be rejected or eaten sparingly.

Medicinal treatment may often be given in the drinking water which
should always be allowed in abundance, pure and clean. In the way of
medication chlorate of potash, not to exceed one-half to one ounce per
day according to the size of the animal, may be added, together with an
antiseptic (carbolic acid, borax, permanganate of potash, common salt,
naphthol, creolin, hyposulphite of soda). In case of severe swelling, a
cap made to fit the head with strips wet in alum and vinegar or other
astringent solution maintained against the intermaxillary space may be
desirable. Support for the tongue may be necessary as mentioned under
glossitis.

In case of complications on the side of the bowels, liver or kidneys,
laxatives, diuretics and antiseptic agents may be called for.


                GENERAL CATARRHAL STOMATITIS IN CATTLE.

  Dense resistant mucosa protective: Affection usually circumscribed.
  Action of violent irritants, and toxins of specific fevers. Mechanical
  irritants. Symptoms: Salivation; congestion; eruptions; erosions;
  ergot; acrid vegetables; caustics. Treatment: Astringents;
  antiseptics; refrigerants; derivatives; tonics. Removal of foreign
  bodies. Lesions and symptoms in sheep.

The mouth of the ox as Cadeae well says has a cuticular epithelium too
thick and resistant to be easily attacked by microbes. It follows that
infected inflammations are far more frequently circumscribed than in the
thinner and softer buccal mucosa of the horse. The more general buccal
inflammations come more particularly from the use of food that is too
hot or that contains strongly irritant agents. The thickness of the
buccal epithelium however, is no barrier to the local action of poisons
operating from within as in rinderpest, or aphthous fever, or in
malignant catarrh, nor is it an insuperable barrier to the local
planting of the germs of cow pox, anthrax, actinomycosis, or cryptogamic
aphtha (muguet). The wounds inflicted by fibrous food make infection
atria for such germs, hence the great liability to such local
inflammations, in winter when the animals are on dry feeding. For the
same reason, perhaps, the prominent portions of the buccal mucosa,—the
papillæ—are sometimes irritated themselves while serving as protectors
for the general mucous surface, and hence they become specially involved
in inflammation, which constituted the “_barbs_” of the old farriers.
Utz records a buccal inflammation occurring in herds fed on green
trefoil, first cutting, showing that even in cattle this agent may
determine a general stomatitis.

_Symptoms._ These do not differ from those of the horse, and resemble,
though often in a milder form, the buccal manifestations of aphthous
fever. There is the difficulty of mastication and indisposition to take
in fibrous aliment, the drivelling of saliva from the mouth, or its
accumulation in froth around the lips, the frequent movement of the
tongue and jaws, and the congestive redness, papular eruption,
vesication, or even erosion of the affected mucous membrane. It is
always necessary to guard against confounding the simple stomatitis, and
the slighter infected inflammations, from the more violent infections
above referred to. The special diagnostic symptoms must be found under
the respective headings. The aphthous fever is not to be expected in
American herds, but the stomatitis which is associated with ergot in the
food is met more particularly in winter and spring, and must not be
confounded with the specific disease, on the one hand nor with the
simpler forms of buccal inflammation on the other. In the case of
ergoted fodder the signs of ergotism in other situations will be found,
in the affected animals, such for example as necrotic sloughs and sores
around the top of the hoof, sloughing of the hoof or of one or more
digits, or of the metatarsus, of the tip of the tail or ear; abortions,
convulsions, delirium, lethargy or paralysis. If not seen in the same
animals some of these forms may be observed in other members of the
herd. Then the buccal lesions are in themselves characteristic: soft,
whitish, raised patches of the epithelium (rarely blisters) are followed
by desquamation and exposure of the red, vascular surface beneath, and
this tends to persist if the ergoted fodder is persisted in.

_Treatment._ Simple stomatitis of the ox generally tends to spontaneous
and early recovery. The simplest astringent and antiseptic treatment is
usually sufficient to bring about a healthy action. Borax given in the
drinking water, not to exceed four ounces per day, or the same amount
mixed with syrup or honey and smeared occasionally on the tongue, or
hyposulphite or sulphite of soda, or weak solutions of carbolic acid
will usually suffice, after the irritant cause has been removed.
Vinegar, or highly diluted mineral acids may be used but are somewhat
hurtful to the teeth. Decoctions of blackberry bark or solutions of
other vegetable astringents may be used as alternatives. When there is
evidence of irritant matters in the stomach or bowels, a saline laxative
will be advisable to be followed by vegetable bitters or other tonics.
Thorns and other foreign bodies imbedded in the tongue or other part of
the mouth must be discovered and removed.


                     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.


                 GENERAL CATARRHAL STOMATITIS IN DOGS.

  Causes: burns; spiced food; bones; sepsis; ferments; pin caterpillar;
  dental and gastric troubles. Symptoms: careful prehension and
  mastication; congestion; swelling; eruption; erosion; furred tongue;
  stringy salivation; fœtor; swelling of lips, cheeks, intermaxillary
  space, and pharynx. Treatment: demulcent foods; antiseptics;
  derivatives; tonics; care of teeth and gums.

_Causes._ Hot food is a common cause in hungry dogs. Spiced food in
house dogs fed scraps from the table tend to congestion of mouth and
stomach alike. Irritation through wounds with bones, especially in old
dogs with failing teeth, and in exceptional cases the impaction of a
bone between the right and left upper molars are additional causes.
Putrid meat must also be recognized as a factor, the septic microbes
seizing upon the wounds and spreading from this as an infecting centre.
Lactic acid and other irritant products developed through fermentation
of particles of food retained about the gums and cheeks soften the
epithelium and irritate the sub-epithelial tissue, causing congestion.
Megnin draws attention to the fact that the pin caterpillar (bombyx
pinivora) found on the stalks of couch grass (Triticum repeus) produces
buccal irritation when chewed and swallowed to induce vomiting. As in
other animals more or less buccal congestion attends on gastric
congestion and inflammation. Dental troubles are often sufficient
causes.

_Symptoms._ The animal becomes dainty with regard to his food, picking
up the smaller or softer pieces and rejecting the larger or harder.
Mastication is painful and selection is made of moist or soft articles
which can be swallowed without chewing or insalivation. The mouth is red
and hot, and at times the mucous membrane eroded, or blistered, the
lesions concentrating especially on the gums and around the borders of
the tongue. The dorsum of the tongue is furred, whitish, yellowish or
brownish. Saliva collects in the mouth and escapes in filmy strings from
its commissures, and the odor of the mouth becomes increasingly foul.
Swelling of the lips, cheeks or intermaxillary space marks the worst
cases.

_Treatment._ Withdraw all irritant and offensive aliments. Give soups,
mushes, scraped or pounded lean meat in small quantities, washing out
the mouth after each meal with a 20 per cent. solution of permanganate
of potash or borax or a two per cent. solution of carbolic acid. Cadeac
advises against chlorate of potash on account of its known tendency to
bring about hæmoglobinæmia in dogs. A laxative and bitters may be called
for in case of gastritis or indigestion, and any morbid condition of the
teeth must be attended to. Decayed teeth may be removed. Tartar
especially must be cleaned off by the aid of a small wooden or even a
steel spud and a hard brush with chalk will be useful. A weak solution
of hydrochloric acid is usually employed to loosen the tartar, but this
is injurious to the structure of the teeth and had best be avoided if
possible. Tincture of myrrh is especially valuable both as a gum-tonic
and as a deodorant and antiseptic. This may be rubbed on the irritated
gums as often as the mouth is washed.




                 GENERAL CATARRHAL STOMATITIS IN SWINE.

  Causes: Irritants; ferments; noose on jaw; specific poisons. Symptoms:
  Careful feeding; thirst; frothy lips; champ jaws; redness; swelling;
  fœtor. Treatment: Cooling, astringent, antiseptic lotions; mushy food;
  derivative; tonics.


_Causes._ Swine suffer from simple stomatitis when exposed to thermal,
mechanical or chemical irritants. Food that is too hot, or that which is
hard and fibrous, or that 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. Thus 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_ are like as 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 odor.

_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, or well kept ensilage may be used,
and clean, cool water should be constantly within reach. In case of
overloaded stomach or indigestion a laxative followed by bitter tonics
will be in order.




                  CATARRHAL STOMATITIS OF BIRDS. PIP.

  Causes: hurried breathing; local irritants; exposure; filthy roost.
  Symptoms: gaping; roupy cry; epithelial pellicle on tongue, larnyx. or
  angle of the bill. Treatment: pick off pellicle; smear it often with
  glycerized antiseptic. Remove accessory and exciting causes.


This form of inflammation of the tongue of birds is characterized by the
increased production and desiccation of the epithelium so that it takes
on a horny appearance. According to Cadeac it may accompany various
inflammatory affections of the air passages, which cause hurried
breathing with persistently open bill, and thus entail evaporation of
the moisture. More commonly it has its primary cause in local
inflammation of the surface in connection with damp, cold, draughty
hen-roosts, and above all, the accumulation of decomposing manure and
the exhalation of impure gas. Even in such cases the abnormal breathing
with the bill open is an accessory cause of the affection.

_Symptoms._ The breathing with open bill should lead to examination of
the tongue, but above all if at intervals the bird with a sudden jerk of
the head emits a loud shrill, raucous sound, which reminds one of the
cough of croup. The tip and sides of the tongue are found to be the seat
of a hard, dry, and closely adherent epithelial pellicle, which suggests
a false membrane.

_Treatment._ The common recourse is to pick or scrape off the indurated
epithelial mass, leaving a raw, bleeding surface exposed. This is then
treated with a solution of borax, or chlorate of potash. Cadeac
deprecates this treatment as useless and dangerous, and advises the
disintegration of the dry epithelial mass with a needle taking care not
to prick nor scratch the subjacent sensitive tissue, and to wash with a
5 per cent. solution of chlorate of potash. A still more humane and
effective method is to make a solution of hyposulphite of soda in
glycerine and brush over the affected surface at frequent intervals.
This may be conveniently applied through the drinking water.

In case of implication of the lower air passages or lungs, the treatment
must be directed to them, and soft, warm, sloppy food and the inhalation
of water vapor will prove of great advantage. Secure clean, sweet, dry
pens, pure air, and sunshine. (See pseudo membranous enteritis.)




                           LOCAL STOMATITIS.

  Division of circumscribed buccal inflammations: palatitis; gnathitis
  gingivitis; glossitis. Causes: injuries; acrid; venomous or caustic
  agents; diseased teeth; foreign bodies in gland ducts; malformed jaws;
  infections, etc. Symptoms: salivation; difficult prehension and
  mastication; dropping half masticated morsels; distinctive indications
  of different caustics; abrasion; abscess; slough; infective disease
  lesions. Treatment: for _palatitis_, massage by hard corn ears,
  scarification, laxatives; for _gnathitis_, care for teeth and ducts,
  astringent washes, eliminate mercury; for _glossitis_, remove cause,
  use antidote to venom, or to chemical irritant, astringent, antiseptic
  lotions or electuaries, evacuate abscess, soft, cool diet, elevate the
  head, suspend the tongue.


Localized inflammations in the buccal cavity are named according to the
portion of the lining membrane attacked;—_palatitis_ if seated in the
roof of the mouth; _gnathitis_ if restricted to the cheeks; _gingivitis_
if to the gums; and _glossitis_ if to the tongue.

=Palatitis. Lampas. Congestion of the hard palate behind the upper front
teeth.= This is usually seen in young horses during the period of
shedding the teeth and is caused by the irritation and vascularity
consequent on teething. The red and tender membrane projects beyond the
level of the wearing surfaces of the upper incisors, and may materially
interfere with the taking in of food. A common practice in such cases is
to feed unshelled Indian corn, the nibbling of which seems to improve
the circulation in the periodontal membrane and by sympathy in the
adjacent palate. Superficial incisions with the lancet or knife will
usually relieve, and may be followed by mild astringent lotions if
necessary. If apparently associated with costiveness or gastric or
intestinal irritation a dose of physic will be demanded. Nothing can
excuse the inhuman and useless practice of burning the parts with a hot
iron.

=Gnathitis. Inflammation of the Cheeks.= Usually resulting as a distinct
affection from irregular or overgrown teeth, or the entrance of
vegetable spikes into the gland ducts, these cause local swelling and
tenderness, slow imperfect mastication, dropping of food half chewed,
accumulation of food between the cheeks and teeth, thickening,
induration and sloughing of the mucous membrane with excessive fœtor.

_Treatment._ Consists in correcting the state of the teeth and ducts and
using one of the washes recommended for glossitis.

=Gingivitis. Inflammation of the gums.= This is either connected with
the eruption of the teeth in young animals and to be corrected by
lancing the swollen gums and giving attention to the diet and bowels; or
it is due to scissor-teeth or to the wear of the teeth down to the gums
in old horses; or it is dependent on diseased teeth, or mercurial
poisoning, under which subjects it will be more conveniently considered.
Barley awns or other irritants must be extracted.

=Glossitis, Inflammation of the Tongue.= _Causes._ Mostly the result of
violence with bits, ropes, etc., with the teeth, or with the hand in
giving medicine; of scalding food, of acrid plants in the food: of
irritant drugs (ammonia, turpentine, croton, lye, etc.), or of sharp,
pointed bodies (needles, pins, thorns, barley and other barbs, etc.)
which perforate the organ. In exceptional cases leech and snake bites
are met with especially in cattle, owing to the tongue being exposed
when taking in food. Local infections and those of the specific forms,
determine and maintain glossitis.

_Symptoms_: Free flow of saliva, difficulty in taking in food or
drinking, and red, swollen, tender state of the tongue, which in bad
cases hangs from between the lips. The mucous membrane may be white,
(from muriatic acid, alkalies, etc.), black, (from oil of vitriol, lunar
caustic, etc.), yellow, (from nitric acid, etc.), or of other colors
according to the nature of the irritant. It may be raised in blisters,
may present red, angry sores where the epithelium has dropped off; may
become firm and indurated from excessive exudation; may swell and
fluctuate at a given point from the formation of an abscess; or may
become gangrenous in part and drop off. Breathing is difficult and noisy
from pressure on the soft palate. There is usually little fever and
death is rare unless there is general septic infection.

_Treatment_ will depend on the cause of injury. In all cases seek for
foreign bodies imbedded in the organ and remove them. If snake bites are
observed use ammonia or potassium permanganate locally and generally, or
cholesterin as a local application. If the irritation has resulted from
mineral acids, wash out with calcined magnesia lime water, or
bicarbonate of soda or potash. If from alkalies (lye) use weak vinegar.
If from caustic salts employ white of egg, vegetable-gluten, boiled
linseed, slippery elm, or other compound of albumen or sheathing agent.
In ordinary cases use cold astringent lotions, such as vinegar and
water; vinegar and honey; borax, boric or carbolic acid, chlorate of
potash, alum or tannin and honey. Poultices applied around the throat
and beneath the lower jaw are often of great value. The bowels may be
relieved if necessary by injections, as it is usually difficult to give
anything by the mouth. If ulcers form touch them daily with a stick of
lunar caustic or with a fine brush dipped in a solution of ten grains of
that agent in an ounce of distilled water. For sloughs use a lotion of
permanganate of potash, one drachm to one pint of water, or one of
carbolic acid, one part to fifty of water. If an abscess forms give a
free exit to the pus with the lancet, and afterward support the system
by soft nourishing diet, and use disinfectants locally. As in all cases
of stomatitis, the food must be cold gruels or mashes, or finely sliced
roots will often be relished.

The mechanical expedient of supporting the tongue in a bag is essential
in all bad cases, as if allowed to hang pendulous from the mouth
inflammation and swelling are dangerously aggravated.


              APHTHOUS STOMATITIS. FOLLICULAR STOMATITIS.

  Causes: in horse, ox, dog; rough, fibrous food, blistering ointments,
  bacteria. Symptoms: general stomatitis, and special; papules with
  grayish centres and red areolæ, vesiculation, ulceration. Treatment:
  Astringent, antiseptic, derivative, tonic, stimulant.

This is a rare affection in ruminants where the thickness of the
epithelial covering appears to be a barrier to infection or injury,
while it is common in the more delicate and sensitive buccal mucosa of
the horse and dog. In the horse the ingestion of irritant plants with
the food and the penetration of vegetable barbs into the mucous
follicles may be charged with causing the disease, while in both horse
and dog the licking of blistering ointments and the local action of
fungi and bacteria are factors in different cases.

_Symptoms._ With the ordinary symptoms of stomatitis, there appear
minute firm, whitish, circular elevations representing the openings of
the inflamed mucous or salivary follicles, having a reddish areola, and
grayish white vesicular centre. They may amount to a line or more in
diameter, and on bursting leave red cores or ulcers. The whole mouth may
be affected or the disease may be confined to the lips, gums or tongue.

_Treatment._ Beside the general astringent washes, this affection is
greatly benefited by the local use of antiseptics, as sulphite or
hyposulphite of soda, 2 drachms in a quart of water. Borax, permanganate
of potash, carbolic acid or other antiseptic in suitable solution may be
substituted. Saline laxatives are often useful to remove sources of
irritation in stomach and intestines, and iron salts (chloride or
nitrate) in full and frequently repeated doses may be given internally.
Ulcers may be cauterized and soft food and pure water given from an
elevated manger.


             ULCERATIVE STOMATITIS. GANGRENOUS STOMATITIS.

  Causes: specific disease poisons; debility; rachitis; cancer; chronic
  suppuration; irritation—mechanical, chemical, thermic, venomous, etc.
  Symptoms: difficult, imperfect prehension and mastication, salivation,
  bleeding, swollen, puffy epithelium, blisters, extending erosions,
  deep or spreading. Duration. Treatment: correct constitutional fault,
  tonics, soft, digestible food, antiseptics, mild caustics.

This is characterized by the formation of necrotic spots and patches of
the buccal epithelium, with desquamation, and the formation of more or
less rodent ulcers of the sub-epithelial mucosa. Like other ulcerative
processes it is usually due to microbic invasion, and in this way it may
supervene on other and simpler forms of stomatitis. It also varies in
its manifestations and nature according to the genus of animal, and the
specific microbe present.




                   ULCERATIVE STOMATITIS IN SOLIPEDS.


_Causes._ Apart from the ulcerations and erosions of specific diseases
(glanders, horsepox, pustulous stomatitis, aphthous fever, etc.,) this
condition is especially liable to appear in anæmic and debilitated
subjects (Cauvet), as in rachitis (Friedberger and Fröhner), cancer
(Cadeac) chronic internal abscess (Cadeac), etc. As an exciting cause
and as a means of furnishing an infection atrium for the microbes of
ulceration all conditions of simple lesion of the mucous
membrane—mechanical, chemical, thermic, venomous, etc., are operative.
Dieckerhoff has described it in connection with diphtheritic rhinitis,
Friedberger with a nasal and conjunctival catarrh, Zeilinger and Kohler
with aphthous fever, Mobius and Hackbarth with trefoil poisoning.

_Lesions and Symptoms._ There is the usual dainty feeding and
disposition to masticate imperfectly or even to drop the partly
insalivated morsels, working of the lips, the formation of froth on
their margins, and the drivelling of saliva in long strings or
filaments. As the disease advances this becomes bloody and fœtid. The
local lesions may be at first like white pulpy spots of softened and
degenerating epithelium, which is exceptionally, raised in blisters.
This is followed by desquamation and the formation of open sores which
are indolent, and show a disposition to further erosion and extension.
They may be rounded or irregularly indented in their borders, and
contain a brownish, blackish or greenish viscid debris. They vary
widely, however, in general appearance and in their disposition to
speedy or sluggish healing, being apparently influenced by the nature of
the pathogenic microbe and the susceptibility of the subject. In some
cases the molecular degeneration extends deeply into the mucosa, and
even over the edges of the lips into the adjacent skin. Recovery and
complete cicatrization may take place in one week, or successive
outbreaks may take place in the same animal lasting in all for months as
in Cadeac’s case associated with chronic abscess of the mesentery.

_Treatment._ The first consideration is to correct the debility on which
the affection is based. Iron and bitter tonics, mineral acids, and
nourishing food given in the form of soft mashes, pulped roots, or
farinas, which will require little mastication, and the antiseptic
cleansing of the mouth after each meal are the main features of the
treatment. As antiseptics, vinegar is inimical to the microbes of the
mouth, which affect alkaline media, borax, boric acid, carbolic acid,
sulphurous acid, the sulphites and hyposulphites, permanganate of
potash, chlorate of potash, creolin, and sulphate or chloride of iron
furnish a sufficient choice of comparatively nontoxic agents. Ulcers may
be touched with tincture of iodine, lunar caustic, or sulphate of
copper.


             ULCERATIVE STOMATITIS (DIPHTHERIA) IN CALVES.

  Accessory causes. Infection. Experimental inoculation. Bacillus, grows
  on blood serum. Lesions in mouth, nose, air passages, intestines,
  digits. Symptoms: difficult sucking, fever, swollen, whitish spots on
  buccal mucosa, phagadenic sores, fœtor, symptoms of extending disease,
  anorexia, debility, prostration. Duration. Diagnosis from foot and
  mouth disease, from actinomycosis, from tuberculosis. Prevention:
  cleanliness, antisepsis, segregation, diet of dam, sterilized milk.
  Treatment: antiseptic and eliminating: locally antiseptic.

This has been observed at frequent intervals in calves, as a serious,
fatal, communicable disorder occurring in the first few weeks of life.

_Causes._ It has been attributed to unhygienic conditions of the dams,
close, damp, impure stables, unwholesome or spoiled food, and privations
of various kinds, and these, in all probability, increase the
susceptibility. The congestion and traumatism connected with the cutting
of the teeth is another predisposing cause. The ultimate cause is,
however, the contagious element and the disease has been conveyed to
healthy lambs by the introduction into their mouths of the necrotic
products from the diseased subjects (Dammann). Sheep inoculated in the
conjunctiva presented violent conjunctivitis in forty-eight hours.
Inoculated rabbits died of septicæmia. Mice showed the same symptoms as
calves, while guinea pigs showed an abscess only at the seat of
inoculation (Löffler).

The identity of the germ has not been fully demonstrated. Dammann found
a micrococcus, but testimony from the inoculation of its pure cultures
is wanting, and the buccal mucosa of the sucking calf is full of varied
germs some of which are irritating and pathogenic to an injured mucosa.

Löffler found in the epithelial concretions (false membranes) of the
mouth and intestines, a bacillus of half the thickness of the bacillus
of malignant œdema, five times as long as broad and usually connected
with its fellows to form filaments. He failed to obtain cultures of this
in nutrient gelatine, but grew it successfully in blood serum from a
calf. Transferred to fresh serum the culture failed. The pure culture
does not seem to have been tried on the calf.

According to Dammann the lesions occur indiscriminately in the mouth,
the nose, the larynx, trachea, lungs, the intestinal canal and the
interdigital space.

It has been suggested that the mouth of the calf rendered susceptible by
the congestion caused by suction, is infected by licking the previously
infected umbilicus.

_Symptoms._ There are the usual symptoms of indisposition to suck,
salivation, redness of the buccal mucosa, and general indisposition. In
two or three days the mucosa shows raised, pulpy, white or grayish
patches about a line in diameter. These gradually soften and break down
and in four or five days leave dark red angry sores one-sixth to
one-third inch in diameter dotted with grayish points and surrounded by
a congested areola. These exhale an offensive odor and tend to extend in
superficial area and in depth, invading indiscriminately the various
subjacent tissues. The lips may be perforated, the muscles, cartilages,
periosteum, and periodontal membrane invaded, the teeth may be shed, and
the alveoli filled with the offensive debris of ulceration. Swelling of
the throat may follow from implication of the pharynx and its lymph
glands, symptoms of laryngitis, bronchitis, and pneumonia may succeed,
also infective gastritis and enteritis. These various parts may be
infected by the direct transference of the infecting saliva, but the
germ is also held to be transmitted through the blood to implicate
distant organs.

Appetite is gradually lost, a blackish, fœtid diarrhœa, sets in and the
calf is sunk in a profound prostration and debility due partly to the
enforced abstinence and colliquative diarrhœa, but much more to the
absorption of toxic matters. Death may ensue from the sixth to the
twelfth day. In case of recovery a month may be requisite for the
completion of convalescence.

_Diagnosis._ This has to be distinguished especially from aphthous fever
by the absence of the large, and clearly defined vesicles of that
disease, by the fact that the mammary region and interdigital spaces
usually escape, and especially by the immunity of the dam and of other
more mature animals. From actinomycosis of the tongue it is diagnosed by
its more rapid progress, by the marked constitutional depression, and
prostration, and by the absence of the marked induration of the
actinomycotic organ (holzzunge) and by the sulphur yellow pin head-like
nodules of actinomyces. Tuberculosis is rare in the first weeks after
birth in calves, and never makes the rapid progress nor causes the
profound depression of this disorder.

_Prevention._ The first object must be to destroy the infection, and the
second to obviate the susceptibility of the young animal. The clearing
away of all accumulations of litter, filth, and even fodder from the
stable proper, including the stalls where the dams lie, should be
followed by a thorough whitewashing or disinfection, with sulphate of
copper or of iron, or even mercuric chloride, (1:500.) If the disease
has already appeared in a stable the calves should be penned singly to
avoid the possibility of infection through sucking each others navels.
In all cases an antiseptic (tannin, carbolic acid) should be applied to
the navel of the new born. The food of the dam and nurse should be
nutritive and free from any suspicion of mustiness or decomposition, and
when possible the calf should be allowed to draw its own milk from the
teat. When this cannot be allowed, artificial feeding should be
surrounded by all the safeguards, named under acute indigestion of
calves.

_Treatment._ Cadeac strongly recommends ½ oz. common salt daily with the
food, or alcohol ¾ oz., or a strong infusion of coffee mixed with the
milk. Lenglen advises quinoa in the form of tincture, ½ to 1 oz.
McGillivray sulphate of soda. Tincture of chloride of iron 30 drops in
an ounce of water with each meal would be an excellent resort.

_Locally_ antiseptics are our main reliance. Naphthol, naphthalin,
salicylic acid, or salicylate of soda, may be applied directly to the
diseased mucous membrane. Tincture of chloride of iron in water (1:2) is
one of the best agents (James). Carbolic acid 1 drachm in 6 oz. water,
and 1 oz. alcohol has been used safely and with excellent results
(Lenglen). Like most other antiseptics, however, this latter must be
used with caution as regards the amount. No actively poisonous
antiseptic is admissible. The antiseptic should be swabbed over the
whole interior of the mouth after each meal.

In case of deep gangrenous masses excision and antiseptics are demanded.


                ULCERATIVE STOMATITIS IN LAMBS AND KIDS.

  Causes: Accessory, locality, youth, debility, unsuitable food, impure
  air, parasitism, contagion. Bacteria. Symptoms: difficult sucking,
  frothing, salivation, buccal redness and swelling, white, softened
  patches, suppuration, granulation, fœtor, emaciation, debility, bowel
  symptoms, respiratory. Duration. Treatment: Artificial feeding,
  antisepsis, disinfection, mild caustics, etc.

_Causes._ This has been noticed as an enzootic affection in young and
debilitated animals, while the mature and more robust ones escape.
Anæmic lambs, those that are fed on watery, innutritious materials
(potatoes, grains, waste of sugar factories), those kept in close
confinement, indoors, and those that suffer from distomatosis show the
disease. Impure air, damp, dark places and impure water have their
influence. The disease is manifestly contagious, but the infecting
microbe has not been demonstrated. It was formerly supposed to be the
_oidium albicans_, the fungus of _muguet_, but Neumann demonstrated its
absence, and though he found _leptothrix buccalis_, _bacilli_,
_spirochcæte_ and _micrococci_ he failed to show that any one of these
in pure culture would cause the disease. Rivolta charged it on
_bacterium subtile agnorum_ and Berdt on the _polydesmus exitiosus_
which according to him the sheep contract from eating rape cake. The
withdrawal of the cake led to a rapid recovery.

_Symptoms._ The disease may begin insidiously without at first very
marked symptoms. Sucking is painful and infrequent, an acid froth
collects about the mouth, and white patches appear on the gums or other
part of the buccal mucosa, with at times redness and swelling, and the
separation of the gums from the teeth. The white epithelial patches
soften and are easily detached, leaving bright red patches, which bleed
easily, and tend to extension and coalescence. These are covered by a
viscid mucopurulent matter, and may become the seat of granulations, or
they may involve the subjacent tissues in ulceration causing evulsion of
the teeth, or necrosis of the jaw bone. The odor of the mouth is fœtid.
Prostration and emaciation set in, and often bear a ratio to the
extension of the disease to the digestive and respiratory organs. This
is manifested by uneasy movements of the hind feet, shaking of the tail,
frequent lying down and rising, constipation or diarrhœa: or by cough,
snuffling breathing, swelling of the submaxillary and pharyngeal glands,
and hurried, oppressed breathing. The complication of vesicular and
pustular eruption has been noticed. Death may occur in eight or ten
days, or more commonly recovery ensues.

_Treatment_ must proceed on the same lines as in the calf. Artificial
feeding on gruels, with antiseptic washes for the mouth at each meal are
indicated. Chlorate of potash, chloride of lime, borax, sulphites and
hyposulphites of soda, carbolic acid, and the salts of iron afford an
ample field for selection. For ulcers, a pointed stick of nitrate of
silver, or a solution of muriatic acid in three times its volume of
water, applied by means of a glass rod or pledget of cotton will serve a
good purpose.




                    ULCERATIVE STOMATITIS IN SWINE.

  Causes: improper food; filthy pens; debility; toxins of specific
  diseases; microbian infection. Symptoms: inappetence; grinding teeth;
  champing jaws; salivation; fœtor; buccal swelling and redness; pulpy
  spots; desquamation; ulcers; pharyngeal, enteric and osseous
  complications. Treatment: Segregation; disinfection; local antiseptic
  washes; tonics.


This is the Scorbutus of Friedberger and Fröhner, the gloss-anthrax 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 dullness 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 on the other animals. Sulphuric or hydrochloric acids in
50 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.


                  ULCERATIVE STOMATITIS IN CARNIVORA.

  Causes: dietary causes; constitutional debilitating diseases; dental
  disorders; microbian infection; microbes. Symptoms: difficult sucking
  or mastication; salivation; dullness; prostration; mucosa red with
  gray patches, erosions, and ulcers; fœtor; loose teeth; excess of
  tartar. Extensions to face, throat, lymphatics, nose, eyes, stomach,
  liver, bowels. Duration. Treatment: clean teeth; antiseptics; mild
  caustics; stimulants.

_Causes._ This affection is more common in this class of animals than in
the herbivora, being apparently dependent in great part on their
artificial habits of life, the sweet and stimulating diet and the
derangement of the digestive organs. The lowering of the general health
in connection with privation or disease and especially canine distemper,
rachitism or indigestion must be recognized as predisposing causes,
while the accumulation of tartar on the teeth, or the decay of the teeth
themselves, constitutes a potent exciting local cause. In connection
with such cretaceous deposits the decomposing elements of the food
collect, and the irritant products of their fermentation lead to disease
of the gums, congestion and ulceration. Superadded to this is the
bacteridian infection of such diseased parts, through which the
ulceration is started, maintained and extended. This infection is not
that of a specific microbe, but usually of a multiplicity of germs, one
or more of the bacteria that live habitually in the healthy mouth,
taking the occasion of the existence of a wound, or of a reduction of
vitality to colonize the mucosa which would otherwise have remained
sound. The microbes actually found in the ulcers are very varied.
Pasteur isolated a spirillum, Fiocca the bacillus salivarius septicus,
others have found pus bacilli, and in sucking kittens the bacillus coli
communis.

But the attempts made to convey the disease to healthy mouths by the
transfer of the microbes have usually failed (Pasteur, Netter, Cadeac).
To establish their pathogenic action therefore, it appears to be
necessary to furnish a susceptible mucosa as well as an infecting
microbe. This explains why the disease does not spread as an infection,
the average mouth is immune and it is only when it becomes the seat of a
wound, bruise or other injury, or when the general system has become so
reduced that the resisting power is a minor quantity, that the hitherto
harmless germ becomes actually pathogenic.

_Symptoms._ There is indisposition to suck or eat, the patient leaves
the teat or the food, and looks dull, depressed and disposed to lie down
apart. There is evident salivation and on opening the mouth we may find
the offensive odor, the tartar covered teeth with red or ulcerated gums,
and on the cheeks, lips and tongue dark red patches of congestion, or
whitish or yellowish gray, soft, pulpy spots of disintegrating
epithelium. This is followed by shedding of these epithelial patches,
and the formation of rounded ulcers of a line in diameter or less. These
are tender, and bleed readily. They may extend to the skin of the lips,
or deeply into the mucosa, the muscles or bones, and the attendant
morbid process may cause loosening and evulsion of the teeth. There may
be implication of the pharynx, the lymph glands, the nose, the eyes, the
stomach, the liver, or the intestines with corresponding symptoms. Death
may supervene in from six to thirty days, or a more or less speedy
recovery may take place.

_Treatment._ The first step as a rule is to remove the tartar from the
teeth. This is often done with a wooden spud dipped in a weak solution
of hydrochloric acid. A steel scraper will usually act well and without
the solvent action of the acid.

Next will come the removal of all diseased teeth which are operating as
local irritants and as centres for infectious microbes and their hurtful
products.

Then antiseptics in the form of liquids applied as in the other animals
with each meal, will be necessary to counteract infective action, and
give the tissues an opportunity to re-establish their integrity. Cadeac
recommends a 10 per cent. solution of oil of thyme, as a safe and
efficient application. Boric acid, borax, salol, salicylic acid, tannic
acid, sulphurous acid, or carbolic acid largely diluted may be
substituted. Internally iron tonics and bitters are of great value in
improving the tone of the system and securing antisepsis of the
intestinal canal. The sulphites too may be given with advantage
internally. In depressed conditions alcoholic stimulants may be used
both as local antiseptics and general stimulants. As in other animals
ulcers may be touched with a rod dipped in tincture of iodine, or a
strong solution of chloride of zinc, or nitrate of silver.


                         MERCURIAL STOMATITIS.

  Animals suffering. Causes: mercurial baths, ointments, blisters and
  surgical dressings; mercurial vapors; deposits on vegetation; rat
  poisons; malicious poisoning. Lethal dose in horse, ox, sheep and
  goat. Mature and old eliminate more slowly. Symptoms; Salivation; red,
  swollen buccal mucosa; gingivitis; loosening of teeth; fœtor;
  ulceration; anorexia; gastro-intestinal tympany; loose, fœtid stools;
  fever; weakness; dyspnœa; langor; blood extravasation in nose, mouth,
  throat, bowels, womb, skin; abortion; skin eruptions. Lesions in
  mouth, stomach, intestines, serosæ, kidneys, muscles, encephalon.
  Treatment; stop the introduction of mercury; as antidote potassium
  sulphide; emetic; cathartic; mucilaginous and albuminous antidotes;
  potassium iodide as an eliminating agent. Locally potassium sulphide
  or chlorate. Iron tonics.

This has been especially seen in the sheep, dog and ox, and less
frequently in other domestic animals.

_Causes._ In sheep the use of baths containing corrosive sublimate, or
of mercurial ointment for acariasis or other cutaneous parasitism. In
other animals it comes mostly from licking mercurial dressings applied
to the skin—calomel, red precipitate, mercurial ointment, protoiodide of
mercury. The red iodide being more irritating is less frequently taken
in. The modern extensive usage of mercuric chloride solutions as
surgical antiseptics opens up a new channel of infection. In the
injection of the uterus or of large abscesses, or in the daily
irrigation of large wounds a dangerous amount may be absorbed. The
application of this agent as a caustic in cases of tumors is
correspondingly dangerous. Vapors from metallic mercury in confined
spaces as in ships’ holds, or from fires on which the mercurial
compounds have been thrown, are ready means of poisoning, acting
primarily on the air passages and lungs and later on the mouth. The
condensation of mercury on vegetation and other food products in the
vicinity of factories where mercury is handled (Idria) affects domestic
animals directly. Finally the small animals are poisoned by eating the
mercurial rat poisons, and all animals are subject to malicious
mercurial poisoning, with sublimate especially.

Stomatitis with fatal pharyngitis and enteritis will result in the horse
from 2 drs. of corrosive sublimate. About one-half of this may poison
the ox, and one-fourth the sheep or goat. Ruminants are more susceptible
to the toxic action of mercury than monogastric animals, one evident
reason being the long delay of the successive doses in the first three
stomachs, so that finally a large quantity passes over at once into the
fourth stomach and duodenum for absorption. The old too are more readily
poisoned than the young, as the functions of the kidneys are more
impaired in age and the poison is not eliminated with the same rapidity.

_Symptoms._ Mercurial stomatitis is a local manifestation of a general
poisoning. Salivation is one of the most prominent phenomena, the watery
saliva falling in streams from the angles of the mouth. The buccal
mucosa generally becomes red and swollen and the tongue becomes indented
at the edges by pressure against the molars. The gums especially suffer
and the teeth raised in their sockets by the swelling of the periodontal
membrane, become loose, and easily detached. The mucosa of the gums
becomes soft and spongy, bleeds readily under pressure and soon shows
erosions and ulcers. This condition extends to the lips, cheeks and
lower surface of the tongue while the upper surface of the latter organ,
the fauces and pharynx commonly escape. The breath and buccal
exhalations are very offensive, and the animal loathes food, and has
little power of mastication or deglutition. Sometimes the ulcers extend
even to the bones.

Along with these local symptoms there are usually gastro-intestinal
irritation, tympany, inappetence, continuous rumbling in the belly;
badly digested fœtid stools, often diarrhœa, small weak pulse,
hyperthermia, accelerated breathing, cough, and great langor and
prostration. A tendency to blood extravasation is shown in sanguineous
fæces, epistaxis, bleeding from the mouth, the throat or the womb and
even into the skin. Pregnant females may abort. The eyes are dull and
sunken, and the conjunctiva yellow. Eczematous or pustular eruptions may
appear on the skin on the nose, lips, neck, back, loins, croup or
perineum.

_Lesions._ In addition to the lesions described above, there are usually
gastro-intestinal inflammation, œdema of the peritoneum and pleura, in
the lung as well as in the serosæ, (pneumonia is not uncommon especially
in sheep), intestines, kidneys and muscles, hæmorrhagic spots are not
uncommon, the blood forms a loose black coagulum, and the encephalon is
anæmic and softened.

_Treatment._ The first consideration is to cut off the supply of
mercury. Mercurial applications on the skin should be washed off with
tepid water and if necessary soap. An application of sulphide of
potassium will precipitate the mercury in an insoluble form. For
mercurial agents in the alimentary canal an emetic may be given (if the
animal is one susceptible to emesis) followed by a saline laxative. This
may be combined with or followed by raw eggs, mucilage, wheat gluten or
other albuminoid, sulphide of potash or sulphur, to precipitate the
mercury and prevent its absorption. Later, when the bowels have been
cleared, iodide of potassium in small doses will serve to dissolve and
remove what mercury may be lodged in the tissues.

Locally one of the best applications is chlorate of potash as a mouth
wash, 2 drs. to the quart of water. To this may be added tannic acid or
other vegetable astringent and even alcohol.

Finally a course of iron and bitter tonics will serve a good purpose in
restoring the general tone.




                       STOMATITIS FROM CAUSTICS.

  Caustic Alkalies; symptoms, lesions and antidotes. Caustic Acids;
  symptoms, lesions and antidotes. Caustic salts; symptoms, lesions and
  antidotes.


=Caustic Alkalies= (soda, potash, ammonia and their carbonates) often
cause stomatitis. What is supposed to be _weak lye_, given to counteract
indigestions, colics, and tympanies often proves dangerously irritating,
and some of the worst forms of stomatitis we have ever seen in the horse
originated in this way. As the animal refused to swallow, the caustic
liquid lay in the mouth and virtually dissolved the epithelium and
surface layers of the fibrous mucosa. The surface in such a case is
usually of a deep red, and where the cuticular covering remains, it is
white and corrugated. The antidote is a weak, non-irritant acid, such as
vinegar, boric, citric, or salicylic acid. When the caustic alkali has
been thoroughly neutralized in this way the ordinary treatment for
catarrhal stomatitis may be followed. The attendant gastritis must
receive its special treatment.

=Caustic Acids.= Sulphuric, nitric and hydrochloric acids act by
abstracting liquids and charring the tissues. The lesions from strong
sulphuric acid turn black, those due to nitric acid, yellow,
(zanthoproteic acid,) and those due to muriatic acid are white, with the
characteristic odor of chlorine. The antidote in such cases is a
non-irritant basic agent, such as chalk, lime water, soapsuds, calcined
magnesia, and mucilaginous liquids, albumen, gluten, flax seed, with
opium. The same agents are applicable to the attendant gastritis and
when the acids are thoroughly neutralized the treatment is as for simple
inflammation.

=Caustic Salts.= Among caustic salts may be named mercuric chloride,
sulphates of copper and iron, chlorides of iron and zinc, tartar emetic.
These may be treated by albumen, blood, white of egg, milk, gluten,
mucilage and other sheathing, protecting agents which will form with the
salts insoluble and harmless coagula. The subsequent treatment will
follow the lines marked out for simple stomatitis. To prevent infection
of the raw surface Cadeac recommends: tannic acid 1 oz., benzo-naphthol
3 drachms, powdered gentian 6 drachms, honey, sufficient to make an
electuary.




     MYCOTIC STOMATITIS IN FOALS, CALVES AND BIRDS. THRUSH. MUGUET.

  Oidium (saccharomyces) albicans; a parasite of the young; cultures.
  Symptoms in foals and calves; congested buccal mucosa; curd-like
  concretions; erosions. Diagnosis from rinderpest. Treatment;
  disinfection; sunshine; open air; exercise; locally antiseptics.


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.

=Foals and Calves.= _Symptoms._ The 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 concretions seen on this mucosa in rinderpest, but
are easily recognized 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._ It is always well to destroy floating germs by cleansing
and whitewashing the stable, and to invigorate the young animals by
sunshine, free air and exercise. Locally the most effective agent is the
old favorite remedy 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 honey or molasses and used
as an electuary. As substitutes boric acid, salol, thymol, chlorate of
potash, or permanganate of potash may be used.

=Birds.= The affection has been twice observed as occurring in the
œsophagus and crop of two chickens. Martin tried in vain to inoculate it
on other fowls, and Neumann failed to convey it from child to chicken by
feeding. The element of individual susceptibility was manifestly
lacking. From its seat in the crop the malady passed unnoticed during
life. In cases that can be recognized, treatment would be the same as in
young mammals.


                 PARALYSIS OF THE TONGUE. GLOSSOPLEGIA.

  Causes: Nervous lesions—central or peripheral, parasitic,
  inflammatory, infectious, traumatic or degenerative. Symptoms:
  unilateral and bilateral. Treatment: remove cause; use nerve
  stimulants, embrocations, blisters, frictions, galvanism, suspension
  of tongue.

Paralysis of the tongue depends on a lesion of the medulla oblongata, or
of the 7th or 12th cranial nerve. The central lesions may be connected
with cœnurus or other parasites in the brain, hydrocephalus, meningitis,
cerebro spinal meningitis, infectious pneumonia, abscess (strangles),
and tumors. The distal or nerve lesions may be due to neuroma, tumors,
traumas, lacerations, bruises, or violent distension of the tongue.
Parotitis, abscess of the guttural pouch and tubercle may be added as
occasional causes. As direct traumatic injuries those caused by wearing
a poke by a habitual fence-breaker, excessive dragging on the tongue in
operations on the mouth, and compression of the tongue by a loop of rope
passed over it, require mention.

_Symptoms._ In =unilateral= paralysis the affected half of the tongue
remains soft and flaccid and is liable to be crushed between the teeth,
the active muscles of the opposite half pushing the organ over to the
paralyzed side. In =bilateral= paralysis the tongue hangs out of the
mouth, and being crushed and torn by the teeth, it swells up, and may
even become gangrenous.

_Treatment._ Will vary according to the cause. After removal of the
central or nervous lesions, the remaining functional paralysis may be
treated by strychnia, internally or hypodermically, by frictions or
stimulating embrocations to the intermaxillary region, or by
electricity. The tongue must be suspended in a sling to prevent œdema,
inflammation and wounds by the teeth. In bad cases of bilateral
traumatic glossoplegia in meat producing animals it has been advised to
have the subject butchered.


                    DISEASES OF THE SALIVARY GLANDS.

Modifications of the secretion are commonly simple excess or deficiency,
with a correspondingly high or low specific gravity of the product.
There may, however, be a virulent element as in the case of rabies.


             SUPPRESSION OF SALIVARY SECRETION. XEROSTOMIA.

  Causes; fever; vascular vacuity, after bleeding, diarrhœa, etc.;
  destruction of glands; Calculus. Symptoms; slow, difficult
  mastication; digestive disorder. Treatment; remove mechanical
  obstruction; correct constitutional disorder; employ stimulation to
  gland—pilocarpin, electricity.

Entire suppression of salivary secretion is usually the result of some
other disease. It may be a manifestation of the general tendency to
retain water in the febrile system, or it may be an indication of
vacuity of the vascular system as after bleeding, profuse diarrhœa,
diuresis, or diaphoresis, or it may be the result of the entire
destruction of a salivary gland or the obstruction of its duct by some
foreign body or calculus. In proportion to the completeness of the
suppression, mastication and deglutition become difficult or impossible.
The condition must be met by the removal of the cause which is operative
in the particular case. The treatment may be surgical for the removal of
obstructions, or medical with the view of overcoming anæmia, fever,
profuse secretions from other emunctories, or the simple physiological
inactivity. To meet the last indication small doses of pilocarpin, or
the application of a gentle current of electricity will usually succeed.




          EXCESSIVE SECRETION OF SALIVA. SALIVATION. PTYALISM.

  Causes; a symptom of other diseases, of the mouth, teeth, throat or
  stomach; rank aqueous vegetation, lobelia, pilocarpin, muscaria,
  tobacco, mustard, and other acrid vegetables; caustic alkalies, acids,
  salts; compounds of mercury, gold, copper, iodine; palsy of lips;
  harsh bit; fungi on clover, sainfoin, etc. Symptoms; salivary escape;
  frequent deglutition; thirst; disordered digestion, etc. Treatment;
  remove cause; astringent washes; sedatives; embrocations to the
  glands.


This is often a symptom of some other affection such as aphthous fever,
dumb rabies, epilepsy, stomatitis, pharyngitis, dentition, caries and
other diseases of the teeth, wounds and ulcers of the mouth, gastric
catarrh, etc. In other cases it is due to direct irritants in the food
or medicine, as very rank, aqueous, rapidly grown, spring grass,
lobelia, pilocarpin, muscarin, tobacco, wild mustard, colchicum, pepper,
garlic, ginger, irritant and caustic alkalies, acids and salts, and the
compounds of mercury, gold, copper, or iodine employed locally or
internally. The application of mercurials to the skin is especially
liable to salivate cattle and dogs, partly because of a special
susceptibility to the action of this metal and partly from the tendency
of these animals to lick the medicated surface. Paralysis of the lips
causes a great flow of saliva from the mouth though no more than the
normal amount is secreted. The irritation of a large or harsh bit will
increase the secretion and still more the former habit of attaching to
it small bags of spicy or irritant chemicals. Certain fungi determine
salivation. Mathieu saw profuse salivation in horses, cattle and sheep
fed on clover and sainfoin which had become brown.

_Symptoms_ consist in the profuse flow of saliva, either in long stringy
filaments, or if there is much movement of the jaws, in frothy masses;
frequent deglutition; increased thirst and disordered digestion
(tympany, inappetence, colics, constipation, diarrhœa). In mercurial
salivation there may be loose teeth, swollen, spongy, ulcerated gums,
tympany, rumbling, and the passage of fœtid flatus and soft ill-digested
stools.

_Treatment_ consists in removing the cause, whether this is to be found
in faulty food or drink, diseased teeth or gums, disordered stomach, or
the irritant food medicine or poison ingested. If more is wanted simple
astringent washes like those recommended for stomatitis and a free
access to pure water will often suffice. Tartar emetic or opium has been
known to succeed in obstinate cases. Friction over the parotid or
submaxillary gland with camphorated spirit, tincture of iodine or soap
liniment is sometimes required. In mercurial salivation chlorate of
potash is especially to be commended, and when the bowels have been
unloaded of the agent, iodide of potassium will hasten its elimination
from the tissues and blood.


      DILATED SALIVARY DUCTS. SALIVARY CALCULUS. SALIVARY FISTULA.

These are all surgical diseases and are to a large extent inter
dependent. The impaction of the calculus in the duct leads to
overdistension of the duct posterior to the obstruction, and the rupture
or incision of the distended duct, determines the fistula. It is only
necessary here to point out the seat of these lesions: the distended
sublingual ducts constituting a more or less rounded swelling to one
side of the frænum lingui, the Whartonian duct forming a tense rounded
cord from the papilla back of the lower incisor teeth backward on the
inner side of the lower jaw, and the Stenonian duct forming a similar
tense cord from near the middle of the cheek down around the lower
border of the jaw in company with the submaxillary artery and backward
on the inner side of its curved border to the parotid gland.

For the more precise lesions, symptoms and treatment of these, see a
work on surgery.




             INFLAMMATION OF THE PAROTID GLAND. PAROTITIS.

  Causes: traumatic; calculus; grains; barley and other beards;
  infecting microbes. Symptoms: fever, dullness, buccal heat,
  salivation, difficult mastication, swelling of gland and duct,
  protruded nose, stiff neck, fœtor, dyspnœa, facial paralysis,
  induration of gland, abcess. Diagnosis from pharyngitis, abcess of
  guttural pouch or pharyngeal glands; from tumors. Treatment: avoidance
  of causes; derivation; astringent, antiseptic washes; wet antiseptic
  bandages to throat; cool pultaceous diet. Open abscess and disinfect.
  For induration deobstruents. For sloughing antiseptics.


This may be caused by traumatism, such as incised punctured or bruised
wounds. Wounds inflicted by the goad, by horns, and even by the yoke in
cattle must be looked on as factors. It occurs from obstruction of the
salivary ducts by calculi, or by grains, seeds, or pebbles introduced
from the mouth; from their irritation by the beards of barley and other
plants (brome, rye, wheat, etc.); and from the localization in the gland
of specific inflammations like strangles, pyæmia, canine distemper,
tuberculosis and pharyngitis. In most of these cases infective microbes
are prominent factors. They enter with penetrating bodies from the skin;
they extend through the weakened and debilitated tissues in bruises;
they penetrate the Stenonian duct with the various foreign bodies from
the mouth; irrespective of foreign objects they make their way up the
duct by continuous growth from the buccal orifice; in case of calculus
or other obstruction their extension is favored by the local congestion
and debility and by the stagnation of the saliva above the point of
arrest. When present these microbes even favor the deposition of the
salivary salts and formation and increase of calculi so that the
affection may advance in a vicious circle, the microbes favoring
calculus and the calculus favoring the increase of microbes.

_Symptoms._ In the horse in particular there may be premonitory symptoms
of fever, dullness, heat of the mouth, ptyalism, slow and imperfect
mastication, and the retention of food in the cheeks.

The Stenonian duct becomes swollen and painful. The parotid becomes
hard, hot, tender, and is surrounded by a softer pitting infiltration
which may extend down around the entire throat, and even along the
intermaxillary region to the chin. When the canal is obstructed it may
stand out as a thick rope-like resilient swelling extending around the
lower border of the jaw and upward toward the cheek as far as the point
of obstruction. When one parotid only is involved, the contrast with the
other is quite marked. The head is extended and carried stiffly. When
the nose is depressed, or when the head is turned to one side or the
other, the patient gives evidence of suffering from compression or
stretching of the inflamed region. The breath and mouth exhale an
offensive odor, determined by the decomposition of mucus and of the
retained food products.

Among remote effects may be named dyspnœa and threatened suffocation
from pressure on the pharynx and laryngeal nerves, and facial paralysis
from pressure on the seventh nerve.

The disease may go on to induration and remain permanently in this
condition, or it may suppurate and discharge through the skin, into the
pharynx or through the duct of Stenon. It may communicate with both the
duct and the skin and determine a fistula. When suppuration occurs there
is an access of fever, a chill may be noticed, the swelling becomes more
tense, harder, more tender to the touch, and even emphysematous, and
finally points internally or externally. This may take place from the
fifth to the tenth day or later. When it opens into the duct it may be
seen oozing from the orifice in the cheek when the mouth is opened, and
in case the jaws are suddenly parted, it may escape in a jet. In such a
case and especially if the microbes have come originally from the food
the odor is very fœtid. The abscess is not always single and when
multiple the pus may escape externally by a variety of orifices. The pus
is usually whitish, yellowish or grayish and creamy, but it may be
grumous or bloody or serous and of a most offensive odor. In exceptional
cases the gland becomes more or less gangrenous and such parts, exposed
in the wound are hard, bloodless and insensible, and add very materially
to the fœtor. This may lead to general septic infection, or the necrosed
masses may slough off and the cavities fill up by granulations.

_Diagnosis._ Parotitis is distinguished from pharyngitis and abscess of
the guttural pouch by the absence of cough and nasal discharge; from
abscess of the pharyngeal glands it is differentiated by the limitation
of the hard swelling to the parotid gland and by the superficial seat of
the resulting abscess. The co-existence of active inflammation serves to
distinguish it from ordinary tumors.

_Treatment._ By way of prevention, the avoidance of injuries by yokes,
forks, pokes, and goads is important. Also the disinfection of the mouth
by a liberal supply of pure water and even by antiseptic washes:—borax,
boric acid, creolin, tannin, chlorate of potash. Also by the removal of
foreign bodies or calculi from the canal.

When the inflammation has set in, a saline laxative is often of value.
Wash the mouth with a solution of vinegar and salt, or other antiseptic,
repeating this at least after every meal. The swollen, painful gland may
be covered with a damp compress or anointed with vaseline to which may
be added a little creolin, naphthol, carbolic acid or salicylic acid,
together with lead acetate and belladonna or other anodyne. The diet
must be soft, cool mashes, sliced or pulped roots or any bland agent
that will demand little or no mastication. Cool, fresh water should be
allowed _ad libitum_. When the laxative has set, it may be followed by
cooling diuretics such as nitrate or acetate of potash.

If suppuration occurs it should be opened as soon as the pus can be
definitely recognized, and the cavity treated antiseptically to prevent
further local or general infection by the microbes. In deep abscess
there is a certain danger of wounding blood vessels and salivary ducts,
but this can be to a certain extent obviated by making an incision
through the skin only and then boring the way into the abscess with a
grooved director or the points of closed scissors. When the cavity is
penetrated the pus will ooze out through the groove or between the
scissor blades. When the pus has been evacuated the cavity should be
washed out two or three times a day with mercuric chloride solution
(1 : 1000), or permanganate of potash solution (1 : 100).

When the gland becomes indurated and indolent seeming to merge into the
chronic form it may be stimulated to a healthier action by a cantharides
blister, or it may be subjected to daily massage, or to a daily current
of electricity for ten or fifteen minutes. If the inflammation is slight
or unrecognizable, the surface of the gland may be daily painted with
tincture of iodine, and iodide of potassium maybe given internally, in
daily doses of ½ to 1 drachm.

Gangrene, the result of septic microbes, a weak system or too severe
treatment, may be met by astringent and antiseptic agents locally, and
by tonics, stimulants and a generous diet internally.

In =cattle= the disease usually responds readily to local antiseptics,
and stimulating germicidal embrocations. Camphorated spirit, alone or
combined with tincture of iodine; cantharides ointment with carbolic
acid; and camphor and phenol may be cited as examples.


                  SUB MAXILLARY ADENITIS. MAXILLITIS.

  Mostly in solipeds and unilateral. Causes; traumatic; calculus;
  infections; ablation of papillæ. Symptoms; tardy mastication;
  salivation; buccal heat and fœtor; submaxillary swelling and
  tenderness; morsels retained under tongue; papilla and duct swollen,
  tender and firm; abscess. Treatment; remove causes; dislodge foreign
  bodies; antiseptic lotions and packing.

This is rarely seen in other animals than solipeds, is mostly
unilateral, and due to the introduction of microbes along with vegetable
spikes (barley awns, brome, wheat or oat spikes or glumes) or other
foreign bodies. It may also be caused by calculi obstructing the duct.
The orifice of each duct, to one side of the frænum lingui, is
imperfectly closed by a triangular valvular projection, which in some
countries is erroneously cut off as a diseased product (barbs), thus
opening the way for the introduction of foreign objects. The microbes
are usually pus germs and tend to abscess of the gland. As in the case
of the Stenonian duct the presence of these germs tends to the
precipitation of the salivary salts and the formation of calculi.

_Symptoms._ The animal may seem hungry, but masticates tardily and
imperfectly, and may even drop morsels partly chewed. He prefers ground
feed to whole, and soft mashes to ground feed, while hay and other
fibrous aliments may be altogether rejected. Salivation may be
excessive, the secretion drivelling from the lips, the mouth may feel
hot and the submaxillary salivary gland swollen and tender. This may be
detected in the intermaxillary space, but is especially noticeable along
the lower and lateral aspect of the tongue. If the mouth is opened and
the tongue drawn to one side a mass of food may be found to one side of
the frænum lingui, and beneath this the projecting, red inflamed papilla
which covers the Whartonian orifice. Extending backward from this the
duct is felt as a thickened cord, and when this is compressed a purulent
liquid flows from the orifice. The mouth becomes offensively fœtid.

The tendency is to suppuration, and if this is determined in the
Whartonian duct only, by the presence of foreign bodies, calculi, or
microbes it may recover in connection with an abundant muco purulent
discharge and a free secretion of saliva. If it occurs in the gland
tissue itself by reason of the penetration of the microbes into the
follicles, the tendency is to circumscribed abscess, which may point and
burst by the side of the root of the tongue, or externally in the
intermaxillary space. In the first case the tongue is displaced upward
and to the other side of the mouth by the hard, firm swelling, which is
felt on one side beneath the back part of that organ, and later there is
the wound, the profuse muco purulent discharge, and intense fœtor. If on
the other hand the abscess forms nearer the skin, there is the firm,
painful intermaxillary swelling, which finally points and bursts
discharging pus of a septic odor. It may be mixed with the foreign
bodies that have penetrated through the canal, with morsels of necrosed
gland tissue and with blood.

_Treatment._ The first consideration is to extract any foreign bodies
which have lodged in the duct causing irritation and infection. The
finger passed along the line of the swollen duct may detect the seat of
such foreign body by the extra swelling, and may extract it by
manipulation from behind forward. This may sometimes be assisted by the
introduction of a grooved director as far as the foreign body, or even
by a catheter which can be made to distend the canal in front of the
object and open the way for its easier passage. In case of failure and
in all cases of the introduction of small bodies like vegetable awns or
spikes pilocarpin may be given to cause an excessive secretion and thus
as it were purge the canal of its offensive contents. Incision of the
canal over the foreign body is the _dernier resort_.

This accomplished, the injection of antiseptic solutions (permanganate
of potash, boric acid), and the liberal use of pure water and detergent
lotions in the mouth (vinegar, borax, carbolic acid or salicylic acid in
solution) will go far to establish a cure. In case of an abscess
bursting internally the antiseptic solutions should be injected into its
cavity. When the abscess bursts externally this is doubly demanded, as
the introduction of aerial germs tends to produce very unhealthy action.
The cavity may be stuffed with carbolized, or iodoform, or acetanilid
cotton, or with boric or salicylic acid.


                SURGICAL LESIONS OF THE SALIVARY GLANDS.

Among these may be named calculi of the Stenonian and Whartonian ducts,
ranula, stenosis and fistulæ of these ducts, tumors, special infections
like actinomycosis.


                 TONSILITIS IN PIGS, AND OTHER ANIMALS.

  Causes; debilitating, climatic, microbian. Symptoms; fever, dullness;
  lies under litter; ears and tail droop; watery eyes; anorexia;
  vomiting; pharyngeal swelling; buccal redness and fœtor; tonsils
  swollen with pus or caseous mass in follicles; cough dry and hard,
  later loose. Abscess. Calculus. Course. Treatment; antiseptic
  electuaries; embrocations; laxatives; diuretics; tonics.

This is seen in both the acute and chronic form. In the former it has
the general causes and symptoms of pharyngitis. There is more or less
fever, dullness, a disposition to lie with head extended and buried in
the litter, ears drooping, eyes watering and red, carelessness of food,
deglutition painful, and liable to be followed by vomiting. The mouth is
red and hot, the breath fœtid and the tonsils swollen, and their alveoli
filled with muco purulent matter or at times with a fœtid cheese-like
product. The cough is at first dry and hard and later loose and
gurgling.

In the chronic form there is general swelling of the tonsils with the
overdistension of the follicles by the above mentioned whitish
putty-like masses, which are often even calcareous. These are due to the
proliferation of microbes which find in these alveoli a most favorable
field for their propagation. A similar condition is found in the
carnivora and to a less extent in the horse, in keeping with the
restricted development of the amygdalæ in these animals. It may be
attended by ulceration, or in rare cases by the formation of veritable
calculi in the follicles of the tonsils.

The gravity of the disease is largely determined by the nature of the
infecting microbe and the debility and susceptibility of the animal
attacked. The affection usually ends in recovery, but may go on to grave
local ulceration, and general infection.

_Treatment_ consists largely in astringent and antiseptic applications
to the buccal mucous membrane. In the acute forms frequent smearing of
the mouth with electuaries of honey or molasses and borax, boric acid,
salammoniac, chlorate or permanganate of potash, and the application of
stimulating embrocations to the skin around the throat. In other cases
solutions of tincture of chloride of iron, or of tincture of iodine can
be used with profit. The iron can be swallowed with advantage, but it is
objectionable to pour liquid rapidly into the mouth of the pig, because
of the danger of its entering the lungs and setting up fatal pneumonia.
A better way is to apply it to the interior of the mouth and fauces on a
swab or sponge dipped in the liquid. Short of this one of these agents
may be mixed with the drinking water, or muriatic acid may be used in
the same way, though at some detriment to the teeth. The general health
must at all times be attended to. Any costiveness may be corrected by
Glauber salts or jalap, and elimination through the kidneys must be
sought through the use of nitrate of potash or other diuretic.




                        CALCULI IN THE TONSILS.

  Diagnosis and treatment of tonsillar calculi; spud; acid dressings.
  Trauma of soft palate by stick, probang, file, molar. Abscess of
  palate. Treatment; laxative; expectorant; antiseptic; lancing. Cleft
  palate and hare lip.


Rudimentary as these organs are in the equine race they are important
enough to have become the seat of hard calculous masses. These have been
found by Goubaux and Blanc in old asses, and by the author in old
horses. They vary in size from a pin’s head to a pea and consist of
concentric layers of a granular material arranged around a central
nucleus, which is usually a foreign body introduced with the food. This
nucleus is usually of a vegetable nature, while the enveloping material
is made up largely of the imprisoned and degenerated epithelium of the
follicle. Both diagnosis and treatment are difficult in such cases. The
adventitious masses should be dislodged by the aid of a smooth, blunt
metallic spud, and the surface thereafter washed or swabbed with an
antiseptic and astringent solution. Swabbing with a solution of
hydrochloric acid will tend to dissolve and remove them.


                INJURIES TO THE SOFT PALATE AND FAUCES.

The region of the fauces is sometimes injured by sharp pointed bodies
swallowed in the food, by the giving of boluses on the end of a pointed
stick, or by the careless use of a probang or of a file upon the
posterior molars. An overgrown last molar will sometimes lacerate the
velum. In other cases the inflammation of sore throat is especially
concentrated on this part, giving rise to cough, difficulty of
swallowing, redness, infiltration and swelling of the parts, and even
abscess. In the dog it is often associated with tonsilitis.

_Treatment._ A laxative is usually desirable to be followed by
salammoniac or chlorate of potash. In case of actual traumatic lesions,
the astringent and antiseptic lotions advised for tonsilitis will be in
order, and if abscess is recognized it should be opened promptly.


                             CLEFT PALATE.

In exceptional cases the soft palate has failed to unite in the median
line, and is represented by two lateral flaps separated by a v-shaped
hiatus in the middle. In a specimen in the N. Y. S. V. College, taken
from a trotting colt, the fissure is continued forward for several
inches between the palatine bones and the palatine processes of the
superior maxillary, establishing a direct communication between the
mouth and nasal chambers. In still other instances the fissure is
continued forward between the maxillary and anterior maxillary bones,
throwing the whole length of the buccal and nasal chambers into one
irregular cavity, and forming harelip.

It would be possible to remedy some of these conditions by plastic
operation, but the value of the young animal will rarely warrant any
such resort.


                         CATARRHAL PHARYNGITIS.

  Causes: traumatic; thermic; gaseous; medicinal; chemical;
  physiological irritants; in solipeds, cattle, swine, dogs; debility;
  exposure; cold baths; youth; age. Microbes in solipeds, cattle, dogs,
  birds; facultative microbes. Symptoms: constitutional; difficult
  swallowing; nasal rejection of water; pharyngeal swelling and
  tenderness; extended head carried stiffly; cough loose; salivation; in
  cattle, grinding of teeth; in dogs, rubbing of chops; buccal heat and
  redness; often fœtor. Course. Duration. Diagnosis from parotitis, from
  abscess of guttural pouch, from pharyngeal tuberculosis, from
  actinomycosis, from adenitis and phlegmonous pharyngitis, from
  specific fevers affecting the pharynx. Lesions: redness and swelling
  of mucosa, epithelial degeneration, elevations, erosions, and ulcers;
  lesions of tubercle, glanders, rabies, anthrax, actinomycosis, etc.
  Prevention. Treatment: soothing; dietetic; laxative; expectorant;
  eliminating; locally antiseptic astringents in solid, liquid, or
  vapor; embrocations and blisters; tonics.

_Causes._ As in stomatitis the starting point of pharyngitis is usually
in a local injury or a systemic condition which lowers the vitality of
the pharyngeal mucous membrane. It may come in all animals from the hot
air of burning buildings, from acrid gases inhaled, food, drink or
medicines given at too high a temperature, from caustic alkalies, acids
or salts, from physiological irritants like croton, euphorbium,
cantharides, from barley and other spikes entangled in the follicles,
from drinking freely of iced water. In _solipedes_ there are the
injuries caused by giving boluses on pointed sticks, and the wounds
caused by tooth files in careless hands, and by coarse fibrous fodder,
which has been swallowed without due mastication. In _cattle_ injury
comes from foreign bodies impacted, from the rough use of probang, rope
or whip and even of the hands in relieving choking. _Swine_ have the
part scratched and injured by rough or pointed objects which they bolt
carelessly with the food. _Dogs_ and especially puppies are often hurt
by solid and irritant bodies that they play with, and swallow
accidentally or wantonly. They also suffer at times from the pressure of
a tight or badly adjusted collar.

The system is debilitated and rendered more susceptible by chills
consequent on exposure to cold blasts, or draughts, or rain or snow,
when heated and exhausted, by cold damp beds, by pre-existing disease,
by underfeeding and by overwork. In the larger animals this may come
from the excessive ingestion of iced water, while in dogs the plunging
in rivers, ponds or lakes may chill.

The weakness of _early age_ and _old age_ have a perceptible
predisposing influence especially in solipeds and carnivora.

Finally as in other catarrhal inflammations the local action of disease
germs on the mucous membrane must ever be borne in mind. These may be
the germs of specific diseases localized in the pharynx;—in =Solipeds=
the streptococcus of strangles, the bacillus of glanders, the
diplococcus (streptococcus) of contagious pneumonia, the germ of
influenza, and actinomyces;—in =Cattle= the bacillus tuberculosis, the
bacillus of anthrax, actinomyces, the germs of aphthous fever and of
pseudomembranous angina; in _dogs_ canine madness and distemper;—in
birds the bacillus of pseudomembranous pharyngitis.

In addition to such specific germs the micrococci, streptococci and
bacilli which are normally present and harmless in the mouth and
pharynx, enter, colonize and irritate the debilitated tissues in case of
trauma, inflammation or constitutional disorder and serve to perpetuate
and aggravate the affection.

_Symptoms._ Acute pharyngitis is manifested by impaired or lost
appetite, dullness, weakness, by difficulty in deglutition, by the
rejection through the nose of water or other liquids swallowed, by
swelling over the parotid and above the larynx, and by a disposition to
keep the head extended on the neck and the nose raised and protruded.
Fever is more or less marked according to the severity of the attack the
temperature being raised in mild cases to 100°, and, in the more
violent, to 104° or 106°. The pulse and breathing may be excited,
amounting sometimes to dyspnœa, the throat is tender to the touch and
its manipulation rouses a cough, the nasal mucosa is congested and the
buccal membrane, and especially along the margin of the tongue may be
red and angry. Salivation is shown more or less, in _solipeds_ the
saliva accumulating especially during mastication in froth and bubbles
at the commissures of the mouth, while in _ruminants_ the grinding of
the teeth or frequent movement of the jaws in the absence of food or
actual mastication leads to a free escape of the filmy liquid at the
same points. _Dogs_ will rub the jaws with the foot as if to remove some
irritating object from the mouth. In the last named animals the swelling
of the tonsils, fauces and pharyngeal mucous membrane, may be seen
marked by patches and spots of varying redness and swelling, covered
with glairy or opaque mucopurulent secretions, or particles of food, or
even showing erosions.

The cough of pharyngitis is painful, paroxysmal, and softer and more
gurgling (even in the early stages) than that of laryngitis or
bronchitis. It is roused by handling the throat, by swallowing, by a
draught of cold air or by passing out of doors, in _dogs_ by opening the
mouth, and in _cattle_ by pulling on the tongue which causes pain and
resistance. The cough is followed by the rejection, mainly through the
nose in _solipeds_, but also through the mouth in other animals, of a
glairy mucus or an opaque mucopurulent discharge often mixed with and
discolored by the elements of food or in bad cases by blood.

The _course_ of the disease is comparatively rapid, and it usually ends
in recovery in seven to fifteen days, in cases that are not complicated
by dangerous local infections.

_Diagnosis_ is mainly based on the stiff carriage of the neck with the
nose elevated, the swelling and tenderness of the throat, manipulation
above the larynx rousing the cough, the soft or rattling nature of the
cough, the ejection of liquids and foods through the nose, the movements
of the jaws apart from mastication and the salivation. From _parotitis_
it is distinguished by the concentration of the swelling and tenderness
to the deepseated region above the larynx, by the abundance of the
discharge, by the ejection of liquids through the nose, and by the
readiness with which the cough is aroused. From _abscess of the guttural
pouch_ it is differentiated by the more continuous discharge from the
nose, rather than the intermittent one. From _tuberculous pharyngeal
glands_ by its acute nature, by the absence of the glandular swellings
in which the tuberculosis is concentrated, also by the absence of
tubercles in other parts of the body. From _actinomycosis_ by its more
rapid progress and by the absence of the hard indurated cutaneous or
subcutaneous swellings, and of the open sores with minute sulphur
colored granules that mark that affection. From _adenitis_ and
_phlegmonous pharyngitis_ it is distinguished by the absence of the
glandular swelling and dyspnœa which attend on that affection. From the
various fatal _febrile affections_, the germs of which may be localized
in the throat, it may be diagnosed by the absence of the more profound
constitutional disturbance, and of the more characteristic local
symptoms of these which are seldom altogether awanting, though often
greatly modified.

_Lesions._ Beside the thick covering of mucopurulent and alimentary
matters, the pharyngeal mucosa, when washed, shows redness, ramified or
reticulated, more or less swelling amounting at times to œdema, a soft
friable consistency, which like the œdema may in bad cases extend into
the submucous tissue, granular elevations, and raw abrasions caused by
the destruction and removal of the epithelium. In some instances the
ulcers may become quite extensive.

In the more specific inflammations (tubercle, glanders, rabies, aphthous
fever, contagious pneumonia, anthrax, actinomycosis), the lesions will
vary according to the specific nature of the disease.

_Prevention._ Avoid the various thermal, chemical, mechanical, and
unhygienic causes already referred to, and the exposure to such
infectious diseases as are liable to localize themselves in the throat.

_Treatment._ A piece of blanket or sheepskin placed round the throat
with the wool turned inward, a moderately warm stall with pure air, and
a diet composed of soft, warm or tepid mashes, (all hard or fibrous
food, oats, hay, etc. being withheld) are important conditions.

If costiveness exists a dose of Glauber salts for the larger animals,
and of jalap for the small, may be useful. Or pilocarpine or eserine may
be given hypodermically. Following this, mild saline diuretics will
serve at once to eliminate offensive products of the disease and lower
the general temperature.

The most important resorts however, are the local applications of dilute
acids, astringents and antiseptics to the pharyngeal mucosa, mouth and
nostrils. In severe cases benefit may be derived from inhalation of
water vapor, but this is rendered far more effective by the addition of
vinegar, carbolic acid, creolin, camphor, tar, or sulphurous acid. The
last may be obtained by the frequent burning of a carefully graduated
quantity of sulphur in the stall, the others by mixing them with hot
water, saturating cloths hung in the stall, or sprinkling them on sand
laid on the floor.

Chlorate of potash or borax may be dissolved in the drinking water, care
being taken not to exceed the physiological dose. Mercuric chloride
(1:2000) may be used to wash the lips and nostrils, but cannot be safely
injected into mouth or nose. Powdered alum or tannic acid may be used by
insufflation.

As a mouth wash and general medicament a saturated solution of chlorate
of potash in tincture of muriate of iron, diluted by adding thirty drops
to the ounce of water, may be given every hour or two. Or a solution of
chlorine water diluted so as to be non-irritating, may be substituted
with somewhat less effect. Even a weak solution of hydrochloric acid may
be employed.

Borax may be used in a solution of 2 per cent., or carbolic acid in one
of 1 per cent., or bisulphite of soda in the proportion of ½ oz. to the
pint, or salicylate of soda ½ oz. to the pint of water. The same agents
may be made into electuaries with honey or molasses and smeared every
hour or two on the tongue or cheek. In such cases the addition of
powdered liquorice, and, if the suffering is acute, of extract of
belladonna will serve an excellent purpose.

The danger of infection of the stomach and bowels may be met by
combining with the above or administering separately salol in doses of 2
to 3 drachms or naphthol in doses of 4 to 5 drachms to the larger
animals. For sheep or swine one-fourth of these doses may be given, and
for a shepherd’s dog one-sixteenth to a twentieth.

As alternate antiseptics may be named, boric acid, permanganate of
potash and salicylate of bismuth. These from their comparative absence
of taste are especially useful in carnivora.

Counter-irritants to the throat are useful. For the horse, sheep, dog
and cat, use equal parts of strong aqua ammonia and olive oil. For the
solipeds a cantharides blister. For cattle or swine equal parts of
strong aqua ammonia and oil of turpentine with a few drops of croton
oil, or grains of tartar emetic.

Finally during convalescence a course of iron and bitters may be useful,
especially in debilitated subjects.


                        PHLEGMONOUS PHARYNGITIS.

  Submucous inflammation and abscess. Solipeds especially. Specific, or
  due to microbian pus infection. Traumatism; from foreign bodies in
  tonsillar and mucous follicles, from rough, fibrous food, instruments,
  etc.

  As a sequel of catarrhal pharyngitis. Symptoms; as in catarrhal form,
  with more swelling and tenderness, glandular swelling, dyspnœa, and
  difficulty in swallowing; local induration followed by fluctuation and
  pointing. Complications; asphyxia, laryngeal œdema, purulent or
  inhalation pneumonia, pharyngeal fistula, palsy of vagus, secondary
  abscesses, septicæmia. Lesions, local, general. Treatment; General and
  local, fomentation—hot or cold and antiseptic. Embrocations. Lancing.
  Tracheotomy.

As distinguished from catarrhal pharyngitis this is inflammation of the
submucous tissue and adjacent lymph glands, tending to abscess.

It is especially common in solipeds and rather rare in other classes of
domestic animals. As a specific infectious disease it has its type in
strangles (infectious adenitis), also in cattle in the complicated
infection of purulent tubercle, but apart from such it is often the
result of the penetration of the pus microbes from a catarrhal pharynx
into the lymph plexuses and lymph glands. Traumatism may play an
important part in causation as when vegetable barbs, awns, chaff or
seeds, or strong hairs or bristles enter the open mouths of the mucous
follicles, or the tonsillar cavities. Similarly trouble may arise from
scratches by tough, fibrous fodder, from pricks by pointed or cutting
instruments, by fractures of the hyoid, or by bruises by probangs, or
tooth rasps. An overgrowth of the last molar, and a resulting wound and
ulcer of the soft palate, and the presence of local deposits like those
of glanders and actinomycosis, are other occasions of the entrance of
the pus organisms. It will be recognized that this affection is not
necessarily due to a difference in the infecting organism, but rather of
the tissue involved, the microbes gaining the submucous tissues and
expending their violence on these instead of confining their ravages to
the surface layers of the mucosa. For this reason the deeper or
phlegmonous affection may supervene on a catarrhal inflammation which
may have already persisted for several days.

_Symptoms._ Beside the general phenomena of catarrhal pharyngitis, this
form of the malady is characterized by a greater swelling and tenderness
of the throat, extending from ear to ear, and from the trachea forward
in the intermaxillary space; by nodular and painful swellings of the
pharyngeal lymph glands, by the greater difficulty of deglutition, the
muscular tissue being involved; by wheezing breathing amounting at times
to violent roaring and threatened asphyxia. Perspiration on the throat,
the ear, the side of the head or neck, of the fore arm, or of the dorsal
region is not uncommon, and has been attributed to the compression of
the vagus, or of the superior cervical ganglion of the sympathetic by
the swelling. Fever usually runs higher than in simple catarrhal
pharyngitis, which may be partly accounted for by the implication of the
deeper and important structures but also in no small degree by the
entrance into the circulation of the ptomaines and toxins, which in the
catarrhal affection escape largely from the inflamed surface.

The resulting abscess is usually in or near a gland or group of lymph
glands. The part passes through the usual succession of changes, of soft
pitting swelling; firm, tense, painful condition in which the exuded
lymph has coagulated; and softening and fluctuation which progresses
from the centre toward the circumference. The abscess points variously
according to its seat. If in the intermaxillary space it opens
externally. If sub-parotidean or peripharyngeal it may burst inwardly
into the pharynx or outwardly through the skin. If supra-pharyngeal
(retro-pharyngeal), it may be so thickly encapsulated in unyielding
walls that it may remain long indolent and inactive becoming a cold or
chronic abscess. When an abscess opens into the pharynx, there is a
sudden and copious flow of pus by the nose, and it may be by the mouth
and a simultaneous subsidence of the inflammation.

Among the _complications_ of the affection are asphyxia, œdema
glottidis; abscess of the guttural pouch; rupture of an abscess into the
larynx, and the descent of pus into the lungs; the entrance of saliva
and alimentary matters into the lungs; gangrenous pneumonia; pharyngeal
fistula; pressure on the vagus and paralysis of the pharynx or larynx;
secondary abscesses; septicæmia.

_Lesions._ Besides the general inflammatory lesions some rather
remarkable ones have been observed. Fractured hyoid, dissection of the
mucous from the muscular coat, by aliments, for nearly the whole length
of the œsophagus (Brückmüller), purulent infiltration of the
supra-pharyngeal muscles (Wakefield), ulceration of the pharyngeal or
guttural sac mucosa, or even gangrene, purulent effusion in the tonsils,
around the hypoglossal nerve, the lingual branch of the fifth, or the
vagus, embolic inflammations, suppurations or gangrene of the bronchia,
and implication of the lung tissue and pleura. Catarrhal enteritis and
fatty liver and kidney are common.

_Treatment._ Beside the general measures advised for catarrhal
pharyngitis, this type demands especially measures to moderate the
intensity of the suffering, and when abscess appears inevitable to
hasten its maturation. The first demand is met by hot fomentations
persistently applied to the throat. This may be done by spongio-piline,
or simply by well washed wool or cotton bound upon the throat and wet at
frequent intervals with water rather hotter than the hand can bear. The
addition of a little carbolic acid will secure at once some local
anæsthesia and a measure of antisepsis. In warm weather the substitution
of cold water has been resorted to with apparently good effect. If
adopted it should be frequently removed so as to keep up the constant
action of cold and moisture. These have been especially recommended in
dogs injured by a tight or ill-fitting collar.

When suppuration appears imminent as shown by the dense, hard,
circumscribed phlegmon, stimulating embrocations may be used to hasten
its progress. Camphorated spirit is suitable for carnivora and sheep. It
may be combined with tincture of cantharides for horses. For cattle and
swine, oil of turpentine may be added, the three being used in equal
proportions. A liniment of ammonia and oil may be used more or less
frequently and energetically according to the relative thickness and
insensibility of the skin of the animal affected.

When matter has formed and fluctuates, it should be at once evacuated
and the cavity treated by antiseptic dressings. In this way secondary
abscesses, septic infections, molecular ulcerations and other injurious
sequelæ may be largely obviated.

In case of threatened asphyxia the _dernier resort_ of tracheotomy is
always available, and this often acts very favorably in improving the
æration of the blood, in restoring the flagging vital functions which
depend on hæmatosis, and in removing the friction and irritation
consequent on the passage of air through the narrowed and tender
passages.




              SUPRA-PHARYNGEAL (RETRO-PHARYNGEAL) ABSCESS.

  A sequel of phlegmonous pharyngitis. Symptoms; masked by its depth;
  pharyngeal wheezing or roaring with little local swelling; difficult
  swallowing; resisting tissues tend to chronicity. Results; pharyngeal
  fistula, burrowing along œsophagus, rupture into chest or
  blood-vessels, lymphadenitis, compression of vagus, or jugulars,
  permanent infected cavity with small orifice. Diagnosis from pus in
  guttural pouches. Treatment; external opening; antisepsis.


This is a natural result of phlegmonous pharyngitis, but it is possessed
of so great importance alike in its chronicity and its results that it
seems to deserve a special article. Like its initial morbid condition it
is especially common in the soliped, and like that may be traceable to
strangles, influenza, and local traumatism.

The _symptoms_ are at first those of phlegmonous pharyngitis, and, if
the local swelling, induration and tenderness are less marked than in
other cases, it is due to the location of the inflammatory lesion deeply
between the pharynx and the atlas and occiput. Indeed the moderate
aspect of the external swelling, conjoined with the noisy wheezing or
violent roaring, may be taken as important diagnostic indications. The
supra-pharyngeal region is so closely confined on its lateral aspects,
by the union of the fascia of the sternomaxillaris and mastoido-humeral
muscles, that the swelling is confined in the early stages just as the
pus is later. As this resistant fascia prevents any relief by lateral
expansion, the engorged tissues press downward on the softer and less
resistant upper wall of the pharynx and seriously impair both
respiration and deglutition. Similarly when pus has formed, these
lateral fibrous barriers, reënforced by organized lymph, stand in the
way of the advance of the pus toward the skin, and lead it to dissect
its way downward toward the pharynx. Even here the thickening of the
tissues by the organized products of the lymph will often interpose a
serious bar, and the pus remains pent up indefinitely, a source of
wheezing, roaring and impaired deglutition, and a constant threat of
secondary abscess or septic infection. Even the dense fibroid tissues
may soften and degenerate and the pus may make its way spontaneously to
the pharynx, or less frequently through the skin of the parotid, or
intermaxillary region, or into the œsophagus or larynx. A fistula of the
pharynx opening externally and allowing the escape of alimentary matters
has been often noticed. These are especially liable to follow puncture
of the abscess.

Among the less common sequelæ are fistula of the œsophagus; purulent
pneumonia in connection with the purulent dissection of the œsophagean
walls and rupture into the chest (Fichet, Schneider); ulceration of the
blood vessels in the cow (Jonge); adenitis and lymphangitis of the neck,
and the thoracic glands, followed by pericarditis and pleurisy (Cadeac);
multiple embolic abscesses of internal organs (Dieckerhoff); compression
and degeneration of the vagus nerve, with consequent respiratory and
digestive troubles (Baudon); and compression and obstruction of the
jugulars with passive congestion of the brain and vertigo. (Delamotte,
Debrade). Even when the abscess opens into the pharynx the orifice is
usually small, the pus escapes imperfectly, and food materials enter and
the fistula may thus persist for a length of time. The same imperfect
discharge is liable to take place with an external orifice and the pent
up pus becomes inspissated, caseated and even calcified.

_Diagnosis._ Supra-pharyngeal abscess is to be distinguished from pus in
the guttural pouches, by the lack of coincidence of the discharge with
the dependence of the head in grazing, eating roots or drinking from a
bucket; by the absence of the intermission when the head is elevated;
and by the fact that the discharge is less frequently limited to the one
nostril. The hearing too is less likely to be affected.

_Treatment._ As soon as the presence of pus can be recognized it should
be evacuated. This is often attempted through the roof of the pharynx,
but with such an opening there is always danger from the entrance and
decomposition of alimentary matters. If fluctuation can be felt
externally, it is better to be opened through the skin. The integument
may be incised with a lancet, and the tissues further penetrated by
manipulations with the finger nail, a grooved sound or the point of
closed scissors. In this way the vessels and nerves are pushed aside and
the dangers of hemorrhage, fistula and paralysis avoided. The cavity
must be irrigated with an antiseptic solution (carbolic acid 3:100; or
acetate of aluminum 1:20).


                PSEUDOMEMBRANOUS (CROUPOUS) PHARYNGITIS.

  False membranes not due to a common microbian cause. Accessory causes
  in solipeds; caustics, smoke infection. Lesions: Congestion, necrosis;
  croupous exudate, extending to patches on bowels and bronchia; kidney
  infarctions; blood altered. Symptoms: fever, dyspnœa, mucous rattle in
  throat, swelling, painful, difficult deglutition, yellow or cyanotic
  mucosæ, pinched face, weakness, prostration. Duration. Diagnosis.
  Treatment, as for catarrhal pharyngitis with antiseptics by inhalation
  and electuary. Iron.

Pharyngites attended by the formation of false membranes are met with in
all the domestic animals and may be grouped together as a special class.
The collection of these in one group, however, must not be taken to
imply that all of these, as met with in the different animals have the
same pathology, and are due to one invariable cause. Above all it must
not be inferred that they are identical with the malignant diphtheria of
the human being. The bacillus diphtheriæ hominis isolated by Klebs in
1883, and proved pathogenic by Löffler in 1884, has not been
successfully inoculated upon any of the larger domestic animals, and has
not been found in any of the casual pseudomembranous pharyngitis of
these animals. The common feature of the group is to be found in the
formation of the false membrane, and the fact that a given disease is
placed in the group must not be held to apply to any special character,
of microbian origin, nor communicability by infection.




               PSEUDOMEMBRANOUS PHARYNGITIS IN SOLIPEDS.


Cases of pharnygitis with false membranes have been seen in horses by
Delafond, Targue, Rey, Bouley, Riss, Sonin, Robertson, Dieckerhoff and
Schneidemühl.

They have been attributed to various causes, as caustic alkalies and
acids, the smoke of a burning building (Bouley, Rey, Riss), to an
infection which operated on dogs and horses (Robertson), to bacteria and
other irritants.

_Lesions._ The mucous membrane of the mouth, pharynx and even the nares
presents active inflammation with branching redness, petechiæ,
circumscribed foci of necroses, and false membranes of a grayish,
yellowish, reddish, greenish or blackish color. These are formed of a
pellicle consisting mainly of fibrine and epithelium, pus globules and
numerous cocci, and ovoid bacteria. The false membranes have been found
on other parts of the intestinal canal (colon, cæcum); and
broncho-pneumonia and pulmonary dropsy have been concomitants. The
effect of the toxic products is seen in hæmorrhagic inflammation and
infarctions of the kidneys, and in a black color of the somewhat
diffluent blood.

_Symptoms._ Besides the usual phenomena of pharyngitis, there is intense
hyperthermia (105°–106°), hurried breathing threatening suffocation,
painful cough roused by the slightest pressure on the swollen throat and
often causing the discharge from the nose of shreds of false membrane.
Auscultation of the pharynx gives a loud gurgling sound. Deglutition is
very difficult and painful, liquids and even solids being rejected
through the nose. The face is pinched and anxious and the mouth is often
held open and the tongue pendant. Weakness and prostration are marked
symptoms from the first, and the walk may be unsteady and swaying. The
visible mucous membranes are congested and usually have a more or less
deep tinge of yellow. The disease makes rapid progress and may prove
fatal under six days. When it takes a favorable turn, recovery and
convalescence may be equally prompt.

Unless the expectoration of false membrane is detected, such cases are
difficult of diagnosis, though a fair inference may be deduced from the
extreme severity of the symptoms, and the unusual degree of prostration
which is present. When a pharyngeal speculum, passing through the nose,
can be availed of, it may become possible to reach a more definite
conclusion.

_Treatment._ Beside the measures advised for catarrhal pharyngitis
(poultice, counter-irritants, laxatives, antithermics, alkalies, etc.),
the main reliance must be placed on antiseptics. Persistent inhalations
of warm water vapor with carbolic acid, creolin, tar, lysol, camphor or
sulphurous acid are in order: also a mixture of one or other of these
agents or of boric acid, bisulphite of soda, or salicylic acid in honey
or molasses to be frequently smeared on the teeth. One of the best
agents is the saturated solution of chlorate of potash in tincture of
muriate of iron, of which a drachm may be added to three ounces of water
and given every hour or two. Calomel may be injected through the nose
during inspiration, by means of an insufflator, care being taken not to
exceed the physiological dose.


                PSEUDOMEMBRANOUS PHARYNGITIS IN CATTLE.

  Most common in calves. Inoculations successful on rabbits, mice and
  sheep. Bacillus: its cultural characteristics. Predisposing causes.
  Symptoms: nasal mucosa congested; false membranes; snuffling, wheezing
  breathing; painful, rattling cough; agonized expression; salivation;
  bowel disorder. Course. Duration. Lesions; intense congestion and
  false membranes. Treatment: as for horse; special antiseptics;
  solvents; anodynes; tracheotomy.

This has appeared especially in calves, and though apparently readily
transmissible among the young, it rarely attacks aged cattle. Cadeac and
others inoculated it on guinea pigs and rabbits without success.
Dammann, on the other hand, had his inoculated rabbits die in
twenty-four hours with hemorrhages in the seat of inoculation. Löffler
inoculated it hypodermically on mice and produced extensive infiltration
of the entire walls of the abdomen, and often of the peritoneum
including the surface of the liver, kidneys and intestines, on which was
formed a thick, yellowish exudate containing the microbe. Damman claimed
to have successfully inoculated the sheep as well.

_Causes: Microbe._ Löffler found in the deeper layers of the exudate a
long delicate bacillus, five or six times as long as broad, and about
half the thickness of the bacillus of malignant œdema. Several bacilli
were usually joined so as to form long filaments. These failed to grow
in nutrient gelatine, or sheep blood serum, but grew readily in the
blood serum of the calf.

Beside the specific microbe Cadeac enumerates as predisposing causes:
sudden chills, rapid changes of temperature, suppression of
perspiration, inhalation of irritant gases, swallowing of irritant
liquids, and traumatic injuries.

_Symptoms._ The nasal mucosa is violently congested, reddened,
thickened, and covered at intervals by false membranes which block the
normally narrow passages and produce snuffling, wheezing, and difficult
breathing. The throat is swollen, and tender, the slightest touch
producing a painful gurgling cough which leads to the discharge of
mucopurulent matter, shreds of false membrane and even blood. These
membranes may be seen on the nose or mouth. There is high fever, rapid,
small pulse, cyanosed mucous membranes, pinched countenance, and usually
open mouth, pendant tongue and drivelling saliva. There may be either
constipation or diarrhœa.

The course of the malady is rapid, death sometimes supervening in 24 to
48 hours. Recovery and convalescence may be prompt, or the disease may
last for weeks.

_Lesions._ The congestion is intense and may invade the mouth, nose,
pharynx, larynx and bronchia, with at intervals the patches of yellowish
white false membranes. These may be soft and diffluent when recent, and
tough and resistant when of longer standing. The deeper layers are often
bloodstained. Preitsch has seen them extend to the gullet, paunch and
manifolds, and attended with considerable ulceration of the subjacent
mucous membrane.

_Treatment._ This does not differ materially from that recommended for
the horse. Among the additional antiseptics employed have been,
iodoform, oil of turpentine, sulphide of calcium, silver nitrate and
coal tar. To loosen and detach the false membranes ipecacuan and
sulphates of soda and magnesia have been largely resorted to. Papayin
and pepsin might be tried. Also as anodynes digitalis, morphia, aconite
and belladonna. Finally tracheotomy has been employed when asphyxia
seemed imminent.


                 PSEUDOMEMBRANOUS PHARYNGITIS IN SHEEP.

  Cause; infected dust on susceptible subject; inoculation. Symptoms;
  movement of jaws; frothy lips; salivation; viscid nasal discharge;
  difficult swallowing and breathing; swollen tender throat; extended
  head; anorexia; cyanosis; open mouth; cough expels shreds of false
  membrane; asphyxia. Lesions. Treatment; Glauber salts or muriatic acid
  in water; antiseptic fumigation and drinking water; antisepsis of the
  pharynx.

Roche-Lubin speaks of this disease as common in flocks, as the result of
moving them around for twenty-four hours in a narrow enclosure covered
with dust which is raised in a cloud and settles in the fleece so as to
increase its weight. The fever and excitement caused by the constant
driving and the local action of the infected dust on the respiratory
mucous membrane is said to bring about the intense exudative
inflammation. It has been seen especially in the spring in young lambs
shortly after weaning. Damman claims that he transmitted the disease to
sheep by inoculating the diphtheritic exudate of the calf.

_Symptoms._ There were constant movements of the jaws, with the
accumulation of frothy saliva round the lips or the drivelling of this
secretion from the mouth, the discharge of a viscid white material from
the nose, difficulty of deglutition, hurried, panting, snuffling
breathing, swelling and tenderness of the throat, and the occurrence of
cough and the discharge of mucopurulent matter whenever it was pressed.
The head and neck are held rigidly extended, the eyes are dull or
glazed, the appetite is completely lost, the mucosæ red and cyanotic and
the animal weak and unsteady upon its limbs. By the third or fourth day
respiration has become so difficult that the mouth is held constantly
open, the tongue protruded and the painful convulsive cough leads to the
expulsion by the nose and mouth of shreds of false membrane. Careful
examination of the nose or of the fauces may detect the grayish or
yellowish patches of false membrane at an earlier stage. Death by
asphyxia is common.

_Lesions_ do not differ materially from those seen in the calf. The
inflammation and pseudomembranous exudate may extend as far as the
trachea and bronchia in which case the indications of death by asphyxia
are clearly marked.

_Treatment_ is the same as for the calf. Tepid drinks slightly acidified
with muriatic acid, or the addition to the drinking water of one pound
of sulphate of soda to every fifty sheep has been especially
recommended. Fumigation with sulphurous acid or chlorine is easy of
application in flocks. As alternatives for addition to the water may be
named hyposulphite or bisulphite of soda, borax, carbolic acid, or
spirits of turpentine. For treatment individually swabbing the throat
with antiseptics and dilute caustics, electuaries, and hot poultices to
the throat may be tried.


                 PSEUDOMEMBRANOUS PHARYNGITIS IN SWINE.

  Prevalence in herds, in close pens, and in young. Relation to swine
  plague and hog cholera. Symptoms: sore throat, prostration, hoarse
  cough, yellowish discharge with shreds of false membrane, pellicles on
  mouth, fauces, tonsils. Diagnosis from swine plague. Treatment:
  Isolation, disinfection, antisepsis to throat, febrifuges.

This has long been recognized as a contagious affection, occurring
especially where the animals were kept in herds and too often in close
and filthy pens. These are more liable in youth than in maturity, partly
no doubt because the older animals have already suffered and attained to
an immunity. Modern observation has shown that pharyngitis with
formation of false membranes is especially 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
those 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.

The _symptoms_ are those of severe sore throat with profound
prostration, a hoarse, painful cough, a yellowish discharge from nose
and mouth, and great muscular weakness. The base of the tongue, tonsils
and soft palate are red and tumid with here and there grayish or
yellowish patches of false membranes. 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 Guinea-pigs
with pure cultures of the germ.

_Treatment_ will depend largely on the nature of the attack—swine plague
or simple pseudomembranous infection. Isolation, cleansing and
disinfection will be demanded in both cases. In swine plague all
additional precautions to prevent its spread must be resorted to. In the
simpler exudative inflammations the antiseptic local treatment and
general febrifuge measures will be demanded.


                 PSEUDOMEMBRANOUS PHARYNGITIS IN DOGS.

  Relation to diphtheria in man and horse. Symptoms; fever, prostration;
  swollen throat; cough; vomiting; false membranes on fauces and
  tonsils; cyanosis. Treatment: local antisepsis; febrifuges.

Rossi and Nicholski claim that dogs contract diphtheria by swallowing
the excrements of diphtheritic infants, but these observations lack
confirmation, and the infrequency of such an occurrence argues against
it. Robertson records cases of canine angina with false membranes
occurring at the same time as a similar affection in the horse. The
victims were puppies and the mortality was high. Exact observations are,
however, lacking.

The _symptoms_ were dullness, prostration, anorexia, a hard cough,
swollen throat, vomiting, diarrhœa, and the presence of grayish or
yellowish false membranes on the fauces and tonsils. The breathing was
difficult and painful and the mucosæ cyanotic.

_Treatment_ has been essentially local, consisting of swabbing with
solution of boric acid (1:200), chlorate of potassa, perchloride of
iron, or nitrate of silver.




          PSEUDOMEMBRANOUS STOMATITIS OF PIGEONS AND CHICKENS.

  Contagious and destructive nature of the disease. Mode of extension
  from the mouth and pharynx. Causes: bacillus diphtheriæ columbarum;
  its characters: pathogenesis to birds, mice, rabbits, Guinea pigs;
  dogs, rats, and cattle immune; diagnosis from bacillus diphtheriæ.
  American disease. Incubation. Symptoms: prostration; wheezing
  breathing; sneezing; difficult deglutition; false membrane on fauces;
  necrotic changes in mucosa; perforations; lesions of internal organs;
  blood infection; nostrils stuffed; bill gapes; lesions on eye, tongue,
  gullet, crop, intestine; diarrhœa; vomiting. Skin lesions. Course,
  acute, chronic. Paralysis. Mortality. Prognosis. Diagnosis from
  coccidiosis, from croupous angina of Rivolta, from aspergillus
  disease. Treatment: isolation; destruction of carcasses; hatching;
  destruction of dead wild birds and rabbits; exclusion of living;
  quarantine of new birds; disinfection; locally, antiseptics by
  inhalation, swabbing, and internally, iron in water.


This affection prevails in certain countries and causes heavy losses
among young pigeons, so that it might with great propriety be included
among animal plagues, which should be dealt with by the State. The
malady is a local inflammation leading to the formation of false
membranes and its usual course is to progress from the mouth and
pharynx, to the nasal passages, lachrymal ducts and sacs, the larynx,
trachea, bronchia, intestines and skin.

_Causes._ The essential cause of the disease is held by Löeffler to be
the _bacillus dipththeriæ columbarum_, which is a short bacillus with
rounded ends, a little longer than the bacillus of fowl cholera and not
quite so broad. It is usually found in irregular clusters, especially in
the interior of the hepatic capillaries. It is ærobic, non-motile,
non-liquifying, and grows on nutrient gelatine, blood serum or potato.
In gelatine it forms a white surface layer, and spherical colonies along
the line of puncture, which show a yellowish brown tint under the
microscope. On blood serum and potato it forms a grayish white layer.

_Pathogenesis._ The bacillus is inoculable on other =pigeons= and as it
usually appears in the young birds in the nest, still fed by the parent
bird, it is probable that no inflammation nor abrasion is necessary to
make it take. Pure cultures inoculated in the mouth gave rise to the
usual local type of the disease. When inoculated subcutem it caused a
local necrotic inflammation.

In =mice= subcutaneous injections proved fatal in five days with general
dissemination of the bacillus. There are congested and hemorrhagic spots
on the lungs, enlarged spleen, and the liver is marbled by numerous
necrotic white masses, in the centre of which the capillaries are found
to be blocked with the bacilli. This is so pathognomonic that Löffler
looks on the inoculation of mice as the best means of diagnosis.

Inoculated =rabbits= showed inflammation in the seat of inoculation and
sometimes fibrinous peritonitis and enlarged spleen. Inoculation on the
cornea produced a false membrane.

In =Guinea pigs= induration and ulceration occurred in the seat of
inoculation but recovery followed in 14 days.

=Sparrows= inoculated in the pectoral muscles died in three days with
yellowish necrotic tissue highly charged with bacilli.

Inoculation of the =chicken= by Löffler and Megnin produced a
circumscribed redness which soon disappeared. On the other hand
Krajewski, Colin, Loir and Ducloux seem to have inoculated chickens
successfully, and Cadeac says that the cultures are infecting for
=sparrows=, =pigeons=, =turkeys=, =chickens= and =ducks=. It rests
uncertain therefore whether the pseudomembranous pharyngitis of hens is
a distinct disease as alleged by Löffler and Megnin or if the chickens
used by these observers were not already immune by reason of a prior
attack.

Löffler’s experiments showed that _dogs_ and _rats_ were immune. Loir
and Ducloux failed to infect cattle.

In infected dove-cots a comparative immunity is attained by the older
pigeons, which continue to harbor the germ, but do not suffer materially
from its presence. They however communicate it to the susceptible young
in the milky secretion produced in the crop and with which they feed
them, and these accordingly perish in large numbers. Thus pigeons that
are themselves in fine condition become the propagators of the bacillus
to the more impressible.

_Sparrows_ and other _small birds_ are also held to be common
propagators of the germ, and if they too can secure an individual
immunity and yet harbor the bacillus, their passage from yard to yard
may be attended with great danger. The grains soiled by their bills and
not swallowed are common media of transmission.

Loir and Ducloux found the affection transmissible between man and
pigeon. The identity of the bacillus with that of genuine diphtheria in
man appears to have been thoroughly disproved by the observations of
Roux and Yersin.

The following differential characters have been noted:

          _Bacillus Diphtheriæ          _Bacillus Diphtheriæ Columbarum_
           (Klebs-Löffler)._


 1. In gelatine cultures grows only  1. In gelatine cultures grows at
      above 23°C.                         15–17°C.

 2. Kills Guinea-pig and dog.        2. Guinea-pig and dog nearly
                                          immune.

 3. Mice immune.                     3. Mice usually die with hepatic
                                          necrosis.

 4. Does not grow on potatoe.        4. Grows luxuriantly on potatoe.

It may be accepted as demonstrated that the common diphtheria of birds
is essentially distinct from the genuine diphtheria of man, and that
when such diphtheria of the bird is conveyed to man as has been often
alleged (Richter, Gips, Bonig, Gerhart, etc.), it is one of the forms of
pseudo diphtheria that is produced, and not that which is caused by the
Klebs-Löffler bacillus. Dr. V. A. Moore, who has cultivated specimens of
the bacillus diphtheriæ Columbarum obtained from Germany, considers the
germ as belonging to the group of the bacillus coli communis, and as not
the cause of the chicken diphtheria in America. Further investigation
must settle whether the bacillus diphtheriæ Columbarum is the one cause
of this affection in Europe, and what is the microbian cause or causes
of the disease in America.

_Incubation._ This is very variable. False membranes may form in
twenty-four hours in some cases; in other cases they may be delayed from
four to fourteen days (Colin, Babes, Puscarin, Marinescu).

_Symptoms._ There is dullness, prostration, sunken head, ruffled
feathers, altered hoarse voice, drooping wings, wheezing breathing,
difficult deglutition, sneezing, and patches of dark red congestion in
the fauces covered with a thin film, at first translucent, but soon
becoming dense, adherent, opaque, whitish or yellowish. As it becomes
older this deposit becomes granular, wrinkled, dry and friable. It is
more adherent in chickens than in pigeons and causes bleeding when
detached. Necrotic changes may take place in the mucosa leading to
considerable loss of tissue, and even to perforations of the soft
palate, pharynx or œsophagus. It may remain circumscribed by the region
of the mouth and end in an early recovery, or it may extend to the
organs of the chest and abdomen, or the germs may proliferate largely in
the blood and induce fatal results. On the other hand it may become
subacute or even chronic, and, as already noted in the case of the
parent pigeons, it may persist as an infecting disease without
materially injuring the general health of a comparatively immune animal.

The affected _nasal passages_ become filled by frothy liquid and blocked
by false membranes, so that the bird is driven to breath through the
open mouth. The skin around the nares, and eyelids and the cavity
beneath the eye may be covered with the false membrane, by the increase
of this product the bones may be driven out of place, so that the
palatines press downward, the eyeball is pressed outward and the root of
the beak may seem swollen. The false membranes that form on the skin or
reach the surface are soft, creamy, cheesy, or dry, granular and
friable.

When the _eye_ is specially affected there are swelling of the lids,
profuse lachrymation, closure of the lids by adhesion, and formation
around their borders or on their inner surface and on the membrana
nictitans of false membranes which press the lids outward more or less
unevenly, and may be easily recognized when the lid is everted. The
cornea and even the interior of the eye may suffer, leading to
perforation, internal tension, and in some cases atrophy, with permanent
blindness.

The _tongue_ may suffer on the tip as in _pip_, or on its dorsum, from
which the disease extends to the larynx, trachea and even the air sacks,
which become filled with false membranes, that are coughed up, and
decomposing in the mouth, add to the infection and fœtor. Dyspnœa and
cyanosis of comb and wattles are marked features.

The extension may take place downward along the alimentary track, the
false membranes forming on the _gullet_ or _crop_ and interfering with
swallowing or digestion, or on the intestine and determining a fœtid,
often greenish or bloody diarrhœa with indications of false membranes.
Vomiting may be a marked symptom.

The _skin_ is usually attacked secondarily around the margin of the
beak, the eyelids, the nares, the ears, the comb, the wattles, the anus,
but it may develop at any point where the infecting material has touched
an abraded surface.

Trinchera found that in acute cases the acme was reached in fifteen days
after which improvement might be looked for. A chronic form affecting
the gullet might however persist indefinitely in pigeons without proving
incompatible with good health.

Paralysis of the wings or limbs may remain after the healing of the
local lesions.

_Mortality. Prognosis._ The disease is very fatal to both pigeons and
chickens, 50, 70 or even 100 per cent. perishing when a flock is
attacked for the first time. In flocks that have previously suffered, on
the other hand, a large number are practically immune, and even if they
contract the disease it assumes a mild form, and they survive but may
retain the germ and continue to communicate it to others. Even the young
of such immune flocks suffer less severely, coming as they probably do
from less susceptible and therefore surviving birds, or having already
perhaps contracted a mild (non-fatal) type of the disease from their
parents.

_Differential Diagnosis._ From _psorospermosis_ (_coccidiosis_) it is
distinguished by its origin on the mucous membranes, and not on the
skin, the skin lesion being a secondary one. In psorospermosis the
primary lesion is usually on the skin, from which it extends to the
mouth and especially along its floor. In psorospermosis the morbid
deposit assumes the form of rounded warty-like masses, on comb or
wattles; is easily propagated by inoculation, is promptly checked by
antiseptics, does not tend to produce internal extension nor
generalization, and on microscopic examination shows numerous spheroidal
coccidia intermingled with the epidermic cells and possessing amœboid
movement. By virtue of this automatic movement they make their way
between and into the epidermic cells in which they multiply.

From the _croupous angina_ of Rivolta it is distinguished by the absence
of the infusoria (monocercomonas gallinæ) to which he, Delprato and
Pfeiffer attributed that affection. The monocercomonas is a flagellate
organism 14 _μ_ to 25 _μ_ in length and 5 _μ_ to 7 _μ_ in breadth. Its
rounded end bears one flagellum as long as the body, and its acute end
three flagella which give it active motions. These are found in the
yellowish white swellings of the mucosa, which vary in size from a
millet seed to a pea, covering a hyperæmic spot and composed of
epithelial cells, blood globules—white and red,—leucocytes, granules and
the infusoria. The false membrane is remarkable for its lack of
consistency and its tendency to invade the mouth and gullet rather than
the air passages. These infusoria are not colored by picrocarminate of
ammonia, but stain by methyl-violet and then appear as round or slightly
irregular hyaline bodies.

From _aspergillus disease of pigeons_, by the absence of the
characteristic, miliary, white nodule of that disease showing caseated
contents intermixed with an abundant mycelium of aspergillus fumigatus.
The aspergillus disease attacks especially the mouth but may also
implicate the gullet, lungs, liver, intestine and kidneys. The
microscopic examination of the exudate is conclusive, by reason of the
presence of the bacillus diphtheriæ columbarum, and the comparative
absence of the filamentous mycelium.

_Treatment._ This is mainly prophylactic. The first step must be to
separate the sick and healthy, destroying the former, or shutting them
up in a special enclosure apart from all other birds. In the case of
valuable chickens, their eggs may be set under other hens and the young
raised apart from the suspected flock. This may even be attempted in
pigeons, the common eggs being removed and the valuable ones put in
their place under a healthy sitting dove. In the case of pigeons that
have been recently through the disease they should be kept strictly by
themselves, even though they may appear to have regained perfect health.
The dead bodies must be burned or deeply buried. Sparrows and even
rabbits dying in the vicinity must be similarly disposed of, and where
the disease prevails sparrows and small birds may be exterminated as
probable bearers of infection.

The purchase of strange birds must be carefully guarded, none being
taken that show weeping eyes, nasal discharge, labored or wheezing
breathing, and all new birds should be placed by themselves in
quarantine for ten to fifteen days. Finally a thorough disinfection of
the place where the sick have been is of first importance. Thorough
cleaning of the poultry house, followed by a coat of white-wash, every
gallon of which contains four ounces of chloride of lime, or one drachm
of mercuric chloride will usually prove effective. The poultry runs
should be liberally sprinkled with a solution of sulphuric or
hydrochloric acid, one part to 1000. The same may be used on the
building, which may further be fumigated by burning sulphur.

Poultry shows should be kept under the most rigorous sanitary
supervision.

_Curative treatment_ is only profitable in the case of specially
valuable birds, and even then only, as a rule, when the disease is
confined to the nose, mouth, larynx and pharynx. The affected parts may
be brushed with a solution of chloride of iron (1 dr. of the tincture to
1 oz. water), nitrate of silver (2 grs. to 1 oz. water), sulphide of
calcium (½ dr. to 1 oz. water), tannin (10 grs. to 1 oz.). Tincture of
iodine may be applied direct, or a solution of carbolic acid or of
creosote or creolin (1 part to 50) will often succeed. Thomassen
recommends the removal of the false membranes and the application of
boric acid followed by dry sulphur. Benoist says the majority recover
when made to inhale the fumes of oil of turpentine evaporated at a
gentle heat twice a day.

As internal medication, or to correct the intestinal affection, sulphate
of iron may be dissolved in the drinking water, or salicylic acid may be
given in pill form with molasses.


                          CHRONIC PHARYNGITIS.

  Sequel of acute: or subacute from the first. Due to œstrus, in cattle
  to summer catarrh, tubercle or actinomycosis. Lymphatic horses
  predisposed; attends chronic indigestion; in swine tonsilitis.
  Symptoms: chronic cough, easily roused, wheezy or mucous; nasal
  discharge; low condition; lack of spirit. Lesions: congestion;
  softenings; erosions; cicatrices; tonsilitis; abscesses; specific
  deposits. Treatment: hygienic; antiparasitic; astringent; antiseptic;
  derivative; counter-irritant; tonic inhalations and electuaries.
  Bitters. Iron.

_Causes and Nature._ Chronic pharyngitis in animals may be a simple
continuation of the acute, in a milder form, or it may assume a subacute
or chronic type from the first and never rise to the intensity that
would characterize the acute. It may be a simple catarrhal affection or
it may become more or less follicular or glandular. Again in horses it
is not infrequently a result of the hibernation form of the œstrus
(bots) attached to the delicate pharyngeal mucosa, and in cattle from
the extension of the chronic summer catarrh, or from the local
development of tubercle or actinomycosis in the walls of the pharynx or
in the adjacent lymph glands. Horses of a soft, lymphatic constitution,
with a heavy coat, confined in close warm stalls, and which perspire
abundantly are especially liable to the affection. It may also be an
accompaniment and result of chronic gastric indigestion. In swine the
affection is commonly associated with tonsilitis.

_Symptoms._ In many cases the main symptom is a chronic cough which is
aroused by any cause of irritation, feed, especially dry or fibrous
fodder, cold drinking water, sudden passing from the hot stable to the
cold outer air, reining in, pressure on the throat, or sudden active
exertion. If the cartilages are calcified it may be impossible to rouse
the cough by pressure. The cough is often dry and wheezy, rather than
soft and gurgling as in the second stage of acute pharyngitis, and is
repeated several times paroxysmally. In the intervals there is more or
less stertor or wheezing, or a distinct rattle especially when the neck
is curved by drawing the nose inward. Deglutition may be interfered with
but this shows most with the first swallow, which in the case of liquids
may be returned through the nose, whereas those that follow go down
without difficulty. A lateral swelling of the parts above the larynx or
a bulging of the parotids is not uncommon. Discharge from the nose of a
mucopurulent character is usually present, but often so scanty as to be
overlooked. There is usually loss of flesh and lack of vigor even if the
subject is well fed.

_Lesions._ In the simple catarrhal form the mucous membrane of the
lateral pharyngeal walls, the posterior pillars of the palate and the
back of the soft palate, is red, congested, with arborescent vessels,
thickening, and puckering into rugæ. The epithelium has lost its
translucency, become opaque and granular, and its desquamation in spots
and patches may leave erosions, ulcers more or less deep, and white
drawn cicatrices. When the follicles and mucous crypts are involved
(follicular) they stand out like millet seed, peas or beans, and may
show ulceration or minute abscess. In pigs especially, tonsilitis is
liable to be present, and the tonsillar follicles are filled and
distended with tenacious mucous, a caseous granular _debris_, or even a
cretaceous material. In the vicinity of the tonsils, minute abscesses
may exist in or beneath the mucosa.

Ulceration may be the result of tubercle, glanders, actinomycosis,
aspergillus, sarcoma, or some local infection, and attendant symptoms of
one or other of these diseases will guide the diagnosis. Thus in
tubercle there will be the implication of the adjacent lymph glands and
usually of distant ones; in glanders the deposits in the nose,
submaxillary lymph glands and lungs will enable one to diagnosticate; in
actinomycosis the hardness of the neoplasm and the presence of the
yellowish tufts which present under the microscope the concentrically
arranged club-shaped elements, will show its nature; and in sarcoma or
carcinoma the structure of the new tissue will decide its character. The
pharyngeal muscles are the seat of granular or fatty degeneration or of
fibroid change. Friedenreich speaks of a fold from the vault of the
pharynx which had nearly closed the passage and had killed the horse by
inability to swallow.

_Treatment._ Chronic pharyngitis is usually a very obstinate affection
and demands careful hygienic as well as medicinal treatment. Hot, foul
stables, unduly thick coats, unwholesome food, irregular feeding,
excessive meals at long intervals, overwork, undue exposure to cold and
wet, lack of sunshine or of grooming are to be corrected. Next, the
removal of mechanical irritants such as pharyngeal bots, actinomycosis
growths, etc., will be in order. Then the use of astringents and
antiseptics internally and of derivatives externally will be demanded.
An occasional embrocation of mustard, or the application of ammonia and
oil, will often serve a good purpose, and in obstinate cases the hot
iron in points will sometimes prove effective.

Internally the inhalation of the fumes of tar, carbolic acid, creolin,
oil of turpentine, or of burning sulphur kept up continually or
frequently repeated. Giving all drink in the form of tar water will
often have a good effect. Electuaries made with boric acid, salicylate
of soda, ammonium chloride or iodide, borax, with honey, molasses,
liquorice, Iceland moss, or gum arabic will often prove beneficial.
Agents that stimulate the mucosa may follow, such as balsams of Peru or
Tolu, copaiba, cubebs, pilocarpin, wild cherry bark, or these may be
combined with the former. Finally a course of tonics are usually of the
first importance; iron sulphate, copper sulphate, arsenious acid,
arsenite of strychnia may furnish examples.


        DEPRAVED APPETITE. STUMP SUCKING. PICA. LICKING DISEASE.

  Common features of group. Ruminants; depraved appetite; objects
  swallowed: hair balls. Sheep eating wool in winter. Pigs eat bristles.
  Puppies swallow marbles, etc., wantonly. Solipeds swallow hair,
  plaster, earth, sand, and lick manger or rack. Fowls eat their
  feathers. Causes: soil exhaustion, lack of lime, soda, potash,
  phosphorous; relation to osteo malacia; granitic or sandy soils, peat,
  muck, causative; digestive disorder; faulty food; yearly breeding and
  heavy milking; constant stabling; dry seasons. Course: chronic.
  Lesions; emaciation; anæmia; serous exudate; catarrh of the bowels.
  Treatment: soil; good fodder; salts of soda, potash and lime,
  phosphates; tonics; apomorphine. Wool eating; example: digestive
  disorders; emaciation. Treatment: open air; good fodder; salts of the
  bones and soft tissues; clip nurses; apomorphine.

_Definition._ We have here a class of morbid habits, which cannot be
referred to any constant lesion or group of lesions, and which appear in
certain cases to result from example and to constitute nothing more than
a bad habit.

_Symptoms._ _Ruminants_ without any appreciable cause, lick the clothes
of their care-takers, chew and swallow articles of clothing of all
kinds, bones, old shoes, gloves, socks, cuffs, collars, small forks,
pocket-knives, nails, wires, needles, coins, stones, lumps of clay,
hair, which may give rise to secondary troubles of a more or less
serious kind. Pregnant cows are especially subject to this infirmity.
The small pointed objects like pins, needles, ends of wires, etc., which
are mostly taken by accident with the food are especially apt to be
entangled in the alveoli of the reticulum and make their way to the
heart, with fatal effect, or through the abdominal walls creating a
fistula. Hair aggregates with saliva, mucus and phosphates, to form
balls in the first two or three stomachs. Other indigestible objects may
also become encrusted and prove sources of irritation. Licking the skin
of another animal is doubtless at times encouraged by the taste of the
salts of perspiration, but in other cases it has all the appearance of a
mutual kind service as the cow with itching head will walk up and
present it to its fellow which rarely fails to respond to the
invitation. Stump licking is not uncommon.

=Sheep= shut up in the winter get in the habit of chewing each other’s
wool, thus virtually depilating their fellows and accumulating wool
balls in their stomachs.

=Pigs= when running at large eat human fæces often infecting themselves
with the cysticercus cellulosa, and devour their own or their fellows’
bristles, which form ovoid and irritating aggregations in the stomach.

=Puppies= are proverbial for swallowing every small object that comes in
their way, coal, pebbles, marbles, leather, hair, etc., with the result
of inducing nausea and vomiting, or more seriously, wounds of the
stomach, gastritis and enteritis. In older dogs the habit is more likely
to imply rabies.

=Solipeds= will lick and swallow each others hair, eat off the hair from
each other’s tails and manes, eat their clothing, lick the wall plaster,
earth or sand, and even the manger or rack. The last named habits are
usually connected with disease.

=Fowls= can digest almost anything they swallow, but if they take to
picking their feathers, they create serious injury to the skin and
indirectly to the general health.

_Causes and Nature._ In general terms it may be said that the causes of
depraved appetite are very numerous, so that the trouble must be looked
upon as a symptom of many morbid conditions in place of a disease _sui
generis_.

_Heredity_ has been invoked as a cause, mainly, it would appear, because
the disease appears enzootically on certain exhausted soils, or in herds
kept in the same unhygienic conditions. In such cases the real cause is
usually to be found in faulty conditions of soil, water, buildings,
food, etc., on the correction of which the trouble disappears. When,
however, from a long continuance of unhygienic conditions, a weakness of
constitution is transmitted from parent to offspring, such hereditary
debility may be accepted as a predisposing factor.

_An exhausted soil_, lacking especially the elements of lime and
phosphorus, is a common cause, though by no means the only one. Nessler
who analyzed the hay and water, furnished to cattle suffering from this
disease in the Black Forest found a notable absence of the soda salts.
In others in which osteo malacia was the prominent symptom the lack was
in phosphate of lime as well. In the nature of things the soil that has
been continuously cropped to exhaustion is robbed of both earthy and
alkaline salts, and the animals fed on its exclusive products suffer not
only as regards the nutrition of the bone, but also of the soft parts.
Hence Trasbot says that in osteo malacia, pica is never absent. Roloff
and Röll hold that it is the first symptom of osteomalacia. In South
Africa where the land has been cropped with oats year after year without
manure and as long as it will bear, the disease became prevalent in the
street car horses fed on the oats, and was corrected by the addition of
phosphates, or phosphate bearing food, to the ration. In the older
dairying farms of New York which have been kept under grass for a great
length of time, and all the milk products sold off, depraved appetite in
all its forms is quite frequent. Where the land is originally light and
sandy and naturally deficient in lime, osteo malacia is often a
concurrent disorder. The two conditions may however occur independently
of each other, and especially may pica appear alone, in keeping with the
greater solubility of the soda and potash salts and the readiness with
which these can be washed out of the soil, while the less soluble lime
salts in part remain.

Lemcke, Haubner and Siedamgrotzky attribute the disease to a nervous
disorder. Lemcke indeed traces the disorder to a lack of phosphorus, and
claims that osteomalacia only supervenes where the rheumatic diathesis
is also present.

It may be shortly stated that the disease prevails especially on
granitic or sandy soils, or on those which are mainly composed of
organic debris (peat, muck). Limestone soils and those which contain any
considerable proportion of potash or soda are usually exempt.

_Digestive disorder_ though starting from a different point may tend to
the same end. A hyperacidity of the stomach has been observed to
coincide with the malady, and by interfering with easy and normal
digestion, it may stand in the way of such assimilation as is necessary
to vigorous health.

_Faulty food_ operates in a similar manner. The exhausted soils, and
their products deficient in alkaline and earthy salts have been already
referred to; we must also note the evil effect of fibrous fodders, the
main nutritive elements of which have been washed out by intemperate
weather after they were cut, the rank aqueous products of wet or swampy
soils, the fibrous and siliceous plants (rushes, carex, equisetums,
etc.) which grow on poor, wet or soured soils, the innutritious and
fermented products of beet sugar factories, and generally the spoilt
food which has undergone fermentation.

_Yearly breeding_ and _constant milking_, by undermining the general
health, predisposes so strongly that in many cases the affection is seen
in dairy cows, while oxen and young cattle escape. The last period of
gestation when the demands for the growing calf are greatest, is the
period of especial danger.

_Permanent stabling_ which denies the invigorating influence of sun,
exercise and pure air contributes toward the general debility and
therefore, in animals that are closely stabled for the winter the spring
is especially to be feared, when compulsory inactivity, poor feeding,
gestation and milking have combined to reduce the system.

_Dry seasons_ have been noticed to increase the affection manifestly by
reducing the supply of food.

_Course._ The affection is chronic and unless arrested by the
supervention of more favorable conditions, may last for a year or more.
Spontaneous recovery may set in when turned out to pasturage and open
air life, and especially if a rich grain feeding is added. Without
change in the conditions however, the tendency is to a fatal result.

_Lesions._ The victims of the disorder are emaciated, the fatty tissue
contains a yellow serum, there is little blood, and that is thin and
watery and coagulates loosely, the muscles are pale and flabby, and the
gastro-intestinal mucous membrane is the seat of catarrh.

_Treatment._ To treat rationally and successfully we must adapt the
measures to the obvious causes. When the soil has been scourged and
exhausted, a change of pasture, and of land used for hay or soiling
crops is the first consideration. If these cannot be secured then grain
and seeds rich in protein, and alkaline and earthy salts should be added
to the ration. Wheat bran, middlings, peas, beans, cotton seed meal,
linseed meal, rapecake may be named among available resorts, or in their
absence, daily doses of phosphate of lime, and sodium chloride or
bicarbonate, or potash salts may be allowed, or even bone dust.

If imperfect digestion is a manifest factor, sodium chloride, or
potassium chloride, calcium phosphate, iron and bitters will serve a
good end. In hyperacidity, limewater, chalk, or magnesia may be given.
If the digestion is torpid, hydrochloric acid with bitters may be
resorted to.

Feser and especially Lemcke strongly recommend apomorphia. It is used
hypodermically in doses of 2 grains for horse or cow repeated daily for
three days.

=Secondary Symptoms in Wool-eating Lambs.= Lambs from two to six weeks
old especially such as suck ewes with woolly udders (merino, Cotswold)
first swallow the wool inadvertently, and then acquire a liking for the
saline matters in the abundant yolk (merino), till finally the
accumulating wool balls produce digestive and nervous disorder and a
craving for the indulgence. Thus the breed must be considered in
estimating the symptoms. For the same reason the wool about the hips or
elsewhere soiled with salts of the urine or liquid fæces prove
attractive to the victim. The proximity of other wool eaters is another
cause which starts others to follow the bad example. The general
conditions of debility, exhausted soil, and the absence of alkaline and
earthy salts must be borne in mind. So too with prolonged confinement
indoors in winter, the absence of invigorating exercise and the
restriction of the animals (dams) to food which is deficient in saline
matters.

Beyond the mere eating of the wool and the destruction of fleeces, the
lambs do not usually suffer seriously. But if the consumption of wool is
excessive the accumulating balls of the size of marbles in the stomach,
and the blocking of the pylorus and small intestine, may give rise to
intermittent constipations and diarrhœas, deranged digestion,
muco-enteritis, mucous covered stools, loss of condition, emaciation and
retarded development.

_Treatment_ consists first in the securing of a more healthy regimen.
This is but one of the evils of the close winter confinement of an
animal preëminently adapted to freedom and exercise. Turning out in a
wide range, especially if pasture is available, is a prime
consideration. The separation from the flock, of the first wool eaters,
will check the propagation of the vice by imitation. Food that is
defective in one or more constituents must be supplemented by that which
will correct the deficiency. Salt, potassic salts and above all
phosphate of lime or bone meal will sometimes benefit. May recommends
the separation of the lambs from the ewes except when nursing, three
times a day. Finally Lemcke claims for apomorphia the same curative
effect as in other animals. The dose is 2 grains, subcutem, as in the
cow and may be repeated three days in succession.


                       LACERATION OF THE PHARYNX.

  Trauma of pharynx from objects swallowed; from whip or other
  instrument in choking; lesions. Symptoms: swelling; rapidly extending;
  dysphagia; salivation; retching; dyspnœa; roaring; asphyxia.
  Treatment: as for pharyngitis; open pouch, suture laceration; use
  antiseptics; liquid diet.

Laceration of the velum palati has been already referred to, and the
remaining walls of the pharynx sometimes suffer in the same way and from
identical causes. Pins, needles, and other sharp pointed bodies taken
with the food sometimes perforate the walls and determine an advancing
ulceration which furnishes a way for their escape externally in the
region of the throat. In other cases a rigid staff, a whip, or even a
probang introduced to overcome choking, is forced through the walls of
the pharynx forming a pouch for the accumulation and septic fermentation
of ingesta, and extensive ulcerative and gangrenous lesions.

_Lesions and Symptoms._ These depend mainly on the extent of the
laceration. If there is a mere abrasion, superficial laceration or prick
of the mucosa, it determines a prompt inflammation, with exudation which
covers or closes the wound and a speedy healing may ensue. When,
however, the whole thickness of the mucosa has been extensively
lacerated and a pouch has been formed beneath it, it becomes filled with
decomposing mucus and ingesta, and the resulting septic products
determine ulceration, abscess, or gangrene. The result is too often a
general and fatal septic infection.

In the milder forms there are only the common indications of a moderate
pharyngitis. In the more severe form, the throat swells at first on the
lacerated side and later all around. This swelling soon fills the
intermaxillary space and extends over the face and the entire head. From
the first, deglutition is extremely difficult or impossible, liquids are
returned through the nose and saliva flows abundantly from the mouth.
Retching is not uncommon and saliva mixed with alimentary matters is
discharged by the nose (solipeds) or mouth (other animals). The swelling
of throat and head has a doughy, œdematous feeling, it is very tender,
and soon causes rattling, wheezing breathing, roaring, dyspnœa and
asphyxia.

_Necropsy_ shows the general œdematous exudate, the laceration of the
pharyngeal walls, and the collection of debris and pus in the lacerated
cavity. The pus may have extended between the muscles following the
course of the gullet and trachea as far as the chest. Extensive patches
of necrosis may also be shown. _Treatment._ In the slighter cases the
ordinary treatment for catarrhal pharyngitis is demanded. In the more
severe the lesions are so redoubtable and their progress so rapid that a
fatal result is virtually inevitable. As a desperate resort the septic
pouch may be opened from without, its contents removed, the pharyngeal
wound sutured if possible, and a thorough irrigation with antiseptics
(acetate of aluminium solution) employed at frequent intervals to check
if possible the septic process. The animal should be fed with well
boiled milk or other liquid which will not add to the fermentation, and
this may be given through a stomach tube, or by the rectum when
deglutition is impossible.




                        PARALYSIS OF THE PHARYNX

  From nervous bulbar lesion, or toxic from the pathogenic bacteria.
  Transient or permanent and fatal. Symptoms: dysphagia: liquids
  expelled by nose or enter lungs. Inhalation pneumonia. Facial palsy.
  Roaring, laryngeal thrill. Atrophy. Gangrene. Treatment: remove cause:
  combat bulbar hyperæmia and cephalic congestion: cold: derivatives,
  electricity: blisters: antiseptics.


This has been described as a rare affection, yet it is often a marked
symptom of cerebro spinal meningitis, and has been observed in
infectious pneumonia, and influenza of the horse (Cadeac, Palat) as well
as in rabies, and traumatic injuries of the brain.

The existence of the condition usually implies disease of the bulb at
the roots of the vagus and glossopharyngeal nerves, or swellings
affecting these nerves or the sympathetic along its course. The morbid
condition may be transient in which case a speedy recovery may follow,
or it may be permanent and end fatally.

_Symptoms._ Swallowing is impossible and the animal refuses food and
drink or if the latter is forced on him it is rejected by the nose or
mouth when the head is lowered or still worse, it enters the larynx and
descends into the lungs. The larynx innervated by the same trunks is
usually involved and the alimentary solids and liquids determine
gangrenous bronchitis and pneumonia, with labored breathing, fœtid
breath and violent dyspnœa. In other cases the facial nerve is involved,
the nostrils and lips are flaccid on one or both sides, and the eyelids
and ears may droop. There may be snuffling breathing from the closure of
the alæ nasi, or roaring from the approximation of the arytenoids and
vocal cords. If the affection is unilateral the difficulty of breathing
is greatly diminished and even deglutition may be effected with some
effort. There is usually, however, the obvious unilateral paralysis of
the face, and especially of the larynx, with the distinct thrill, during
inspiration, conveyed to the finger placed on the larynx.

Complications in the form of gangrene and atrophy of parts supplied by
the same nerves, or those adjoining the pharynx, have been recognized in
different cases.

_Treatment._ This must depend on the obvious cause of the affection. If
due to an infectious disease the first attention must be given to that.
If due to tumors or abscesses pressing on the nerves they may be
removed. If there is bulbar hyperæmia or effusion attention must be
devoted to derivation and other means of combating that. Cephalic
congestion and heat may be met by cold applications. Derivation toward
the bowels may be secured by eserine, pilocarpin or physostigmine
administered subcutem. Reabsorption of exudate may be sought by
pilocarpin, or diuretics—the latter administered by the rectum.
Electricity in weak current may be tried when the acute febrile symptoms
have moderated, accompanied by hypodermic injection of strychnia (2
grs.). Frictions around the throat with essential oils or even a
cantharides blister may be used to advantage. Antiseptic washes may be
injected into the mouth,—vinegar, boric acid, borax, sulphite of soda.
Finally the animal must be nourished by rich gruels and soups given by
the rectum, or in the smaller animals by the stomach tube.


                         TUMORS OF THE PHARYNX.

  Varieties of neoplasms. Malignant invade adjacent and distant parts.
  Symptoms: sore throat; stertor; dyspnœea; dysphagia. In cattle,
  lymphadenoma, tubercle, actinomycosis. Cause cough, ptyalism,
  discharge, fœtor, dysphagia. Dogs and pigs vomit. Treatment: medical;
  surgical.

Tumors of the pharynx are not common in the _horse_ yet they
occasionally appear as either primary or secondary neoplasms. They are
of various kinds, as, epithelioma (Labat, Mathis), carcinoma (Casper,
Dupuy, Mathis), sarcoma (Siedamgrotzky, Johne), lipoma (Fricker),
cystoma (Degive) and melicerous (Lesbre). The malignant forms tend to
invade the surrounding tissues and spread widely into the nose, palate,
tongue, pharyngeal glands, and, secondarily, into the small intestines.
The simple tumors like the lipomata and fibromata tend to detach
themselves and hang by a pedicle (see pharyngeal polypi). The same is
true of the melicerous cyst which originating in an obstructed mucous or
salivary duct projects as a mass as large as a hen’s or pigeon’s egg
into the fauces or pharynx.

_Symptoms._ There are symptoms of intense sore throat with stertor
continuous or intermittent, increasing to dyspnœa at intervals or on
exertion. In case of pediculated tumors these attacks correspond to the
displacement of the tumor into the glottis. Deglutition is difficult or
impossible, liquids or even solids returning through the nose, mixed
with mucus and at times tinged with blood. Nasal discharge and ptyalism
are present.

In =cattle= pharyngeal tumors may be of the same nature as mentioned for
the horse, but they are far more frequently lymphadenoma, and above all
tubercle or actinomycosis. Zimmer found that of seventy-three such
tumors fifty-four were actinomycosis.

The _symptoms_ are wheezing breathing, cough, nasal discharge, ptyalism,
bleeding from the nose, fœtid breath, difficult deglutition attended by
cough and rejection of the ingesta through the nose, and the presence of
a solid body in or on the pharynx which may be manipulated from without
or within and tends to increase in size.

In =dogs= there are the same general symptoms with vomiting. The vomited
material is usually remasticated and swallowed. The swelling in the
pharynx can be felt from without, or seen through the open mouth. The
tonsils are usually enlarged. Pressure on the pharynx or gullet produces
instant regurgitation.

_Treatment_ consists in the removal of the tumor when possible.
Malignant growths and multiple tumors are not favorable for treatment.
Actinomycosis can be treated throughout by iodides, or these may
supplement the surgical measures. In the short-faced animals an
ecraseur, or a wire-snare passed through a tube may be employed. (See
pharyngeal polypi).




                ESOPHAGITIS. INFLAMMATION OF THE GULLET.

  Causes: Alimentary and therapeutic; parasitic and accidental
  traumatisms; mechanical irritants; acrids; caustics;
  parasites—gongylonema, coccidia, spiroptera. Extension inflammations.
  Lesions: hyperæmia; epithelial degeneration and desquamation; erosion;
  petechiæ; suppuration; fibroid contraction; sacculation; polypi.
  Symptoms: dysphagia, difficult deglutition; eructation; cough; upward
  wave motion in jugular furrow; colicy pains; probang arrested; fever.
  Treatment: liquid or semi-liquid food; for caustics, antidotes; cold
  water; ice; antiseptics; derivatives; open abscess; potassium iodide.


_Causes._ This usually arises from injury to the mucous membrane and in
the milder forms remains confined to this structure. In the more severe,
it extends to the muscular coat and even to the periœsophagean tissues.
The causes may be divided into alimentary and therapeutic irritants;
parasitic or accidental traumatisms; and extension of inflammation from
the pharynx or other adjacent part.

Among _irritants_ taken as food, may be named hot mashes, bolted by a
hungry and gluttonous horse, and temporarily arrested in the gullet by
reason of the resulting irritation of the mucous membrane. In other
cases, coarse fibrous fodder is bolted without previous mastication, and
scratches and abrades the œsophagean mucosa leading to transient or
progressive inflammation. In other instances diseases of the teeth,
jaws, temporo-maxillary joint, or salivary glands prevent the necessary
trituration of the food, and it is swallowed in a rough, fibrous, or
even a dry condition. Again the impaction of a solid body (turnip,
apple, potatoe, egg) or of a quantity of finely divided grain or fodder
so as to obstruct the lumen of the gullet, is an occasional cause. The
density of the epithelium reduces these dangers to the minimum, yet a
too rough morsel, or an undue detention of the less irritating material
will determine hyperæmia and even inflammation and infective invasion.
Acrid and irritant vegetables in the food are less injurious when
thoroughly insalivated, as their contact with the œsophagean walls is
then very slight and transient.

_Irritant and caustic chemical agents_ given for therapeutic purposes,
attack the mouth, pharynx and stomach, more severely than the gullet
through which they are passed with great rapidity. In some cases,
however, the agent will adhere by reason of its powdery, gummy or
balsamic character and will then act as a direct irritant. Solutions of
caustic alkalies (weak lye) given to correct acid gastric indigestion in
the horse, and ammonia to remedy tympany in cattle, when insufficiently
diluted, will dangerously attack the œsophagean mucosa.

_Parasitic irritation_ is not so common here as in other parts of the
intestinal canal where the contents are longer delayed and are passed
with less friction, yet certain parasites are found in this region and
may even produce considerable irritation. The gongylonema of the
thoracic œsophagean mucosa of ruminants and swine are apparently
harmless. The psorospermia of the œsophagean muscles of the same animals
are alleged to cause œdema of the glottis, asphyxia and epilepsy. The
spiroptera microstoma of the horse has in one instance known to us
caused extensive denudation of the muscular coat within a foot of the
cardiac end of the gullet. Finally we have found bots hooked on to the
œsophagean mucosa close to the cardia, causing much irritation and
spasm. The spiroptera sanguinolenta is often present in chambers
hollowed in the œsophagean mucosa of the dog.

_Traumatic causes_ appear in the form of contusions and bruises from
without, but much more frequently from foreign bodies, and probangs
operating from within. The use of a whip or of a rope without a
cup-shaped end for the relief of a choked animal. Short of the
occurrence of laceration this often produces contusion and abrasion
which results in local inflammation. Even the too forcible dislodgment
of a solid body by a probang of approved pattern, may bruise and scratch
the gullet when the seat of violent spasm. Pins, needles, wire, thorns
and other sharp bodies are liable to do serious damage during their
passage in an ordinary bolus and when they transfix the mucosa violent
infective inflammation may ensue.

_Extension inflammations_ from the throat, and from phlegmous,
abscesses, tumors, etc., in the jugular furrow need only be mentioned in
this connection, as the primary disease will be clearly in evidence.

_Lesions._ These are usually circumscribed when due to a traumatic
injury and extended when caused by caustics or irritants. The affected
section is swollen, and surrounded by some serous effusion. When the
muscular coat is involved it is often paler than normal, and
microscopically shows extensive granular and fatty degeneration. The
mucosa usually sloughs off its epithelial layer, sometimes over an
extensive area (thoracic portion, Renault; whole gullet, Bertheol), and
the exposed raw surface is of a deep red or violet. When the epithelium
is not shed, it is infiltrated, swollen and friable breaking down under
the slightest manipulation. Petechiæ and slight blood extravasations are
abundant, and diffuse suppuration is not uncommon. In traumatic injuries
necrosed areas are found in the muscular and mucous coats. Strictures,
dilatations, and polypoid growths are liable to follow as sequelæ.

_Symptoms._ These usually manifest themselves from two to four days
after the operation of the cause. There is much difficulty in
deglutition, the effort to swallow either solids or liquids causing
acute suffering, with extension of the head on the neck and strained
contraction of the facial muscles. If the liquid succeeds in passing the
pharynx, it is arrested at the seat of inflammation and regurgitated
through the nose and mouth, or in solipeds through the nose only. This
takes the appearance of emesis even if nothing actually comes from the
stomach. The animal shakes the head violently, breathes hurriedly, and
has fits of paroxysmal coughing. A wave extending from below upward
along the jugular furrow and followed by nasal discharge is a marked
symptom, as the violence of the inflammation increases. Uneasy movements
of the limbs, pawing and lying down and rising, indicate the existence
of colic, and this is aggravated by the administration of anodynes or
antispasmodics by the mouth. In cattle, rumination is arrested, froth
accumulates around the lips, the rumen becomes tympanitic, and colicy
movements appear. Oftentimes a swelling extends upward in the jugular
furrow, and even in its absence, pressure with the fingers along the
furrow will often detect an area of tenderness with or without local
swelling. Fever with more or less elevation of temperature, is a general
symptom. There may be wheezing breathing or loud stertor. The passage of
a probang is arrested by the swelling or spasm at the diseased part and
when withdrawn may be covered with pus or fœtid _debris_. In the horse a
small probang may be passed through the nose.

_Treatment._ In a slight congestion at the seat of a recent obstruction
and which tends to renewed obstruction, little more is necessary than to
restrict the feed for a few days to soft mashes so that irritation of
the sensitive surface, spasm and the arrest of the morsel may be
obviated. Plenty of pure water or of well boiled linseed or other gruel
should be allowed.

In cases in which the obstruction is still present in the gullet, its
removal by probang or looped wire is the first consideration, to be
followed by the measures mentioned above.

In case of the swallowing of a caustic agent, no time should be lost in
giving an antidote. For the mineral or caustic organic acids, lime
water, magnesia, or other bland basic agent is demanded. For caustic
alkalies or basic agents, bland acids, such as vinegar, citric acid, or
even a mineral acid very largely diluted will be in order. In both these
cases and in that of caustic salts, albuminous and mucilaginous agents,
eggs, linseed tea, slippery elm, gums, and well boiled gruels are
indicated. To these may be added small doses of laudanum when the
irritation is great. Iced drinking water, iced milk, or iced gruels are
often soothing to the suffering animal, and cold compresses, snow or ice
applied along the jugular furrow is often valuable. To counteract the
septic developments on the affected mucous membrane, chlorate of potash,
boric acid, salol, naphthalin, naphthol, pyoktannin, or even weak
solutions of phenic acid or creolin may be used. In the slighter forms
of inflammation or when the acute form threatens to persist, an active
counter-irritant of mustard or cantharides may be applied along the
jugular furrow.

In case of abscess, as manifested by fluctuation following a hard,
indurated, painful swelling, a free incision should be followed by
frequent injections of antiseptic lotions or by the packing of the
cavity with such bland antiseptics as salol, boric acid, or iodoform on
cotton.

As inflammation subsides, potassium iodide may be given, both as an
antiseptic and a resolvent, to counteract the tendency to fibroid
contraction and stricture of the gullet.




                 SPASM OF THE ŒSOPHAGUS. ŒSOPHAGISMUS.

  Causes: nervous disorders or lesions, pharyngeal, œsophagean, or
  gastric disease, œsophagean parasites, choking, tumors, ulcers, cold
  drinks. Symptoms: extended drooping head, working jaws, frothing,
  pawing, attempts at swallowing, alkaline regurgitation, cries, rigid
  gullet, tenderness. May be paroxysmal with intervening dullness.
  Treatment: by sound; by removal of obstruction; by antispasmodics.
  Embrocations. Tonics.


_Causes._ This has been noticed as a concomitant of certain diseases of
the nervous centres, such as rabies, tetanus, or epilepsy, and those of
the pharynx or stomach. Cadeac has seen it in connection with stricture,
and the present writer has observed it as a result of larvæ of œstri
hooked on to the mucosa above the cardia. It is an important factor in
most cases of choking, and may depend on tumors, ulcers, or even cold
beverages. Animals with a specially nervous organization are
particularly subject to it and it may thus be an hereditary family
trait. It has been especially noticed in solipeds and calves.

_Symptoms._ A feeding animal suddenly ceases to eat, extends the head on
the neck, drops the nose toward the ground, moves the jaws constantly,
froths at the mouth or lets the saliva drivel to the ground, moves the
fore feet uneasily pushing the litter under the belly, makes efforts at
deglutition during which, waves may be seen to descend along the jugular
furrow, followed by regurgitation and discharge of the liquid as by
emesis. The act is often followed by a slight cry. Manipulations of the
left jugular furrow detects the gullet as a firm, rigid cord, unless
when liquids are passing as above, and auscultation reveals a rattling
or gurgling noise as if in jerks. Pressure on the gullet is often very
painful, increasing the spasm and rigidity, and causing the animal to
cry out. Wheezing breathing may attend the discharge of saliva through
the nose, and violent paroxysms of coughing may be caused by the
entrance of this liquid into the larynx.

In the majority of cases no food is swallowed and nothing but saliva is
disgorged, which together with the absence of an acid odor distinguishes
this from true vomiting. In an exceptional case of the author’s,
occurring in a colt, the animal continued to masticate and swallow green
food which gradually filled the whole length of the gullet, practically
paralyzing it. In ordinary cases a small sound can usually be passed
into the stomach. In cases of obstruction, however, by a solid morsel,
or by an accumulation of soft solids, the probang will enable one to
detect the condition. The acute symptoms may occur in paroxysms of a few
minutes in length, between which, the animal remains dull and
disspirited until the new attack supervenes. Recovery is at times as
sudden as the onset, though there remains, for a length of time,
liability to a relapse. Cadeac has seen a succession of such attacks
which extended over a year and a half.

_Treatment._ In many cases the passage of a probang or sound, will, by
the mere distension of the gullet, overcome the local spasm, though it
may be necessary to repeat the operation several times. In case the
sound causes much pain the end of the instrument may be well smeared
with solid extract of belladonna, and after passing this as far as the
obstruction a short time may be allowed, before its passage is again
attempted. In case obstruction by soft solids has taken place, the
passage of the wire loop will serve to break up the mass and even to
draw it up toward the mouth.

The administration of antispasmodics is the next indication. Chloroform
or ether by inhalation or in solution in water, chloral hydrate as an
enema, morphia or atropia hypodermically may be used according to
convenience. Bromide of potassium and other antispasmodics given by the
mouth, too often fail to pass the obstruction and thus prove useless,
except in the intervals of the spasms.

Fomentations of the lower border of the neck with warm water, and
frictions over the region of the gullet with camphorated spirit,
essential oils, ammonia, or in calves with oil of turpentine, often
contribute to relieve the spasm.

Finally after the severity of the attack has passed, a course of bitter
tonics and above all of nux vomica will fortify the system against a
relapse.




                      PARALYSIS OF THE ŒSOPHAGUS.

  Causes: nervous lesions and disorders; arytenectomy; over distension;
  stricture; parasites. Symptoms: dysphagia; regurgitation; cough;
  dyspnœa; hard packed gullet. Inhalation pneumonia. Lesions. Treatment:
  remove cause; liquid food; dilatation; nerve sedatives and stimulants;
  electricity; counter-irritants.


_Causes._ This has been noticed in a number of cases in solipeds, and
attributed to central nervous lesions, cerebral concussion (Straub),
encephalitis (Hering, Bornhauser), paralysis of the fore extremities
(Meier), pharyngeal paralysis (Puschmann). Möller has seen it several
times consequent on arytenectomy, while Dieckerhoff and Graf have seen
it occur without any clearly defined cause. In a case referred to above,
the present writer found it connected with the attachment of larvæ of
œstri in the lower end of the gullet. Stricture and impaction may be a
further cause.

_Symptoms and lesions._ There is more or less interference with
deglutition, culminating in complete inability to swallow, and the
rejection of morsels of masticated food by the nose. Cough may also
occur from the descent of food toward the lungs, with more or less
dyspnœa and oppression of the breathing. Manipulation along the left
jugular furrow, detects the œsophagus as a prominent hard, rope-like
mass which fills up the groove unduly. When death occurs rapidly the
gullet is found gorged with masticated food throughout its entire
length. In certain instances gangrenous pneumonia is found, the result
of the penetration of food into the bronchia. In other cases there are
lesions of the medulla oblongata, or of the vagus or glossopharyngeal
nerves or their œsophagean branches.

Death usually results from obstruction, inanition, or, in case the
paralysis is partial, from pneumonia or exhaustion.

_Treatment._ First remove or correct the existing cause of the disease.
Impaction may be broken up by the use of the wire loop, or pincer
probang; parasites may be expelled by passing a cupped probang; the
impactions following arytenectomy can be obviated by feeding gruels,
milk and other liquid foods only, and from a bucket set on the ground;
stricture may be dilated by the use of graduated sounds; and nervous
diseases may be dealt with according to their specific nature in each
several case. When any definite cause of this kind has been overcome the
persistent use of strychnia, subcutem, or by the mouth, may be effectual
in overcoming the paresis of the gullet. Hypodermic injections are best
made along the left jugular groove, and frictions, stimulating
embrocations, and galvanic currents may be employed with excellent
effect.


                           ŒSOPHAGEAN TUMORS.

  Forms of neoplasm in gullet of horse, ox, sheep, pig, dog. Symptoms:
  dysphagia; eructation; vomiting; bloating; cough; dyspnœa; stertor;
  fœtor; palpitation. Treatment.

These have been often noticed in the lower animals. In the _horse_ have
been noticed _melanoma_ (Olivier, Röll, Kopp, Besnard, Pouleau),
_fibroma_ (Dandrieu, Dieckerhoff), Carcinoma (Chouard, Lorenz, Cadeac,
Laurent), epithelioma (Blanc, Lorenz), Leiomyoma (Lucet, Lothes),
cystoma (Caillau, Legrand), mucous cysts (Lucet).

In =cattle papilloma= is especially common, having been noted by
_Johne_, Mons, Fessler, Schütz, Lusckar, Gratia, Beck, Cadeac and Kitt.
=Tubercles=, and =fibroid masses= with cystic purulent centres are not
uncommon. =Actinomycosis= is also frequent, sometimes hard and warty and
at others soft and vascular.

In the =Sheep=, Dandrieu found between the muscular and mucous coats a
hard tumor as large as a hen’s egg, the removal of which put a stop to a
persistent choking. In both =cattle= and =sheep=, swellings from
=coccidiosis= are common; in =cattle= and =swine= from =gongylonema=,
and in =sheep= from =filaria= (Harms) or =spiroptera= (Zurn).

In =pigs=, =fibroma= is met with in the walls of the gullet (Raveski)
and in =dogs= =fibroma=, =papilloma=, and the tumors of spiroptera.

_Symptoms._ The coccidia and spiroptera usually cause few symptoms or
none, but neoplasms usually develop symptoms of obstruction, dysphagia,
eructation, vomiting, and all the indications of choking according to
their seat. These do not come on suddenly and recover as in simple
choking, but even though there may be periodic obstructions, spasms and
paroxysms, there is a slow, progressive advance as the neoplasms
increase. Stertorous or mucous breathing, cough, dyspnœa and fœtid
exhalations are common, the symptoms may be aggravated when the head is
bent, and the tumor may even be felt on palpation of the throat or left
jugular furrow. In ruminants tympany occurs after feeding.

_Treatment_ is surgical and consists in the removal of the tumors by
incision and ecraseur or otherwise. Thoracic œsophagean tumors are
usually inoperable.


             IMPACTION OF THE CROP. INGLUVIAL INDIGESTION.

  Gallinaceæ and Palmipeds. Causes; Overfeeding after privation;
  fermentation; lack of water; green food in geese and chickens; food
  containing paralyzing element. Symptoms; dull; motionless; erect
  plumes; drooping wings and head; gapes; ejects liquid from bill; firm
  cervical swelling. Treatment; manipulation; incision; surgical
  precautions. Convalescent feeding.

The cervical dilatation of the œsophagus known as the crop is well
developed in all granivorous birds, (Gallinaceæ, etc.;) and like the
macerating cavities of the ox (first two stomachs) is subject to
overdistension and paralysis. In the palmipeds (ducks, geese) there is
no distinct crop but in its place the cervical portion of the gullet has
a fusiform dilatation, and under given conditions this may be also the
seat of impaction.

_Causes._ The impaction may result from overfeeding when the bird has
been starved, or when it suddenly gains access to food of a specially
appetizing kind and to which it has been unaccustomed. The crop like
every other hollow viscus is rendered paretic by overdistension. Then
the food undergoes fermentation still further distending the cavity,
affecting the brain by reflex action, and paralyzing the vagus and its
peripheral branches in the lungs, heart, stomach, liver, intestines,
etc. When the food is dry as in the case of beans, peas, bran, farinas,
it may be a simple firm impaction which the muscular walls of the crop
are unable to break up or move onward. When green food is taken there is
often superadded the additional evil of active fermentation from the
great number and activity of the bacterial ferments contained in it and
the soft aqueous fermentescible nature of the food (See _tympany in
ruminants_). Dupont states that young geese led out to fresh spring
grass may lose two-thirds of their number in a few hours from such
overloading and that some species of _Carex_ and cynodon dactylon are
particularly injurious. Chickens also gorge the crop with clover, etc.
In all such cases, plants that contain a paralyzing principle like
lolium temulentum, ripening lolium perenne, chick vetch, etc., are to be
specially dreaded. (See Trichosoma Contortum).

_Symptoms._ There are first dullness and sluggish movements, followed by
indisposition to move, the bird standing in one place with ruffled
feathers and drooping wings, and at intervals, projecting the head
forward with open beak and in some cases a little liquid is rejected. If
the bird is now caught and examined the crop is found to be firmly
distended, and more or less compressible or indentable according to the
nature of the food impacted. In most cases and especially if the food
has been green or aqueous, there is a certain resiliency from the
presence of gas outside the solid impacted mass.

_Treatment._ This must be in the line of seconding the physiological
efforts of regurgitation which is a normal and common act in birds. The
duck which has gulped a mouse half-way down the cervical part of the
œsophagus will readily disgorge it when he finds it impossible to pass
it further. The carnivorous birds often reject by vomiting the
indigestible debris such as feathers and bones, after all the more
soluble parts have been disposed of in the stomach. The pigeon even
feeds its young by disgorging into their open bills, the semi-digested
food and milk from its crop. Following these indications we must break
up the contents of the crop by manipulation and force them in small
masses upward into the bill and downward to the proventriculus. The
rejection by the bill may be further stimulated by introducing the
finger into the fauces to rouse the reflex active emesis. Usually the
crop can be quickly and satisfactorily emptied in this way.

When this proves impossible there remains the operation of direct
incision through the walls of the crop and the evacuation of its
contents. This can be done by a pocket knife or even a pair of scissors.
The crop is punctured in its lower part and the incision is continued
upward as far as may be necessary to allow the escape of the contents.
Usually half an inch will suffice. Then the crop is squeezed so as to
press the contents through this opening and it is emptied by a process
of enucleation. If the contents are fibrous it may be necessary to
employ forceps to dislodge the material. The empty crop may be washed
out with tepid water, any food attached to the raw edges of the wound
must be removed and the skin stitched accurately together. The wound
rarely fails to heal by first intention. To avoid stretching it, the
food for a day or two should be restricted to milk, gruels, or a little
soft mash.

Lerein notices jaundice as a sequel of impacted crop, and recommends
treatment by sulphate of soda in the water.


             TYMPANITIC INDIGESTION IN THE RUMEN. BLOATING.

  Definition. Susceptible Genera. Causes; gastric paresis, overloading,
  cold, fear, exhaustion, poisons, fermentescible food,—new grain,
  leguminosæ, frosted vegetables, ruminitis, foreign bodies in rumen,
  microbian ferments. Symptoms, abdominal, general. Gases formed under
  different aliments—carbon dioxide, marsh gas, hydrogen sulphide,
  nitrogen, oxygen. Lesions, rupture of rumen or diaphragm, compression
  or rupture of liver or spleen, petechiæ, congestion of lungs and right
  heart, of cutaneous and cerebral vessels. Prevention, avoid
  indigestible and fermentescible aliments, correct adynamic conditions,
  tonics, avoid injurious ferments, make alimentary transitions slowly.
  Treatment, exercise, bath or douche of cold water, rubbing and
  kneading, rope round abdomen spirally, gag in mouth, dragging on
  tongue, movement of a rope in fauces, probang, stimulants,
  antiseptics, alkalies, ammonia, oil of turpentine, oil of peppermint,
  alcohol, ether, pepper, ginger, soda, potash, lime, muriatic acid,
  carbolic acid, creosote, creoline, sulphites, kerosene, chloride of
  lime, chlorine, tar, common salt, hypochlorite of soda, magnesia,
  eserine, pilocarpin, barium chloride, colchicum, lard, trochar, Epsom
  salts, rumenotomy. Treatment of diseased gullet, mediastinal glands,
  stomach or intestines.

_Definition._ The condition is a combination of paresis of the rumen and
gaseous fermentation of its contents. The initial step may be the
paresis or in the more acute forms the fermentation.

_Genera susceptible._ While all ruminating animals are subject to this
disorder, it is much more frequent in cattle and sheep than in goats.

_Causes._ It commences in _paresis of the rumen_ in the weak,
debilitated, convalescent or starved animals which are suddenly put on
rich, and appetizing food. Hence it is common in animals that break into
a cornbin, a store of potatoes, a field of growing corn or small grain,
or that are turned out on green food in early spring. Cadeac maintains
that paresis of the rumen is the essential cause in all cases, while the
nature of the aliments ingested fills a secondary and comparatively
insignificant rôle. According to this view the torpid stomach can
neither relieve itself through regurgitation for rumination, nor expel
through the œsophagus the constantly evolving gas which therefore
distends the viscus to excess. In support of this view may be adduced
the occurrence of tympany through fatigue, fear, cold, enlarged
(tubercular) mediastinal glands pressing on the gullet and vagus,
obstruction of the œsophagus by a solid body (choking), impaction of a
morsel of solid food in the demicanal of the calf as noticed by
Schauber, and the cessation of the normal vermicular movements of the
rumen in connection with inflammation of its coats, or extensive
inflammation elsewhere or finally of fever. Even in paralysis of the
stomach by poisons like lead, tympany may be a result. Cadeac attributes
tympany following the ingestion of green food wet with a shower, or
drenched with dew, of frosted potatoes or turnips, or of iced water, to
the paralyzing action of the cold on the rumen. This view is manifestly
too extreme, as the bloating occurs often after a warm summer shower, or
after the consumption of potatoes and other roots and tubers which have
been spoiled by frost but which are no longer at a low temperature when
consumed.

_Tympany_ may also start from the ingestion of certain kinds of _food_
which are _in a very fermentescible condition_. Green food, especially
if the animal has been unaccustomed to it, is liable to act in this way.
Clover and especially the white and red varieties, lucern (alfalfa),
sainfoin, cowpea and other specially leafy plants, which harbor an
unusual number of microbian ferments, and which contain in their
substance a large amount of nitrogenous material favorable to the
nourishment of such ferments are particularly dangerous in this respect.
All of these are most dangerous when wet with dew or when drying after a
slight shower, partly no doubt at times by reason of the chilling of the
stomach, but mainly because the ferments have been stimulated into
activity by the presence of abundance of moisture. Drenching and long
continued rains are less dangerous in this respect than the slight
showers and heavy dews, manifestly because the former wash off a large
portion of the microbes, which under a slight wetting multiply more
abundantly.

Frosted articles act in a similar way, partly when still cold by the
chilling and paralyzing of the stomach, but cold or warm, by reason of
the special tendency of all frozen vegetables to undergo rapid
fermentation when thawed out. This is true of green food of all kinds
when covered by hoarfrost, of turnips, beets, potatoes, carrots, apples,
cabbage, etc., which have once been frozen, and of frosted turnips and
potato tops, though, in the case of the latter agent, a narcotic
principle is added.

In the case of Indian corn, the smaller cereal grains, and certain
leguminous plants (vetches, tares, peas, beans) which have the seed
fully formed but not yet quite hardened nor ripened, there is the double
action of a paralyzing constituent and an aliment that is specially
susceptible of fermentation.

Inflammation of the rumen, already quoted as a cause, may be determined
by hot as well as cold food, by irritant drugs and poisons, and by
narcotico-irritant and other acrid plants in fodder or pasture. In the
same way the inflammation caused by the introduction of foreign bodies
into the rumen, such as nails, tacks, needles, pins, wires, knife
blades, and masses of hair or wool may at times cause tympany.

The two main causative factors, of paresis of the rumen on the one side
and of specially fermentescible food and a multiplicity of microbian
ferments on the other, must be recognized as more or less operative in
different cases, and in many instances their combined action must be
admitted. The tympany is the symptom and culmination of a great variety
of morbid causes and conditions, and its prevention and treatment must
correspondingly vary.

_Symptoms._ The whole left side of the abdomen being occupied by the
rumen, its distension leads to an uniform swelling of that side,
differing from that caused by simple excess of solid ingesta in being
more prominent high up between the last rib and the outer angle of the
ilium, and in giving out in this region a clear tympanitic or drumlike
resonance on percussion. It has also a tense resiliency, like that of a
distended bladder, easily pressed inward by the finger but starting out
to its rotundity the moment the pressure of the finger is withdrawn. The
distension caused by overloading with solids bulges out lower down, is
not resonant but dull or flat when percussed, and yields like a mass of
dough when pressed retaining the indentation of the finger for some
time. The swelling of tympany, when extreme, rises above the level of
the outer angle of the ilium and even of the lumbar spines on the left
side, and if no relief is obtained the right side may undergo a similar
distension.

Auscultation detects an active crepitation over the whole region of the
rumen, finer in some cases and coarser in others, according to the
activity of evolution and the size of the bubbles of gas. The
crepitation is especially coarse and loud in fermentation of green food,
and of spoiled potatoes or other tubers or roots.

In all acute or severe cases, there is anorexia, suspension of
rumination, and the normal movements of the compressed bowels seem to be
largely impaired, though the anus is protruded and a little semi-liquid
fæces or urine may be expelled at intervals. The breathing is
accelerated, short, and labored. The nostrils are dilated, the nose
extended, the face anxious, the eyes bloodshot and the back arched.
Froth may accumulate around the lips, or the mouth may be held open with
the tongue pendent. Sometimes a quantity of gas may suddenly escape with
a loud noise, but without securing permanent relief. The heart beats are
violent and accelerated, the pulse increasingly small and finally
imperceptible, and the visible mucous membranes are congested and
cyanotic. Pregnant females are very liable to abort.

When the right flank as well as the left rises to the level of the
lumbar spines death is imminent, and this may take place as early as
fifteen or thirty minutes after the apparent onset of the attack. Death
may result from nervous shock, from suffocation, or from the absorption
of deleterious gases, or from all of these combined.

In the less acute cases the animal may live several hours before the
affection terminates in death or recovery. As a rule he stands as long
as he can and finally drops suddenly, the fall often leading to rupture
of the diaphragm or stomach, to protrusion of the rectum, or the
discharge of ingesta by the mouth and nose.

In still slighter cases relief comes through vomiting or more commonly
through frequent and abundant belching of gas, the swelling of the
flanks subsides, rumbling of the bowels may again be heard, and usually
there is a period of diarrhœa.

_Gases present._ When the rumen is punctured before or after death so as
to give exit to the gas in a fine stream it proves usually more or less
inflammable, the lighted jet burning with a bluish flame. The usual
inflammable ingredients are carbon monoxide, hydrogen carbide (marsh
gas) and hydrogen sulphide, yet the relative proportion of the gases
varies greatly with the nature of the food and the amount of gas
evolved, carbon dioxide being usually largely in excess. The following
table serves to illustrate the variability:

 ─────────┬─────────┬─────────┬──────────┬─────────┬─────────┬─────────
          │         │         │          │Lameyran │         │
          │         │ Gmelin, │          │   and   │         │
   Gas.   │Pflüger. │  from   │Lassaigne.│ Fremy,  │ Vogel.  │ Raiset.
          │         │ clover  │          │  from   │         │
          │         │         │          │ clover. │         │
 ─────────┼─────────┼─────────┼──────────┼─────────┼─────────┼─────────
 CO       │    60–80│        5│        29│        5│       27│    74.23
 CO       │    28–40│         │          │         │         │
 CH       │         │       15│         6│       15│       48│    23.46
 HS       │         │       80│          │       80│         │
 O        │         │         │      14.7│         │         │
 N        │         │         │      50.3│         │       25│     2.22
 ─────────┴─────────┴─────────┴──────────┴─────────┴─────────┴─────────

The most elaborate observations on this subject are those made by
Lungwitz on the different aliments kept in closed vessels at the body
temperature, and on similar agents fed for days as an exclusive aliment
to oxen provided with a fistula of the rumen for purposes of collection.
He found carbon dioxide to be the predominating gas in all cases, but
that it was especially so in extreme tympanies and varied much with the
nature of the food. The following table gives results:

                                         Percentage of CO_{2}.
         Buckwheat (Polygonum fagopyrum)                    80
         Alfalfa (Mendicago Sativa)                      70–80
         Clover (Trifolium pratense)                     70–80
         Meadow grass                                    70–80
         Indian corn (Zea Maïs)                          70–80
         Spurry (Spergula arvensis)                      70–80
         Hay of alfalfa or clover                        70–80
         Oats with cut straw                             70–80
         Yellow Lupin (Lupinus luteus)                   60–70
         Vetch (Vicia sativa)                            60–70
         Oats cut green                                  60–70
         Potato tops                                     60–70
         Potatoes                                        60–70
         Meadow hay                                      60–70
         Leaves of beet                                  50–60
         Leaves of radish                                50–60
         Cabbage                                         40–50

The marsh gas varied from 16 to 39 per cent., being especially abundant
in cases of abstinence. It should, therefore, be in large amount in the
tympanies which accompany febrile and other chronic affections. Hydrogen
sulphide was found only in traces, recognizable by blackening paper
saturated with acetate of lead. Oxygen and nitrogen were in small amount
and were attributed to air swallowed with the food. In the work of
fermentation the oxygen may be entirely used up.

_Lesions._ These are in the main the result of compression of the
different organs, by the overdistended rumen. Rupture of the rumen is
frequent. The abdominal organs are generally bloodless, the liver and
spleen shrunken and pale, though sometimes the seat of congestion or
even hemorrhage. Ecchymoses are common on the peritoneum. The right
heart and lungs are gorged with black blood, clotted loosely, and
reddening on exposure. The right auricle has been found ruptured.
Pleura, pericardium and endocardium are ecchymotic. The capillary system
of the skin, and of the brain and its membranes, is engorged, with, in
some instances, serous extravasations.

_Prevention._ This would demand the avoidance or correction of all those
conditions which contribute to tympany. In fevers and extensive
inflammations, when rumination is suspended, the diet should be
restricted in quantity and of materials that are easily digested (well
boiled gruels, bran mashes, pulped roots, etc.,) and all bulky, fibrous
and fermentescible articles must be proscribed. In weak conditions in
which tympany supervenes on every meal, a careful diet may be
supplemented by a course of tonics, carminatives and antiseptics such as
fœungrec oxide of iron, hyposulphite of soda and common salt, equal
parts, nux vomica 2 drs. to every 1 ℔. of the mixture. Dose 1 oz. daily
in the food, or ½ oz. may be given with each meal.

Musty grain and fodder should be carefully avoided, also mowburnt hay,
an excess of green food to which the stock is unaccustomed, clover after
a moderate shower, or covered with dew or hoarfrost, frosted beet,
turnip, or potato tops, frosted potatoes, turnips or apples, also
ryegrass, millet, corn, vetches, peas with the seeds fairly matured but
not yet fully hardened. When these conditions cannot be altogether
avoided, the objectionable ration should be allowed only in small amount
at one time and in the case of pasturage the stock should have a fair
allowance of grain or other dry feed just before they are turned out.
Another precaution is to keep the stock constantly in motion so that
they can only take in slowly and in small quantity the wet or otherwise
dangerous aliment.

When it becomes necessary to make an extreme transition from one ration
to another, and especially from dry to green food, measures should be
taken to make the change slowly, by giving the new food in small
quantities at intervals, while the major portion of the diet remains as
before, until the fæces indicate that the superadded aliment has passed
through the alimentary canal. Another method is to mix the dry and green
aliments with a daily increasing allowance of the latter. Some have
avoided the morning dew and danger of fermentation by cutting the ration
for each succeeding day the previous afternoon and keeping it in the
interval under cover.

_Treatment._ Various simple mechanical resorts are often effective in
dispelling the tympany. Walking the animal around will sometimes lead to
relaxation of the tension of the walls of the demicanal and even to some
restoration of the movements of the rumen with more or less free
eructation of gas. The dashing of a bucket of cold water on the left
side of the abdomen sometimes produces a similar result. Active rubbing
or even kneading of the left flank will sometimes lead to free belching
of gas. The same may be at times secured by winding a rope several times
spirally round the belly and then twisting it tighter by the aid of a
stick in one of its median turns.

A very simple and efficient resort is to place in the mouth a block of
wood 2½ to 3 inches in diameter and secured by a rope carried from each
end and tied behind the horns or ears. This expedient which is so
effective in preventing or relieving dangerous tympany in choking
appears to act by inducing movements of mastication, and sympathetic
motions of the œsophagus, demicanal and rumen. It not only determines
free discharge of gas by the mouth, but it absolutely prevents any
accession of saliva or air to the stomach by rendering deglutition
difficult or impossible. A similar effect can be obtained from forcible
dragging on the tongue but it is difficult to keep this up so as to have
the requisite lasting effect. Still another resort is to rouse
eructation by the motions of a rope introduced into the fauces.

The passing of a hollow probang into the rumen is very effective as it
not only secures a channel for the immediate escape of the gas, but it
also stimulates the demicanal and rumen to a continuous eructation and
consequent relief. Friedberger and Fröhner advise driving the animals
into a bath of cold water.

Of medicinal agents applicable to gastric tympany the best are
stimulants, antiseptics and chemical antidotes. Among stimulants the
alkaline preparations of ammonia hold a very high place. These, however,
act not as stimulants alone, but also as antacids and indirectly as
antidotes since the alkaline reaction checks the acid fermentation which
determines the evolution of the gas. They also unite with and condense
the carbon dioxide. Three ounces of the aromatic spirits of ammonia, one
ounce of the crystalline sesquicarbonate, or half an ounce of the strong
aqua ammonia may be given to an ox, in not less than a quart of cold
water. Next to this is the oil of turpentine 2 oz., to be given in oil,
milk, or yolk of egg. But this too is an antiferment. The same remark
applies to oil of peppermint (½ oz.), the carminative seeds and their
oils, and the stronger alcoholic drinks (1 quart). Sulphuric or nitrous
ether (2 oz.) may be given in place. Pepper and ginger are more purely
stimulant and less antiseptic. Other alkalies—carbonate of potash or
soda, or lime water may be given freely.

Among agents that act more exclusively as antiseptics may be named:
muriatic acid 1 to 1½ drs. largely diluted in water; carbolic acid,
creosote or creolin, 4 drs. largely diluted; sulphite, hyposulphite or
bisulphite of soda 1 oz.; kerosene oil ½ pint; chloride of lime 4 drs.;
chlorine water 1 pint; wood tar 2 oz. The latter agent is a common
domestic remedy in some places being given wrapped in a cabbage leaf,
and causing the flank to flatten down in a very few minutes as if by
magic. The extraordinarily rapid action of various antiseptics is the
most conclusive answer to the claim that the disorder is a pure paresis
of the walls of the rumen. The affection is far more commonly and
fundamentally an active fermentation, and is best checked by a powerful
antiferment. Even chloride of sodium (½ lb.) and above all hypochlorite
of soda or lime (½ oz.) may be given with advantage in many cases.

Among agents which condense the gasses may be named ammonia, calcined
magnesia, and milk of lime for carbon dioxide, and chlorine water for
hydrogen.

Among agents used to rouse the torpid rumen and alimentary canal are
eserine (ox 3 grs., sheep ½ gr. subcutem), pilocarpin (ox 2 grs., sheep
⅕ gr.), barium chloride (ox 15 grs., sheep 3 to 4 grs.), tincture of
colchicum (ox 3 to 4 drs.). Trasbot mentions lard or butter (ox 4 oz.,
sheep ½ oz.), as in common use in France.

In the most urgent cases, however, relief must be obtained by _puncture
of the rumen_, as a moment’s delay may mean death. The seat for such
puncture is on the left side, at a point equidistant from the outer
angle of the ilium, the last rib and the transverse processes of the
lumbar vertebræ. Any part of the left flank might be adopted to enter
the rumen, but, if too low down, the instrument might plunge into solid
ingesta, which would hinder the exit of gas, and would endanger the
escape of irritant liquids into the peritoneal cavity. In an extra high
puncture there is less danger, though a traumatism of the spleen is
possible under certain conditions. The best instrument for the purpose
is a trochar and cannula of six inches long and ⅓ to ½ inch in diameter.
(For sheep ¼ inch is ample.) This instrument, held like a dagger, may be
plunged at one blow through the walls of the abdomen and rumen until
stopped by the shield on the cannula. The trochar is now withdrawn and
the gas escapes with a prolonged hiss. If the urgency of the case will
permit, the skin may be first incised with a lancet or pen knife, and
the point of the instrument having been placed on the abdominal muscles,
it is driven home by a blow of the opposite palm. In the absence of the
trochar the puncture may be successfully made with a pocket knife or a
pair of scissors, which should be kept in the wound to maintain the
orifice in the rumen in apposition with that in the abdominal wall,
until a metal tube or quill can be introduced and held in the orifices.

When the gas has escaped by this channel its further formation can be
checked by pouring one of the antiferments through the cannula into the
rumen.

When the formation of an excess of gas has ceased, and the resumption of
easy eructation bespeaks the absence of further danger, the cannula may
be withdrawn and the wound covered with tar or collodion.

When the persistent formation of gas indicates the need of expulsion of
offensive fermentescible matters, a full dose of salts may be
administered. If the presence of firmly impacted masses can be detected,
they may sometimes be broken up by a stout steel rod passed through the
cannula. If the solid masses prove to be hair or woolen balls,
rumenotomy is the only feasible means of getting rid of them.

In _chronic tympany_ caused by structural diseases of the œsophagus,
mediastinal glands, stomach or intestines, permanent relief can only be
obtained by measures which will remove these respective causes.




                     CHRONIC TYMPANY OF THE RUMEN.

  Causes: catarrh of rumen, impaction of manifolds, debility, paresis,
  peritoneal adhesions, neoplasms, concretions, sudden change in diet,
  gastric congestion, lesions of gullet, or of mediastinal glands.
  Symptoms are usually after feeding only, inappetence, rumbling,
  costiveness, rumen indentable. Treatment: obviate causes, give
  salines, acids, bitters, and water, laxative food, carminatives,
  antiseptics, electricity, emetic tartar, eserine, pilocarpin, barium
  chloride, apomorphin.


_Causes._ The persistence of causes of acute tympany may lead to the
appearance of the condition after each meal, or even in the intervals
between meals. Among the more specific causes may be named catarrhal
inflammation of the rumen, impaction of the third stomach, paresis of
the rumen, general debility, peritoneal adhesions affecting the viscus,
tuberculosis, actinomycosis or other morbid productions in its walls,
hernia of the reticulum into the chest, hard stercoral, hair or wool
balls, or masses or foreign bodies in the rumen, and the ingestion of a
very fermentescible quality of food. When the rumen is affected by
catarrh or paresis or debility, even ordinary food will lead to tympany,
but much more so any food to which the animal has been unaccustomed
(green for dry, or dry for green, grain for grass or hay, or beans or
peas for grain). Also food in process of fermentation, or the seat of
fungoid growth.

Again, so intimately related are the different stomachs that derangement
of one instantly impairs the functions of the other, and thus a slowly
progressive impaction of the third stomach leads to torpor of the first,
and the aggregation of more or less of its contents into solid,
fermenting masses. In the same way congestion of either the third or
fourth stomach impairs the functions of the rumen and induces tympany.

Morbid conditions affecting the functions of the œsophagus and
interfering with rumination and eructation of gas are familiar causes.
For example, strictures and saccular dilations of the tube, and
enlargements—tubercular, sarcomatous, actinomycotic,—of the mediastinal
glands.

The _symptoms_ do not differ from those of acute tympany excepting that
they are less severe; and are continuous or remittent, suffering a
material aggravation after feeding. Rumination may be suppressed or
tardy, the bowels also are torpid, the fæces glazed, and the ordinary
intestinal rumbling little marked. When the tympany has temporarily
subsided, the knuckles, pressed into the left side, can often be made to
strike against the hard, solid impacted mass of ingesta. Symptoms of
impacted manifolds may also be patent and the patient steadily loses
condition.

_Treatment_ must be directed toward the removal of the special cause of
the trouble, and if this cannot be secured, as in tuberculosis, the case
is hopeless. In cases of solid masses in the rumen the free use of
common salt with a drachm of hydrochloric acid, and one grain strychnine
with each meal, and a free access to water may succeed. The food had
best be restricted to gruels and sloppy mashes. The daily use of
electricity through the region of the paunch is an important accessory.
The common salt may be increased as required, so as to keep up a very
relaxed condition of the bowels.

In obstinate cases of this kind puncture may be resorted to and an
attempt made to break down the impacted masses with a steel rod
introduced through the cannula. Should this also fail the solid masses
or foreign bodies may be extracted by rumenotomy.

In simple catarrh of the rumen the continued use of strychnine with
gentian, and sulphate of iron, may prove successful under a carefully
regulated diet. Oil of turpentine, balsam of copaiba, or balsam of tolu
may also prove useful, or in other cases extract of hamamelis, or of
wild cherry bark. While strychnine and electricity are to be preferred
to rouse the muscular activity of the viscus, such agents as tartar
emetic, emetine, apomorphin, eserine, pilocarpin and barium chloride are
recommended and may be resorted to in case of necessity.




                      OVERLOADED (IMPACTED) RUMEN.

  Definition. Causes, excess of rich unwonted food, gastric torpor,
  paresis, starvation, debility, partially ripened, poisonous seeds,
  paralyzing fungi or bacteria, lead, cyanides, congestion of rumen,
  chlorophyll, acrids, dry, fibrous innutritious food, lack of water,
  enforced rest on dry food, over-exertion, salivary fistula or
  calculus, diseased teeth or jaws, senility. Symptoms, suspended
  rumination, inappetence, anxious expression, arched back, bulging
  pendent left flank, impressible, no friction sounds, excessive
  crepitation, hurried breathing, colics, grunting when moved, diarrhœa,
  stupor, cyanosis. Signs of improvement. Phrenic rupture. Diagnosis
  from tympany, pneumonia, or gastro-intestinal catarrh. Treatment,
  hygienic, antiseptic, stimulants, puncturing, purgation, rumenotomy.


_Definition._ The overdistension of the rumen with solid food is
characterized by two things, the excess of ingesta which produces the
torpor or paresis which is common to all over-filled hollow viscera, and
the comparative absence of fermentation and evolution of gas. If the
ingesta is of a more fermentescible nature the rapid evolution of gas
occurs before this degree of repletion with solid matters can be
reached, and the case becomes one of tympany, but if the contents are
comparatively lacking in fermentability they may be devoured in such
quantity as to cause solid impaction.

_Causes._ Overloading of the rumen is especially common as the result of
a sudden access to rich or tempting food to which the animal has been
unaccustomed. Accidental admittance to the cornbin, breaking into a
field of rich grass, clover, alfalfa, corn, sorghum, vetches, tares,
beans, peas, or grain, or into a barrel of potatoes or apples will
illustrate the common run of causes. A pre-existing or accompanying
torpor or paresis of the stomach is a most efficient concurrent cause,
hence the affection is especially common in animals debilitated by
disease or starvation, but which have become convalescent or have been
suddenly exposed to the temptation of rich food. For the same reason it
is most likely to occur with food which contains a paralyzing element,
as in the case of the following when they have gone to seed but are not
yet fully ripened: Rye grass, intoxicating rye grass, millet, Hungarian
grass, vetches, tares and other leguminosæ, and to a less extent, wheat,
barley, oats and Indian corn. The same may come from the paralyzing
products of fungi or bacteria in musty fodder or of such chemical
poisons as lead, and the cyanides.

A catarrhal affection of the rumen, and the congestion produced by
irritant plants, green food with an excess of chlorophyll, and the whole
list of irritants and narcotico-acrids, will weaken the first stomach
and predispose to overdistension.

Anything which lessens the normal vermicular movements of the rumen and
hinders regurgitation and rumination tends to impaction, and hence an
aliment which is to a large extent fibrous, innutritious, and
unfermentable, such as hay from grass that has run to seed and been
threshed, the stems of grasses that have matured and withered in the
pastures, fodder that has been thoroughly washed out by heavy rains,
sedges, reedgrass, rushes, chaff, finely cut straw, and in the case of
European sheep, the fibrous tops of heather contribute to this
affection. Lack of water is one of the most potent factors, as an
abundance of water to float the ingesta is an essential condition of
rumination. Hence pasturage on dry hillsides, prairies or plains, apart
from streams, wells or ponds is especially dangerous unless water is
supplied artificially, and the winter season in our Northern states,
when the sources of drinking water are frozen over, and when the chill
of the liquid forbids its free consumption, is often hurtful.

Gerard attributes the affection to constant stabulation. This, however,
has a beneficial as well as a deleterious side. It undermines the health
and vigor, and through lack of tone favors gastric torpor and impaction,
but it also secures ample leisure for rumination, which is so essential
to the integrity of the rumen and favors the onward passage of its
contents. With dry feeding and a restricted water supply it cannot be
too much condemned, but with succulent food and abundance of water the
alleged danger is reduced to the minimum.

Active work and over exertion of all kinds must be admitted as a factor.
At slow work the ox can still ruminate, but in rapid work or under heavy
draft this is impossible, and the contained liquids may pass over from
rumen to manifolds conducing to impaction of the former, or
fermentations may take place, swelling up the mass of ingesta and
distending the walls of the first stomach. Similarly, cattle and sheep
that are hurried off on a rapid march with full stomachs are greatly
exposed to both tympany and impaction.

In speaking of dry, fibrous food and lack of water as factors, we must
avoid the error of supposing that succulent or aqueous food is a sure
preventive. In a catarrhal condition of the rumen or in a state of
debility, impaction may readily occur from the excessive ingestion of
luscious grass, wheat bran, potatoes, apples, turnips, beets, or
cabbage.

Finally defects in the anterior part of the alimentary tract may tend to
impaction. Salivary fistula or calculus cutting off the normal supply of
liquid necessary for rumination, tends to retention and engorgement.
Diseased teeth and jaws interfering with both the primary and secondary
mastication has the same vicious tendency. Old cows, oxen and sheep in
which the molar teeth are largely worn out, suffer in the same way,
especially when put up to fatten or otherwise heavily fed. In this case
there is the gastric debility of old age as an additional inimical
feature.

_Symptoms._ These vary with the quantity and kind of ingesta also to
some extent with the previous condition of the rumen, sound or diseased.
They usually set in more slowly than in tympany. On the whole the
disease appears to be more common in the stable than at pasture. The
animal neither feeds nor ruminates, stands back from the manger, becomes
dull, with anxious expression of the face, arching of the back and
occasional moaning especially if made to move. The abdomen is distended
but especially on the left side, which however hangs more downward and
outward and tends less to rise above the level of the hip bone than in
tympany. If it does rise above the ilium this is due to gas and it is
then elastic, resilient and resonant on percussion at that point. The
great mass, and usually the whole of the paunch is nonresonant when
percussed, retains the imprint of the fingers when pressed, and gives
the sensation of a mass of dough. The hand applied on the region of the
paunch fails to detect the indication of movements which characterize
the healthy organ. The ear applied misses the normal friction sound, but
detects a crepitant sound due to the evolution of bubbles of gas from
the fermenting mass. This is especially loud if the impaction is one of
green food or potatoes, even though the gas remains as bubbles
throughout the entire fermenting mass, instead of separating to form a
gaseous area beneath the lumbar transverse processes.

The respiration is hurried, labored and accompanied with a moan, the
visible mucosæ are congested, the eyes are protruded and glassy from
dilatation of the pupils, the feet are propped outward, and the head
extended on the neck. There may be signs of dull colicy pains, movements
of the tail and shifting of the hind feet, in some cases the patient may
even lie down but never remains long recumbent. There may be occasional
passages of semi-liquid manure, though usually the bowels are torpid and
neither passages nor rumbling sounds on the right side can be detected.
When moved the animal usually grunts or moans at each step, and
especially when going down hill, owing to the concussion of the stomach
on the diaphragm. In cases due to green food the irritation may extend
to the fourth stomach and intestines and a crapulous diarrhœa may ensue.
The temperature remains normal as a rule. The disease is more protracted
than tympany, yet after several hours of suffering and continual
aggravation the dullness may merge into stupor, the mucosæ become
cyanotic and death ensues from shock, asphyxia, or apoplexy.

_Course. Termination._ Many cases recover in connection with a
restoration of the contractions of the rumen, the eructation of gas, in
some rare cases vomiting or spasmodic rejection of quantities of the
ingesta, and the passage of gas by the bowels. This may be associated
with a watery diarrhœa, and loud rumbling of the right side, which may
continue for twenty-four hours or longer. With the subsidence of the
diarrhœa there comes a return of health, or there may remain slight
fever, inappetence, suspended or impaired rumination, dullness,
listlessness, and a mucous film on the fæces. This indicates some
remaining gastro-enteritis.

In some instances there is rupture of the diaphragm with marked increase
in the abdominal pain and the difficulty of breathing. In others there
is a laceration of the inner and middle coats of the rumen so that the
gas diffuses under the peritoneum and may even be betrayed by an
emphysematous extravasation under the skin.

_Diagnosis._ From tympany this is easily distinguished by the general
dullness on percussion, the persistence of the indentation caused by
pressure, the outward and downward rather than the upward extension of
the swelling, and the slower development of the affection.

It is far more likely to be confounded with pneumonia, which it
resembles in the hurried, labored breathing, the moans emitted in
expiration, in the dullness on percussion over the posterior part of the
chest, it may be even forward to the shoulders, and in the cyanotic
state of the mucosæ. The distinction is easily made by the absence of
hyperthermia, and of crepitation along the margins of the nonresonant
areas in the lungs, by the fact that the area of chest dullness covers
the whole posterior part of the thorax to a given oblique line, and by
the history of the case and the manifest symptoms of overloaded stomach,
not with gas but with solids. From gastro-intestinal catarrh it may be
distinguished by the more rapid advance of the symptoms and by the
absence of the slight fever which characterizes the latter.

_Treatment._ Slight cases may be treated by hygienic measures only.
Walking the animal uphill, injections of cold water, friction on the
left side of the abdomen to rouse the rumen to activity, antiseptics as
in tympany to check further fermentation, and stimulants to overcome the
nervous and muscular torpor, may be employed separately or conjointly.
When it can be availed of, a rubber hose may be wound round the abdomen
and a current of cold water forced through it.

When further measures are demanded we should evacuate any gas through
the probang or a cannula, as in tympany, and thus relieve tension and
then resort to stimulants and purgatives. Common salt 1 ℔. is of value
in checking fermentation, and may be added to 1 ℔. Glauber salts in four
or five quarts of warm water. A drachm of strong aqua ammonia or 2 oz.
oil of turpentine and ½ drachm of nux vomica may be added. Bouley
advocated tartar emetic (2 to 3 drachms), and Lafosse ipecacuan (1 oz.
of the wine) to rouse the walls of the rumen, and more recently
pilocarpin (ox 3 grs.), eserine (ox 2 grs.) and barium chloride (ox 15
grs.), have offered themselves for this purpose. The three last have the
advantage of adaptability to hypodermic use, and prompt action. The
repetition of stimulants and nux vomica may be continued while there
appears any prospect of restoring the normal functions of the paunch,
and when all other measures fail the only hope lies in rumenotomy.

=Rumenotomy.= The warrant for this operation is found in the entire lack
of movement in the rumen, the absence of eructation, the cessation of
rumbling and motion of the bowels, and the deepening of the stupor in
which the patient is plunged. The longer the delay and the deeper the
stupor and prostration the less the likelihood of a successful issue
from the operation. The animal is made to stand with its right side
against a wall, and its nose held by the fingers or bulldog forceps. If
judged necessary a rope may be passed from a ring in the wall in front
of the shoulder around the animal to another ring behind the thigh and
held tight. Or a strong bar with a fulcrum in front, may be pressed
against the left side of the body, and well down so as to keep the right
side fast against the wall. A line may be clipped from the point of
election for puncture in tympany down for a distance of six inches. A
sharp pointed knife is now plunged through the walls of the abdomen and
rumen in the upper part of this line, and is slowly withdrawn, cutting
downward and outward until the opening is large enough to admit the
hand. The lips of the wound in the overdistended stomach will now bulge
out through to the wound in the abdominal walls, and three stitches on
each side may be taken through these structures to prevent displacement
as the stomach is emptied and rendered more flaccid. A cloth wrung out
of a mercuric chloride solution may be laid in the lower part of the
wound to guard against any escape of liquid into the peritoneal cavity.
The contents may now be removed with the hand, until the organ has been
left but moderately full. Two or three stable bucketfuls are usually
taken, but it is by no means necessary nor desirable that the rumen be
left empty, as a moderate amount of food is requisite to ensure its
functional activity. As a rule at least fifty pounds should be left.
Before closing the wound and especially in cases due to dry feeding, it
is well in a tolerably large animal to introduce the hand through the
demicanal to ascertain if impactions exist in the third stomach and to
break up these so far as they can be reached. This done, the edges of
the wound in the stomach are to be carefully cleansed, washed with the
mercuric chloride solution and sewed together with carbolated catgut,
care being taken to turn the mucosa inward and to retain the muscular
and peritoneal layers in close contact with each other. It will usually
be convenient to cut first the two lower stitches through the abdominal
walls, and suture from below upward. When finished the peritoneal
surface of the gastric wound may be again sponged with the mercuric
chloride solution, together with the edges of the wound in the abdominal
walls. Finally the abdominal wound is sutured, the stitches including
the skin only or the muscular tissues as well. The smooth surface of the
paunch acts as an internal pad and support, and with due care as to
cleanliness, antisepsis and accuracy of stitching, it is rare to find
any drawback to continuous and perfect healing. It is well to restrict
the animal for three days to well boiled gruels, and for ten days to
soft mashes in very moderate amount lest the wound in the paunch should
be fatally burst open before a solid union has been effected.


                 RUMINITIS. INFLAMMATION OF THE RUMEN.

  Prevalence in different genera. Causes, as in tympany and impaction,
  irritants, specific fevers. Symptoms: impaired rumination, tympanies,
  impactions, depraved appetite, fever, nervous disorders. Lesions:
  hyperæmia, petechiæ, exudates, ulcers, desquamation, swollen or
  shrunken papillæ. Treatment: remove cause, mucilaginous food, or
  gruels, sodium sulphate, or chloride, bismuth, bitters, mustard
  cataplasm, electricity.

This is not a prevalent disease but affects animals at all periods of
life and is a cause of tardy and difficult digestion and rumination. It
usually shows itself as a catarrhal inflammation and by favoring
fermentation in the food, and torpor of the muscular walls of the organ
contributes to tympany and impaction. It is more common in the ox than
in the sheep owing, perhaps, to the more habitual overloading of the
stomach and to the hurried, careless manner of feeding. In the goat it
is rare.

_Causes._ Among the causes may be named tympany and overloading, so that
all the dietary faults that lead to these may be set down as causes of
inflammation. Irritants taken with the food, whether in the form of
acrid plants (ranunculaceæ, euphorbiaceæ, etc.), musty fodder, irritant
products in spoiled fodder, aliments which are swallowed while very hot
or in a frozen state, and foreign bodies of an irritating kind are
especially liable to induce it. Congestions of the paunch are not
uncommon in specific infectious diseases like Rinderpest, malignant
catarrh, anthrax, and Texas fever, and specific eruptions sometimes
appear in aphthous fever and sheeppox.

_Symptoms._ Rumination is slow and irregular, appetite capricious,
tympanies appear after each feed, and there is a marked tendency to
aggregation of the ingesta in solid masses, which resist the
disintegration and floating which is necessary to rumination, and favor
the occurrence of putrid fermentation. There is usually a tendency to
lick earth, lime from the walls, and the manger, and a depraved appetite
shown in a desire to chew and swallow foreign bodies of many kinds.
Vomiting or convulsive rejection of the contents of the rumen is not
unknown (Vives, Pattaes). There is slight fever with heat of the horns
and ears, dry muzzle, and tenderness to pressure on the left flank. The
bowels may be alternately relaxed and confined, and bad cases may end in
a fatal diarrhœa. In other cases the disease may become acute and
develop nervous symptoms, as in tympany and impaction. When the disease
takes a favorable turn, under a careful ration, recovery may be complete
in eight or ten days.

_Lesions._ These are violet or brownish patches of hyperæmia on the
mucosa of the rumen, circumscribed ecchymoses, exudates in the sense of
false membranes and even pin’s head ulcerations. On the affected
portions the mucosa is swollen, puffy, dull and covered with mucus, and
epithelium may desquamate. The papillæ are often red, and thickened or
shrunken and shortened. In the specific affections like aphthous fever
and sheeppox the lesions are rounded vesicles containing liquid. The
ingesta is more or less packed in masses.

_Treatment._ If irritant foreign bodies have been taken rumenotomy is
demanded. If caustic alkalies, acetic or other mild acid. If acids, lime
water or magnesia. Feed well boiled flax seed, or farina gruels, and
wheat bran or middlings in limited quantity. Solids may be at first
withheld, coarse or indigestible food must be. It may be necessary to
rouse the organ by 10 or 12 ozs. of sulphate of soda with a little
common salt and abundance of thin gruels as drink. As a tonic the animal
may take nitrate of bismuth ½ oz., powdered gentian ½ oz., and nux
vomica 20 grains, twice a day. The application of a mustard pulp or of
oil of turpentine on the left side of the abdomen may also be resorted
to. A weak current of electricity through the region of the paunch for
twenty minutes daily is often of great service.


          HAIR BALLS IN THE RUMEN AND RETICULUM. EGAGROPILES.

  Balls of hair, wool, clover hairs, bristles, paper, oat-hair,
  feathers, chitin, mucus, and phosphates. Causes: Sucking and licking
  pilous parts, eating hairy or fibrous products. Composition. Symptoms:
  Slight, absent, or, gulping eructation, vomiting, tympany, in young
  putrid diarrhœa, fœtid exhalations, emaciation. Diagnosis. Treatment.

_Definition._ The term egagropile, literally goat-hair, has been given
to the felted balls of wool or hair found in the digestive organs of
animals. The term has been applied very widely, however, to designate
all sorts of concretions of extraneous matters which are found in the
intestinal canal. In cattle the hair licked from their skin and that of
their fellows rolled into a ball by the action of the stomach and matted
firmly together with mucus and at times traces of phosphates, are the
forms commonly met with. In sheep two forms are seen, one consisting of
wool matted as above and one made up of the fine hairs from the clover
leaf similarly matted and rolled into a ball.

In pigs the felted mass is usually composed of bristles, (exceptionally
of paper or other vegetable fibre), and in horses felted balls of the
fine hairs from the surface of the oat, mingled with more or less mucus
and phosphate of lime make up the concretion. These are found in the
stomach, and intestines. In predatory birds the feathers and in
insectivorous birds chitinous masses are formed in the gizzard and
rejected by vomiting.

_Causes._ Suckling animals obtain the hair from the surface of the
mammary glands hence an abundance of hair or wool on these parts favors
their production. The vicious habit of calves of sucking the scrotum and
navel of others is another cause. In the young and adult alike the habit
of licking themselves and others especially at the period of moulting is
a common factor.

_Composition._ Hair, wool, and the fine hairs of clover are the common
predominant constituents, but these are matted together more or less
firmly by mucus and phosphates, the ammonia-magnesian phosphate uniting
with the mucus and other matters in forming a smooth external crust in
the old standing balls of adult animals. The centre of such balls is
made up of the most densely felted hair. In balls of more recent
formation the external crust is lacking and the mass is manifestly hairy
on the surface, and the density uniform throughout. These have a
somewhat aromatic odor, contain very little moisture, and have a
specific gravity approximating .716 (sheep) to .725 (ox). Ellagic, and
lithofellic acids, derivatives of tannin, are usually present, and are
abundant in the egagropiles of antilopes.

In the balls of recent formation, as seen especially in sucking calves,
the hair is only loosely matted together, and often intermixed with
straw and hay, and is saturated with liquid and heavier than the old
masses. These are usually the seat of active putrefactive fermentation,
and being occasionally lodged in the third or even the fourth stomach,
the septic products act as local irritants, and general poisons. They
are therefore far more injurious than the consolidated hairballs of the
adult animal, and often lay the foundation of septic diarrhœas and
gastro-enteritis.

The balls may be spherical, elliptical, ovoid, or, when flattened by
mutual compression, discoid.

_Symptoms._ Generally these balls cause no appreciable disturbance of
the functions of the stomach. This is especially true of the large, old
and smoothly encrusted masses. The museum of the N. Y. S. V. College
contains specimens of 5½ inches in diameter, found after death in a fat
heifer, which had always had good health and which was killed for beef.
This is the usual history of such formations, they are not suspected
during life, and are only found accidentally when the rumen is opened in
the abattoir.

The smaller specimens, the size of a hen’s or goose’s egg, or a billiard
ball, have produced severe suffering, with gulping, eructation, vomiting
and tympany from obstruction of the demicanal or gullet, and such
symptoms continued until the offending agents were rejected by the
mouth. (Caillau, Leblanc, Prevost, Giron). Again they may block the
passage from the first to the third stomach (Schauber, Feldamann,
Adamovicz, Tyvaert, Mathieu).

In calves on milk they are especially injurious as beside the dangers of
blocking the passages already referred to, the unencrusted hairs and
straws irritate the mucous membranes and still worse, the putrid
fermentations going on in their interstices, produce irritant and
poisonous products, and disseminate the germs of similar fermentations
in the fourth stomach and intestine. Here the symptoms are bloating,
colics, impaired or irregular appetite, fœtid diarrhœa, fœtor of the
breath and cutaneous exhalations, and rapidly progressive emaciation.

_Diagnosis_ is too often impossible. Tympanies, diarrhœa, colics, etc.,
may lead to suspicion, but unless specimens of the smaller hair balls
are rejected by the mouth or anus there can be no certainty of their
presence. If arrested in the cervical portion of the gullet they may be
pressed upward into the mouth by manipulations applied from without. The
looped wire extractor may be used on any portion of the œsophagus. If
lodged in the demicanal the passage of a probang will give prompt
relief. If retained in the rumen and manifestly hurtful, rumenotomy is
called for as soon as a diagnosis can be made.


               FOREIGN BODIES IN THE RUMEN AND RETICULUM.

  Common. Harmless or injurious. Perforating objects. Traumatisms of
  contiguous organs. Causes; hurried primary mastication, morbid
  appetite. Bodies found. Lesions; catarrh, perforations, congestions,
  ulcerations of mucosa, abscess, trauma of liver, spleen, diaphragm,
  abdominal and thoracic walls, lung, pleura, pericardium, heart.
  Symptoms; absent, or, indigestion, tympany, eructations, hepatic,
  respiratory or circulatory disorder, colics, local tenderness,
  crepitation, substernal exudate, costiveness, difficult urination or
  defecation, bloody fæces, nervous disorder. Treatment; Prevention;
  avoidance of causes, gravitation methods, incision.

These are so frequent that they can hardly be looked on as abnormal, but
they must be accepted as pathological when they cause serious irritation
or digestive disorder. This result is seen especially in the case of
cutting or sharp pointed bodies, which beside wounding the walls of the
rumen, show a marked tendency to advance to the heart and penetrate it,
or to perforate the liver, diaphragm or abdominal walls and even to
cause a fistula through which the ingesta escapes.

_Causes._ The common cause in cattle is the habit of swallowing, after
one or two strokes of the teeth, any small object that is mixed with the
provender. Next to this comes the habit of stabled cows, and of such as
suffer from a lack of phosphates or other important element in the food,
of licking, chewing, and swallowing articles that can in no sense be
considered as alimentary.

Among the rounded or smooth bodies found in the rumen and reticulum may
be named coins, rivets, fragments of wood, cords, pieces of rope,
leather, gloves, cloth, small garments like vests or caps, ribbons,
bones, pieces of lead, dried paints, cotton waste used as packing for
machinery, shot, and even small animals such as frogs, toads, and
snakes; also sand and pebbles.

Among sharp or pointed bodies the most common are nails, pins, needles,
baling wire, pieces of iron or other metals, knives, scissors, forks,
fragments of glass, thorns, etc.

_Lesions._ These are as varied as the nature of the traumatic agent, the
seat and nature of the trauma. The rounded bodies, if non-poisonous, act
merely by attrition of the walls and tend to induce a local catarrhal
inflammation. Yet even sharp pointed bodies may prove comparatively
harmless. The museum of the N. Y. S. V. College contains a pocket knife
which had remained open in the rumen for a length of time without
producing any visible injury.

Sharp and pointed bodies are especially liable to be entangled in the
cells of the reticulum; so that this viscus is the most common seat of
the resulting trauma. Around this there occur hyperæmia, exudation,
thickening and centrally ulceration, which may lead into a fistula or
abscess, confined it may be to the wall of the viscus, or continued into
the surrounding organs. In this way may be implicated, the liver, the
spleen, the diaphragm, the abdominal or thoracic walls, the lung, the
pericardium or the heart. The pus is always fœtid and usually mixed with
alimentary matter. If it approaches the surface it may burst and allow
exit to the offending body. If it encroaches on the liver, symptoms of
hepatic disorder supervene. Its progress through the lung or pleura is
marked by objective symptoms of pulmonary or pleural inflammation
(crepitation, flatness or percussion, creaking or friction sounds), but
without the customary amount of hyperthermia, and with some evidence of
gastric disorder. When the pericardium is reached there are the usual
signs of pericarditis, attended by comparatively little fever, and a
doughy swelling beneath the sternum is added to the objective signs of
exudation in the pericardium.

Among the peculiar routes followed by such bodies may be named the
following: to the side of the ensiform cartilage; through an intercostal
space; into a chondro-costal articulation; through the muscles of the
flank; and even in the region of the croup. If the attendant abscess or
fistula bursts into a serous cavity it determines septic peritonitis or
pleurisy, while in the lung it may cause septic pneumonia. As a rule,
however, this is prevented by the excessive quantity of exudation.

_Symptoms._ These are extremely variable according to the seat and
nature of the lesion. So long as the foreign body is confined in the
rumen there is usually no symptom. Even when it has penetrated
surrounding organs the symptoms are usually for a time very obscure. A
few years ago a cow entered the prize ring, at the New York State Fair,
was awarded first prize, and died a few minutes later from a piece of
baling wire penetrating the pericardium. When symptoms are patent there
are usually early indications of indigestion in the rumen, capricious
appetite, sluggish and imperfect rumination, dullness, tardy movements,
frequency and fœtor of eructations, colicy pains, grunting when moved,
and wincing under pressure in the left hypochondrium. Pressure below, to
the left of the ensiform cartilage is sometimes particularly painful.

If the object is advancing toward the heart a broad area or line of
dullness may often be detected by percussion on the left side of the
chest and under the acts of respiration or walking, gurgling sounds may
be heard along this line. The movements of the ribs on the same side are
limited as compared with the other side, and straining in defecation or
urination may be manifestly painful and accompanied by groaning. For the
same reason costiveness is liable to set in.

When the body approaches the skin there is formed a large, hot,
phlegmonous swelling similar to that which marks the advance of an
intercostal abscess.

In special cases there are symptoms of disease of the particular organ
penetrated. Hepatitis, splenitis, and peritonitis are occasionally seen.
Eggeling notes a fatal hemorrhage from the wounding of the œsophagus by
a nail, and Brauer bloody fæces from penetration of the pylorus by a
piece of glass. In other cases fatal results have followed on trauma,
thickening and obliteration of the pylorus. (Olivier).

In cases of the ingestion of shot, the spray of bullets, white or red
paint or other form of lead, the special symptoms of lead poisoning
supervene. (See lead poisoning).

_Treatment._ As a rule this is unsatisfactory and especially in cases
implicating the pericardium, as the symptoms may be entirely overlooked
until sudden death occurs. Hence the great value of preventive measures,
and above all the careful removal of all nails from the vicinity of
fodders. Bailed hay is always dangerous, and when used, each bale should
be carefully freed from its wires and any short pieces removed. Pointed
metallic bodies of all kinds should be removed from the pastures and
stables.

In case the migrating foreign body leads to the formation of a
superficial phlegmon at any point, this should be freely opened and the
offensive agent extracted.

If the lesion in the reticulum has been diagnosed, the combined methods
of Kolb and Schobert should be tried. Turn the animal on its back with
the head and shoulders up hill, and employ strong pressure, with the
foot, in jerks, over the ensiform cartilage. The object is to slide the
foreign body back into the viscus, and success is claimed in seven cases
out of nine.

Failing in such methods there remains only the operation of rumenotomy
and the removal of the offending bodies so far as they can be reached.




                   TUMORS OF THE RUMEN AND RETICULUM.


Tumors of different kinds have been found in the walls of these organs,
though by no means frequently. Epithelial hypertrophy and papilloma have
been found in the ox the former undergoing necrotic changes. Chondroma
is reported by Kitt, Sarcoma by Cadeac and Beylot. There seems to have
been a special tendency to invade the demicanal, and to interfere with
deglutition, rumination, and the passage of food into the third stomach.
The impairment and loss of appetite and of rumination, the presence of
tympany, and the general loss of condition are suggestive. If the
disease of the demicanal leads to antiperistaltic movements of the
œsophagus which can be felt by the hands pressed on the jugular furrows
the diagnosis may possibly be made.

_Treatment_ is manifestly hopeless. To be effective it must be surgical
and would too often entail excision of the affected part of the viscus
and careful suture of its walls. This would be even more hopeless when
the demicanal was the seat of disease.

Temporary palliation might be secured by a sloppy diet, the withholding
of all rough food which would demand rumination, and the use of common
salt, saline laxatives and abundance of water.


              ANIMAL PARASITES OF THE RUMEN AND RETICULUM.

  Infusoria. Amphistomum Conicum. Actinomycosis. Tumors: Papilloma,
  Chondroma, Sarcoma. Treatment—palliation or surgical.

Colin describes and figures as many as eight varieties of infusoria
found habitually in the first two stomachs. All appear to be introduced
with the food, in the infusions of which they also appear, and they find
in the fermenting mass of ingesta in the first two stomachs a favorable
medium in which to grow and multiply. It cannot be shown that they are
in any way detrimental and they have even been supposed to be beneficial
to digestion as glycogen has been demonstrated in their protoplasm. Like
the bacterial ferments they doubtless assist in the disintegration of
the mass of food.

_Amphistomum Conicum._ This is a trematode worm about the size of an
apple-seed (10 millimetres long by 2 millimetres thick), rounded at both
ends, slightly curved on itself, and, as usually found, of a bright red
color. It attaches itself by its sucker (on thick end), usually in the
vicinity of the demicanal. Its life history is closely allied to that of
the distomata, but as it is not known to prove at all injurious to its
host, it possesses no pathological importance.

=Actinomycosis of the Rumen and Reticulum.= Tumors of this fungus are
sometimes found in the walls of the two first stomachs projecting in the
form of polypi, or imbedded in the thickness of the coats. Where they
are completely covered by the mucous or serous membrane their true
nature is not readily recognized. When incised they show the
characteristic yellow granules made up of club-shaped cells, though the
usual stellate arrangement may be somewhat imperfect. From the serous
surface the growth may invade the different adjacent organs. It is
impossible to diagnose a primary actinomycosis of the rumen, if
unaccompanied by more superficial lesions, but, if the disease is
recognized elsewhere, the same general treatment with iodide of
potassium will dispose of these formations as well.


                IMPACTION OF THE OMASUM (THIRD STOMACH).

  Definition. Synonyms. Causes, torpid action, defective insalivation,
  inactive rumen, fever, inflammation, spinal paresis, dry, fibrous,
  innutritious food, fungi, ergot, smut, privation of water, or of
  succulent food, microbian ferments and their products, chronic heart
  disease, dry farinas, extreme changes of diet, brain disease.
  Symptoms: slight or violent; ill health, impaired appetite and
  rumination, grunting, tympany, diarrhœa, constipation, baked coated
  fæces, percussion signs, separation from herd, red eyes, stiffness,
  agalactia, fœtid eructations, paralysis, drowsiness, stupor, delirium,
  nervous symptoms mostly in acute cases. Course in chronic and acute
  cases. Diagnosis; from pneumonia, and overloaded rumen. Lesions; solid
  impacted omasum, baked contents, shedding of epithelium, congestion,
  petechiæ, ulceration, empty, and congested abomasum and small
  intestine. Treatment: laxative food, purgatives, stimulants,
  antiseptics, enemata, stimulants of peristalsis, counter-irritants,
  mucilages, laxative diet, tonics.

_Definition._ This may be defined as 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.

_Synonyms._ As the disease has been long popularly known it has received
a variety of popular names which are more or less characteristic. Dry
murrain, Clewbound, Fardelbound, Stomach staggers, Grass staggers,
Vertigo, Chronic dyspepsia, and Chronic indigestion may serve to
illustrate these.

_Causes._ Torpor of the manifolds and the suppression of secretion of
saliva, together with the absence of a continuous access of waves of
liquid floating the finely divided food from the mouth or rumen to the
third stomach are prime conditions of dessication of the contents. The
third stomach, like the two first, has no provision for liquid
secretion, but is dependent for its supply on constant flushing from in
front. If therefore feeding and rumination are interrupted as the result
of a febrile disease, if the secretion of saliva is in great part
suppressed, if the vermicular movements of the rumen and resulting
overflow into the third stomach are checked, and if in addition the
omasum itself is rendered torpid, the ingesta compressed between its
folds becomes drained of its liquid, and in no great length of time, to
such an extent that it may be rubbed up into a dry powder. All this is a
necessary result of an acute febrile condition, and therefore all
febrile and inflammatory affections tend to drying and impaction of the
contents of the omasum. If therefore the observer were to go no further
than this he would have a very simple pathology, for all or nearly all
fevers and inflammations would be to him simply impacted omasum. In the
great majority of cases this condition is to be looked on as a secondary
and subsidiary affection, while the real primary disease has still to be
sought for.

Some explanation of the special susceptibility of the third stomach in
such constitutional troubles, is found in the source of innervation of
the viscus. Colin and Ellenberger could rouse the movements of the first
two stomachs but not of the third by electric stimulation of the vagus,
while the third stomach was excited to action by excitation of the
spinal cord and of the sympathetic twigs proceeding from this to the
manifolds. Ellenberger indeed avers that the walls of this viscus are
abundantly furnished with ganglionic cells which are called into action
by this sympathetic stimulus. The innervation being derived from an
independent source, derangement of the third stomach may be quite
independent of any primary disorder of the first, and the omasum
deriving its motor supply from sources so closely related to the
vaso-motor ones, may give an additional explanation of the intimate
connection of its disorders with febrile and inflammatory diseases.

But while acknowledging the controlling influence of torpor or paresis
of the omasum, it would be an error to follow Cadeac in denying the
influence of food as a cause of impaction. It has long been notorious
that impaction of the omasum is preëminently a disease of winter, or of
the period of dry feeding. It occurs in cattle fed on dry, fibrous,
innutritious fodder, and especially when there is a scarcity of water,
or when in connection with severe frost the usual water supply has been
frozen up. It prevails in stock turned in spring or autumn on pastures
in which the fresh green grass grows up among the dead, dried and
withered stems of a previous growth and tempts them to eat them. It
appears when the stock consumes corn or cornstalks affected with smut or
certain other fungi, or the cereals or grasses suffering from ergot or
smut, but this is especially the case when there is also a privation of
water, whereas, with an abundant water supply or a partial ration of
roots, potatoes or ensilage the danger is greatly reduced. Sometimes a
change from soft to very hard water appears to act as a cause but
whether from a special astringent action or a disinclination to consume
the usual amount has not been made clear.

It must be allowed that the sheep and goat which habitually drink
little, suffer far less from this affection than the ox which drinks
freely, yet allowance must be made for the constitution and long settled
habits of the genus, and we must not forget that it is usually under
privation of water or a restricted supply that the ox suffers.

Among other causes must be named fermented food, the microbian ferments
and their products, serving to render the organ torpid, but also to
produce fever, lessened secretion and an arrest or retardation of liquid
supplies from the mouth or rumen.

Chronic heart disease, causing blood stasis in the omasum, appears to
induce torpor and favor impaction.

The ingestion of lead has a very direct action in producing paralysis
and consequent impaction.

Finally, finely divided dry food like meal or bran, swallowed hastily,
tends to pass in large amount directly into the omasum, and, before the
animal has become accustomed to the ration, is liable to clog the viscus
and induce impaction.

In nearly all cases, the commencing impaction entails a certain rise of
temperature and suppression of secretions, so that the malady tends to
move in a vicious circle, each new step tending to aggravate the already
existing condition. In chronic cases, which are very common, a careful
record of bodily temperature shows oscillations, above and to the
normal, at irregular intervals, each rise tending to add to the
impaction.

The most acute and fatal forms of the affection 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.

_Symptoms._ These vary according to the degree of impaction or gastric
torpor, from simple, irregular, or suspended rumination (loss of cud) to
the most severe gastric and nervous disorder.

The slighter or less acute cases are marked by a failure to re-establish
regular rumination on partial convalescence from a fever or
inflammation. The hyperthermia subsides, but the appetite remains poor
and capricious, the muzzle dry, the eyes dull, the spirits low,
breathing quickened and occasionally accompanied by a moan, especially
when moving down hill, slight tympanies of the rumen may appear and the
contents of that organ seem consolidated and may be felt as solid masses
when pressure is made by the hand. The mouth is hot, clammy and fœtid,
and the bowels costive, the fæces being passed in small amount and in
the form of hard, black pellets, covered by a film of mucus, or streaks
of blood, and containing particles of undigested food. This not
unfrequently merges into a transient diarrhœa to be followed in turn by
renewed constipation, and such alternations may repeat themselves again
and again. The omasum is so deeply seated under the ribs on the right
side that exploration is unsatisfactory, especially in the milder cases,
yet pressure of the closed fist upward and forward below the middle of
the chest will give the impression of a specially solid resistance and
the patient may indicate suffering by a moan. Percussion with the closed
fist has the same effect. There may be slight tremors of the body, the
horns, ears and limbs are cold, and the hair erect in patches, dry and
lustreless.

In cases occurring independently of previous disease, diarrhœa may be
the first symptom noted, the malady being preceded by local irritation
and congestion, but this soon gives place to constipation with
alternating diarrhœa and the general train of symptoms above mentioned.
The animal leaves the herd and is found lying apart on its left side
with the nose in the right flank, the pulse and breathing quickened, the
eyes congested, and a moan emitted occasionally in expiration. This is
increased if the patient is raised and driven, especially down hill. He
walks with stiff, arched back, unsteady gait and dragging limbs.
Appetite may not be entirely lost at first, but only impaired and
irregular, and as rumination ceases, grinding of the teeth becomes
common. The secretion of milk is diminished or altogether arrested, and
emaciation advances day by day. Fœtor of the eructations, the result of
prolonged and septic fermentation in the rumen, is often 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 the more acute cases resulting from a sudden access of green food, a
change of water, or the ingestion of irritant plants, the affection
partakes more or less of the nature of congestion or inflammation of the
viscus, and may run a rapidly fatal course. The animal may be seen apart
from the herd in the characteristic recumbent position, with eyes red
and glassy, eyelids semi-closed, and much drowsiness and stupor, but
when raised he may still feed in a sleepy, listless manner. The bowels
may be loose or confined, the pulse and breathing accelerated, the right
hypochondrium firm and tender, and as in the other forms the crepitating
sound of fermentation is slight or absent over the region of the
manifolds. Soon nervous disorder appears, the eyes glare wildly, the
animal seeks relief in motion, it may be in a straight line, or to one
side, and being blind and unconscious of obstacles he may fall into
pits, or ditches, dash against trees, fences or buildings, and if they
offer sufficient resistance he will continue pushing, breaking teeth or
horns, and subject to violent muscular contractions, causing even the
grubs to start from the back. The nervous disorder is often further
shown in loud and terrified bellowing as if chased by a dog or gored by
one of its fellows.

_Course._ Chronic cases may continue almost indefinitely the victims
showing merely poor health, impaired digestion, and steady loss of
condition. After death the omasum is sometimes found to contain dried
materials, such as the animal has not had access to for from three to
five months.

In those which end in an early recovery there occurs a free and abundant
diarrhœa, the fæces containing solid flattened masses with black baked
or polished surface, the result of the detachment of the impacted layers
from between the folds of the third stomach. The tympany of the rumen
subsides, crepitation is renewed in the rumen and omasum, there is free
rumbling in the bowels, and the appetite gradually improves. The
softening and removal of the dessicated contents are slow and it may be
weeks before there is a complete restoration to normal conditions.

_Diagnosis._ The hurried pulse and breathing and the grunting with
expiration may be mistaken for pneumonia or pleurisy, but the
distinction can be made as in impacted rumen. There is at first no
fever, the tenderness is confined to the right side, the percussion
dullness of the chest is in the posterior part and distinctly referrible
to the loaded abdominal viscera, it is attended by no pulmonary
crepitation, indeed crepitation in rumen and omasum is lessened or
abolished, there is no pleural effusion, but there are the
unquestionable signs of gastric and intestinal disorder.

It may be confounded with overloading of the rumen, but in the latter
case the distension occurs rapidly, there is little or no indication of
movement of the viscus, appetite and rumination are usually early
suspended and the gaseous eructations are not putrid.

_Postmortem Appearances._ These are essentially connected with the
impaction of the omasum. This organ is gorged to twice its normal size
or larger, firm, solid and resistant, not easily taking an impression of
the finger, and having at times an almost stony hardness. When incised
the intervals between the folds are sure to be packed with dessicated
food, often so dry in the upper part that it may be rubbed down into a
grayish powder, and it has been compared to the cakes of linseed as they
come from the press. The surface of such cakes is smooth and dark, and
usually covered by a layer of epithelium which has detached itself from
the surface of the fold. This is usually quoted as a morbid
desquamation, but inasmuch as we frequently see it in perfectly healthy
conditions in animals killed in abattoirs, it must be admitted to occur
also as a normal physiological exfoliation. The exposed mucosa shows
spots and patches of congestion, extravasation, and even at times
ulceration, or slight areas of necrosis.

The rumen shows the result of torpor and inactivity. The ingesta is
largely packed into solid masses, which have advanced from the simple
acid fermentation, to evident putrefaction with offensive emanations.
The abomasum is empty or nearly so of ingesta, but contains abundance of
mucus and shows patches of congestion as in prolonged abstinence.

The small intestine is also empty and collapsed, with considerable
redness and congestion. The larger intestine contains a small quantity
of feculent matter, dry, massed in small pellets and with smooth
glistening surface. Mucus is abundant and dense.

_Treatment._ This must follow the same lines as in impaction of the
rumen with the understanding that the response is less certain and the
result somewhat more tardy in reaching complete convalescence. In mild
and chronic cases a liberal allowance of flaxseed tea, several
bucketfuls per day, will often succeed.

In using purgatives those are usually the best which lead to drinking
abundantly. For the ox a pound each of Epsom and common table salt, with
an antiseptic stimulant like aqua ammonia (3 to 4 drachms) or oil of
turpentine (2 oz.) will often act favorably. The sodium chloride is
antiseptic, and induces ardent thirst and if there is free access to
water, tepid or not too cold, purgation is early secured and the
impacted cakes in the manifolds are slowly softened, detached and
removed. But unless water is given freely the salt will prove irritating
and even injurious.

In obstinate cases, and in the absence of indications of gastric or
cerebral congestion the addition of 20 croton beans or 20 drops of
croton oil will be excellent. Nux vomica (½ drachm) is also of value in
rousing the torpid nervous action. Injections are always in order, and
it is recommended to use these cold so as to rouse the muscular action
of the intestine and stomach.

Some of the newer remedies which rouse the contractility of the
digestive organs and at the same time stimulate secretion serve an
excellent purpose in these cases. Eserine 1½ grain, veratrine 1 grain,
barium chloride 10 to 15 grains, or pilocarpin 3 grains may be given
hypodermically in addition to the usual purgative. The pilocarpin is
theoretically the best as its tendency is to cause free secretion from
all mucous surfaces, and even a slight secretion from the omasal folds
will greatly favor detachment and discharge of the impacted plates.
These as well as the stimulants may be repeated as the effects pass off.
The purgatives on the other hand should be given at first in a large
dose, and not repeated except under the stress of necessity as their
constant repetition in small doses seems to nauseate the animal and even
to retard action. In the case of profuse secretion from the kidneys
however it may be supposed that the saline agents have passed off in
that way and a purgative may be safely repeated. It may be well however
to use one which is less likely to stimulate the kidney, such as castor,
olive, or raw linseed oil or senna.

The patient may be several days or even a week without alvine discharge
and yet do well. If there are fever and other indications of gastric
congestion a blister to the right hypochondrium may be of value. Rub
well with oil of turpentine and then with a pulp of the best ground
mustard and tepid or cold water and cover with sheets of thick paper to
prevent evaporation.

If nervous, symptoms are manifested by dilated pupils, blindness,
congested conjunctiva, hot horns and ears, and drowsiness, or
excitability apply cold water or an icebag to the head and continue as
long as may be needful. If the patient should become violently delirious
he may be fastened to a beam overhead in the centre of the stall so as
to prevent him from injuring himself or others.

In these cases the more violent and irritant purgatives are to be
avoided, and decoctions of slippery elm, linseed or gum may be given to
sheathe and protect the irritated membrane.

Even though a free action of the bowels has been secured it is not to be
assumed that all impacted material has been removed. A specially
laxative diet of roots, ensilage, or succulent green food, with a
liberal supply of salt, and free access to water should be kept up for
some weeks to secure a complete softening and expulsion of the impacted
material. Repeated small doses of laxative medicine may be requisite to
bring this about. As a rule a course of tonics, and above all of nux
vomica is valuable in re-establishing the normal tone of the stomachs
and intestines.


                      INFLAMMATION OF THE OMASUM.

  Involved in rinderpest, Texas fever, malignant catarrh, etc.
  Diphtheritis, Tuberculosis, Irritant poisons, Traumatisms, Impactions,
  change to green food, etc. Lesions: Congestion, ramified redness,
  petechiæ, desquamation, softening, necrosis, false membranes,
  ulcerations, pigmentation, papillary growths, impaction. Symptoms:
  those of impaction with fever. Course, Treatment: demulcents,
  laxatives, blisters, bismuth, eserine, veratrine, pilocarpin,
  electricity, careful diet.

Like the rumen the omasum is the seat of local inflammatory lesions in
certain specific fevers. Thus in Rinderpest, and Texas fever it is
almost always the seat of patches of congestion and blood extravasation,
and in the latter of necrosis and perforation of the folds. Similar
lesions sometimes appear in malignant catarrh and anthrax. Dieckerhoff
describes exudates, ulcerations and even perforations in
pseudo-diphtheritis, and Brückmüller, congestions and ecchymoses in
connection with a cutaneous rash. Tuberculosis of the organ is somewhat
rare and is held to be due to the swallowing of bronchial secretions in
cases of pulmonary tuberculosis.

Cases of primary inflammation are rare, in keeping with the soft finely
divided condition in which the food reaches the organ. It may, however,
occur in case of the ingestion of arsenic and other irritant poisons, or
of goring, kicks and other injuries on the right hypochondrium, or from
the irritation attendant on impaction, or again from the stimulus of a
sudden change to rich green food.

The _lesions_ in such a case are congestion of the folds with patches of
ramified redness, blood extravasations, desquamation, softening or even
gangrene. False membranes, perforating ulcers, and erosions are
sometimes present. In the chronic forms grayish or slate colored
pigmentation of the mucosa, congestions and papillary growths are
common.

In both acute and chronic forms the congestion entails loss of
contractility and thus impaction and drying of the ingesta between the
folds of the organ are constant.

_Symptoms._ These are the symptoms of impaction of the manifolds,
impaired appetite and rumination, formation of solid masses in the
rumen, tympany, tenderness or pressure on the right hvpochrondrium,
irregularity of the bowels, arching of the back and grunting when made
to walk. The addition of fever, as evidenced by rectal hyperthermia, hot
horns, ears, legs and muzzle, serves to diagnose it from simple
impaction.

The _course_ of the malady is the same as in impaction, but with an even
greater tendency to aggravation and a fatal result as the inflammation
entails a paresis of the walls of the viscus which favors a constant
accumulation and dessication of the interlaminar material.

_Treatment._ This must be largely on the same line as in impaction,
laxatives of sulphate of soda, a diet of flaxseed or barley gruel, and
drinking water rendered demulcent with slippery elm. These must be
supplemented by a mustard or other blister to the right hypochondrium,
by soothing doses of nitrate of bismuth (½ ounce), and hypodermic
injections of eserine (1½ grain), veratrine (1 grain), or pilocarpin (3
grains). A current of electricity sent through the right hypochondrium
once or twice a day, will further be desirable. When convalescence has
set in, mashes of wheat bran and middlings may be allowed, to keep up
the flagging vigor, and the patient should be returned to solid, fibrous
food by slow degrees only.


                         TUMORS OF THE OMASUM.

  Papilloma. Sarcoma. Actinomycosis.

Tumors of the omasum have been seen only as papilloma, and sarcoma.

The =papillomata= result from hypertrophy of the normal papillæ, and
their general appearance resembles those of the pharynx, gullet and
paunch. They sometimes grow to the size of the fist or larger, with a
cauliflower appearance, their increase and the formation of pedicles
being favored by the active contractions of the muscular coat of the
manifolds. They may be red and vascular if recent, are usually white if
older, and may become somewhat horny on the surface, but soft and
friable within. When they attain a large size they may obstruct the
passage to the fourth stomach, tending to impaction of the manifolds and
arresting digestion and nutrition.

=Sarcoma= of the third stomach has been recorded by Paule, Kitt and
Schütz as developing in the subserous tissue and forming a layer on the
surface of the organ. This bulges out in rounded swellings of irregular
sizes, and may show various degenerations—caseous, calcic or necrotic.
The structure shows fusiform and rounded cells more or less numerously
imbedded in a fibrous stroma.




                     ACTINOMYCOSIS OF THE ABOMASUM.


This has been seen once by Professor Axe. Its true nature is
unrecognizable during life, but if other formations of the same kind
betray the nature of the lesion, the treatment by iodide of potassium
may be resorted to with good hope of success.


                      INDIGESTION OF THE ABOMASUM.

  Causes: excess of water—ice cold, or after privation. Symptoms: colicy
  pains, local perspirations, right flank gurgling, diarrhœa, arched
  back, anorexia, or nervous symptoms. Prevention: Treatment:
  stimulants, carminatives, exercise, electricity, friction, stimulants
  of peristalsis.

This has been observed as the result of ingestion of an excess of water,
and especially ice cold water, by work oxen, or overdriven animals which
have been long exposed to the heat of the sun and subjected to violent
exertions without drink. The habit of allowing water only at long
intervals, though it is being abundantly eliminated not only by kidneys
and bowels, but also by the accelerated breathing and the sudation,
causes consuming thirst, and when brought to the drinking place, the
subject drinks inordinately before eating. Much of this liquid is passed
at once into the abomasum, which with a capacity of 20 to 25 quarts,
becomes overdistended and irritated. Much of the water passes speedily
into the bowels, rousing these also into unwonted action. The sudden
distension appears to cause spasmodic contractions of the abomasum,
which are aggravated if the liquid is cold, and a violent though
transient suffering is induced.

_Symptoms._ These appear suddenly after the drinking of the cold water
and consist in the most violent colicy pains, twisting of the tail,
kicking at the belly, lying down and rising at short intervals, moaning,
looking at the flanks, anxious countenance, and the breaking out of
perspirations around the ears, on the neck or belly. There is no tympany
of the rumen but there are some fullness and active gurgling on the
right side of the abdomen. The attack does not usually exceed one or two
hours in length, and a profuse diarrhœa brings relief, the alvine
discharges being very watery with considerable mucus and some undigested
food principles.

In exceptional cases it has lasted for six hours and even in the more
transient cases, there is liable to remain for a time dullness and
prostration, advancing of the hind legs under the body, anorexia and
suspended rumination. Cruzel records two cases in which the small
intestine was ruptured as the result of too vigorous driving of the
patients. Other cases have perished from the coexistent diarrhœa.
Nervous symptoms also may appear as in other gastric disorders. The
usual result is recovery after a very transient illness. This short and
favorable course, and the evidence of cause and symptoms sufficiently
identify the disease.

_Treatment._ Prevention should be sought by avoidance of cold water in
excess, when the animal is heated, fatigued and thirsty. A little food,
an occasional mouthful of water, or a drink of warm water and meal will
act prophylactically. When the animal is attacked alcoholic drinks,
ammonia, carminatives (pepper, ginger, fennel, caraway, peppermint,
chamomile) or even strong tea or coffee may be used to advantage.
Careful walking exercise is also useful with friction to the abdomen, or
the use of electricity. Cadeac advises stimulants of the
peristalsis—eserine, veratrine or pilocarpin subcutem; senna,
podophyllin, or castor oil by the mouth.




            INDIGESTION OF THE FOURTH STOMACH IN THE YOUNG.

  Causes: Symptoms: Dullness, recumbency, inappetence, colic, acid
  eructations, abdominal tension, costiveness, diarrhœa, emaciation.
  Lesions: Sour coagula in stomach, puffy or congested mucosa,
  undigested casein in bowels and fæces. Prevention as in infector
  gastro-enteritis. Treatment: Elimination, antacid, antiseptic,
  carminative, stimulant, rennet.


While the fourth stomach in the mature animal is protected against
danger by the preparatory work of the first three, and by their action
in retarding the food in its progress, and allowing it to pass into the
fourth only when thoroughly comminuted and then only in small quantity
at a time; in the suckling on the other hand the milk passes at once
into the abomasum, which is thus rendered as susceptible as in the
monogastric animal.

_Causes._ The causes are almost identical with those set forth under
_infective gastro-enteritis_ of the suckling, acting however with less
force, or on a less susceptible system. Overloading and the resulting
paresis; unsuitable milk from another genus, or from unhealthy,
overworked, or over-fed specimens of the same genus; the ingestion of
hard, insoluble, indigestible or toxic aliments, and exposure to cold
and wet are among the most common direct causes. As secondary causes are
overfeeding of the cows, and bringing up the calves on the pail with all
kinds of substitutes for the milk of the mother.

_Symptoms._ Dullness, lack of sportiveness and of appetite. The patient
lies down a good deal, but is nervous or restless, and when up shows
colicy pains by movements of the tail and hind limbs. He may moan gently
or bellow frequently. The muzzle is dry, the mouth clammy, hot and sour,
the abdominal muscles rigid and the belly often somewhat swollen, and
resonant on percussion. Acid eructations are common. At first there is
costiveness, but in a few hours diarrhœa sets in and usually proves
critical, clearing away the offensive and irritant materials and paving
the way for recovery. The tension of the belly lessens, by degrees, the
appetite returns, the bowels resume their normal tone and in twenty-four
or forty-eight hours health may be fully restored.

There is, however, always danger of the supervention of gastro-enteritis
of which in many instances the above-named symptoms indicate the first
stage. In all cases it interferes with the growth and fattening of the
subject.

_Lesions._ We observe the presence in the stomach of masses of
coagulated milk, undigested, mixed with an excess of mucus, and exhaling
a sour or even a septic odor. The mucosa is more or less red and
congested with swelling and opacity of the epithelium. The bowels also
contain the undigested flocculi of casein, more or less fermented and
which have escaped the action of the peptic liquids.

_Prevention._ This consists in the avoidance of the causes, and as these
are in the main the accessory causes of infective gastro-enteritis in
the suckling, it will save repetition to refer to the article on that
subject.

_Treatment._ In an attack which is caused and maintained by undigested
and irritant materials in the stomach, the first consideration must be
the elimination of these offensive matters. An ounce of castor oil with
a teaspoonful of laudanum for calf or foal will usually effect this
purpose. Or ½ oz. calcined magnesia or carbonate of magnesia, or of
manna 2½ drs. or cream of tartar may be substituted for the oil. The
addition of a carminative or stimulant (1 dr. syrup of anise, or
tincture of cinnamon, 1 oz. whisky or brandy, or ½ oz. oil of turpentine
for calf or foal) will often check the diarrhœa and fermentation.

In weak subjects the stimulant may be used with a drachm of chalk or of
bicarbonate of soda, and 5 grains powdered nux vomica.

In all cases alike the use of rennet is very advantageous. One-eighth of
a calf’s rennet being steeped in a bottle of sherry wine and the liquid
given to the amount of a tablespoonful (½ oz.) with each drink. This
secures proteid digestion and checks fermentation thereby hindering the
formation of the offensive products which maintain the irritation and
disorder.




  INFECTIVE GASTRO-ENTERITIS IN CALVES, LAMBS AND FOALS. WHITE SCOUR.

  Causes: early life, exclusive activity of fourth stomach, faulty milk,
  absence of colostrum, milk from advanced lactation, milk of other
  genus, or altered by excitement, or unwholesome food, excess on hungry
  stomach, soured, fermented, feverish milk, putrid milk, leucomaines,
  overdistension of stomach, farinaceous food, hair balls, morning and
  evening milk, milk after first calf, composition of milk by genus,
  ruminant’s milk to monogastric animal, infectious microbes—bacilli,
  micrococci. Symptoms: costiveness, inappetence, listlessness, tense
  abdomen, acid eructations, fœtid diarrhœa, becoming yellow or white,
  general fœtor, staring coat, pallid mucosæ, tucked up tender abdomen,
  weakness, emaciation, fever, bloating, frothy dejections, arthritis,
  peritonitis, pneumonitis, hepatitis, ophthalmia, laminitis, etc.
  Mortality: in foals, calves, lambs. Lesions: gastric and intestinal
  congestions, exudations, necrosis, incoagulable blood in foals,
  anæmia. Prevention: normal feeding, expulsion of meconium, care of
  nurse, adapt composition of cow’s milk to genus of nursling, warmth,
  lime water, rubber teat, Pasteurizing, disinfection, separation from
  infected animals and places, breed from robust parents. Treatment:
  elimination, antiseptics, boiling milk, rennet, ipecacuan,
  carminatives, astringents, tar, calomel and chalk, gum, flaxseed, elm
  bark.


_Causes._ The abomasum in the adult is protected against disorder, by
the normal activity of the first three stomachs, macerating the food,
presiding over the second and more perfect mastication, grinding it
between the omasal folds into a firmly attenuated pulp and delaying its
progress so that it arrives at the fourth stomach at short intervals and
in small quantities only at a time. It follows that this organ is rarely
involved in serious disorder unless as the result of the ingestion of
poisons, or of excess of water, or from the presence of parasites. In
the very young ruminant, however, the condition is reversed, the first
three stomachs are as yet undeveloped, and incapable of receiving more
than the smallest quantity of food or of retaining the same, and the
abomasum alone is functionally active and receives at once practically
everything that may be swallowed. In the first few weeks of life
therefore the ruminant is exposed to almost the same dangers, from
overloading, indigestion, inflammation and poisoning as is the
monogastric animal. For the time, indeed, the undeveloped ruminant is in
its physiological and pathological relations, a monogastric animal. For
this early life therefore whatever applies to the soliped applies
equally well to the ruminant.

When allowed to suck at will from a healthy nurse, which completed its
gestation about the time the young animal was born, indigestion is rare.
But whatever interferes with the normal supply is liable to cause
derangement. The withholding of the first milk—colostrum—the laxative
properties of which are essential to clear away the intestinal
accumulations of fœtal life—meconium; the placing of new-born offspring
on the milk of nurses that bore their young many months before; bringing
up of foals on cow’s milk; working, overdriving, hunting, shipping by
rail, or otherwise exciting the dams; allowing too long intervals
between the meals—feeding morning and night only, or morning, noon and
night, the nurse being kept at work or pasture in the interval; feeding
unwholesome food to the nurse; bringing up by hand, on cold and even
soured milk, or that which has become contaminated by putrid leavings in
the unscalded buckets. Some of these causes should be emphasized, for
example the milk of excitement and fever, milk that is soured or putrid,
and milk suddenly swallowed in excess. The nurse which is fevered or
subjected to over-exertion has produced an excess of tissue waste and
leucomaines which largely escape from the system in the milk. This milk
is therefore at times unwholesome and even poisonous. Mares subjected to
severe work or that fret much under lighter work, cows carried by car or
boat, or driven violently, and any nursing animal which has been thrown
into a fever from any cause whatever, is liable to yield toxic milk.
This would include the milk of all severe diseases, as being liable to
become charged with toxins and ptomaines and thus poison the young
animal, which subsists upon it as an exclusive diet, even though the
actual pathogenic microbe may not be present in the secretion.

With regard to fermented milk, that which has been simply soured,
relaxes the bowels and the attendant congestion contributes to further
derangement and even infection by any pathogenic germ which may be
present, or by microbes which are habitually saprophytic, but take
occasion to dangerously attack the weakened mucosa. If the milk has
undergone putrefaction in the feeding bucket, the co-existence of the
septic germ and the septic ptomaines and toxins, often determines
indigestion and irritation of the mucosa. These poisons may further be
absorbed and produce general constitutional disorder which reacts most
injuriously on the stomach and digestion.

Milk swallowed rapidly and in excess by a hungry calf or foal,
overdistends the stomach, which, like other hollow viscera in such
conditions, is rendered paretic or paralytic, and suffers from
suspension of both the vermicular contractions and the peptic
secretions. Under these conditions the milk, which is one of the most
admirable culture media for bacterial ferments, undergoes rapid
decomposition, with the production of a series of toxins and ptomaines
varying according to the different kinds of microbes that may be
present. Under such conditions microbes which are normally harmless,
vigorously and destructively attack the mucous membrane and determine
some of the worst types of juvenile diarrhœa.

In artificial feeding there is another serious danger. Calves in
particular are brought up largely on gruels made from farinaceous
material. These contain a large quantity of starch which requires the
action of the saliva (ptyaline) to resolve it into glucose, and fit it
for absorption. But in the early days of life the salivary glands are
almost entirely inactive, and it is only as the first three stomachs
develop that this secretion becomes normally abundant. This is sought to
be met by fixing in the feeding bucket a rubber teat, which the young
animal is made to suck so as to solicit the secretion of saliva. The
benefit obtained is however more from the slower ingestion of the milk
than from any material increase of saliva from the as yet functionally
inactive glands.

The presence of hair balls in the stomach, derived from the skin of
themselves or others is one of the most injurious of the causes of
juvenile indigestion. Lying as these do at this early age in the one
well developed stomach they interfere with its normal secretions, and
being at first open in texture they become saturated with putrefying
ingesta, which gives out the most poisonous products.

The milk is materially affected by the food eaten by the nursing animal
and such variations in the milk tend at times to derange a weak stomach.
The following table from Becquerel and Vernois gives the results of dry
and succulent food on the amount of the different proximate principles
in the milk.

 ───────────────────────────────┬──────┬──────────┬──────┬───────┬──────
                                │      │Casein and│Milk, │       │
                                │Water.│extractive│Sugar.│Butter.│Salts.
                                │Parts │ matter.  │Parts │ Parts │Parts
                                │  in  │ Parts in │  in  │  in   │  in
         Nature of Food.        │1,000.│  1,000.  │1,000.│1,000. │1,000.
 ───────────────────────────────┼──────┼──────────┼──────┼───────┼──────
 Cows on winter feed:           │      │          │      │       │
    Trefoil or lucerne 12–13    │      │          │      │       │
      lbs.; oat straw, 9–10     │      │          │      │       │
      lbs.; beets, 7 lbs.;      │      │          │      │       │
      water, 2 buckets          │871.26│     47.81│ 33.47│  42.07│  5.34
 Cows on summer feed:           │      │          │      │       │
    Green trefoil, lucerne,     │      │          │      │       │
      maize, barley, grass and 2│      │          │      │       │
      buckets water             │859.56│      54.7│ 36.38│  42.76│  6.30
 Goats milk on different        │      │          │      │       │
   rations:                     │      │          │      │       │
    Straw and trefoil           │858.68│     47.38│ 35.47│  52.54│  5.92
    Beets                       │888.77│     33.81│ 38.02│  33.68│  5.72
 ───────────────────────────────┴──────┴──────────┴──────┴───────┴──────

The decrease of the solids but especially of the casein, sugar, and
salts is very marked in the cow on poor winter feeding. In the goat fed
on beets alone the increase of sugar and decrease of other solids is
striking.

To the same effect speaks the following table giving the results of an
experiment with a ration of corn and cob meal, in contrast with one of
sugar meal. Each cow had a common ration of 12 lbs. corn fodder and 4
lbs. clover hay, in addition to the test diet which was 12½ lbs. corn
and cobmeal in the one case, and 10 lbs. sugar meal in the other. To
avoid the misleading effects of a sudden transition from one food to the
other, each special ration was fed for seven days before the
commencement of each test period.

 ───────────────────────────┬──────┬─────┬──────┬─────┬──────┬──────────
                            │      │     │      │     │      │ Ratio of
                            │      │Fat. │      │     │      │  fat to
                            │Milk. │ Per │      │Fat. │Solids│solids not
     Animal and Ration.     │ Lbs. │Cent.│Solids│Lbs. │ Lbs. │   fat.
 ───────────────────────────┼──────┼─────┼──────┼─────┼──────┼──────────
 Grade Shorthorn Cow:       │      │     │      │     │      │
   1st 21 days: Corn and cob│      │     │      │     │      │
     meal                   │631.25│ 3.43│ 11.57│21.67│ 73.02│422. :1000
   2d 21 days: Sugar meal   │641.50│ 4.04│ 12.53│25.93│ 83.38│476.2:1000
   3d 21 days: Corn and cob │      │     │      │     │      │
     meal                   │559.00│ 3.22│ 11.86│17.97│ 66.32│371.7:1000
 Grade Shorthorn Cow:       │      │     │      │     │      │
   1st 21 days: Corn and Cob│      │     │      │     │      │
     meal                   │604.75│ 3.57│ 11.95│21.56│ 72.28│425.1:1000
   2d 21 days: Sugar meal   │582.00│ 3.91│ 12.37│22.74│ 72.57│456.3:1000
   3d 21 days: Corn and cob │      │     │      │     │      │
     meal                   │527.00│ 3.37│ 12.05│17.78│ 63.48│389.1:1000
 Grade Shorthorn Cow:       │      │     │      │     │      │
   1st 21 days: Sugar meal  │753.50│ 3.97│ 12.43│29.94│ 93.67│469.8:1000
   2d 21 days: Corn and cob │      │     │      │     │      │
     meal                   │601.50│ 3.15│ 11.45│18.97│ 68.89│380.0:1000
   3d 21 days: Sugar meal   │560.50│ 3.85│ 12.16│21.58│ 68.16│463.3:1000
 Grade Shorthorn Cow:       │      │     │      │     │      │
   1st 21 days: Sugar meal  │487.50│ 4.15│ 13.27│20.25│ 64.69│455.6:1000
   2d 21 days: Corn and cob │      │     │      │     │      │
     meal                   │379.00│ 3.51│ 12.00│13.30│ 48.09│382.3:1000
   3d 21 days: Sugar meal   │374.50│ 3.72│ 13.01│13.95│ 48.74│401.0:1000
 ───────────────────────────┴──────┴─────┴──────┴─────┴──────┴──────────

Here we find a material increase of the solids and particularly of the
fat whenever the sugar (gluten) meal, rich in fat and albuminoids was
furnished. It is interesting to note the relative amount of fat and
albuminoids in the corn and cobmeal mixture as compared with the sugar
meal.

           _Constituents_. _Corn and cob meal_. _Sugar meal._
                               _Per Cent._       _Per Cent._
           Water                          13.37          6.10
           Salts                           1.43          1.17
           Fat                             2.81         11.16
           Carb-hydrates                  65.99         52.66
           Woody fibre                     8.03          8.64
           Proteids                        8.37         20.27
                   —_Bulletin_: _Iowa Agricultural Experiment
                                                    Station_.

Such variations in the quality of the milk under different rations,
occasionally affect the weak stomach of the new born, and as the same
constitution is likely to predominate in the same herd, a number may be
attacked together as a result of some change in feeding.

Other conditions, however, lead to variation in quality. Hassall found
that the morning milk of the cow furnished 7.5 per cent. of cream, while
the evening milk gave 9.5 per cent. Boedecker found that morning milk
had 10 per cent. of solids and evening milk 13 per cent. The first drawn
at any milking is poorer in cream than that which is drawn last. The
first may have only one-half or in extreme cases one-fourth of the cream
that the strippings have. When the cow is in heat the milk not only
contains more of the solids, but has granular and white blood cells like
colostrum and often disagrees with the young animal. The milk of the
young cow with her first calf is usually more watery than that of the
adult, and that of the old one has a greater tendency to become acid.
The longer the period which has elapsed since calving the greater the
tendency to an excess of salts. Certain breeds like the Channel Island
cattle produce an excess of butter fat (4–5 per cent.), whereas others
like Holsteins, Ayrshires and Short Horns have less on an average (3–4
percent.), the casein and, it may be, the water predominating. Hence
Jersey and Guernsey milk will scour calves which do well on that of one
of these other breeds.

Overkept, fermented and soured food tends to produce acidity and other
changes in the milk. Old brewers’ grains, swill, and spoiled gluten
meal, or ensilage, especially such as has been put up too green, are
especially injurious to the milk. The milk of cows fed on raw Swedish
turnips or cabbage acquires a bitter taste and odor.

The milk of different genera of animals offer such strong contrasts that
it is always dangerous to attempt to bring up the young of one genus
upon the milk of another. The following table giving the composition of
the milk in woman and each of the domestic mammals serves to illustrate
this and to furnish a basis for adjustment:

 ───────────────┬───────┬───────┬───────┬───────┬──────┬───────┬───────┬──────┬───────
                │Woman. │ Cow.  │ Goat. │ Ewe.  │Camel.│ Mare. │ Ass.  │ Sow. │Bitch.
 ───────────────┼───────┼───────┼───────┼───────┼──────┼───────┼───────┼──────┼───────
 Density        │1032.67│1033.38│1033.53│1040.98│      │1033.74│1034.57│      │1041.62
 Water          │ 889.08│ 864.06│ 844.90│ 832.32│      │ 904.30│ 890.12│854.90│ 772.08
 Solids         │ 110.92│ 135.94│ 155.10│ 167.68│134.00│  95.70│ 109.88│145.10│ 227.92
 Butter         │  26.66│  36.12│  56.87│  51.31│ 36.00│  24.36│  18.53│ 19.50│  87.95
 Casein and     │       │       │       │       │      │       │       │      │
   extractive   │       │       │       │       │      │       │       │      │
   matters      │  39.24│  55.15│  55.14│  69.78│ 40.00│  33.35│  35.65│ 84.50│ 116.88
 Sugar          │  43.64│  38.03│  36.91│  39.43│ 58.00│  32.76│  50.46│ 30.30│  15.29
 Salts(by       │       │       │       │       │      │       │       │      │
   incineration)│   1.38│   6.64│   6.18│   7.16│      │   5.23│   5.24│ 10.90│   7.80
 ───────────────┴───────┴───────┴───────┴───────┴──────┴───────┴───────┴──────┴───────
                                                              _Becquerel and Vernois_.

Not only does the milk vary so widely with the genera, but that of the
ruminating animal with its great excess of casein coagulates in the
stomach into large dense clots which are not easily penetrated and
digested by the peptic juices while that of woman or soliped forms loose
clots, easily permeable by the gastric fluids and therefore much more
readily digestible. Indeed the milk of these monogastric animals often
form loose floating flocculi only, instead of solid clots. As cows are
usually selected for foster-mothers to the orphaned animals of other
genera this becomes a source of danger to the young and must be obviated
by modifying the milk more in keeping with that of man or soliped.

As predisposing causes, must be named a weak constitution and damp,
dark, filthy, or otherwise unwholesome buildings. Buildings with no
drainage nor ventilation beneath the floors, standing on filth-saturated
soil, and those with double walls holding dead rats and chickens are
especially to be dreaded. In breeds of inconstant color the lighter
colored calves (light yellow, light brown) are more subject to such
attacks than the darker shades (dark browns, reds, blacks). The weak
constitution may be a result of close breeding, without due
consideration of the strength and vigor of the parents. Then young
animals kept indoors in impure air, damp and darkness are more
susceptible than those that are kept in pasture and are invigorated by
exercise, pure air and sunshine.

Aside from the general run of causes, predisposing and exciting, we must
recognize the contagious element. Jensen has sought to identify the
microbe as a small ovoid bacillus united in pairs, or in long chains.
This was present not only in the ingesta, but in the lesions of the
mucosa, and in the lymph glands. Its cultures ingested in milk, or
injected into the rectum sometimes produced the affection.
Microscopically it resembled the bacillus fœtidus lactis, but the latter
failed to produce the disease. He looks upon it as a sport of the
bacillus coli communis.

Perroncito found micrococci, usually arranged in pairs and comparable to
the cultures of those obtained from the blood in the pneumonia of
calves. The injection of the cultures into the thorax of a Guinea-pig
caused pleuro-pneumonia with or without dysentery. The rabbit proved
immune. At the necropsy the Guinea-pig like the calf showed the
diplococci in the blood. Nikolski who studied the affection in lambs
seeks to incriminate both micrococci and bacilli.

It is premature to specify any particular microbe as the sole cause of
the affection. It seems not improbable that bacterial ferments of one or
more specific kinds, which in a healthy animal have no injurious effect,
may by special combination, or by growth in a mucosa in a given morbid
condition, acquire properties which render them not only violently
irritating, but may retain such properties so as to render them actively
contagious. In this condition they may overcome the resistance of the
most healthy stomach and bowels and attack all young animals into which
they may secure an entrance. Certain it is that the infection may
persist in the same stable for years, will enter a new herd with a newly
purchased cow or calf bought out of a previously infected lot, and will
follow the watershed and affect in succession the different herds
drinking from a stream as it flows downward.

The similarity of the germ found by Jensen to the bacillus coli
communis, suggests that in this as in a number of other contagious
affections a pathogenic sport from this common saprophyte is at least
one of the microbian factors in this disease.

_Symptoms._ These may set in just after birth but usually the disease
occurs within the two first weeks of life. When delayed for a few days
after birth it may be preceded by some constipation, the fæces appearing
hard, moulded, and covered with mucus. This is especially the case when
the meconium has been retained and has proved a cause of irritation. The
young animal is careless of the teat or refuses it (or the pail if
brought up by hand), yawns and seems weary. The abdominal muscles are
tense and the belly may be swollen if fermentation has already set in
but this is rarely excessive. Straining to defecate usually causes
eructations of an acid odor, and sometimes vomiting of solid
soursmelling clots. Abdominal pain may be manifested by uneasy movements
of the tail and hind limbs, by looking toward the flank and even by
plaintive cries. This is followed within six hours by liquid dejections,
at first merely soft, slimy and sour but soon complicated by a peculiar
odor of rotten cheese which becomes increasingly offensive as the malady
advances. The tail and hips become soaked with the discharges and as the
putrid fermentation goes on after their discharge of the fæcal matters,
the air becomes more and more repulsive. The same odor pervades the
mouth and the breath and the tongue is coated with a whitish, grayish or
yellowish fur.

The fæces become more watery and slimy, with much casein in course of
putrefaction, and the patient is rapidly run down by the profuse
discharge and the general poisoning by absorbed putrid products. In the
worst cases this may prove fatal in one or two days.

When the illness is more prolonged the alvine passages which at first
number five or six per day, increase to fifteen or twenty and are passed
with more effort, usually leaving the anus in a liquid stream. The color
of the stools changes from a yellow to a grayish yellow or dirty white,
hence the common name of _white scour_, and the fœtor is intensified.

Appetite may be in part preserved for a time but is gradually lost, and
the subject becomes dull, listless and weak, indisposed to rise and
walking unsteadily when raised. A general appearance of unthriftiness,
staring coat, scurfy, unhealthy skin, pallor of the mucous membranes,
arching of the back, tucking up and tenderness of the abdomen,
excoriation of the margins of the anus, and congestion of the rectum as
seen everted during defecation, mark the advance of the disease.
Emaciation becomes very marked, and weakness and prostration extreme.

Fever usually sets in as the disease advances, as marked by
hyperthermia, hot dry muzzle, hot ears, accelerated pulse and breathing.

When the intestinal fermentation is extreme there may be distinct
bloating, more acute colicy pains, rumbling of the bowels and a frothy
and even bloody condition of the dejections. The prostration may become
extreme and the temperature reduced to the normal or below.

Death may result from inanition and exhaustion, or from nervous
prostration and poisoning.

The affection may be complicated by purulent arthritis, peritonitis,
pneumonia, hepatitis, keratitis or laminitis. It may prove fatal in from
three to ten days.

_Mortality._ This is always high. For foals it has been set down at 80
per cent. of the numbers attacked, for calves at 54 to 90 per cent., and
for lambs at 66 per cent. In 500 lambs Beresow found 300 attacked and
200 died. Kuleschow sets the losses at 30 to 40 per cent. of the lambs,
and Cadeac advises that even the survivors should be fitted for the
butcher as they are unfit for reproduction.

_Lesions._ In foals these are mainly confined to the intestines which
show a more or less extended area of redness and congestion with
catarrhal or pseudomembranous exudate on the mucosa, and the submucous
connective tissue is infiltrated softened and marked by intense
punctiform redness. The epithelium is swollen, opaque and easily
detached, and Peyers patches infiltrated and prominent. The blood in the
intestinal vessels is incoagulable. Exudation into the peritoneum and
softening of the liver are not infrequent.

In calves the lesions are very similar, but the 4th stomach is usually
implicated, the congestion and epithelial desquamation being most marked
in the pyloric region. The contents of the intestines are mucopurulent,
grayish, yellowish or red, and intensely fœtid. The follicles of the
small intestine are red and projecting with an areola of congestion.
Softening and even necrotic centers are found in the liver and kidneys
and the mesenteric glands are swollen, red and softened.

In lambs the lesions are nearly the same in the 4th stomach, intestine,
lymph glands, liver and kidneys. There is usually marked emaciation and
the spleen and nerve centres are anæmic.

_Prevention._ The first consideration is to avoid the various causes
which have been enumerated. Give the young the warm milk of its dam or
of a nurse of the same species and at the same time after parturition.
If it is necessary to give older milk to the new born don’t fail to
clear out the bowels by a tablespoonful or two of castor oil (foal,
calf,) or two teaspoonfuls (lamb), or to add manna or linseed decoction
to the milk. Protect both nurse and nursling against cold storms,
overheating, overwork, excitement, and sudden changes of diet, (dry to
green, etc.). If the nurse has been overheated or overexcited draw off
the first milk by hand and let the nursling have only that which is
secreted later. Avoid the milk of diseased and especially fevered
animals. If the milk of one nurse disagrees, correct any obvious cause
in the food or general management, and if none can be found get another
nurse. If fungi appear in the milk (inducing ropiness or not) withold
the food or water from which they have been probably derived and give
bisulphite of soda (cow or mare 2 to 4 drs., ewe ½ dr. daily). When an
animal of one genus has to be brought up on the milk of another, let the
milk be so modified by the addition of water, sugar, cream, etc., as
will approximate it somewhat to the normal food. The milk of the cow may
be given unchanged to lambs or kids, while for the foal it should be
diluted by adding ⅖ of water, and sugar enough to render it perceptibly
sweet. Even more sugar is wanted for the young ass. In place of simple
water, barley water may be used, as this not only loosens the coagulum
formed in the stomach, but renders it especially open and permeable to
the digestive fluids. Another method of special value for puppies is to
let the cow’s milk stand for several hours and then take only the upper
half (containing most of the cream) for feeding. This must be watched
lest it should unduly relax the bowels. In all cases the milk
artificially prepared should be given milk warm. To retard the acid
fermentation which is liable to occur early and injuriously in adapted
milk, the addition of an ounce of lime water to each quart of milk is of
great advantage. Pigs and puppies can usually adapt themselves readily
to the milk of the cow. In all cases in which a young animal is raised
by hand and especially if on the milk of another species, it is
desirable to provide against sudden overloading of the stomach. The
artificial rubber teat fixed in the feeding pail serves a good purpose
in this respect. Pasteurizing is admissible but boiling of the milk is
objectionable, as rendering the milk constipating and thereby favoring
irritation. In condensed milk this tendency is largely reduced by reason
of the excess of sugar and consequent looseness of the clot, only care
should be taken to dilute it sufficiently with boiled water.

Among the most important measures of precaution, is the separation of
the sick from the healthy, and to disinfect thoroughly the buildings in
which the infected have been. Straw, and when possible dung should be
burned; if not, they should be buried together with the urine. The
stalls should be thoroughly cleansed and then saturated with mercuric
chloride (1 : 1000), or sulphuric acid (3 : 100), or a saturated
solution of sulphate of copper. Here as elsewhere chloride of lime (4
oz. to the gallon) with as much quick lime as will make a good white
wash, does admirably, as it is at once seen if any part has been missed.

Esser remarked that the calves of cows that had been removed to another
stable some time before parturition, usually remained healthy, provided
they were kept from the other and sick calves.

Lastly, it is important to use for breeding purposes such animals only
as have a strong, vigorous constitution, and to furnish a healthful,
abundant aliment and to allow a sufficient amount of exercise during
gestation. Vigor and stamina are the great desiderata, but these are
usually found with the darker colors.

_Treatment._ The old treatment of eliminating offensive matter by a
laxative is still good, and thus castor oil (2 ozs. for a foal or calf,
2 drs. for lamb), or rhubarb (1 dr. foal or calf, 1 scr. for lamb), or
manna (½ oz, foal or calf, 1 dr., lamb), may be given with laudanum (1
dr., foal or calf, 10 drops, lamb), and salicylate of soda (16 grs.,
foal or calf, 5 grs.,lamb). The milk should be given boiled. An old and
excellent remedy to follow the laxative is solution of rennet made by
adding ⅛ of a calf’s abomasum to a quart of 20 per cent, alcohol (or
sherry). A tablespoonful may be given with each meal. The value of this
as an antiferment is liable to be overlooked, yet both the hydrochloric
acid and pepsin are strongly antiseptic, and neither of these is
produced to any extent in the diseased stomach. In addition to this
ipecacuan has been used and by its stimulant action on both stomach and
liver it furnishes the two most important natural disinfectants of the
alimentary canal (foal or calf 1 dr., lamb 10 drops ipecacuan wine,
thrice a day).

In addition to these or separately, antiseptics, carminatives and
astringents may be employed. An excellent preparation is prepared chalk
1 oz., white bismuth 1 oz., tincture of cinnamon 8 ozs., gum arabic ½
oz. A tablespoonful thrice a day will often check the disorder.

Cadeac advises, subnitrate of bismuth 5 grains, salicylic acid 5 grains,
naphthol 20 grains, syrup 150 grains, distilled water 100 grains. One or
two tablespoonfuls in the mouth after each drink (foal or calf).

Filliatre obtained excellent results in calves, with a solution of tar
150 grams in 6 litres boiling water, given in the dose of ⅓ litre every
half hour. It may also be used as an enema. The diarrhœa is promptly
checked, and the tar water may then be restricted to ¼ litre mixed with
the milk of the next two days. One-tenth of the dose may be given to
lambs.

Among other antiseptics in use may be named salicylic acid and tannin,
salol, boric acid, betol, diaphthol, bruzonaphthol, salicylate of
bismuth, creolin, naphthalin, and lactic acid.

When icteric membranes, white discharges and extreme fœtor indicate
hepatic disorder, calomel 1 part and chalk 12 parts may be resorted to
three or four times a day (foal or calf 6 grs., lamb 1 gr.).

Among the carminatives may be named anise, fennel, dill, cinnamon, and
chamomile. Beside their stimulant action these are all more or less
antiseptic.

In addition to the boiling of the milk, and in certain cases as a
temporary substitute, may be used sterilized mucilaginous agents, gum
arabic, flax seed, and slippery elm.


       ACUTE GASTRIC INDIGESTION IN SOLIPEDS. TYMPANITIC STOMACH.

  Definition. Causes: overloading, lessened secretion, mastication or
  insalivation, frosted food, fermenting food, appetizing food, cooked
  food, debility, disease, starvation, overwork, fatigue, violent
  exertion after a meal, anæmia, parasitism, injury to vagi or their
  centres, iced water, wading or swimming in iced water, food with
  excess of proteids, drink after grain, alkaline waters. Symptoms: in
  slight cases, in severe, violent colic, weariness, pinched
  countenance, acid mouth, bloating of abdomen, anorexia, dysphagia, no
  rumbling of bowels, no fæces, tries to eructate, dullness, stupor,
  coma, vomiting. Rupture of stomach. Recovery. Lesions: overdistended
  stomach, ruptured peritoneal hemorrhage, ruptured diaphragm, small
  bloodless liver and spleen. Diagnosis. Treatment: Aromatics,
  stimulants, antiferments, laxatives, stimulants of peristalsis,
  exercise, friction, electricity, chloral hydrate, puncture of stomach
  and colon, probang, stomach pump, dieting, tonics.

_Definition._ Suspension of the normal functions—motor and secretory—of
the stomach and the supervention of fermentation in its contents.

_Causes._ The small size of the stomach in the soliped (26 quarts) and
the rapidity with which the alimentary matters normally traverse it,
render this organ much less subject to disorder than the complex
stomachs of ruminants. In his native state the horse eats at frequent
intervals and digestion is constantly going on, so that the viscus is
never distended to paresis, nor the secretions, nor vermicular movements
retarded by excess of ingesta. But the limited capacity of the viscus
becomes in its turn a cause of indigestion whenever the animal is
tempted by hunger to hurriedly swallow too great a quantity of food;
when the decreased secretions fail to act with sufficient promptness on
the contents and leave them to undergo fermentation; when from imperfect
mastication and insalivation the food is left in large masses
comparatively impermeable to the gastric juice, and accumulates in
firmly packed masses; when frosted food (roots, potatoes, apples, turnip
tops, etc.), taken in quantity temporarily chills and paralyzes the
stomach, and starts a speedy and gaseous fermentation; when the food
swallowed is already in process of fermentation (musty or covered by
cryptogams) and full of toxic fermentation products which tend to
paralyze the stomach. Old animals are especially liable because not only
are the teeth and salivary glands ineffective, but the functions of the
stomach are habitually below par.

The paralysis of the stomach by overloading is seen especially in
animals that have been fasting for too great a length of time, and are
then furnished with a food, rich, appetizing and abundant. Few horses
are proof against the temptation to overeating when they get to the
cornbin, the ripening grain or maize, or the field of rich red clover.
Some are natural gluttons and on gaining access to grain or green food,
will suddenly overload the stomach beyond its power of active
contraction on its contents, and without sufficient mastication or
insalivation. The food is literally bolted whole, with no admixture of
saliva, and no facility for admixture of gastric juice, even if the
overloading had left the stomach capable of secreting the latter. Cooked
food is especially dangerous by reason of its bulk, the facility with
which it is swallowed, and the rapid and excessive dilatation of the
stomach caused by it, rather than from lack of trituration and saliva.
If fed judiciously, cooked food is more fattening for both horse and ox,
any lack of ptyaline being counterbalanced by the presence of amylopsin
in the intestines.

Such paresis and indigestion, however, are more common as the result of
a general debility or a special gastric atony caused by disease,
starvation, overwork or fatigue. In all acute febrile and inflammatory
diseases the gastric functions are weak or suspended, and if the animal
is tempted to eat, the ingesta is unaffected by the digestive fluids and
forms a suitable fluid for injurious fermentations. In convalescence
especially, when the starved system once more craves support, tempting
food is liable to be taken to excess, unless the attendant is especially
judicious and careful in grading the feed as the stomach can dispose of
it. The horse that has been starved must be fed little and often, of
easily digested material until the gastric functions are restored. Long
continued severe work, exhausts the motor and secretory power of the
stomach, as it debilitates the system at large, and the animal may be at
first unable to digest a feed of grain even if he will take it. In such
a case as in that of the very hungry glutton a drink of gruel or a
handful of hay which he must masticate will often obviate the danger.

Violent exertion immediately after a meal arrests digestion, and tends
to a fatal indigestion. An animal fed grain and immediately put to
severe work, or subjected to confinement for a painful operation, may
die in two hours from tympanitic indigestion.

This weakness of the digestion may come from profuse bleeding, from the
anæmia caused by parasites (sclerostomata), or from injuries to the
pneumogastric nerves or their centres. It can be produced experimentally
by cutting both vagi; the gastric contents then remain packed and solid,
without peptic juices and without digestion.

Iced water, like frozen food, may temporarily arrest the gastric
functions and entail fermentation. It acts most dangerously on the
overheated and exhausted horse, and though the indigestion may not prove
fatal, it may induce a sympathetic skin eruption or laminitis. The mere
exposure to external cold is less to be dreaded as there is a
compensating stimulus which drives the blood to internal organs, the
stomach included. Standing in cold water or wading or swimming a cold
river, is commonly less injurious than a full drink of iced water, when
heated and fatigued.

Certain kinds of food are far more dangerous than others, and especially
such as should be digested in the stomach. Thus the different
grains—barley, rye, buckwheat, wheat, oats, Indian corn, and even bran,
have been especially objected to. The amount of proteids in oats, for
example, is 11.9 per cent., while those of hay are but 7 per cent. The
same bulk of oats, therefore, demands nearly double the work of the
stomach to reduce its nitrogenous constituents to peptones than does
hay. But when fully insalivated the difference is even greater, for oats
take but the equivalent of their own weight of saliva, whereas hay takes
four times its own weight. There is 1 part of proteids in 16.7 parts of
insalivated oats, and but 1 in 71.4 of insalivated hay. If the oats are
bolted without mastication, which can never be the case with hay, the
discrepancy becomes greater still. Grain is best fed often, in moderate
amount, and without further loading of the stomach immediately with
either solids or fluids. Above all never feed grain to a thirsty horse
and then lead him direct to the watering trough. Even should he fail to
have the stomach paralyzed by the cold water, and indigestion developed,
yet much of the proteids will be washed out into the small intestine to
threaten indigestion there.

Selenitic waters may induce indigestion by neutralizing the hydrochloric
acid of the stomach and interrupting digestion.

Finally all forms of gastritis—catarrhal, toxic, and phlegmonous—induce
atony, fermentation and indigestion.

_Symptoms._ There may be simply tardy digestion or grave disorder with
impaction or tympany.

In the former case there is impairment or perversion of appetite,
refusal of food, irregular feeding, licking earth or lime, or eating
filth, even fæces, with some dullness, apathy, or signs of pain such as
pawing with the fore feet, or looking round at the flanks. There is
rumbling of the bowels, followed in favorable cases by the passage of
flatus, of softened fæces containing imperfectly digested food, and
distinct diarrhœa which proves curative.

The more violent attacks set in suddenly, usually within one or two
hours after feeding. There are usually colicy pains, pawing, looking
back at the flank, kicking of the abdomen with the hind feet, lying
down, rolling, rising again quickly, yawning, anxious pinching of the
countenance, rigid loins insensible to pinching, and heat and dryness
with an acid odor in the mouth. There is soon observed some swelling and
tension of the belly with tympanitic resonance on percussion in the left
hypochondrium. There is no elevation of temperature as in gastritis, and
no complete intermissions of pain as in spasmodic colic, but pain is
continuous, though worse at one time than another. There is an utter
indisposition to eat or drink and if liquids are given by force there is
manifest aggravation of the sufferings. As a rule there is no rumbling
of the bowels, and though the animal may strain violently, little or
nothing is passed, except at the first a few moulded balls of dung. The
bowels like the stomach are paralyzed. In some cases there are attempts
at regurgitation, the fore feet are placed apart, the neck arched, the
lower cervical muscles are contracted and the nose drawn in toward the
breast. In some instances relief is obtained by belching gas or by
actual vomiting of solid matters. Vomiting in the horse is always ground
for suspicion, since it usually occurs when the muscular coat of the
stomach is ruptured. An important hindrance to vomiting lies in the
loose folds of the mucosa covering the cardia, in the flaccid condition,
and as these folds may be entirely effaced in hernia of the mucosa
through the muscular coat as well as in the overdistended condition,
vomiting may be either a fatal or a favorable indication. If vomiting
takes place, without attendant prostration and sinking, and if on the
contrary there is manifest improvement after it, it may be looked on as
a beneficent outcome.

If no such relief is obtained the patient becomes increasingly dull and
stupid; the breathing is accelerated, short, moaning or wheezing; the
nostrils dilated; the nasal mucosa dark red; the superficial veins,
especially those of the face, are distended and prominent.

The nervous symptoms may vary. Usually the dullness increases to stupor,
the animal rests his head on the manger or against the wall, or if at
liberty he may move forward or around blindly until some obstacle is met
and he stumbles over it or pushes against it. In some instances there is
champing of the jaws, or irregular motions of the limbs, but more
commonly the dullness goes on to stupor and coma, the animal falls
helpless and dies in a state of profound insensibility.

If the _stomach should become ruptured_ there is often vomiting, the
ingesta escaping by the nose, without any relief of the general
symptoms, but with an increasingly haggard expression of countenance,
sunken eye, and accelerated, weak, and finally imperceptible pulse. Cold
sweats, which may have been already present, become more marked and the
prostration becomes more extreme and the abdominal tenderness more
marked. There are muscular tremblings of the shoulders and thighs,
dilatation of the pupils, rapid breathing and stupor which presages
death.

Recovery may be hoped for if rumbling in the bowels commences anew, if
defecations continue and become soft and liquid, if urine is passed
abundantly and if the general symptoms are improved. Complete relief may
be had in five or six hours, and even in protracted cases in two days.

_Lesions._ The body is swollen, tense and resonant; the rectum usually
projects somewhat and is dark red; the intestines, small and large, are
tympanitic; the stomach is double or triple its usual size, tense and
resistant, and with its contents may weigh as much as 40 pounds. When
cut open its contents are seen to be disposed in the order in which they
were eaten, in stratified layers, the motions of the stomach have not
operated to mix them. There is no sign of digestion, unless it be in a
thin surface layer or film which may be white, pulpy and chymified. The
cuticular mucosa is usually unchanged further than its attenuation by
stretching, the alveolated mucosa also attenuated is congested, opaque
or slightly inflamed. The great curvature may be the seat of a rupture
the edges of which are slightly swollen, congested and covered with
small blood clots. The escaping ingesta usually remains enclosed in the
omentum, which thus looks like a larger stomach with extremely thin
gauze-like walls. If this is ruptured then the food floats in masses
among the convolutions of the intestines. The peritoneum is red,
hemorrhagic and covered with more or less exudation.

Another occasional lesion is rupture of the diaphragm. The liver and
spleen are usually small and comparatively bloodless, owing to the
compression.

_Diagnosis._ This is largely based on the speedy supervention of the
attack on a feed, the animal having been apparently well before, on the
onset by slight colics, rapidly passing into great and continuous
suffering and stupor, with tympanitic tension of the abdomen, and
suppression of the intestinal movements, in the absence of any distinct
or marked hyperthermia. The rapid progress to death or recovery is
equally characteristic.

_Treatment._ In mild cases the prompt use of aromatics will sometimes
succeed; tincture of pimento, anise or coriander 2 to 3 ounces, oil of
peppermint, 20 to 30 drops. Stimulants, aqua ammonia, 1 to 2 drachms,
largely diluted, ether 1 ounce, brandy or whisky 1 pint, will sometimes
succeed. A good combination is dilute hydrochloric acid, 1 drachm, oil
of turpentine 1 ounce, olive oil ½ pint.

Still more effective in the rousing of the torpid vermicular movements
are eserine sulphate 1.5 grain or pilocarpin 2 grains, or barium
chloride 7 grains subcutem.

These largely replace the old plan of giving a dose of aloes in bolus,
yet in case of need aloes may still be given in ounce doses in cold
water injections. The cold serves to rouse the vermicular movements of
the bowels and sympathetically of the stomach.

Walking exercise, friction over the abdomen, and even electric currents
through the epigastrium and left hypochondrium may be helpful.

In very urgent cases, 1 ounce to 2 ounces chloral hydrate is often
effective. It acts as a powerful antiferment, checking further
extrication of gas, and counteracts spasms of the bowels, so that gas
passes more freely per anum, vermicular movements are resumed and
recovery may be hoped for.

Puncture of the stomach through the external abdominal wall can only be
effected by transfixing the transverse colon above which it lies and few
have the hardihood to undertake this. It may, however, be punctured with
comparative safety through the fourteenth to the seventeenth intercostal
space in its upper half (Scammel). The overdistended stomach pressing
forward on the left half of the diaphragm, applies that against the
inner surface of the ribs, the lung being driven forward out of the way,
and the liver and colon are also displaced, so that the trochar
transfixes the skin, intercostal muscles, costal and phrenic pleura,
diaphragm, peritoneum and stomach. The marked drumlike resonance on
percussion indicates the best point for the puncture, and the trochar
should be directed inward and slightly backward and pushed until solid
resistance at its point ceases. As the intestines are usually tympanitic
as well it may be requisite to puncture also the cæcum and colon, to
restore the peristalsis of the alimentary tract generally. Antiseptics
such as sulphurous acid, the sulphites, or hyposulphites, calcium
chloride, bleaching powder, potassium permanganate or chloral hydrate,
may be introduced through the cannula or by the mouth.

As far as the stomach is concerned, an effective relief can be had
through the probang or stomach pump. A small one-half inch hollow
probang may be safely passed through the nose and gullet into the
stomach, and any gas or liquid allowed to escape. With proper
attachments this may be fixed to a stomach pump and the viscus exhausted
of all available liquid, after which an equal amount is pumped in and
again withdrawn, until the contents are reduced to a normal amount. The
water pumped in may be rendered antiseptic by sodium chloride, sodium
bisulphite, or other antiferment, so that further extrication of gas
will be prevented. If it is necessary to use the ordinary probang or
stomach tube introduced through the mouth, great care must be taken in
introducing it to see that the soft palate does not deflect it downward
into the larynx. Its presence in the gullet above and beyond the larynx
can be felt by manipulation from without, and until this is ascertained
it should on no account be pushed onward.

The importance of a measure of mechanical relief such as this, is the
greater that the stomach of the soliped is non-absorbing, and relief
from undue pressure of contents can only be had by their passage upward
or downward. Then again, the horse cannot vomit like the carnivora and
omnivora, nor regurgitate like ruminants, and if left to himself with
engorged stomach, his case is hopeless indeed.

The contingent weakness in cases of recovery may demand careful feeding
and a course of bitter tonics.




                   GASTRIC INDIGESTION IN CARNIVORA.

  Causes: too frequent feeding, indigestible food, epidermic products,
  bones, tendons, rubber, cords, marbles, pebbles, catarrh,
  inflammation, intestinal lesions, fever. Symptoms: dullness,
  restlessness, eating grass, vomiting, seeks seclusion, colics,
  giddiness, tense, tender abdomen. Treatment: emetic, diluents,
  dieting, tonics.


_Causes._ Unintermittent work of the organ wears out its tone and
indigestion follows. The more indigestible the food, and the admixture
with the food of indigestible materials the greater the tendency to this
fatigue and atony. Thus epidermic materials, hair, horn, wool, bristles,
feathers are often injurious; also bones, tendons, and above all pieces
of rubber, caouchouc, cords, marbles, pebbles and other small objects.
Fortunately such agents are usually rejected by vomiting, but if
retained, the movements of the viscus become tardy and its secretions
defective, and fermentation, indigestion and irritation ensue. The evil
effects however mostly come of catarrhal and other inflammations of the
stomach, and serious lesions of the intestines, (inflammation,
obstruction, volvulus, intussusception, tumors, strangulated hernia,) or
acute fever. In any such case the stomach ceases to act, and its
contents become a center of active fermentation with more or less
irritation.

_Symptoms._ In transient cases the dog will appear dull and restless,
moving about, and, if opportunity affords, perhaps eating grass so as to
hasten emesis and relief. With this relief the subject may remasticate
and swallow the very materials he has vomited.

If relief is not secured by vomiting, the animal remains dull, anxious,
retiring, seeking perhaps seclusion and darkness, is taciturn, moves
continually, lying down first on one side and then on the other, or
successively in different places, looks round at the belly, starts up
suddenly with a piercing cry, and may appear giddy and uncertain in his
gait. The abdomen is usually tense or even full and tender to touch.

_Treatment._ The first resort is the evacuation of the stomach by
vomiting. Give tepid water and tickle the fauces with a feather or the
finger. Or ½ to 1 gr. tartar emetic in a tablespoonful tepid water, or a
teaspoonful of ipecacuan wine. Or ½ dr. of a ¹⁄₁₀₀ solution of
apomorphia hypodermically. Beyond this, little is wanted except careful
feeding as regards quantity and quality. Nux vomica ½ gr. twice a day
will serve to restore tone. Further treatment will come naturally under
catarrhal gastritis.


                  ACUTE GASTRIC INDIGESTION IN SWINE.

  Causes: fermented or putrid swill, spoilt vegetables, frozen aliments,
  caustic alkalies (powdered soaps) from kitchen, indigestible
  materials, poisons. Symptoms: dullness, grunting, restlessness,
  seeking seclusion, colics, vomiting, rumbling, tense, tucked up
  abdomen, diarrhœa. Treatment: emetic, bland acids, laxative, dieting,
  bitters, iron.

_Causes._ Swine have such a varied dietary, are so constantly fed swill
containing all manner of ingredients and often kept in barrels, etc.,
that are never emptied and cleansed, and therefore so often the seat of
septic fermentation, that both gastritis and enteritis are often
produced. Spoilt turnips, potatoes, apples and other succulent
vegetables, or those that have been exposed to frost, or which are
devoured while frozen are additional causes of irritation. The various
caustic alkaline powders used in washing the table dishes and the
product added to the swill is another cause of such outbreaks which,
attacking a whole herd at once, is attributed to hog cholera. Then
indigestible materials (hoofs, hair, bristles, tree bark, etc.) when
they fail to be rejected by vomiting cause gastritis and indigestion.
Finally a long list of medicinal and toxic substances act in this way.

_Symptoms_ are like those seen in dogs, dullness, arching of the back,
drawing the feet together, erection of the bristles, hiding under the
litter, grunting, restlessness, frequent movement from place to place,
lifting of the hind feet, grubbing in the litter with the snout, tension
of the abdomen, and often abdominal rumbling followed by diarrhœa and
recovery. More commonly, however, relief comes from early rejection of
the irritant matters by vomiting.

_Treatment._ Induce emesis as in the dog. Give vinegar in case of
alkaline poisoning. Follow this by a laxative if the irritants have
gained the intestines, and finally a course of iron or bitters. Careful
dieting is absolutely essential.


                ACUTE CATARRHAL GASTRITIS IN THE HORSE.

  Causes: wet fermented food, cryptogams, bacteria, sprouted green
  potatoes, sand, irritants, hot food, frosted food, ill health,
  starvation, anæmia, siliceous plants, diseased teeth or salivary
  apparatus, parasites, calculi, specific inflammations. Symptoms:
  depraved appetite, licking soils, walls, filth, etc., clammy mouth,
  red bordered tongue, eructations, colic, rumbling, tympany, icterus,
  costive, coated fæces, tender hypochondrium, anorexia, emaciation.
  Lesions: stomach full or nearly empty, pyloric sac congested, mucosa
  thickened, petechiated, with excess of mucus and desquamated
  epithelium, cells swollen opaque, congested duodenum, pale yellow
  liver, with excess of pigment in cells, also in urine, ruptured
  stomach, hemorrhagic infiltrations. Treatment: careful dieting,
  laxative, stomachics, pepsin, antiferments, bitters, ipecacuan.

_Causes._ This is a much less common affection in horses than dogs and
is usually charged on some fault in diet. Fodders that have been badly
harvested or wet from any other cause and are musty, dusty, rusty, or
covered with any irritant or poisonous cryptogams or bacterial ferment,
sprouted oats, or potatoes that have become green by exposure to the
sun, sand and gravel in the grain, irritant plants like ranunculus,
euphorbium, veratrum, etc.; cooked food given too hot, or vegetable food
given frosted; putrid water, and indeed all the causes of indigestion
tend to produce gastric catarrh. Weakness of the stomach and gastric
functions from any cause is a concurrent factor. Thus extensive
inflammations and violent fevers, prolonged abstinence, starvation,
anæmic and parasitic affections, the action of frozen food on the
viscus, are to be feared. A horse which has been for a week or more
without food is extremely subject to such attacks unless fed with the
greatest caution at first. Irritant plants like carex, equisetum, etc.,
which act mechanically by reason of the contained silica, food
imperfectly masticated on account of disease of the jaws, teeth or
salivary glands, parasites like spiroptera and bots and phosphatic and
oat-hair calculi, act mechanically. Finally certain affections like
petechial fever, influenza, pneumonia, pustulous stomatitis and horse
pox may develop local foci of inflammation in the stomach. When once
started, microbian infection tends to maintain and aggravate it.

_Symptoms._ These are very indefinite, depending very much on the
complications. Some loss or perversion of appetite, a licking of the
soil or walls, eating litter, filth and even manure, a clammy mouth, a
redness along the margin of the tongue, eructations or attempts to
eructate, or actual vomiting, colicy pains which are usually dull until
the bowels are implicated, more or less rumbling in the bowels,
sometimes icterus, in other cases tympany, and nearly always tardy
passage of hard and scanty mucus-covered fæces. The colics may be
intermittent, appearing only just after food is taken, or they may be
continuous, the animal pawing incessantly hour after hour. A slight
hyperthermia and a distinct tenderness of the epigastrium and left
hypochondrium to pressure are valuable symptoms. Percussion causes even
keener suffering.

If the gastric contents are abundant and fermentation active, death may
ensue from gastric tympany. In other cases, the persistence of colics at
the time of feeding, of impaired appetite, constipation and loss of
condition are the main symptoms. In the last named cases the patient may
die of marasmus.

_Lesions._ In cases terminating in fermentation and fatal tympany the
stomach is full; in other types it is empty of all but water, mucus, and
perhaps some irritant contents, or decomposed food. The alveolar mucosa
of the right sac and above all of the pylorus is red, congested,
petechiated, macculated, thickened to double its normal thickness or
more, thrown into rugæ, and covered with tenacious mucus. This mucus is
highly charged with detached epithelial cells, and at different points
the mucosa is abraded by their desquamation. The epithelium generally
shows swollen, opaque cells. The red congested spots show active
engorgement of the capillaries, and this is especially marked around the
glandular follicles, with more or less formation of embryonic cells. The
duodenum is often implicated with similar lesions of the mucosa and its
epithelial layers, which may block the orifices of the pancreatic and
especially of the biliary duct. In this case there is a yellowish
discoloration of the liver, excess of pigment in the hepatic cells, and
hemorrhagic spots in the liver and even in the kidneys. The urine may be
yellow or reddish brown from the presence of bile or blood pigment. In
ruptured stomach, spiroptera, bots, and other irritants, we find their
characteristic lesions, and in petechial fever there is excessive and
partly hemorrhagic infiltration of the mucosa and submucosa. In
protracted cases ulcers may be present on both stomach and intestine.
When it is a localization of some specific fever the characteristic
lesions of that affection will be found.

_Treatment._ If appetite continues, diet should be restricted to a very
moderate allowance of green food, pulped roots, bran mash, boiled
flaxseed, boiled middlings, with pure water or whey. If there are
irritants in the stomach they may be got rid of by a laxative (aloes 4
drachms, or sulphate of soda ½ pound). Sodium bicarbonate (½ drachm 2 or
3 times daily) is desirable to stimulate peptic secretion and check acid
fermentations. Pepsin (2 drachms) should be given at equal intervals.
Fermentations should be checked by the use of salol (1 to 2 drachms),
naphthalin (1 to 2 drachms), benzo-naphthol (1 to 3 drachms), or calcium
salicylate (2 drachms).

In this connection bitters are of value to improve the tone of the
gastric mucosa, nux vomica, gentian, quinia and quassia in combination
with ipecacuan giving good results.


             PHLEGMONOUS (PURULENT) GASTRITIS IN THE HORSE.

  Definition: deep inflammation tending to abscess. Causes: invasion by
  pus microbes, infectious diseases, parasitism, traumas. Symptoms:
  hyperthermia, colic, tenderness, icterus, coincident disease,
  hæmatemesis. Lesions: submucous or subperitoneal abscess, parasites,
  peritonitis, exudation, thickening, neoplasm of mucosa, catarrhal
  complications. Treatment: careful diet, antiseptics, bitters,
  laxatives.

_Definition._ This is a gastric inflammation affecting the membranous
layers, and tending to submucous or subperitoneal abscess. It is much
less frequent than the catarrhal form.

_Causes._ It may be attributed to invasion of the gastric walls by pus
microbes, and appears as secondary abscess in pyæmia and above all in
strangles. The microbes are introduced more directly through the wounds
inflicted by the larvæ of œstrus, or by the burrowing of these (Argus,
Schlieppe, Schortmann), or of spiroptera (Argus). Wounds by sharp
pointed bodies taken in with the food, furnish other infection—atria,
and in their turn ulcers connected with catarrhal or toxic inflammation
may furnish a means of entrance.

_Symptoms._ These resemble those of catarrhal inflammation, but are
usually attended by greater hyperthermia, and the colicy symptoms are
more marked. There is also greater tenderness in the epigastrium and
left hypochondrium, and icterus is more marked. When it occurs as an
extension of strangles or pyæmia the symptoms of these affections
elsewhere are pathognomonic. When the abscess bursts into the stomach
there may be vomiting of bloody mucus (hæmatemesis) which is not
necessarily followed by a fatal result.

_Lesions._ As these are seen only in fatal cases, the presence of an
abscess is the characteristic feature. This is usually submucous, or
less frequently subperitoneal, and may vary in size from a hazelnut
upward. The tendency appears to be to open into the stomach, though it
may burst into the peritoneum and cause general infection of that
membrane. In case of parasites, the spiroptera or œstrus larva may be
found in the abcess cavity having a narrow opening into the stomach. In
certain cases the abscess on the pyloric sac has been found opening into
the duodenum. Congestion, thickening, puckering into rugæ and laceration
of the adjacent mucosæ may be a marked feature, a circumscribed
catarrhal gastritis complicating the local phlegmon.

_Treatment._ This is less hopeful than in catarrhal gastritis, but
should be conducted along the same lines. The same careful diet, with
daily antiseptics and bitters may prove valuable in limiting the
inevitable suppuration, and, if the pus should escape into the stomach,
in healing the lesion. Sulphites of soda, sulphide of calcium,
chamomile, and quinia, are to be commended and pepsin may be added to
secure at once proteid digestion and antisepsis. Laxatives may be
required to counteract constipation or expel irritants, and these may be
combined with the antiseptics already named or with salol, eucalyptol,
sodium salicylate or other non-poisonous agent of this class.




                      TOXIC GASTRITIS IN SOLIPEDS.

  Causes: caustics or irritants acting on mucosa, accidently, or
  maliciously. Symptoms: colics, pinched face, small rapid pulse,
  hurried breathing, hyperthermia, sometimes salivation, color of buccal
  mucosa, odor, congestion of tongue, thirst, urination, icterus,
  albuminuria, analysis of urine or vomited matter. Lesions: congestion,
  corrosion, necrosis or ulceration of gastric mucosa, discoloration.
  Treatment: antidote, stomach pump, demulcents, coagulants.


_Causes._ Toxic gastritis in solipeds is peculiar in this that it must
be due to one or other of the more caustic or irritant agents, which act
chemically on the tissues, while those agents that require to be
absorbed to establish a physiological irritation are comparatively
harmless. This depends on the fact that few or none of the poisonous
agents are absorbed by the gastric mucosa of the soliped, and if
ingested they must pass on into the duodenum before they can be absorbed
into the tissues and blood-vessels. Hence the horse is injured mainly by
actual caustics like mercuric chloride, zinc chloride, ferric or cupric
sulphate, the caustic alkalies or earths, or alkaline carbonates, and
the mineral acids. These may be taken accidently or administered
maliciously, or as medicines.

_Symptoms._ Morbid symptoms vary according to the agent swallowed. There
are colics, anxious countenance, small accelerated pulse, rapid
breathing, hyperthermia, and salivation, especially marked with mercuric
chloride. The buccal mucosa may give valuable indications, becoming
white with muriatic acid, or zinc, or antimony, or mercuric chloride,
yellow with nitric acid, and white changing to black with sulphuric acid
or silver nitrate. Ferric or cupric sulphate may give their respective
colors to the saliva, and the former will darken the fæces.

The mouth is usually dry, hot, and clammy, and the edges of the tongue
red. Temperature is usually elevated, yet with tartar emetic it may be
distinctly reduced. Thirst is usually marked, and urination frequent.
Icterus and albuminuria attend on phosphorus poisoning. When vomiting
takes place the appearance or analysis of the matters rejected, or
otherwise of the urine, will often indicate the nature of the poison.

_Lesions._ The gastric mucosa is congested and discolored, but the
corrosion and even the ulceration are especially characteristic. Patches
of necrotic mucous membrane may be more or less detached exposing a deep
red submucosa. The coloration otherwise varies;—white or black with
sulphuric acid or silver nitrate; white with muriatic acid, the caustic
alkalies, or zinc chloride; yellow with nitric acid; or green with salts
of copper.

Similar lesions are found on the buccal, œsophagean and intestinal
mucosæ, and even at times on the respiratory.

_Treatment._ In the treatment of this form of gastritis the first
consideration is to expel, or use an antidote to, the poison. In the
soliped, emetics are useless. The stomach pump or tube may, however, be
applied with good effect in nearly all cases, alternately throwing in
water and drawing it off. Demulcents and coagulants are also universally
applicable. Milk, eggs beaten up in milk, blood albumen, flaxseed tea,
well boiled gruels, or slippery elm bark, may be used as may be most
convenient. Next come the other chemical antidotes the use of which
however demands a previous knowledge of the poison present. For the
mineral acids one can make use of calcined magnesia, lime water, chalk,
or carbonate of soda in weak solution. For alkalies the appropriate
antidote is vinegar. For carbolic acid, vinegar, alcohol, or failing
these a weak solution of soda or oil. For tartar emetic, gallic or
tannic acid. For bichromate of potash or chromic acid, calcined
magnesia, magnesia carbonate, or lime carbonate. For phosphorus, old oil
of turpentine and demulcents—no oil. For ammonia, vinegar followed by
almond, olive or sweet oil. In case of œdema glottidis, tracheotomy. For
copper salts yellow prussiate of potash, which precipitates the copper
in an insoluble form, and demulcents. For mercuric chloride, demulcent
drinks can be resorted to, there is no other reliable antidote. In all
cases after the evacuation of the stomach and the use of the antidote,
mucilaginous agents must be given freely with morphia or other anodynes.




             CATARRHAL INFLAMMATION OF THE FOURTH STOMACH.

  Usually a complication. Causes, predisposing, exciting, changes of
  food or water, spoiled, frosted or fermented food, green potatoes,
  caterpillars, nitrogenous food, irritants. Symptoms: Separation from
  herd, grinding teeth, eructation, depraved appetite, fever, tender
  epigastrium, coated dung, red eyes, fixed or retracted, dilated, blind
  eyes, drooping ears, nervous symptoms, reckless unconscious movements,
  bellowing, tender skin, tremors. Lesions: Congestion and exudate in
  gastric mucosa, hemorrhagic discoloration, desquamation, excess of
  mucus, resemblance to rinderpest, Texas fever and malignant catarrh.
  Treatment: Empty stomach by bland laxatives, stimulants of
  peristalsis, calmatives, cold to head, counter-irritants, enemata,
  bitters.


This affection is by no means rare in cattle, though it is usually
complicated with inflammation of the first three stomachs or of the
intestines. Nevertheless, when the disease appears to be concentrated on
the fourth stomach mainly, it may well take its name accordingly.

_Causes._ A predisposition to the affection occurs in the weak and
debilitated, the overworked oxen, underfed cattle, in those that are
just recovering from a severe illness and in which the gastric
secretions and functions are still poor. The usual exciting cause is
some fault in the food, it may be a sudden change from one kind to
another, and especially from dry to green, or from one kind of green
food to another and more tempting one, as when the animal breaks into a
field of grain which is advancing to maturity. Even a sudden change of
water, as from soft to hard has seemed in our experience to contribute
to its development. Next come spoiled aliments, frosted or frozen
turnips, beets, carrots, potatoes, apples, turnip tops, fermented
grasses, musty hay, sun-exposed potatoes, putrid vegetables, and
caterpillars on cabbages, tree leaves and other vegetables. Next come
products that are highly nitrogenous, like vetches, alfalfa, sainfoin,
clover, and the cakes of linseed, rape and cotton seed. Irritant plants
such as colchicum, digitalis, yew, radish, etc., have been charged as
causative agents.

_Symptoms._ These are often difficult to distinguish from those of
indigestion or acute lead poisoning, and they vary in different cases
according to the severity of the attack. In the milder cases there may
be loss of appetite and rumination, some tympany, arching of the back,
uneasy movements of the hind limbs and tail, a disposition to leave the
herd, grinding of the teeth, and frequent gaseous eructations. Some show
a depraved appetite, picking up and chewing various non-alimentary
substances. Somewhat more characteristic are the dry, hot muzzle, the
hyperthermia of the body, the tenderness to pressure of the epigastrium,
and the baked appearance and glistening surface of the fæces. In the
more severe forms the suffering is increased and the nervous system
participates in the disorder. The eyes are congested, fixed or rolled
back, the pupils dilated, the vision appears to be abolished, the ears
are pendant, if tied the subject attempts to get loose, if at liberty he
moves steadily in some one direction regardless of obstacles or dangers,
he bellows, pushes against walls or other obstructions and may seriously
injure himself or others. There is, however, no mischievous purpose, he
is simply impelled to blind motion, and no regard is had to anything
which may be in his way. In some instances the nervous disorder is
manifested by a sensitiveness of the skin, so that the animal shrinks
when handled or pinched along the chine or back. Tremors is another
marked symptom.

_Lesions._ These consist mainly in congestion and swelling of the
gastric mucosa, which is further covered by a thick layer of mucus. The
folds are especially thickened and discolored, and the seat of
hemorrhagic extravasations (petechiæ) and exudations in spots and
patches. Desquamation of the epithelium may be met with at points and
even distinct ulcers. Exudation in the submucous tissue, and petechiæ in
the peritoneum are common. The condition may bear a close resemblance to
what is seen in rinderpest or malignant catarrh.

_Treatment._ The first desideratum is the elimination of the irritant
ingesta from the stomach. But for this purpose emetics are useless and
we must fall back on laxatives. Again we are met by the consideration
that the inflamed stomach will neither readily absorb nor respond to a
stimulus. Yet as a rule the viscus is not equally inflamed throughout,
and even the affected parts do not necessarily have the whole muscular
coat involved and paralyzed. We can therefore hope for a measure of
response which once started will deplete and improve the adjacent and
more violently affected parts. But irritant and drastic purgatives like
croton, podophyllin or gamboge are proscribed as very liable to
aggravate the inflammation. Pilocarpin 3 grs. hypodermically may be
given or in default of this, 1 lb. each of Glauber and common salt in
not less than six quarts of water, free access being allowed to pure
water until it shall have operated. Bismuth may also be given as a
calmative. Active rubbing of the abdomen will assist in rousing the
stomachs to action, and hasten the action of the purgative. If there
should be any sign of cerebral disorder, cold water or ice may be
applied to the head, and oil of turpentine, followed by a pulp of the
best ground mustard may be applied to the epigastrium and right
hypochondrium. This may be accompanied and followed by copious enemata,
and doses of quinia, gentian or still better nux vomica three times a
day.


                     CATARRHAL GASTRITIS IN SWINE.

  Definition. Causes, irritants, fermented, putrid swill, spoiled
  vegetables, irritant molluscs or larvæ, hot or cold food, alkalies,
  indigestible food, specific germs and toxins, parasites. Symptoms:
  inappetence, restlessness, vomiting, colic, constipation, diarrhœa,
  fever, stiffness, tender abdomen, arched back, chill, plaintive
  grunting, drooping tail. Lesions. Treatment: change diet,
  mucilaginous, milk, protection from saprophytes, change pen, emetic,
  laxative, calomel, bismuth, cleanliness, washing.

_Definition._ Inflammation of the gastric mucosa with mucopurulent
discharge.

_Causes._ Irritants of various kinds, fermented or putrid swill, spoiled
vegetables, irritant molluscs or larvæ, too hot or too cold aliment,
excess of brine, excess of alkalies, in swill (dishwashings),
indigestible foods of all kinds. The stomach may also be the seat of
catarrhal inflammation in hog cholera, swine plague, rouget,
diphtheritic affections and in the case of gastric parasites, so that it
is very important to distinguish the affections due to simple irritants,
from those dependent on plagues and parasitism.

_Symptoms._ There is inappetence, vomiting, restlessness and constant
movement, colics, vomiting, constipation or diarrhœa, hyperthermia,
stiffness, tenderness of the abdomen to handling, arched back, a
disposition to hide under the straw, plaintive grunting when roused,
drooping of the tail. The tendency is to a rapid recovery after the
evacuation of the stomach by vomiting, though it may persist under a
continuance of the irritating ingesta.

In these last cases the _lesions_ may closely resemble those of the
contagious affections of the abdomen, but the disease may be
distinguished by its indisposition to spread beyond the herd which is
subjected to the unhealthy dietary.

_Treatment._ Change the diet to one of pure and easily digestible
materials, soups, mush, fresh whey or buttermilk, boiled farinas or flax
seed, and even fresh grass. If there is violent diarrhœa boiled milk is
often of great value.

Whatever food is given should be furnished in a vessel into which the
animal can’t get his feet, as these are usually charged with septic
germs which are pathogenic to the diseased stomach, though they may have
started from ordinary saprophytes.

For the same reason it is usually desirable to change the pen, as the
animal grubbing in the ground charges the snout with the same offensive
microbes.

If vomiting is not already established, 30 grains of ipecacuan may be
given, or tepid water may be used to assist the process. If constipation
is present 10 to 30 grains of calomel (according to size) may be given.
In case of diarrhœa a combination of calomel 1 part and chalk 12 parts,
may be given in 3 grain doses, two or three times a day. Or ½ to 1
drachm nitrate of bismuth may be substituted.

Cleanliness in food and surroundings is among the most important
measures, and if the skin has been filthy, repeated washing with soap
and warm water may be resorted to with great benefit.


                  CHRONIC GASTRIC CATARRH IN SOLIPEDS.

  Causes: Debility, age, anæmia, leucæmia, lymph gland, kidney, heart or
  lung disease, parasitism, dental or salivary disease, coarse, fibrous
  food, spoiled food, putrid water, gastric neoplasms. Symptoms:
  Impaired appetite, eating lime or earth, weariness, costiveness,
  coated dung, tympanies, diarrhœas, fatigue, sweating, unthrifty hide,
  pallid mucosæ, emaciation, colics. Lesions: Thickened right gastric
  mucosa, discoloration, mucus, petechiæ, opaque granular epithelium,
  gastric dilatation. Treatment: Remove causes, diet, watering,
  exercise, sunshine, bismuth, pepsin, acids, bitters, electricity,
  antiseptics, stomachics.

_Causes._ These are in the main the causes which operate in producing
the acute affection. In most chronic cases they act continuously on a
system rendered susceptible by debility or otherwise. Among predisposing
causes may be named: The debility of old age, anæmia, leucæmia, chronic
diseases of the lymph glands, of the liver, kidney, heart, or lung,
parasitic diseases, diseases of the jaws, teeth, or salivary glands
which interfere with proper mastication and insalivation. Among exciting
causes may be named: A coarse, fibrous, innutritious diet, a too bulky
diet, spoiled fodders of all kinds, putrid drinking water, and stomach
parasites (spiroptera, œstrus larva). Actual disease of the
stomach—papilloma, cancer, actinomycosis, tumors, and oat-hair or other
concretions are further causes.

_Symptoms._ Impaired or capricious appetite, a disposition to lick the
walls or earth, or to drink impure water, yawning, constipation with
glossy mucus-covered fæces, and slight tympany, alternating with
diarrhœa, small, accelerated pulse, susceptibility to perspiration and
fatigue on slight exertion, unthrifty skin and hair, hide-bound, dry,
hot mouth, coated tongue, pallor of the mucous membranes, loss of
condition, and increasing weakness. Slight colics may occur at
intervals, and the sluggishness may deepen into stupor or vertigo.

_Lesions._ The right sac is usually the seat of more or less hypertrophy
of the mucosa, which is thickened, rugose, with patches of dark red,
gray and slate color, and covered with a layer of tenacious mucus. The
surface may show warty-like elevations, or papillary projections, with
here and there patches of blood extravasation. The epithelial cells are
increased, opaque and contain many fatty granules.

Dilatation of the stomach is not uncommon especially in old horses, and
then the mucosa may be attenuated and smooth.

Hyperthermia may be present, but is so slight that inflammation cannot
be predicated from it and it is difficult to establish a diagnosis from
chronic dyspepsia.

_Treatment._ It is important to first correct any curable predisposing
disorder, in teeth, jaws, salivary glands, blood, or internal organs, to
carefully regulate feeding, watering and work, to secure as far as
possible an outdoor life, and to employ bitter and other tonics. All
over-exertion or fatigue must be carefully avoided. The food may be as
advised for the more acute affection. Costiveness may be best met by
boiled flaxseed, or in case of necessity by bran mashes, or green food.
The irritation of the stomach may be benefited by nitrate of bismuth (3
to 4 drs.) and pepsin, and dilute muriatic acid with each meal are often
of value. Nux Vomica (10 to 25 grs. twice daily) will help to restore
the lost tone, and a current of electricity may be sent through the
epigastrium daily. As alternatives, sulphate of quinia or gentian may
replace the nux, and salol or salicylate of bismuth may take the place
of the nitrate. Bicarbonate of soda in ½ dr. doses, common salt in ½ oz.
doses, and fennel in ½ oz. doses are sometimes useful in re-establishing
gastric functions.


                    CHRONIC GASTRITIS IN RUMINANTS.

  Causes: As in acute form, parasites, gravid womb, insufficient ration,
  overwork, exhaustive milking, chronic diseases. Symptoms: deranged
  appetite, rumination, pica, eructations, regurgitations, tympanies,
  colics after feeding, coated dung, diarrhœa, fever, hot clammy mouth,
  sunken eyes, small weak pulse, palpitations, emaciation, weakness,
  tender hypochondrium. Lesions: hypertrophy of gastric mucosa, granular
  epithelium. Treatment: tonic regimen, diet, green food, roots,
  sunshine, bismuth, salol, strychnia, pepsin, muriatic acid, common
  salt, counter-irritants.

_Causes._ These are in the main the causes of the acute affection. There
may, however, be special persistent factors like parasites (strongylus
contortus and filicollis, spiroptera) in the stomach, the pressure of a
gravid womb, an alimentation deficient in lime or phosphorus, overwork,
exhausting milking, or chronic disease of important organs (heart,
liver, lung, kidney).

_Symptoms._ These are indefinite and not easily distinguished from those
of disorders of the third stomach. There is impaired or capricious
appetite, a disposition to eat lime, earth, and all sorts of
non-alimentary objects, rumination is rare or altogether suspended,
efforts to regurgitate are ineffectual, or result in gaseous eructations
only, there are tympanies and abdominal pains especially after feeding,
and constipation with a firm glazed appearance of any fæces passed, may
alternate for a short time with diarrhœa. The mouth is hot and clammy,
the eyes sunken and semi-closed, the pulse small and weak, though the
heart may palpitate, and there is a constantly progressive emaciation
and prostration. Among the more characteristic symptoms are tenderness
of the right hypochondrium to manipulation and percussion, and the
presence of slight hyperthermia.

_Lesions._ The changes consist mainly in hypertrophy of the gastric
mucosa, with changes in the epithelium and submucosa such as are already
described in the horse. The pyloric region suffers most, and here ulcers
are not at all uncommon.

_Treatment._ The main aim must be to remove the causes, and to build up
the general health, so that the patient may rise above the debilitating
conditions. More is to be expected from the change of diet to green
food, roots, mashes, etc., and an outdoor life than from the action of
medicines, which are liable to disappear by absorption in the first
three stomachs, so that they can only act on the fourth through the
system at large. Yet benefit may be expected from the use of nitrate of
bismuth, and salol, as calmatives and antiferments, nux vomica as a
tonic and even from pepsin and muriatic acid as digestive agents. The
two last are not dependent on the fourth stomach for their activity but
will digest the contents more or less in the first three, and the finely
disintegrated and partly peptonized ingesta coming to the fourth stomach
in a less irritating, and less fermentescible condition, lessens the
work demanded of that organ and gives a better opportunity for
recuperation. Small doses of common salt and one or other of the
carminative seeds may be added. The application of mustard or oil of
turpentine to the right hypochondrium will sometimes assist in giving a
better tone to the organ.




                      CHRONIC GASTRITIS IN SWINE.

  Causes. Symptoms: inappetence, dullness, arched back, colic, irregular
  bowels, fever, emaciation. Treatment: diet, green food, milk, mashes,
  cleanliness, bismuth, salol, sodium bicarbonate, strychnia, pepsin,
  muriatic acid, sunshine, washing.


_Causes._ These are like those producing the acute affection which may
easily merge into this by a continuation of such causes.

The _symptoms_ too are alike. Inappetence, dullness, prostration, arched
back, vomiting, colic, constipation, with alternating diarrhœa. There is
hyperthermia with hot dry snout, thirst, increasing emaciation, and
anæmia.

_Treatment._ An entire change of diet, to green food, roots, fresh milk,
and soft mashes in limited quantity. Allow pure water freely. Adopt all
precautions against contamination of the food by the feet or snout. The
stomach may be quieted by oxide of bismuth (20 grs.) or salol (10 grs.)
two or three times daily, and the tone and secretions of the stomach may
be stimulated by bicarbonate of soda (1 dr.) and nux vomica (1 to 2
grs.) thrice daily. In addition pepsin and muriatic acid may be given
with each meal in proportion adapted to its amount. A life in the open
air, and an occasional soapy wash will do much to restore healthy
gastric functions.


                     CHRONIC GASTRITIS IN THE DOG.

  Causes: faults in diet, musty food, foreign bodies, poisons, lack of
  sunshine, retained fæces, parasites, ill health, chronic diseases, icy
  bath, septic drink. Symptoms: irregular appetite and bowels, fever,
  foul breath, red tongue, tartar on teeth, dullness, prostration,
  vomiting of mucus or bile, tender epigastrium, arched back, fœtid
  stools, emaciation. Treatment: regulate diet, sunshine, pure water,
  scraped muscle, soups without fat, antiseptics, calomel, pepsin,
  muriatic acid, strychnia.

_Causes._ The irregularity and variability of the food, overfeeding,
highly spiced foods, putrid or spoiled food, musty food, the swallowing
of pieces of bone, and of indigestible bodies, the consumption of
poisons, the absence of open air exercise, the compulsory suspension of
defecation in house dogs, and the presence in the stomach of worms
(spiroptera, strongylus), are among the common causes of the affection.
As in other animals, ill health, debility, lack of general tone, and
chronic diseases of important organs (liver, kidney, heart, lungs) must
be taken into account. The plunging into cold water when heated and the
licking of septic water must also be named.

_Symptoms._ Appetite is poor or irregular, the nose dry and hot, the
mouth fœtid, the tongue reddened around the borders and furred on its
dorsum, the teeth coated with tartar, the animal dull and prostrate,
vomits frequently a glairy mucus mixed with alimentary matters or yellow
with bile, and there is constipation alternating with diarrhœa. The
epigastrium is tender to the touch, the back arched, the fæces glazed
with mucus or streaked with blood, and offensive in odor. Emaciation
advances rapidly and death may occur from marasmus.

_Treatment._ Adopt the same general plan of treatment. Stop all
offensive and irritating food, give regular outdoor exercise, free
access to pure water, and every facility to attend to the calls of
nature. Give plain easily digestible food in small amount. In the worst
cases pulped or scraped raw meat, in the less severe mush, or
well-prepared soups with the fat skimmed off, and bread added. Check the
irritant fermentations in the stomach by salol, bismuth, salicylate of
bismuth, or naphthol. In case of constipation give 8 to 10 grs. calomel.
Then assist digestion by pepsin (5 grs.) and hydrochloric acid (10
drops) in water with each meal. If the bitterness is not an objection 1
gr. nux vomica may also be added.




                       ULCERATION OF THE STOMACH.

  Causes: peptic digestion, paresis, caustics, irritants, acids,
  alkalies, salts, mechanical irritants, hot food, parasites,
  thrombosis, embolism, specific disease poisons, aneurism, tumors,
  infective growths, nervous disorder, debility, toxins of diphtheria,
  staphylococcus, etc. Symptoms: slight colics, tympany, emaciation,
  vomiting blood, tender epigastrium, dark or bloody stools, irregular
  bowels; in carnivora abdominal decubitus, arched back, bloody, mucous,
  acid vomit, colics after meals. Lesions: in horse erosions, ulcers,
  parasites, neoplasms, discolorations, extravasations; in cattle and
  dogs on folds, nature of ulcer. Treatment: restricted, digestible
  diet, lavage, anodynes, bismuth, antacids, antiseptics, salol,
  naphthol, chloral, pure water.


_Causes._ Gastric ulcers may arise from quite a variety of causes which
determine necrotic conditions of the mucosa and the gradual invasion of
the resulting lesion by destructive microbes. One of the simplest
factors is the peptic juice, the stomach, being struck with paresis (in
inflammation, fever, nervous disorder), while containing a quantity of
its secretion, undergoes an autodigestion which affects particularly the
lowest (pyloric) portion, toward which the liquid gravitates, and the
free edges of the folds which are the most exposed to its action.

The swallowing of irritant and caustic agents (the mineral acids or
alkalies, mercuric chloride, tartar emetic, antimony chloride, Paris
green, arsenious acid, etc.) by corroding or causing destructive
inflammation of the exposed mucous membrane may similarly operate. This
is especially the case with monogastric animals, (horse, pig, dog, cat),
as in the ruminants such agents tend to be diluted in the first three
stomachs and rendered more harmless.

Mechanical irritants may cause the lesion and infection atrium in any of
the domestic animals, pins, needles, nails, pieces of wire and other
sharp pointed bodies being swallowed by horse and ox, and small stones,
pieces of bone, and all sorts of irritant objects picked up by the puppy
or rabid dog.

Cooked food swallowed hurriedly at too high a temperature is especially
liable to start necrotic changes in the single stomach of horse, pig or
dog, the ruminant being in a measure protected by the food passing first
into the rumen.

The wounds caused by gastric parasites may become the starting points of
molecular degeneration and ulceration. In the horse the spiroptera
megastoma, s. microstoma, and the larvæ of the various œstri; in cattle
and sheep the strongylus contortus, s. convulutus, s. filicollis and s.
vicarius; in swine the spiroptera strongylina, Simondsia paradoxa, and
gnathostoma hispida; in dogs spiroptera sanguinolenta, and in cats the
ollulanus tricuspis act in this way.

Gastric catarrh debilitates the affected mucosa and lays it open to
necrotic microbian infection especially in the pyloric sac and on the
summit of the folds.

Interruption of the local circulation in the deeper parts of the mucosa
as in inflammation and capillary thrombosis, arterial embolism, venous
thrombosis, may lead to local sloughing and ulcerous infection. This may
be seen in the petechial fever of the horse, malignant catarrh,
rinderpest, and anthrax in cattle and sheep, and in canine distemper in
dogs. Vogel found ulcers resulting from a gastric aneurism in the dog.

Tumors and infective growths in the walls of the stomach may prove an
occasion of ulceration. Thus sarcoma, epithelioma, actinomycosis and
tubercle may be the primary morbid lesion in different cases.

Gastric ulcers have also been attributed to morbid nervous influences as
in dogs they have been found associated with lesions of the dorsal
myelon, and the corpora quadrigemini, and faradisation of the vagus has
apparently led to their production.

General constitutional debility has been alleged as a factor, and
experimentally in dogs, the hypodermic or intravenous injection of
various microbes or their toxins (diphtheritic toxin, Enriquez and
Hallion, staphylococci, Panum, Lebert, Letulle, and a bacillus of
dysentery in man, Chantemesse and Widal), have produced gastric ulcers.

_Symptoms._ In _horses_ and _cattle_ these are very obscure, being
mainly in the nature of chronic gastritis. In both there are recurrent
attacks of slight colicy pains, with tympany in cattle, and gradual
emaciation. Vomiting has been exceptionally seen in both class of animal
and if the rejected matters are very acid and above all if mixed with
blood it is more suggestive of ulcer. In the horse the attacks of colic
are mostly in connection with eating. or (in case the ulcer is duodenal)
an hour or two after a meal. In this animal it is possible to withdraw
liquids from the viscus by the stomach pump, and any hyperacidity or
blood may be almost diagnostic. Tenderness to pressure on the
epigastrium or hypochondrium is often present, yet the colics of
ulceration are often relieved by pressure and friction. Blood is
sometimes present as such in the excrements, but more commonly these are
simply blackened by the exuded blood as acted on by the gastric acid and
intestinal liquids. The bowels may be alternately constipated and
relaxed. A gradually increasing feebleness is a characteristic feature
and in cattle paraplegia may precede death.

In the _carnivora_ the symptoms are less obscure. The animal is dull,
prostrate, weak, lies on its belly, but rarely long in one place, and
when up has arched back, stiff movements, and tucked up abdomen. The
epigastrium is painful to touch, which tends to arouse vomiting of food
or bloody mucus. As in the horse the rejected matters are very acid.
Constipation may alternate with diarrhœa, the fæces being blackened
(melæna) or even streaked with blood. The occurrence of suffering after
meals, the constancy and persistency of the symptoms and the steadily
advancing emaciation and weakness are very characteristic. If the
tenderness is referable to a given point, it is even more distinctive.

_Lesions._ In the _horse_ ulcers and erosions occur in the cardiac sack
in connection with œstrus larva and spiroptera which destroy and remove
the cuticular covering, or with sarcoma or epithelioma growing in the
gastric walls. In the right sac there may also be round ulcers from the
hooklets of the œstrus, or irregular excavations on the summits of the
folds in connection with catarrhal inflammation. Ulcers from
autodigestion are usually in the right sac, in the most dependent part
of the viscus, between the folds, and of a more or less circular
outline. The raw surface is black, brown, slaty gray or white. The
ulcers which result from petechial fever are irregularly notched and
marked by a mass of dark blood coagulated in their depth.

In _cattle_ and _dogs_ the ulcers are most frequent near the pylorus,
and when of catarrhal origin may be round or irregular, and on the
summit of the fold, or if peptic, may be round and between the folds. In
malignant catarrh and rinderpest, they are mostly formed on the summits
of the folds. They may vary in size from a pea to a quarter of a dollar.
The surrounding mucosa is usually congested, swollen, and projecting,
and the surface of the ulcer itself of a dark red, black, yellowish,
slaty or gray.

The round ulcer is usually marked by surrounding infiltration and by a
tendency to become deeper and to perforate the gastric walls, with the
result of inducing an infective peritonitis. This is more common in
cattle and carnivora than in solipeds.

_Treatment._ If a reasonably certain diagnosis can be made the patient
should be put on a restricted diet of easily digested materials, given
at regular intervals. For the carnivora scraped or pulped raw meat, and
milk, and for the herbivora milk and well boiled flax seed or other
farina are appropriate.

Violent emesis in carnivora may demand washing out of the stomach with
tepid water with or without the aid of a stomach tube. This may be
seconded by anodynes, chloral, cyanide of potassium, or even morphia.

Bismuth trisintrate or oxide is appropriate in all animals, also sodium
bicarbonate, chalk or magnesia to neutralize the muriatic acid.

As antiseptics calculated to obviate the formation of irritant products
from the gastric contents and to check the progress of the microbian
infection in the wound such agents as the following may be used: Salol
(horse or ox 1 dr., dog 5 grs.), naphthol or naphthalin (same doses),
chloral (horse 2 drs., dog 5 grs.).

Sometimes it is well to relax the bowels by small doses of Glauber
salts, and in all cases an abundance of fresh water, butter milk, or
other bland drink.

Cases of the kind are slow in their progress and unless the animal is
specially valuable, treatment may be a source of loss.




                    PERFORATING ULCER OF THE STOMACH

  Causes: round ulcer, foreign bodies, parasites. Symptoms: those of
  ulcer, followed by infective peritonitis, fistula, pleuritis,
  pericarditis. Treatment: of fistula.


This may be the result of the gradual deepening of the round ulcer, yet
in the domestic animals it mostly comes from the presence of sharp
pointed bodies. These may be enumerated as needles, pins, nails, wires,
sharp bones (dog), whalebone (horse), forks, knives (cattle), and even
gravel. The burrowing of the spiroptera has seemed to cause perforation
in the horse. All causes of ulceration may, however, lead to
perforation.

The _symptoms_ are those of gastric ulcer, already given, followed by
the more specific ones of perforation. These in their turn differ
according to the parts involved. In the horse and dog the perforating
ulcer usually opens into the peritoneum, inducing a fatal infective
peritonitis. In cattle the foreign body sometimes passes toward the
heart, enveloped in a protecting mass of new formed tissue and proves
fatal by heart disease. In other cases it has been found to proceed
downward toward the sternum and to escape by a fistula formed beside the
ensiform cartilage. In other cases it has taken a direction toward the
right wall of the abdomen where it formed a fistula, discharging
alimentary matters. In still other cases it has opened into the
peritoneal cavity with fatal effects.

_Treatment_ in the case of external fistula, without implication of the
peritoneum, consists in the removal of the foreign body, and the
stimulation of granulations along the tract of the fistula by the
application of an ointment of tartar emetic to the interior. Should this
fail the fistulous tract may be scraped to make it raw, and the edges
may then be drawn together with sutures taking a deep hold of the skin.




                       DILATATION OF THE STOMACH.

  Adaptability to bulk of food. Dilatation with atony. Eructation.
  Cribbiting. Vomiting. Age. Rare in cattle. Catarrh, overloading,
  nervous lesions, intestinal obstructions, tumors, calculi, volvulus,
  invagination, hepatitis. Symptoms: overfeeding, pot-belly, unthrifty
  hide, emaciation, eructations, cribbiting, fatigue, perspiration,
  indigestion, colic after meals, tympanic resonance. Lesions: varying
  distension, contents, action of calculus or pebbles, cardiac
  dilatation. Treatment: nutritive, digestible, concentrated food,
  lavage, strychnia, iron, faradisation, antiseptics.


The stomach has a great power of accommodation to the amount of food
habitually taken. In the horse fed mainly on grain with only a little
hay, it is habitually small, while in one fed on cut straw with a little
grain, on hay alone, or on green food, it is very much more capacious
though within the physiological limits of health. The cow wintered on
grain alone, has all four stomachs lessened in capacity, and though she
maintains good condition she is ill fitted to change at once to the
bulky grass diet of spring. The heavily fed swine, and the farina fed
dog and cat, have both stomach and intestines increased in capacity over
those of the wild boar, or the purely carnivorous wolf or wild cat.

The condition becomes pathological when associated with atony, and this
may occur directly from over distension. It is especially common in the
horse by reason of the difficulty of relieving the over distension by
eructation or vomiting, and also by reason of the habit of swallowing
air (cribbiting). The dog, which has great facility in vomiting, should
be correspondingly protected from the condition, yet it is very common
in old dogs, doubtless from their common vice of gourmandizing and lack
of exercise. Cattle are rarely attacked, the fourth stomach being
protected by the others which stand guardian over it and prevent the
sudden access of excess of food even if that is rapidly swallowed.

Other _causes_ are: chronic catarrh which renders the stomach atonic,
lessens its peptic secretion and determines indigestions and over
distensions: habitual overfeeding which results in chronic indigestions
and fermentations; lesions of the brain, and tumors of the jugular
furrow or mediastinum which interfere with the functions of the vagus
nerve; obstructions of the intestines which force the contents back into
the stomach or hinder their exit. Thus tumors on the duodenum, calculi
in stomach or intestines, volvulus and invagination have been charged
with producing overdistension. Chronic hepatic disorder has also been
quoted as a cause.

_Symptoms._ The subject may eat naturally or excessively yet is
unthrifty, the belly is habitually distended, the hair dry and rough,
there is loss of flesh, there may be eructations or (in the horse)
swallowing of air, lack of endurance, a disposition to perspire easily,
a tendency to indigestion and colics after meals, and hurried breathing
sometimes marked by a double lifting of the flank in expiration. In the
_dog_ which has the stomach more accessible to examination its outline
may be followed by percussion, a tympanitic resonance being produced
from the eighth rib back to the umbilicus or further. If there is any
difficulty the organ may be emptied of water by a stomach tube and then
pumped full of air by means of a Davidson’s syringe, and percussed in
each condition. Or a half a teaspoonful of bicarbonate of soda may be
given in a little water followed by an equal amount of tartaric acid,
and the stomach percussed.

_Lesions._ The distension of the stomach may reach ten times its normal
size in the horse (Leisering). Kitt found a stomach with a capacity of
84 quarts. Fitzroy Philipot took from a dilated equine stomach 140 lbs.
of contents. The contents of the viscus are usually largely of solids
which the weakened and attenuated walls failed to pass into the
duodenum. On the contrary and as if by compensation, the pylorus and
duodenum are constricted and the latter has liquid contents which pass
from the stomach with very little of the solids.

Special dilatations are sometimes met with, thus an equine stomach has
been found largely dilated at the greater curvature where concretions
formed in the viscus or pebbles introduced with the food had habitually
lodged. In other cases the cardia has been dilated like a funnel, so
that the animal could eructate or vomit with great facility. This last
dilatation is especially common in cribbiters.

_Treatment._ This must necessarily be prolonged as time must be allowed
for a tonic contraction of the viscus. Food must be given often in small
quantity, of easy digestion, and of aqueous composition. For dogs, milk,
eggs and soups, or pulped raw meat furnish examples. For horses milk
gruels, boiled flax seed, pulped roots may suffice. If the stomach is
loaded as is usually the case, it should be washed out with the stomach
tube, which when passed into the stomach should be raised at its free
end and filled with tepid water; it is then suddenly lowered so as to
act as a syphon in evacuating the liquid contents of the stomach. This
may be repeated again and again, the stomach in the case of the dog
being manipulated so as to mix and float the solids and favor their exit
through the tube. Daily washing out of the stomach by the tube is of the
greatest possible value.

Meanwhile we should seek to improve the tone of the stomach by strychnia
(horse 2 grs., dog ¹⁄₆₀ gr. daily), by salts of iron, and by
faradisation.

To counteract fermentation, antiseptics (salol, naphthol, freshly burned
charcoal) may be given with each meal, along with pepsin and
hydrochloric acid.


                  RUPTURE OF THE STOMACH IN SOLIPEDS.

  Mainly in solipeds. Causes: overloading, fermentation, impossibility
  of eructation, violent concussions, falls, galop, concretions,
  dilatation, catarrh, ulcers, cicatrices, abscesses. Symptoms:
  Anamnesis, colic relieved, followed by prostration, sinking, complete
  anorexia, tender abdomen, vomiting, no abdominal rumbling. Lesions:
  tear in greater curvature, most extensive in outer coats, shreddy,
  bloody edges with clots, contents in omentum, other seats, partial
  ruptures. Treatment: in partial ruptures, stomach pump, diet.
  Prevention.

This is pre-eminently a disease of solipeds for the reason that they
alone of domestic animals are especially liable to overload the
comparatively small stomach and are mostly unable to relieve the
overloaded viscus by eructation or vomiting.

_Causes._ These are in the main overloading of the stomach and
overdistension, by the gases of indigestion. To this are usually added
violent concussions when the animal throws itself down violently. The
stomach distended to the fullest possible capacity, and lodged in a
cavity which is not all equally tense, is comparable to a very tense
bladder which is liable to burst when forcibly struck, or suddenly
compressed.

Apart from such indigestion, cases are recorded in which the full
stomach has been burst by a sudden fall in the shafts or elsewhere.
Miles even records a case which occurred during a rapid galop after a
full drink of water.

The presence of solid bodies (calculi, gravel) in the stomach or even in
the intestines has appeared to cause rupture by blocking the outlet of
ingesta and determining indigestion.

Certain conditions predispose to rupture, notably dilatation of the
stomach with attenuation of its walls, cribbiting, old standing catarrh
of the viscus, pre-existing ulcerations, cicatrices and abscesses.

_Symptoms._ There is usually the history of a full feed of grain,
followed by violent colic, and indications of gastric overdistension,
tense abdomen, dullness, then the rejection of the gastric contents by
vomiting, the matters escaping by the nose, and then collapse. The
violence of the colics may cease, but the pulse becomes rapid, small,
and finally imperceptible, the breathing hurried, the head depressed,
eyelids, ears and often the lower lips drooping, the face becomes heavy
and expressionless, the belly distended and tender, the skin covered
with cold sweat, and the temperature exalted above or depressed below
the normal. There is never any disposition to eat nor drink. Death
follows in a few hours.

In the vomiting which is independent of rupture, the symptoms are
usually at once relieved, when the emesis occurs, since not only liquid
and solid matters escape but also gaseous material. The pulse retains
its fullness, the facial expression is that of intelligence and comfort,
rumbling may be resumed in the bowels, fæces and urine may be passed,
and colics are less acute. In favorable cases the animal may even desire
to eat or drink.

_Lesions._ The usual seat of rupture is on the great curvature and may
extend longitudinally for from six to ten inches. The laceration is
usually most extensive in the outer coats, and the mucosa is carried
outward with the escaping ingesta, which helps to efface the normal
mucous folds at the cardia, and to render vomiting possible. The edges
of the wound are more or less shreddy, and of a dark violet color from
blood extravasation and clots. The escaping contents are rarely diffused
in the cavity of the abdomen, but remain enclosed in the omentum through
the thin meshes of which they can be easily seen, and which has
sometimes been mistaken for the walls of the stomach reduced to this
attenuated condition by disease. When the omentum gives way the contents
are at once diffused through the abdominal cavity between the
convolutions of the intestines. In exceptional cases the rupture has its
seat in the lesser curvature, or even at the cardia. In still others the
laceration implicates the muscular and peritoneal coats only, and the
looser mucosa, filled with ingesta bulges outward as a hernia. In such a
case a recovery seems possible if the viscus could be relieved of its
contents.

_Treatment_ is virtually hopeless. Yet a moderate laceration of the two
outer coats only might be followed by recovery through the formation of
a cicatrix. The first consideration would be the unloading of the
stomach spontaneously or by the aid of the stomach pump, and thereafter
the adoption of a rigidly restricted diet of easily digestible food
(such as gruels) in small quantities at a time.

_Prevention_ is much more available. In violent colics with overloading
or tympany of the stomach, employ anodynes to keep the animal from
throwing himself down violently, give a soft bed of litter where the
shock on lying down will be lessened, employ antiferments to prevent
gaseous distension, and whenever possible relieve the plenitude of the
viscus by the stomach pump or tube.


                   TORSION OF THE STOMACH IN THE DOG.

  Causes: mobility of dog’s stomach when empty, leaping, running down
  stairs. Lesions: viscus doubled forward, pylorus in front of cardia,
  duodenum compresses cardia, liver, spleen and omentum displaced,
  stomach tympanitic, lungs and heart compressed, latter gorged with
  dark blood. Symptoms: tympanitic abdomen, and half thorax, no
  rumbling, murmur in front of thorax, abdomen tender, patient stands,
  dyspnœa, emesis impossible. Course: violent symptoms in twelve hours,
  death in thirty-six. Diagnosis: sudden, severe seizure, complete
  anorexia, tympany, tenderness, dyspnœa, no vomiting, arrest of
  peristalsis. Obstruction. Peritonitis. Choking. Treatment: tapping,
  laparotomy, replacing the viscus.

This has been demonstrated by Kitt and Cadeac who believe that it is
quite a common occurrence.

_Causes._ The predisposing cause is the extreme mobility of the canine
stomach which hangs from the œsophagus like a pear from its stalk, the
remainder of the viscus being only attached to the loose omentum,
spleen, and commencement of the duodenum all of which it can carry with
it easily when it rolls on itself. Its mobility is, however, very
restricted when full, the liver on the one side and the spleen and
intestines on the other proving almost insuperable obstacles to
rotation. But when empty it moves with great freedom and by a sudden
shock in leaping, gamboling or running rapidly down stairs the pylorus
is carried forward and to the left until it and the commencement of the
duodenum are jammed in front of the cardia. The result is the
obstruction of the cardia and duodenum by their mutual pressure in
crossing each other, and the interruption of the gastric circulation and
functions.

_Lesions._ As just stated the stomach which would normally extend from
the cardia downward and to the right is bent forward and doubled upon
itself, the pylorus lying in front of the cardia, the duodenum extending
from before backward above the cardia and tightly compressing it, the
liver drawn to the left by the hepato-duodenal peritoneum, and the
spleen displaced to the right by the traction on the omentum. The
stomach enveloped in its omentum is distended by gas to perhaps ten
times its normal dimensions and appears to fill the entire abdominal
cavity while the intestines are pushed aside and concealed. The chest is
compressed by the strong pressure on the diaphragm, and the lungs are
congested of a deep blue and the right heart distended with dark blood.
The animal appears to have perished of apnœa.

_Symptoms._ In fully developed cases the abdomen is greatly distended
and tympanitic. The drumlike resonance is met with in the anterior part
of the abdomen including the umbilical region. It extends forward over
one-half of the thorax, excepting only a space of 5 or 6 inches square
in the right hypochondrium, which represents the situation of the liver,
and spleen. Auscultation furnishes no sound in the abdomen, and only in
the anterior portion of the thorax is there a distinct respiratory
murmur. The heart may beat strongly and rapidly, or weakly and slow, and
the pulse is small and thready. The abdomen is tender. The animal
stands, dull, and breathes with great effort. If made to walk it is done
slowly, stiffly and with head extended, mouth open and tongue
protruding. There is no sign of vomiting and this cannot be brought
about by tickling the fauces, or even by giving apomorphine subcutem,
though retching may be induced.

_Course._ The disease may develop into dullness and anorexia in two
hours after boisterous health; in twelve hours there may be considerable
tympany and dyspnœa; and a fatal result is reached in about thirty-six
hours.

_Diagnosis._ This is based on the transition from vigorous health to
sudden illness, with complete anorexia, inability to swallow or to
vomit, tympany of the stomach as shown by percussion, tenderness of the
abdomen, dyspnœa, disturbed heart-functions, and inactivity of the
bowels. With intestinal obstruction on the other hand there is free
vomiting of bilious and feculent matters. With peritonitis there is much
greater and more uniform abdominal tenderness, vomiting and higher
fever, but less tympany in the anterior abdominal region, and no such
complete suspension of defecation. With choking there is no such
progressive tympany, appetite and defecation are not so completely
suspended, and liquids may often pass the obstruction in small
quantities in both deglutition and vomiting. Choking is by no means so
speedily fatal.

_Treatment_ is essentially surgical. When tympany is already established
the gas must be evacuated by a small cannula and trochar. Then resort is
had to laparotomy, the incision is made on the right side large enough
to introduce the fingers, which must follow the great curvature of the
stomach as far as the pylorus which is pulled back into its normal
position on the right. The incision is now closed by an ordinary
continuous suture.




 FOREIGN BODIES IN THE STOMACH. HAIR, WOOL, BRISTLE, CLOVER AND COTTON
                                 BALLS.

  Hair balls, wool balls, bristle balls, cotton balls, clover-hair
  balls, oat-hair balls, paper balls, phosphatic calculi, sand and
  gravel, nails, wires, needles, pins, etc., cloth, leather, whalebone,
  playthings, etc. Symptoms: of catarrh or colic, dullness,
  restlessness, arched back, in dog vomiting of blood, fistula.
  Diagnosis. Treatment: emetic, feed potatoes, laparotomy.


=Hair Balls.= These are common in the rumen of cattle and have been
found in the fourth stomach. They are especially injurious to young
animals by reason of their irritating the gastric mucosa, but they also
occasionally block the pylorus, producing indigestion, gastric
dilatation, gradually advancing emaciation and even a fatal result.

=Wool Balls.= These are found in sheep and are especially injurious in
young lambs.

=Bristle Balls.= These are found in swine as round, or ovoid balls or
long ellipses bent upon themselves. The sharp projecting ends of the
bristles render them very irritating, especially to young pigs.

All of these are caused by licking themselves or their fellows, and
particularly during the period of moulting or as the result of some skin
affection. Lambs which are nursed by ewes with an excess of wool on and
around the mammæ, and old sheep with a disposition to eat wool are
frequent victims.

=Cotton Balls.= These have been found in lambs fed on cotton seed cake.
A certain amount of the cotton fiber is incorporated in the cake, and
this is rolled together and felted by the movements of the stomach and
agglutinated by mucus.

=Clover-hair Balls.= The fine hairs from the clover leaf have been found
rolled into balls in the abomasum of lambs producing all the evil
effects of the other pilous masses.

=Oat-hair Balls.= The fine hairs which cover the seed of the oat are
found matted together and cemented by mucus in the stomach of horses fed
on the _dust_ of oatmeal mills. They are especially common in Scotland,
where oatmeal has been so extensively used.

=Paper-ball.= In the museum of the N. Y. State Veterinary College is a
conglomerate ball of paper taken from the stomach of a hog by Dr.
Johnson, Sioux City.

=Phosphatic Calculi= have been described as found in the stomach, but
this is evidently an error, as the acid secretion would have speedily
dissolved them. The error doubtless came from mistaking the transverse
colon for the stomach.

=Sand and Gravel= arrive in the stomach of the _horse_ from pasturing on
loose sandy land, the plants being pulled up by the roots and swallowed
together with the sand adherent. Also from drinking water from shallow
streams with sandy bottoms. Feeding of grain from the ground is a cause
of swallowing sand, earth and pebbles. Licking the soil in acidity of
the stomach is another cause. Fodder that has been packed down and mixed
with earth, and that which has been blown full of sand or dust, and
roots eaten from the ground in wet weather lead to the ingestion of much
sand or earth. Shetland ponies taken from the islands pass sand for some
weeks. Dogs taught to fetch and carry, swallow stones, pebbles, marbles,
etc., accidentally.

=Nails, Wires, Needles, Pins, etc.= More or less pointed metallic
objects are often taken in with the food by gluttonous horses and though
usually arrested in the intestines they sometimes irritate or wound the
stomach.

=Fragments of cloth, leather, or whalebone= are similarly taken with the
food, or in case of depraved appetite are deliberately chewed and
swallowed.

=Playthings and small household articles= are especially taken by
puppies through mere wantonness. Rubber balls, pieces of metal, thread,
cord, cloth, bits of leather, sponge, horse hair, human hair, corks,
bits of wood and everything obtainable of small size may be swallowed
and found in the stomach.

=Pigs= swallow pieces of wood and other objects.

=Birds= habitually swallow pebbles and ordinary objects are ground down
in the gizzard. They also readily vomit feathers, bones and other
offensive matters that have proven indigestible.

_Symptoms._ In =horses= there are no especial symptoms, though the
foreign bodies sometimes cause gastric catarrh, and in other cases
produce wounds and ulcers or block the pylorus causing violent colic.
Most commonly the foreign bodies pass on into the intestines, where they
may directly wound the walls, form nuclei for the deposition of earthy
salts in the form of calculi, or in case of fibrous materials (cords)
roll into firm balls.

In =dogs= the foreign bodies may cause gastric catarrh, or puncture or
abrasion of the mucosa, and they may be rejected by vomiting. The more
rounded, smooth bodies may lie for a length of time in the stomach
without doing any manifest injury, as in the case mentioned by Nichoux
in which a dog carried in its stomach for twelve years a four franc
piece and a large sou. Sometimes the objects block the pylorus. Then the
subject is dull, depressed, inclined to lie on the right side but
continually changing his position, gives a stifled yelp when he lies
down or occasionally when he stops walking. He carries the back arched,
and the abdomen tucked up, and drags his hind limbs. Vomiting, is
frequent and accompanied by violent and painful retching. The vomited
matters may be mixed with blood. The epigastrium is tender to pressure.
Death may ensue in twenty-four hours or not until after weeks or even
months.

In other cases there is gastro-enteritis with vomiting, colic, anorexia,
trembling, hyperthermia, constipation or diarrhœa, and finally the
passage of the offending agent per anum, when recovery ensues.

In other cases sharp pointed bodies perforate the walls of the stomach,
and determine the formation of abscess or fistula opening at any point
around the abdominal cavity. This may be followed by recovery, by
gastric or intestinal fistula, or by chronic disease of some important
organ like the liver.

In =dogs=, _diagnosis_ is often possible by manipulation of the stomach
through the walls of the abdomen. If the belly is very lax it may be
compressed between finger and thumb, or between the two hands; if more
tense, pressure with both hands just behind the sternum may detect the
resistance of a solid body.

_Treatment._ In the =horse= this is hopeless.

In the =dog= much may be expected from the use of emetics, (ipecacuan,
tartar emetic, apomorphine, tepid water, tickling the fauces). In some
cases of sharp pointed bodies an exclusive and abundant diet of well
boiled potatoes proves successful. The object is to pass much of the
starchy matter through the small intestines undigested, so that it may
envelop the sharp body and protect the mucosa. When it reaches the
colon, the ingesta as a whole becomes more solid and invested by this,
the body is often passed without danger. Other methods failing
laparotomy remains. The dog is stretched on his back on a table with the
forelimbs held well apart. The skin of the epigastrium is denuded of
hair and washed with antiseptics (mercuric chloride solution 1:500).
Hands and instruments are also made aseptic. Then an incision is made in
the epigastrium or in the situation where the offending body has been
felt, and the finger is introduced to locate the body. At this point a
thread is passed through the walls of the stomach, and these are drawn
well out through the abdominal wound and incised to the extent of an
inch or more. Through this orifice the foreign body can be easily felt
and extracted. Then in case the stomach is over-filled it may be
emptied, and the edges washed with the antiseptic and carefully sutured
with sterilized catgut. The usual care must be taken to turn the mucosa
inward and bring the muscular and serous coats in accurate opposition.
Finally the abdominal wound is closed by a continued suture of silk or
catgut.

The greatest care must be taken to prevent the escape of any of the
gastric contents into the abdominal cavity, to render both wounds
aseptic and to protect the external wound especially against infection.
A wash of carbolic acid (1:100) with a little of some intense bitter
(quassia) will often succeed in preventing licking or gnawing.

Even greater care must be given in the matter of diet. At first a few
teaspoonfuls of cold water only need be given. After twenty-four hours a
little well strained beef tea; later milk or gruel may be added, and by
degrees more solid food. In three weeks the ordinary food may usually be
resumed.

In case the foreign body has escaped into the peritoneal cavity, the
same method may be pursued, the edges of the gastric or intestinal wound
being made raw, treated antiseptically and carefully sutured, and the
abdomen washed out with an antiseptic solution (aluminum acetate
solution) and closed.




                         TUMORS OF THE STOMACH.

  In horse—sarcoma, papilloma, lipoma, adenosarcoma, epithelioma, in
  cattle—scirrhus, in dog—sarcoma, lipoma, epithelioma. Symptoms:
  chronic gastritis, periodic indigestions, colics, vertigo, salivation,
  impacted gullet, blackened fæces, eructations, vomiting, rumbling,
  stiffness, emaciation. Treatment: laparotomy in dog.


The peptic stomach in the different animals is subject to a great
variety of tumors. In many of the recorded cases, however, the true
nature of the tumor has been left uncertain.

=Sarcoma.= In the =horse= this is the common tumor of the pylorus, and
less frequently it is found on the cardia and body of the stomach,
especially on the greater curvature. These are usually firm and
resistant, though sometimes soft and friable; they tend to swell out in
lobules, and show areas of ulceration, or even suppurating excavations
opening through the mucosa. In some instances, however, they start under
the serous coat, and the ulcerous surface may open into the peritoneum.
At other times they are but a local manifestation of a general
affection.

In the =dog= multiple sarcomata have been found on the stomach varying
in size and easily mistaken for recent tubercles. In these cases the
small round cells were especially numerous in the centre of the tumor
rendering it soft and predisposing to degeneration.

=Papilloma.= In the horse these are found as branching or filamentous
dependent projections from the mucosa of the left sac having evidently
started from the sores formed by the attachment of the œstrus larvæ.
They are also found around the pylorus and of such size as to seriously
obstruct that orifice (Stadler).

=Lipoma.= Fatty tumors have been seen on the stomach of the =dog= and
=horse= in the submucosa.

=Adenosarcoma.= This formation in the =horse= leads to a thickening of
large patches of the mucosa. It also grows out in mushroom like masses,
or is irregularly lobulated.

=Epithelioma.= In the =horse= epithelioma has been found at the pylorus
and on the great curvature of the stomach. It usually grows out as a
rounded mass varying in size from an egg to an infant’s head, and may be
even a diffuse thickening of the mucosa. Microscopically the individual
lobules, are composed of cylindroid cells surrounding a central mass of
epidermoid cells. The stomach may be greatly contracted, and the surface
of the neoplasm, ulcerated or even excavated. In the =dog= similar
formations are found.

=Carcinoma.= In =cattle= _Scirrhus_ of the abomasum is described. Small
tumors rise to a height of ½ to 3 inches, and are closely packed
together so as to assume polygonal forms. The surface is smooth, or
perforated by orifices leading into ulcerous or suppurating cavities. On
section the mass shows a fibrous or a lardaceous consistency. They are
most common in the pyloric region, and may partially obstruct this
orifice.

_Symptoms._ These are necessarily obscure. In the =horse= periodic
gastric indigestions and colics may be the sole indications, which are
certainly not pathognomonic. In other cases, have been noticed: vertigo,
salivation, impacted gullet, and blackish, sanguinolent fæces due to
ulceration and hemorrhage from the tumors.

In =cattle= have been observed variable and capricious appetite,
imperfect rumination, tympany, eructations, vomiting, rumbling of the
bowels, constipation, slow painful walk, progressive emaciation and
debility. When blood is discharged by emesis or defecation the suspicion
of gastric tumor may be strengthened.

In the =dog= there are the usual signs of chronic gastritis, thirst,
anorexia, stiffness, a disposition to lie, sunken eye, dyspnœa,
vomiting, often of blood. The discharge of blood by mouth and anus, the
distended abdomen, the tumor usually easily detected by manipulation,
and the progressive loss of condition are strongly suggestive.

_Treatment_ of these cases is hopeless. In the dog alone for a
circumscribed tumor, laparotomy, the removal of the tumor and closure of
the wound may be tried.




     ACUTE INTESTINAL INDIGESTION IN THE HORSE. INTESTINAL TYMPANY.

  Definition. Causes: Debility—general and local, and its causes,
  fermentescible food, legumes, new grain, paralyzing seeds, musty
  fodder, defective teeth, jaws and salivary glands, iced water after
  grain, verminous embolism, chill. Symptoms: Anamnesis, colic, gaseous
  distension, stupor, death, diagnosis from spasmodic colic. Course:
  Fatal in two hours, or more. Recovery. Lesions: Distension of bowels
  with carburetted hydrogen, carbon dioxide, and nitrogen, redness of
  intestinal mucosa, anæmia of abdominal organs, congestion of cutaneous
  and surface vessels. Treatment: Stimulants, antiseptics, enemata,
  chloral hydrate, puncture, eserine, pilocarpin, friction, massage,
  exercise, dieting, bitters.


_Definition._ A gaseous overdistension of the intestines, from
fermentations in the ingesta, but also in part from air that has been
swallowed, and from carbon dioxide exhaled from the blood circulating in
the intestinal mucosa.

_Causes._ These are to a large extent the same as those of gastric
tympany. General and digestive debility resulting from former disease,
from spare diet, from unsuitable or indigestible food, from anæmia, from
parasites, from hemorrhages, is a potent predisposing cause.

Weakness of the alimentary canal from catarrh, or other persistent
disease, from impaired innervation, from embolism of the vessels and
imperfect circulation also predisposes, or again the lack of vermicular
movement and of the mingling of the digestive fluids with the food,
leaving the latter in a specially fermentescible condition. As direct
_exciting causes_ may be named:

Very _fermentescible food in excess_, such as the leguminous products
(beans, peas, vetches, cowpea, alfalfa, sainfoin, clover) in their green
condition. These contain an excess of protein compounds, which should be
mainly digested in the stomach, and if passed rapidly in large quantity
into the intestines, they fail to be sufficiently acted on by the
trypsin, and are specially liable to fermentation. Very rapidly grown
and aqueous grasses are similarly liable to decomposition.

_New grain_ is specially liable to fermentation the more so that it
sometimes contains a paralyzing agent, which acts like intoxicating
ryegrass. The ripening seeds of many forage plants often act in this
way, (annual and perennial ryegrass, millet, Hungarian grass, chick
vetch, vetches generally). The same has been observed of the leaves of
growing maize, grapevine leaves, and potato plants.

_Musty and spoiled fodders_ of all kinds are very dangerous, the toxic
principles of the fungi and bacterial ferments paralyzing the
sympathetic nervous filaments.

_Fodders_ that are _imperfectly masticated and insalivated_ owing to
defective teeth or diseased jaws or glands are liable to prove hurtful
in a similar way.

_A full drink of water_ and especially of ice cold water _after a feed
of grain_ is one of the most potent factors. The stomach and intestines
are both roused to violent peristaltic action, the undigested food is
washed on into the bowels, and too often the action of the cold induces
congestion and partial paresis, and exposes the undigested mass to the
uncontrolled action of ferments.

_Circulatory troubles_ caused by verminous embolism (see intestinal
congestion) is another very prolific factor. _A sudden chill_ in an
animal that is perspiring and fatigued may precipitate an attack, by
causing a retrocession of blood from the skin to the intestines, with
resulting paresis of their coats.

_Symptoms._ The condition is usually complicated with gastric tympany,
so that we have a complication of symptoms. The history of the case is
often diagnostic, showing one of the above mentioned causes, and above
all a full drink after a feed of grain, speedily followed by abdominal
pain, gaseous distension of the abdomen, causing death in two hours or
upward. The distension of the abdomen usually shows more on the right
than the left, and the resonance on percussion is greater. Colics are
usually less violent than in intestinal congestion, and the actions of
the animal are less precipitate or disorderly. He may lie down, roll and
rise, but the constant restless movement, the sitting on the haunches,
and the frequent agonized turning of the nose toward the flank are
rarely shown. The animal is rather dull and prostrate, passing finally
into a stupor, the face is pinched and anxious, the back arched, the
head pendent, the walk slow and unsteady, and respiration and pulse
accelerated. There is no complete intermission of pain, though it is
more acute at one time than another, for some time there is rumbling in
the bowels followed by complete silence, as they are fully paralyzed,
fæces may be passed at first, but this ceases as the floating colon is
emptied and the gaseous distension becomes extreme, and urination which
may take place in the early stages is no longer effected in the advanced
ones. The compression of the thorax causes severe dyspnœa, accompanied,
when the patient is down, by a slight groan.

_Course_. In the advanced stages the animal may sink to the ground
oppressed by the shock, poisoned by the carbon dioxide which can no
longer be exhaled through the lungs, and by hydrogen sulphide and other
toxic products of intestinal fermentation. Death may follow two hours
after a hearty meal and is rarely long delayed in fatal cases.

Improvement may be recognized by the termination of the paresis, the
lessening of the abdominal tension, the return of the rumbling in the
abdomen, the passage of fæces and flatus, and of urine and by general
relief.

_Lesions_. In case of death the overdistension of the intestines and
abdomen is the most marked lesion, the composition of the gas varying
with the nature of the ingesta and the duration of the illness.
Carburetted hydrogen compounds abound as a rule in the early stages,
while carbon dioxide predominates later. Pinner found 49 per cent. of
carburetted hydrogen, 8 per cent. of carbon dioxide, and 42 per cent. of
nitrogen.

The contents of the large intestines are usually in considerable amount
and in an undigested condition. The walls of the distended bowels are
greatly attenuated and may show congestion, petechiæ, or rupture.
Rupture of the diaphragm is not uncommon. Congestion of the lungs, but
especially of the skin and superficial structures of the body, and of
the brain are natural results of the expulsion of blood from the
abdominal cavity.

_Treatment_. The desiderata are: relief from existing gaseous tension;
arrest of further fermentation; and the restoration of the vermicular
movement of the intestine.

The two first indications may sometimes be successfully met by
stimulants and antiseptics. Formerly, mild cases were successfully
treated by oil of peppermint and oil of turpentine in oil, and a free
use of enemata. A more modern resort is a large (virtually soporific)
dose of chloral hydrate (1 oz.) given in solution. This is at once a
powerful antiferment and an antispasmodic. It is moreover highly
volatile and in the heat of the stomach is readily passed on into the
duodenum and absorbed. Employed early it not only checks the production
of gas, but it relaxes the whole intestinal tract and allows the free
passage of accumulated gas which passes off rapidly per anum.

But in severe cases the gaseous distension is too great to hope for
relief by such measures and puncture of the cæcum or double colon is the
only hopeful resort. This is made with a small trochar and cannula not
more than ¼ inch in bore, which is inserted at the point of greatest
resonance. The point usually advised, as in the ox, is the centre of the
space circumscribed by the last rib, the ilium and the transverse
processes of the lumbar vertebræ. A better plan is to percuss and
puncture the point where the drumlike resonance is greatest. The higher
the puncture the more promising as the cannula is less likely to be
blocked by the ingesta which accumulates in the lower part of each
viscus. The cannula may be left in place for some time to keep the bowel
flaccid and allow time for the restoration of its contractile functions.
The cannula may be utilized to inject antiferments (chloral) and
peristaltic stimulants (eserine, pilocarpin, barium chloride). In cases
in which puncture is not imperative these agents may be used
hypodermically, eserine 1½ gr., pilocarpin 2 grs. or barium chloride 7
grs.

Enemata of soapsuds, with or without stimulants prove effective in
emptying the floating colon and soliciting the action of the large
intestines generally and the passage of flatus. Friction of the abdomen
and walking exercise are desirable. After recovery a restricted diet,
laxatives and bitters serve to restore the lost tone of the alimentary
canal.




 ACUTE INTESTINAL INDIGESTION WITH IMPACTION OF THE LARGE INTESTINES IN
                               THE HORSE.

  Definition. Causes: dessication of ingesta in colon, sacculation,
  constriction at pelvic flexure, debility, ill health, local
  peristalsis, diseased teeth, jaws or salivary apparatus, excess of
  food, heating grain, hard fibrous indigestible fodder, green
  leguminosæ, privation of water, inactivity, verminous aneurisms,
  tumors, strictures, obstructions. Symptoms: colics after meals,
  becoming more severe, tension and firmness of right side, sitting on
  haunches, stretching, small, hard, dry coated stools, obstruction felt
  on rectal exploration, frequent attempts to urinate, tympany. Course:
  six hours to six days or more, signs of aggravation and improvement.
  Lesions: large intestines tympanitic, impaction often at pelvic
  flexure, or other constriction, adherent mucosa has thick mucus or
  blood, is discolored, friable, necrosis, perforation, liquid contents
  of distended bowel in front, rupture, invagination, volvulus.
  Treatment: laxative diet, injections, aloes, pilocarpin, eserine,
  barium chloride, chloral hydrate, morphia, henbane, belladonna,
  puncture, cold or oleaginous enemata, empty or knead rectum and colon,
  cold compress, electricity, friction, laparotomy.


_Definition._ This is an impaction and obstruction of the colon, and
usually of the pelvic flexure with dried and badly digested alimentary
matters.

_Causes._ Certain anatomical and physiological conditions contribute to
this disease in the horse. The ingesta as it leaves the stomach is
liquid or pultaceous and throughout the small intestines it remains so,
so that they are little liable to impaction. But by the time the cæcum
is reached much of the liquid has been absorbed, and as the contents
pass into the double colon they are usually a soft solid, which
gradually becomes dried as it advances through the double and floating
colon. The sacculation of cæcum and colon tends to delay the masses and
favors absorption. The pelvic flexure, the narrowest part of the double
colon, is formed by an acute bend of the viscus on itself so that the
dried masses advancing from in front are especially liable to become
arrested and impacted at this point. Impaction may, however, occur at
any part of the large intestine.

Any debility or atony of the intestines predisposes to the condition.
The ingesta accumulates in the portion which does not contract
sufficiently to pass it onward, and this soon becomes distended to a
state of absolute paresis. All conditions of debility, and all prolonged
ill health tend to operate in this way by lessening vermicular movement.

Again in cases of nausea or intestinal disorder the supervention of
antiperistaltic movements, will tend to accumulate the ingesta at one
point and favor impaction (Ernst).

As in the case of other indigestions the imperfect preparation of the
food is an active factor. Diseased teeth, jaws or salivary glands, act
in this way and a functionally weak stomach contributes to this as to
other intestinal disorders.

An excess of food and especially indigestible food will contribute to
impaction. Heating grain, like corn, wheat, buckwheat, passed rapidly
through the stomach in an imperfectly digested condition, tends to
accumulate in the larger intestines. Hard, fibrous fodders like hay and
straw that have run to seed, or which have been washed out by rains,
bleached or heated, rye-straw, the stalks of beans, peas, vetches, which
have been similarly spoiled, and clover hay affected with cryptogams or
other ferments act in the same way. Even clover eaten green, produces in
foals impactions to which the hairs of the leaves and chalices
materially contribute (Verrier). The allied plants alfalfa and sainfoin
when passed rapidly through the stomach tend to impaction of the large
intestines. But any fibrous, indigestible and innutritious fodder, taken
in excess to make up the deficiency of nutriment is liable to act in
this way.

Other conditions that contribute to impaction are lack of water,
especially at night when much hay is consumed, and lack of exercise
which tends to torpor of both liver and bowels.

Finally verminous aneurisms and embolism of the intestinal arteries
induce congestion, paresis, spasms, and other disorders which tend to
aggregation and impaction. Also tumors, strictures and obstructions of
all kinds tend to impaction.

_Symptoms._ A certain amount of impaction is not incompatible with
ordinary health, but as this increases all grades of colic may be met
with from the most simple and transient to the most persistent and
severe.

In the milder forms slight and transient colics come on after meals, for
days in succession, before any serious attack is sustained. These are
especially marked under dry bulky fodder (hay), less so on grain, and
less on green food or roots. The animal paws, moves the hind limbs
uneasily, looks at the flanks, he may even kick at the abdomen, lie down
and roll, rise, pass a little manure or flatus, and seeming relieved may
resume feeding, until the next attack. The intermissions may last a few
minutes, a quarter of an hour or longer, and they gradually become more
prolonged until they disappear for the time. Sooner or later, however,
the obstruction becomes more complete and the colic more severe and
persistent. To the ordinary symptoms of violent abdominal pain there are
added symptoms which point to bowel impaction or obstruction. There is a
special tension of the right side of the abdomen, with flatness on
percussion. When down there is a tendency to sit on the haunches to
relieve pressure on the diaphragm and lungs. When standing there is a
disposition to stretch the fore limbs out forward and the hind ones
backward. Fæces may be passed at first in a few small round balls at a
time, but this soon ceases, and very little or none can be obtained even
by the use of enemas. The straining is usually so violent as to expel
the enemata as soon as introduced. The hand introduced into the rectum
can easily detect the solid impacted pelvic flexure of the colon
pressing backward into the pelvis or impinging on the right pubis.
Another common symptom is the frequent passage of urine in dribblets,
due to the irritation of the bladder by the pressure upon it of the
impacted colon during straining. In cases of this kind the colon and
cæcum become tympanitic as first shown by a resonant distension of the
right flank obliterating the hollow in front of the ilium, and later by
a similar condition of the left flank.

The abdominal pain is usually less acute than in simple spasmodic colic
or intestinal congestion. The face is less pinched and anxious, the eye
less frightened, the kicking at the belly less violent, and the lying
down more deliberate and careful. Very commonly the patient merely rests
on his belly or side without attempting to roll.

_Course._ The disease may last six to twelve hours, or even as many days
before it ends in recovery or death. The colicy symptoms usually
increase, with the complication of dyspnœa when tympany becomes well
marked, hyperthermia in case of the supervention of enteritis, and signs
of general peritonitis and collapse in case of rupture of the bowel. A
sudden increase of the pain may otherwise indicate the occurrence of
invagination.

As indicating a favorable termination there may be restoration of the
rumbling, the passage of fæces at first perhaps in the form of solid
cylindroid masses, and later as a mixture of broken up ingesta, liquid
and gas, the tension of the abdomen disappears, the pains lessen and
cease, and there is a gradual restoration to health.

_Lesions._ The abdominal walls are tense and more or less drumlike, and
when these are cut through the large intestines protrude strongly. When
punctured there is a free discharge of gas. The most common seat of
obstruction is the pelvic flexure, but it may occur in the floating
colon, or rectum, in the double colon even at other parts than its
pelvic flexure, in the cæcum or in the ilio-cæcal opening. The impacted
mass is firm, rather dry, covered with mucus and sometimes blood, and
manifestly only partially digested. Its size and form vary greatly as it
is moulded into the affected viscus. The mucosa in contact with the
impacted mass is covered with a thick layer of viscid mucus sometimes
streaked with blood. The mucosa itself is congested, thickened, friable,
and marked with spots or patches of various colors (white, gray, green,)
indicating commencing necrosis. In old standing cases this may extend to
the other coats of the bowel determining perforation or laceration.

The portion of the bowel immediately in front of the obstruction is
filled with liquid which has been forced down upon the barrier by the
active peristaltic movements, and the distension by liquid and gas may
have increased until rupture has ensued with the escape of the contents
into the peritoneal cavity. Invagination, volvulus and peritonitis are
common.

_Treatment._ This will vary according to the stage and degree of the
illness. In slight cases with transient colics only after meals, a more
laxative diet may suffice. Boiled flaxseed, roots, potatoes, apples,
green cornstalks, silage, or even sloppy bran mashes, with an abundance
of good water and active exercise may prove efficient. Copious
injections of warm water, soapsuds, or linseed oil emulsion may be
added.

In the more violent cases we must resort to more active measures and yet
drastic purgatives are full of danger. The free secretion from the
vascular small intestines and the active vermicular movements, lead to
the speedy overdistension of the bowel just in front of the obstruction,
the current being strong and active all around the contracting gut in
contact with the mucosa, while a weaker return current sets in in the
centre, but is effectually checked and arrested at no great distance in
front of the impaction by the strong backward peripheral stream. If
therefore the impaction is not broken up, it is inevitable that the gut
above must be more and more distended until a rupture ensues.

Yet in a certain number of cases a moderate dose of aloes or castor oil
supplemented by frequent enemata and other measures, succeeds in safely
overcoming the obstruction. The solid impacted mass is gradually
softened and removed, and finally after perhaps three or four days of
complete obstruction the fæces begin to pass and recovery ensues.

With or without the aloes, the hypodermic use of pilocarpin or eserine
or both will often succeed in obtaining successful peristalsis. Barium
chloride while inducing more active peristalsis is, on that account,
somewhat more dangerous.

Pain may be moderated and fermentation checked by chloral hydrate (½
oz.), or, an anodyne, morphia (2–4 grs.), may be given hypodermically.
In the absence of these, extract of hyoscyamus or belladonna (2 drs.)
may be given by the mouth, and repeated as may be necessary. If tympany
is dangerous use the trochar and cannula. Enemata and other accessory
measures must not be neglected.

W. Williams has resorted to rectal injections of 2 oz. aloes forced into
the rectum by a syringe furnished with a long elastic tube, and repeated
when expelled. Brusasco has used copious liquid injections poured into a
rectal tube the end of which is raised at least ten feet above the
croup, so as to gain the requisite force. Schadrin uses injections of
cold water to stimulate the bowels to contractions. Injections of oils
or mucilaginous matters when they can be carried far enough lubricate
the walls and favor the passage of solid matters. Castor oil which acts
to a large extent locally is especially applicable.

Mechanical applications are often valuable. If the obstruction is lodged
in the rectum or floating colon it can usually be reached by the oiled
hand and carefully extracted. If this is not successful, impactions in
the floating colon or pelvic flexure may still be to a large extent
broken up and loosened by the knuckles of the oiled hand in the rectum.
I have often resorted to this with excellent effect. Impactions in the
cæcum or elsewhere in the double colon are however inaccessible for such
treatment. For these, external measures are available. Wilhelm wraps the
abdomen in cold compresses. Causse and Lafosse recommend the electric
current. Friction to the skin of the abdomen is a common resort.
Rudofsky turns the animal on his side or his back, to remove the weight
of the small intestines from the impacted cæcum or colon, and favor the
exit by gravitation of the contents from the cæcum into the colon.
Kneading of the abdomen with the fists or knee when in this recumbent
position may also be resorted to.

As a _dernier resort_, Gaullet performed laparotomy but with no success
as the animal died the following day. The horse was, however, in
extremis at the time of the operation and a portion of the intestinal
wall was blackish and gangrenous. To be successful such an operation
should be practiced before there is any probability of gangrene, and
while the patient is still in good condition for recuperation. But these
are just the cases in which success is to be hoped for from less
dangerous measures. Again the conditions for its success are best in
case of obstruction of the pelvic flexure, as that could easily be drawn
out through a spacious abdominal wound, incised, emptied and sutured
with careful antiseptic precautions, and with little risk of infection
of the peritoneum. But this is just the point where an obstruction can
be efficiently dealt with in a less dangerous way, by kneading through
the rectum for example. The operation, however, is not one to be utterly
condemned, but in any case in which it is certain that the obstruction
is otherwise irremediable, it should be adopted at as early a stage as
possible, under anæsthesia, and with antiseptic precautions. The after
treatment would consist in a restricted diet of milk or gruel with
antiseptics to prevent fermentation and bloating.




                  IMPACTION OF THE COLON IN RUMINANTS.

  Causes: Debility, hard, fibrous food, dry winter feeding, privation of
  water, astringents, smut, ergot. Symptoms: Hard, moulded, coated dung,
  blood-streaked, and in small quantity, tympany, dullness, debility,
  splashing sound when right flank is pressed, rectal exploration.
  Treatment: Laxative food, water, salt, strychnia, eserine, barium
  chloride, enemata, oils.


This is not a common affection in cattle, yet it does occur in weak and
debilitated conditions, and in animals fed on fibrous and innutritious
aliments. The ingesta are delayed in the gut, their liquid portion
absorbed and the remainder accumulates in a hard mass, which distends
and weakens the bowel. Dry winter feeding, with a scarcity of water
strongly contributes to its production. Astringent plants in the hay, or
smut or ergot may add to the tendency.

_Symptoms._ The fæces are hard and firm, glazed on the surface, coated
with mucus and sometimes stained with blood. They are passed in small
quantity and with much effort and straining, and finally the bowels
become completely blocked, nothing whatever being passed. Tympany of the
rumen now appears, especially after feeding, appetite and rumination
fail, there is much dullness, debility, and loss of flesh and unless
relieved, the animal dies in marasmus. Pressure on the right side of the
abdomen made suddenly and forcibly produces a sound of liquid splashing
in an air space, derived apparently from the accumulation above the
obstruction. The oiled hand introduced into the rectum may feel the
solid impaction, but in any case causes pain and moaning when the seat
of the impaction is pressed upon.

_Treatment._ In the milder cases and earlier stages a change to sloppy
food, green food, or boiled flaxseed, with plenty of salt, free access
to water, and scruple doses of nux vomica may prove successful.

In the more advanced conditions with complete obstruction, give ½ lb. to
1 lb. each of sodium chloride, and sodic sulphate, and ½ dr. nux vomica,
inject hypodermically 3 grs. eserine or 7 grains barium chloride, give
water _ad libitum_, and frequent and large injections of soapsuds. If
these latter are given cold they will still further stimulate the
missing peristalsis. In obstinate cases a second dose of the salts, or 1
quart of castor oil may be given with the addition of 20 drops of croton
oil.

When relief has been obtained, a laxative and nutritive diet and a
course of bitters should follow.


          INDIGESTION WITH OBSTRUCTION OF THE COLON IN SWINE.

  Causes: green leguminosæ, dew, rain, dry indigestible food, lack of
  water or exercise, debility, torpid liver. Symptoms: firm, small,
  coated stools, obstruction, straining, tympany, rumbling, vomiting,
  anorexia, lies on belly, secludes himself, restless, grinding teeth,
  diarrhœa. Diagnosis from hog cholera. Treatment: laxatives, enemata,
  antiferments, rubbing, massage, mechanical unloading of rectum,
  puncture, dieting, bitters.

_Causes._ The leguminosæ in their green state are liable to produce
indigestion and flatulence in the pig. If covered by dew or rain this
tendency is increased. Dry, fibrous or indigestible food with privation
of water and of exercise tends to intestinal impaction. Debility from
any cause, by weakening the contractility and secretory power of the
bowel strongly predisposes to this condition. Torpid liver with
diminished secretion of bile is another common factor.

_Symptoms._ The defecations are infrequent, and small, and covered by a
mucus film on a glazed surface. This increases steadily until they cease
altogether, when straining, tympany, rumbling and vomiting follow. The
animal refuses food, and lies on its belly, hiding under the straw when
that is available. Restlessness with frequent change of place and
grinding of the teeth are noticed. A spontaneous cure may take place by
a free secretion of liquid in which the impacted mass is loosened,
disintegrated and floated off, the costiveness being succeeded by
diarrhœa. Once established this diarrhœa may become persistent, causing
serious loss of condition, and simulating hog cholera. It may be
distinguished by the fact that it occurred without the introduction of a
_contagium_, is easily accounted for by the nature of the food and is
not communicated to adjacent herds treated in a different way. There is
also the absence of the petechiæ on the skin, and, on post mortem, of
the specific round necrotic intestinal ulcers of hog cholera.

_Treatment._ The first object is to rid the intestines of the irritating
impacted masses, and this may be secured by giving 1 oz. castor oil, 2
drs. jalap, or 3 grs. croton farina to a 150 lb. pig. This may be
seconded by frequent and copious injections of soapsuds. If fermentation
and tympany are troublesome 30 grs. chloral hydrate may be given and
repeated as circumstances demand it. Active rubbing of the abdomen or
kneading of the same will prove useful. If tympany becomes dangerous the
gas may be safely evacuated by trochar and cannula, the point of
puncture being selected by the clearness of the resonance. When the
impaction has reached the rectum and prevents the use of enemata, it may
be extracted with the oiled fore finger. An injection of sweet oil may
then be given and the finger may be used again and again as the impacted
fæces come within reach. When diarrhœa has set in it may be checked by
doses of 30 to 60 drops of laudanum, and a diet of boiled milk, well
boiled flaxseed or other starchy gruel or mush. A course of bitters with
chalk, bismuth or antiseptics will prove serviceable during
convalescence.


          INTESTINAL INDIGESTION IN THE DOG WITH CONSTIPATION.

  Usual seat. Causes: house life, neglect of call to defecate, lack of
  exercise, overdistension, atony, watch dogs, over feeding, obesity,
  ill health, debility, loss of teeth, paraplegia, spiced and sweet
  food, matting of hair over anus, tumors round anus. Symptoms: small,
  hard, white, glazed stools, straining, no stools, hot, tender,
  swollen, bulging anus, abdominal manipulation, dullness, laziness,
  seeking seclusion, colics, tender abdomen, stiffness, arched back,
  drooping head and tail, vomiting—sometimes feculent, fever. Lesions:
  impacted mass of hard, gritty particles, catarrhal congested or
  necrotic mucosa, and outer coats, perforating ulcers. Treatment: air,
  exercise, laxative diet, mechanical extraction, purgatives, enemata,
  demulcents, laparotomy, enterrectomy.

In the dog, atony and impaction are common especially in the rectum,
where the fæces are unduly retained in connection with house life until
accumulated and dried. The impaction tends to extension forward, the new
material adding continually to the old, and the overdistended rectum
becoming more and more atonic in proportion to the increase of the
distension.

_Causes._ The most prominent factor is denial of nature’s call to
defecate, on the part of house dogs trained to habits of cleanliness.
The accumulated mass distends and weakens the rectum, enabling it to
hold more without suffering, making the call of nature less imperious,
and diminishing the power of expulsion. Lack of exercise usually
operates in the same animals, as it also does in watch dogs, the
movements of which are limited by the length of their chains.

Overfeeding contributes, in various ways, by increasing the amount of
feculent matter passed on into the rectum, by hastening the food through
stomach and small intestine imperfectly digested and therefore in a more
irritating condition, and by contributing to obesity and lack of tone.

In mastiffs, hounds, bull-dogs, etc., which are naturally gluttonous and
swallow animal food in large masses without tearing apart, or
mastication, portions pass into the intestine undigested and tend to
disturb and block the terminal bowel.

Dogs that are out of health, and which lack tone in general have usually
torpid bowels and suffer from delay and impaction of contents. Hence all
chronic and debilitating diseases are liable to become aggravated by
this troublesome complication.

Old dogs with the teeth worn out and the general tone of the stomach and
intestines low are habitual sufferers.

Paralysis of the posterior limbs is usually associated with paresis of
the rectum and accumulation, and various other atonic nervous disorders
act in the same way.

The sympathy between the skin and alimentary tract shows itself in
common disorders, indigestions and catarrh becoming complicated by skin
eruptions acute and chronic, by indigestions and impactions. To both
conditions the nature of the food of house dogs largely contributes, the
habit of eating abundantly at each meal time of the master, the
consumption of highly spiced meats, of sweet cakes, pastry and puddings,
and even the exclusive diet of white bread or farinaceous and starchy
aliment.

In long haired dogs, the matting of these hairs together across the anus
proves a factor by rendering defecation difficult and painful.

The formation of tumors around the anus, or inflammation and swelling of
the anal glands are additional causes.

_Symptoms._ As in other animals this condition may be chronic, lasting
for a long time without leading to complete obstruction. The fæces are
passed in hard fœtid, whitish masses, often partly divided, in pellets,
dry, and polished on the surface and covered with a film of mucus,
sometimes blood. They are passed at considerable intervals, slowly and
with painful effort and straining.

In the more advanced and violent cases defecation becomes absolutely
impossible, though the animal strains violently and frequently. The anus
and rectum bulge as a rounded swelling and the congested and bleeding
mucous membrane may be exposed, but nothing is passed. The anus is hot
and tender to the touch and the anal glands swollen. Manipulation of the
abdomen between the two hands can detect the impacted gut extended
forward for a considerable distance, and even implicating the colon. The
oiled finger in the rectum may detect the impacted matter as a
conglomerate mass of gritty materials. If the appetite continues this
becomes all the more extensive. The affected animal is dull, prostrate
and indisposed to exertion, seeking a dark retired place where he can
rest undisturbed curled up into a ball. Sometimes he starts with a sharp
yelp. Especially does he shrink and complain when the belly is handled.
If made to walk, he does so stiffly, hangs head and tail, arches the
back and tucks up the belly. The face and eyes express severe suffering.
Vomiting is a frequent complication, the rejected matters being often
feculent. Colicy pains are indicated by yelping or moaning, enteritis
and peritonitis by hyperthermia and extreme abdominal tenderness. The
acute disease may last from one to two weeks, and death may be preceded
by auto-infection, by nervous symptoms of various kinds or by enteritis
or peritonitis.

_Lesions._ These may be stated shortly as impaction, catarrh or necrotic
changes of the mucosa, more or less extensive inflammations of the
bowels and peritoneum, perforations, and congestions of the liver and
kidneys.

_Treatment._ In the milder cases plenty of open air exercise and a
laxative diet may succeed. In the more severe cases it is usually
requisite to unload the rectum mechanically. The dog is laid on a table,
and the oiled finger introduced through the anus, lubricates the mucosa
as far as it can be reached. Then little by little the firm mass may be
disintegrated and removed being steadied by the other hand applied on
the abdomen. The handle of a teaspoon or a special spoonshaped curette
may at times replace the finger to advantage, but must be used with due
judgment, in view of the thinness and friability of the walls of the
gut.

When the gut has been emptied in this way, or in the less severe cases
without this preliminary, purgatives and frequent injections can be used
to advantage. Jalap ½ dr. and calomel 5 grains, or castor oil ½ oz., or
syrup of buckthorn have been usually employed. The impaction is usually
too firm for the transient action of eserine or pilocarpin. As
injections, castor oil, soapsuds, decoctions of flaxseed, mallow or elm
bark may be employed being repeated as often as they are expelled and
supplemented by the mechanical removal of all solid matters that come
within reach.

In cases so extensive as to resist the above measures we can resort to
laparotomy. The incision can be made close and parallel to the linea
alba, the rectum, or floating colon drawn out through the wound, the
other intestines being carefully held back by an assistant, the gut is
then incised longitudinally and its solid contents removed. The wound is
thoroughly cleansed, washed with an antiseptic (mercuric chloride
1:2000), and sutured with catgut, the mucosa being carefully turned in
and the muscular and peritoneal coats kept in accurate contact. Finally
the abdominal wound is closed by silk sutures. The patient must be
placed for a week or ten days on well boiled gruels and the rectum
frequently emptied by injections of tepid water.

In case the bowel is found to be necrotic, the gangrenous section may be
excised and the ends brought together by Murphy’s button, or simply
sutured with catgut over a hollow tube of raw potato.




            INTESTINAL INDIGESTION AND OBSTRUCTION IN BIRDS.

  Causes: Age, debility, atony, matting of feathers, dry or indigestible
  food, lack of water, diseased oviducts, sand or gravel, lack of
  pebbles or power in gizzard. Lesions: masses of egg, uric acid, or
  fæces in cloaca, implicating colon and cæca. Symptoms: dullness,
  stupor, vertigo, staggering, erect plumage, trailing wings and tail,
  bulging anus, covered with matted feathers, impaction felt by finger.
  Treatment: extract mass, castor oil, laudanum, chalk, bismuth, pepper,
  demulcents, phenol, exercise, silage, green food, pebbles.


_Causes._ These resemble those already noted for the dog. Old age,
debility, and atony of the bowel, the matting together of feathers
across the anus, dry feeding, indigestible food, scarcity of water, and
lack of exercise are especially to be noted. Malformations or other
changes lead to obstruction of the cloaca, and of defecation. Sand and
gravel passing from an atonic gizzard accumulate in the small intestine
or in the cæca distending them to great excess. Imperfect trituration in
the gizzard, from lack of pebbles, may prove a factor in stoneless
prairies.

_Lesions._ The most common seat of obstruction is at the cloaca, and the
impacted matter may be yellow partaking of the nature of yolk of egg, or
it may consist of feculent matters and uric acid in various proportions,
white, hard and fœtid. As in the dog this distension may be continued
forward blocking the colon and cæca as well. Lucet mentions a case in
which the impacted mass measured seven inches long, and eight in
circumference at its posterior and larger end.

_Symptoms._ The bird is dull, sluggish, stupid, giddy or unsteady on its
limbs, with feathers erect, wings, tail and head pendent and loses flesh
rapidly. Often a felted mass of feathers and fæces cover the anus. In
its absence there appears the rounded swelling or on manipulation the
impacted cloaca or rectum can be felt firm and resistant.

_Treatment._ Soften and remove the external mass of fæces by the aid of
tepid water, clip off the feathers, which would tend to restore it, then
by the oiled finger and warm water injections break up and extract the
contents of cloaca and rectum. If impaction remains farther forward give
a teaspoonful of castor oil. If diarrhœa has already set in, give 5
drops laudanum, and mix chalk or bismuth and pepper in a mush to be fed
to the patient. Injections of slippery elm containing a teaspoonful of
carbolic acid in the pint will prove useful.

The bird should be allowed plenty of exercise, its grain being fed on a
floor covered lightly with straw to encourage scratching, and silage or
green food should be allowed. On the prairies where pebbles cannot be
secured, imported gravel or vitrified brick broken into small pieces
should be allowed.


   COLIC IN SOLIPEDS FROM VERMINOUS EMBOLISM. INTESTINAL CONGESTION.

  Definition. Causes: presence of sclerostoma in arteries, form, habit,
  nature, immature, biology, life in bowel, in submucosa, in arteries,
  outside the mammal, pathogenesis, blood-sucking, verminous cysts,
  verminous aneurisms, seats of latter, coagula, embolism, stagnation of
  blood, œdema and thickening of intestine, mesentery, fermentations,
  tympany, infective inflammations, blood extravasations, infection of
  liver and spleen. Symptoms: sudden attack, violent colics, reckless
  movements, frequent defecation followed by its arrest, palsy of
  peristaltic movement, of pain, prostration. Course: two to twenty-four
  hours, death from indigestion, tympany, obstruction, hemorrhage,
  poisoning, recovery, sequelæ, laminitis, intestinal catarrh or atony,
  debility. Treatment: aneurism worms beyond reach, treat lesions,
  venesection, anodynes, stimulants of peristalsis, antiseptics,
  compresses, sinapisms. Prevention: expel intestinal worms, exclude
  embryos, tartar emetic, iron sulphate, arsenic, phenol, pure water,
  occasional vermifuges.

_Definition._ Congestion and spasms of the intestines in connection with
blocking (thrombus or embolism) of the mesenteric arteries, and
verminous aneurism.

_Causes._ The essential cause is the migration of the sclerostoma
equinum (strongylus armatus, Rud.) into the mesenteric arteries in its
agamous condition. It seems appropriate therefore to here notice the
life history of this parasite.

The =sclerostoma equinum= (_strongylus armatus_) is one of the common
pin worms of the horse. It is distinguished by its dull gray or reddish
brown body, thickest at the cephalic end and tapering off toward the
caudal, but ending in a blunt point; by the round, open mouth furnished
with several firm chitinous rings, of which the _outer_ bears six short
symmetrically arranged papillæ, an _intermediate_ row of rounded blunt
tooth-like projections, and the _innermost_ a row of fine, closely
aggregated and very sharply pointed teeth for penetration of the mucosa.
Male ¾ to 1½ inches long, with caudal membranous alæ in two lateral
lobes, joined by a rudimentary central lobe: two delicate spicula.
Female ¾ to 2 inches long, blunt pointed tail, vulva in posterior half
of the body. Eggs ovoid with slightly raised ring around the centre:
oviparous.

_Habitats._ They are found in solipeds in two stages of existence, the
_mature worms_ in the cæcum and colon, and the _immature_ in the same
organs encapsuled in little pellets of manure, and in cysts in the
mucosa but also apart in the arterial system especially in the anterior
mesenteric artery and other gastric or intestinal trunks.

The =mature sclerostomata= are found attached to the mucosa of the large
intestine into which the head is sunk for the purpose of sucking the
blood, and they may be gray, brown or red according to the quantity of
blood which they have imbibed. The author has found them in little
hernial sacs of the mucosa hanging from the peritoneal surface.

The =sexually immature sclerostomata= are found in little pill-like
masses of ingesta in the large intestines and from which they project
part of the body through a narrow opening. Another habitat is in cysts
of the mucosa of the cæcum and colon and less frequently of the small
intestine, individual cysts varying in size from a pin’s head to a hazel
nut, and containing the young worm rolled upon itself, and varying in
size but always less than the intestinal worm and always asexual. In
some cases the cyst is found empty but with a small opening toward the
lumen of the bowel showing the means of escape of the parasite. A third
habitat of the immature worm is in the blood-vessels, especially the
posterior aorta and its divisions, and still more constantly the
anterior and other mesenteric arteries.

=Biology.= The ova of the sclerostoma are segmented in the oviduct but
are hatched out after they have been laid. The hatching may be effected
in the intestine or in manure or water external to the body. When
hatched out in the intestine they may pass out at once with the manure
or they may envelop themselves in pellets of the finer ingesta and
remain for a time in the bowel and finally pass out in this condition.
Baillet has traced their development out of the body. In a watery or
damp medium they are hatched out in a few days as a cylindroid worm ¼ to
⅓ mm. long, thick in front and with a filiform tail. In moist
environment but especially in damp manure they grow to 1 mm. or 1.5 mm.
and continue for months in this condition, but remain small and asexual,
until taken in, in the drink or green food of the soliped. Reaching the
intestine and especially the cæcum and colon they bore their way into
the mucosa and encyst themselves, or if they happen to perforate a
blood-vessel they make a habitat of that. In the cyst, development
proceeds and when it has reached a certain stage the worm once more
bores its way through the mucosa and reaching the intestine becomes
sexually mature.

In this last migration the young worm is liable to perforate a
blood-vessel in which case it is destined to a period of existence in
the blood. It may, however, have blundered upon a blood-vessel at an
earlier stage when seeking a temporary home in the mucous membrane, so
that the sclerostomata of aneurisms may be derived from two separate
sources. In the blood-vessels the parasite attains a length of 1 to 8
lines, whereas in the mucous cysts it does not exceed 3½ lines. Yet
Neumann holds that after leaving the blood-vessels they may again encyst
themselves in the mucosa before escaping into the intestine.

Several moultings take place in the asexual condition.

Other views have been advanced as to the development of the
sclerostomata. Colin believed that the ova deposited in the ducts of the
mucous glands and in the perforations made by the parasite in
blood-sucking, hatched in this situation and the embryo at once encysted
itself in the mucosa.

Leuckart imagines that the embryo found in the fæces or in water outside
the body of the soliped, should pass through an intermediate host before
it can return to gain sexual maturity in the horse. But no evidence of
the existence of such intermediate host is furnished, and the encysted
intestinal worms show no indication of a special development which would
have been accomplished in such host.

Willach holds to a hermaphrodite stage passed in the intestine of the
soliped. He found in the bowel small worms apparently related to the
sclerostomata by the appearance of the head and the caudal membrane, but
not exceeding three to five lines in length. Some were evidently females
and contained not only eggs with soft shells, but in one case embryos.
Others had the caudal membrane of the male, yet contained also a few
eggs. There is no vulva and the embryos escape by rupture of the
oviducts. These embryos he supposes are developed in the same host into
the familiar mature sclerostomata.

Whatever may be said of those alleged modes, the first described series
of changes and migrations may be taken as the usual and regular method
of development.

=Pathogenesis.= _Lesions._ These embrace perforations of the mucosa,
cysts, aneurisms, embolisms and congestions.

=Irritation of the mucosa.= The adult worms, like so many leeches are
continually biting and sucking blood from the mucosa and when present in
large numbers, hundreds, thousands, or a million create an aggregate of
irritation which may determine violent indigestions and congestions.

=Verminous Cysts.= These are like a pin’s head, a pea or hazel nut,
containing the asexual worm in a mass of purulent debris, or if empty,
presenting a small orifice where it made its exit.

=Verminous Aneurisms.= These are perhaps the most important lesions
caused by the sclerostome as they are the steppingstone to the dangerous
embolisms, and too often fatal colics and congestions of the intestines.
They are very common in some localities, and rare in others following
the distribution of the sclerostomata. Bollinger found them in 90 to 94
per cent. of adult horses, and Ellenberger in 84 out of 85 horses
dissected. They are found in all ages from six months up, and are nearly
always in the short, stubby trunk of the anterior mesenteric artery.
Often two or three exist in the same animal, the whole length of the
posterior aorta showing patches of disease, exudations, neoplastic
elevations alternating with depressions, and aneurisms and thrombosis in
its different branches. In 100 horses Bollinger found 168 aneurisms, 153
in the anterior mesenteric, and its divisions, 4 in the cœliac axis and
its divisions, 3 in the hepatic artery, 3 in the posterior mesenteric
artery, 3 in the renal arteries and 2 in the posterior aorta.

The special predisposition of the anterior mesenteric artery is
variously accounted for: 1st. There is the obvious fact that its
branches are distributed to the cæcum and double colon, the home of the
mature parasite, and to the small intestines which are first reached by
the young parasites that are taken in with the water and the food. These
are therefore most likely to get into the branches of this vessel and to
follow them up toward its origin. 2nd. The anterior mesenteric artery
distributes its branches to the small intestines the most motile portion
of the intestinal tract, and the cæcum and colon the most heavily loaded
with solid ingesta, it is therefore the most subject to traction, and
distensions, and the more so that the parent trunk is extremely short
and the divisions pass in all directions and to a large extent at right
angles, so that there is a dragging of the walls apart as well as an
obstruction to the blood flow and an increase of internal tension. The
distension, laceration, inflammation and softening of the internal coat
have accordingly been regarded as the starting point of an endarteritis
upon which the parasites have been implanted as a further cause of
trouble. We must not forget, however, that the sharp circle of teeth of
the parasite, by which it fixes itself on the intima of the vessel are
quite enough to produce initial endarteritis, without any assistance
from distension, traction or laceration.

The irritation of the intima from whatever cause determines here as
elsewhere exudation, and coagulation, and the inflamed walls losing
their tone yield more and more readily to the internal tension.
Sometimes the coagulum lines the aneurism or vessel all round, leaving a
narrow central passage through which the blood still flows; in other
cases the clot extends into the adjacent smaller vessels, completely
blocking them and disturbing circulation and innervation in the parts
which they supply. As a rule the parasites are found in galleries
hollowed out in the clot, and heads or tails may be seen to project into
the circulating blood. Sometimes they are found imbedded in the arterial
coat, or in an adjacent small abscess. The formation of aneurisms in the
other arterial trunks may follow the same method.

=Embolisms.= These come very naturally from the formation of thrombi in
the various arteries. The coagulum determined by the presence of the
worms, tends to undergo retrogressive changes notably fatty
degeneration, to which germs brought on the worms or in their alimentary
canals contribute. This together with the movements of the parasites
tends to break up the mass, and minute portions are washed on into the
different smaller vessels. Soon these reach divisions which are too
small to admit them, which are accordingly occluded and the circulation
through them abolished. The presence of microbes as well as fibrine
contributes to cause further coagulation, more absolute embolism and
arrest of the circulation.

It is further alleged that the sexual instinct in the summer months (May
to August) leads the worms to leave the aneurisms, to pass through the
smaller divisions to the cæcum or colon where alone full sexual
evolution is possible. In these migrations they cause the thrombosis of
the smaller trunks and determine the verminous congestions of the bowels
which are especially common in these months.

=Disturbances of the Intestinal Circulation.= As these usually occur in
the lines of distribution of the anterior mesenteric artery a knowledge
of its divisions and their destination and anastomosis, is essential to
an intelligent understanding of the pathogenesis and lesions. As first
pointed out by Lecoq the anterior mesenteric artery is divided into
three primary bundles: (a) a _left_ of 15 to 20 trunks which are
destined to the small intestine; (b) a _right_ which gives off cæcal
branches, one to the double colon, and one to the ilium to anastomose
with the last trunk of the left bundle; and (c) an _anterior_ which
gives one branch to the second division of the double colon and
anastomosis with the colic branch of the right bundle at the pelvic
flexure; and a second branch to the floating colon to anastomose with
the posterior mesenteric artery.

The divisions of the left bundle anastomose so freely with each other in
the mesentery and immediately above the intestine that the blocking of
any one branch cannot entirely arrest the circulation in the
corresponding part of the intestine. It may however produce a partial
local stagnation in the vessels of a short loop of intestine, resulting
in œdematous infiltration and thickening with resulting induration and
stricture of the gut. Chronic and permanent lesions are produced by such
blocking, but only rarely acutely fatal ones. Acute and fatal congestive
lesions of the small intestine from verminous embolism, occur only when
several adjacent divisions of the artery are blocked at once, and this
is a rare occurrence.

The right bundle of branches furnishes the only two arteries which are
supplied to the cæcum and the only artery furnished to the first half of
the double colon. The ileo-cæcal branch is less involved, first, because
being less dependent and smaller, it is less likely to receive an
embolus, and, second, because any lack of blood supply is
counterbalanced by the free anastomosis with the last iliac division of
the left bundle. When the embolus blocks the undivided trunk of the
right bundle this same principle comes into play, the free supply of
blood from the posterior branch of the left bundle supplying blood
through its anastomosis with the iliac and cæcal branches of the right.

But when the emboli are lower down, in the cæcal branches of the right
bundle, or in these and the colic branch, arrest of the circulation in
the intestinal walls ensues, followed by paresis, passive congestion and
hemorrhage. The cæcum and double colon thus become the seats of the
grave and fatal lesions of verminous embolism.

The resulting lesions are to be variously accounted for. The stagnation
of blood in the vessels below the embolus, determines a speedy
exhaustion of its oxygen and increase of its carbon dioxide, so that it
is rendered unfit to maintain the normal nutrition and functions of the
part, and the capillary and intestinal walls are alike struck with atony
or paresis. The blood filters into the stagnant vessels slowly from
adjacent anastomosing trunks, and the liquor sauguinis exudes into the
substance of the tissues and lumen of the intestine, leaving behind the
greater part of the blood globules so that the stagnant blood is
rendered more and more abnormal in composition. The walls of the
capillaries soon lose their cohesion as well as their contractility, and
giving way at different points, allow the escape of blood into the
tissues, bowels and peritoneal cavity. It has been further claimed that
the emboli already infected and in process of degeneration communicate
this to the walls of the vessels and to the stagnant blood, hastening
the process of degeneration and rupture.

Another series of circulatory disorders are liable to take place. The
blocking of the vessels of the right bundle, tends to increase the blood
pressure in the left bundle and the anterior one, and thus to determine
congestions, paresis and inflammations in the small intestines, the
second division of the double colon and the floating colon. The
resulting inflammation and increased vascular tension may lead
indirectly to implications of the brain and lung.

Extravasations so extensive as to appear like blood clots may be present
between the layers of the mesentery or in the mucosa and submucosa, and
blood, liquid or coagulated, may have accumulated in the abdominal
cavity. Blood effusion into the intestine gives a dark red coloration to
the contents which are further mixed with distinct clots.

The atonic bowels are always the seat of extensive fermentations and
tympany. The microbes engaged in these fermentations and their toxins,
are accountable for toxic changes occurring in the locally diseased
parts and in distant organs. To this may be attributed the congestion
and softening of the liver and the engorgements and hemorrhagic centres
in the spleen.

_Symptoms._ An animal, perhaps known to harbor the sclerostoma equinum,
is suddenly attacked with violent and persistent colic. He trembles,
paws, moves his hind feet uneasily, kicks the abdomen, throws anxious
looks at the flanks, crouches, lies down, rolls, gets up, and at once
gets down again. The intensity of the suffering rapidly increases, the
face is drawn and pinched, the eye is extremely anxious, the patient no
longer lies down, but throws himself down reckless of consequences, when
down he is not quiet for an instant, but now on his breast, then on his
side, then on his back, the limbs struggling and jerked violently, the
head turned first to one side and then to the other, he is a picture of
extreme agony. If made to walk the same indications continue; he walks
with head down and limbs semiflexed ready to drop at any moment, and
often he will drop suddenly in spite of every effort to keep him on his
feet. The pulse is at first strong and full, but as extensive effusion
takes place into the bowels or abdomen, or as the animal is poisoned by
toxins, it becomes small, weak, and it may be imperceptible. Breathing
is quick and catching, and the mucous membranes are dark red. Sweating
which shows first about the elbows or flanks or back of the ears finally
becomes general, the surface cold and the limbs especially so. Fæces may
be passed at first, a few dry balls at a time from the floating colon or
rectum, but soon they are suppressed entirely. Some patients strain
frequently to micturate but pass little at a time.

In some instances the acute pain seems to suddenly cease, but there is
no general improvement, the patient stands with head depressed, eyes
sunken and expressionless, ears lopped, cold perspiration, chilly limbs,
unsteady gait and imperceptible pulse. It implies merely a paralysis of
the affected bowels in connection with the extensive congestion and
extravasation.

_Course._ _Duration._ The more acute cases reach their acme with great
rapidity, death may occur after two hours illness, and in other cases it
may be delayed ten or even twenty-four hours. It may be caused by
indigestion and tympany, by volvulus or invagination, by excessive
hemorrhage, or by poisoning with toxic matters.

Recovery occurs when the vessel blocked is an unimportant one as a
branch of the left bundle so that circulation may be reëstablished from
collateral trunks; or when a more important trunk has been but partially
blocked, and after a time it either clears itself, or collateral
circulation comes in with sufficient compensation. There is a more or
less rapid disappearance of the colics and other symptoms, a free
passage of urine, the rejection of fæces, it may be in a liquid,
semi-liquid or sanguineous condition, yet enough to indicate the
restoration of intestinal tone. The patient begins to pick morsels of
food and soon acquires his former appetite.

In some instances, however, the recovery is not complete. Trasbot has
noted a case of laminitis occurring within fifteen hours after the
improvement, and in other cases there remain chronic debility and
catarrh of the intestines. The appetite remains poor, there are
occasional colics, the bowels are irregular, loose or costive, and the
fæces are dry, glossy and covered with mucus. The back is arched, the
belly tucked up, strength and vigor are both lacking, and the patient
spends much time in the recumbent position.

Complications of various kinds may follow as in other diseases of the
intestines. After even the best recoveries, a relapse is always to be
apprehended as the original cause remains and the animal is liable to be
cut off at any time.

_Treatment._ This is very unsatisfactory as the original source of
trouble, the worms, being in the blood-vessels, cannot be reached by
vermifuges that would be harmless to the host, and clots blocking the
smaller intestinal vessels, cannot be dissolved and removed. Moreover,
although we could compass the death of the worms in the aneurisms, we
would leave their dead bodies as sources of septic change, blood
coagulation and embolism.

A certain number of cases, however, are not necessarily fatal, and the
worms of the blood-vessels have not an indefinite period of life, so
that there is some encouragement for both therapeutic and preventive
treatment. During the attack we must be content to treat symptoms.
French veterinarians still trust largely to general bleeding, adopted at
the very outset and to the extent of 6 to 10 quarts. It will temporarily
lessen the vascular tension, more permanently dilute the blood, and calm
nervous excitement, and in the most violent cases, as a kind of forlorn
hope, it might be tried with the view of tiding over the acute stage
until a freer collateral circulation could be established.

The use of anodynes will be more generally acceptable to American
practitioners. Two to four grains of sulphate of morphia or codeine may
be given hypodermically in combination with 1½ gr. eserin, 7 grs. barium
chloride, or 2 grs. pilocarpin, to secure a speedy movement of the
bowels.

To counteract intestinal fermentation perhaps no better agent can be got
than chloral hydrate, ½ oz. of which may be given by the mouth in water,
and ½ oz. more by the rectum.

Wet compresses to the abdomen, or fomentations with water rather hotter
than the hand can bear or even the application of mustard is sometimes
useful as a soothing or derivative agent.

In the absence of morphia or chloral, laudanum, ether, chloroform,
camphor or assafœtida have been recommended.

It is important to keep the patient on a soft, littered floor to prevent
injury from his throwing himself down, and walking him around may be
resorted to for the same purpose.

_Prevention._ After a non-fatal attack and in every case in which a
horse is found to harbor the sclerostoma equinum in quantity, measures
should be taken to expel those present in the bowels and to prevent the
entry of embryos. The infested horse may be purged and put on two
drachms each of tartar emetic and sulphate of iron every morning in a
handful of feed half an hour before the first meal. After six doses he
may take a second active purgative. In case of need the addition of 6
grains arsenious acid and a drachm of carbolic acid to each dose will
render them much more effective. All water must be withheld that comes
from streams running by farm-yards, from ponds or open wells in
barn-yards, from uncovered cisterns and from any source which receives
drainage or leaching from land occupied by solipeds or spread with their
manure.

A course of vermifuge medicine should be given at intervals of two or
three months to get rid of the worms which have passed in the interval
from the cysts of the colon, into the intestine.


            NON-VERMINOUS INTESTINAL CONGESTION IN SOLIPEDS.

  Causes: sudden changes to green food, or leguminous fodder, newly
  harvested fodder, frosted food, iced water, microbian infection, toxin
  poisoning, intestinal fermentations, experiments, volvulus,
  invagination, strangulation, compression, atony. Symptoms: as in
  verminous aneurisms. Diagnosis: absence of worms, presence of other
  causes. Treatment.

_Causes._ Acute intestinal congestion apart from verminous aneurisms is
ascribed to a variety of causes. Sudden changes of food especially to
green food, in spring, or to some of the leguminous fodder plants
(alfalfa, cowpea, clover, tares, vetches), newly harvested grain or hay,
fodders covered with hoarfrost, iced water, and microbian infection or
poisoning with toxins or other irritant products of intestinal
fermentations. Experimentally the injection into the circulation of
pyogenic toxins and putrid matters has determined intestinal congestion
and hemorrhage. In the same way musty hay or grain have proved the
occasion of these attacks. Finally mechanical blocking of the
circulation of the intestine as by volvulus, invagination, strangulated
hernia, or even compression by bulky food has seemed to operate in this
way.

It ought to be borne in mind that the habitual microbes of the healthy
bowel may become pathogenic when brought in contact with a mucosa which
is the seat of irritation, atony or any condition of debility.

_Symptoms and Lesions._ The verminous aneurisms and thrombosis aside,
the symptoms and lesions of this form of congestion so closely resemble
those of the verminous affection that it seems needless to repeat them.

_Diagnosis_ is difficult but the absence of worms in the affected
animals and their fellows, and the presence of some one of the other
recognized causes may lead to a fair conclusion.

_Treatment_ of the affection is more hopeful than in the verminous
affection, and may be conducted on the same general lines.


           PSEUDOMEMBRANOUS (CROUPOUS) ENTERITIS IN SOLIPEDS.

  Definition. Causes: As in ordinary enteritis, with added infections or
  toxins. Symptoms: As in enteritis, nervous symptoms, diarrhœa.
  Lesions: Congested mucosa, whitish or grayish false membranes, in
  patches or tubular casts, granular, mucous, albuminoid, fibrinous.
  Diagnosis: False membranes in stools. Treatment: Glauber salts,
  calomel, alkaline carbonates or tartrates, oils, antiferments,
  demulcents, careful diet, bitters.

_Definition._ An inflammatory affection of the bowels characterized by
the ejection with the fæces of false membranes.

_Causes._ It has been long attributed to the causes which produce other
forms of enteritis and indigestions, as youth, rich stimulating feeding,
sudden change to green food in spring, sudden chills, over-fatigue,
confinement indoors, and prolonged costiveness. In man it is found as a
sequel of infectious diseases (pneumonia, pyæmia), in Bright’s disease,
cirrhosis of the liver and cancer, and in poisoning by lead, mercury or
arsenic (Osler). Cadeac, who found great numbers of streptococci in the
false membranes in animals, is certain it is a microbian disease, and
this is doubtless true, if qualified by the statement that the microbe
as is so often the case with other intestinal affections, requires an
occasion in the form of a diseased or debilitated condition of the
mucosa to enable it to become pathogenic. The disease is not known to
propagate itself indefinitely or without such a predisposing occasion.

_Symptoms._ There are dullness, prostration, langor, hyperthermia,
accelerated pulse, and colics which may be slight or very severe. In
some cases nervous symptoms have been observed, such as irritability or
stupor and somnolence with icterus and fœtid stools. The fæces are
usually semi-liquid, implying an excessive liquid secretion as well as
the exudation of the membranous matter.

_Lesions._ There is a pink congestion of the intestinal mucosa more or
less generally distributed. Whitish false membranes cover patches
chiefly on the terminal portion of the small intestine, but frequently
also on the cæcum and colon, covering an especially red and angry
mucosa. They may occur as simple patches, as ribbon shaped pieces, or as
hollow cylinders lining the entire circumference of the intestine. They
appear as if fibrillated, but contain abundance of granular matter and
seem to be composed mainly of mucus with albuminoid matter and probably
a little fibrine. The deeper layers, in contact with the inflamed
surface are soft and gelatinoid. It is alleged that coexisting wounds on
other parts of the body become covered by a soft pultaceous false
membrane.

_Diagnosis_ is based on the presence of the false membranes of a
considerable thickness, so that they can be distinguished from the film
of mucus which covers the fæcal balls in constipation or enteric
catarrh.

_Treatment._ Facilitate the secretion from the mucosa, and the
separation of the false membrane by giving 1 lb. Glauber salts, or give
this agent in doses of 5 or 6 ozs. per day. Calomel 1 dr. may be used
instead and has the additional advantage of acting as a disinfectant.
The alkaline carbonates or tartrates or even olive or castor oil may be
used as substitutes. Antiferments like salol, naphthol, salicylic acid,
and salicylate of soda have been prescribed to check the multiplication
of the germ. Flaxseed tea, elm bark, and other mucilaginous agents may
also be given. An easily digestible and laxative diet and a course of
bitters may follow.




            PSEUDOMEMBRANOUS (CROUPOUS) ENTERITIS IN CATTLE.

  Causes: as in solipeds, youth, overfeeding, plethora, dietetic
  blunders, temperament, over-exertion, chill when heated, gestation,
  foul water, irritants, drastics, infections. Symptoms: as in enteritis
  with false membranes, complications. Duration. Lesions: false
  membranes, extent, color, structure, composition, congested mucosa.
  Treatment: Glauber and other salts, pilocarpin, potassium iodide,
  antiseptics, sulphites, sulphides, borax, bismuth, naphthol, creolin,
  muriatic acid, bitters.


_Causes._ The same causes are quoted as in solipeds, youth, extra high
condition, rich feeding, sudden change to the green food of spring,
climatic vicissitudes of the same season, a sanguineous (Reynal) or
lymphatic (Friedberger and Fröhner) temperament, overwork, exhausting
travel, suppressed perspiration, gestation, plethora, foul drinking
water, special irritant plants (chicory, Huzard), and drastic
purgatives. Cadeac suggests bacteria, quoting instances of a fifth or a
fourth of a herd suffering at once. The same would come from any other
cause acting on the whole herd and it seems probable that a microbian
factor is present but can find occasion for its pathogenesis only in
given morbid conditions of the mucous membrane. This would explain the
failure of the affection to propagate itself like a plague, and at the
same time its tendency to manifest itself extensively in given herds
with a common predisposing condition.

_Symptoms._ There are indications of enteric inflammation and fever,
rigors, slight hyperthermia, drying up of the milk secretion, impaired
or suspended appetite and rumination, constipation, colicy pains,
increasing dullness and prostration. As the disease advances the
excrements become soft, pultaceous or watery, with floating hard baked
pieces, dark and even glistening on the surface and more or less false
membranes. These are sometimes stained with blood, which may also be
mingled with the liquid debris. As in solipeds these membranes
constitute the only true diagnostic symptom. They may appear as shreds,
bands or complete cylindroid casts of the intestine.

Other complications, like pseudomembranous exudate on wounds, abortions
and profound weakness are sometimes noted. The disease may last eight
days before ending in recovery. When death takes place it is about the
fourth or sixth day.

_Lesions._ The false membranes are found on the ilium and colon, in thin
films or in thick masses, or tubular casts. In extreme cases the
membrane has covered an extent of 24 feet in length, and if recent it is
soft and friable. If older it may be firm, consistent and yellow or
stained by the blood or ingesta. As in solipeds it shows a reticulated
network and a fine granular structure, and is composed mainly of
inspissated mucus with albuminoids and fibrine. The exudate covers a
surface of extreme redness, with points of darker blood-staining and
even abrasion or ulceration. The surrounding mucosa is also congested,
the villi hypertrophied, the mucous follicles swollen.

_Treatment._ In the early stages a laxative of soda sulphate is of
especial value in depleting from the inflamed mucosa, liquefying the
secretions and dissolving and loosening the false membranes. Epsom
salts, cream of tartar, Rochelle salts, calomel, and pilocarpin are more
or less valuable substitutes. Iodide of potassium is most valuable in
dissolving the exudate and acting as a microbicide (dose 3–4 drs.).

Other alkaline salts may be substituted or as antiseptics the sulphites,
hyposulphites, or sulphides of potash or soda. Borax, bismuth, naphthol
and creolin have also been recommended. Enemata of warm water are
desirable.

In very adynamic conditions, muriatic acid (½ dr. doses) may be given
with vegetable bitters and the same may be allowed during convalescence.


            PSEUDOMEMBRANOUS (CROUPOUS) ENTERITIS IN SHEEP.

  Causes: As in cattle, draughts in folds, overfeeding. Symptoms: fever,
  inappetence, weakness of hind parts, diarrhœa, tenesmus, false
  membranes, blood in stools, tympany. Treatment: change diet of dam,
  exercise, Glauber salts, potassium iodide, bismuth, flaxseed, elm
  bark, mallow, gum, carminatives, bitters, antiseptics.

_Causes._ The same causes are claimed as for cattle. Clavel attributed
it to too rich milk, and exposure to cold draughts, in folded lambs.

_Symptoms._ To the general symptoms of fever are added refusal of the
teat, weakness or paresis of the hind limbs, looseness of the bowels and
the ejection of false membranes with an unusual amount of straining. The
dejections may be watery and mixed with blood. In some cases defecation
is suppressed, the intestines being blocked by the membranes, and then
acute indigestion and fatal tympany may follow.

The pathological anatomy and lesions resemble those seen in the ox.

_Treatment._ Change the diet of the ewe, and allow more outdoor
exercise. Give the lamb Glauber salts (½ to 1 oz.) with potassium iodide
(10 grs.), and bismuth (1 dr.). Decoctions of flaxseed, or solutions of
elm bark, mallow or gum arabic are desirable, and infusions of aromatic
plants or oils of peppermint, anise, or fennel may be added with quinia.
As in the other animals such antiseptics as salol, naphthol, naphthalin,
boric acid, or salicylate of soda may be administered.


             PSEUDOMEMBRANOUS (CROUPOUS) ENTERITIS IN DOGS.

  Complication of other diseases like distemper. Symptoms: fever,
  retching, vomiting, tense, tender, tympanitic abdomen, irregular
  bowels, false membranes. Lesions: stomach empty, congested, croupous
  exudate, extravasations. Treatment: sodium sulphate, boric acid,
  sodium salicylate, salol, bismuth, by mouth or enema, strychnia,
  vermifuges.

In dogs the formation of false membranes on the intestinal mucosa seems
to have less of an individual character, and is found associated with
other affections, like canine distemper and parasitism. In the absence,
however, of accurate knowledge of the specific cause of croupous
enteritis in other animals it seems permissible for the present, to
arrange the whole in one class characterized by the presence of false
membranes.

_Symptoms._ Along with the general symptoms of fever and the special
ones of the existing specific disease there is more or less disturbance
of the digestive organs, anorexia, vomiting, tense, tender, perhaps
tympanitic abdomen, irregularity of the bowels and the passage of the
false membranes. A morose disposition and tendency to snap has been
noticed by Röll.

_Lesions._ The stomach is empty with red or dark mottled mucosa, the
intestinal mucosa is congested covered with a layer of mucopurulent
exudate, and at intervals patches of false membranes which are also
found in shreds floating in the glairy contents. The exudates are of a
yellowish gray color, more or less streaked with blood, and the mucosa
infiltrated, swollen, highly congested and with spots of extravasation
of blood.

_Treatment._ Small doses (1 to 2 drachms) of sulphate of soda may be
given by the mouth, or boric acid (1 scruple), salicylate of soda (10
grains), salol (5 grains), or bismuth nitrate (½ drachm). Injections of
boric acid, borax, sodium hyposulphite, or even Glauber salts prove
useful, and powdered nux vomica (1 grain twice daily) may be added.

In case of intestinal parasites vermifuges must be resorted to.


            PSEUDOMEMBRANOUS (CROUPOUS) ENTERITIS IN BIRDS.

  In pigeons: Ærobic, non-motile bacillus, in lesions, membrane and
  internal organs, pathogenesis, in chickens pathogenesis differs, also
  in man, parts attacked, exudate, other symptoms, mortality early and
  late in outbreak, American form, pathogenesis to rabbits and
  Guinea-pigs. Prevention: Avoidance of infection, quarantine of birds,
  separation of sick, disinfection, accidental bearers of infection,
  pigeons, buzzards, carrion crows, dogs, men, cleanliness. Treatment:
  Locally antiseptics, phenol, boric acid, generally, phenol.

This has been especially seen in pigeons in which it has been studied by
Löffler, Cornil and Megnin, and Babes and Puscarin. Löffler found an
ærobic, non-motile, non-liquefying bacillus in the false membranes,
inflamed tissues, liver, lungs and blood, even in the leucocytes. It
formed irregular masses, and grew in nutrient gelatine, blood serum and
potato. It proved pathogenic to pigeons, linnets, rabbits and mice, but
not to hens, Guinea-pigs, rats or dogs. Chickens, however, suffer from
an acute diphtheritic affection caused by a nearly allied bacillus, and
it remains to be seen whether the varying pathogenesis may not be due to
the habit of long continued growth in a particular genus and an acquired
unfitness for growing in the other. The pathogenesis is also different
from the bacillus of diphtheria of man, and the two diseases are not
usually inter-communicable, in spite of the fact that in rare instances
infection has appeared to have taken place from man to birds.

In pigeons and fowls the upper parts of the air passages and digestive
tract are mainly involved, the tongue, fauces, corners of the mouth,
nares, larynx, and conjunctiva. The bowels suffer less frequently and
mostly concurrently with the mouth, nose and throat. The mucosa is
deeply congested and in part covered by a yellowish exudate which may
accumulate in masses, and dry into a firm substance. The disease affects
particularly high bred birds, kept in close warm houses, and is often
imported by prize animals returned from a show. There may be dullness,
listlessness, sunken head, trailing wings and tail, erect plumage,
diarrhœa, and, if the nose and throat are affected, a modification of
the voice as in roup. Death may occur from asphyxia from the second to
the fourth day near the beginning of an outbreak or the illness may last
twenty days, after the more susceptible birds have been killed off.

In investigating a series of outbreaks of roup in chickens in America,
Dr. V. A. Moore found a non-motile bacillus allied to the colon bacillus
which proved much more deadly to rabbits and guinea pigs than to
chickens, and which was not found in the blood nor internal organs but
only in the local lesions where inoculated. The disease tended to assume
a chronic type in place of the acute form as seen in Europe. Three
inoculated chickens escaped the disease altogether. It would appear
therefore that we have here a disease distinct from that described by
Lœffler, or that there was an absence of some unknown predisposing or
contributing conditions that were present in the European outbreaks. In
both diseases however infection is an undoubted factor and similar
measures of prevention and even of treatment may be followed.

_Prevention._ The first consideration is the seclusion of flocks from
outside animals in affected localities. Newly purchased birds or those
returning from a poultry show should be placed in strict quarantine for
a few weeks until the absence of infection shall have been demonstrated.
Different flocks should not be allowed to mingle, nor the members of a
healthy flock to wander where the manure of another flock has been laid.
Birds having diarrhœa, or any discharge from eyes, nose or beak, or any
false membrane on such parts should be excluded from the flock, and the
house and yard disinfected. It should not be forgotten that rabbits,
guinea pigs and mice may be bearers of the infection, and that it may be
introduced on the feet of dogs or their masters. Pigeons, buzzards, and
carrion crows are especially dangerous as possible bearers of the
infection. Cleanliness as regards food and water, buildings and yards is
of vital importance.

_Treatment._ The sick birds should be strictly secluded and handled by a
special attendant. When the lesions appear on visible mucosæ they should
be painted several times a day with a 5 per cent. solution of phenol, or
a saturated solution of boric acid, or salicylic acid, potassium
permanganate, iodine, or some other germicide may be used. For the bowel
affection one or two drops phenol in water may be given daily, and the
drinking water should be slightly charged with the same. Cleanliness,
pure air, warmth, dryness and sloppy food are all important.


                 ACUTE CATARRHAL ENTERITIS IN SOLIPEDS.

  Definition. Causes: Irritants swallowed, debility, improper,
  insufficient food, congestions, parasitisms, impaired innervation or
  circulation, iced water, chills, perspirations, fatigue, hot, damp
  weather, overfeeding, cryptogams, bacteria, newly harvested fodder,
  septic, or fermented food, leafy fodder, toxins, stagnant, septic
  water, lack of pepsin, muriatic acid and bile, diseased teeth or jaws
  or salivary glands. Lesions: Gastritis, congestion of small intestine
  and colon, in striæ, thickening, ecchymosis, ulceration, necrosis,
  excess of mucus with pus, villi, follicles and glands swollen.
  Symptoms: Fever, high colored urine, costiveness, coated tongue, red
  eyes, inappetence, sluggishness, emaciation, weakness, unthriftiness,
  colics, rumbling, diarrhœa; or more fever, suffering, anorexia,
  icterus, hurried breathing, pleuritic ridge, arched back, tender
  abdomen, rumbling, flatus, diarrhœa, critical or bloody, anxiety,
  debility, prostration, collapse. Prognosis. Treatment: In mild cases,
  careful diet, and laxatives with antiferments, in severe cases,
  laxatives, anodynes, antiseptics, demulcents, stimulants of
  peristalsis, enemata, counter-irritants, fomentations, compresses,
  mustard, in profuse diarrhœa antiseptics, anodynes, demulcents,
  calomel and chalk, bismuth, astringents, boiled flour or starch, gums.
  Dieting during convalescence.

_Definition._ Inflammation of the intestinal mucosa.

_Causes._ Irritants of all kinds taken in with food, or as medicine or
otherwise and acting on the mucosa. Debilitating conditions (chronic
disease, starvation, overwork, close indoor life) which lower the tone
of the system at large, and local debilitating conditions like coarse,
dry, fibrous, innutritious food, congestions, parasitisms, impaired
innervation and troubles of the circulation are strongly predisposing.
Drinking iced water may operate by lowering the tone of the intestines
but seems to habitually act rather by inducing reaction and congestion.
Chills of the surface, especially when perspiring and fatigued, act in
the same way. The relaxation and atony attending on long continued hot
weather, predisposes to enteritis, but is doubtless even more injurious
by the abundance of ferments which it propagates in food and water.

Overfeeding and stimulating aliments thrown on an alimentary canal in
such an atonic condition become especially hurtful. The injury, however,
comes most commonly from food that contains an excess of cryptogams or
bacterial ferments or from water similarly charged. Newly harvested
fodders in which the microbes are still in a state of vigorous life,
when added to the poisonous principles in certain immature seeds
(leguminosæ, gramineæ, etc.); fodders that have undergone fermentative
changes (rotten potatoes, turnips, musty hay or oats); fodders that are
leafy and harbor an excess of microbes (alfalfa, sainfoin, cowpea,
clover) are especially dangerous at times. If musty or otherwise altered
they often contain besides, dangerous toxins.

In taking into account the fungi and microbes in spoiled foods, we need
not give exclusive attention to the particular species of microbe
present. An extended observation shows that the same ferments may be
present in the dry, well cured, wholesome fodder, and in the musty or
spoiled specimen, the main difference being in the excess found in the
latter case as compared with the former. With the excess too, there is
always present a large amount of toxins, ptomaines and other more or
less poisonous products, which, acting on the intestinal mucosa or even
on the system at large, tend to reduce its vitality and to lay it open
to the attacks of bacteria which had otherwise remained perfectly
harmless. Porcher and Desoubry, Achard and Phulpin and Wurz have shown
experimentally that intestinal microbes can enter the chyle and blood
from even a healthy bowel. The streptococcus of pneumoenteritis equi of
Galtier and Violet appears to be a common fodder and intestinal microbe,
which has become pathogenic, because of its excess or on account of a
lack of resistance on the part of the animal. In the same way the
various intestinal cocci and the common colon bacillus may become
pathogenic when the normal antagonism of the bowels and their contents
is lessened.

In the same way stagnant and septic water may be harmless to one animal
of great vigor and good tone and pathogenic to another which lacks these
qualities; or the excess of the ferment and its toxins may overcome the
natural resistance of the animal. The lack of the natural antiferments
of the intestine, pepsin and hydrochloric acid, on the one hand and bile
on the other, will also conduce to multiplication of the microbes and
their products, so that they can successfully attack the mucous
membrane.

Other accessory causes operate more or less, thus any impairment of the
process of mastication, through diseased teeth or jaws tends to the
escape of undigested food through the stomach, as a specially favorable
culture media for the microbes, and irritants of the mucosa.

_Lesions._ As the disease very often implicates the stomach
(gastro-enteritis), the usual lesions of gastritis will be seen. Most
commonly the lesions are best marked in the small intestine, and again
in other cases in the colon, but usually there is more or less change in
all parts of the intestinal canal. The small intestine is almost devoid
of aliments and the mucosa deeply congested in patches or striæ, with at
points thickening, softening so that it crushes under the finger,
hemorrhagic discoloration, and even ulceration, and necrotic changes. It
is covered with a layer of mucus, thin and mucilaginous or thick and
glutinous, containing many granular and pus cells. The villi are
swollen, the follicles of Lieberkuhn puffed up, and the agminated and
solitary glands widely dilated, filled with exudate, and surrounded by
an area of congestion. Proliferation of small, round cells has produced
embryonic tissue in the mucosa and especially between the glands.

_Symptoms._ In the _mildest form_ there is hyperthermia, thirst,
insensible loins, scanty, high colored urine, costive bowels, a few
small pellets only being passed at a time, hard, dry and covered with a
mucous film, hot, clammy mouth, coated tongue, with redness along the
edges and tip, yellowish red eyes, impaired appetite, dull, sluggish
habit, a tendency to hang back on the halter, and a steady loss of flesh
and increased dryness and unthriftiness of the coat. Slight,
intermittent colics occurring especially after meals and attended by
loud rumbling of the bowels are marked features. This may be followed by
slight relaxation of the bowels and recovery in about a week, unless it
should become complicated by intestinal indigestion or impaction, or
should merge into the acute form.

In the _more intense forms_ all symptoms are aggravated. There is
anorexia and even refusal of water, dullness and prostration are well
marked, the head carried low, and the gait is unsteady. The mouth is hot
with tenacious mucus, and a fœtid odor; the tongue is furred and red at
the tip and margins, the eye is sunken, the conjunctiva icteric, the
face pinched, and the pulse accelerated. Hyperthermia may reach 104° F.
Breathing may be almost normal, or with fever, may become rapid and
accompanied by a pleuritic ridge on the flank. The back is slightly
arched and rigid, the belly drawn up and tender, after meals it may be
tympanitic, and colics set in or are aggravated, pawing, uneasy
movements of the hind limbs, and lying down to rise again shortly, with
frequent looking at the flanks being noticeable.

Defecations are at first abundant and coated with mucus, later the balls
are small and scanty and expelled with much effort. From the first the
everted rectum is of a very deep red. Toward the end of the first day or
later the intestinal rumbling increases, flatus passes freely, and
diarrhœa may set in and prove critical. This usually indicates disease
in the colon and tends to recovery; it may be entirely absent if the
inflammation is confined to the duodenum, the effused liquid being
re-absorbed from the cæcum and colon. If the diarrhœa should prove
critical there is a return of appetite and spirit, the fæcal discharges
become firmer and recovery takes place in a week. If, however, the
diarrhœa becomes more profuse and bloody, the colics more intense, the
eyes more sunken and hopeless, the face more pinched and anxious, and
the temperature reduced to or below the normal, with great weakness and
debility, the near approach of death may be feared. This state of
collapse may be further marked by extreme coldness, or dropsy of the
limbs, increased icterus, hurried breathing and rapid loss of flesh.

A prominent icterus indicates implication of the liver from the ascent
of the infecting germs through the bile ducts, or the passage of
microbes or their products or both through the portal vein. In either
case it is a serious complication.

_Prognosis._ In its uncomplicated form the disease is not very fatal to
vigorous, mature horses, though more trying to the young. If infective
germs or their products implicate the liver producing marked jaundice,
or if the general system is poisoned by the microbes or their toxins,
producing marked depression and prostration the danger is enormously
enhanced.

_Treatment._ In the _mildest cases_ a limitation of the food to moderate
bran mashes, and a dose of ½ lb. of sodic sulphate, with salicylate of
soda (3–4 drs.) or bismuth will usually suffice.

In _severe cases_, at the outset, while constipation exists give 3 or 4
drs. of cape aloes, or ½ lb. Glauber salts or ½ pint olive oil, combined
with 2 drs. of extract of hyoscyamus or belladonna and 3 drs. salicylate
of soda. This serves to deplete from the inflamed vessels and the whole
portal system, to soothe suffering, to expel much of the offensive and
infective matters from the bowels, and to check fermentation in that
which remains. They should be given with, or followed by mucilaginous
liquids like solutions of slippery elm or gum arabic, flaxseed tea, or
well boiled farinaceous gruels.

Pilocarpin, 3 grs., or eserine, 2 grs., or both have been recommended
and may be resorted to when action of the bowels is urgently demanded.
They need not supersede the other laxatives. In manifest impaction of
the large intestines, salts, aloes, pilocarpin and eserine may form an
effective combination.

Copious enemata with mucilaginous liquids or warm soap suds should be
given at frequent intervals.

Counter-irritants and derivatives to the abdomen are most important. Hot
fomentations may be persisted in for an hour at a time, or a damp
compress around the abdomen covered closely by dry blankets and held in
place by elastic circingles. Mustard pulp made with cold water rubbed in
against the hair and at once covered by paper and a thick blanket is
often of great value as drawing blood and nervous action to the skin and
relieving the suffering intestine.

In all cases the diet and drink must be carefully supervised. A little
thoroughly scalded wheat bran, or farina, and decoctions of flaxseed,
farinas, slippery elm or mallow, or a solution of gum arabic will
refresh the animal without overloading the digestive organs or favoring
further fermentation.

In case of the onset of diarrhœa which threatens to prove excessive and
persistent, the giving by mouth and anus of antiseptics and anodynes
with mucilaginous agents may be resorted to. Calomel may be given in 10
grain doses twice daily mixed with five times the amount of chalk. Or 2
drs. each of nitrate of bismuth and salicylate of soda and ½ oz. of
laudanum may be given three times a day. Or quinine, 2 drs. and nux
vomica 10 grs. may be added to the above. A choice may be made of other
anodynes, (hyoscyamus, belladonna), antiseptics, (salol, chloral,
naphthol, naphthalin, creolin), and bitters, (gentian, calumba,
cascarilla).

Antiseptic and even astringent injections must be given, and well boiled
farinas and mucilaginous agents may be given by the mouth. Wheat flour
boiled for several hours; starch prepared with boiling water as for the
laundry, (1 pint); gum arabic, or slippery elm may suffice as examples.

The patient should have a dry comfortable box and warm clothing
according to the season of the year. He must be kept for a week on
linseed gruel or other equally simple demulcent agent and brought back
to his customary food by slow degrees.




                CHRONIC CATARRHAL ENTERITIS IN SOLIPEDS.

  Causes: As in acute: troubles of circulation, heart, lungs, verminous
  embolism, parasitism, skin disease. Lesions: thickening of mucosa,
  pigmentation, rigidity, hypertrophy of villi, follicles and glands,
  ulceration, polypi. Symptoms: impaired appetite, buccal fœtor,
  retracted flank, unthrifty skin, pallid mucosæ, colics, tympanies,
  rumblings, irregular bowels, emaciation, perspiration, fatigue.
  Treatment: dietetic, tonic, bitters, salines, aromatics, enemata,
  bismuth, laudanum, calomel and chalk, iron, astringents,
  counter-irritants, electricity, sunshine.


_Causes._ This may occur from a continuance of the same causes as in the
acute, or from an imperfect recovery from the acute form. It may result
from troubles in the circulation, as valvular disease of the heart, or
emphysema of the lungs, which forces the blood back on the venous
system, including the liver and portal vein. Or the lesions that come
from verminous embolism may leave such alteration in the intestinal
walls as entail chronic congestion of the mucosa, or intestinal
parasites may be the cause. Severe and inveterate skin diseases appear
to affect the intestinal mucosa by sympathy, just as diseases of that
mucosa usually entail skin diseases.

_Lesions._ Attenuation of the coats of the small intestine and
thickening of the mucosa of the large have been noticed. The mucosa is
darkly pigmented and covered with excess of mucus. The thickening of the
mucosa may extend into the submucous tissue, giving a firm leathery
feeling to the part, and entailing a loss of elasticity. The villi are
hypertrophied and the follicles of Lieberkuhn and Peyers’ patches may be
congested, ulcerated or otherwise altered. Polypoid growths are not
uncommon on the mucosa, and the mesenteric glands are enlarged and
pigmented.

_Symptoms_ are by no means very definite. Disturbance of the digestive
functions, capricious or impaired appetite, dry fœtid mouth, tucked up
abdomen, dry hair and skin, pallor of the visible mucous membranes,
slight intermittent colics and tympanies, loud rumblings in the bowels,
and relaxed bowels, or alternate costiveness and diarrhœa, with some
tenderness on manipulation of the abdomen are the usual symptoms. The
animal loses flesh, has dry, unthrifty coat, and sweats and is easily
exhausted at work.

_Treatment._ Dietary care is the first essential. Boiled oats, barley,
rye or bran, in small amount and flaxseed tea may indicate the kind.
These should be given in small amount often, and at regular intervals.

A failing appetite may be stimulated by nux vomica (10 grains) twice
daily, or by gentian or other bitter, along with common salt and
aromatics.

Constipation may be combated by fresh green food in small quantities, or
by an ounce each of Glauber salt and common salt given every morning
before feeding, in a drink of water (half to a bucket, if possible), and
10 to 20 grains of nux vomica may be advantageously added. Soapy
injections with salt or glycerine may also be given.

Diarrhœa may be moderated or checked by nitrate of bismuth (2 drachms),
with laudanum (1 ounce), repeated as may be demanded. A combination of
calomel and chalk (1:12) will often serve a good purpose in drachm doses
several times a day. For persistent diarrhœa Cadeac recommends the
following: Iron carbonate 4 drachms, lime water 10 ounces, alum 1
drachm, powdered oak bark 1 ounce, given in water and farina.

Sepsis and fermentation must be combated by the same means as in the
acute type, and the same counter-irritants may be resorted to. A life in
the open air or sunshine, but without undue exertion is of great
importance.


                  ACUTE CATARRHAL ENTERITIS IN CATTLE.

  Causes: atony, debility, starvation, overfeeding, innutritious food,
  close, foul buildings, ill health, over-exertion, hot weather, sudden
  changes, chills, privation of water, irritants, spoiled and newly
  harvested grain, foul water, parasitism, chest diseases, thrombosis.
  Lesions; in small intestine mainly, tympany, congestion, thickened
  mucosa, epithelial degeneration, desquamation, enlarged villi,
  follicles and glands, erosions, ulcers, perforations. Symptoms: solid
  masses in rumen, impaired rumination and appetite, rumbling,
  tenderness, costiveness, fever, arched back, tender, tucked up
  abdomen, colics, in severe cases, agalactia, tremors, rigors, drooping
  head, ears, eyelids, tender abdomen, straining, expulsion of mucus,
  foul eructations, later diarrhœa, critical or exhausting. Death from
  tympany, bleeding, infection, inanition. Diagnosis: by concurrence of
  symptoms, hyperthermia, tender abdomen, no blood nor coccidia in
  stools, no frothy bloody mucus with tenesmus. Treatment: dietetic,
  friction, synapism, atropia, chloral hydrate by rectum, salines,
  demulcents, nux, tartar emetic, eserine, pilocarpin, sulphites, salol,
  sodium salicylate, naphthol, etc., bitter tonics, carminatives,
  stimulants, sodium chloride, ipecacuan, hygiene during convalescence.

_Causes._ As in solipeds the various conditions which lower the general
tone, and those which especially debilitate the bowels predispose to
catarrhal inflammation. Underfeeding and overfeeding, fibrous,
innutritious, indigestible food, an indoor life in close, foul stables,
chronic and debilitating diseases, overwork, overdriving, long continued
hot weather, sudden changes of weather, chills, long railway journeys
without water, exposure in hot stockyards in midsummer, all lessen the
resisting power of the system and of the bowels.

As more direct irritants, may be named irritant plants, weedings and
culls from gardens, musty and spoiled fodders of all kinds, newly
harvested grain, and putrid drinking water. Also intestinal parasitism,
diseases of the heart and lungs, and thrombosis of the mesenteric
arteries.

_Lesions._ These predominate in the small intestine in catarrhal
enteritis as they do in the large intestine in dysentery. The small
intestine and cæcum may be distended by gas, and reddened more or less
deeply on their outer surface. The mucosa is the seat of congestion,
punctiform and ramified redness, thickening, infiltration and softening
so that the epithelium breaks down into a pulp under the pressure of the
finger. Desquamation may be extensive leaving a raw angry surface. The
villi are infiltrated, erect, and ulcerated showing dark bloody points,
and ecchymoses, and circumscribed sloughs and eschars are present. The
solitary glands are congested, hypertrophied and projecting. The
submucosa is infiltrated with a gelatinoid material and the same may be
found around the swollen and congested mesenteric glands. Perforations
have been met with in some cases, and coexistent inflammatory lesions in
the stomachs are common.

_Symptoms._ In the _mildest forms_ there is inactivity of the rumen,
aggregation of the contents into hard masses, easily felt through the
surrounding gases, appetite and rumination are greatly impaired, and
there is much rumbling and considerable tenderness of the right side of
the abdomen, and more or less costiveness, with hard, glazed
mucus-covered fæces. There is some rise of temperature, ardent thirst,
injected mucous membranes, dry, hot muzzle, weeping eyes, a small, hard,
weak pulse, arched back, tender to pinching, and tucked up abdomen.
There may be slight colicy pains, uneasy movements of the hind feet and
tail, and sometimes lying down and rising at short intervals.

In _more severe cases_ the impaction and tympany of the rumen are more
marked, the hyperthermia runs high, appetite and rumination cease, the
milk dries up, rigors and tremors appear, the head and ears droop, the
eyes are sunken, the mouth is clammy and fœtid, the colicy pains are
severe or extreme, the right side of the abdomen is very tender,
defecation may be altogether suspended and rumbling in the right side of
the abdomen ceases or becomes rare. Straining may continue but seldom is
anything but mucus passed. Eructations from the rumen are distinctly
fœtid.

After the third day the violence of the pains may abate, and sometimes
diarrhœa sets in and may be regarded as critical, and portending
recovery. If rumbling in the right side is resumed, if the fever
subsides, the spirits revive, and some appetite and rumination return
they will herald improvement.

If on the other hand the pulse becomes smaller, the temperature higher,
the eyes sunken and fixed, the urine scanty, red and acid, the animal
constantly recumbent on its left side, if when raised it omits the
healthy stretching of its hind limbs, and walks sluggishly and painfully
with frequent moaning, if when down it rests its head on the ground, the
prospects are very unfavorable.

Death may occur early from tympany and asphyxia; it may follow profuse
intestinal hæmorrhage; or it may be the result of general infection and
inanition.

_Diagnosis_ must depend on the combination and succession of the
above-named symptoms. From acute intestinal congestion it is
distinguished by the more moderate type of the colic, and the more
gradual advance of the disease. From acute indigestion and tympany of
the rumen by the early and marked tenderness of the right side of the
abdomen, and the decided hyperthermia. From hemorrhagic enteritis by the
absence of the black sanguineous discharges from the bowels at an early
stage of the malady, and of coccidia from the droppings. From dysentery
it is distinguished by the absence of the mucous and bloody discharges,
which are passed with much straining in that affection from the
beginning.

_Treatment._ The first consideration is dietetic and hygienic. If the
animal will still eat, he ought to have boiled flax seed or other well
boiled gruel, rendered palatable by salt. Even if he refuses food, this
may be diluted largely and will be taken on account of the thirst. If he
refuses all, a bottle may be given at intervals to refresh him. Or
better—milk may be given from a bottle in the same way. Active friction
to the abdomen with straw, or the application of oil of turpentine or
mustard may abstract blood to the skin and favor the restoration of the
intestinal functions. To calm the pains and control spasms, sulphate of
atropia (½ gr.) may be given subcutem and repeated if there is no action
on the pupil in fifteen minutes. Or extract of belladonna (2 drs.), or
chloral hydrate (½ oz.) may be given by rectal injection.

To overcome the intestinal torpor 1 lb. each Glauber and common salt may
be given in four to six quarts of warm water and followed by frequent
mucilaginous drinks, as much as the animal will take, but only two or
three quarts at a time. The addition of ½ dr. nux vomica will serve to
rouse peristaltic action. Harm advises 1½ dr. tartar emetic by rectal
injection for the same end. Next to Glauber salts, Castor oil (1 qt.) is
to be recommended. Along with these or independently of them sulphate of
eserin (1½ gr.) or pilocarpin (2 gr.) may be employed subcutem.

Frequent rectal injections of soap or mucilaginous liquids, with or
without laxatives will be useful.

As antiferments beside the salt may be used bisulphite of soda in ½ oz.
doses, salol 3½ drs., salicylate of soda 3 drs., betol 3½ drs., or
naphthol 3½ drs., by the mouth and rectum.

When free movement of the bowels has been secured, attempts should be
made to restore appetite and rumination by tonics and stimulants:
gentian ½ oz., nux vomica ¼ dr., ipecacuan 2 drs., common salt 1 oz.,
may be given three times a day.

The diet should at first be restricted to flax seed gruel or that of
other farinas, with a mere handful of fresh grass or bran mash and the
restoration of the previous diet should be slow and gradual, care being
taken meanwhile that no costiveness of the bowels supervenes.


                 CHRONIC CATARRHAL ENTERITIS IN CATTLE.

  Causes: As in acute chest diseases, abdominal tuberculosis. Lesions:
  Thinning, discoloration, degeneration of mucosa, fœtid, mucous
  contents, black baked masses, lymph glands pigmented. Symptoms:
  Impaired appetite, irregular bowels, tympanies, lies with nose on
  right flank, unthrifty coat, prostration, emaciation, weakness, tender
  flank. Treatment: Dietetic, laxative, stimulant of peristalsis,
  bitters, antiseptics, aromatics, muriatic acid, treat concurrent
  disease.

_Causes._ This may result from a continuance of the causes that are
operative in the acute, or from the latter merging into the chronic
form. Chronic diseases of the heart and lungs, local disturbances of the
circulation, and tumors or tubercles of the intestines or mesentery are
additional causes.

_Lesions._ These embrace attenuation of the intestinal walls at Peyers’
patches, a dark, slaty discoloration of the mucosa, more or less
congestion, an accumulation of fœtid mucus in the small intestines, of
mucus and black baked fæcal matters in the large, and discoloration of
the mesenteric glands. Inter-dependent diseases of the heart, lungs and
liver are not uncommon.

_Symptoms._ Following the acute form there remain impaired or capricious
appetite and rumination, costiveness alternates with relaxation of the
bowels, intermittent slight tympanies occur, the subject inclines to lie
much with his nose in his flank, has dull coat, erect on back and neck,
sunken eyes, drooping ears, and rapidly loses flesh and strength.
Tenderness of the right side of the abdomen when the fist or knee is
pressed into it is a marked feature.

_Treatment._ The diet must be cared for as in the acute form, yet fresh
green grass, a little at a time, is calculated to stimulate appetite and
rumination and to prove laxative to the bowels. The same purgatives may
be given in one-fourth the doses and repeated daily or reduced as may be
found best to secure a moderate secretion and discharge from the bowels;
eserine or pilocarpin may be used for the same purpose; the bitters and
antiseptics may be given in the same way. As calmative aromatics, oil of
peppermint 30 drops, powdered anise ½ ounce, or ginger ½ ounce, may be
given twice or thrice daily.

Cadeac strongly recommends a drink slightly acidulated with hydrochloric
acid to assist the digestion and stimulate the stomach to action.

Attention must of course be given to any curable concurrent or
inter-dependent disease.


                          DYSENTERY OF CATTLE.

  Definition. Attacks ox mainly. Causes: accessory causes, chills, rain
  storms, night dews, hoar frost, foul or iced water, alimentary
  irritants, spoiled fodder, over exertion, hot damp weather, odors of
  carrion, crowding, swamps, foul stables, germs or pathogenic ferment,
  in man catarrhal, diphtheritic and amœbic, amœba dysenterica, other
  microbes, effect of better hygiene. Symptoms: attack sudden, languor,
  trembling, weakness, weeping eyes, fever, buccal epithelial softening,
  erosions, tenesmus, fœtid, liquid stools, involuntary defecation,
  hemorrhoidal congestion, open anus, colics, tender right flank,
  splashing on handling, anorexia, salivation, unthrifty skin,
  hide-bound, cracked muzzle, later prostration, low temperature, sunken
  glazed eyes, drooping head, ears, eyelids, weakness, emaciation,
  alkaline, fœtid, frothy, bloody, mucous stools, with sloughs, saliva
  acid, gastric liquids alkaline, bile suppressed. Duration: three days
  to three weeks or chronic. Mortality 50 to 80 per cent. Complications:
  mostly septic, abscess, gangrene of other organs, lungs, joints,
  glands, etc. Lesions: rapid sepsis, blood deep red, coagulum loose,
  venous congestion, large intestines congested, tumefied, softened,
  desquamated, eroded, sloughing, necrotic, folds perforated,
  cicatrizing, contents mucopurulent, bloody, putrid, microbes,
  glandular lesions, implication of small intestines, stomach mouth,
  liver, spleen, hepatic abscess. Diagnosis: from rinderpest by
  tardiness and comparative weakness of contagion, absence of general
  mucous congestion and epithelial concretions, from toxic enteritis by
  same. Prevention: avoidance of causes, separation of sick,
  disinfection, careful feeding. Treatment: Demulcents, antiseptics,
  astringent tonics, opiates, ipecacuan, calomel, sodium sulphate with
  antiseptics, antiseptic enemata of glycerine, phenol, creolin, iron
  sulphate, silver nitrate, salicylic and boric acids, rest,
  gravitation, careful dieting.

_Definition._ An infective, ulcerative inflammation of the large
intestine but especially of the colic and rectal mucosæ.

It is well recognized as a disease of the ox, and the older writers
allege its existence also in horses, swine and dogs, though this is not
admitted in all modern veterinary works.

_Causes._ It was formerly ascribed to improper hygiene, chills, cold
rain storms, night dews, hoar frost, malarious emanations, putrid,
stagnant or iced water, irritants in food, green, fermented or musty
food, a too liberal diet after starvation, overtaxation in very hot
weather, and bad odors from decomposing carcasses. These can only be
accepted as predisposing causes begetting a general debility, or
debility of the alimentary canal and laying that open to the attacks of
specific microbes. The close aggregation of cattle on ship-board, in
besieged cities, and in the parks of armies in the field, has apparently
contributed to the propagation of the dysentery. The removal of a victim
to a herd with free healthy range seldom starts a new center of the
disease. In all infected herds huddled in small compass there is every
facility for the propagation of a germ already present, and especially
in the commissariat of a belligerent army there are enough privations,
over-exertions and other trying conditions to favor predisposition.
Faulty food like stale bread, musty hay, have been supposed to cause it.
For man and beast alike dysentery is preëminently a disease of the
tropics, and of hot seasons, and will often subside on the advent of
cold weather.

Its propagation on given (swampy) soils, and in particular (foul)
stables strongly suggests a special germ, though for the cow this has
not been perfectly identified. Gerlach vainly attempted to inoculate it,
and it does not often propagate itself beyond the foul and infected
localities or stables, yet its persistence in them for years bespeaks
unequivocally the operation of a special pathogenic ferment.

It may also be fairly assumed that it is not necessary that the same
factor should be present in all cases alike, but that one operates
predominantly in one case and another in another. In other words
dysentery must be recognized as not one disease, but several, of which
the true pathogenic microbes have not yet been fully demonstrated, but
which are classed together because of the similarity of the attendant
lesions.

In man three distinct forms are recognized. 1. =Catarrhal dysentery=,
with frequent small stools of rosy mucus, and blood; and later pus,
scybala, passed with tenesmus, but no sloughs and little odor; 2.
=Diphtheritic dysentery=, with thin watery bloody discharges having a
pronounced cadaveric odor; also tenesmus, sloughs, and increasingly
offensive smell; 3. =Amœbic dysentery= with frequent bloody mucus
stools, tenesmus sloughs and fœtor, but with distinct remissions or
intermissions. With the latter, amœbæ are found abundantly and more so
in the more acute cases with alkaline stools. They are found in the
fresh warm stools, 5 to 8 times the size of a red blood globule and
oval, pyriform or irregular in form, with nucleus and nucleolus.
Kartulis and Hlava succeeded in inducing dysentery in cats and dogs by
injecting pure culture of the amœba, and the former testifies that dogs
in Egypt take the disease spontaneously, and their stools contain the
same amœba coli as is found in man.

Cunningham who investigated the subject in India found amœba in the
bowels of healthy men, and also abundantly in the fæces of horses and
cows, which have naturally the requisite alkaline reaction.

The mere presence of the amœba therefore may not be sufficient to cause
the disease, but with the requisite predisposition and an alkaline
condition of the intestinal contents, it is manifestly an important
factor in the disease.

The causative microbes in other forms of dysentery have not been
identified, but under the requisite irritation and local debility one
can easily conceive of the ordinary bacterial ferments of the intestine,
concurring with others introduced from without, in determining the
morbid condition. With better hygiene the disease is steadily
diminishing in man and beast, though violent epizootics (in cattle)
still appear in connection with wars (siege of Belfort, 1870, Zundel),
and carriage by sea in hot climates (Mediterranean trade, Bouley).

_Symptoms._ The disease sets in suddenly, yet prodromata may
occasionally be observed, such as dullness, langor, trembling over the
flanks and elbows, weakness, prominent, weeping, congested eyes, and low
moans when moved. Then follow hyperthermia, at first slight, heat of the
mouth without injection, epithelial concretions or erosions and diarrhœa
(sometimes there is straining without passage at first). Then follows a
period of profuse and fœtid discharge, with relaxed or open anus, the
liquids escaping involuntarily and smearing the tail, perineum, thighs
and hocks, and the protruded mucosa showing dark red congestions and
even commencing erosions. Colicy pains, slight at first, have now become
intense, and the right side of the abdomen is very tender to the touch
and fluctuates noisily when manipulated. Appetite and rumination are
lost. Salivation may be present, the saliva falling in films to the
ground. The buccal epithelium is softened, loosened and easily detached
by the finger, leaving raw sores. The temperature which has risen slowly
(not as in rinderpest abruptly) may reach 106°. The hair becomes dry,
the skin harsh, rigid, and firmly adherent to the deeper parts, and
often cold, while the muzzle is hot, dry and even cracked.

At a still more advanced stage, the pulse is small, the temperature
lowered, the animal very weak and unsteady and inclined to lie, great
emaciation, sunken glazed eye, drooping head, ears and eyelids, and a
general fœtor from the skin as well as the dejections, which attracts
crowds of flies. By this time there may be passed only bloody mucus
mixed with eschars, and having a most repulsive odor.

It is a noticeable fact that the fæces are alkaline, and in man the
saliva is acid and destitute of its glycogenic properties, the stomach
secretions are alkaline and no longer peptogenic, and the secretion of
bile is arrested until improvement sets in.

_Course._ _Duration._ Some mild cases recover in two or three days, and
in violent cases death may occur at this early date. More commonly the
disease continues for two or three weeks before ending in death or
recovery. Some merge into the chronic form and may last for months and
die in a condition of marasmus. These last cases become mere walking
skeletons, with pallid mucosæ, sunken eyes, scurfy hide-bound skins
covered with vermin, and the frequently everted rectum is congested and
covered with ulcers and eschars. _Mortality_ is _from_ 50 to 80 per
cent.

_Complications._ Most complications are in the direct line of septic
infection. Among the most common are hepatic abscess, gangrenous
pneumonia, and extensive gangrene of the intestinal walls. In man
arthritis, paralysis, parotitis and other secondary affections are seen.
In the animal as well we may expect necrotic centres in any organ, from
the supervention of a general septicæmia.

_Lesions._ The carcasses putrefy with extraordinary rapidity being as a
rule pervaded by septic microbes and their toxins. The blood is of a
deep red, loosely and imperfectly coagulated, and accumulated in the
veins and subcutaneous connective tissue.

The large intestines are the special seat of the disease, the walls
being found hyperæmic, with concentration especially on the mucous
surface which is red, congested, infiltrated, tumefied so that it is
easily detached under pressure by the finger, or broken down into a
putrid pulp. At other points the epithelium or the whole mucosa has been
detached leaving ulcers, varying from mere erosions to the deep and even
perforating sores, through which the putrid contents escape into the
abdominal cavity. At other points the surface is covered by necrotic
masses surrounded by a swollen margin of living mucosa. Elsewhere the
eschars have been detached and the granulating base and margin have
contracted into more or less perfect cicatrices. The contents of the
affected bowel may be largely mucopurulent, or it may be mixed with
blood, with eschars and putrilage from the sores and at times with small
packed masses of food, but in all cases it is very putrid and repulsive.
It always contains the elements of blood and exudation, together with
many microbes, the predominance of individual species suggesting the
main factors in the pathogenesis. Peyers’ patches and the solitary
glands are often the seat of infiltration and ulceration. Virchow points
out that in man the lesions are largely concentrated in the flexures of
the colon in which the ingesta is longer delayed, and the very
convoluted arrangement of the viscus in cattle may be one reason of
their special predisposition to the disease.

The small intestines are exceptionally implicated, and the abomasum red,
congested, ecchymosed and even ulcerated. The mouth and pharynx are
often congested, with erosions and ulcerations on the gums and tongue.

The mesenteric glands are red and swollen or pigmented of a dark gray
color, and these or the adjacent connective tissue may be the seat of
abscess. The liver is enlarged congested, of a yellowish red color, with
granular degeneration and softening. Hepatic abscess is rare in cattle.
The spleen is engorged with black blood and distinctly enlarged.

_Diagnosis._ Dysentery is distinguished from rinderpest by the slower
advance of the hyperthermia, by the absence of buccal concretions of
epithelium, and of vaginal congestion, and above all by the absence of
the virulent contagion by which the rinderpest spreads widely and
rapidly, irrespective of special unwholesome environment. The lesions of
dysentery are concentrated on the large intestines, while in rinderpest
they are extended over the whole alimentary canal, and do not spare
other mucosæ.

From toxic gastro-enteritis it is distinguished by the absence of any
history or lesions showing the ingestion of a poison and by the
concentration of the lesions on the large intestines whereas in
poisoning with irritants, the stomach and small intestines are the most
liable to suffer.

_Prevention._ Precautions against overcrowding on board ship in hot
seasons, and the maintenance of cleanliness are prime considerations. In
commissariat herds close crowding must be avoided, feeding should be
done at different points for six or eight cattle at each, the yards
should be frequently changed, or carefully cleared of manure and
sprinkled with a solution of 3 per cent. sulphuric acid. In case an
animal is attacked it should at once be removed and killed, and its
offal and the yard where it has been, disinfected. Food and drinking
water should be specially wholesome.

_Treatment._ Mild cases may be successfully treated by the use of
mucilaginous draughts, (boiled flaxseed, mallow, slippery elm, gum
arabic) with antiseptics (salicylic acid or salicylate of soda 2 to 3
drs., salol 1 dr., creosote 1 dr., sulphate or chloride of iron 1 dr.)
every three hours.

In the more severe cases the most varied treatment has been resorted to.
Formerly opiates and astringents were largely employed, practically
shutting up the poison in the intestine. Ipecacuan in large and
frequently repeated doses had the advantage of soliciting the action of
both liver and bowels, but however useful, it has gradually declined in
public confidence.

An eliminating and antiseptic treatment has at present the most general
acceptance. Seven grains of calomel has been given every two hours for
two or three days in succession. Still more recently 2 to 4 ozs.
sulphate of soda every three hours with hot water and antiseptics
(salicylates, sulphites, salol, boric acid, creolin, naphthol) have been
substituted. Even more important is the washing out of the large
intestine by antiseptic enemata. These should be very copious and
frequently repeated so as not only to render the contents of the rectum
and colon antiseptic but to secure the discharge of the offensive
matters as they are produced. The agents may be glycerine, carbolic
acid, creolin, sulphate of iron, nitrate of silver, salicylic or boric
acid. If the animal can be made to stand on an inclined plane with its
hind parts elevated it will favor the penetration and retention of the
liquid. Perfect rest is a most important accessory.

In case of recovery the return to ordinary diet should be gradual.


                 CATARRHAL ENTERITIS IN SHEEP AND GOAT.

  Causes: Symptoms: Moping apart, inappetence, tympany, hard masses in
  rumen, constipation, colics, straining, stretching, fever, no rumbling
  nor defecation, diarrhœa, critical, or exhaustive. Treatment:
  Laxative, antiseptic, counter-irritant, demulcent antiseptic
  injections, in diarrhœa antiseptics, carminatives, bitters, diet, well
  boiled farinas.

_Causes._ These are unknown apart from those given for the ox.

_Symptoms._ Moping alone in place of following the flock, inappetence,
suspended rumination, tympany, hard masses in the rumen, cold ears,
horns and limbs, obstinate constipation, weary movements of the hind
limbs, lying down and rising, looking at the flanks, and tenderness of
the right side of the abdomen, frequent straining, stretching,
hyperthermia, rapid pulse, and suppression of movement and rumbling in
the bowels are prominent symptoms. The constipation may be followed by
diarrhœa, which may presage recovery or hasten death, the symptoms of
improvement or aggravation indicating which. The diarrhœa may be simply
serous or mucopurulent and inoffensive or it may be black, bloodstained
and fœtid. It may cause extensive losses, with pathological changes as
in the ox.

_Treatment_ in the early stages with inactive bowels, must be laxative
and antiseptic, sodic sulphate 4 ounces with 1 drachm chloral hydrate in
a quart of warm water will serve to largely expel offensive ingesta and
bacterial ferments and pave the way for recovery. A counter-irritant of
aqua ammonia to the abdomen, under the wool, will have a good effect,
and soapy or mucilaginous and antiseptic injections are desirable.

If the bowels are already acting freely, ½ drachm each of boracic acid
and nitrate of bismuth may be given at least thrice daily, with the
addition of 60 drops of laudanum, and antiseptics (salol, naphthol,
naphthaline). Carminatives like chamomile, anise, cardamons, peppermint
may be added, and bitters such as quinia or nux vomica.

Well boiled gruels of barley, oats, linseed, or rye should be given and
little or no solid food until appetite and digestion have been restored.


                     CATARRHAL ENTERITIS IN SWINE.

  Causes: decomposing swill, ferments from snout and feet in swill,
  toxins, salt, brine, powdered soaps, etc. Symptoms: dullness,
  inappetence, fever, burrowing under litter, stiffness, drooping head,
  ears and tail, arched back, tender abdomen, constipation, diarrhœa,
  petechiæ, rumbling, tympany, weakness, emaciation, paraplegia, not
  actively infectious. Duration: one to eight days or more. Lesions:
  mucopurulent exudation in alimentary canal, congestion, extravasation,
  hemorrhages, ulcerations, congestion of peritoneum, mesenteric glands
  and other organs. Diagnosis: presence of alimentary causes, many
  attacked at once, no spread to better kept herds, no germ fatal to
  guinea-pigs nor rabbits. Treatment: eliminate, oil, calomel, flaxseed,
  gruels, enemata, antiseptics, revulsives, diet during convalescence,
  antidotes.

_Causes._ The enteritis of swine has been long considered as infective
or septic, yet this is perhaps mainly due to the nature of the food too
often furnished to this animal in a state of domestication. Not only is
he fed on swill containing all kinds of over-kept food, in a state of
more or less advanced decomposition, but he is kept in a pen or yard
which soon becomes offensive, and following his natural instincts he
roots around with his nose in the accumulating filth. When fed he
plunges this foul snout in his liquid food, and as if this were not
enough the fore feet follow, and if the trough is long enough the hind
feet as well. Every available saprophytic microbe therefore finds its
way down his throat, and the toxins from their growth outside the body
accompany them to irritate or benumb the mucosa and fit it for the
attacks of bacteria, which would otherwise have proved harmless. But in
addition to all this, chemical irritants get into the swill and pave the
way for the microbes. Salt, brine, and the various caustic washing
powders used in washing dishes and tables find their way into the swill
barrel often in quantity sufficient to irritate and poison. In
experiments conducted at the N. Y. State Veterinary College the washing
powders have been proved to be most deadly, and upon different farms, a
mortality attributed to hog cholera, has again and again been arrested
by preventing the entry of these powders into the swill barrel.

_Symptoms._ There is dullness, inappetence, hyperthermia (105°), a
tendency to lie under the litter, leaving the herd, when raised the pig
arches his back, moves stiffly with grunting, the tail and ears pendent,
and the belly tender to the touch. The bowels are at first constipated,
and thirst ardent, later diarrhœa may set in, and the skin and snout may
have red blotches or patches as in hog cholera. Tympanies and abdominal
rumblings are frequent. The animal becomes very dull, weak, emaciated,
staggers in walking or is completely paraplegic.

It may end fatally in twenty-four or forty-eight hours, or death may be
deferred for six or eight days or the disease may merge into the chronic
form, or recover. The usual foul surroundings of the pig and the
abundance of microbes and toxins taken in, serve to make enteritis in
this animal much more redoubtable than in other domestic animals.

The _lesions_ are usually common to stomach and intestine, and consist
in abundant mucopurulent discharge, extensive congestion, points and
extensive patches of blood extravasation, and of lymph infiltration,
ulcers, congested peritoneum and mesenteric glands, and congestions and
ecchymosis in distant organs.

The _diagnosis_ between this affection and hog cholera on the one hand
and swine plague on the other is not always easy, but it occurs in herds
where no introduction of infection can be shown, there is always the
evidence of a foul or unwholesome food, drink or environment, and the
history of a number having been attacked at once and not one by one at
varying intervals, as in infection, the disease does not spread to
neighboring herds kept in better conditions, and there is an absence of
the specific germ of hog cholera, motile, ærobic, non-liquefying,
asporogenous, gas producing with glucose and fatal to guinea-pigs; or of
that of swine plague, non-motile, ærobic, non-liquefying, asporogenous,
not gas producing and not fatal to guinea-pigs, but fatal to rabbits.

_Treatment._ If the bowels are costive give castor oil 2 ounces, with
great care to avoid choking, or shake 15 to 30 grains of calomel on the
tongue and give flaxseed tea, or solution of slippery elm or gum which
the animal will usually drink to slake its thirst. Or well boiled gruels
may be substituted. Injections of soapsuds or Glauber salts with
salicylate of soda should be added until the bowels respond, after which
the salicylate alone may be given by both mouth and anus, or it may be
replaced by one of the other non-poisonous antiseptics. Oil of
turpentine alone or with ammonia may be applied on the abdomen and
covered up until the skin is red and angry.

When appetite returns, gruels, linseed tea, boiled milk and other easily
digested food may be given for some days until the stomach reacquires
tone, when the patient may be slowly returned to its accustomed diet.

If the disease can be traced to alkaline washing powders, these should
be first neutralized by vinegar, after which laudanum, antiseptics and
mucilaginous gruels will be in order.




                      CATARRHAL ENTERITIS IN DOGS.

  Causes: faulty feeding, close confinement, youth, distemper,
  over-exertion, meat diet, chills when heated and fatigued, ferments,
  bacteria, debility, ill health. Lesions: congested, softened,
  ulcerated, thickened mucosa, mucopurulent exudate, swollen intestinal
  and mesenteric glands, hyperplasia, polypi, follicular degeneration.
  Symptoms: dullness, segregation, inappetence, fever, arched back,
  abdominal rumbling, tenderness, retraction, constipation, diarrhœa,
  colics, vomiting, tenesmus, swollen red excoriated anus, icterus,
  weakness, debility, paralysis, if chronic, unthrifty skin, with
  eruptions, pallor, foul breath, tongue and gums, emaciation. Course:
  may recover in vigorous, or run down and die in old, young, weak,
  debilitated or ill. Relapses. Treatment: dietetic, laxative, in
  icteric, calomel, manna, enemata, warm bath, synapism, antiseptics,
  bismuth, sodium salicylate, in diarrhœa, bitters, astringent
  antiseptic tonics. Demulcents.


_Causes._ The dog is susceptible because of its varied, irregular,
stimulating, often excessive diet, and its close confinement and lack of
wholesome outdoor exercise. The conditions which predispose to or excite
gastritis tend equally to enteritis. Youth, canine distemper,
over-exertion, an exclusive meat diet, and chills from plunging into
cold water when exhausted with hunting are to be specially noted.
Spoiled meats charged with the germs of infection, or with putrefactive
bacteria and their toxic products are common causes. Then any old
standing disease or other cause of general debility will predispose to
the attacks of such otherwise harmless germs. The irritation caused by
intestinal parasites is an occasional factor.

_Lesions._ The mucosa is congested, ramified, spotted or dark and slaty;
it together with the submucosa is swollen and infiltrated, and with
points of ecchymosis, extravasation or even ulceration. The surface has
a thick layer of mucopurulent matter. The solitary glands are swollen
and charged with small lymphoid or pus cells and have a congested
areola. The mesenteric glands are congested and the liver usually
congested softened or mottled. In chronic cases there may be
hyperplasia, polypi, cystoid degeneration of the follicles, etc.

_Symptoms._ There may be dullness, drowsiness, a seeking of seclusion,
inappetence, hyperthermia (102 to 104°), ardent thirst, arched back,
abdominal rumbling, tympany or tucked up tender abdomen, and a very
temporary constipation, early giving place to diarrhœa. If however the
inflammation is confined to the rectum and floating colon, constipation
may persist. There are intermittent colics, frequent lying down and
rising, or rising on the hind limbs only and when the belly is handled
the patient may whine. The mouth is sour, hot, clammy, and red, and the
dorsum of the tongue furred. The nose is dry and burning, the eyes
congested, sunken and watery.

The fæces may be early soft or liquid and bilious, then as the
defecations increase they pass through shades of gray to black or
reddish black from the admixture of effused blood, and show bubbles and
fœtor. Vomiting is usually an early symptom (septic matters in septic
poisoning) and as the disease advances there is much fruitless straining
and even protrusion of the congested and excoriated rectum. Icterus is
common from infection of the gall ducts or the absorption of toxins into
the portal vein. Weakness and debility amounting even to paresis may
appear in the end.

In chronic cases there are emaciation and debility, unthrifty hair and
skin, cutaneous eruptions, pallor of the mucosæ, fœtid breath, foul
teeth and tongue, with irregular appetite, alternate constipation and
diarrhœa, and, in case of implication of the duodenum and liver,
icterus. The abdomen is retracted and tender.

_Course._ In strong vigorous dogs a spontaneous recovery is the rule,
which is greatly favored by elimination through vomiting and purging.
Fatal cases occur in puppies, in old, debilitated animals, or in such as
have disease of the heart, lungs, or liver. Relapses are common and
dangerous.

_Treatment._ Mild cases may respond to a purely dietetic treatment.
Boiled milk, hot soup, or well cooked mush, and biscuit, are indicated,
and with ½ oz. castor oil and 5 to 10 drops laudanum may suffice for
treatment.

In the more severe cases, with some icterus, calomel 1 to 2 grs. with
the oil, or with manna 5 drs. may be followed by emollient or soapy
injections, and a warm bath or fomentations, the body being afterward
carefully dried and warmly covered. This may be followed by a mustard
poultice.

The usual antiseptics (salol 10 grs., naphthol 20 grs., creoline 20
drops, creosote 7 drops, or naphthaline 20 grs.) may be given with the
laxative and should be given by both mouth and anus several times daily,
in combination with nitrate of bismuth. In case of icterus give a
mixture of calomel 5 grs., chalk 60 grs., in doses of three to five
grains three or four times a day. Or salicylate of soda (10 grs.) may be
given at the same intervals.

Quinia sulphate 5 grs., nux vomica 1 gr., tannic acid 1 gr., or silver
nitrate ½ to 1 gr., or iron chloride 3 to 5 grs., may be employed when
the bowels are much relaxed. Injections of well boiled rice or starch,
or of gum or slippery elm, may be employed as adjuvants.


                HEMORRHAGIC GASTRO-ENTERITIS OF THE DOG.

  Definition. Causes: Spring, toxins, irritants, inflammation. Symptoms:
  Vomiting, diarrhœa, pendent head, arched back, retracted belly, black,
  bloody glairy frothing fæces, circulation excited, mucosæ red, yellow,
  or brown, death in two or three days. Diagnosis. Lesions: Stomach and
  intestines empty, mucosa of a dark blood red, thickened, liver and
  kidneys congested. Treatment: Little successful, intestinal
  disinfection, elimination, laxatives, wet compresses, enemata, heart
  stimulants, ergot, iron chloride.

_Definition._ A special form of septic enteritis, occurring as an
epizootic and not transmissible by ingestion.

_Causes._ These are not well known. Occurring in a few dogs at one time
in the same place, and time (by preference in spring) and then
disappearing for months, and not being appreciably communicable by
contagion or ingestion, it has the aspect of being caused by poisons,
probably of the nature of toxins taken in with the food or water.
Preëxisting inflammation has been alleged as a predisposing cause, the
attack having followed superpurgation, or the administration of a
handful of salt. Guinard found that the intravenous injection of
tuberculin, mallein and other products of microbian growth produced
lesions analogous to those of this disease.

_Symptoms._ The attack is usually sudden. The dog is seized with
vomiting and diarrhœa and stands with head depressed, back arched and
belly tucked up. The vomit is at first of alimentary matters, then of
glairy mucus, or black and bloodstained material. The fæces are black,
bloody, glairy, frothy, and abundant, fouling the tail and the hips. The
abdomen is at first tense and extremely tender. The pulse is
accelerated, the heart beats tumultuous, the breathing slow and
temperature elevated. Redness of the visible mucosæ, often tinged more
or less deeply with yellow, implies hepatic disorder or destruction of
blood globules. Death may occur in two or three days.

The abruptness and violence of the attack, the violent vomiting and
purging and the staining of the discharges with blood are to a large
extent diagnostic.

_Lesions._ These are most noticeable in the stomach and intestines which
are empty and of a dark blood red. The mucosa is thickened, gorged with
blood, and showing deeper shades here and there where extravasation has
occurred. The liver and kidneys are also deeply congested.

_Treatment_ has been almost constantly a failure. Cadeac recommends
disinfection of the intestinal canal, with salol, cresyl or dinaphthol,
but in the absence of contagious germs this seems the less called for.
The indications would seem to point to elimination of the chemical
poisons, the soothing of the irritation and the tiding the animal over
the period of weakness. Agents that will at once eliminate the poisons
and sustain the heart’s action appear to be called for, hence digitalis
2 grs. or tincture of strophanthus 10 drops are particularly indicated.
Laxatives are rather hopeless considering the congestion and paralysis
of the bowels, and yet if they can be made to operate on any
comparatively healthy part of the intestine they will serve a good
purpose in eliminating the poisonous contents, in securing secretion and
elimination of poison from the blood, and in depleting from the
overcharged portal system. Glauber salts by mouth and anus, or jalap, or
castor oil may be resorted to. In the absence of these a free use of
watery enemata and the ingestion of water by the mouth may be resorted
to. A damp compress around abdomen and loins will be at once soothing
and stimulating to the secretions of both kidneys and bowels.

To counteract congestion and extravasation Cadeac advocates ergotine 2
grs. subcutem, or iron perchloride, 2 ozs., to 1 quart of water to be
given in doses of two or three tablespoonfuls every two hours. It might
also be used in enema.




                     CATARRHAL ENTERITIS IN BIRDS.

  Causes: microbes, diagnosis from fowl cholera, less virulent rapid and
  deadly, and comparatively harmless to the rabbit, debility, youth,
  age, unsuitable food, ill health: bacillus gallinorum, bacillus coli
  communis, bacillus of duck cholera, spirillum Metchnikowi. Symptoms:
  dullness, fever, langor, inappetence, thirst, pale comb, greenish
  fæces, erect plumage, drooping wings and tail, sunken head, gaping,
  staggering, somnolence, bloody fæces, violet comb, low temperature,
  death in one to three weeks. Diagnosis: by restriction to one flock,
  or species, and immunity of rabbits. Mortality 80%. Prevention:
  separation of sick and healthy, disinfection of roosts and yards, pure
  food and water boiled or acidified, immunization. Treatment: boiled
  food with antiseptics, antiseptic enemata, stimulants, tonics.


_Causes._ A number of different microbes are implicated in producing and
maintaining catarrhal enteritis in the domestic poultry. All forms of
the disease are therefore closely related to the well known fowl
cholera, which is however to be differentiated, by its more intense
virulence, rapid progress, and its deadly effect when inoculated on the
rabbit. As in other forms of microbian enteritis, that of fowls is
undoubtedly favored by general and local debility, youth, old age,
unsuitable food and other health depressing causes, yet as the specific
pathogenic microbe has been in many cases identified, it is well to
consider some of the different species.

=Bacillus gallinorum= found by Klein (1889) in the blood of chickens
suffering from an infective diarrhœal enteritis, is ovoid, with rounded
ends, from 0.8 to 2_μ_ long and 0.3 to 0.4_μ_ thick; often in pairs.
Stains in the aniline colors. Ærobic (facultative anærobic)
non-liquifying, non-motile, asporogenous. Culture easy in neutral,
alkaline or slightly acid media at room temperature, or better in
thermostat. On gelatine plate films, it forms grayish white, superficial
colonies, becoming flat homogeneous white discs, brownish under
transmitted light. The deeper colonies are small spherical and brown or
yellowish by transmitted light. On agar it forms a thin gray layer with
irregular margins, which extends over the entire surface. In bouillon it
causes turbidity and in 24 hours a precipitate of bacilli to the bottom.

=Pathogenesis.= Chickens inoculated hypodermically or intravenously die
in 1 to 5 or 6 days with peritonitis and intense intestinal congestion.
Fed in vegetable food it is harmless, but with animal food virulent.
Rabbits and pigeons are immune.

Pond water is a common source of casual infection, also dung heaps in
which carcasses of little chicks have been buried. Summer is the period
of greatest prevalence, as there is the best opportunity for the
multiplication of the germ, and the drying of the ponds concentrates the
product.

The bacillus is found on the intestinal mucous membrane, and in the
mucus and in advanced stages, in the blood, spleen, liver and kidneys.

=Bacillus Coli Communis=, the familiar bacillus of the healthy bowel, is
charged by Lignieres with causing a fowl enteritis and probably does so
as in mammals when the mucosa has become diseased and non-resistant. At
the same time there are so many closely allied forms or varieties of
this bacillus found in different intestinal diseases, that it may well
be that the pathogenic agent is a modified form or “sport” from the
parent microbe, though no clearly defined peculiarities can be
established by cultures.

The typical colon bacillus is 2 to 3 _μ_ long by 0.4 to 0.6 _μ_ broad,
with rounded ends, but it may be ovoid or even round, or it may be 5 _μ_
long. It stains readily with aniline colors, bleaches with iodine. It is
ærobic, facultative anærobic, non-motile, non-liquifying, and
asporogenous. It ferments all sugars producing gas, acidifies its
culture fluids, and coagulates milk. It grows freely at room
temperatures in peptonized gelatine, agar and bouillon and on potato.
Stab cultures in gelatine have a moss-like tufted appearance.

=Pathogenesis.= Injections subcutem, and into the veins and ingestion
with food all failed to infect the chicken, while the pigeon died in 24
hours from intravenous injection and in 12 to 18 days from 1 c.c. given
subcutem. In rabbits and guinea-pigs hypodermic injection caused
abscess, while pleural and peritoneal injections killed in 24 to 48
hours. Rabbits are unaffected by intravenous injection, while
guinea-pigs die in 1 to 3 days.

=Bacillus of Duck Cholera= found by Cornil and Toupet in the blood of
ducks suffering from a diarrhœal enteritis, is 1 to 1.5μ long, by 0.5μ
broad, with rounded ends. It is ærobic, non-liquifying, non-motile and
asporogenous. Stains in the aniline colors and bleaches in iodine.

=Pathogenesis.= In morphology and cultures it resembles the bacillus of
fowl cholera, but it fails to infect chicken, pigeon or rabbit. It
infects ducks readily by ingestion or hypodermic inoculation.

=Spirillum Metchnikowi= was found in 1888, by Gamaleia in the ingesta of
chickens dying in Russia of a choleræic enteritis. It resembles the
cholera spirillum, but is shorter, broader and more curved. Its size
varies, being twice as broad as the cholera spirillum, when found in
pigeons. It may be 0.8μ long, by .5μ broad, furnished with one polar
flagellum and very motile. It stains in aniline colors and bleaches in
iodine. Grows readily in common media at room temperature, and is killed
in five minutes by 122° F.; renders milk strongly acid, coagulating it,
and perishes in the acid. In eggs turns the albumen yellow and the yolk
black. In gelatine it forms transparent colonies and in potato pale
brown.

=Pathogenesis.= By inoculation it infects chickens, pigeons and
guinea-pigs, while rabbits and mice are refractory except to large
doses. By ingestion it infects chickens and guinea-pigs but not pigeons.
Infection takes place easily by the air passages. In all cases alike the
lesions are concentrated in the intestines.

_Lesions._ These are very similar in the different forms. The intestine
is violently congested and contains a quantity of yellowish green
mucopurulent or serous fluid. The mucosa is infiltrated, softened and
even abraded by the desquamation of epithelium. The liver is greatly
enlarged and softened and gorged with blood, and the gall bladder
filled. The spleen is enlarged and pale, contrary to what is seen in
fowl cholera, and the kidneys are congested. The heart is flaccid, soft,
petechiated, and the pericardium is the seat of serous effusion.

_Symptoms._ In the _acute form_ there is dullness, langor, inappetence,
ardent thirst, pale comb, and greenish fæces. Later the feathers are
erect, the wings and tail droop, the head sinks, the patient gapes
frequently, walks unsteadily, and a liquid bluish green diarrhœa sets
in, which later becomes yellow and bloody. The somnolence increases, the
walk becomes more unsteady, or the patient sinks down with eyes half
closed and refuses to rise. As the disease advances the comb becomes
violet, the dark shade constantly increasing and a glairy grayish mucus
is discharged from the nose and bill. The temperature which was at first
raised 1° or 2°, falls 2° or 3° below the normal prior to death, which
may be deferred to near the end of the second week.

In the chronic cases the disease may drag along for three weeks, the
emaciation, pallor and weakness constantly increasing and the feathers
around the anus soiled and matted together by the fœtid liquid
discharges. There may be remissions which go on to complete
convalescence but more commonly an exacerbation occurs which proves
fatal in a day or two.

_Diagnosis._ From fowl cholera this may be distinguished by the fact
that it is confined to one farm or flock of turkeys, chickens or ducks,
proving most deadly in early summer, to the broods of the same spring,
and at the commencement of the epizootic, and proving less and less so
as time passes. The immunity of rabbits even when inoculated is a
further distinguishing feature. From intestinal parasitism it is
distinguished by the color of the discharges, and the absence of worms
and their eggs from these liquids.

_Mortality_ is often very high. Klein found it 80 per cent.

_Prevention._ Remove the infected from the flock (with ordinary fowl it
is often best to kill and burn or bury them), keep the poultry house and
yard scrupulously clean of droppings and sprinkle it occasionally with a
3 per cent. solution of sulphuric acid. The poultry house may be
fumigated with sulphur (1 ounce to the cubic yard), or the walls and
roosts may be washed with a solution (1:12) of bisulphide of carbon in
liquid vaseline. The diseased must be removed as soon as they are
detected and food and water must be given pure. If pure water is not
available, boil it or render it acid by sulphuric acid (1:33), and feed
grain, cooked roots, bran and bread with more or less green food.

In the case of valuable birds immunization may be secured by inoculating
with the virulent blood or culture so diluted that not more than one or
two of the germs shall be inserted in each case or the virulent liquid
may be heated for 20 minutes to a temperature of 55° C (121° F) and then
injected in a dose of 2 drops.

_Treatment._ If it is decided to treat the sick they should be placed
together in safe seclusion from all others. Feed with mush or cooked
roots or vegetables adding salol ½ dr. naphthol 1 dr. and quinia 1 dr.
to the food of 15 or 20 fowls. Nitrate of bismuth and powdered charcoal
may be added in moderate quantities. As drink give water containing 2%
of sulphuric acid. Antiseptic enemata may be added in the case of very
valuable birds, salol, naphthol, boric acid, salicylate of soda, or
solution of carbolic acid or creosote. Stimulants and tonics are highly
esteemed by some, and Cadeac recommends the free use of the following
mixture: powdered fennel, anise, coriander and quinia of each 5 drs.,
gentian 10 drs., ginger 12 drs., ferric sulphate 2½ drs.


       COCCIDIAN ENTERITIS IN CATTLE. COCCIDIOSIS. RED DYSENTERY.

  Definition. Distribution: Switzerland in summer. Causes: weakness,
  debility, youth, cold, heats, spoilt fodder, protozoa, coccidium
  oviforme, coccidium perforans. Lesions: reddening, thickening and
  desquamation of alimentary mucosa and lungs, congested mesenteric
  glands, liver and spleen, coccidia in discharge and epithelium,
  staining, anæmia. Symptoms: chill, fever, grinding teeth, fœtid
  diarrhœa becoming bloody, tenesmus, stiffness, red ulcerated rectum,
  emaciation, false membranes. Duration: death in one to fourteen days
  or more. Complications. Diagnosis by coccidia. Prevention: avoidance
  of affected soils, water and fodder. Treatment: antiseptic, by mouth
  and as enemata, demulcents. Flesh safely eaten by man. Coccidium
  bigeminum in dogs, coccidium oviforme in rabbits, coccidium tenellum
  and gregarina avium intestinalis in birds.

_Definition._ Enteritis affecting chiefly the colon and rectum, and due
to the presence of the protozoa, coccidium oviforme, and coccidium
perforans.

_Distribution._ This affection was found in 1885 in the cantons of
Berne, Lucerne and Argovi where it attacked 5 per cent. of the cattle
and destroyed from 2 to 4 per cent. of those that suffered. It prevailed
mainly in the summer (May to October) on the pastures, though not
unknown at other seasons. Sucking calves were immune and the ages of a
year to two and a half years were the main sufferers.

_Causes._ Predisposing causes embrace such as induce weakness or
debility, youth, low condition, cold intemperate weather, extreme heats,
musty or spoilt fodders.

The essential cause, the coccidium, appears to be taken in with food or
water as sucking calves are largely exempt. The parasite is found in the
gastric and intestinal epithelium of the diseased animals, in numbers
proportionate to the severity of the attack, being very abundant when
the disease is at its height, diminishing during convalescence, and
disappearing entirely on recovery. Two species are found in this
disease.

=Coccidium Oviforme= is 40 to 50μ long by 22 to 28μ thick, ovoid, with a
double outlined limiting membrane enclosing a refrangent protoplasm with
a nucleus two or three times as large as that of an epithelial cell, and
staining with hæmatoxylon or aniline colors. The young coccidia appear
as round granular protoplasmic masses, without a capsule but provided
with a nucleus. At first of a diameter of 9 to 10μ they increase to 26μ
retaining the spherical form and acquiring the membrane of the mature
parasite. As it grows the protoplasm separates from the wall and forms a
globular nucleated mass, which after fifteen days divides into two and
later into four masses or sporoblasts. Each sporoblast in its turn
divides into two falciform corpuscles lying in contact but in an inverse
sense to each other. Each of these under favorable conditions becomes a
new amœboid individual capable of invading an epithelial cell and
passing through the same stages of development as its predecessor.

The coccidium oviforme is found in the epidermis in cutaneous
psorospermosis of birds, and in the coccidian hepatitis in rabbits.

=Coccidium Perforans.= In its mature form this is 25μ to 35μ long, by
14μ to 20μ broad. Its different stages of evolution are essentially the
same as for the Coccidium Oviforme. It is a cause of intestinal
Coccidiosis in both dog and rabbit as well as in cattle, usually killing
the rabbit in from eight to ten days.

_Lesions._ In the first reported cases in calves in 1877 (Proger and
Zurn), there was catarrhal inflammation of the upper air passages as
well as the bowels. There was thickening, redness and desquamation of
the abomasum near the pylorus of the small intestine and colon. In the
intestines there were patches of thickening and softening of the mucosa
and miliary ulcers with yellowish contents. The mesenteric glands, liver
and spleen were enlarged, softened and ecchymosed. In all the lesions
coccidia were found. In the cases reported by Hess, Zschokke, Guillebeau
and Cadeac the abomasum and large intestine principally suffered. There
was a diffuse inflammation of the mucosa and in the rectum and portion
of the colon a great degeneration and desquamation of the epithelium.
The columnar cells of the mucous glands especially suffered. A single
cell would contain five or six psorosperms, in different stages of
development. If the parasites have escaped, the cell walls are pressed
together. Among the diseased glands others with healthy epithelium were
found, their orifices plugged with mucus. Both forms of coccidia above
described are found in two conditions, in the epithelial cells with
granular nuclei staining in hæmatoxylon, and violet or black with iodine
(Lugol’s), and outside the cells with granular nucleus or simple hyaline
contents which do not stain. Zschokke considers the latter as in process
of degeneration. Other organs are anæmic.

_Symptoms._ The disease is ushered in by cold extremities, weakness,
dullness, suspended rumination, ardent thirst, hyperthermia, 102° to
104° and even 106°, small, weak thready pulse beating 100 to 140 per
minute, sunken eyes, grinding of the teeth, and defecation in small
quantity only. Toward the fourth day or earlier a fœtid diarrhœa sets
in, watery, bloody and fibrinous. The bloody discharges last to the
seventh day, the diarrhœa to the end of the second or fourth week.
Straining may be violent, exposing or everting the irritated or
ulcerated rectum, the hind parts may be stiff, the patient rises with
difficulty, he winches if pressed on the back or right side of the
abdomen, loses flesh rapidly and becomes a walking skeleton. when the
discharges are less profuse cylindroid croupous casts are sometimes
expelled.

_Course._ _Duration._ In the weak and young a violent attack may prove
fatal in 24 hours. In others the malady lasts for two or more weeks and
sometimes relapses, and the patient becomes very weak and anæmic.
Complications of various kinds may also supervene and cut off the
animal, the lesions and debility alike favoring the introduction of the
germ. Thus black quarter, bronchitis, pneumonia, convulsions, paralysis,
phthiriasis and ring-worm have been noted as sequelæ.

_Diagnosis_ can always be made by microscopic examination of the fresh
warm fæces.

_Prevention._ This will consist in the avoidance of water and of green
food from soils where the disease has been found to prevail.

_Treatment._ Antiseptics given by the mouth have proved of very little
avail having as a rule lost their power through dilution in the contents
of the stomachs. They may still be given to keep in check the
propagation of the coccidia in the fourth stomach. Silver nitrate, iron
sulphate, lead acetate, tannic acid, oak bark, carbolic acid, cresol,
lysol, salicylic acid, hydrochloric acid, sulphuric acid, hyposulphite
of soda have been used in this way. The same agents may be used with
better effect as enemata being forced as far as is consistent with
safety and frequently repeated. Quinia and iodide of potassium may also
be given as parasiticides. Mucilaginous gruels and decoctions should be
given at first, followed by mashes as they can be borne, but the food
must be moderate and easily digestible until full convalescence has
taken place.

The flesh of animals killed while suffering from this affection has been
eaten by man with impunity.


        COCCIDIAN ENTERITIS IN THE DOG. INTESTINAL COCCIDIOSIS.

_Causes._ Two parasites have been found in connection with this disease
in the dog; the =Coccidium penetrans=, already described, and the
=Coccidium bigeminum=.

=Coccidium Bigeminum, var. Canis.= This is elliptical and from 12 to 15
μ long by 7 to 10 μ broad. They are usually found in pairs lying side by
side, and sometimes both in the same envelope indicating multiplication
by division along the longitudinal axis.

The bigeminum is held to be harmless, but the perforans, as in the cow
and rabbit is very injurious and even fatal. The _symptoms_ are those of
digestive disturbance, dullness, loss of appetite, retching, vomiting,
colic and fœtid and bloody diarrhœa. Irritability, and a morose
disposition and loss of control over the hind limbs have been set down
as rabiform indications.

_Diagnosis_ depends on the inveteracy and sanguineous nature of the
diarrhœa, but especially on the discovery of the amœboid organisms in
the recent, warm discharges.

_Treatment_ should be along the same line as in cattle.


        COCCIDIAN ENTERITIS IN RABBITS. INTESTINAL COCCIDIOSIS.

_Causes._ In rabbits the coccidium perforans is the psorosperm which
usually attacks the bowels. The coccidium oviforme which produces
hepatic coccidiosis is also occasionally found in the intestines. The
perforans is smaller than in cattle being 15 to 25 μ long, by 12 to 15 μ
broad, approximating to the variety found in man.

_Lesions._ There is extensive congestion of the intestinal mucosa, with
thickening and softening of the epithelium so that it breaks down into a
pulp under pressure, also free desquamation with the formation of
abrasions, sloughs and ulcers. In some instances extensive croupous
casts of the intestine are found. As in the other animals the coccidium
is found abundantly in the epithelial cells of the affected parts which
swell up and degenerate. When the parasite has escaped from the cells it
lives free in the abundant mucopurulent and sanguineous secretions of
the bowels.

_Symptoms._ There are loss of appetite, swelling of the abdomen, profuse
diarrhœa, the fæces yellowish in color and containing mucopurulent
matters and blood. The disease may prove fatal in a few days without
much loss of flesh, but if protracted it leads to extreme anæmia,
emaciation and debility and the animal dies in marasmus.

_Diagnosis_ is always to be certified by the profusion of coccidia found
in the fresh liquid discharges.

_Prevention_ must be secured if possible by the removal of the healthy
rabbits from the infected and from the hutch or warren in which the
latter have been. The greatest care must be taken to prevent them from
obtaining access to the droppings of the sick, or to streams, ponds or
wells, into which the drainage from such manure can have found its way.
The safest course is to destroy the sick and burn up them and all their
droppings, as the latter ground into powder can blow on the wind.

_Therapeutic treatment_ has proved unsatisfactory but may be attempted
along the same lines as for the larger animals.


         COCCIDIAN ENTERITIS IN BIRDS. INTESTINAL COCCIDIOSIS.

Two sporozoa are known to be pathogenic in the intestines of birds: the
=coccidium tenellum= and the =gregarina avium intestinalis=.

=Coccidium Tenellum.= This has a nearly globular body 21 to 25 mm. long
by 17 to 19 mm. broad, a very thin, delicate investing membrane, and has
been found in the mucosa of the cæca of birds, producing a fatal
typhlitis. The sporoblasts are developed in water outside the animal
body and when taken in with the food colonize in the intestinal mucosa.

=Gregarina Avium Intestinalis.= When mature this is in form of a
granular body with hollow spaces or utricles, is oval, or globular and
measures 40 to 48 μ in diameter. The spores are 11 to 14 μ. They are
found in the submucosa of the intestines in chickens, being taken in
with food or water, and attack not the intestines only but the skin, the
buccal and pharyngeal mucosa and even the liver and lungs. They traverse
the mucous membrane and become encysted in the submucosa as white
isolated or confluent points, disturbing the circulation and nutrition
and destroying the nutritive and other functional activities of the
mucosa.

_Lesions._ From the coccidium tenellum these are mainly found in the
cæca and consist in intense inflammation, white lines formed by the
parasitic colonies, desquamations of the epithelium and erosions and
ulcers. In the early stages and in the absence of diarrhœa there may be
simply thickening and induration of the mucous membrane and whitish
colonies of the parasites. When there has been diarrhœa the contents are
serous, or seropurulent, brick red, and filled with epithelial cells,
red globules, leucocytes, fat globules and coccidia.

The gregarinæ are not confined to the cæca but scattered over the whole
intestinal canal as white spots in the submucosa surrounded by
congestion and degenerative changes. It has been found complicated with
false membranes.

_Symptoms._ Dullness, anorexia, ruffled feathers, sunken head, trailing
wings, slow uncertain gait, plaintive cries, with diarrhœa, passing
through serous, brick red, and bloody. In small chicks it may be whitish
and followed by constipation. Death is usually an early result.

_Treatment._ Hyposulphite of soda with carminatives (fennel anise,
coriander, ginger, and gentian) has been given in boiled milk or bread.
Quinia and iodine might be tried.

_Prevention._ Avoidance of infected roosts and runs, and above all of
infected streams, wells and ponds, and the removal and cremation of the
sick, followed by thorough disinfection, are much more promising than
therapeutic treatment.


       GASTRO-ENTERITIS FROM CAUSTIC ALKALIES AND ALKALINE SALTS.

  Ammonia: Counter-irritation, fauces, larynx, bronchia, congestion and
  softening of the gastric mucosa, loose blood clots, solution of
  globules, dysphagia, salivation, in carnivora and omnivora vomiting,
  diarrhœa, white fumes with muriatic acid.—Ammonia carbonate: less
  corrosive, same symptoms.—Potash lye, deep corrosion, gastric
  congestions, fluid, blackish red blood.—Soda lye.—Carbonates of potash
  and soda, less violent, tests for potash and soda. Treatment: weak
  acids, demulcents, anodynes.

=Aqua Ammonia.= Lethal dose pure, horse 1 oz. and upward; cattle 2 ozs.;
dog ½ dr. There may be sudden death from abstraction of water and
cauterization of the fauces and larynx including at times the bronchial
mucosa. In other cases death occurs later from gastro-enteritis, the
mucosa of the alimentary canal being congested, softened and covered
with bloody mucus. The blood in the vessels is of a dark red, coagulates
imperfectly and the blood globules are dissolved changing the color to
black, and then brownish red. Prior to death there is great distress,
salivation, inability to swallow, swollen tongue, frequent pulse and
respiration, cough, spasms, and sometimes the odor of ammonia. Retching
and vomiting may be a feature in carnivora and omnivora, and diarrhœa if
the case is not promptly fatal. The urine is not rendered alkaline.
White fumes with muriatic acid indicate ammonia.

=Ammonia Carbonate= gives rise to the same symptoms and lesions with the
exceptions that there is less corrosion of the mucosa, and no pure
ammonia exhales in the breath.

=Caustic Potash, Lye.= Lethal dose, 5 grs. dog intervenous. In strong
solution this is one of the most potent caustics, which penetrates
deeply into the tissues and abstracting water cauterizes everything with
which it comes in contact. It therefore produces the most destructive
changes on the walls of the stomach, and intestines, with violent
gastro-enteritis, retching, or vomiting of alkaline matters. The
congested, ashen and even black color of the tongue, and (post mortem)
of the gullet, stomach and intestines, and the intense alkalinity of
contents are characteristic. The blood is fluid, gelatiniform, and
blackish red. Later, erosions and contractions are common.

=Caustic Soda= is only less destructive than potash, and produces the
same general lesions and symptoms.

The =Carbonates of Potash and Soda= have the same general properties
only they act with very much less energy. Potassium can be recognized by
its purple color in an alcohol or Bunsen flame and sodium by an intense
yellow.

_Treatment._ Weak acids (acetic, vinegar, citric, malic, lactic, boric,
benzoic, salicylic) or the stronger mineral acids largely diluted.
Mucilaginous solutions (flaxseed, elm bark, gruel, mallow). Anodynes
(opium).




                  GASTRO-ENTERITIS FROM CAUSTIC ACIDS.

  Sulphuric acid, corrodes, blackens, dysphagia, salivation, retching,
  vomiting, colics, collapse. Lesions. Test, barium nitrate. Nitric
  acid, corrodes, stains yellow, or brown. Test, reddish fumes with
  copper and sulphuric acid. Muriatic acid, corrodes, whitens. Test,
  chlorine odor, white curdy precipitate with silver nitrate. Oxalic
  acid, colic, emesis of black bloody matter, gastric mucosa red or
  black, blood bright red, lowered respiration, innervation,
  temperature. Acetic acid, congestion, softening of gastric mucosa, may
  stop heart. Treatment: weak bases, magnesia, lime or their carbonates,
  soap, lime water, demulcents.


=Sulphuric Acid.= This acts on stomach and intestine as on the mouth
abstracting water and blackening the tissues. It produces dysphagia,
salivation, retching, vomiting in carnivora and omnivora, colics, and
collapse. Sometimes the urine becomes albuminous or bloody. The post
mortem blackness of the contents and walls of stomach and intestine and
their intense acidity are characteristic. Nitrate of baryta will
precipitate the insoluble sulphate.

=Nitric Acid.= In concentrated state this acts in the main like the
sulphuric acid, but stains the lips yellow, and the mucosæ white
changing to citron yellow or brown and does not precipitate baryta. It
gives reddish fumes with copper and strong sulphuric acid.

=Muriatic Acid.= This is less caustic than nitric or sulphuric acid, and
may be recognized by its white cauterized patches on the mucosa of the
mouth, stomach and intestines, its chlorine odor, and the curdy
precipitate which it throws down with silver nitrate. It does not
corrode the skin. In the stomach this acid is normally present in the
free state.

=Oxalic Acid.= Lethal dose, dog 15 grs., cat 2 grs. When swallowed this
causes colics, emesis in vomiting animals, the rejected matters being
black and perhaps bloody. After death the gastric contents and walls and
those of the bowels are congested and more or less blackened, and the
blood of a bright red color. Heart is arythmic, respiration slow,
paresis of limbs, spasms, temperature subnormal.

=Acetic Acid.= This causes congestion and softening of the gastric and
intestinal mucosa, colics, emesis in vomiting animals. It may kill by
suddenly arresting the heart’s action.

_Treatment_ for the acids consists in alkaline or basic antidotes;
magnesia, or its carbonate, lime, or its carbonate, soapsuds, carbonates
and bicarbonates of potash and soda. Lime water is the one appropriate
antidote to oxalic acid, precipitating the insoluble oxalate.
Mucilaginous drinks may be added freely.


                     POISONING BY SODIUM CHLORIDE.

  Poisonous with privation of water. Dose: horse, ox, pig, dog, hen.
  Symptoms: anorexia, thirst, emesis, colics, diarrhœa, dysuria,
  weakness, spasms, palsy, death in six hours to two days or more.
  Lesions: gastric congestion, ecchymosis, blood fluid, bright red,
  cerebral congestion. Treatment: emesis, water, demulcents, enemata,
  oils, cold to head. Brine: salt, ptomaines, toxins, from salt meat and
  fish. Strongest at three months old. Dose: horse, pig, dog. Symptoms:
  nervous, disorder, mainly spasmodic. Lesions: congestion of
  encephalon. Treatment: anodynes, stimulants, wine, camphor.

Common salt is especially irritant if given in concentrated solution and
with subsequent deprivation of water. The poisonous dose for the horse
is 2 to 3 lbs. (Gohier), for cattle 4 to 5 lbs. (Hertwig), for the pig 7
to 8 ozs. and for the dog 6 to 7 ozs. Chickens are poisoned by picking
up broken pieces of salt instead of pebbles, or by salted food.

_Symptoms._ Anorexia, intense thirst, dullness, emesis in vomiting
animals, colics, watery diarrhœa, frequent urination, muscular weakness,
spasms, paralysis, weak pulse, red buccal mucosa, dilated pupils. Death
may take place in six hours or it may be delayed two days or longer. In
chickens giddiness and rotary movements are common.

_Lesions._ Congestion of the stomach and intestines with points of
ecchymosis. The mucosa of the bladder is reddened. The blood is fluid
and of a bright red. There is more or less congestion of the cerebellum
and medulla and their meninges.

_Treatment._ Emetics (tepid water, tickling fauces) and the stomach
pump. Abundance of water or of mucilaginous drinks. The same liquids by
the rectum. Bland oils may be given as emollients and eliminating
agents. Cold to the head is usually desirable.


                          POISONING BY BRINE.

This is partly due to the toxic effects of common salt but also to the
ptomaines and toxins formed in old brine. It has been seen most
frequently in hogs fed on salted kitchen waste and on the liquids from
salt meats, (beef, pork, fish). Herring-brine is a common source of
poisoning for hogs and dogs, also the brine from the salted meats of the
butcher’s shops. Reynal found it to be especially poisonous when at
least four or five months old. He gave as the fatal doses for horse 3½
pints, for pig ½ pint, for dog 6–7 ozs. The lethal dose however will
vary with the concentration of the fluid and its age.

_Symptoms._ In addition to the direct irritation caused by the sodium
chloride there are marked nervous symptoms, nervous irritability,
spasms, rolling of the eyes, convulsive winking, dilated pupil,
blindness, vertigo, staggering gait, epileptiform seizures, trismus,
oposthotonos, pleurosthotonos, stupor.

_Lesions._ In addition to those of the stomach and intestines there is
marked congestion of the encephalon, especially the medulla and
cerebellum.

_Treatment._ In addition to that for common salt, anodynes and
stimulants (wine, camphor) may be demanded.


                      NITRATES OF POTASH AND SODA.

  Lethal dose. Symptoms: Colics, tympany, emesis, salivation, pupillary
  dilatation, diarrhœa, diuresis, hypothermia, stupor, palpitations,
  trembling, spasms, palsy. Lesions: Congested gastro-intestinal mucosæ,
  erosions, ecchymosis, congested kidney and bladder. Blood fluid,
  bright red. Treatment: Emesis, stomach pump, water and mucilaginous
  liquids, stimulants.

Nitrate of soda being used largely as a top dressing for grass and other
crops is more liable to be taken in toxic doses than nitrate of potash.
The former is also given in mistake for common salt. The toxic dose is
high. Morton gave 2 pounds saltpeter to a horse with only a temporary
purgative and diuretic effect. Huzard found that 3 doses of 16 ounces
each, given at intervals of 8 days sufficed to kill a horse. Cattle are
said to have died from taking 5 to 6 ounces.

_Symptoms._ There are colics, tympany, emesis in vomiting animals,
salivation, dilated pupil, diarrhœa, diuresis, hypothermia, stupor,
palpitations, weak pulse, trembling, convulsions, tetanic symptoms,
paralysis.

_Lesions._ Congestion of a cherry red, brown or purple of the gastric
mucosa and that of the small intestine, erosions and ecchymosis,
congestion and ecchymosis of the kidney and of the mucosa of the
bladder. Blood uncoagulated and of a bright red.

_Treatment._ Favor emesis or use stomach pump according to the species
of animal. Give abundance of water or mucilaginous fluids by mouth and
anus. Stimulants may be resorted to in case of sinking or collapse.


        ACUTE ARSENICAL POISONING, ARSENIOUS ACID, PARIS GREEN.

  _Acute poisoning._ Sources. Lethal dose, horse, ox, sheep, dogs, pigs.
  Endermic. Symptoms: colic, weak pulse, rapid breathing, red eyes,
  dilated pupils, purging, weakness, trembling, stupor, convulsions,
  paralysis, green or yellow vomit, test of urine. Lesions:
  gastro-intestinal inflammation, ropy, bloody mucus, ecchymosis,
  extravasation, ulceration. Treatment: emesis, stomach pump, hydrated
  iron oxide, calcined magnesia.—_Chronic poisoning._ Excessive
  administration, arsenical fumes from smelting furnaces. Symptoms:
  indigestion, emaciation, hide-bound, depilation, red eyes, diarrhœa,
  agalactia, weakness, paraplegia, salivation. Lesions: as in acute,
  fatty liver, test of urine. Tests: on hot charcoal garlic odor,
  Marsh’s test by zinc and sulphuric acid. Treatment: avoidance of
  cause, antidotes demulcents, diet.

Arsenious acid given recklessly as medicine, rat poison, arsenite of
soda made into a sheep dip and left within reach of animals, and
arsenite of copper used for potato bugs, or other insect pests and
carelessly left where animals can get it are the most common sources of
acute arsenical poisoning. Horses die from 140 grains in solution, or 3½
drs. in the solid form, cattle from 3½ to 7 drs., sheep are killed by 2
drs., dogs may die from 2 grs., but larger doses usually cause vomiting
and the animal is saved. Hogs may die from 15 grs. but they often save
themselves by vomiting with much larger doses. The poisonous effects may
be induced by putting arsenic on a raw sore.

_Symptoms._ Violent colic, quick, feeble, irregular pulse, hurried
respiration, emesis in vomiting animals, ardent thirst, purging,
tenesmus, lowered or unevenly distributed temperature, red eyes, dilated
pupils, and nervous symptoms, weakness, trembling, stupor, convulsions
and paralysis. The urine is albuminous and may be bloodstained. In case
of Paris green, the green color of the vomit, and of arsenious acid, a
yellow color may be looked for. Test urine for arsenic.

_Lesions._ Inflammation of the stomach and small intestine, with ropy,
often bloody mucus. Ecchymosis, and extravasations appear in the
stomach. Ulceration is not common in very acute cases, but in protracted
cases, it is usually present in the stomach (abomasum in cattle).
Petechiæ may be met with in different internal organs and in protracted
cases, fatty degeneration of liver, heart, or kidney.

_Treatment._ In vomiting animals encourage emesis by tepid water,
tickling the fauces, or giving ipecacuan. For non-vomiting animals the
stomach pump may be tried. The available antidotes are hydrated oxide of
iron, or a solution of calcined magnesia. To make the first, mix 100
parts sulphate of iron in solution with 250 parts magnesia in solution.
This should be given liberally and often: horse or ox 1 qt., sheep or
pig 2 ozs., dog 1 oz. A simple aqueous solution of calcined magnesia
also forms with arsenic an insoluble combination.




                      CHRONIC ARSENICAL POISONING.


This comes from continuous injudicious dosing with arsenic, or from the
condensing on the grass of the vapors from the smelting of ores
containing arsenic.

_Symptoms._ There is chronic indigestion, emaciation, hide-bound,
depilation, red or weeping eyes, chronic diarrhœa, suppression of milk
in cows, muscular weakness, paraplegia, soreness of the gums,
salivation.

The _lesions_ are essentially the same only less intense than in the
acute form. Hugo found in the intestines of poisoned animals a slimy,
serous, grayish white fluid, and a false membrane like a frog spawn
streaking the intestine. Later this may be dense like a diphtheritic
membrane. There was fatty degeneration of the liver and of the gall
bladder epithelium. Injection of the capillary vessels of the brain and
pia, and effusion into the ventricles and on the surface of the brain
were found in dogs.

_Elimination._ Arsenic is eliminated mainly in the urine, but also in
part in the bile and perspiration.

_Tests for Arsenic._ When taken in the solid form it may be found
undissolved on the gastric mucosa.

If burned on red hot charcoal or iron it gives out the odor of garlic.

Marsh’s test consists in evolving arseniureted hydrogen from zinc and
sulphuric acid to which a little of the suspected liquid has been added.
A flask is taken having a cork conveying two tubes, one a funnel
reaching nearly the bottom of the flask, and the other a delivery tube
of some length and provided with a chloride of calcium bulb, and at its
end turned up at right angles and drawn out to form a narrow orifice.
Pieces of zinc are placed in the bottom of the flask, and sulphuric acid
is poured upon these through the funnel. This causes the evolution of
hydrogen. The suspected liquid is now added, and the gas issuing from
the delivery tube having been lighted, a piece of cold white porcelain
is held above and a short distance from the flame. A dark metallic spot
of arsenic is obtained. The stain obtained by antimony differs in being
formed more closely to the flame, in volatilizing less rapidly under
heat, and in forming a black or orange instead of the canary yellow
sulphide when subjected to a stream of H_{2}S. with gentle heat.
Chloride of lime dissolves the arsenic stain but has no effect on the
antimonial one.

_Treatment._ Avoid the causes. Employ the antidotes in small doses once
or twice daily. Check the diarrhœa by mucilaginous agents, and nourish
the animals well.


                        POISONING BY PHOSPHORUS.

  From matches, rat poisons, fatal dose, horse, ox, pig, dog, chicken.
  Symptoms: Anorexia, dysphagia, swelled tongue, thirst, colic, emesis,
  vomit phosphorescent, or bloody, diarrhœa, icterus, agalactia,
  trembling, weakness, choreic spasms, hemorrhages. Lesions:
  Buccal-gastro-intestinal inflammation, fatty degeneration of
  epithelium, liver, kidneys, heart and muscles, black blood,
  ecchymosis, hemorrhage, phosphorescent ingesta. Treatment: Emesis,
  stomach pump, oil of turpentine in mucilage.

Phosphorus is usually taken in the form of matches or more frequently as
one of the pastes sold for the destruction of vermin. Almost all of the
latter contain 1 to 2 per cent. of phosphorus, in combination with
flour, sugar, and fatty or oily matters. The lethal dose of phosphorus
is: Horse or ox 7 to 30 grains; pig 2 to 4 grains; dog ¾ to 1½ grain;
chicken ⅓ grain.

_Symptoms._ Anorexia, dysphagia, swelling of the tongue, intense thirst,
colic, emesis in vomiting animals, vomited matters may shine in the
dark, and may be tinged with blood, diarrhœa is common though not
constant, icterus, and suppression of the milk. Trembling, weakness,
acceleration of the pulse and breathing and hyperthermia may be noted.
Chickens have been noticed to have choreic movements in walking.
Hemorrhages are common.

_Lesions._ Inflammation of the mucosa of the alimentary canal from the
mouth to the stomach and intestines. Fatty degeneration of the
epithelium very noticeable in the gastric glands. Enlargement and fatty
degeneration of the liver and kidneys, and degeneration of the heart and
muscles. The blood is black and ecchymosis and hemorrhages appear on
various internal organs. The contents of stomach and bowels shine in the
dark. Phosphorus may be recognized by its luminosity when distilled at a
very low heat from an acid solution and received into a refrigerated
condenser. This must be done in perfect darkness, and the
phosphorescence will be seen in the condenser or connecting tube.

_Treatment._ Empty the stomach by emetic or stomach pump, and then give
oil of turpentine in mucilaginous liquid: Horse 1 to 2 ounces; ox 2 to 3
ounces; pig ½ ounce; dog 20 to 30 drops; chicken 5 to 10 drops. This may
be repeated several times and if used early enough will probably
succeed.


                      POISONING BY TARTAR EMETIC.

  Fatal doses, large in herbivora. Symptoms: vomiting, diarrhœa,
  ulcerative stomatitis, salivation, thirst, colic, tremors, palsy.
  Lesions: gastro-intestinal inflammations, ulcerations, lung
  infarctions. Treatment: emesis, antidote tannic acid.

This is mainly seen in the smaller vomiting animals. To kill horses or
cattle much larger doses are necessary than are likely to be taken.
Barlow and Dun gave 4 drs. to a horse thrice a day, and in all 10 ozs.
in 10 days, yet it improved in condition. Ten and a half ounces given in
6 days proved fatal. An old sow was killed by 2 drs., a 5 months pig by
80 grs., (Hertwig). Dogs were killed by 3 to 7 grs.

_Symptoms._ Vomiting, diarrhœa, ulcerative stomatitis, salivation,
vertigo, thirst, dullness, cold surface, colicy pains, trembling,
paralysis of the hind quarters, and early death.

_Lesions._ General inflammation of the gastric and intestinal mucosa,
sometimes ulceration especially if the agent has been taken in the solid
form. Congestions and infarctions of the lung are not unknown.

_Treatment._ Encourage vomiting by tickling the fauces, and by the
ingestion of tepid water. The best known antidote is tannic acid in any
one of its combinations. Solution of tannin, decoctions of oak bark, oak
galls, catechu, kino, rumex, sumac, or even strong tea will serve to
render it insoluble and non-irritant.


                POISONING BY CORROSIVE SALTS OF MERCURY.

  Calomel with muriatic acid, corrosive sublimate, mercuric chloride,
  iodide, nitrate, cyanide. Fatal dose. Symptoms: anorexia, salivation,
  thirst, emesis, colic, diarrhœa, rumbling, debility, tremors, stupor,
  death. Lesions: corrosive whitening of gastro-intestinal mucosa,
  congestion, ulceration, blackening, bloody, glairy ingesta. Treatment:
  albumen, emesis, demulcents, chlorate of potash, bitters, iron
  sulphate. Test: copper and muriatic acid.

Calomel in itself cannot be looked on as corrosive, but in ruminants in
which it is retained in the system for 3 or 4 days it is largely
resolved into mercuric chloride by the free gastric acid and alkaline
chlorides. It has therefore been largely excluded from the materia
medica of these animals. When in these or other animals it produces
corrosive action, the operation is essentially that of corrosive
sublimate.

The corrosive salts of mercury likely to be taken by animals are
corrosive sublimate now so largely used as an antiseptic, the nitrates
and iodides, and cyanides of mercury used as local applications or as
antiseptics.

=Mercuric chloride= may be taken as the type. It has proved fatal to the
horse in a dose of 2 drs.; to the ox in 1 to 2 drs.; to the dog in doses
of 4 to 6 grs.

_Symptoms._ Loss of appetite, salivation, thirst, emesis in vomiting
animals, colics, diarrhœa, often bloody, weak perhaps imperceptible
pulse, hurried breathing, much rumbling of the abdomen, debility,
trembling, stupor and death.

_Lesions._ Escharotic whitening in patches of the mucosa of the mouth,
throat, gullet, stomach and intestines, with acute congestion,
ulceration and ecchymosis, and sometimes blackening by the formation of
the sulphide. The contents of the bowels may be serous or bloody and
more or less glairy. Like arsenic, mercuric chloride concentrates its
action on the intestinal canal by whatever channel it may have entered
the body.

_Treatment._ The mercury should be precipitated in an insoluble form and
then eliminated by emesis or by the stomach pump. White of eggs is
usually the most available agent producing the albuminate of mercury.
This is, however, still soluble in acid and alkaline liquids, in
chlorides of potassium, sodium or calcium and even in excess of albumen.
Vomiting may be favored by tickling the fauces, or by hypodermic
injection of apomorphia. This may be followed by boiled flaxseed or
copious drinks of rain water. When the mercury has been largely
eliminated the salivation may be controlled by chlorate of potash, and
the digestive disorder met by bitters and iron sulphate.

_Test for Mercury._ Place a few drops of the suspected solution on a
clean surface of copper; acidulate with muriatic acid; then touch the
copper through the liquid with a piece of zinc; a silver colored stain
will be formed easily dissipated by heat.


                         POISONING BY SULPHUR.

  Fatal dose, horse 16 ozs. Symptoms: dullness, anorexia, colic,
  diarrhœa, sulphur odor. Lesions: congestion, desquamation, ulceration
  of gastro-intestinal mucosa, sulphur odor in flesh, blood nearly
  fluid, blackens silver. Treatment: chloride of lime, oil, puncture
  rumen or colon, stimulants.

In excessive doses this is irritant. The horse is poisoned by 16 ozs.
(Tabourin): violent colics follow a dose of 12 ozs. (Collaine). Cattle
are less susceptible.

_Symptoms._ Dullness, anorexia, colic, pulse small and quick, skin cold
and clammy. Fœtid flatus and profuse diarrhœa, are marked symptoms.

_Lesions._ Injection of the gastro-intestinal mucosa, shedding of the
epithelium, ulceration, and sometimes gangrene. Sulphur is found in the
ingesta and fæces and a sulphur odor is prominent, not only in the
bowels but also in the flesh. Tympany from H_{2}S is common. The blood
is mostly fluid, and ecchymosis is shown on heart, lungs and other
internal organs. The tissues blacken silver.

_Treatment._ Chloride of lime, oleaginous laxatives, use trochar and
canunla for tympany. In prostrate conditions give stimulants (alcohol,
ether).




                    POISONING BY BROMINE AND IODINE.


Poisoning by these agents is rare in domestic animals. Bromine 2 drs.
killed a dog in 5 hours: 10 to 12 drops in 1 oz. water intravenously
killed a dog suddenly, and 5 to 6 drs. of iodine by the mouth killed in
a few days (Orfila). A horse had colic from taking ½ oz. iodine
(Tabourin), others died from the effect of 2 drs. doses intravenously
(Patu).

_Symptoms._ Violent colicy pains, salivation, emesis in vomiting
animals, diarrhœa, iodine or bromine odor, acute coryza, red eyes,
dilated pupils, weakness, debility, vertigo, convulsions. If the patient
survives the glandular system undergoes atrophy, with emaciation and
scaly skin eruptions.

_Lesions._ After large doses there are congestion, ulceration, corrosion
and sloughing of the œsophagus, gastric and intestinal mucosa, and more
or less yellow discoloration of the parts. The odor is characteristic.
With iodine there may be blue iodide of starch in the ingesta.

_Treatment._ Favor emesis by tickling the fauces and giving tepid water,
or apomorphia subcutem. Boiled starch is the best antidote and may be
given freely, both by mouth and rectum. Opium is often called for to
relieve suffering.


                          POISONING BY COPPER.

  Copper sulphate: Fatal dose, horse, dog. Symptoms: Dullness, colic,
  blue or green vomit, diarrhœa, straining, weakness, spasms, palsy,
  albuminuria, icterus, hæmoglobinuria, impaired appetite, emaciation,
  spasms. Lesions: Redness, softening, ulceration, sloughing of
  alimentary mucosa, methe-globinæmia, fatty liver, enlarged spleen,
  ingesta give copper film on polished iron. Treatment: Albumen, milk,
  mucilage, iron filings, sulphur, magnesia, laxatives, opium. Avoid
  acids.

The common copper poisons are the sulphate and acetate. Copper alum,
oxide or carbonate of copper and paints with a copper base are less
frequently taken.

=Sulphate of copper= 1 ounce has proved fatal to the horse. In dilute
solution or with mucilaginous liquids it is much less injurious. Ten
grains to 2 drachms subcutem have killed the dog. (Tabourin.)

_Symptoms._ Dullness, colics, emesis of blue or greenish matter in
vomiting animals, diarrhœa, tenesmus, weakness, trembling, spasms,
trismus, paralysis, small, weak pulse, hurried breathing. In
experimental chronic poisoning in the sheep, albuminuria, icterus,
hæmaglobinuria, hæmaturia, impaired appetite and rumination,
constipation followed by diarrhœa, great emaciation and weakness and
finally convulsions. (Ellenberger and Hofmeister).

_Lesions._ Redness and softening of the alimentary mucosa, ulceration,
sloughing, perforation. In the chronic forms methe-globinæmia, free
hæmatin as crystals in liver, spleen and kidney, nephritic
extravasation, fatty degeneration of the liver, enlarged spleen, and
catarrhal changes in the intestinal mucosa. Polished iron placed in the
gastric or intestinal contents becomes coated with copper.

_Treatment._ White of egg, milk, mucilage, iron filings, sulphur,
calcined magnesia, laxatives. Opium may be required to calm suffering,
but acids must be carefully avoided.


                           POISONING BY ZINC.

  Sulphate and chloride poisonous, less potent oxide and carbonate.
  Symptoms: colics, emesis, congested alimentary mucosa, diarrhœa,
  cramps, weakness, paresis, anæmia, emaciation. Lesions: white,
  leathery, sloughing or ulcerated alimentary mucosa, strictures.
  Treatment: emesis, demulcents, tannic acid, sodium carbonate.

The =sulphate= and =chloride= are the most likely to be taken in
dangerous amount, the former being mistaken for Glauber salts. Three
ounces of sulphate intravenously in the horse has proved fatal, or 10 to
50 grains in the dog. In the vicinity of zinc ore furnaces the agent is
taken in on the fodder as oxide or carbonate.

_Symptoms._ There is much abdominal pain, emesis in vomiting animals,
quick pulse, congested mucosæ, diarrhœa, cramps, weakness, and paresis,
and if the patient survives, anæmia and emaciation.

_Lesions._ The mucosa of mouth, gullet, stomach and perhaps duodenum is
white, opaque, hard, corrugated, leathery, sloughing, or ulcerated.
Congestion is well marked. Strictures may appear in chronic cases.

_Treatment._ Give tepid water and tickle the fauces. Use white of egg or
milk freely and mucilaginous agents. Tannic acid, or carbonate of soda
are antidotal by tending to precipitate insoluble compounds.


                          POISONING BY SILVER.

Toxic doses of silver come mostly from materials used in the arts. The
photographer uses chiefly the nitrate, iodide, bromide, cyanide and
chloride. Taken into the stomach the silver salts are less poisonous
because they are largely precipitated as insoluble chloride or
albuminate. The chloride and albuminate are, however, soluble in
solutions of alkaline chlorides and hence even they may poison.

_Symptoms._ Colic, emesis in vomiting animals the vomited matters
blackening in the light, diarrhœa, great muscular weakness, paresis,
weak clonic spasms, and disturbed respiration. The nervous symptoms are
very prominent (Rouget and Curci). Chronic poisoning produces emaciation
and fatty degeneration of liver, kidneys and muscles (Bogoslowsky).

_Lesions._ Patches of congestion and of white corrosion on the buccal
œsophageal and gastric mucous membrane, the presence of the curdy white
chloride of silver adherent to the gastric mucosa. In chronic cases the
visible mucosæ and white skin may have a slaty color.

_Treatment._ Emetics in vomiting animals. White of egg, common salt
largely diluted and followed by milk as antidotal, demulcent and
nutritive agent.




                          POISONING BY BARIUM.

  Poisonous salts. Symptoms: spasms, peristalsis, defecation, urination,
  restlessness, prostration, emesis, weak pulse, coma. Lesions: Moderate
  congestion of gastro-intestinal mucosa. Treatment: alkaline sulphate,
  anodynes, demulcents.


The salts of barium are irritant with a special action on the nervous
system shown by weakened action of the heart and spasms or paresis of
the muscles. The chloride is used in staining wool, the nitrate and
chlorate in producing green colors in fireworks, the oxide and carbonate
in glassmaking, the chromate by painters, and the sulphate for giving
weight and body to various white powders. The chloride is now largely
used to stimulate intestinal peristalsis in animals.

_Symptoms._ Barium chloride hypodermically produces tonic and clonic
convulsions, increased peristalsis, discharges of urine and fæces, great
restlessness, muscular prostration, emesis in vomiting animals, hurried,
shallow respiration, weak, thready pulse, asthenia, coma, and death.

_Lesions._ There is congestion of the gastric and intestinal mucosa, but
this is rarely violent, and corrosion and ulceration are almost unknown.
The agent indeed seems to act more energetically upon the nervous system
than on the mucosa of the alimentary tract.

_Treatment._ This consists in giving an alkaline sulphate (sulphate of
soda, potash, or magnesia), to precipitate the insoluble barium
sulphate, with anodynes (opium) and mucilaginous agents.


                           POISONING BY IRON.

  Sulphate and chloride on empty stomach poisonous. Symptoms: Colic,
  emesis, rumbling, purging. Treatment: Alkaline or earthy carbonates,
  tannic acid, albumen. Opium.

Sulphate and chloride are the principal poisonous compounds. Both are
comparatively harmless even in large doses taken on a full stomach,
while on an empty stomach they may cause violent gastro-enteritis.

_Symptoms._ Colicy pains, purging, emesis in vomiting animals, more or
less tympany and rumbling of the bowels, and surface coldness.

_Treatment._ Give carbonates of the alkalies, magnesia or lime to
precipitate the comparatively insoluble carbonate or oxide; or tannic
acid or infusion of oak bark or galls. White of egg, milk and
mucilaginous agents, and opium may be required to allay irritation.


                         POISONING BY CHROMIUM.

  Chromic acid, chromate and bichromate of potash. Corrosive. Cause:
  Gastro-intestinal inflammation, albuminuria, hæmaturia, emaciation,
  digital ulcers and sloughs, colic. Diarrhœa, vertigo, stiffness,
  weakness. Lesions. Treatment: Emesis, stomach pump, demulcents.

Bichromate of potash is used extensively in dyeing, calico printing, in
the manufacture of porcelain, in chemistry and photography, and to a
slight extent in medicine, while lead chromate (chrome yellow) is a
valuable pigment. Chromic acid is one of the most potent caustics, at a
moderately high temperature dissolving all animal products that may be
subjected to it. The chromate and bichromate of potash are only less
violently caustic, producing deep and fistulous sores on the hands of
the dyers, and acting in a similar manner on the mucosa of the
alimentary canal. Twenty-eight grains of the bichromate given by the
stomach killed a rabbit in two hours, while 45 grains of the chromate
had no such effect (Gmelin). Pelikan found that the bichromate acted
like arsenic or mercuric chloride, producing violent irritation of the
stomach and intestines, followed by albuminuria, hæmaturia and
emaciation: 1 to 5½ grains proved fatal to rabbits and dogs.

Workmen inhaling the bichromate dust, have inflammation, ulceration and
finally destruction of the nasal septum, together with skin eruptions
and ulcerations.

Horses working at the factories have intractable ulcers of the skin and
sometimes shed the hoofs (B. W. Richardson).

_Symptoms._ Taken by the mouth the bichromate causes colicy pains,
emesis in vomiting animals, diarrhœa, great prostration, cold
extremities, vertigo, stiffness or weakness of the hind limbs, dilated
pupils, weak pulse and death. If protracted the urine may be bloody and
albuminous.

_Lesions._ There is more or less intense congestion of the stomach and
intestine, yellow shrunken mucosa, abrasions, sloughs, and ulcers, and
congested kidneys with yellow cloudiness of the epithelium of the
convoluted tubes and congestion of the glomeruli.

_Treatment._ Wash out the stomach by emesis or the stomach pump and use
albuminous and mucilaginous agents freely.


                      POISONING BY CARBOLIC ACID.

  Susceptibility of cat and other animals. Fatal dose. Effect of
  dilution and gastric plenitude. Concentrated is corrosive. Symptoms:
  Salivation, dysphagia, anorexia, thirst, emesis, colic, arched back,
  odor of the acid, dark, greenish brown, albuminous urine, tremors,
  lowered temperature, debility, stertor, stupor, coma. Lesions:
  Whitened corroded mucosa, inflammation, ecchymosis, dark, liquid
  blood, brain effusions or extravasations, nephritic congestion.
  Treatment: Vinegar, alcohol, emesis, demulcents, Glauber salts.

The cat is the most susceptible to this poison. For dogs, cats and
rabbits from 3 to 4 drops per pound, is the minimum fatal dose. For an
ordinary dog the lethal dose is ½ to 1 drachm. The horse has taken 3
ounces without fatal results, and 15 ounces in a week (Munk). Much
depends on the dilution of the agent and the plenitude of the stomach.
In a concentrated state it acts at once on the mucosa as a caustic
abstracting the water and forming a white eschar.

_Symptoms._ The concentrated acid causes salivation, dysphagia,
anorexia, thirst, emesis in vomiting animals, colics, arched back,
retracted abdomen, odor of the acid in the breath, dark or greenish
brown albuminous urine, trembling, lowered temperature, debility,
stertorous breathing, clonic or tonic spasms, paralysis of the hind
limbs, stupor, coma and death.

_Lesions._ In the mouth, throat, stomach and intestines are whitish,
cauterized patches, with active inflammation beneath and around them,
and ecchymosis. The blood is fluid and dark colored, extravasations or
effusions on the brain or in the lateral ventricles, with pulmonary
congestion and parenchymatous nephritis.

_Treatment._ If available, give vinegar proportionate to the amount of
carbolic acid taken. Alcohol is a good substitute. Emesis should be
encouraged when available. Next mucilaginous agents and bland oils to
dilute the acid are required. Glauber salts may assist in neutralizing
and expelling the acid.


                         POISONING BY CREOSOTE.

  Irritates, coagulates albumen, and blood, arrests heart, colic,
  emesis, salivation, labored breathing, vertigo. Lesions: Congestion,
  corrosion, dark clotted blood, odor. Treatment: Mucilaginous agents,
  emesis, oily laxatives.

On the mucous membrane creosote has a very irritant action, coagulating
the albumen, causing violent inflammation. It also coagulates the blood
and when injected into the veins, stops the action of the heart. Taken
by the mouth it causes violent colics, emesis in vomiting animals,
salivation, laborious breathing, convulsions, vertigo and death. At the
necropsy the stomach is found congested of a dull red color, and
corroded, and the vessels contain dark clotted blood. A dog died from a
dose of 2 drachms. The odor of creosote is marked.

_Treatment._ Emesis, white of eggs, mucilaginous liquids, and oily
laxatives.


                POISONING BY SEEDS OF RICINUS COMMUNIS.

  Superpurgation. Poison in seeds. Diluents, demulcents, stomach pump,
  laxatives if necessary.

An overdose of castor oil may kill by gastro-intestinal congestion and
superpurgation. Apart from the oil however the seeds contain a very
active poison, which has been fatally ingested by horses with grain or
otherwise. Five and a half ounces of the seeds have proved fatal.
(Pelletier. Wende).

The _symptoms_ are those of acute colic and gastro-enteritis. The
indications are to wash out the stomach by abundant demulcents and the
stomach pump, and if necessary to hasten the expulsion of the offensive
matters by bland laxatives (olive oil, Glauber salts).


                   POISONING BY CROTON SEEDS AND OIL.

  Fatal dose without water. Vomiting animals. Superpurgation. Lesions.
  Treatment: diluents, demulcents, stomach pump. Opiates.

One drachm of croton seeds given to a horse, without water proved fatal
in 24 hours (Morton); 2 drachms followed by all the water the horse
would drink produced most violent catharsis followed by recovery
(Hughes). Twenty to thirty drops of croton oil proved fatal; 8 drops in
the jugular vein caused death (Hertwig). It is much less fatal to
cattle. Dogs and pigs vomit it so readily that they usually survive with
profuse catharsis.

The _symptoms_ are profuse watery diarrhœa with tenesmus, congested
mucosæ, rapidly increasing weakness and small pulse, becoming
imperceptible.

The _lesions_ are violent congestion of the mucosa of stomach and
intestines, concentrated very largely on the cæcum and colon.

_Treatment_ consists in abundance of mucilaginous liquids, which the
animal readily drinks, and washing out the stomach with the stomach tube
or pump. Opiates may be demanded to calm the pain.


                        POISONING BY EUPHORBIA.

In Europe _euphorbia lathyris_ has been found to produce in animals,
colic, constipation, tympany, followed by bloody diarrhœa, stupor and
hæmaturia. In America the euphorbia corollata (large flowering spurge)
and euphorbia ipecacuanhæ (ipecacuanha spurge) though less potent have a
similar action. _Treatment_ consists in favoring elimination by emesis,
and abundant mucilaginous and demulcent agents.




                        POISONING BY BOX LEAVES.


The leaves of buxus sempervirens, used as a border in gardens, contains
an acrid principle. After eating 1½ lb. a horse had colic, tympany and
enteritis. After death the lesions of gastro-enteritis were found
(Weiss). _Treatment_ would be by stomach pump, laxatives, demulcents and
anodynes.


   POISONING BY DAFFODILS. (NARCISSUS POETICUS, AND NARCISSUS PSEUDO
                              NARCISSUS).

These common denizens of gardens produce intense gastro-enteritis,
profuse diarrhœa, spasms, stupor and weakness. _Treatment_ will not
differ materially from that advised in box poisoning.


                        POISONING BY RANUNCULUS.

The _ranunculus acris_ (tall crowfoot), _repens_ (creeping crowfoot),
_sceleratus_ (cursed crowfoot), and _bulbosus_ (butter cup), are all
more or less acrid and liable to produce gastro-enteritis when taken in
quantity. They are usually avoided by animals but will sometimes be
taken by accident with other vegetation. Sheep are said to eat
ranunculus bulbosus with impunity (Daubenton). Both cattle and sheep
suffered from the other species (Delafond, Lipp, Brugnone, Delplanque).
There were salivation, colic, emesis in vomiting animals, diarrhœa,
vertigo, spasms, grinding of the teeth, arched back and staring coat.
_Treatment_ would be emesis or the stomach pump when available,
mucilaginous drinks and enemata. Johnson (Medical Botany of North
America) had a herd of cows abort for years on a field thickly set with
ranunculus acris, but which ceased to abort when removed to a field from
which this weed was absent.




           POISONING BY VERATRUM. VIRIDE. AMERICAN HELEBORE.


Used in the early days by New England farmers to destroy birds in the
cornfields (Osgood). Taken internally it reduces the fullness and
frequency of the pulse, and if the dose be large excites nausea,
vomiting and purging with great prostration. In the horse I have found
anorexia, irritability of the bowels, and frequent retching. The action
is primarily on the heart and nervous system and incidentally as an
irritant on the gastro-intestinal mucosa. _Treatment_ consists in
evacuation of the stomach and the free use of mucilaginous drinks and
diffusible stimulants. Helleborus Niger, viridus and fœtidus have
analogous effects.


                     POISONING BY CICUTA MACULATA.

The American water hemlock is an energetic poison acting not only as a
narcotic but as a violent irritant to the gastro-intestinal mucus
membrane.


                   POISONING BY COLCHICUM AUTUMNALE.

This agent expends its energy mainly on the digestive and urinary
systems. The symptoms are suppression of appetite and rumination,
thirst, ptyalism, grinding of the teeth, colic, emesis in vomiting
animals, profuse, watery fœtid and often bloody diarrhœa, the frequent
passage of a clear urine, abortion in pregnant females, with short
difficult breathing, weak pulse, pale mucosæ, coldness of the
extremities, trembling, muscular weakness, sunken eyes, dilated pupils,
spasms and death. The activity of the plant is greatest in July and
August. On post mortem examination the gastric and intestinal mucosa are
violently congested and the lumen of the bowel filled with a thin bloody
mucus. Congestion of the kidneys and bladder is usually present.

_Treatment._ Evacuation of the stomach, and abundance of demulcents.




                          POISONING BY SAVIN.


The tops of the juniperus sabina when powdered and given to dogs produce
violent colic, vomiting, bloody fæces and urine, spasms, paralysis, and
death, with lesions of gastro-intestinal and uro-genital inflammation.
In cattle and sheep they caused tympany, anorexia, colic, hyperthermia,
and constipation followed by a bloody diarrhœa. Horses took 4, 8 and
even 12 ozs. twice daily for eight days without any ill effect (Sick).

_Treatment._ Evacuate the stomach and give demulcents.


                       OTHER VEGETABLE IRRITANTS.

  List of gastro-intestinal irritants. Common Symptoms. General
  treatment: emesis, stomach pump, diluents, demulcents, laxatives,
  enemata, anodynes, antiseptics, tannic acid. Prevention.

Among vegetables which produce more or less disturbance of the
digestion, or congestion of the digestive organs Cadeac names the
following: =Acorns= in horses (Morton); =tares=; =bird’s trefoil= (lotus
corniculatus, Colin); =vetches= at ripening (Gerlach); =laburnum=
(cytissus) horse and ox (Cornevin); =hybrid= and =sweet trefoil= (Pilz);
=officinal melilot= (Carrey); the =field poppy=, =digitalis= and
=snapdragon= often mixed with wheat and rye (Cornevin); =conium
maculatum=, =cicuta virosa=, =yew leaves=, =lolium temulentum=, and
other forms of =ryegrass when ripening=; =chickweed= (stellaria) killed
60 horses in 200 (Semmer); =clematis=, =aconite=, =tobacco=, =male
fern=, =aloes=, =horsetail= (equisetum) when full of silica;
=mercurialis annua=, =wild radish=, =resinous plants=, =potato tops=,
=potatoes in excess, or green= from exposure to the sun; =Œnanthe
Crocata= (water dropwort); =giant fennel=, =anemone=, =phytolacca= (poke
root); =buckwheat= in flower (Moisant); =St. John’s wort=, various
species of =lathyrus=, =rhododendron=, =artichokes= in excess, =spurry
seeds=, =galega=, =bryony=, the fruit of =melia azedarach= (in pigs)
(Dreux); =nux vomica=, =podophyllum=.

It may be added that the plants credited with causing the “loco” disease
(=Astragalus mollissimus=, =Hornii=, and =lentiginosus=, the =oxytropis
Lambertii=, =mutifloris= and =deflexa=) cause diarrhœa and sometimes
ulceration of the intestines.

The farina of =mustard= is sometimes mixed with linseed cake and
(developing the active principles of that agent) produces a severe or
even fatal gastro-enteritis in cattle and sheep. The wild mustard of the
fields, being allowed to grow with the flax, or rape, the seeds mingle
when harvested and thus the cake comes to contain an injurious quantity
of the mustard.

_Symptoms._ These will vary much according to the predominating action
of the individual poison on other organs, but when they irritate the
gastro-intestinal mucosa they have this in common, that they impair
appetite and rumination, produce colicy pains (perhaps salivation and
vomiting), and constipation or diarrhœa of varying intensity.

_Treatment._ Apart from the individual treatment demanded by the special
symptoms of disorder of other organs, it may follow the same general
line for all: Unload the stomach by tepid water, ipecacuan, with
tickling of the soft palate, or by the stomach pump or tube, and follow
this by abundance of mucilaginous drinks. In cases attended by
constipation a laxative of Glauber salts, or aloes may be demanded, or
assiduous mucilaginous injections. With an excess of irritation anodynes
may be indicated. When there is tympany and fœtor of the discharges
these must be met by non-irritant antiseptics, such as naphthalin or
salol. For many of the vegetable poisons tannic acid proves
advantageous, being at once an antiferment, and fitted to unite with
organic alkaloids, rendering them less soluble and otherwise often
changing their properties.

_Prevention_ should be sought by removing all such poisonous plants from
pastures, or land used for raising fodder crops.




              POISONING BY CANTHARIDES AND OTHER INSECTS.

  Action on genito-urinary and alimentary tracts. Dysphagia, congestion,
  retching, diarrhœa, with mucus and blood, diuresis, enuresis,
  albuminuria, retracted testicles, prostration. Lesions: urinary and
  gastro-intestinal congestion, ecchymosis. Treatment: emesis with
  ipecacuan, demulcents, avoidance of oils, alcohol and chloroform.
  Other vesicant beetles and larva.


Spanish flies have a primary physiological action on the genito-urinary
organs, but when introduced by the stomach they prove direct and violent
irritants to the gastro-intestinal mucous membrane. They cause redness
of the buccal mucous membrane, difficulty of swallowing, retching,
emesis in vomiting animals, diarrhœa with mucus and bloody fæces,
diuresis or enuresis with albuminous urine, retraction of the testicles,
prostration, perspiration, paresis and death.

_Lesions._ Active gastro-intestinal congestion with ecchymosis, marked
congestion of the genito-urinary mucosa especially that of the bladder.

_Treatment._ Emesis with ipecacuan and tepid water, followed by abundant
mucilaginous or albuminous liquids. Flaxseed tea, gum arabic, and white
of eggs are useful. Avoid oils, alcohol and chloroform which dissolve
the cantharides.

Among other insects which act as vesicants may be named the =cockroach=
(blatta orientalis) and the =potato beetle= (cantharis vitatta), also
the _cantharis cinerea_, _cantharis marginata_, _cantharis atrata_, and
_cantharis nuttalli_. The larvæ of various lepidoptera, thus =army
worm=, =Cnethocampa primivora=, =Cnethocampa processionea=, =liparis
auriflua=, =lithosia crinola=, and the =larvæ= of the =artica cassus
ligniperda=, and =pieris brassica= are covered with stinging hairs
charged with formic acid and perhaps an enzyme, which are shed with the
skin in passing into the state of chrysalis, and getting mixed with
fodders produce violent stomatitis, hemorrhagic gastro-enteritis and
nephritis.




        POISONING BY FUNGI, BACTERIA AND THEIR PRODUCTS IN FOOD.

  Poisons in spoiled food: Moulds, rust, smut, bacteria, toxins. Action
  of moulds on rabbits, on alimentary and nervous systems. Smuts, ergots
  and their congeners. Tetanizing and paralyzing products. Duration of
  symptoms.


Food is usually spoiled by the growth of moulds, rust, smut, bacteria
and the toxins which they produce.

Kaufman has experimented with moulds on rabbits. He found that
=aspergillus glaucus= (green mould) grown on bread produces a fatal
infection in the rabbit even in very minute doses (⅒ milligramme); that
it will attain this in a neutral or even slightly acid medium as well as
in an alkaline one; and that the spores retain this pathogenic activity
for six months at ordinary temperatures. The aspergillus glaucus,
penicillium glaucum, and mucor mucedo affect the intestinal organs only,
while ascophora oidium aurantiacum affect the nervous system as well.
The =smuts= (ustilago) and =ergots= (claviceps purpurea) vary
considerably in their potency according to the conditions of their
growth and the stage of their development, yet experiment has shown a
special action on the vaso-motor nerves leading to nervous disorders,
circulatory troubles, and trophic disease. In connection with =ustilago
maidis= (corn smut) there are usually found bacteria, such as =bacillus
maidis= and =bacillus mesentericus fuscus=, and the combined products of
these and the ustilago have been studied by Lombroso, Dupre and Erba.
These observers isolated a red oil with the tetanizing action of
strychnia, and oleo-resinous substances having bases which they named
maïsine and pellagrozeine, and which had a paralytic action on the nerve
centres. Pellizi and Tirelli cultivated the bacteria of damaged maize
and found that the sterilized cultures, introduced into rabbits
hypodermically or intravenously caused muscular jerking, exaggeration of
the reflexes, tetanic spasms and paralysis which lasted for fifteen days
after the injection. This is exactly in line with the causation of
contagious bacteridian diseases in which the ptomaines and toxins are,
as a rule, the immediate pathogenic factors.




                   CRYPTOGAMIC POISONING IN SOLIPEDS.

  Prominent symptoms, asthenia and vertigo. Vary with cryptogam, merge
  into zymotic diseases. Causes: grain harvested damp and moulded,
  bluish or greenish, hay greenish white, brown or black, clover
  reddish, musty fodder, and diuresis, indigestion, gastric intestinal
  and systemic paresis, somnolence, delirium. Rusts, spring and summer,
  their evolution. Bunt, smut, produce fever and paralysis, spasms,
  abortions and dry gangrene, buccal erosions; evolution of ergot, honey
  dew on leguminous plants causing skin disease, bacterial ferments,
  diplococcus, streptococcus from foul water, causing enteritis.
  Symptoms: _adynamic_, dullness, blunted sense, pendent head, ears,
  eyelids, congested, yellow, ecchymosed conjunctiva, fever, tympany,
  colic, constipation, dung small, round, coated masses, vertigo,
  sometimes fatal diarrhœa, or colliquative diuresis; _vertiginous_:
  fever, anorexia, yellow mucosæ, tardy breathing, costiveness colics,
  stupor, somnolence, giddiness, heavy steps, stumbling, delirium, push
  head against wall, clinch jaws, grind teeth, make walking or trotting
  or plunging motions, or pull on halter and fall, amaurosis, paralysis,
  coma. Remissions. Death in one day or upward. Resumption of functions
  and recovery. Diagnosis: from meningo-encephalitis. Lesions:
  gastro-intestinal congestion, infiltration, ecchymosis, fermenting
  ingesta, congestion of mesenteric glands, liver, brain and meninges.
  Leucin and tyrosin in urine. Treatment: stomach pump, antiferments,
  potassium iodide, purgatives, enemata; for brain, bleeding, sedatives,
  ice, snow, elevation, derivatives, prevent mechanical injury.


The most prominent features of cryptogamic poisoning in these animals
are asthenia and vertigo. In dealing with such poisoning, however, we
must bear in mind that we have in hand, not one particular disease but a
group, differing among themselves according to the cryptogam and its
products which may be present:—a group moreover which overlaps more or
less the true zymotic diseases.

_Causes._ Oats, barley and other grain or fodder which has been put up
damp, and especially ground feed, becomes speedily overgrown and
permeated with moulds, especially =penicillium glaucus=, =aspergillus
flavus= and =glaucus=, =mucor racemosus=, and =ascophora mucedo= which
give a bluish or greenish color and heavy odor, rob it of its nutritive
constituents and charge it with toxic products. On mouldy hay it is
common to find =aspergillus candidus=, =botrytis grisea=, =torula
herbariorum=, and =eurotium herbarium= which form a greenish white or
brownish dust. The =spœria herbarium= is characterized by small black or
brown spots with yellowish, brown or black spores. The peronspora
trifolium attacks growing clover (clover sickness) and =isaria
fuciformis= the fescue grasses. The latter has a red color and mucous
consistency and is charged with producing fatal poisoning in cattle.

=Mouldy= or =musty= oats, or other grain or fodder have long been
notorious for producing diuresis in horses with excessive elimination of
phosphates, extreme emaciation, weakness and death. In other seasons,
and probably because of a difference in the fungi or their products they
have caused widespread enzootics of indigestion with paresis of stomach
and bowels, and of the systemic muscles. Paraplegia is a common
manifestation, suggesting lesions of the spinal cord, and in other cases
there are general paresis, somnolence and delirium suggesting cerebral
lesions, (Staggers).

Gillespie records an enzootic of gastro-intestinal indigestion and
tympany among the horses of a battery of artillery in Afghanistan from
eating mouldy grass. Fröhner, Martin and Varnell have seen cases of
poisoning by moulds without digestive, urinary or febrile troubles.

Of =rusts= growing on grain crops there are two chief varieties; the
=spring rust= (_uredo rubigo vera_) which commences as light yellow
patches on the leaves and stems, which change to black as the fungus
approaches maturity; and the =summer rust= (_uredo linearis_) which
grows to a larger size and assumes a browner color. Each of these passes
through an evolutionary cycle, the small preliminary patches (=uredo=)
passing into the mature fungus (=puccinia rubigo vera= and =puccinia
graminis=.) Then it must pass through an alternate generation on another
family of plants before it can again grow on the gramineæ.

=Bunt= produced by the _tilletia caries_ attacks the grasses and small
grains. The growing seed (wheat especially) is changed into a black or
olive colored powder, having a fishy odor. If the stems are attacked the
leaves become pale, withered and dry. It can only be detected by
carefully examining the individual seeds.

Other forms of smut are the =ustilago carbo= and =ustilago maidis= the
familiar black smuts of small grains and maize. These develop by
preference in the growing seeds, but also in the stem and leaves. The
_tilletia caries_ is as a rule more poisonous than the _ustilago_ the
effects being mainly hyperthermia and paralysis. There is, however, a
tendency to spasmodic contractions, and abortions, and dry gangrene will
occur from smut. The author has seen a large herd of cattle attacked
with gangrenous sores around the coronet, which were promptly stopped
when the light, smutty ears of corn were no longer given. In other cases
the hoof was in part separated from the quick and creaked when the
animal walked.

In connection with the gangrenous ergotism of cattle, the author has
found on the same farms and feed, horses with ulcers on the buccal
mucosa and gastro-intestinal indigestion. =Ergot= affects the seeds in
nearly all the small graminaeæ and is produced by the _claviceps
purpurea_ which first attacks the ovary of the seed (_sphacelia_ stage),
then it invades the whole seed which grows out from the glumes as a
hard, dark or purple spur-like process (_ergot_ stage), then falling on
the ground it grows up as a minute stalk with rounded head containing
spores.

=Honey dew= growing on leguminous plants is reputed to cause skin
disease in white horses and on the white spots of dark horses, from
which those not eating the diseased plants escaped.

_Bacterial ferments_ have an equally bad reputation. Bastin records the
poisoning of five foals by fermented rye; Dieckerhoff describes an acute
gastro-enteritis with congestion and swelling of liver, spleen and
kidneys, as the result of microbes and their products in the fodders.
Galtier traced a pneumoenteritis in the horse to two cocci, a motile
_diplococcus_ and non-motile _streptococcus_. Both stained in aniline
colors, and were bleached by iodine. They grew in ordinary culture media
above 50° F. but most freely at 98° F. The animals were infected by
drinking putrid water or spoiled fodders in which the microbes were
contained. The change to boiled water in the former case led to their
prompt disappearance. Reynal, Cailleux and Foucher have also adduced
instances of severe enteritis in the horse from drinking putrid water.
These animals showed active congestion of the intestinal mucosa with
abundant infiltration of the submucosa.

Bouley found 14 cases in one stable, the owner of which had marketed the
good fodder and kept the spoiled for home use. Barthelemy, Alasonniere,
Lombroso and Hausmann, Clichy, Rey, Gamgee and others give similar
examples.

A large number of observations show the dangerous results on the horse
of mouldy bread, inducing colics, vertigo, profuse sweating.

_Symptoms_. When =Adynamia= prevails there is great dullness and
depression, the senses are blunted, the head depressed resting on the
manger, the eyes sunken, weeping and half covered by the drooping upper
lid, the conjunctiva is congested, sometimes yellow or marked by
petechiæ. The mouth is hot, the lower lips pendent, the tongue furred,
the abdomen somewhat tympanitic, with slight colics, but with little
rumbling or indication of peristalsis. There is a primary constipation,
a few small, hard pellets being passed with effort. The temperature may
be 102° to 104°, breathing short, pulse small, weak; the walk unsteady,
the animal preferring to stand, completely apathetic. In some cases a
profuse diarrhœa sets in and may prove fatal.

In the cases attended by diuresis, the weakness is extreme, emaciation
advancing rapidly, but the other symptoms of nervous depression are less
marked, the poisons being apparently eliminated by the kidneys (see
_diuresis_).

In the =Vertiginous form= the disease may set in with more or less
hyperthermia, anorexia, a dislike particularly of the spoiled fodder,
yellowness of the visible mucosæ, slow breathing, small accelerated
pulse, costiveness, tympany, colics more or less intense, tenderness of
the belly, and sooner or later marked nervous disorder. This may be in
the form of stupor, the head resting in the manger, the senses are
manifestly clouded, the animal walks unsteadily, staggers, steps
heavily, striking the feet against obstacles, and stumbling. At the end
of a variable number of hours (2 to 6 or 8 after feeding) nervous
excitability and vertigo may supervene. He may push the head against the
wall, the jaws clenched, grinding the teeth, the eyes fixed, pupils
dilated, facial muscles contracted, respirations hurried, heart
palpitating and the skin perspiring. He may continue in this position,
moving his feet as if walking, or he may rear plunging his feet into the
manger or fall back over, and rising push anew against any object he may
come in contact with. Coulbaux speaks of rabiform symptoms such as
attempts to bite but any such deliberate purpose is rare.

There may follow complete amaurosis, insensibility to pricking of the
skin, and even paralysis or coma. Hyperæsthesia may also be temporarily
present.

_Course._ Remissions and exacerbations usually alternate, the duration
of the former furnishing some criterion by which to establish a
favorable prognosis. Death may take place in 24 hours or it may be
delayed for several days. Recovery is usually heralded by the resumption
of defecation and urination, and the return of appetite. It is liable to
be at first only partial, some of the senses remaining dull, or a
general stupor persisting.

_Diagnosis._ In all such forms of poisoning there is the history of
the ingestion of the toxic matters, and in any suspicious looking
cases a careful examination of the food should be made. From
meningo-encephalitis the presence of the abdominal disorder will serve
to identify and to incriminate the food.

_Lesions._ These vary much with the poison. There is always, however,
inflammation of the gastro-intestinal mucous membrane, usually with
ecchymosis, and infiltration of the submucosa. The contents of the
bowels are imperfectly digested, the mesenteric glands congested and
enlarged, the liver congested and softened, and the brain and its
meninges hyperæmic or infiltrated. The leucine and tyrosine present in
the urine during the acute attack is said to disappear when improvement
sets in (Pellagi, Azzaroli).

_Treatment._ The first object must be the removal or neutralizing of the
poison. In some instances the stomach pump or tube might be tried.
Usually one must fall back on antiferments such as naphthol, naphthalin,
salol, salicylic acid, and above all iodide of potassium. The last
checks the growth of the fungi or bacteria and favors elimination of the
toxins. It may be given freely to act on the kidneys. Creolin, 1¼
drachm, repeated three times a day has been found effective (Albrecht).
In addition the action of the bowels may be solicited by full doses of
sulphate of soda and abundance of water.

When the brain is implicated Cadeac recommends bleeding as an
eliminating as well as a sedative measure. In any case use cold water,
snow or ice to the head, elevation of the head, and purgatives which may
as a rule be doubled. Potassium iodide or other antiseptics should be
pushed, and diuresis as well as a relaxed condition of the bowels
maintained. Counter-irritants such as mustard may be applied to the
abdomen, and enemata used at frequent intervals. It is important to fix
the patient to a ring in the centre of a box stall or barn to keep him
from injuring himself.


                  CRYPTOGAMIC POISONING IN RUMINANTS.

  Moulds and bacteria in brewer’s grains, or the marc of beet sugar or
  cider factories derange digestion, or cause abortion. Spoiled potatoes
  cause enteritis, vertigo, palsy, in sheep, nephritis and cystitis.
  Mouldy bread causes indigestion, urinary and nervous disorder. Mildew.
  Musty grain and fodder as in the horse. Ergot causes winter and spring
  gangrene of skin, feet, limbs, ears or tail, lethargy, palsy, spasms,
  delirium, abortion; variation in toxicity with stage and condition of
  growth, privation or liberal supply of water, or succulent vegetables.
  Symptoms: varying, mouldy bread causes digestive and urinary trouble,
  with marc or ensilage, develops slowly, impaired appetite, salivation,
  tympany, colic, diarrhœa, debility, paresis, spasms, delirium.
  Duration, 5 hours to 2 weeks. Gangrenous ergotism, necrotic sore,
  slough hard, dry, leathery, black, living parts at demarcation line
  pink or purple, puffed up, tender, necrosis involves all soft tissues
  and bone; nervous form: abortion form. Lesions: congestion of stomach,
  bowels, mesenteric glands, brain and meninges, petechiæ. Diagnosis,
  from anthrax, from coccidian hemorrhagic dysentery, from foot and
  mouth disease, from rinderpest. Prevention, stop or regulate the
  injurious fodder, salt and pack the fresh grains or marc. Treatment:
  antiferments, potassium iodide, saline purgatives, stimulants, oil of
  turpentine, injections, derivatives.

_Causes._ The growth of =moulds= on or in brewer’s grains, which have
been preserved without salting and close packing, has at times rendered
them dangerous poisons (Duvieusart, Wehenkel, Schütz). The refuse or
marc of beet sugar factories, or of cider works may act in a similar
manner. These products, at first neutral or only slightly acid, undergo
an acid fermentation, with an abundant production of acetic, lactic or
butyric acid which adds materially to their action in deranging
digestion. These agents usually require a large amount to prove
deleterious, about 150 to 200 lbs. a day. Arloing found three active
microbian ferments in the pulp of the sugar factories, and four in that
of the distilleries. The marc of apples has even caused abortion
(Cornevin).

=Spoiled potatoes= have caused adynamic enteritis, with vertigo and
paralysis (Zimmermann, Grabin, Holme) and in sheep symptoms of nephritis
and cystitis as well (Kloss).

=Mouldy bread= has been found to cause indigestion and cerebral
disturbances in cows (Cagny) or nervous disorders without digestive,
urinary or febrile trouble (Fröhner, Martin and Varnell).

=Mildew= on the leaves of a grapevine has also poisoned six cows
(Bisseauge).

=Musty= grain and fodder has the same general action as on the horse and
produces paraplegia and other nervous disorders with or without
digestive troubles.

The =isaria fuciformis= has caused the death of cattle which ate the
grasses infested by it.

When we come to the ergots and smuts we find even more evidence of
poisoning than in the horse. Toward the end of our long winters in the
Northern States we occasionally find widespread =gangrenous ergotism=
from eating infested hay, the lesions varying from simple sores around
the top of the hoofs, in the interdigital spaces or on the teats and
mouth, to loosening of part of the sole or wall, shedding of the entire
hoof or sloughing of the entire limb—just above the hoof, at the
fetlock, or in the metatarsal region. Portions of the tail or ears will
similarly slough. This appears to be mainly due to the lessening of the
calibre of the capillaries by contraction of their walls, under the
action of the ergotin and secalin, seconded by the cold of the season.
Cold is, however, by no means essential to its production. The other
most common form of ergotism is the action on the nervous system. The
contraction of the cerebral capillaries and disturbance of the
circulation lead in some cases to a condition of lethargy and apathy in
which the animal fails to eat or ruminate and gradually falls into
marasmus, or paralysis may be induced, or delirium and spasms. Then
finally there is the familiar form of abortion induced apparently by the
contraction of the involuntary muscles of the womb and of its capillary
vessels.

There is, however, a great difference of opinion as to the deleterious
action of ergot. Various experiments with large doses of ergot on
pregnant animals have failed to produce any sign of abortion. The agent,
however, varies in its nature according to the conditions under which it
grew and the stage at which it was collected, so that the failure to
produce the expected result in a given case can by no means be accepted
as disproving its pathogenic properties under other conditions.

The same remarks apply largely to the action of the smuts, which are
often eaten in large quantities with impunity, especially if plenty of
water or succulent vegetables are allowed, whereas under other
conditions as in winter, under the action of cold, with the usual water
supply frozen up, and no succulent food, it proves very destructive.

_Symptoms._ These vary with the particular poison: With mouldy bread the
symptoms may come on promptly with indigestion, tympany, constipation,
marked irritation of the urinary organs, and it may be nervous disorder.
Sometimes, as noted above, the narcotic action is shown with paresis or
paralysis and stupor without any manifest disorder on the part of the
digestive or urinary functions.

Most commonly with mouldy fodders, grains, marc, or ensilage the results
are tardily developed and only after long continued use of the spoiled
food. There is then loss of appetite, and rumination, drivelling of
saliva, some tympany, and abdominal pain shown by frequent movement of
the hind limbs, lying down and rising. The bowels may be costive at
first, but this early gives place to a fœtid diarrhœa, with weak rapid
pulse (100 per minute) palpitations and hurried breathing. The walk
becomes weak, unsteady, staggering or stumbling, and there may appear
marked paresis especially of the hind parts. When nervous excitement
sets in there may be twitching of the muscles of the neck, shoulders or
thigh; the eye rolls or becomes fixed and the pupils are dilated; the
muscles of the face are contracted and the jaws clinched, with grinding
of the teeth. Bellowing or pushing of the teeth and nose, the forehead
or horns against the wall or other obstacles, or the dashing violently
against obstacles is occasionally observed, and indicates in most cases
an unfavorable termination.

The duration of the malady is uncertain. It may not be over five or six
hours in acute cerebral cases, and especially in sheep, and again it may
be prolonged for one or two weeks. Death often takes place in
convulsions.

In =gangrenous ergotism= a necrotic sore with more or less surrounding
swelling may be seen, and a line of demarcation forms of a pink or
purplish aspect along which the separation of the dead tissue takes
place. The slough is usually of a dark red or black color, the red
globules having apparently migrated into the tissues and piled up in the
capillaries in the early stages of stagnation. When the line of
separation is higher, the line of demarcation completely encircles the
limb, the inflammation and swelling is very marked just above this line,
the skin and soft tissues beneath drying and withering up into a dark
red leathery mass, and this is gradually separated by the formation of a
granulating surface above. The process of separation takes place much
more slowly through the bony tissues, and not unfrequently the soft
tissues having become detached, the lower part of the limb is separated
at the first joint below the line of demarcation and the bone from that
line down to its free end remains as a projecting necrosed stump. In the
ear or tail the necrotic portion withers up into a stiff rigid shrunken
slough which becomes detached sooner or later by mechanical violence.

In the =nervous ergotism= the symptoms are largely those of the
adynamia, paresis and convulsions already described.

In =abortion from ergotism= there are usually few premonitory symptoms,
and the occurrence is to be explained by the number of victims in a herd
eating ergot or smut.

_Lesions._ These vary greatly. Usually the congestion and inflammation
are most prominent in the abomasum and small intestine, complicated by
ecchymosis and even extravasation which may so thicken the mucosa as to
block the intestine (Walley). The mesenteric glands are usually gorged
with blood and of a deep red. The brain may be nearly normal or
violently congested and with its meninges covered with petechiæ.

_Diagnosis._ From anthrax this affection is distinguished by the absence
of the specific large bacillus in the blood and of the marked
enlargement of the spleen, by the great prominence of the nervous
symptoms in many cases, and by the history of a dietetic cause.

From the coccidian hemorrhagic dysentery it is diagnosed by the absence
of the coccidia in the stools and the predominance of the nervous
systems.

From foot and mouth disease, the gangrenous ergotism is distinguished by
the facts that the sores are in the nature of sloughs, and not vesicles,
and that some members of the herd are almost certain to show sloughing
of the limb at some distance above the hoof. More important still is the
fact that the daintily feeding sheep and the pig kept in the same yards
do not suffer from the ergotism.

From rinderpest it is differentiated by the fact that the sores on the
mouth (when present) are not of the nature of epithelial concretions,
and they do not appear on the vulva, and more significant still there is
no indication of the introduction of the disease by contagion nor of its
rapid progress from herd to herd. The immunity of sheep from gangrenous
ergotism is another significant feature.

_Prevention_ consists in putting a stop to the supply of the altered
food or, if it must be given, in giving it in small quantities only with
abundance of water or fresh succulent aliment. In the case of grains or
marcs the fermentation may be checked by adding ¼ per cent. of common
salt and packing the material firmly in a close box or silo.

  In ergotism, succulent food, water ad libitum, stimulants, poultices,
  fomentations or wet bandages, a warm building and pure air are all
  important. Usually ergot and smut can be safely fed in relatively
  large amount with a liberal ration of potatoes, turnips, beets, green
  food or ensilage.

_Treatment_ does not differ materially from that advised for the horse.
Antiferments including potassium iodide, and saline purgatives stand at
the head of the list. Stimulants may be demanded to rouse the torpid
bowels and nervous system and unless contraindicated by
gastro-intestinal inflammation oil of turpentine offers itself as at
once stimulant, antiseptic and eliminating. Injections and
counter-irritants are of use. Then cold (ice, snow, water) to the head,
and the confinement of the patient so that he cannot injure himself or
others are not to be neglected.




                    CRYPTOGAMIC POISONING IN SWINE.

  Spoiled foods. Toxic rye. Botulism. Brine poisoning. Flesh of
  overdriven (leucomaines). Symptoms: from mouldy bread, brain disorder,
  gastric, urinary, hæmatic: from brine, restlessness, convulsions,
  eructations, vomiting, weakness, paresis. Lesions: congestion of
  stomach, bowels and mesenteric glands; with brine, heart and skin
  charged with black blood, congestion of brain, kidneys and bladder.
  Petechiæ. Treatment: empty stomach, emetics, purgatives, potassium
  iodide, antiferments, sedatives, cold to head, enemata,
  counter-irritants. Prevention.


_Causes._ Spoiled foods of all kinds such as mouldy bread, musty meal,
spoiled grains of all kinds, or rotten potatoes, or apples are common
causes of poisoning. In specimens of toxic rye Woronin found four
fungi:—=fusarium roseum=, =gilberella Sanbinetti=, =belminthosporium=,
and =cladosporium herbarium=. Prilleux and Delacroix have obtained a
fifth, =endoconidium temulentum=. Rye so affected produced nervous
disorder in swine, dogs, birds and even in man. Pigs often die from
botulism, being fed flesh in a more or less advanced stage of
putrefaction. Old meat brine is also a source of toxin and ptomaine
poisoning since its toxic property increases with age which is not the
case with a mere solution of common salt. Yet this is very deadly to the
pig, a half a pint often proving fatal. Kuhnert records that the flesh
of an overdriven horse proved fatal to the pigs that ate it.

_Symptoms._ From mouldy bread the pig becomes dull, stupid, sluggish,
stiff, stilty and staggering in his gait, and usually costive. There are
usually signs of colicy pains, inappetence, frothy lips, champing of the
jaws, yawning, retching and vomiting. The mucosæ become yellow and the
urine red and albuminous.

The symptoms caused by old brine are more violent. There are dullness,
prostration, and inclination to lie, but at short intervals the animal
gets up and wanders round, moving stiffly, is seized by tremors and
finally convulsions, in which he falls to the ground, dashes his head
from side to side, champs his teeth, rolls his eyes and froths at the
mouth. There are usually eructations and often vomiting which does not,
however, give the desired relief. The animal becomes rapidly weaker and
though unable to rise has frequent paroxysms of trembling and other
nervous symptoms.

_Lesions._ With mouldy bread the congestion of the gastric and
intestinal mucosa, and of the mesenteric glands are marked features.
With brine there is in addition the heart gorged with black, tarry
blood, the skin and subcutaneous connective tissue shows a similar dark
congestion, also the brain and its membranes and the kidneys and
bladder. Petechiæ are abundant on the serous membranes and other parts
of the body.

_Treatment._ Evacuate the stomach by tickling the fauces, giving tepid
drinks, or ipecacuan. Follow with purgative of sulphate of soda and
diuretics especially potassium iodide. Potassium bromide, sodium
salicylate or salol may be given to calm nervous excitement and check
fermentation. Degoix recommends chloral hydrate, enemata, cold to the
head, and counter-irritants and in very prostrate conditions stimulants
may be employed.

The most important measure, however, is the cutting off of the supply of
the poison and the administration of a wholesome diet. Medicinal
treatment is too often unsatisfactory and will seldom pay for the
trouble; prevention is the one rational and economical measure.


                  CRYPTOGAMIC POISONING IN CARNIVORA.

  Botulism. Racial immunity. Acquired immunity. Gastric secretions,
  protective. Bacteria in septic beef, old brine, stale fish, privy air.
  Symptoms: sudden onset, colic, nausea, retching, vomiting, septic
  vomit, fever, tender abdomen, bloody, fœtid, mucous diarrhœa,
  prostration, death in three to twenty-four hours. Lesions: of
  gastro-enteritis, ingesta fœtid, congestions and petechiæ of other
  organs. Treatment: emetic, laxative, diuretics, potassium iodide,
  antiseptics, demulcents, stimulants.

_Causes._ What is called _botulism_ in man is not uncommon in carnivora.
Eating carcasses of animals that have died of disease, of poisoning,
etc., in a raw condition and too often in an advanced state of
putrefaction, they are liable not only to infection by the pathogenic or
poisonous microbes, but also to direct poisoning by the ptomaines and
toxins. There are however certain protective conditions. Accustomed as
this class of animals is to the consumption of such food, they have by
selective evolution acquired an insusceptibility to many such poisons
which would prove deadly to the herbivora. Again the mature dog or cat
has already been subjected to many of these poisons and having survived
them has acquired an immunity which renders it comparatively safe for
the future. The antiseptic power of the gastric secretion of the dog may
be easily shown, by letting him bolt a moderate piece of putrid meat,
and killing him ten or fifteen minutes later when the mass will be found
in the stomach without odor of decomposition. He succumbs to the poison
either when the quantity ingested is too large, or when the digestion is
from any cause deranged and the gastric secretion impaired. Anthrax
flesh may produce pharyngeal or intestinal anthrax in the dog. In the
animal with temporarily impaired immunity the more virulent septicæmias
may prove infecting. From putrid beef the following pathogenic bacteria
have been isolated: 1. Gärtner and Basenau have independently isolated
=bacillus bovis morbificans= which forms clear colonies on the surface
of peptonized gelatine, and brownish ones beneath the surface, and
coagulates milk in 24 hours. This is short with rounded ends, very
motile, non-liquefying, and capable of surviving the freezing
temperature. Its toxins are not destroyed by boiling. It causes
enteritis, or, subcutem, debility, somnolence, and stupor. This bacillus
was pathogenic to mice, rats, guinea-pigs, rabbits, goats and calves but
had little effect on dogs or cats. 2. The =bacillus of Poels= which
produces paralysis. 3. The =bacillus of Gatky= which performs very rapid
gyratory movements only, and is not found in the muscles.

=Old Brine= is as poisonous for the dog as for pigs. Six to nine ounces
proved fatal, (Reynal).

=Stale Fish= has been known to prove poisonous in the same way.

Three dogs that were made to breathe the air over a foul privy were
seized with vomiting, fever and diarrhœa.

_Symptoms._ These usually develop six or more hours after a feed. The
earlier symptoms are those of digestive disorder. There is colic,
nausea, retching, vomiting of septic or bilious matter, ardent thirst,
dry mouth, furred tongue, redness of the buccal mucosa, and tenderness
of the abdomen. Diarrhœa sets in early and may become bloody, fœtid and
dysenteric. There is usually much prostration and debility so that apart
from his compulsory movements under the colics the animal remains most
of the time curled up. Fever is usually slight but the temperature may
rise to 105° F. Death may take place in 3 hours, or may be deferred 24
hours or longer.

_Lesions._ There is usually gastro-enteritis, the mucosa being
congested, red œdematous, with petechiæ, and congestion and swelling of
Peyer’s patches, the solitary glands, the mesenteric glands, the liver
and kidneys. The contents of the bowel are brownish red, and an effusion
into the peritoneum is common. The spleen is often engorged and
enlarged. Congestions of the lungs and brain are common.

_Treatment._ Evacuate the stomach by ipecacuan, etc., and the bowels by
a purgative. Next seek elimination of the toxins by potassium iodide and
other diuretics. Antiseptics (calomel, salol, naphthalin) to counteract
the further formation of toxins, and demulcents by draught and enema are
indicated. In cases of great prostration, heart and nerve stimulants may
be useful.


                          DIARRHŒA, SCOURING.

  Definition. Concomitant of other affections. Causes: Congestion,
  effusion from small and large intestine, irritants in bowels, or
  blood, chill or other shock acting as reflex, cold drink and violent
  exercise, aqueous food, cooked, pulped; irritants, feculent
  concretions, parasites, fermentation products, diseased teeth, jaws or
  salivary glands, drink after grain, gastric hepatic or pancreatic
  disease, spoiled food, purgative agents in food, fever products,
  purgative waters, rains, dews, damp stalls, etc., fear, “washy”
  horses, nervous animals, root diet, œstrum, hepatic torpor, equine
  susceptibility. Symptoms: with root diet, with much or little bile,
  slight cases do not affect system, in severe cases, tympany, pawing,
  straining, fœtor, in infective diseases; complications, laminitis,
  enteritis, pneumonia. Treatment: remove or expel cause, demulcents,
  laxatives, anodynes, antiseptics; chronic cases, iron, bitters,
  antiseptics, astringents, dietetics, rest.

_Definition._ A frequent discharge of fluid or semi-fluid evacuations
from the bowels without excessive griping or painful straining.

This is a common condition attending many diseases, rather than a
specific disease of itself yet it is such a prominent feature of these
various affections, and one so very characteristic that it seems well to
give it a special place, even at the risk of repeating much of what must
necessarily appear elsewhere.

The immediate cause of diarrhœa is a congestion of the intestinal mucous
membrane and a profuse secretion into the intestinal canal. When such
congestion occurs in the small intestine alone, it may be
counterbalanced by increased absorption in the large, so that the
secretion must be excessive to produce liquid alvine discharges. When on
the other hand it occurs in the large intestine or in both large and
small, the product is likely to escape in the liquid form.

In its turn the congestion of the intestinal mucosa may result from
irritants in the bowels, from the presence in the blood of irritant
agents which being secreted stimulate the intestinal glands to excessive
secretion, and from reflex nervous action, starting from a distant point
as in chilling or irritation of the skin or other organ.

Among direct irritants of the intestinal mucosa may be named a full
drink of cold water especially if the horse is trotted or galloped for
twenty minutes immediately after;—soft, juicy, rapidly grown green food,
to which the animal is unaccustomed, as the first grasses of
spring;—cooked or pulped food or ensilage in hard worked animals;—many
irritant and acid plants;—accumulations of hard feculent masses in the
intestines;—irritation caused by intestinal worms especially the
blood-suckers;—the presence in the intestines of undigested matters, and
resulting fermentations, the result of diseased teeth and jaws and
imperfect mastication, of disease of the salivary glands or ducts and
imperfect insalivation, of a drink of water after a grain feed, washing
a part out of the stomach in an undigested condition, of disease of the
stomach, liver or pancreas interfering with their proper functions;
unwholesome and fermenting food like spoiled grain, or fodder, or
decomposed potatoes, apples, turnips, pumpkins, carrots, cabbages,
etc.;—stagnant and putrid water;—tumors, ulcers, volvulus,
invaginations, adhesions and other serious lesions of the bowels may act
in the same way.

As examples of the secretion of irritant matters from the blood may be
mentioned almost all the different agents used as purgatives, and
purgative agents accidentally taken in, these being as a rule absorbed
and later secreted again on the intestinal surface, increasing the
secretions in their passage:—also the morbid products of fevers which
irritate the intestinal mucosa and glands as they are thrown out by them
(rinderpest, lung plague, Southern cattle fever):—the purgative waters
on certain “scouring lands” act in a similar way. Under the head of
reflex action may be named the chills from exposure to cold rains, night
dews, damp stalls or beds, and damp, hot buildings, seasons and
localities. Under the head of nervous causes must be included strong
emotions as excitement, fear, etc., which lead to increase of both
secretion and peristalsis. Some horses are very subject to this and are
known as “washy”. These have usually a slim abdomen and long loin, and
scour whenever they are put to hard work. Other nervous animals with
good conformation, but which fret under saddle or in harness will scour
under specially severe work or under excitement. This is especially
common in young colts while being “broken”, and will occasionally show
in mares which are in _heat_. Cattle that have been on a specially
succulent diet (turnips, beets, ensilage, grass) are liable to scour
profusely if driven far or fast, and stock men seek to obviate this by
feeding some dry bran, meal, and above all fresh dry brewer’s grains
just before starting. Cows running at large when in heat are very liable
to scour. An exclusive diet of turnips or beets will keep cattle in a
chronic condition of mild diarrhœa, though not enough to interfere with
rapid improvement in flesh. Chronic diseases of the liver by obstructing
the flow of blood through the portal vein, cause intestinal congestion
and predispose to diarrhœa.

Of the various domestic animals horses are the most liable to
superpurgation, from an undue dose of aloes acting on the very large
colon and cæcum. Hence the importance of using such an agent carefully
in the young, fat or debilitated especially, of the avoidance of cold
drinks or exercise to excess after the aloes has been given, and of
keeping from work during its operation or immediately after.

_Symptoms._ These are of all degrees of severity from the frequent pulpy
evacuations of animals fed exclusively on roots, (beets, turnips,
potatoes), to the excessive and almost constant discharge of a dark
colored liquid mingled with more or less mucus. The discharge may be of
a light color and fœtid, indicating deficiency of bile, or of a dark
yellowish brown and odorless.

Slight diarrhœa does not affect the appetite nor general health, nor
check improvement in condition. In the more severe and continued forms
there is loud rumbling in the abdomen, loss of appetite and condition, a
rapid small pulse, accelerated breathing, pallid mucous membranes,
sunken glassy eye, and increasing debility even to an unsteady gait.
Distension of the abdomen with pawing and other indications of abdominal
pain may appear in bad cases. In the milder cases due to simple
irritation and congestion there is no tenesmus, no excess of mucus, no
formation of bubbles or froth in the stools, as occurs in active
intestinal fermentation and dysentery. In symptomatic cases on the other
hand there are superadded the marked symptoms of intestinal
inflammation, or fermentation, and the fæces become putrid and
offensive, which they do also in the different infectious diseases
(influenza, contagious pneumonia, rinderpest, lung plague, hog cholera,
swine plague, canine distemper, fowl cholera), when the toxins and waste
matters of the food and decomposing tissues are being thrown off by the
bowels.

Diarrhœa may be complicated with other diseases and especially in the
horse with laminitis.

In mild cases it tends to a spontaneous recovery, and is followed by
some slight costiveness, and if this should prove extreme there may be
some danger of complicating sequelæ such as indigestion, enteritis,
pneumonia or laminitis.

_Treatment._ The first consideration for the practitioner is to discover
if possible the immediate cause of the diarrhœa. If this is found to
reside in some infectious or other disease aside from the bowel, the
attention must be directed to that even more than to the diarrhœa. If it
depends on an overdose of some purgative agent or of acrid purgative
plants taken with the food, any further laxative is to be avoided, and
yet astringents and other agents which tend to lock up the offending
material in the alimentary canal must be equally guarded against. An
abundance of mucilaginous and demulcent liquids (mallow, flaxseed gruel,
boiled starch, etc.) may be given both by the mouth and anus, to sheathe
and protect the irritable mucous membrane and to dilute and carry off
the irritant contents. Moderate doses of opium may be required to allay
the violence of the spasms and peristalsis, but this should not be
pushed to the extent of locking up the irritants. Sometimes antiseptics
(naphthalin, salol) are useful to check fermentation, and pepsin may be
given to assist digestion.

In ordinary cases due to the presence of an irritant the first object
must be to relieve the bowels of this, and the second to soothe the
irritated mucous membrane. A laxative is usually all that is required,
but it must be a mild one so as not to add to already existing
irritation. Olive or castor oil are to be preferred as a rule (horse and
ox 1 pint; sheep and swine 4 ounces; dog ½ ounce), alone or with a
moderate dose of laudanum. Or rhubarb or aloes may be substituted if
desired. A dose of whisky or brandy, or oil of turpentine will often do
much to allay the secretion and peristalsis. These should be followed by
moderate doses of flaxseed gruel, or solution of slippery elm or mallow,
or simple well boiled gruels.

If the discharge persists after the laxative has had time to operate,
these mucilaginous agents may be replaced by solutions of boiled starch,
or of gum arabic, and small doses of calmatives such as laudanum (horse
or ox 1 ounce, sheep or pig 2 drachms, dog 20 drops), or prussic acid or
cyanide of potassium (30 drops of the acid or grains of the salt for
horse or cow). Sub-carbonate of bismuth, chalk, and carminatives and
antiseptics may also be given. According to the indications the
practitioner must combat persistent intestinal fermentation, or a
relaxed adynamic condition of the intestinal mucosa, or general weakness
and exhaustion, with such agents as seem best adapted to the individual
case.

_Chronic_ cases will demand the exercise of much judgment. After a
gentle laxative, salts of iron (sulphate, chloride) and pure bitters may
be given with antiseptics. Or vegetable astringents (catechu, kino) with
freshly burned charcoal and essential oils (peppermint, cloves, cajeput)
may be employed. In some instances calomel and chalk (1:12) will serve a
good end. In others silver nitrate, or arsenite of copper succeeds.
Quinine, nux vomica, pepsin, may be used to improve tone. The diet is
usually all important. Well boiled gruels, boiled milk, arrowroot,
pulped or scraped raw flesh may be demanded in different cases. The
patient should be kept at perfect rest, and all excitement avoided.


                  COLIC, ENTERALGIA, INTESTINAL SPASM.

  Definition. Colicy pains from spasm, enteralgia, tympanitic
  indigestion, overloading of bowels, impaction, calculi, concretions,
  sand, foreign bodies, intestinal and arterial parasites, irritants,
  enteritis, catarrhal, bacteridian, protozoan, chemicals,
  strangulation, adhesion, volvulus, invagination, hernia, trauma of
  stomach or intestine, peritonitis, pleuritis, metritis, ovaritis,
  hepatitis, biliary calculus, nephritis, urinary calculus, neoplasms,
  lead poisoning. Causes of enteralgia or spasm, idiosyncrasy,
  nervousness, cold, wet, high condition, debility, cold, rain, dew,
  perspiration, fatigue, indigestion, rheumatism. Symptoms: horse—sudden
  attack, paws, kicks, anxious look at flank, crouches, goes down,
  rolls, sits, rises, shakes himself, feeds, repeats at intervals,
  rumbling, defecations. Complications. Diagnosis, symptoms violent,
  transient, completely intermittent, no fever, no tenderness; from
  acute indigestion by absence of faulty feed, loaded or tympanitic
  abdomen, crepitation, continuous pain, and of careful decubitus; from
  constipation by complete intermissions and freer passages; from
  intestinal worms by absence of fur on anus, of rubbed rump, and of
  parasites in stools; from verminous thrombosis by complete
  intermissions and absence of prostration, cold sweats and of bloody
  stools; from enteritis and other inflammations by absence of fever;
  from intestinal anthrax by the intermissions, the absence of brownish
  mucosa, and perhaps of anthrax from the district; from hepatitis by
  absence of icterus, tender hypochondrium, and fever; from kidney
  affections by lack of stiff, straddling gait, tender loins,
  stretching; from pleurisy by absence of catching breathing, tender
  intercostals, and friction sound; ruminants—similar symptoms except
  sitting up or rolling; swine—sudden starting with grunt or scream,
  vomiting, etc.; Carnivora—frequent moving, yelps, snapping, straining,
  looking at flank. Treatment: solipeds, morphia subcutem, anodynes,
  laxative, friction, walking, enemata, chloral hydrate: ruminants,
  walking, enemata, morphia, laxative; swine, morphia, laxative,
  antispasmodics, injections, derivatives; dog,—purgative, injections,
  chloral hydrate, ether, olive oil.

The term colic is loosely applied to all abdominal pains from whatever
cause they may arise. It is thus allowed to embrace all diseases of the
abdomen. In its more restricted sense in which it will here be
considered it may be held to indicate =abdominal pain without
inflammation or any structural lesion=.

It may however be well to note the most common causes of abdominal pain
so that the distinction may be more definitely reached by a process of
exclusion.

1st. =Simple spasmodic colic.= 2d. =Enteralgia or neuralgia of the
intestines.= 3d. =Colics from indigestion=, _a_ =tympanitic=, _b_ =from
overloading with ingesta=, _c_ =from impaction or constipation=, _d_
=from calculi or concretions= or from =sand=, or =gravel= taken with the
food or from =foreign bodies= swallowed, _e_ from =worms in the
intestines=, _f_ from =worms in the mesenteric vessels=
(thrombo-embolic), _g_ from =irritants taken with the food or
otherwise=. 4th. Colics from =structural lesions of the intestines=; _a_
from =inflammation of intestine=, _b_ from =bacteridian inflammation of
the bowels=, _c_ from =protozoan inflammation=, _d_ from =chemical or
other irritants=, _e_ from =intestinal strangulations=, _f_ from
=adhesions=, _g_ from =volvulus=, _h_ from =invagination=, _i_ from
=mesenteric omental or phrenic hernia=, _j_ from =strangulated inguinal,
femoral ventral or umbilical hernia=, _k_ from =wounds=, =ruptures or
perforations of stomach or intestines=, _l_ from =peritonitis or
pleuritis=, _m_ from =metritis or ovaritis=, _n_ from =hepatitis or
biliary calculus=, _o_ from =pancreatitis or pancreatic calculus=, _p_
from =nephritis=, =nephritic=, =uretral=, =cystic or urethral calculus=,
_q_ from =neoplasms affecting any of the abdominal organs=. 5th. Colic
due to =lead poisoning=.

_Causes of enteralgia and spasmodic colic._ Enteralgia may be defined as
a neuralgic pain of the bowel which may therefore be free from spasm or
any other appreciable structural or functional change. Its existence in
the lower animal is necessarily somewhat problematical, as it can only
be inferred from the analogy of the animal with man, and of the enteron
with the superficial parts that are more frequently attacked with
neuralgia, and also from the absence of visible spasmodic contractions
in the bowel which has been the seat of intense pain, yet shows no
inflammatory lesion. But whether this is accepted or not, the occurrence
of spasm is undeniable and as both are functional nervous disorders the
same causative factors will apply to both.

In some nervous animals, especially high bred horses and dogs, there is
undoubtedly an idiosyncrasy which shows itself in a special
susceptibility of the nervous system. In such animals an exposure to
cold or wet, or the presence of a local irritant which would have been
without effect under other circumstances, lights up the nervous disorder
and produces an explosion, it may be as spasm or it may be as nervous
pain. Animals that are kept under the best care, that are least
accustomed to exposure and neglect, that are highly fed, and maintained
in high spirits and are impatient of control are more susceptible than
those that become inured to change and exposure, yet are kept in
moderately good condition. On the other hand the subject which has
become debilitated by overwork, underfeeding, exhausting disease, or the
generation in the system of some depressing poison is likely to show a
similar nervous susceptibility, so that at the two extremes of plethora
and nervous susceptibility, on the one hand, and anæmia and neurasthenia
on the other, we find a corresponding tendency to nervous disorder under
comparatively slight causes. Thus it happens that a drink of ice cold
water, an exposure to a cold blast or a drenching rain or a heavy night
dew may seem to be the one appreciable cause of the trouble. If the
animal has been perspiring and fatigued the attack is more likely to
occur. In other cases a slight indigestion unattended by impaction or
tympany, or the ingestion of an irritant which on another occasion, or
in another animal would have been perfectly harmless, will induce a
violent nervous colic. In some instances the attack is supposed to be of
a rheumatic nature the causative action of the cold giving color to the
theory.

_Symptoms._ The attack usually comes on suddenly especially if it has
followed on a drink of cold water or a cold exposure.

=Solipeds.= The _horse_ leaves off feeding or whatever he may have been
engaged in, paws with his fore feet, moves uneasily with his hind ones
or kicks with them, one at a time against the abdomen or out backward,
he looks back at the abdomen with pinched, drawn, anxious countenance,
bright anxious eye, and dilated nostrils, he moves uneasily from side to
side of the stall or box, crouches for a few seconds with semi-bent
knees and hocks and then throws himself down violently with a prolonged
groan. When down he may roll from side to side over the back, and
struggle in various ways, he may start to rise, sit for a moment on his
haunches, then go down and roll as before. Or he may get up, shake
himself and resume feeding as if entirely well. Soon the spasms
reappear, suddenly as at first, and after a time subside as before. Thus
the disease proceeds, each succeeding paroxysm diminishing in violence
until they permanently subside, or increasing until the animal dies worn
out with shock, suffering and exhaustion. If the paroxysms are severe
the skin is usually bathed more or less in perspiration. Usually the
peristalsis continues more or less, a rumbling is heard in the bowels
and more or less fæces are passed in small solid balls or semi-liquid.

The _course_ of the disease is usually rapid and followed by recovery.
When prolonged it may become complicated by volvulus, invagination,
indigestion or even enteritis.

_Diagnosis._ The characteristic symptoms are the suddenness of the
onset, the extreme suffering during the paroxysm, the reckless manner in
which the animal throws himself down, the intermissions with complete
absence of pain, the natural condition of the pulse and temperature in
the intermissions, the comfort with which the patient shakes himself,
and the absence of all abdominal tenderness, manipulation and friction
seeming to give relief rather than discomfort.

In the colic of =acute indigestion= there is the previous excessive or
unwholesome meal, or the full drink after feeding; there is tympany, or
a loaded state of the abdomen proving flat on percussion, there may be
crepitation on auscultation, there is continuous pain with exacerbations
(not complete intermissions), and there is rather a careful mode of
lying down.

In =intestinal constipation= or other =obstruction=, fæces may be passed
at first in small pellets coated with mucus or they may be at first
passed freely but in steadily lessening quantities until they stop
altogether. The pain is constant but worse at one time than another and
in case of external hernia the swelling will be visible.

In =helminthiasis= there is the general unthriftiness, irregular
appetite, frizzled broken hair on the base of the tail, a fur of dried
mucus around the anus and the presence of parasites in the droppings.

In =verminous thrombosis=, to the symptoms just named there are added
the reckless method of throwing himself down, hyperthermia, constancy of
the pain, rapidly running down pulse, cold sweats, and profound
prostration. When blood is passed per anum it is all the more
significant.

In =enteritis= or =peritonitis= the hyperthermia and the constancy of
the pains are sufficiently pathognomonic.

In =intestinal anthrax= there are the dusky brownish yellow mucosæ, the
marked prostration, the hyperthermia and the constancy of the suffering.
There is also the fact that the region is subject to anthrax and bacilli
may be present in the blood.

In =acute hepatic disease= there is hyperthermia, dusky or icteric
mucous membranes, great tenderness when percussion is made over the
short ribs, and sometimes lameness of one shoulder (usually the right).

In =disease of the urinary or generative organs= the stiff or straddling
gait, tender loins, and the frequent stretching as if to urinate, are
nearly pathognomonic.

In =pleurisy= the hyperthermia, the transient duration of the colic, and
the tenderness on manipulating the intercostal spaces will usually
differentiate.

=Ruminants.= In cattle, as in the horse, the symptoms of spasmodic colic
are restlessness, constant movement, looking round at the flanks,
wriggling of the tail, uneasy lifting of the hind feet, kicking at the
abdomen, and abruptly lying down and rising again. The animal does not
roll on the back nor sit on the haunches. Fæces may be passed in small
quantity or entirely suppressed, and there may be a slight tympany of
the paunch.

=Swine.= The animal is attacked abruptly, starts with a grunt or scream,
moves around uneasily, lies down, rolls, gets up, and repeats the
motions. Vomiting is not uncommon, and the belly may be tense,
tympanitic and even tender. The bowels may be confined or relaxed.

=Carnivora.= The colicy dog is very restless, changing from place to
place, sitting on his haunches, lying down curled up, starting up
suddenly with a yelp, and repeating the restless movements. He looks
anxiously at his flank, sometimes bites at it, and cries plaintively.
The bowels are usually torpid, and defecation effected with straining.

There are distinct intermissions but these are cut short by a new
accession of pain.

The attack is usually transient and ends in recovery.

_Treatment._ =Solipeds.= For nervous colic the hypodermic injection of
sulphate of morphia (2 grs.) is very effective. This will commonly bring
relief in less than five minutes. Should there be no effect at the end
of this time it may be repeated with advantage, but should a second dose
fail, it is well to resort to other measures. Eserine and barium
chloride are contraindicated as being liable to increase the spasm, and
if there is no irritant to expel there is no object in their exhibition.
The old prescriptions of laudanum and turpentine; laudanum and ether;
sweet spirits of nitre with belladonna, or hyoscyamus, and other
stimulants and narcotics are of little avail as they are not absorbed
from the horse’s stomach and cannot operate until they have reached the
duodenum. If given at all, their action may often be hastened by
injecting them into the rectum.

When the morphia fails it is the safest treatment to give a moderate
dose of aloes or other laxative, in combination with extract of
hyoscyamus or chloral hydrate. This takes time to pass into the
duodenum, and be absorbed and secreted anew in order to have its full
effect, and therefore it may be necessary to keep up a moderate action
of the morphia as a palliative. In four hours, however, at the latest,
the aloes can be counted on to bring permanent relief. This appears to
come as soon as the active principles have been absorbed, the nauseating
effect operating at once on the overexcited nerve centres. The action is
more perfect still when a free secretion has been started from the
intestinal mucosa, and the circulation and innervation in the intestinal
walls are essentially changed. This measure which was long successfully
practiced and advocated by the late Joseph Gamgee, is even more
perfectly adapted to the colics of indigestion and irritation, of
impaction and fermentation. There are of course cases of complete
obstruction in which it must fail, but it is probably the most
successful method for colicy affections in general.

In addition to the above, other methods of correcting the disordered
innervation are available. Active friction of the abdomen with straw
wisps is often effective, also fomenting the abdomen with hot water.
Simply leading the animal around acts as a nervous derivative, and may
be employed to prevent his dashing himself down so suddenly as to injure
himself. Then copious injections of warm water soothe the rectum,
solicit its peristalsis and by sympathy affect the other intestines in
the same way. They may often be made more effective by the addition of
antispasmodics (extracts of belladonna or hyoscyamus or chloral
hydrate).

In all cases a soft bed should be provided to secure the animal against
injury in his sudden reckless movements.

=Ruminants.= Simple spasmodic colic is usually transient and may be
successfully treated by driving around, giving copious warm water
injections, and using morphia subcutem. Frictions to the abdomen with
straw wisps, or with oil of turpentine should be tried. Should these
fail there is a presumption of further trouble and no time should be
lost in giving a laxative (Glauber salts) 1 to 2 pounds, or castor oil 1
quart, with antispasmodics and stimulants as for the horse.

=Swine.= The antispasmodic treatment may be tried on the pig, but
usually it is well to give a purgative at once in combination with the
narcotic. Castor oil 4 ounces, laudanum ½ drachm, or jalap 2 drachms,
and extract of hyoscyamus 20 grains in electuary. Warm injections and
embrocations to the abdomen are desirable.

=Dog.= It is usually well to give a purgative at once (jalap ½ drachm)
with 10 to 20 drops laudanum according to size. Copious injections of
warm water and a warm bath may follow. Chloral hydrate 20 to 60 grains,
may be exhibited by the rectum; also ether 1 drachm, in olive oil.


                  CONSTIPATION FROM INTESTINAL ATONY.

  Definition. Symptomatic. Causes: habit of retention in horse, dog and
  cat, indigestible matters in colon, calculi, dry food, lack of water,
  fever, diuresis, diaphoresis, milking, bleeding, hepatic torpor,
  verminous thrombi, old age, debility, nervous disease, matting of
  hairs, hæmorrhoids, abdominal suffering. Lesions: dilatation and
  catarrh of bowel, disease of rectum. Symptoms: solipeds—small, dry,
  coated, infrequent stools, straining, inappetence, tympany, colic,
  stretching as if to urinate; dog, fruitless straining, or dry, earthy
  looking fæces, coated, bloody, fœtid, anus swollen, tender, moist,
  palpitation, colic, vomiting, diarrhœa may fruitlessly occur, male
  urinates like bitch, foul, fœtid mouth; may last days or months;
  complications, sequelæ. Treatment: solipeds—exercise, pasturage, cold
  water before morning feed, regular regimen, bran, flaxseed, carrots,
  turnips, ensilage, common salt, Glauber salts, nux, cold injection,
  glycerine, barium chloride, purgative, enemata; dog:—mechanical
  unloading of the rectum and colon, injections, exercise, water,
  regular habits, laxative food, eserine, oil, calomel, jalap,
  podophyllin, colocynth, belladonna, nux vomica, abdominal massage,
  electricity.

_Definition._ Constipation consists in dryness, hardness, and undue
retention of the fæces. It has of course many grades and may lay claim
to many different causes, so that it might, like its antithesis
diarrhœa, be held as merely a symptom of another disease. It has however
such a definite character, that it is convenient to retain the name to
designate those cases in which the torpor or atony is the most prominent
and dominating feature, while other forms of obstruction will be treated
under different heads.

_Causes._ Defecation is immediately due to the active peristaltic
movements of the rectum overcoming the resistance of the sphincter.
There is also the concurrent closure of the glottis and contraction of
the diaphragm and abdominal walls, and it is usually the voluntary
operation of these forces that rouses the rectum to effective
peristalsis. The excitability of the rectum depends greatly on habit,
hence the habitual retention of fæces, gradually dulls that organ and
renders it less and less disposed to respond. In _horses_ this is seen
largely in connection with abundant dry feeding and lack of exercise. In
house _dogs_ and _cats_ on the other hand, inculcated habits of
cleanliness, compels the suppression of the natural instinct, and the
habitually overloaded bowel becomes less and less responsive. The
retained excrements meanwhile give up more and more of their liquids
until they become so dry, and incompressible as well as massive that
they can be expelled only by violent efforts. Inflammation of the mucosa
naturally follows the retention and this in its turn adds to the
weakness and torpor.

Acting in a similar way the partial obstruction, by accumulations of
bones and other undigested matters in the colon, and by calculi, tends
to continued accessions of new material and to gradually increasing
intestinal paresis. So with the other forms of obstruction which will
not be further referred to here.

In all animals dry feeding and a lack of water are potent causes of
inspissation of the ingesta and torpor of the bowels.

All or nearly all febrile affections, leading as they do to suppression
of secretions, cause drying and tardy movement of the contents of the
bowels.

The excessive loss of liquid through other channels,—by diuresis, by
profuse perspirations, by excessive secretion of milk, or by
bleeding—has a similar tendency.

The suppression of the biliary secretion through liver disease, or
obstruction of the biliary duct, withholds from the intestine, the most
important of the stimuli to peristalsis, and tends to constipation,
unless the resulting irritation should cause excessive secretion.

The derangement in the circulation in the intestinal walls caused by
verminous thrombi in the horse, acts in the same way, the imperfectly
nourished walls not only losing the normal power of peristalsis, but
sometimes contracting so as to cause a stricture. Parasites encysted in
the walls of the bowels, like catarrhal and other inflammations of these
parts tend to atony and tardy peristalsis.

A weakness of the nervous system attendant on old age, or debility, or
chronic lead poisoning often tells with force on the alimentary canal,
and the loss of nervous power through disease of the great nerve centers
(ganglionic system, brain, spinal cord) impairs the vermicular motion.
This is notoriously the case in paraplegia, chronic hydrocephalus, and
vertigo.

Finally among the causes of constipation must be noted the matting of
the hairs around the anus (in dogs), and painful affections of the anus,
or the abdominal walls, which render efforts at defecation painful and
deter the animal from attempting them.

_Lesions._ These are as varied as the diseases which give rise to
constipation, or result from it. Permanent dilatation or sacculation of
the intestine, and the structural changes attendant on intestinal
catarrh are the most common local lesions. But proctitis, hemorrhoids
and ulcers of the anal follicles are met with in canine patients and
ulcers of the colon in the seat of impaction are common.

_Symptoms._ In =Solipeds= the fæces are passed, at long intervals, in
small quantity, usually only a very few balls at a time, firm, dry,
moulded smooth and black on the surface, often covered with mucus, or
with streaks of blood. They are passed with unusual effort and
straining, and even with groaning, and one or more balls that may be
exposed in the act are often drawn back and retained by the inversion of
the rectum and closure of the sphincter. It is liable to be complicated
by impaired appetite, tympanies, slight recurrent colics, and dryness,
scurfiness and unthriftiness of the skin. Not unfrequently the pressure
of the impacted colon (pelvic flexure) irritates the bladder causing
stretching as if to urinate, and the passage of urine often in small
quantity. There may be the symptoms of any one of the different nervous
affections that lead to impaired peristaltic action, or of the local
diseases which tend to obstruction of the bowels.

In =dogs= there are violent and painful efforts to defecate, which may
be fruitless, or may lead to the expulsion of small masses of dry,
earthy looking fæces, smoothly moulded on the surface, coated with
mucus, streaked it may be with blood and highly offensive in odor. The
anus may be puffy and swollen with mucopurulent secretion from the anal
glands, which soils the hair of the hips and tail. If the abdomen is
flaccid, manipulation with both hands on opposite sides usually detects
a solid mass representing the impacted rectum and colon, and extending
from the pelvis forward, often to the sternum. The same mass will be
reached by the oiled finger introduced into the rectum. Both methods of
exploration are painful and may call forth cries from the patient. The
abdomen is usually distended, largely from the impacted fæces, in which
case it gives a flat sound on percussion, or from gaseous emanation, in
which case it is tense, resilient and resonant. Colicy pains are liable
to appear, and vomiting at first of food only, then more or less yellow
and bilious, and finally of distinctly feculent matters. For a time
appetite may be retained, but this is gradually lost. There may
supervene diarrhœa, which in favorable cases may lead to expulsion of
the impacted mass, but in others it fails to completely dislodge it. The
patient is dull and spiritless, inclined to lie curled up in dark
corners, and when raised walks slowly and stiffly, with the tail carried
straight or slightly to one side. The male urinates like a bitch without
lifting the leg. The nose is dry, the tongue furred, the teeth usually
covered with tartar, and the breath fœtid. There is at first no
hyperthermia, but some rise of temperature attends on the advance of the
disease, and the auto-poisoning by absorbed products of the putrefaction
of retained fæces.

The disease may last a few days only or it may continue for weeks or
months. In the last case intestinal catarrh, ulceration, and
circumscribed necrosis are likely to supervene and the animal may die of
auto intoxication, acute peritonitis or enteritis. Yet the majority of
cases in the dog reach a favorable termination, or recover with
remaining cicatrices, strictures or dilatations.

_Treatment._ In =solipeds= accustomed to an idle or pampered life,
plenty of daily exercise will often correct the torpor. A run at pasture
will often effectually counteract the tendency. If the patient must be
kept in the stable a full drink of cold water every morning before
feeding will often succeed. Regularity in feeding and watering is of the
utmost importance, and the addition of a little wheat bran or flaxseed
to the grain is often of material advantage. Next may be added a
moderate allowance of carrots, turnips, or ensilage to furnish the
needed succulence and organic acids. If in addition medicinal measures
are wanted, a small handful of common salt, or of Glauber salts, in the
morning drink to be taken ten or fifteen minutes before the first feed,
will usually operate well. This may be continued for a length of time if
necessary, without the ill effects of purgatives given at other times.
It may be rendered slightly more effectual by the addition of 10 grains
nux vomica on each occasion. A morning injection of a quart or two of
cold water with one or two ounces of glycerine may be tried. Another
resort is 2 or 3 grains of barium chloride in the morning drink or
hypodermically repeated daily for some time.

In the more severe cases with already existing impaction of the colon,
purgatives and copious injections will be demanded as advised under that
disease.

In =dogs= the first object is the unloading of the rectum and colon and
this usually demands direct mechanical intervention. (See Intestinal
Indigestion with Constipation.) In case of hypertrophied prostate this
may be rendered somewhat difficult, yet with a free use of oily, soapy
or mucilaginous injections it can usually be accomplished.

The further treatment is on the same line as for the soliped. An
abundance of exercise in the open air is a prime essential, together
with a free access to fresh water. House dogs must be taken out for
urination and defecation at regular times that are not too far apart.
The food must be of a laxative nature. At first fresh whey or buttermilk
only may be allowed, but as some action of the bowels is obtained well
salted beef tea, pulped or scraped red muscle seasoned with salt, or
milk treated in the same way is permissible. If the bowels fail to
respond when the dog is taken out at the regular times an injection of
cold water may be given. Sulphate of eserine (⅕ gr.) may be given daily
by the mouth or hypodermically, or castor oil (½ to 1 oz.) may be
administered at one dose to be followed by careful dietary and hygienic
measures. Or sweet oil, calomel and jalap, podophyllin, or colocynth may
be substituted. When the bowels have been freely opened a daily morning
dose of a drop of the fluid extract of belladonna and ½ gr. of nux
vomica will often materially improve the peristalsis. Active
manipulation of the abdomen may be employed, or, if available, a current
of electricity through the torpid bowels for 10 or 15 minutes daily.


                         CONSTIPATION IN BIRDS.

  Causes: Matted feathers, impacted cloaca, arrest of eggs, debility,
  catarrh, parasites, nervous disorder. Symptoms: swelling of anus,
  pendent abdomen, waddling gait, straining without effect. Treatment:
  remove obstruction by mechanical means, cut off matted feathers, egg
  matter may demand laparotomy, castor oil, tincture of rhubarb,
  enemata, green food, ensilage, roots, onions.

In birds torpid and obstructed bowels may come from the effects of a
previous diarrhœa, which has led to the matting together of the feathers
over the anus at once obstructing defecation and rendering it painful.
It may result in and be aggravated by a slow accumulation of
indigestible matters in the intestine or cloaca (pebbles, feathers,
etc.), and the arrest of eggs in the oviduct, pressing upon and
obstructing the bowel. In a recent case the author removed 18 ozs. of
impacted egg matter from the oviduct of a hen, which when divested of
this load weighed barely 2 lbs. Debility of the general system and
particularly of the walls of the bowels, and its various causes (old
age, exhausting disease, intestinal catarrh, parasites, nervous
diseases, etc.) retard defecation and favor impaction as in the mammal.

The _symptoms_ may be; hard dry droppings, matting of the feathers over
the anus with feculent matters, a firm swelling surrounding the
sphincter, a pendent condition of the abdomen which when manipulated is
felt to be firm and resistant, ruffling of the feathers, drooping of the
head, wings and tail, walking sluggishly with legs half bent and a
waddling gait, and ineffectual attempts to defecate.

_Treatment._ As in dogs remove the obstructing mass by mechanical means.
Matted feathers may be clipped off, and feculent accumulations may be
dislodged by the aid of the finger, or in small birds of a blunt prob.
This may be favored by manipulation through the abdominal walls, and the
injection of soapy or oily enemata. Accumulations of impacted egg matter
may be similarly removed, or, failing this, by an incision made through
the abdominal walls and oviduct. As a purgative give one or two
teaspoonfuls castor oil according to the size of the hen, or a few drops
to a small cage bird. For the latter Friedberger and Fröhner advise a
few drops of tincture of rhubarb in the drinking water. Injections of
warm or cold soapsuds or water may be continued as symptoms demand.
Green food, ensilage, roots, worms, snails and insects are indicated to
correct the tendency to costiveness and may be continued until the
bowels have acquired their proper tone. A moderate allowance of onions
is often of great value.


            HAIR BALLS IN THE INTESTINES—HORSE. EGAGROPILES.

  Seat, colon, cæcum; hair of oat seed, clover leaf, vine tendrils, hair
  of horse, nucleus, calcic admixture, straw, in horses on dry food,
  with depraved appetite, or with skin disease. Symptoms: none, or
  torpid bowels, colics, recurring, fermentations, tympany, obstruction,
  rupture, peritonitis, rectal exploration. Lesions: impacted ball, with
  excess of liquid and gas in front, rupture, ragged bloody edges.
  Treatment: extraction, enemata, eserine, barium chloride.

Hair balls, received the name of egagropiles because of their discovery
in the alimentary canal of the wild goat, but they are found in various
forms in all the domestic animals. In _horses_ they occupy the cæcum and
colon and are most frequently composed of the fine vegetable hairs that
surround the grain of the oat, or the leaf of clover, of the woody
tendrils of vines, and of the hairs of themselves and their fellows
taken in at the period of moulting. They sometimes contain a nucleus of
leather or other foreign body which has been swallowed but in many cases
no such object can be found, the hair having become rolled and felted by
the vermicular movements of the stomach and intestines. An admixture of
mucus assists materially in the felting, and calcareous and magnesian
salts may make up the greater part of the mass, rendering it virtually a
_calculus_. They may further have a large admixture of straw and
vegetable fibres of larger size than oat or clover hairs. They are most
frequent in horses kept on dry food, (sweepings of oatmeal mills) and at
hard work, and which show depraved appetite and lick each other. Omnibus
horses suffer more than army horses. Skin diseases, by encouraging
licking, contribute to their production.

_Symptoms._ In the great majority of cases hair balls do not seriously
incommode the horse. They do not attain a large size, and being light do
not drag injuriously on the intestine and mesentery. They do, however,
retard the movement of the ingesta, and when grown to a considerable
size they may block the intestine, more particularly the pelvic flexure,
the floating colon or rectum. Under such conditions they produce colics
which may be slight, transient, and recurrent, or severe and even fatal,
having all the characteristics of complete obstruction from other
causes. Fermentations, tympanies, and straining without defecation are
common features. When the obstruction takes place in the pelvic flexure,
the floating colon or rectum, it may often be detected by rectal
exploration. When complete obstruction occurs all the violent symptoms
of that condition are present, and these may pass into those of rupture
(Peuch, Leblanc, Neyraud), and shock or peritonitis. If the animal has
passed hair balls even months before, the colics may with considerable
confidence be attributed to other balls of the same kind.

_Lesions._ In case of death there are the usual lesions of gaseous
indigestion, with or without enteritis, but with the accumulation of a
great quantity of liquid contents, above the ball, which is felt as a
firm body impacted in the gut. In other cases the distended bowel has
given way and the liquid contents and often the hair ball as well are
found free in the abdominal cavity. In such a case the edges of the
laceration are covered with blood clots and thickened with inflammatory
exudation, and there is more or less peritonitis.

_Treatment._ Relief may sometimes be obtained by the extraction of a
hair ball lodged in the rectum or adjacent part of the floating colon.
In other cases abundant soapy or oily enemata, and the employment of
eserine or barium chloride subcutem are indicated.


                 HAIR AND BRISTLE BALLS IN DOG AND PIG.

  From licking in skin disease. Symptoms: of obstruction. Treatment:
  manipulation, enemata, oil, antispasmodics, eserine, barium chloride,
  laparotomy, diet in convalescence.

The hair balls of _dogs_ come mainly from licking themselves when
affected with skin diseases or parasites. In _pigs_ they are mostly
attributed to depraved appetite.

The hair balls of the _dog_ are small, open in texture, and easily
disintegrated, having little mucus and no earthy salts in their
composition.

The bristle balls of _pigs_ take the form of straight or curved rods of
firm consistency, but without earthy salts. The projecting ends of the
bristles render them particularly irritating.

The _symptoms_ are those of obstruction of the bowels, and the
_treatment_ consists in efforts to dislodge them. If situated near the
anus they may sometimes be reached with the finger, or copious oily
injections may facilitate their passage. Manipulations through the
abdominal walls may be helpful in the dog. Oleaginous laxatives and
antispasmodics may be tried, or these failing, eserine or barium
chloride. As a last resort laparotomy may be performed, the ball
abstracted and the intestine and abdominal wall carefully sutured
(Siedamgrotzky). In such a case the diet should be restricted for a week
to beef soups, buttermilk, and well boiled gruels, especially flaxseed.




               INTESTINAL CALCULI. ENTEROLITHS. BEZOARS.

  Earthy basis, nucleus, stratification, in cæcum or colon, multiple,
  size, number up to 1000. Composition, phosphates of lime, magnesia,
  and ammonia, silica, mucus, epithelium, organic matter.
  Ammonio-magnesian tend to crystalline form, common phosphate of lime
  to smooth forms. Concretions. Source in food. Ammonia from bacteridian
  fermentation, action of colloids, varied nuclei, rapid growth.
  Lesions: catarrh, dilation, obstruction, rupture, peritonitis.
  Symptoms: intermittent colics with obstruction, tympany, bowel
  distension, liquid and gaseous, before obstruction. Diagnosis: by hand
  in rectum, hard obstruction with distension in front. Treatment:
  purgative dangerous, but exceptionally successful, extraction,
  oleaginous enemata, laparotomy.


=Horse.= Intestinal calculi have an earthy basis (ammonio-magnesian
phosphate, or oxalate of lime, and more or less silica) glued together
by mucus and having a central nucleus usually of some foreign body, (a
particle of sand, pebble, morsel of hair, lead, cloth, nail, coin, blood
clot, or inspissated mucus) around which the earthy salts have been
deposited layer after layer. They are usually formed in the cæcum or
double colon and may be multiple and moulded upon each other, so that
they become discoid, angular or otherwise altered from the globular
shape. The worn, flattened surface in such cases shows concentric rings
representing the layers as deposited in succession.

The _size_ of the masses may be from a pea or smaller, up to calculi of
six inches in diameter.

In _number_ there may be a single calculus or there may be an indefinite
quantity. Zundel counted 400 in a single colon, and Gurlt 1,000.

_Composition._ They are usually composed of phosphate of lime and of
magnesia, of ammonio-magnesian phosphate, with a little silica, mucus,
epithelium, and organic matters from the ingesta. Traces of sodium
chloride, and iron oxide may also be present.

The phosphates of lime, magnesia, and of ammonia and magnesia usually
constitute the main part of the calculus. Fürstenberg found specimens in
which the ammonio-magnesian phosphate amounted to 72 to 94 per cent.

The calculi containing an excess of ammonio-magnesian phosphate tend to
assume a crystalline or coralline form which causes them to be specially
irritating to the mucosa. When broken they show a radiated structure
from the centre to the circumference in addition to the concentric
rings. These are usually of a yellowish brown or a gray color and have a
specific gravity of 1694 to 1706.

Calculi in which the common phosphate of lime abounds are likely to be
smooth on the surface and on section show the concentric rings more
distinctly and the radiating lines less so. The brownish calculi of this
variety are much more compact, and harder than the crystalline or
mulberry calculi, and have a higher specific gravity—(1823).

Bluish calculi with a smooth glistening surface and lower specific
gravity—1681—, have been found of small size and in great numbers in the
colon (1000 in the colon, Gurlt).

In some calculi there is a large admixture of alimentary matters, and a
low specific gravity (1605 to 1674). These were designated as _pseudo
calculi_, by Fürstenberg.

In still other cases a calculous looking mass, when broken into, is
found to be composed of a mass of dried alimentary matter enclosed in a
thin layer of lime salts. These have a low specific gravity (1446 to
1566) and have been named _concretions_ by Fürstenberg.

_Causes._ As a large proportion of the calculus is phosphate of lime or
ammonio-magnesian phosphate, we must look for the source of these in the
food and then at the conditions which determine their precipitation.

The percentage of ash and of phosphoric acid in the common foods of
horses may be seen in the following table:

                                       PO_{5} in the     PO_{5} in the
                         Ash.              Ash.          entire food.
                       Per cent.         Per cent.         Per cent.
 Wheat bran                      7.3                50              3.65
 Wheat grain                     3.0             46.38            1.3914
 Oats grain                     2.50              26.5            0.6625
 Barley grain                   3.10              39.9            1.2276
 Bean grain                     3.10              31.6            0.9864
 Pea grain                      2.75              34.8             0.957
 Tare grain                     3.00              36.2             1.086
 Indian corn grain               1.5
 Rye grain                       1.6              39.9            1.0384

The source of the magnesia may be found to a large extent in the grains
represented in the following table:

                                  Ash.     Mg. in Ash.
                                Per cent.   Per cent.
                 Oat, grain           2.50         7.3
                 Barley, grain        3.10         8.5
                 Rye, grain            1.6         2.4
                 Wheat, grain         2.12        9.98
                 Wheat, bran           7.3        11.2
                 Bean                  3.1         6.6
                 Pea                   2.7         5.6

The amount of magnesia in each of these grains is amply sufficient to
furnish the material for the constant growth of a calculus. Wheat bran
is preëminent in the amount of its magnesia and therefore wheat bran has
been charged with predisposing to calculi. In the perisperm as a whole,
Fürstenberg found 1 per cent. of phosphate of magnesia, and in coarse
bran not less than 2.5 per cent.

The ammonia which is essential to the precipitation of the phosphate of
magnesia in the form of the compound salt (ammonio-magnesian) can be
found wherever proteids are in process of septic fermentation. The
slightest failure to peptonize every particle of such proteids, implies
septic change and the evolution of ammonia, which on coming in contact
with magnesia phosphate instantly precipitates the insoluble salt.

This fully agrees with the doctrine of the formation of urinary calculi
through the agency of bacteria, since the ammonia is essentially a
fermentation or bacterial product.

It may also be noted that the experiments of Rainey and Ord showed that
in the presence of colloids (mucus, epithelium, pus, blood) the earthy
salts are precipitated as minute globular bodies which by further
accretions become calculi. In the absence of colloids the salts tend to
precipitate in angular crystalline forms, so that the mulberry and
coralline calculi may possibly have been precipitated in the absence of
such bodies. From the solvent quality of ammonia, however, the contents
may easily pass from a fermenting liquid containing colloids to a
non-fermenting and noncolloid mixture.

The presence of a solid body which may act as a nucleus is an essential
element, and the condition of the food or drink will often supply this.
It has been noticed that army horses in the field, feeding from the
ground and taking in sand and pebbles, are unusually liable to
intestinal calculus. Horses which lick earth in connection with acidity
of the stomach or other dyspepsia are specially subject to it. Horses
watered from shallow streams with sandy bottoms, where they take in sand
with the water, have been similarly affected. Millers’ horses, in the
days of old process milling, suffered not alone because of the abundance
of oat hairs in the feed but also on account of the grit from the
millstones. Hay and other fodders that have lain on the ground and which
contain earth and sand furnish other sources of such nuclei. Shingle
nails and other small nails, pins, needles, coins, etc., which have
mixed with the feed are common causes of trouble, and indeed any foreign
body may become the centre and starting point of a calculus.

Catarrhal affections and other lesions of the mucosa, which furnish
excess of mucus, beside pus, lymph and even blood as nuclei, are invoked
as starting points of the calculi, but however true this may be in
particular cases, irritation and catarrh appear to be much more
frequently the result than the cause of the calculus.

Attempts have been made to estimate the time taken in the formation of a
calculus by allowing a ring for each feed and successive deposit
therefrom (Fürstenberg, Colin). Thus a calculus of 14 pounds with 720
layers, it was estimated could be formed in one year at two feeds per
day. More definite evidence was found in the case of Pastore in which a
coin with the mint mark of 1847 was found as the nucleus of a calculus
the size of the fist in 1848.

_Lesions._ Formed in the most spacious parts of the colon and cæcum,
calculi usually rest there for a length of time without visible injury,
and it is only when they are moved onward and get arrested at a narrow
part of the gut (pelvic flexure, floating colon, rectum) that they cause
appreciable trouble. Yet it is claimed that by their weight they drag
upon the yielding walls of the bowel, causing dilatation and
attenuation, weakening the peristalsis and predisposing to rupture. The
compression of the vessels also tends to anæmia and atrophy. In the case
of rough crystalline calculi the mucosa is subjected to attrition,
irritation, and inflammation. The more serious and urgent trouble is
that of obstruction of the narrower portions of the colon and rectum,
which may be absolute and persistent, leading to rupture and death or a
fatal inflammation on the one hand, or may end in recovery on the other,
in connection with a displacement onward or backward of the calculus as
the result of peristalsis or anti-peristalsis.

_Symptoms._ These are intermittent colics, each reaching a climax and
followed by a sudden recovery as the calculus is displaced into a more
spacious part of the colon. A significant feature is the complete
obstruction, fæces being passed for a short time at first and then
suddenly and absolutely stopped. Coincident with this are tympany,
violent colics, straining, rolling, sitting on the haunches,
perspirations, anxious countenance, and all the symptoms of obstruction.

_Diagnosis_ is never quite certain unless the practitioner with his
oiled hand in the rectum can detect a hard stony mass obstructing the
pelvic flexure of the double colon with a tense elastic distended bowel
immediately in front of it, or a similar hard obstruction of the
terminal part of the floating colon with a similar distension in front
of it. The pelvic flexure may usually be felt below and to the right at
the entrance to the pelvis, and the floating colon above, under the
right, or more commonly the left kidney. Calculi in the more spacious
parts of the double colon or in the cæcum are inaccessible to
manipulation. The feed (bran, ground feed) will be suggestive, as will
the occupation of the proprietor (miller, baker).

_Treatment._ This is rather a hopeless undertaking. No effective solvent
of the calculus can be given, and purgatives usually increase the danger
by increasing the peristalsis and dangerously distending the bowel above
the point of obstruction. It is true that this is sometimes followed by
a temporary recovery the calculus being loosened and falling back into
the dilated portion of the bowel. Less frequently the increase in the
peristalsis forces on a moderately sized calculus to complete expulsion.
It is a desperate though sometimes successful resort. A more rational
course of treatment is the dilation of the bowel back of the obstruction
by copious mucilaginous, soapy or oleaginous enemata. Trasbot suggests
CO_{2} produced by injecting sodium bicarbonate and tartaric acid. This
may be seconded by the hypodermic injection of barium chloride or of
atropia. When the calculus is lodged in the floating colon or rectum it
may be possible to reach it with the hand and extract it at once. The
last resort, is by laparotomy for the removal of the calculus. One such
successful case is on record in which Filizet removed a calculus as
large as an infant’s head. In other cases the horses failed to survive.
Desperate as the resort may be it is not to be neglected in a case of
undoubted calculus, solidly impacted and of such a size that its passage
is impossible. A fatal result is imminent, and even if the present
attack should pass off it can only be looked on in the light of an
intermission, so that there is practically nothing to lose in case the
result should prove fatal. Anæsthesia and rigid antiseptic measures
should of course be adopted.


             FOREIGN BODIES IN THE INTESTINES OF SOLIPEDS.

  Sand, pebbles, earth, lime, nails, pins, needles, coins, shot, cloth,
  leather, rubber, sponge, tooth, bone, wood, twine. Symptoms: as in
  intestinal indigestion or calculi, or sand or pebbles in fæces;
  peritonitis, phlegmon. Lesions: congestion, catarrh, ulceration,
  abscess, needles may travel to other organs. Treatment: laxative,
  enemata, or as for calculi.

All sorts of foreign bodies are taken in with food and water and find
their way to the intestines. Sand from drinking from shallow streams
with sandy bottoms, from browsing on sandy pastures where the vegetation
is easily torn up, or from feeding grain from sandy earth will sometimes
load the intestines to an extraordinary extent so that such horses will
pass sand for some weeks after leaving the locality. Small stones and
gravel are taken in in the same way or from the habit of eating earth or
licking crumbling lime walls. Nails, pins, needles, coins, shot, pieces
of cloth, leather, caouchouc, sponge, and even a molar tooth and a piece
of a dorsal vertebra have been thus taken. Recently the author saw a
small twig of hard wood transfixing the pylorus and duodenum with fatal
effect. In another case were balls of binding twine which had been taken
in with the fodder on which it had been used.

The _symptoms_ are usually those of intestinal indigestion or calculi.
In some cases, however, they are peculiar, thus there may be a constant
passage of sand, there may be indications of peritonitis, or there may
form a phlegmonous swelling of the abdominal walls in the abscess of
which the foreign body is found.

_Lesions._ Pechoux found 56 lbs. of a brownish earth in the cæcum and
colon. Congestion and ulceration of the intestines are common, with
occasionally abscess. All the lesions that attend on or follow
obstruction may be met with. Boullon saw a remarkable case of the
ingestion of needles in which these bodies were found in the small
intestine, liver, pancreas, diaphragm, kidney and lung.

_Treatment_ varies with the character of the bodies ingested, sand and
gravel may be passed on by a laxative diet and even by the use of mild
laxatives. Bernard gave 10 quarts of water and 4 oz. Glauber salts every
hour for eight days, and the same amount by enema. For the larger solid
bodies which obstruct the intestines the treatment is the same as for
calculus. For sharp pointed bodies causing abscess and fistulæ, we must
follow the indications, ever aiming at the discovery of the whereabouts
of the offending object and its removal.


             FOREIGN BODIES IN THE INTESTINES OF RUMINANTS.

Foreign bodies are usually arrested in the rumen of cattle and unless
sharp, pointed or rough so as to cause mechanical trouble or caustic so
as to act chemically, rarely do much harm. The most extraordinary
objects that have found their way into the intestine are snakes.
Gherardi claims that he found in the intestines a snake of 25 inches
long; Jager found one of 21 inches in length, in an advanced state of
decomposition, in the rectum of a calf. It is supposed that both had
been taken in with the food. In each case there was obstruction of the
intestine with severe colicy symptoms.




             FOREIGN BODIES IN THE INTESTINES OF CARNIVORA.

  Small bodies, especially playthings, feathers, hair, bristles, bones
  of prey. Lesions: congestion, inflammation, hemorrhage, ulceration,
  perforation, invagination. Symptoms: colic, vomiting, tucked up belly,
  straining, palpitation, rabiform symptoms, cough, convulsions. Course:
  emaciation, prostration, death in five days or two weeks according to
  seat of obstruction. Treatment: Oleaginous injections, laparotomy.


_Causes._ The dog is especially liable to this form of trouble, in
consequence of his habit of carrying objects in his mouth and of playing
with different objects especially the playthings of children. Marbles,
pebbles, spinning-tops, corks, coins, nuts, peach stones, pieces of
rubber, cloth or leather, bits of wood, sponge, needles, pins, potato,
bone, cord, hair, bristles, feathers, wire, and a number of other
objects. Some of them like feathers, hair, and bones are swallowed with
food, and when that has been digested, they are either vomited or
failing in this, are passed on into the intestine. Lately the author
made a post mortem of a house dog with over 24 inches of the jejunum
virtually blocked with fragments gnawed from a caouchouc ball and pieces
of twine.

=Cats= also swallow a variety of objects. Benjamin and Megnin record
three cases of intestinal obstruction by the crystal drops of shades.

_Lesions._ When the lumen of the intestine is blocked with a round solid
body like a marble or peach stone there occur active congestion,
inflammation, blood stasis and hemorrhage, with in many cases necrosis,
ulceration and perforation. Similar lesions occur from cord. In a recent
case of impaction with gnawed fragments of caouchouc and cord, the 24
inches of the bowel implicated were the seat of extended patches of
necrosis and of deep, and even perforating ulcers on the lesser
curvature of the intestine, evidently caused by the tension of the
stretched cord on the shorter attached border of the gut. Cadeac says
the lesions from cord are always at the point of attachment of the
mesentery, whereas those coming from round or cubical solid bodies are
mainly on the greater curvature. Mathis found at the pylorus a piece of
net from which a cord extended through the small intestine and ended in
a ravelled mass near the ileo-cæcal valve. The dragging of the cord on
the intestine often causes invagination at one or several points.

_Symptoms._ There may be slight colic, dullness, a disposition to lie
curled up in some secluded place, loss or caprice of appetite, vomiting,
tucked up abdomen, arching of the back, straining, and unless the bowels
are distended with gas, the obstruction can usually be felt by the two
hands applied on opposite sides of the abdomen. The matters vomited are
at first alimentary, then bilious and in the advanced stages always
feculent.

The French veterinarians assure us that rabiform symptoms are very
common as the result of obstruction of the intestines with foreign
bodies. The indications are signs of fury without the barking which
characterizes genuine rabies. The patient becomes wicked, cross and
excitable, sometimes dull and morose, and snappish, his eyes glittering
and his mouth frothy. He has alternate paroxysms of fury and torpor, at
one time flying at and biting any living thing he meets, or tearing some
object to pieces, and at another hiding away in secluded and dark
corners. Massenat saw two dogs supposed to be affected by rabies, but
which recovered promptly after having vomited the foreign bodies which
they had swallowed. In a country where rabies is so prevalent as in
France, it would be interesting to see the results of inoculation with
some of the most pronounced of these rabiform cases.

Beside the rabiform symptoms cough and epileptic seizures occasionally
result from the foreign bodies.

_Course._ _Termination._ Unless relief is obtained by vomiting or
purging, appetite ceases altogether, emaciation advances rapidly, the
animal becomes dull and stupid, being evidently poisoned by the absorbed
toxins, and death may ensue in four or five days if the obstruction is
near the stomach, or in one or two weeks if in the large intestines.

_Treatment._ The general treatment advised for the horse is applicable
to the carnivora. Purgatives are always dangerous as threatening the
overdistension and rupture of the bowel above the obstruction.
Oleaginous and mucilaginous injections with manipulations are more
promising if the obstruction is in the colon or rectum.

In many cases laparotomy is the only hopeful resort. Felizet and Degive
have been quite successful in removing corks in this way, and Fröhner
advises the operation to be performed under opium narcosis, and with
antiseptic precautions. Make an incision of 1¾ inch near the umbilicus
and parallel to the linea alba, extract the blocked loop of intestine,
ligature it in front of the foreign body and behind it, incise, remove
the offending mass and carefully close by sutures, bringing the muscular
and serous coats in accurate opposition. Remove the ligatures,
disinfect, return the bowel into the abdomen, close the abdominal wound
with sutures and apply an antiseptic bandage.

If such cases are to be operated on it is important that it be done
early, before the occurrence of necrosis, ulceration, perforation, or
general infection.


                  RUPTURE OF THE INTESTINE. SOLIPEDS.

  Causes: overdistensions in front of obstructions, softening,
  friability, necrosis, suppuration or ulceration, Duodenum from worms
  or perforation by pointed bodies, exudate in verminous embolism,
  petechial fever. Jejunum and ileum, by disease of walls, ulcers,
  abscesses, neoplasms, caustics in umbilical hernia, clamping of
  hernia. Cæcum, falls, blows, kicks, blows of horn, tusk, stump,
  calculi, abscesses, cauterizing of hernia. Colon, external traumas,
  calculi, worms, verminous thrombosis, neoplasms, abscesses,
  overdistensions, violent straining, arsenic. Symptoms: follow
  accident, signs of obstruction, no rumbling, tympany, stiffness, great
  prostration, fever. Death in short time.

_Causes._ Ruptures occur as we have already seen from overdistensions of
the bowel in front of some obstruction, by ingesta, concretions,
calculi, foreign bodies, etc., and this may take place in the most
healthy organs. In other cases, however, there has been some
pathological process at work rendering the intestinal wall soft,
friable, necrotic, suppurative or ulcerative, by which its substance is
attenuated or its consistency or cohesion reduced.

=Duodenum.= Lacerations of the duodenum are often connected with
obstruction by tumors or the ravages of worms. These latter are mostly
the ascaris megalocephala, accumulated in mass, and sometimes engaged in
pouches outside the walls of the gut. In other cases, the walls of the
intestine have been perforated by hard woody stalks of straw or hay
(Mollereau) or of still more woody plants as in a case observed by the
author, and in which the pylorus was perforated. Sometimes the exudate
or blood extravasation attending on petechial fever, or verminous
embolism will pave the way for the rupture. Perforations by pieces of
wire (Schmidt) or other metallic bodies are also observed. Adhesive
peritonitis has also rendered the walls friable and predisposed to
rupture.

=Jejunum and Ileum.= Lesions are most frequent toward the termination of
the ileum and resulting from obstructions of the bowel or the weakening
of the walls by disease, or both. Ulcerations, abscess of the closed
follicles opening into the peritoneum, and neoplasms of various kinds
are to be especially noted among the causes. The impaction of the cæcum,
blocking the ileo-cæcal valve is also among the observed factors. Other
instances have been traced to deep cauterization of an umbilical hernia,
the enclosed loop of small intestine becoming inflamed and perforated.
The author has observed one instance from clamping of a hernia in which
the contained intestine was adherent to the hernial sac.

=Cæcum.= From its position on the lower part of the abdomen and from its
habitual plenitude with food or water, this organ is especially exposed
to direct mechanical injuries and ruptures. A sudden fall, more
especially if the umbilical region strikes on a stone or other
projecting solid body, kicks with heavy boots or with the feet of other
animals, blows with a cow’s horn or a boar’s tusks, and violent contact
with stumps, poles and other objects may be the occasion of the rupture.
These are usually found near the base of the viscus and across its
longitudinal direction.

Inflammations, connected with punctures, calculi, parasites, etc., may
render the walls so friable that they give way under slight strain or
injury. Abscesses have been found in the walls of the viscus leading to
perforation, and extension of inflammation from an umbilicus cauterized
for hernia has determined adhesion and perforation.

=Colon.= The loaded colon is even more liable to mechanical injury than
the cæcum. Occupying as it does the more lateral parts of the abdominal
floor, it is even more exposed to kicks and blows, and extending as it
does back toward the inguinal regions, it is especially in the way of
blows of horns so often delivered in this region. From the solid nature
of its contents the presence of calculi, the presence of blood sucking
worms, and its implication in the congestions and extravasations of
verminous thrombosis, this organ is especially liable to degenerations
and inflammations which render its walls particularly friable. Neoplasms
of various kinds, cancerous, tubercular, etc., have been found on its
walls as occasions of rupture. Abscesses of strangles have ruptured into
the viscus. Overdistensions in front of an obstruction in the pelvic
flexure, floating colon or rectum are the most frequent causes of
rupture. Again, cases have been seen as the result of violent exertions,
as during straining in dystokia. It has been a complication of phrenic
hernia, of volvulus of the double colon, and of ulceration caused by the
prolonged ingestion of arsenic. In severe impaction the necrosis of the
intestinal walls has proved a direct cause of laceration. The seat of
these ruptures may be at any point, but it is most frequent in front of
the pelvic flexure, or in the floating colon, or directly in the seat of
impaction.

_Symptoms._ The attack comes on suddenly, perhaps in connection with
some special accident or injury, and is manifested by violent colicy
pains which show no complete intermission. In many respects the symptoms
resemble those of complete obstruction of the bowel, there is a
suspension of peristalsis, rumbling, and defecation, a tendency to roll
on the back and sit on the haunches, an oblivion of his surroundings and
pain on pressing the abdomen. Usually the shock is marked in the dilated
pupil, the weak or imperceptible pulse, the short, rapid breathing, cold
ears, nose and limbs and the free perspirations. Tympany is usually
present as the result of fermentation. Signs of infective peritonitis
and auto-intoxication are shown in the extreme prostration, unsteady
gait, dullness and stupor, and general symptoms of collapse. The
temperature, at first normal, may rise to 105° or 106° as inflammation
sets in, and may drop again prior to death.

_Termination_ is fatal either by shock or by the resulting peritonitis
and auto-intoxication. Exceptions may exist in case of adhesion of the
diseased intestine to the walls of the abdomen and the formation of a
fistula without implication of the peritoneum.


                RUPTURE OF THE INTESTINES IN RUMINANTS.

  From blows of horns, tusks, etc., from rectal abscess. Symptoms:
  colic, resulting in septic peritonitis and sinking. Treatment.

Lesions of this kind usually come from blows with the horns of others.
They may lead to artificial anus as in a case reported by Rey, or the
formation of a connecting sac as in that of Walley. In a case seen by
the author a large abscess formed above the rectum, from injuries
sustained in parturition. This ruptured into the gut leaving an immense
empty cavity in which the hand could be moved about freely, but which
gradually contracted so that the cow made a good recovery.

André furnishes an extraordinary record of rupture of the colon, blocked
by a potato. It seems incredible that a potato could have traversed the
stomachs and intestine without digestion.

The _symptoms_ are those of violent colic suddenly appearing in
connection with some manifest cause of injury, and going on to septic
peritonitis and gradual sinking.

_Treatment_ is manifestly useless excepting in the case of some such
fortunate condition as in the case of abscess of the rectum in which the
free use of injections and the antisepsis of the abscess cavity proved
successful.


                 LACERATION OF THE INTESTINE IN SWINE.

This is rare and appears to have been observed only in connection with
scrotal and ventral hernias, with adhesion. It may lead to an artificial
anus which in its turn may cicatrise and close, or to the discharge of
fæces into the peritoneal cavity with fatal effect. If seen early
enough, laparotomy with suture of the bowel and careful antisepsis will
be indicated.




               LACERATION OF THE INTESTINE IN CARNIVORA.

  Obstruction and overdistension, necrosis, ulceration, feculent
  impaction, kicks, parasites, caustics, abscess, tubercle, cancer.
  Symptoms: peritonitis following accident, vomiting, no defecation.
  Treatment: laparotomy.


The most common cause of intestinal rupture is obstruction by foreign
bodies, with overdistension of the bowel immediately in front, or
necrosis and ulceration of the portion of the bowel pressed upon.
Feculent impaction acts in a similar way. Kicks and other external
injuries sustained on a full intestine will lead to rupture. Perforation
by parasites, by caustic agents swallowed, by abscesses, and by tubercle
or cancer is also to be met with.

The _symptoms_ are those of sudden peritonitis, with marked abdominal
tenderness, tucking up of the abdomen, bringing the legs together under
the body, vomiting, suspension of defecation and peristalsis. Rabiform
symptoms have been noted.

_Treatment._ As in swine there is every hope of success by suture of the
intestinal wound if done early. The same general method may be followed
as in closing the wound after extraction of a foreign body.


                   ABSCESS OF THE BOWEL IN SOLIPEDS.

  In strangles, from puncture, kicks, blows, foreign bodies in food,
  larva, cysts, large or small, creamy or cheesy, open into bowel or
  peritoneum, infective peritonitis. Symptoms: rigor, ill health,
  unthrift, colics, tender abdomen, tympany, painful movements, lying,
  rising, turning, going downhill, rectal exploration, phlegmonous
  swelling, pus passed by anus. Treatment: open when it points on
  abdominal wall, or when near rectum, antiseptics, support strength,
  careful dieting, antipuruleut agents.

This is most common as an irregular form of strangles, the abscess
forming in connection with the mesenteric glands or on the walls of the
intestine. Small abscesses may also implicate the mucous glands or
Peyer’s patches as a result of catarrhal enteritis. Less frequently an
abscess forms in the seat of the puncture of the colon for tympany, or
in connection with blows, kicks, punctures with stable forks, nails and
other pointed objects. Foreign bodies entering with the food and the
cysts of the larvæ of the sclerostomata will also give rise to
suppuration.

These abscesses may attain a large size, especially in strangles, and
involve adhesions between the bowel and other viscera, or the walls of
the abdomen. Or they may be small like peas or beans scattered along the
coats of the intestine or between the folds of the mesentery. They may
be inspissated to the consistency of thick cream or rich cheese, and
they may rupture into the intestine, through the abdominal walls or into
the peritoneum. In the last case infective peritonitis sets in usually
with fatal results.

_Symptoms._ These are generally obscure. There may have been noticed a
rigor, and there are always marked indications of ill health, dullness,
lack of spirit or appetite, dryness and erection of the hair, hide
bound, insensibility of the loins to pinching, colics after meals,
tenderness of the abdomen, tympany, groaning when lying down or rising,
when turned around short, or when walked down hill. Sometimes the
abscess can be distinctly felt by the hand in the rectum. When it
implicates the abdominal walls there is usually a diffuse phlegmonous
swelling, at first soft and pasty, then firm and solid, and finally
softening and fluctuating in the center. Sometimes there is the
evacuation of pus by the anus or of the investing membrane of the
abscess, and this may be expected to herald recovery. In case of
infective peritonitis there are the usual symptoms of stiff movement,
the bringing of the feet together under the belly, abdominal tenderness,
trembling, hyperthermia, cold ears and limbs, cold perspirations, great
dullness and prostration, small, weak or imperceptible pulse, hurried
breathing and gradual sinking.

_Treatment._ This is most favorable when the abscess approaches the
surface so as to be punctured through the abdominal walls. In other
cases it is so situated that it can be punctured with trochar and
cannula through the rectum. In such a case it may be evacuated and
injected with a nontoxic antiseptic, the puncture and injection being
repeated as wanted. In the internal and deeply seated abscesses we must
seek to support the general health, give pure air, easily digestible and
nourishing food, and agents that may be hoped to retard suppuration.
Hyposulphite of soda in ½ oz. doses, or sulphide of calcium in scruple
doses, may be repeated two or three times a day.




                     ULCERATION OF THE INTESTINES.

  Symptom or sequel of other disease, or from traumas, caustics,
  neoplasms, peptic ulcers, verminous thrombosis, tubercle. Catarrhal
  erosion, peptic, deep, round ulcer, calculi with irregular ulcers,
  cord ulcer at mesenteric attachment, small, follicular, grouped
  ulcers, sloughing ulcers of infectious diseases, circular projecting,
  button like ulcers of hog cholera, microbes. Symptoms: diarrhœa,
  black, or red, sloughs, fever, blood stained vomit, manipulation.
  Treatment: for foreign body, poison, or infectious disease, careful
  diet, antiseptics.


Ulceration of the intestines is commonly a symptom or sequel of other
intestinal disorder, such as intestinal catarrh, impaction, calculus,
foreign body, parasites, petechial fever, influenza, glanders,
rinderpest, Southern cattle fever, hog cholera, pneumoenteritis, rabies,
canine distemper. Then there are ulcers, caused by sharp pointed bodies,
by caustic agents ingested, and by obstructive changes in neoplasms.
Peptic ulcers may occur in the duodenum as in the stomach. Finally local
disturbances of the circulation and especially such as attend on
verminous thrombosis, are at once predisposing and exciting causes of
ulceration. Tuberculosis and other neoplasms are additional causes.

The ulcers may vary in different cases. In catarrh there is usually
superficial desquamation of the epithelium, and erosions rather than
deep ulcers. The peptic ulcer forms on the dependent wall of the gut,
where the gastric secretions settle, and assumes a more or less
perfectly circular outline (round ulcer). Those due to calculus or
impaction, may be irregular patches mostly on the unattached side of the
intestine and resulting from necrosis of the parts most exposed to
pressure. The ulcers resulting from cords stretched along inside the
bowel, are in the form of longitudinal sores on the attached or
mesenteric side of the intestine, where the wall being shorter the cord
continually presses. Follicular ulcerations are usually small, deep
excavations, commonly arranged in groups. Ulcers connected with
neoplasms have an irregular form determined by that of the morbid
growth. In infectious diseases the ulcers are round or irregular,
resulting from circumscribed sloughs. In most of the infectious diseases
the tendency appears to be to attack the intervals between the folds of
the mucosa, probably because the bacteria of ulceration find a safer
lodgement in such places. In the hog cholera ulcers the older ulcers
tend to the circular form with thick mass of necrotic tissue in the form
of plates or scales imbedded in the bottom and projecting above the
adjacent surface of the mucosa. As a rule the microbes which in the
different cases preside over the necrobiosis are found in the depth and
walls of the ulcers.

The _symptoms_ are largely those of the diseases of which the ulcers are
a concomitant or result. There is usually diarrhœa, which is generally
black from extravasated blood, and may be marked by fresher red bloody
striæ. Sloughs of variable size are not at all uncommon in the fæces.
Hyperthermia is usually more intense than in ordinary chronic enteritis,
indicating the action on the heat producing centres of the necrosing
microbes and their toxins. In pigs and dogs there may be vomiting of
dark blood stained material or of feculent matter. In the small animals
it may be possible to feel through the walls of the abdomen the
thickening of the intestine at and around the seat of any extensive
ulcer.

_Treatment._ So far as this is not the treatment of the foreign bodies,
poisons, or specific fevers which cause the ulcers, it consists mainly
in careful dieting and the use of antiseptics such as subcarbonate of
bismuth, salol, salicylic acid, sodium salicylate or naphthol.




                       DILATION OF THE INTESTINE.

  Capacity adapted to ingesta, rich and nutritious food improves breeds,
  excessive filling renders paretic, dilates; obstructions, impactions,
  strangulations, hernias, invaginations, twisting, tumors,
  compressions, calculi, lowered innervation, impaired circulation,
  verminous aneurism, peritonitis, persistent umbilical vesicle in horse
  and ox, hernia of mucous through muscular coat, cæcal dilatation,
  colic, rectal, with atresia ani, diseased end of cord, retained fæces.
  Symptoms: colics after meals, abdominal and rectal exploration, softer
  than impaction. Treatment: empty mechanically or by laxatives,
  demulcents, kneading, stimulants, nux vomica, ergot, barium chloride,
  eserine, rich concentrated food, electricity, enemata, laxatives.


It is a physiological law that the intestine developes in ratio with the
demands made upon it, provided these demands are not too sudden and
extreme. Thus the domestic pig and rabbit have intestines at once longer
and more capacious than those of the wild varieties. The same is true of
cattle and even of horses, heavy, rich feeding, generation after
generation, increases the capacity to take in and utilize more, and to
attain to a larger size and earlier maturity. In such a case the walls
of the intestinal canal retain their primary thickness and strength and
the whole change is in the direction of physiological improvement for
economical ends.

When, however, the retention or habitual accumulation of food in the
alimentary canal exceeds the self-adapting powers of its walls a true
pathological dilatation takes place, and attenuation or thickening and
paresis or actual paralysis of the walls ensues.

Whatever interferes with the normal active movement of the ingesta
predisposes to this. Thus partial obstructions of all kinds, strictures,
impactions, strangulations, hernias, invaginations, twisting, tumors,
compressions, calculi, contribute to the overfilling of the bowel in
front of them and to its more or less speedy dilatation. Whatever
weakens the muscular walls of the bowels or the nerves presiding over
these has a similar effect. Thus pressure on the solar plexus or its
branches from any cause, or degeneration of the same, a tardy and
imperfect circulation resulting from verminous aneurism and thrombosis,
and a circumscribed peritonitis extending from the serous to the
muscular coat of the bowel act in this way.

The persistence of the canal of the umbilical vesicle has been
repeatedly observed in solipeds, in the form of a pouch or dilatation
connected with the ileum three or four inches in front of the ileo-cæcal
valve. Rauscher records one of these of thirteen inches long and having
a capacity of seven quarts. These have been noticed in cattle as well.

Another form of sacculation results from rupture of the muscular coat
through which the mucous forms a hernial sac in the peritoneal cavity.
On a small scale these sacs are not uncommon, the size of a pea, a bean,
or a marble, and very often containing larval or mature worms. Degive
records an enormous dilatation of the horse’s cæcum, Peuch, one of the
pelvic flexure of the colon having a capacity of forty pounds, and
Simonin one of the floating colon. Dilatations of the rectum always take
place in the new born affected with atresia ani.

Dilatation of the rectum into a cloaca is found in the horse and ox,
often connected with disease or injury of the terminal part of the
spinal cord, and is very common in dogs and cats in connection with the
compulsory retention of the fæces indoors. Pigs also present instances
of the kind.

The _symptoms_ are in the main slight colics, with or without tympany
and recurring after each meal. In the small animals the distended gut
may often be recognized by palpation through the abdominal walls, and in
the larger animals by rectal exploration. The distended viscus has not
the firmness nor hardness of impaction or calculus and is mainly
recognizable by its bulk and form. When the distension is in the rectum
it may be easily reached and contents dislodged with the effect of
giving complete relief for the time being.

_Treatment._ Treatment is necessarily mainly palliative and consists in
the removal of abnormal accumulations. From the rectum this can be done
with the hand, or in the smaller animals with the finger. For abnormal
dilatations more anterior, purgatives and mucilaginous injections are
required, with kneading of the bowels through the abdominal walls, or
through the rectum in the larger animals, and stimulation of the
peristalsis by nux vomica, ergot, barium chloride or eserine.

Having unloaded the dilated portion of any undue collection, further
accumulation should be guarded against by giving nutritious food in
small compass, and of a laxative nature, by stimulating peristalsis by
nux vomica or other nerve stimulant and by the daily application of
electricity. Enemata and laxatives should be employed when necessary.


                      STRICTURE OF THE INTESTINE.

  From healing of ulcers, inflammation or infiltration, neoplasms, ring
  like or sacculated, in small intestine in horse preceded by a
  dilatation, an effect of verminous thrombosis; in cattle; in dog.
  Symptoms: Progressive, if in duodenum can’t eat full meal, belches
  gas, has colics and tympany; in cattle tympany, unthrift; in dog
  vomiting, tympany, colic, accumulations. Treatment: Gradual stretching
  by bougies if within reach.

Strictures of the intestine are in the main the result of ulceration of
the intestinal walls which contract in healing, or inflammation, and
infiltration which leads to contraction in their organization into
tissue. Neoplasms of the walls (cancer, myxoma, lipoma, polypus,
melanosis, actinomycosis, tubercle) are additional causes of
constriction. If resulting from a lesion which completely encircled the
bowel there is an uniform constriction in the form of a circular ring;
if on the other hand it started from a longitudinal ulcer or lesion the
bowel is shortened on that side and puckered.

In =solipeds= strictures are most frequent in the small intestine, or
rectum. The pylorus is often affected. When on the small intestine there
is constantly a dilatation just in front of the obstruction. The
constricted portion is usually short, but as seen from outside of the
gut may be duplicated a number of times. Cadeac mentions seventeen such
strictures in the same animal, each preceded by a dilatation. The
individual stricture may be less than two inches in length and so narrow
as just to allow the passage of the index finger. The walls of many
times their natural thickness, are still further thickened by an
external layer of adipose tissue. It may be the seat of a small abscess,
or of a tumor. Internally the mucosa may show ulcerations.

The stricture or strictures in solipeds often depend on the disturbance
of the circulation which results from verminous thrombosis, the exudate
into the intestinal walls, undergoing organization, at once thickens and
constricts the tube, and determines as secondary result the dilatation
in front of it.

Professor Mauri of Toulouse records the case of a horse with a rectal
stricture 4 inches from the anus, and a great dilatation in front. The
removal of the stricture, secured normal defecation, (whereas before
this the fæces had to be removed by hand) and the colics entirely
disappeared.

In =cattle= strictures have been found mainly at or near the pylorus,
less frequently in the rectum, and on one occasion (Revel) in connection
with a cancerous tumor, in the colon.

In the dog the pylorus is also the favorite seat of thickening and
stricture, yet it may occur in the small intestine, the rectum, or the
colon.

_Symptoms._ These are gradually advancing, as the stricture approaches
more and more nearly to a complete stenosis. If the stricture is in the
pylorus or duodenum, the patient can not eat a full feed of grain
without discomfort. He stops, hangs back on the halter, plants the fore
feet in front, arches the neck, drawing in the nose and eructating gas.
If he cannot eructate he is liable to show colics, tympany, and the
general symptoms of gaseous indigestion of the stomach.

In =cattle= there is tympany, partial loss of appetite, tardy
rumination, and loss of condition.

=Dogs= show vomiting as a prominent symptom. When the stricture is in
the rectum there is a gradual lessening of the amount of fæces passed at
a time and an accumulation of feculent masses in advance of the
obstruction, recognizable by rectal exploration. When in the terminal
part of the small intestine or in the colon, a gradual lessening of
defecation, with tympanies and colics, culminating in complete
obstruction, may afford a suggestion of the trouble but no means of
certain diagnosis. In the smaller animals some additional indications
may be had from abdominal palpation.

_Treatment_ is usually hopeless unless the stricture is in the terminal
portion of the rectum. In the latter case gradual dilatation by the
passage of the hand, the finger, or of bougies which are used larger and
larger, as they can be forced through with moderate pressure may secure
a sufficient dilatation. Forced dilatation, or even careful incision at
several different points of the circumference of the stricture may give
good results in certain cases.


         INTESTINAL INVAGINATION. INTUSSUSCEPTION IN SOLIPEDS.

  Definition. Seat: ileum into cæcum, rectum through sphincter, duodenum
  into stomach, floating small intestine into itself, cæcum into colon.
  Lesions: blocking, or tearing of mesentery, dark congestion,
  peritoneal adhesions, incarcerate gut, necroses, sloughing of
  invagination. Symptoms: colics of obstruction, enteritis, and septic
  infection, eructation, emesis, tenesmus, signs of sepsis and collapse,
  death in seven hours or more, or recovery by disinvagination or
  sloughing. Diagnosis: by rectal exploration or passing of slough.
  Treatment: oily laxatives, demulcents, enemata, mechanical restoration
  of everted rectum, laparotomy.

_Definition._ The sliding of one portion of an intestine into a more
dilated one, as if a few inches of the leg of a stocking were drawn
within an adjoining portion which is continuous with it.

_Seat._ It is most commonly seen in the inversion of the small intestine
into itself or into the cæcum, or next to this the passage of the rectum
through the sphincter ani, to constitute eversion of the rectum. It
would appear to be possible at any part of the intestinal canal in the
horse, in which the bowels are more free to move than they are in
ruminants. Peuch records a case of invagination of the duodenum into the
stomach and Cadeac gives a woodcut of such a case, which one would
suppose the fixed position of the duodenum would render impossible. It
is conceivable that the jejunum could be invaginated into the duodenum,
and that this should have continued until it extended into the stomach,
but it is difficult to see how the duodenum itself could have passed
into the stomach without tearing itself loose from its connections with
the pancreas, liver and transverse colon.

Schrœder, Serres and Lafosse describe cases in which the small intestine
was everted into the cæcum and thence through the colon and rectum until
it protruded from the anus.

The invagination of the floating small intestine into itself is common
at any point, and extensive and even repeated. Marcout records a case in
which 24 feet were invaginated, and Rey a case of quadruple invagination
at the same point.

The invagination of the cæcum into the colon is frequent, the blind end
of the cæcum falling into the body of the same organ, and this
continuing to increase until it passes on into the colon, and even
carries a portion of the small intestine with it. This lesion is more
rare in solipeds because the cæcum has its blind end lowest and
gravitation opposes its invagination.

_Resulting Lesions._ In any case of invagination it must be noted that
it is not the intestine alone which slips into its fellow, but it
carries with it its attaching mesentery, which, dragging on one side of
the invaginated gut, shortens and puckers that and turns its opening
against the wall of the enclosing gut so as to block it, while the
opposite or free side passes on and tends to form convolutions. If the
outer and enveloping intestine is too small to allow of this, the
detaining mesentery of the invaginated mass must be torn or stretched
unduly and its circulation and innervation correspondingly impaired.
When the invagination occurs of one portion of the small intestine into
another of nearly equal size, the resulting mass is firm like a stuffed
sausage, and this enlargement and consolidation ends abruptly at the
point of visible entrance of the smaller contracted portion, into the
larger dilated one.

If recent, the invaginated mass is still easily disengaged from the
enveloping portion, though considerably congested and dark in color in
proportion to the duration of the lesion. When it has been longer
confined the incarcerated portion is the seat of extreme congestion, and
extravasation, and has a dark red or black color. The exudation into its
substance, which is especially abundant in the mucosa and submucosa,
produces a thickening which may virtually close the lumen, and on the
opposing peritoneal surfaces leads to adhesions which prevent the
extraction of the imprisoned mass. The interruption of the circulation
and the compression of the invaginated mass, leads soon to necrosis and
thus a specially offensive odor is produced, and if the animal survives
the whole may be sloughed off and passed with the fæces, the ends of the
intussuscepted portion and of that receiving it meanwhile uniting and
becoming continuous with each other.

_Symptoms._ These are the violent colic of obstruction of the bowels,
soon complicated by those of enteritis and finally of septic infection.

The animal looks at his flank, paws, kicks with his hind feet, lies
down, rolls, sits on his haunches, waves the head from side to side, and
sometimes eructates or even vomits. Straining may be violent, with the
passage of a few mucus-covered balls only, and rumbling may continue for
a time if the small intestines only are involved.

The partial subsidence of the acute pains, the presence of tremors,
dullness and stupor, the coldness of the ears and limbs, the small, weak
or imperceptible pulsations, the cold sweats, dilated pupils, and loss
of intelligence in the expression of the eye and countenance may
indicate gangrene, and bespeak an early death which may take place in
seven hours.

The subsidence of the acute symptoms with improvement in the general
appearance and partial recovery of appetite may indicate a spontaneous
reduction of the invagination, an issue which may happily arrive in any
case in the early stages, but especially in those implicating the cæcum
and colon.

An absolutely certain _diagnosis_ is rarely possible, unless the lesion
is a protrusion of the rectum, or unless as the disease advances the
invaginated part is sloughed off and passed per anum.

_Treatment._ The failure to make a certain diagnosis usually stands in
the way of intelligent treatment. Oleaginous laxatives and mucilaginous
gruels are advised to keep the contents liquid, and favor their passage
through the narrowed lumen of the invaginated bowel. In cases
implicating the floating colon and rectum abundant watery or
mucilaginous injections may assist in restoring a bowel which has not
been too long displaced. In case of eversion of the rectum, the hand
should be inserted into the protruding gut and carried on till it passes
through the sphincter ani. Then, by pushing it onward, the arm carries
in a portion of the invaginated gut and usually of the outer portion
next to the anus as well, and this should be assisted by the other free
hand, and even if necessary by those of an assistant, and whatever is
passed through the sphincter should be carefully retained, while the arm
is withdrawn for a second movement of the same kind, and this should be
repeated until the whole protruding mass has been replaced.

Invaginations situated more anteriorly and which can be correctly
diagnosed by rectal exploration or otherwise, will sometimes warrant
laparotomy, especially those of the cæcum into the colon, where adhesion
of the peritoneal surfaces is less common or longer delayed. The patient
should be given chloroform or ether, the abdominal walls should be
washed and treated with antiseptics, and the incision made back of the
sternum and to one side of the median line, and large enough to admit
the exploring hand. It has also been suggested to introduce the hand
through the inguinal ring, or behind the posterior border of the
internal oblique muscle.


            INTESTINAL INVAGINATION IN RUMINANTS AND SWINE.

  Double colon cannot be invaginated, floating small intestine, cæcum
  and floating colon can. Causes. Lesions. Symptoms: Acute, violent,
  persistent colic, palpation of right flank causes gurgling, rectal
  exploration, prostration, collapse. Duration 1 to 5 weeks. Treatment:
  Laxative, enemata, injections of sodium bicarbonate and tartaric acid,
  laparotomy.

In these animals the double colon is rolled around itself between the
folds of the great mesentery the free border of which supports the small
intestine. The arrangement is as if a piece of rubber tubing were first
doubled upon itself, and the end of the loop were then turned inward and
the remainder wound round it as a centre. If this were then sewed
between two pieces of cloth, the stitches passing between the different
windings of the tube at all points, we would have an arrangement fairly
representing that of the double colon of ruminants, and, for our present
purpose, of swine as well. It must be evident that no portion of a tube
arranged in this way can slide into another. It would also appear that
the small intestine cannot become invaginated to any extent into another
portion or into the cæcum without extreme stretching or laceration of
the small portion of mesentery left between it and the coils of the
double colon above. The anatomical arrangement is therefore opposed to
the formation of invaginations in a way that is not the case in the
horse.

Yet invaginations are by no means unknown in these genera. The small
intestine can be invaginated into itself or into the cæcum. The cæcum,
which floats loose at the right side of the mesentery that envelopes the
double colon, can be invaginated into the colon, and the floating colon
can be invaginated into the double colon on the one hand and into the
rectum and through the anus on the other. Invagination into the rectum,
for eight inches, in a bull calf, of six days old, is reported by
Cartwright in the _Veterinarian_ for 1829. In a similar case of Youatt’s
the intussuscepted portion sloughed off and was discharged per anum.

The _causes_ are like those acting in solipeds, and which give rise to
excessive and irregular peristalsis. A drink of ice cold water,
indigestions and colics of various kinds, diarrhœa, chills, the
irritation caused by poisons or parasites, and the paresis and
dilatation of portions of the intestine into which the more active
portions can easily pass. Almost any irritation or congestion may cause
intussusception, and young animals in which peristalsis is most
energetic are the most liable.

_Lesions._ The intussusception is usually found in the ileum and to a
less extent in other parts of the small intestine, or involving the
cæcum and colon, or again the floating colon and rectum. The successive
conditions of congestion, exudation, adhesion, obstruction, necrosis,
sloughing, and repair by union of the remaining ends are the same as in
the horse.

_Symptoms._ There is acute, agonizing and dangerous colic in an animal
in which these troubles are usually comparatively slight and transient.
The animal looks at the right flank, paws or stamps with fore feet as
well as hind, lies down and rises often, strains to pass manure but
passes only mucus or a few small hard masses, if anything. If pressure
is made on the right side of the abdomen and the hand suddenly withdrawn
there is a significant gurgling and the corresponding hind foot is
lifted or moved forward or backward, appetite and rumination are lost,
the pulse becomes rapid and weak, and the animal becomes prostrate, dull
and stupid, often remaining recumbent in spite of all efforts to raise
him. Rectal exploration may detect the firm tender mass in the seat of
the invagination. The disease may last from one week to five, according
as the obstruction is complete or partial. The usual termination is a
fatal one, though a certain number of spontaneous recoveries are met
with.

_Treatment._ By a happy accident the peristalsis or anti-peristalsis
determined by a purgative will sometimes disengage the intussuscepted
bowel. Copious injections into the rectum may also prove useful in case
of intussusception of the floating colon or rectum. Or the disengagement
of carbon dioxide from the injection of solutions of sodium bicarbonate
and tartaric acid may be tried. Laparotomy is however the most radical
measure when a certain diagnosis has been made and this is less
dangerous in the cow than in the horse in which peritonitis is so grave.
Under antiseptic precautions an incision is made in the right flank and
the invagination found and reduced. In case firm adhesions have already
taken place, and above all if the included gut is apparently gangrenous,
the latter may be exposed by breaking down the connections at the side
opposite to the attachment of the mesentery, or where the adhesions are
least firm, then cutting out and removing the incarcerated gut and
carefully closing the opening between the ends by suture. The use of a
sublimate or carbolic acid solution and careful suturing and bandaging
of the external wound with carbolated cotton wool will often give a
successful issue.


               INTESTINAL INVAGINATION IN DOGS AND CATS.

  Anatomical conditions favor. Causes: as in other animals, common in
  icterus, and surgical operations from deranged peristalsis. Lesions:
  most common in small intestines, congestion, inflammation, necrosis,
  sloughing. Symptoms: may be colic, but not always, dullness, anorexia,
  vomiting, constipation, palpation, swelling firmer than from impacted
  twine. Treatment: shot, castor oil and exercise on hind legs.
  Demulcents. Laparotomy.

The intestines of the carnivora are more open to invagination than in
other domestic animals for even the colon is free enough throughout its
course to allow of one part sliding into another. The _causes_ to which
it is attributed are in kind the same as in other domestic animals. The
swallowing of ice cold water in excess when heated, diarrhœa,
superpurgation, intestinal worms, the active peristalsis of early life,
and jaundice have been especially blamed. Reynal found intussusception
twenty times in forty cases of icterus and Rancilla four times in five
cases. It has been frequently seen after severe surgical operations, and
it is surmised that in both cases alike the deranged peristalsis
attendant on severe suffering was the cause of the accident.

_Seat and Lesions._ The most common seat of invagination is in the small
intestines, and less so in the cæcum and colon, or rectum. The lesions
are as in the other animals, congestion, infiltration, adhesion,
necrosis, gangrene and sloughing.

_Symptoms._ There may be colics as in the larger animals, but in some
instances there are simply prostration, dullness, inappetence, vomiting,
constipation, or the passage of a little liquid and fœtid excrement.
Palpation of the abdomen detects a firm, cylindroid and very tender
swelling on the line of the softer intestine which taken with the other
symptoms is nearly pathognomonic. If situated in the small intestine and
disconnected from the rectum and pelvis the diagnosis is more
satisfactory. Impaction is most commonly in the rectum and floating
colon and can be traced into the pelvis and even felt by the finger
introduced into the anus. It might be confounded with obstruction of the
intestine by the ingestion of twine, but the swelling is usually firmer
and the cylindroid outline more uniform in intussusception.

_Treatment._ The measures recommended for the larger animals are
applicable to the dog. Cadeac has had four recoveries in seven cases
after the use of leaden shot and castor oil. Three balls of No. 16
calibre are dipped in castor oil and given to the dog. This is followed
by ½ oz. of castor oil slightly heated, and walking or running exercise,
or take the dog by his fore limbs and walk him around on his hind. No
drink is allowed for 24 hours, and a quart of decoction of flax seed on
the day following.

Should these measures fail, laparotomy is available, yet it is more
promising in proportion as it is resorted to early, before ulceration,
or gangrene has set in. The manipulations are practically the same as in
the ox and the outcome is even more promising. The diet should be
restricted to milk or mucilaginous gruels for a week after the
operation.




           VOLVULUS (TWISTING) OF THE INTESTINE IN SOLIPEDS.

  Definition: rolling of a loop on its mesenteric axis, bending in a
  vicious direction, rolling of one loop round another. Causes: laxity
  of mesentery in hernia, relaxation or rupture of linea alba, pot belly
  in old breeding mares, sudden movements in falls, leaps, draught,
  galop, slipping, mounting, warm weather, casting, rolling, rising,
  sudden filling of a loop, heavy feeding and fermentescible food, cold
  drinks, chills. Lesions, most in double colon, next in jejunum, cæcum
  wrapped in small intestine, floating colon, tympany and pallor of
  obstructed loops, later congestion, infiltration, extravasation,
  adhesions, necrosis, sloughs, infective peritonitis. Symptoms: sudden
  severe attack, violent, reckless colicy movements, pain constant with
  exacerbations, fever, prostration, collapse. Diagnosis: only by rectal
  exploration and exceptionally. Treatment: by rectal manipulation,
  eserine, castor oil, laparotomy.


Strictly speaking this lesion consists in the twisting of a loop of
intestine upon its mesenteric axis, so that the portion which is drawn
spirally over the mesentery of the other is more or less completely
obstructed. The term has, however, been applied as well to the turning
of a viscus at a sharp angle from its normal direction so as to
interfere more or less with the passage of its contents and with its
circulation. This has been especially seen in a vicious direction given
to the cæcum, but also at times to the double colon. The simple twisting
on the mesenteric axis is common to the floating portion of the small
intestines, the double colon, floating colon and rectum. A third form of
twisting which is, however, rather a strangulation, consists in the
rolling of one loop of intestine round the loop of another, the
mesentery of which has become unduly long.

_Causes._ The predisposing cause is a certain laxity or undue
lengthening of the mesenteric attachment of the intestine. This is
sometimes formed in connection with the existence of hernia, into which
the bowel protrudes, or short of this a relaxation or rupture of the
linea alba so that the whole of the intestinal mass hangs down unduly,
or finally in unthrifty pot-bellied animals and in breeding mares in
which the abdomen is unduly pendent.

Next comes the question of sudden movement as in falls, in leaping, in
violent exertions of draught, or galop, in sudden slipping upon wet or
icy ground, and of stallions in mounting mares. In the Omnibus Company’s
(Paris) horses Palat found 35 cases in entire horses, 23 in mares, and
11 in geldings. The stallions in the stables were fewer than the mares
and geldings put together, but it does not appear that the difference
was sufficient to make the above figures very significant. These
stallions it should be added, are not used for breeding, so that the
statistics have no bearing on the effect of mounting.

Palat’s figures show a greater number of cases in summer, than in
winter. There were 58 cases from April to October and but 21 from
November to March. It would seem as if the relaxation of the system and
mesentery in summer more than counterbalanced the combined effect of
slipping on ice and sudden chills.

A large proportion of the cases have been found in horses that have died
of colic, or which have been cast for operation, and the recent
character of the lesions has often shown that we must look upon them as
the result of the tumultuous peristalsis, and the lying, rolling,
sitting and other sudden and unwonted movements performed. A heavily
loaded portion of bowel, occupying a position slightly lower than a
lighter portion or parallel to it, suddenly moves by gravitation when
their relative positions are altered as in rolling, decubitus, or
rising, and it thereby becomes twisted upon itself. Or a portion of
intestine filled with liquid or gaseous contents is suddenly emptied by
the passage of these onward into another and the latter portion of
intestine or some other lodged alongside it, in moving to fill the
place, rotates upon itself and establishes a volvulus.

Hard worked horses which are subjected to stimulating feeding are much
more frequently attacked than those which have light work and feeding.
In the same way newly harvested hay or oats, spoiled or otherwise
indigestible food have apparently been productive causes. Cold drinks,
and exposure to cold draughts have been similarly charged. Indeed any
cause of indigestion and colic may be held to predispose to volvulus.

_Lesions._ _Seat._ Twisting of the small intestine is impossible in the
duodenum, and for the floating portion it is far more common in the
ileum and terminal portion of the jejunum where the mesentery is long
than in the anterior jejunum where it is short.

The double colon from the sternal portion to the pelvic flexure being
free from any restraint by omental or mesenteric bands is especially
liable to torsion. Palat found four cases of torsion of the colon to one
of the small intestine, and Schutze gives the ratio as 56 of the first
to 13 of the second.

The cæcum has been frequently found twisted upon itself with a portion
of the small intestine rolled round it.

The floating colon like the small intestine is rolled around its
mesenteric axis, but cases are much more rare than in the case of the
small intestine.

In a recent and complete twisting with obstruction of the bowel, the
loop of intestine is distended with gas the result of fermentation of
its contents, and its walls may be thin and pale. Much more commonly and
when the lesion is of longer standing there is hyperæmia, and
infiltration and thickening with inflammatory products, and blood
extravasations. At the seat of torsion the compressed intestine is
congested, covered with petechiæ, and its peritoneal surface with
fibrinous exudate tending to bind the parts together. Later there may be
seen spots of necrosis and perforating sores and semi-detached sloughs,
or the whole mass of twisted bowel may be gangrenous. The patient
usually dies before this last stage has been reached. If the animal
survives long enough the lesions of infective peritonitis are constantly
present.

_Symptoms._ The disease usually sets in suddenly with intense severity.
In exceptional cases there is an insidious onset, the twist being at
first but partial and gradually increasing and for a time the contents
pass on in a restricted but still physiological manner. Colics at first
slight become by degrees more and more intense until all the symptoms of
obstruction and acute inflammation are developed.

More commonly symptoms of extreme gravity appear at once, the patient
stops, paws, kicks at his belly, tries to lie down, strains to defecate
or urinate, lies down, rolls, sits, gets up and moves round uneasily
trying to lie down again. He looks at the flank with anxious eye and
countenance and has all indications of the most violent colic. Pain is
constant, but worse at one time than another, the pulse is from 50 to 90
and becomes weak and even imperceptible as the case advances, and
hyperthermia, at first slight or absent rises with the onset of
inflammation. Finally great prostration, depression and stupor, sunken,
glazed eye with dilated pupil, and cold sweats and extremities bespeak
collapse or general infection.

_Diagnosis_ is rarely certain. The sudden onset, extreme violence of the
symptoms, and rapidly fatal progress are significant and in exceptional
cases rectal exploration will detect obstruction in the rectum or
floating colon, or a tympanitic condition of the pelvic flexure.

_Treatment._ A rational treatment is only possible in those rare cases
in which the diagnosis is certain. When the lesion can be reached in the
rectum or adjacent part of the floating colon, the oiled hand may be
made to drag on the interior of the viscus so as to restore it to its
normal position.

Cadiot has had recoveries from supposed volvulus by the use of eserine
hypodermically, and Trasbot by the use of castor oil and it is just
possible that active peristalsis, and plenitude of the bowel running
into the volvulus, may serve to unwind slight cases. When the diagnosis
is certain and the case, as usual, intractable the resort of laparotomy
and the attempt at untwisting is fully warranted. The case is a fatal
one if unrelieved.


                         VOLVULUS IN RUMINANTS.

This condition is almost unknown in ruminants, Reichert recording a
single case of volvulus of the ileum involving 8 inches of the gut. The
reason for the habitual immunity is to be found in the arrangement of
the small intestine at the end of a mesentery which is strengthened and
stiffened by the winding folds of the colon until twisting is
practically impossible. There remains, therefore, only the floating
colon and rectum at all exposed to the lesion. The isolated case of
Reichert only proves the rule.




                           VOLVULUS IN DOGS.

  Rare. Short mesentery hinders. Occurs with hernia. Symptoms:
  obstruction, prostration, colic, tense, painful abdomen, retching,
  anorexia, exhaustion. Treatment: laparotomy.


The carnivora seem to be protected against volvulus by the shortness of
their mesentery, the comparative lightness of the intestinal contents,
and the restricted area of the abdominal cavity. Cadiot, Müller, and
Friedberger and Fröhner agree in ignoring the subject as a canine
disease, while Cadeac mentions only such cases as are complicated by
mesenteric hernia, the protruding loop becoming twisted in the wound
through which it has protruded.

“The _symptoms_ are those of invagination or intestinal obstruction;
sometimes the animal is dull, anxious, resting almost constantly down on
his belly, and this prostration dominates the table of symptoms;
sometimes, on the contrary, the subject manifests signs of excitement
and intestinal pain; it trembles, lies down, glances at its flanks;
sometimes it even lets itself fall abruptly, straightens out stiffly its
limbs and head, clenches its jaws and rolls its eyes.”

“In all cases the belly is hard, drawn up, painful to pressure or
palpation; but these means of exploration are insufficient to feel the
intestinal knot.”

“Constipation is persistent, obstinate, and efforts at vomiting
continuous; anorexia is incomplete, or the animal rejects the solid and
liquid aliments immediately after their ingestion. Vomited matters, when
they exist, become glairy, bilious toward the end of the attack; but
sometimes the animal becomes exhausted in his fruitless efforts; one is
rendered uncertain and hesitates to confirm his diagnosis by
laparotomy.”

The only treatment advised is by laparotomy.




            INTESTINAL STRANGULATIONS BY ADVENTITIOUS BANDS.

  Result of circumscribed peritonitis. Extends from one part of
  abdominal wall to another, around or between intestines, on omentum,
  or adhesion of omentum to inguinal ring. In cattle tubercular products
  strangulate bowels. Symptoms: the colic of obstruction, rectal
  exploration. Treatment: laparotomy, removal of constricting band.


Adventitious fibrous bands in the abdomen are the result of a
pre-existing peritonitis of a circumscribed area. The fibrinous exudate
thrown out on the parietal peritoneum is detached in its median part but
remains adherent at the ends, and when organized into tense resistant
white fibrous tissue remains as a trap to entangle and strangulate the
intestinal folds. In other cases they form on or between intestines or
other viscera which are for the moment torpid and inactive, and
contracting as they become organized, they bind these together and
hamper their movements, and endanger the integrity of all movable
viscera in the vicinity. Again they form on the omentum and threaten the
integrity of the bowels by strangulation. The omentum protruding at
castration becomes adherent to the inguinal ring and forms a dangerous
band.

In _cattle_ the growth of peritoneal tubercle often binds the small
intestines together in an inextricable tangle leading to considerable
compression, and obstruction without a complete stenosis.

_Symptoms._ These vary with the organ constricted, but they are usually
those of a more or less perfect obstruction of some portion of the
intestine small or large, which has passed over or under the
constricting band and fails to return, often undergoing a torsion which
renders its imprisonment still more secure. The author has found the
double colon fatally constricted in this way, and Leblanc furnishes a
similar case. Cases are on record of the binding of the duodenum to the
right lobe of the liver by a strong fibrous band, of the binding of the
double colon to the right flank and in another case to the floor of the
abdomen, and of the ileum to the meso-rectum and in another case to the
left flank. These give rise sooner or later to obstruction of these
viscera or, to incarceration of adjacent ones so that the animal dies of
intestinal obstruction with its attendant symptoms.

_Treatment._ If the true nature of the case can be made out by rectal
exploration the appropriate treatment is by laparotomy and the removal
of the constricting band.


                   PELVIC HERNIA IN THE OX. GUT TIE.

  Cause: laceration of parietal peritoneum by tearing through the
  spermatic artery, a loop of intestine is strangulated in the resulting
  pouch. Diagnosis: patient is a steer castrated by the method named,
  rectal exploration confirms. Treatment: turn on back, jump from a
  height, trot down hill, dislodge incarcerated mass by hand in rectum,
  pass cannula through rectum, introduce probpointed bistoury and cut
  through the band, or laparotomy. Second Form: adhesion of stump of
  spermatic cord to intestine, or abdominal wall or formation of a
  pediculated tumor, and resulting strangulation of intestine. Third
  Form: weight of testicles tears the peritoneum from the abdominal wall
  forming pouch. Treatment: laparotomy.

_Causes._ This is a peculiar affection said to be connected with a
faulty mode of castration in calves. When the testicle has been exposed,
the spermatic cord is torn through by sheer force, or the posterior
portion having been cut across the anterior division is dragged upon
violently until torn apart. The gelders usually estimate the quality of
the operation by the length of the artery which can be torn out. The
artery which is the most resistant portion of the cord and the last to
give way takes its origin from the posterior aorta opposite the
posterior mesenteric artery, extends outward by a curvilinear course
just in front of the brim of the pelvis, and when stretched violently it
is straightened out and carries with it the peritoneum, tearing it from
the portion immediately in front and forming a sac, or tearing it
completely apart from the abdominal wall in its median part and leaving
it attached above and below. Into this sac, or above this band, which is
just below the sacral transverse processes, a loop of intestine may
pass, and becoming strangled there, produces all the symptoms of
intestinal obstruction.

_Diagnosis_ is helped by the fact that the animal is a steer, and in a
locality where the above-named mode of castration is in vogue. It is
completed by feeling the imprisoned intestine and the constricting cord
just under the right or left transverse processes of the sacrum.

_Treatment._ The gut will sometimes escape from the sac if the animal is
turned quickly on its back. Another method is to invoke the influence of
gravitation by jumping the animal from a high step down to a lower
level, or by trotting him down a steep incline. A still more effective
method is to introduce the hand into the rectum and press the palm
upward and forward against the soft mass of the imprisoned intestine. In
this way the gaseous, liquid and solid contents are passed over into the
portion of the gut in front of the constriction, and by continuing the
process the intestine itself can usually be pressed out and the
suffering relieved. It is further suggested to press the thumb or the
whole hand forward against the constricting band and tear it in two. A
certain amount of to and fro movement is usually required and in
exceptional cases the cord is so strong that the measure has to be
abandoned.

Another resort is to pass a cannula and trochar through the adjacent
part of the rectum, and withdrawing the trochar, to pass a probpointed
bistoury through the cannula, and beneath the cord and cut it in two.

These measures failing an incision must be made in the right flank,
following the line of the fibres of the external oblique, and the hand
being introduced and passed round the posterior border of the omentum
the seat of the disease is found and the constricting cord is cut with a
probpointed bistoury or a bistouri caché. The wound is then sutured,
disinfected and covered with antiseptic gauze or cotton and bandage. The
sounds of peristalsis are resumed and in five or six hours defecation is
restored.

=2nd Form.= Another alleged condition vouched for by English and
continental veterinarians depends on drawing down the spermatic cord as
far as possible, cutting it off and allowing it to be retracted into the
abdomen. Having been detached by the traction from the abdominal wall it
is alleged to float free, sometimes establishing an adhesion to one of
the intestines of which it later limits the movements; sometimes forming
a connection with the abdominal wall and forming a sling in which the
intestines may be snared, and sometimes swelling at its free end to form
a pedunculated tumor, and winding around a loop of intestine so as to
strangle it. For these conditions incision of the abdominal wall and
section of the offending cord are recommended.

=3rd Form.= Lobbe tells us that the disease is common in bulls as well
as oxen in mountainous regions, being determined by violent exertions,
or by the struggle to rise, when the animal has accidently fallen. In
this alleged form there is the suggestion of the heavy pendent testicles
as factors in detaching the cord with its vessels and nerves from the
abdominal wall, so as to form a loop or snare for the intestine.


        DIAPHRAGMATOCELE. DIAPHRAGMATIC HERNIA. PHRENIC HERNIA.

  Definition. Susceptibility by genera, horse, dog, ox. Enterocele,
  epiplocele, gastrocele, hepatocele. Congenital, arrest of development
  and of closure of foramen or elsewhere, diaphragm absent. Traumatic,
  blows on false ribs by pole, shaft, buffer, gate, bars, beams, kicks,
  blows with horns, tusks, clubs, fractured rib perforating diaphragm,
  falls on projecting bodies, muscular strains in draught, plunging,
  falling, slipping, casting, parturition; trotting or galloping down
  hill, jumping to lower level, slipping to knees, dystokia, colic,
  tympany. Symptoms: extreme dyspnœa and asphyxia; or difficult
  breathing slowly increasing, colics, dilated nostrils, retracted angle
  of mouth, projecting eyeballs, shallow, rapid catching respirations,
  gurgling in chest, drumlike percussion sounds, with perhaps flat
  areas; in slight cases, listlessness, colics, double lift of flank,
  tender intercostals; in chronic cases, short wind on exertion,
  sluggishness, colics after meals. Hernia through intercostal space.
  Lesions: unduly large foramen sinistrum or dextrum, lacerations of all
  forms and sizes, edges ragged, thickened, bloody, broken rib, inflated
  stomach causes shreddy tear; post mortem lacerations show no
  inflammatory products; chronic cases have edges devoid of inflammation
  and often smooth, serosæ usually perforated, nature of hernial mass,
  omentum, intestine, colon, cæcum, stomach, spleen, liver, congestion
  of viscera involved. Prognosis: slight cases may survive, to be
  fattened or to breed, but are useless for work. Treatment: quiet,
  sedatives, antiferments, cathartic, concentrated food, lift by fore
  limbs, incline stall backward and downward, laparotomy in cattle,
  dogs, and swine.

As this lesion is shown by symptoms referable to internal organs only,
and as it is considered irremediable by surgical measures, it may be
properly considered in the class of medical affections.

_Definition._ A displacement of one or more of the abdominal organs into
the cavity of the thorax.

_Frequency in different animals._ It has been found most frequently in
the horse, and less so in the dog and ox. Severe exertions conduce to it
in horse and dog, while in the ruminant the great bulk of the gastric
cavities, covering the whole posterior surface of the diaphragm, tends
to prevent protrusion even if a slight rupture has taken place. On the
other hand, the weight of the gastric cavities in the ox and the tension
upon the œsophagus, when the animals ride each other, sometimes cause
laceration of the foramen sinistrum and hernia of the reticulum.

_Hernial mass in different animals._ In the horse the protruding organ
is most commonly the small intestine (enterocele), omentum (epiplocele),
colon, or less frequently the cæcum, stomach (gastrocele), or liver
(hepatocele). In the ox the reticulum most commonly protrudes, and after
that the liver, abomasum, the omentum or the small intestine. In the dog
the mass is usually formed by the stomach or liver, or less frequently
by the small intestine or omentum.

_Causes and mode of formation._ The hernia is either congenital or
acquired after birth. Again, it may result from imperfect development or
from a trauma. Congenital cases usually depend on an arrest of
development, the foramen sinistrum fails to close and the abdominal
organ passes through by the side of the œsophagus into the chest; or the
diaphragm is left imperfect at some other point, and the two cavities,
abdominal and thoracic, communicate. In some instances there is left not
a distinct opening but a mere relaxation of the parts and under
traction, as, for example, by the gullet, an orifice is torn and a
hernia protrudes. Such cases are very rare. Other lacerations may be
almost all referred to external injuries on the posterior ribs, violent
muscular exertions, sudden shocks in connection with falls, or throwing
for operations, and overdistension of the abdominal viscera.

=1st. External Violence.= In the larger animals this may come from blows
on the last ribs, by poles or shafts of carriages, the buffers of cars,
the end of a gate and the gatepost, projecting ends of bars or beams
against which they run, kicks by horse or ox, blows by the horns of
cattle or tusks of boars. In the smaller animals in addition to the
above, blows with heavy clubs and kicks with heavy boots. In all such
cases there is usually a fracture of one or more ribs, the sharp broken
ends of which are forced into the diaphragm, which they tear when they
again spring outward. The same occurs as the result of falls on hard
projecting bodies of any kind.

=2nd. Muscular Strain.= In heavy draught the fixing of the glottis, ribs
and diaphragm and the extreme contraction of the abdominal muscles often
lead to extraordinary tension of the muscular septum by the mere
violence of which, or when there is superadded a sudden shock, (in
plunging in harness, or displacement of the feet or slipping and
falling,) the diaphragm is torn, usually in its tendinous portion, and
the abdominal viscus protrudes into the chest. If the diaphragm is
momentarily relaxed the lesion may take place in the peripheral muscular
portion. In still other cases the lesion is at one of the natural
openings. The same accident occurs in animals thrown for operation, the
abdominal viscera being full, the hind limbs drawn forward so as to
further compress the belly, and the muscles being subjected to violent
contraction in the efforts to get loose. Violent straining in dystokia
is another cause which, however, usually partakes of a sudden shock on
the diaphragm when a violent pain sets in.

=3rd. Sudden Shocks on the diaphragm, and pressure by the abdominal
organs.= In the horse especially the weight of the abdominal viscera is
very great and the floor of the abdomen inclines downward and forward so
that the whole mass presses with great force against the concave
diaphragm. In cattle the great weight of the stomach and liver is
especially important and in dog and pig of the liver mainly. In trotting
or galloping down hill or jumping from a higher to a lower level, or in
slipping back on the fore feet so that the horse falls on the knees or
shoulders, this pressure is suddenly greatly enhanced and the tense
diaphragm may give way in its tendinous portion or the relaxed organ
through its muscular tissue. A similar danger attends on the violent
straining which attends on difficult cases of parturition, and even in
cases of overloaded stomach and tympany and especially when the tortured
animal throws itself suddenly and recklessly on the ground. In cattle
and sheep this is usually the result of tympany of the rumen, and in
solipeds of stomach and intestines.

Rupture by simple overloading or overdistention is, however, a rare
occurrence, and many cases attributed to this are in reality instances
of _post mortem_ lesions, to be identified by the seat of the laceration
in the muscular portion, and by the absence of blood clots, exudate,
thickening or other sign of inflammation on the torn border.

_Symptoms._ These bear a direct relation to the size of the laceration
and the mass of abdominal organs that protrude into the chest.

In _very grave, recent cases_, with a great phrenic rupture and a most
extensive protrusion of abdominal organs into the chest, there may be
simply the indications of extreme dyspnœa, nostrils and chest widely and
persistently distended, nasal mucosa darkly congested, countenance
pinched, eyes protruding and fixed, pupils dilated, breathing rapid,
shallow and oppressed, and in a few minutes the animal staggers and
falls in the death agony.

In _cases_ which are _less rapidly fatal_, the patient lasting for hours
or even days, there occurs, after the accident, deep, difficult and
oppressed breathing, but not so violent as to threaten instant
suffocation, or more commonly, these symptoms increase slowly as more
and more of the hernial mass protrudes through the narrow opening into
the chest. This form is usually seen only in animals of a specially
quiet disposition, and which have not been subjected to active exertion
or excitement after the accident and the hernia has increased by slow
degrees only. The patient becomes listless, or very restless, paws,
looks at his flanks, shifts from one hind foot to the other or even
kicks at the abdomen, lies down carefully, rolls, sits on his haunches
(though no more than in other forms of colic), and manifests the
anxious, pinched, colic-countenance. The advance of the pain is constant
but slow, and usually it is not characterized by that intensity which
drives the animal to throw himself down recklessly and to roll and kick
with violence. There is also usually an absence of the weak running down
pulse of hemorrhagic congestion (thrombosis) and of the pallor of the
surface mucosæ which usually attend on the extensive blood
extravasations of that disease. An exception may be made in those cases
in which the hernial mass is strangulated, as these may closely resemble
spasmodic colic or hemorrhagic congestion.

The respiration furnishes more distinctive symptoms. The breathing which
may be hurried and almost panting in colic and acute congestion, is
changed in this lesion to a condition of extreme oppression, the
nostrils remain widely dilated in expiration as well as inspiration, the
angle of the mouth is retracted so as to show the teeth and gums, all
the facial muscles stand out, the eyes are protruding and fixed, with
dilated pupils, the head is held extended on the neck, and the ribs are
not allowed to fall in freely, as after ordinary inspiration, but like
the nostrils they remain permanently drawn out. The efforts at
inspiration are violent though shallow and marked by lifting of the
flanks. There are usually one or two nervous catches in each expiration
and sometimes in inspiration as well. This is partly due to the
impotence of the deeply lacerated diaphragm as an organ of respiration,
but also to the pressure of the displaced and overdistended abdominal
organs on the lungs, and to the profound nervous shock. The whole work
has been suddenly thrown on the costal muscles, and the depressed
nervous system proves unequal to sustaining them in the unwonted toil.

Still clearer indications may be obtained from auscultation and
percussion. These are gurgling, rumbling and clucking, or a coarse
mucous râle which seem abnormally close to the ear, and a drumlike
resonance, much greater than that of emphysematous lung and enormously
in excess of what is given out by the sound lung tissue. These may be
heard at points where only pulmonary murmurs naturally occur or where
abdominal sounds, if heard at all, are distant in health. There may also
be areas of abnormal flatness on percussion by reason of the protrusion
of a solid viscus like the liver or spleen or one with solid contents.
These symptoms are only clear when there is a large intrusion of
abdominal organs into the thorax, and they increase rapidly until
asphyxia supervenes.

In _cases which do not immediately threaten life_ the extent of the
phrenic laceration is usually small and the orifice may be blocked by a
bulky organ like the rumen, double colon, stomach or liver, so that any
protrusion takes place only to a limited amount and the function of the
diaphragm can still be carried on to a reasonable extent. In these cases
there may be no very marked symptom at the outset, though the animal is
dull, listless and without appetite, or, if he eats or drinks, it is
liable to be followed by slight colics and a double action of the flank
in expiration as in pulmonary emphysema (heaves). Pressure or percussion
in the posterior intercostal spaces is painful. Cough when roused by
pinching the larynx is broken and abortive. These symptoms are not
distinctive, however, and unless there is a protrusion of a loop of
small intestine, to give gurgling and drumlike sounds the diagnosis of
the case is liable to fail. The fact of a recent injury may however
assist in the recognition of the lesion.

The _chronic cases_ are even more difficult to recognize as there is no
record of recent injury and no fever. There may be _short wind_, the
animal breathing hurriedly on slight exertion, and showing a double lift
of the flank in expiration (Girard). In place, however, of the
tympanitic bowels and frequent passage of flatus which characterize
heaves, there is a tendency to colic, especially after meals, and in a
certain number of cases there are all the symptoms of fatal
strangulation, due to the contraction of the diaphragmatic wound. When
the hernia is made by a loop of intestine there are the characteristic
symptoms of thoracic gurgling and drumlike resonance.

Cases are on record in which the intestine protrudes through one of the
last intercostal spaces or between the ends of the broken rib as a
hernia and diagnosis becomes easy by auscultation, palpation and
percussion. But in a large proportion of cases the lesion escapes
recognition and is only found on _post mortem_ examination.

_Lesions._ The lacerated orifice in the diaphragm varies much as regards
situation, extent, form and the nature of its border. In congenital
cases due to an imperfect closure of the natural openings there may be
simply a round or ovoid opening, too spacious to be filled by the
gullet, vena cava or aorta as the case may be, and capable in the
different cases, of containing an organ of any size from the omentum to
the liver or stomach. Its margins may be perfectly smooth and even,
without any thickening, irregularity, fringe, clot or exudate. In
traumatic cases on the other hand the orifice may be of almost any form,
size or situation. It may be round, elliptical, triangular, or irregular
in many ways. It may be so small as to admit nothing more than a small
fold of the omentum, or it may be large enough to open the two cavities,
thoracic and abdominal into one common space, and to practically abolish
the function of the diaphragm. If the lesion is a recent one the torn
margin is irregularly indented or fimbriated and marked by small black
blood clots, and somewhat later by exudate and irregular thickening or
swelling. When due to a broken rib, the existence of the fracture is
patent and the laceration extends along two lines often radiating from
point of perforation by the rib. When the laceration has resulted from
tympany of the stomach or intestines or from other overdistension of the
abdominal organs, the general and comparatively equable pressure has
determined the independent laceration of numerous tendinous or muscular
bundles all over the diaphragm, so that the divided ends stand out at
intervals each bearing its little clot of dark blood, but without actual
perforation. The actual orifice in such cases is confined to one point
where the tension has been greater or the resistance less. _Post mortem_
lacerations, from tympany or other cause, are easily distinguished from
those occurring during life, in that the edges of the wound are pale and
bloodless, without clot or exudate.

When the hernia is chronic there is an absence of exposed fringes, and
of indications of inflammation, the margins of the orifice being in some
cases smooth, even and fibrous, and in others irregularly notched or
indented with nodular, fibroid swellings of various sizes at intervals.
In such cases the orifice is always relatively small and the hernial
mass inconsiderable.

As a rule the peritoneum and pleura, being firmly adherent to the
diaphragm, are involved in the laceration so that the hernial mass is
not retained in a special sac, but simply protrudes into the pleural
cavity, after the manner of an eventration. In exceptional cases they
become detached from the muscle, and becoming distended, envelope the
hernial mass in a distinct sac.

In hernia with a very small orifice the omentum alone may pass through,
even the small intestine proving too large for admission. In such cases
it is usual to find the band of omentum adherent to the callus formed by
the repair of a fractured rib. When the orifice is somewhat larger a
portion of small intestine or of the double colon or cæcum may be
engaged, while with a still larger opening the stomach, spleen, or liver
may form the hernia. In cattle the reticulum is most likely to be the
hernial mass, as noted in an article below. In rare cases the small
intestines, omentum or liver protrude (Youatt, Lafosse). The protruding
organ is liable to be constricted and strangulated sooner or later by
increase in its bulk in connection with its vermicular movements, the
accumulation of its contents or the extrication of gas in its lumen, or
by the gradual contraction of the orifice in process of healing. Then
there may be dark red venous congestion, blood extravasation and
effusion, friability and even rupture of the intestinal walls, and
adhesions to the wound or the lungs. Once started this congestion and
extravasation may extend backward into the abdominal cavity involving a
great part of the contiguous intestinal canal.

_Prognosis._ The worst cases are promptly fatal, while others destroy
life in one or two days and such are always to be recognized by the
extreme dyspnœa which appears soon after the accident. The slight cases
with small orifice and little protrusion may merge into the chronic
form, and the animal may even be fit for work, notwithstanding existing
dyspnœa, which closely resembles that of chronic emphysema (heaves), but
is not benefited by the same treatment. In the ruminants even
considerable lacerations and protrusions may not be incompatible with
fattening provided the animal is kept from all causes of excitement or
over-exertion.

_Treatment._ Surgical treatment has not proved successful. Expectant and
medicinal treatment are the only available resorts and then only in the
slighter cases. Quiet and the absence of all excitement is the first
consideration to allow of an arrest of any increase of the hernia and
the establishing of a healing process in the torn margins. Bouley
strongly advises bleeding to allay abdominal pain. Chloral hydrate (1
ounce for the larger animals) will often meet the same end, with the
additional advantage that it counteracts fermentation and tympany. The
unloading of stomach and bowels by a cathartic, and the use of flaxseed
meal or other concentrated food of a laxative nature are indicated.
Small animals may be lifted by their fore limbs, and the abdomen may be
meanwhile manipulated to favor the return of the hernial mass by
gravitation. Large animals should be placed in a stall having an
inclination downward and backward for the same reason. When it can be
ascertained that the hernia consists of a loop of small intestine only,
it is permissible, especially in cattle, carnivora and omnivora, to make
an incision in the flank and with the disinfected hand to attempt the
reduction of the hernia and the placing of a bulky viscus, like the
rumen, stomach or liver in the way of its return. In case of violent
abdominal pain Bouley advises active counter-irritation over the
abdomen, but as strangulation is usually present in such cases, this
measure may be held to be inferior in value to gravitation, anodynes,
antiseptics, unloading of the gastro-intestinal organs and absolute rest
or surgical interference.


                 DIAPHRAGMATIC HERNIA OF THE RETICULUM.

  Anatomical reasons. Gullet, weight of stomach, riding, dystokia.
  Symptoms. Tendency to chronicity. Treatment.

In ruminants this is the most common phrenic hernia of a hollow
abdominal viscus. On the right side the gastric and intestinal organs
are separated from the diaphragm by the flat mass of the liver. A
laceration in this region must therefore be extensive to allow of the
protrusion of any abdominal organ into the chest. The left half of the
diaphragm, however, comes in direct contact with the reticulum and any
opening large enough to admit of this viscus is likely to entail hernia
of the second stomach. The lesion is further favored by the fact that
the gullet passes through this part of the diaphragm and is connected
with the stomachs in the furrow between the first and second stomachs.
In case, therefore, that the gullet is violently dragged upon by the
weight of the contents of the overloaded or tympanitic paunch, or when
the animal rises on its hind limbs, in riding its fellow, the foramen
sinistrum is liable to be enlarged by laceration, and the second stomach
most naturally protrudes through the opening. The strain thrown on the
diaphragm in violent abdominal contraction, as in difficult parturition,
is mainly expended on this left half, and the laceration takes place
around the œsophagus, or as in cases reported by Schurinck and
Siedamgrotzky through the aponeurotic portion. The protrusion may be
composed of the second stomach alone, or together with portion of the
paunch as observed by Schmidt in a goat, or of the third and fourth
stomachs as in a case in a bull reported by Baraillé. The edges of the
orifice may show, in recent cases, the fringed or irregular jagged
outline with blood clots and thickening, or in chronic cases the pale,
fibrous, smooth, even outline already described under diaphragmatic
hernia.

The _symptoms_ are like those of other forms of phrenic hernia, in ratio
with its extent. The tendency to survival, and chronicity is greater
than in the monogastric animals, 1st because the entrance of the smaller
viscera is barred by the great gastric masses applied against the wound,
and 2nd by the quiet uneventful life of the ox and the absence of active
work and violent excitement.

_Treatment_ will not differ from that of other forms of phrenic hernia.


   HERNIA THROUGH THE MESENTERY, OMENTUM OR OTHER FOLD OF PERITONEUM.

  Definition. Causes: Concussions in horse especially, anatomical
  conditions in cattle, pediculated tumors, dystokia, hernia of small
  intestine in horse, ox, broad ligament, pelvic hernia. Lesions:
  Congestion, hemorrhage of hernial viscus, adhesions, softening,
  thickening, strangulation. Symptoms: Intestinal obstruction, rectal
  exploration. Treatment: Laparotomy.

_Definition._ This consists in a protrusion through an opening,
congenital or acquired, in the double fold of peritoneum (mesentery)
which passes off from the abdominal wall to support a viscus, or that
which passes from organ to organ (omentum).

_Causes._ The lacerations of mesentery or omentum are attributed to
sudden concussions of various kinds (falls, blows, leaps, violent
efforts), and have been especially found in horses in which the bulk and
weight of the contents of the digestive organs furnish a special
predisposition. In ruminants in which the contents of the abdomen are
equally bulky and heavy the lesion is rarely seen, probably because the
great bulk of the ingesta lies in the first three stomachs, and because
the large intestines are folded up in the mesentery which supports the
small, thereby strengthening this means of support and restricting the
freedom of movement on the part of the intestines themselves. In
carnivora the limited bulk of the intestines and their contents, and the
relative shortness of the mesenteric folds largely obviate the
predisposition.

Pediculated tumors of mesentery or omentum may drag on the delicate
membrane so as to cause laceration, and circumscribed peritonitis, by
producing softening and friability, may act as a causative factor.
Violent straining in defecation or parturition is another cause of
laceration.

_In solipeds_ the loosely suspended and eminently mobile small intestine
is the viscus which most commonly forms a hernia through such
adventitious openings, either through the great mesentery, the great
omentum, the gastro-splenic omentum, the mesentery of the umbilical vein
(falciform ligament of the liver), or the gastro-hepatic omentum. Cases
are on record, however, in which the floating colon, the double colon
and even the cæcum formed herniæ through the peritoneal lacerations.

In _cattle_ the most common lesion is the hernia of a knuckle of
intestine through a laceration in the mesentery, but, the rupture has
also occurred in the great omentum and exceptionally in the broad
ligament of the uterus which is very extensive in these animals. Pelvic
hernia or gut tie as usually described is dependent on a laceration of
the mesentery of the spermatic artery.

_Lesions._ The fold of intestine which makes the hernia is liable to
become strangled, and sometimes twisted in the opening, so that the
circulation of blood and ingesta is interrupted, congestions and
hemorrhages set in, and necrosis and general infection follow.
Oftentimes a fibrinous exudate is thrown out, binding together the
intestinal convolutions, and attaching them to the margins of the
mesenteric or omental opening. Similarly the lips of the lacerated wound
in the mesentery become covered with blood clots, or congested, or
infiltrated, and sometimes the seat of extensive extravasations. The
inflamed membrane may soften, become friable and tear more extensively,
or if the patient survives, the exudation becomes organized, thickening
and strengthening the margins of the wound and causing them to contract
so as to strangle the enclosed loop of intestine.

_Symptoms._ The indications are those of intestinal obstruction, to
which accordingly the reader is referred. The only possible indication
of the exact nature of the lesion is to be obtained by rectal
exploration. Herniæ through the meso-colon or broad uterine ligament may
be reached in this way, and possibly diagnosed.

_Treatment._ Laparotomy alone gives any hope of success, and this will
only be warranted when a certain diagnosis has been reached.


          HERNIA THROUGH THE FORAMEN OF WINSLOW IN THE HORSE.

  Anatomical considerations, small size and elevated position of
  foramen, length and freedom of mesentery of jejunum; spare diet,
  draught, straining, rolling, colic. Symptoms: of intestinal
  obstruction only, lesion found at necropsy.

The foramen of Winslow is a comparatively small opening between the
lesser curvature of the stomach and the liver, and between the gullet
and its cardiac ligament on the left side and the gastro-hepatic omentum
on the left. With its elevated and anterior position in the abdomen it
would seem to be little exposed to this kind of accident, yet a number
of recorded instances in the horse, show that it is certainly not
immune. The great mobility of the jejunum, owing to the extra length of
its mesentery is believed to be the essential predisposing cause. A
spare diet, or one which is in small bulk, allows the comparatively
empty gut to pass more readily through the small opening. Severe efforts
in draught and straining in defecation and parturition are also invoked
as means of pressing the jejunum through the orifice. So with the
concussions attendant on falls and the unwonted positions taken in
decubitus and rolling on the back in wantonness or colic.

_Symptoms_ of this lesion are essentially those of intestinal
obstruction, with usually a rapid and fatal course. An accurate
_diagnosis_ is impossible during life.


                         OTHER FORMS OF HERNIA.

The other forms of hernia (umbilical, inguinal, scrotal, femoral,
ventral, vaginal, ischiatic) are essentially surgical and need not be
further referred to here, than to guard the reader against overlooking
them as factors in producing intestinal and omental strangulation and
colic. They are all to be recognized by the presence of a local
swelling, which may often be obliterated by returning its contents into
the abdominal cavity, which sensibly enlarges when the animal is made to
cough, and which, if made up of intestine, is subject to gaseous
distension, and gurgles when manipulated and returned. A violent colic
occurring in a male animal should never be considered as certainly
diagnosticated until the scrotal and inguinal region have been carefully
examined for hernia.


                        PARALYSIS OF THE RECTUM.

  In solipeds, ruminants, swine, carnivora. Injuries to loins and croup.
  Palsy of tail and sphincters. Nerve centres in end of cord. Fractures
  and dislocations of the pelvis. Hæmoglobinuria. Advanced gestation.
  Sclerosis. Ovariotomy by vagina. Impaction of rectum. Neoplasms.
  Thrombosis of internal iliac artery. Ptomaines and toxins in fevers.
  Symptoms: tardy defecation, impaction, over distension, fæces firm,
  dry, roller like, liquid oozing, excoriation, foul tail and thighs,
  bulging of anus, incontinence of urine. Paresis and wasting of
  quarter. Treatment: remove cause, for sprains and fractures sling,
  treat myelitis, debility, poisoning, unload rectum often, oily or
  soapy enemata, strychnia, eserine, ergot, barium chloride,
  derivations.

This is much more common in the horse than in ruminants, swine or
carnivora, mainly because the soliped is more exposed to traumatic
injuries of the loins, croup, and pelvic bones. It is noticeable that in
the majority of cases the paralysis of the rectum is connected with
palsy of the tail, anus, and sphincter vesicæ. This comes from the
anatomical fact that the centres presiding over the motions of these
different parts are situated close to each other in the terminal portion
of the spinal cord, and any lesion of that part by traumatism or disease
is likely to affect all of these parts alike.

The condition has been especially noticed in fractures or severe sprains
of the loins causing pressure on the spinal cord. In some cases injury
to the nerves supplied by this part of the cord, leads to an extension
of inflammation to the nerve centres, thus paralysis of the rectum has
followed on fracture of the ischium, dislocation of the sacro-iliac
joint, or even of the first bone of the coccyx. Again, congestions and
effusions on the terminal part of the cord, which occur in certain cases
of hæmoglobinuria and in old hard worked horses is a cause of these
local paralyses. Advanced gestation appears at times to produce the
disease through pressure on the nerves, though it has also been noticed
in non-breeding animals, and is doubtless traceable to sclerosis or
other degenerations of the cord. It sometimes follows vaginal
ovariotomy.

Sometimes the condition is traceable to local lesions as over distension
of the rectum in horse or dog or in rectitis, but the result in such
cases is usually partial, a paresis rather than a paralysis. The same
may at times result from the growth of the neoplasms, and from the
debility of old age. In other cases thrombosis of the aorta or internal
iliac artery, implicates the hemorrhoidal vessels and paresis occurs as
a result of the limited blood supply.

It may further result from the action of toxins and ptomaines on the
spinal cord as when it supervenes in the course of debilitating fevers.
This usually shows itself first as paresis of the sphincter ani, and
later implicates the rectum as well.

_Symptoms._ In the slighter forms defecation is retarded, the fæces
accumulate and overdistend the organ, adding to the paresis; they escape
only under violent straining and apparently by the peristaltic
contractions of the anterior portion of the rectum; the ejected matters
are discharged usually in the form of a cylindroid mass; and they are
dry, and firmly compressed. In some cases the irritation caused by the
impaction leads to a free secretion, which escapes through the widely
open anus and runs down the thighs, leading to excoriation of the skin.

In the more severe cases the accumulation is more complete, the
expulsion still more difficult, and as the tail is often implicated, it
lies flaccid between the thighs, and is smeared with the discharges. The
peristalsis in front and the forcible compression by the abdominal
muscles may be entirely inadequate to effect defecation so that the
fæces have to be removed by the hand. The pressure on the bladder often
leads to incontinence of urine, if the paralysis of the vesical
sphincter has not already brought this about.

The trouble is not unfrequently associated with paresis and wasting of
the muscles of the quarter.

_Treatment._ The first consideration is the removal of the cause. If
fracture of the loins or pelvic bones, or severe sprain of the lumbar
region, slings are usually requisite to obviate renewed injury in lying
down and rising. Simple inflammation of the cord or its membranes may be
met by laxatives, blisters and perhaps bromides. In the old and
debilitated, tonics, rich food, open air, and sunshine, with locally,
blisters or stimulating embrocations, will be demanded. In case of
poisoning by ptomaines or toxins the disease which produces them must be
attended to, and elimination favored as far as compatible with existing
weakness. In all cases the rectum must be frequently unloaded with the
hand or soapy injections, and its walls may be stimulated by giving of
nux vomica, or by the hypodermic use of eserine, ergotin or barium
chloride. Blisters or stimulating embrocations may be applied over the
croup or between the thighs, or mustard or tobacco may be added to the
injections.




            NEOPLASMS. TUMORS OF THE INTESTINE IN SOLIPEDS.

  Lipoma: sessile or polypoid, pediculated, strangulation, stenosis,
  size. Sarcoma: on bowel or peritoneum. Fibroma: flat or pediculated,
  obstruction, stenosis, degeneration, fatty, calcic. Myoma: hypertrophy
  of muscular coat, degeneration, stenosis. Myxoma: small translucent,
  oval, intestine mesentery. Carcinoma: extension from urocyst in horse,
  intestine, lymph glands, spleen, stomach, liver, mesentery, omentum.
  Epithelioma: colon, stomach. Cystoma: may contain sand or
  sclerostomata. Lymphadenoma: rectum, colon. Undetermined neoplasms.
  Causes: foreign bodies, microbes, constitutional, hereditary.
  Symptoms: tardy defecation, obstruction; in malignant, pallor, anæmia,
  emaciation; peritonitis, ascites; fœtid irregular stools, bloody,
  sloughs, rectal exploration. Treatment: surgical removal where
  possible, recovery by sloughing, laparotomy, useless in multiple or
  malignant tumors.


Tumors of the intestine are very varied in kind (lipoma, sarcoma,
fibroma, myoma, myxoma, carcinoma, epithelioma, cystoma), and are found
on all portions of the canal.

=Lipoma= or _fatty tumor_ is most frequent in connection with the small
intestine or rectum, and on the mucosa it may assume a pediculated or
polypoid form and may more or less perfectly block the intestine. When
situated under the peritoneal surface it is usually sessile and
flattened apart from the mesentery, but if growing from the latter or at
its connection with the bowel it tends to become pediculated, sometimes
hanging at the end of a very long cord which may roll around a loop of
intestine and strangle it. Similarly the sessile masses, as they
increase press inward so as to diminish the calibre of the bowel and
finally close it. They are often found no larger than a coat button,
while in other cases they grow to enormous size (25 lbs. Vogt, 42 lbs.
Semmer). Semmer’s case bound the cæcum and colon to the abdominal wall.
The structure is essentially fatty tissue, though in some cases the
fibrous stroma is more dense than in others.

=Sarcoma.= Small round cell tumors have been repeatedly found in
connection with the intestine or mesentery. Baranski found one over 4
inches in length in the wall of the large intestine producing a serious
constriction. Lucet found one of 18 lbs. weight and Mouquet one of 7
lbs. attached to the omentum. They are found to follow in certain cases
the irritation and exudation of peritonitis.

=Fibroma.= Pediculated fibrous tumors have been found in the rectum of
the horse and when large may threaten obstruction. They are usually of a
loose fibrous texture, soft and elastic, and are often situated between
the mucous and muscular coats. Quite frequently they are already in
process of fatty or calcareous degeneration at particular points, the
debris tending to fall into the intestine and be discharged with the
fæces.

=Myoma= in the form of hypertrophy of the muscular coat of the bowel,
the muscular fibres being increased in number and the wall further
thickened by an intermixture of fibrous tissue, with areas of fatty
degeneration. This may be confined to one side of the bowel and assume a
spherical form, but it tends to contract the lumen until it is little
more than half an inch in diameter. Mollereau records one case of myoma
of the double colon which measured nearly a foot in diameter.

=Myxoma.= These are small, pale, translucent, round or oval neoplasms
having a sparse network of fusiform cells and fibres, filled in the main
with small round mucus corpuscles. They are not frequent in man and
appear to be less so in the lower animals, but Friedberger and Mollereau
have recorded two cases of myxoma in the intestines of the horse, and
Chassereaud one case connected with the mesentery. In one case a mare
passed such a tumor three inches long and nearly an inch in thickness.
Chassereaud’s case caused torsion of the floating colon.

=Carcinoma.= Cadeac says it is not rare to see cancer spread from the
urinary bladder to all the abdominal organs in the horse. Conté
describes a case in the duodenum, Marty one on the pelvic flexure of the
colon, Latour on the ileo-cæcal valve, Mario on the floor of the rectum,
and Casper in the lymphatic glands of the spleen, stomach, liver,
mesentery and omentum, the last showing a mass of 28 lbs.

=Epithelioma.= When in a growing neoplasm, epithelial cells are arranged
not only on the surface, but also in the form of cylinders extending
into the substance of the tissues the growth is looked upon as
epithelioma. Morot records a growth of this kind on the horse’s colon,
and which had grown to enormous dimensions. Röll also mentions it as
occurring on the gastric and intestinal mucous membrane.

=Cystoma.= As seen in the horse these have usually been determined by
the presence of foreign bodies. Redieux describes a cyst of the small
intestine which enclosed 30 lbs. of sand. Charlot speaks of a cyst
placed between the stomach and sternal arch of the double colon,
furnished with a smooth serous lining. Vernant and the author have found
on the walls of the cæcum and double colon small cysts, each
communicating with the interior of the intestine by a narrow opening.
Beside mucopurulent matter, these have often in our experience contained
the sclerostomata or their larvæ.

=Lymphadenoma.= Wuth describes a case of obstruction of the rectum by an
adenoid tumor as large as the closed fist, which induced a fatal
hemorrhage. It was connected with the terminal part of the floating
colon. Jobelot records another case.

=Tumors of uncertain kinds.= A large number of tumors are described in
veterinary literature, the true nature of which has not been made out.
If these could be successfully differentiated they would add to the
above list materially, and other forms not referred to above.

_Causes._ The causes of these neoplasms are not always traceable. In the
case of some an occasion may be found in the presence of an irritant,
like worms, sand, gravel, oat seed, etc., found in their interior, in
others like the carcinomata we may accept the presence of the protozoön
of that disease, and in still others there is an unknown cause, perhaps
constitutional or hereditary which predisposes to the new growth. This
last cause was probably operative in producing the fatty neoplasm in the
rectum of Pritchard’s fat Hereford heifer, seeing that her grandsire
also died from a similar lesion.

_Symptoms._ These usually culminate in the classic symptoms of
obstruction of the bowels, but there is sometimes a train of significant
symptoms leading up to this climax. Thus in the malignant tumors in
particular, though in some other forms as well, there is anæmia, pallor
or yellowness of the mucosæ, weakness and emaciation. In other cases
there are symptoms of peritonitis and ascites. In others there is
obstinate constipation or diarrhœa, the excretions having a peculiar
fœtid odor, often suggesting the decomposition of animal matter. They
may be mixed with fresh blood, or sloughs from the surface of a tumor,
or the whole tumor may be passed at once. Rectal exploration may be
intercepted by a rigid stricture, by a tumor blocking the lumen, or a
mass may be felt projecting in from one side. Aside from these the
situation, form and size of the tumor can sometimes be felt through the
flaccid walls of the rectum. In other cases the blocked and distended
bowels may be felt, without the identification of a tumor as the cause.

_Treatment._ For tumors situated in the rectum, the removal by surgical
measures (torsion, ecraseur, etc.) is indicated. If the tumor is simple
a permanent cure may be hoped for; if malignant it is likely to recur.
Tumors situated more anteriorly are usually desperate cases. Yet a
certain number of pediculated tumors are detached spontaneously and
discharged. In the absence of this, and when a tumor can be certainly
diagnosed, there remains a resort to laparotomy, which in the horse is
too often unsuccessful. If the tumor can be made out to be malignant and
multiple it is useless to resort to removal.


                   TUMORS OF THE INTESTINE IN CATTLE.

  Sarcoma: usually near lymph glands. Lipoma: mucosa, serosa,
  pediculated, strangulation, obstruction. Fibroma: floating colon.
  Carcinoma: generalized cancer, colon. Cystoma; reticulum, omasum,
  abomasum. Undetermined tumors. Symptoms: discovery by rectal
  examination, in case of debility or digestive disturbance. Treatment:
  removal through rectum or by laparotomy, spontaneous sloughing.
  Hyperplasia of intestinal mucosa.

=Sarcoma.= Multiple sarcomata have been found in nearly all parts of the
abdominal cavity but above all in or near the lymph glands. They are
from a small size up to masses of 60 lbs. (Revel).

=Lipoma.= Fatty tumors are found attached to the mucosa, and peritoneum,
but above all as masses with long elastic pedicles which are liable to
wind round and obstruct the intestines. Tannehauer records a case of
fatal obstruction of the small intestine from a lipoma of the mucosa,
and Pritchard two cases of fatal obstruction of the rectum by a fatty
neoplasm occupying its walls.

=Fibroma.= Furianetto furnishes an interesting case of a fibrous tumor
connected with the mucosa of the floating colon, on which it had dragged
so as to cause a fatal invagination.

=Carcinoma.= Mauri relates a case of multiple cancer involving not only
the intestines but also the lymph glands, the heart, the brain, the
muscles, etc. Landis also records the case of a cancerous tumor of six
inches in circumference attached to the floating colon of a calf.

=Cystoma.= Tumors of this kind have not been found to any extent in the
intestines of cattle. Reboul describes a large cyst weighing 20 lbs.,
attached to the reticulum, omasum and abomasum and containing a
pultaceous fœtid debris. There was attendant congestion of the colon.

=Tumors of Uncertain Kind= have been recorded by other observers.

_Symptoms._ As in the soliped the one diagnostic symptom is the
discovery of the neoplasm and its effects by rectal examination, in
those cases in which the tumor is within reach. Apart from this there
are the general symptoms of ill health, anæmia, pallor of the mucosa and
emaciation in malignant cases, and recurrent colics, tympanies, impaired
rumination and appetite, with dark colored liquid or bloody fæces, or
complete suspension of defecation. In Pritchard’s cases one animal was
in the highest possible condition, having been in preparation for the
Smithfield (London) fat stock show.

_Treatment._ If the tumor has been diagnosed with certainty, it may be
removed by surgical means from its seat in the rectum, or even from
other parts if not multiple or malignant. Laparotomy is better borne in
cattle than in horses.

=Hyperplasia on the Intestinal Mucosa in Cattle.= In a Jersey heifer
presented at the clinic of the New York State Veterinary College a
hyperplasia of the mucosa of the duodenum, which blocked the lumen, was
removed and the bowel resected. On examination the mass was found to be
the result of productive inflammation, and undergoing necrosis and
separation.




                   TUMORS OF THE INTESTINES IN DOGS.

  Sarcoma: lymph glands. Epithelioma, intestine. Adenoma, rectum.
  Undetermined tumors. Diagnosis by abdominal palpation or rectal
  exploration. Removal by rectum or laparotomy. Chickens: Sarcoma.
  Epithelioma.


Cadeac records the frequent existence of sarcoma of the lymph glands,
and epithelioma of the intestines and Friedberger an adenoma close to
the rectum. Born describes a tumor of uncertain kind, and with a number
of smaller adjacent rounded masses.

The _diagnosis_ is usually easier than in the larger animals, the
flaccid walls of the abdomen facilitating a satisfactory manipulation.

In the case of isolated and non-malignant growths, laparotomy should be
resorted to without hesitation. Even resection of the intestine may be
resorted to for the removal of a neoplasm the ends being reunited by
sutures or by Murphy’s button.


                   TUMORS OF THE INTESTINES IN BIRDS.

In chickens it is no uncommon thing to find sarcomata, and other tumors
of less determinate structure in connection with the intestine. Pommay
and Bizard record a case of cylindroid epithelioma in an ostrich, almost
completely blocking the intestine.

The _treatment_ in birds may be very heroic, the tendency to infection
by pyogenic and other common bacteria of wounds being reduced to a
minimum.




  STRANGULATION OF THE INTESTINE BY THE OVARIAN LIGAMENT IN SOLIPEDS.

  Pediculated ovary in mare. Strangulation. Diagnosis by rectal
  exploration. Castration.


In most healthy animals the ovary is light and its situation in the
anterior border of the broad ligament so firm that it is impossible for
it to enwrap and constrict the intestines. In the mare, however, the
healthy ovary may be almost as large as the closed fist, and when
further enlarged by cystic or other degeneration, it drags upon and
lengthens the ligament until that may form a long pedicle which can
easily be wound round the floating colon or small intestine.

_Diagnosis_ of this trouble can often be satisfactorily made by rectal
exploration, and _treatment_ will consist in the removal of the
offending body by castration through an incision made in the anterior
part of the roof of the vagina close behind the os uteri.


                              PERITONITIS.

  Acute: Chronic; general; local; idiopathic; traumatic; surgical;
  accidental; perforation; strangulation; cachexia; microbian almost
  always; aseptic foreign bodies escape into bowel: Castration; gastric
  or intestinal rupture or ulcer, enteritis, obstructions, cold storms,
  draughts, chills, all lower resisting power of tissue; generalization
  through peritoneal serum. Non-infective peritonitis from chemical
  irritants. Paves the way for microbes of ingesta. Rheumatic
  peritonitis, tuberculous, actinomycotic, microbes differ.

All inflammations of the peritoneum go under this general name. At the
same time clinical and pathological distinctions have been made with the
view of distinguishing more precisely different classes of cases. Thus
it is described as _acute_ and _chronic_, _general_ and _local_,
_idiopathic_ and _traumatic_, _surgical_, _accidental_, or by
_perforation_, _by strangulation_ and _by cachexiæ_.

The advance of bacteriology has greatly simplified our views of the
disease, as microbes are found to be at work in practically all cases.
If we could exclude microbes from this membrane, peritonitis would be
practically abolished, portions of aseptic powdered glass, sponge or
gauze can be left in the abdominal cavity with comparative impunity, the
tendency being, as shown in the dog, to coat themselves with a fibrinous
exudate, and to make their way into the intestines through which they
escape (Sternberg, Jalaguier and Manclaire). Hence it is that
peritonitis is to a very large extent the result of a traumatism
(castration, penetrating wound of the abdomen, contused wound of the
abdomen), or of a rupture or ulceration of the stomach or intestine,
through which the microbes make their way into the peritoneal cavity. In
enteritis, congestions, strangulations, intussusceptions and
obstructions of the bowels, the cause is the same, the microbes making
their way with greater ease through the coats of the bowels in which the
circulation and nutrition are impaired and the power of resistance
diminished. Finally the occurrence of the disease as a consequence of
exposure to cold or wet, of exposure in a cold rain or snow storm, of
standing in a draught when perspiring, or plunging into cold water when
heated and fatigued, or drinking ice cold water when in a similar
condition, may in most cases be explained on the same grounds. The germs
in this case had already gained access to the blood, but were helpless
to accomplish much harm, until by chilling, the resisting power of the
system was lowered and an occasion furnished for their successfully
colonizing the peritoneum. Parallel cases are found in the frog which is
immune from anthrax until it is heated, and in the chicken which is
immune from anthrax until chilled. Reduce the vitality of the system and
the germ which was already present, and up till now harmless, takes
occasion to colonize more or less destructively.

This view also furnishes an explanation of the tendency of local
peritonitis to become generalized. In the scanty liquid which bedews the
surface of the abdominal organs, the microbes grow, multiply and spread;
by the constant peristaltic movements of the bowels and their rolling
upon each other this extension is largely favored; and the tendency to
generalization will be in ratio with the potency of the invading germ,
and the general or local weakening of the invaded tissues. With a
limited infection wound in an otherwise healthy peritoneum and system,
and invasion by a pus coccus only, the infection may not succeed in
extending from its primary centre, but with a debilitated system, an
extended enteritis, or when the invasion is made by septic germs it is
likely to become speedily and fatally generalized.

Pernice has shown, however, that peritonitis may occur independently of
infection. The injection into the cavity of concentrated mineral acids,
acetic acid, phenol, nitrate of silver and other powerful antiseptics
determine inflammation by their purely irritant action. By weakening the
tissues of the bowels these in their turn pave the way for the escape of
the microbes from the contents, and to the occurrence of a secondary
infective inflammation.

Cases occur as a manifestation of rheumatism, tuberculosis,
actinomycosis and other affections which will be treated at greater
length under these respective heads.

The microbes would seem to vary greatly. Soula attributes infection of
castration wounds mainly to the bacillus of malignant œdema which is 3
to 3.5 μ long and 1 to 1.1 μ broad often bearing a refrangent spore at
one end (is sporeless in the peritoneal cultures), and growing out into
chains in artificial cultures. They are anærobic, liquefying, motile,
easily stained by aniline colors, but bleached by iodine.

In other forms of peritonitis the bacillus coli commune is found and
probably comes from the intestinal contents where it is present in all
our domestic animals.

In man Fränkel found the bacillus coli communis 9 times, streptococcus
pyogenes 7 times, bacillus lactis aerogenes 2 times, micrococcus
pneumoniæ crouposæ 1 time, staphylococcus pyogenes aureus 1 time.
Flexner found the proteus vulgaris.




                     ACUTE PERITONITIS IN SOLIPEDS.

  Susceptibility to pyogenic bacteria, infection simple or complex.
  Traumatic injuries: accidental, omphalitis, operations, strangulation,
  wounds in rectum or vagina, coition, hernia, castration of mare, or
  horse, infected from 2d to 6th day, later granulation protects,
  ruptured stomach, perforating ulcer, perforation of parturient womb,
  ruptured abscess, microbes in circulation, debility. Symptoms: trauma
  with spreading swelling, œdema, tenderness, stiffness, arched back,
  tucked up abdomen, fever, prostration, colics, careful decubitus and
  rising, tense tender belly, ridge along flank, breathing short,
  inspirations catching, straddles, steps short, costive or later
  diarrhœa, enuresis, abdomen fluctuates, death in 1 to 8 days. With
  ruptured stomach or intestine prostration extreme, collapse, vomiting.
  Resolution. Ascites. Diagnosis: trauma, gastric or intestinal lesion,
  followed by specific symptoms. Lesions: trauma, rupture and escape of
  ingesta, congestion, ecchymoses, false membranes, adhesions, liquid
  effusion, bloody, pink, or straw colored, albuminous, fibrinous,
  granules, cells, salts, bacteria, pus, fœtor, bowels tympanitic, later
  fibrous bands, strangulations, degenerations. Prevention: fatal in
  solipeds, avoid abdominal congestions, inflammations, traumas,
  infections, accumulation of serum, blood, etc., also debility, ill
  health, chill. Treatment: old methods, by anodynes and checking
  peristalsis. Modern method: antisepsis, iodoform, carbolic acid,
  mercuric chloride, irrigation with boiled water, drainage; internally,
  saline laxatives, eliminates from bowels, blood, peritoneum, favoring
  phagocytosis, and innervation, antiseptics, sodium salicylate, chloral
  hydrate, morphia, enemata, hot fomentations, or ice, in suppuration
  drainage and washing with normal salt solution at body temperature,
  derivatives, laparotomy, puncture in tympany.


_Causes._ Solipeds are especially subject to peritonitis in its acute
and dangerous forms largely because this class of animals is
preëminently obnoxious to the attacks of pyogenic bacteria. The disease
may however be dependent on a great variety of different organisms, and
these may cause different forms through invasion by one specific microbe
or by a complex invasion. It is convenient to note the different
channels of invasion.

_a._ =Traumatic injuries.= Wounds are not uncommon from pricks with
forks, pickets, broken rails, prongs of stump fences, poles or shafts of
wagons, nails, barbed wire, horns of cattle, tusks of boar, and other
sharp or pointed objects, which carry infecting germs, or in any case
make an entrance for those found in the dust of the stable, on the
horses skin, comb, brush, rubber or clothing. Inflammation of the
umbilicus and resulting abscess may prove an entrance way for the germs
either by rupture into the peritoneum or by causing adhesions between
two loops of intestines from which the microbes escape through the
weakened tissues. Wounds made in operations on hernias may have a
similar ending and as Dieckerhoff has pointed out the onset of the
peritonitis may be delayed for one or two weeks while the abscess is
maturing or the walls of the bowels are being traversed by the microbes.
Strangulated hernias and those in which the intestine is congested are
especially subject to such peritonitis, as the germs may enter by the
external wound and through the intestinal wall as well. The author has
seen artificial anus formed through inclusion in the clamps of an
adherent loop of small intestine, and at such a point peritonitis is
liable to start.

Wounds of the rectum or vagina are sometimes the starting point of the
inflammation. The penis of a stallion entering and lacerating the rectum
of a mare, or the large penis of an ardent male rupturing the roof of
the vagina are occasional causes. The latter may occur without fatal
consequences, yet the author has seen a generalized and rapidly fatal
attack follow such an injury when the mare had at once thereafter made a
journey of nine miles in a cold rainstorm. The horse was a Percheron
with very large penis and the mare would weigh about 900 lbs. The
castration of mares, even through the vagina may be followed by
peritonitis from sepsis of the instruments, hands or arms.

The castration of the horse is more liable to be followed by this
infection. Too often no attempt at asepsis is made, implicit trust being
placed in the defensive power of the tissues. In other cases even a very
careful local antisepsis fails, the germ being already present in the
circulation and the extensive wound and resulting local congestion and
debility are seized upon as an opportunity for colonization and growth.
This infection usually takes place from the second to the sixth day
while the inguinal canal and vaginal sheath are still open to the cavity
of the abdomen. Later when these have closed by adhesion, and when
protective granulation has formed the implication of the peritoneum is
rare.

_b._ =Rupture of the Stomach or Intestine.= This comes as already shown
from gaseous distension, overloading, sudden shock or concussion,
obstruction by dried ingesta, calculi, foreign bodies, parasites, etc.,
and by abuse of too powerful purgatives in cases of obstruction. The
resulting infection is very abundant and varied, and the microbes
accustomed to an anærobic existence in the intestines, multiply with
extreme rapidity in the peritoneum and prove rapidly fatal. Beside the
bacillus coli commune, there are usually staphylococcus and
streptococcus pyogenes and not unfrequently the bacillus of malignant
œdema.

_c._ =Perforating ulcer.= Though having a separate point of origin the
effect of this is precisely the same as in rupture, the same bacteria
escaping and the nature of the infection being identical. Inasmuch,
however, as the perforation is usually small at first and the escape of
contents very limited the symptoms advance more slowly and reach their
acme later.

_d._ =Perforation of the Parturient Womb.= This usually depends on a
case of dystokia in which the organ is torn by a foot of the fœtus or by
some ill-directed instrument. The infection has usually been carried in
on the hands or instruments, or introduced as dust by an aspiratory
movement in the intervals of labor pains. The healthy womb is usually
sterile as regards microbes, yet Lignieres claims that he has found
staphylococcus pyogenes albus and aureus and in contagious abortion the
specific bacillus of this affection can always be found. In woman
peritonitis following rupture of the womb usually shows streptococcus
pyogenes.

_e._ =Rupture of Abscess into the Peritoneum.= As an abscess is nearly
always the product of pus microbes it follows that its rupture into the
abdominal cavity will determine infection. If the abscess contains some
special infective germ like that of strangles or glanders the resulting
inflammation partakes of their nature.

_f._ =Penetration of Microbes through the Circulation.= Healthy blood is
free from germs, yet it is not uncommon to find a few circulating in the
blood in given conditions. Debility, toxin and ptomaine poisoning and
other conditions render it possible for bacteria to successfully invade
the circulating blood, hence, many infective diseases are at first
local, and later on become generalized. Under these circumstances any
cause of debility operating especially on the peritoneum opens the door
to their infection. Under such debilitating causes all those already
referred to as chills must be recognized, together with kicks, blows,
local congestions and other injuries.

_Symptoms._ The existence of a penetrating wound or sore of the abdomen,
a kick, an open abscess, or a recent exposure to severe cold when heated
and fatigued, or finally some serious affection of the abdominal organs
will give definiteness to some of the symptoms which follow. There may
have been noticed a rigor, or trembling of the muscles may still
continue. There is swelling around the external wound, which in case of
castration is usually œdematous and more or less tense, affecting the
entire sheath and extending forward on the abdomen. In any such case
there is tenderness to pressure around the margin of the wound, for a
distance that constantly increases. The animal moves stiffly and the
back is more or less arched. The temperature is raised two or three
degrees and may go on till it has reached 107. The patient becomes dull
and listless, with drooping head and ears, sunken, lustreless, pale eye,
more or less fixed, lips drawn up firmly and muscles of the face
contracted and prominent. He stands with back arched, loins insensible
to pinching, and legs drawn somewhat toward each other under the belly.
There are indications of colic, pawing, looking toward the flanks, and
shifting of the hind feet without the violent kicking motion of
spasmodic colic or intestinal congestion. When he lies down it is
comparatively slowly and carefully and he is more inclined to lie on the
side with hind legs, or at least the one on the affected side extended
backward. The rolling on the back and the sudden jerking movement of the
hind limbs, seen in spasmodic colic are rarely noticed. There are
exceptions to this rule when violent spasms or acute congestion is
present as well as in some cases following castration and with
strangulated cord.

The abdominal walls are always tense from muscular contraction, and
often also from tympany, in which case there is marked drumlike
resonance, on percussion. An elevated ridge like that seen in pleurisy
extends from the outer angle of the ilium to the lower end of the last
rib. The breathing is hurried and carried on mainly by the ribs, the
diaphragm being kept as fixed as possible. The inspirations are short
and catching as in pleurisy, the expirations a little more prolonged. In
standing the hind legs are held apart, and in moving the animal
straddles and moves them stiffly avoiding advancing them far forward.
Constipation is the rule the rectum containing a number of small, round,
dry balls, yet after a day or two diarrhœa may set in. Urine is usually
suppressed, or passed in small amount and of a high color. The pulse is
usually small, hard, and at times thready, the skin perspires more or
less generally, prostration and dullness set in and death may occur
within 24 hours or more commonly in 4 to 8 days. After the 1st day there
may be fluctuation of the abdomen from liquid effusion.

In case of infection from perforated or ruptured stomach or intestine
the symptoms are more severe from the first, and the issue is more
rapidly fatal. With marked trembling, there occur extreme weakness and
prostration, dull, sunken eyes, flaccid facial muscles, cold
perspiration, chilly ears and limbs, entire cessation of defecation,
small, weak accelerated pulse, breathing rapid, broken in inspiration or
expiration, and more or less tympany. Yet the tenderness of the abdomen
is less marked, and the animal may move with somewhat less stiffness,
and gets up and down with less apparent suffering. The temperature is
less elevated than in the external traumatism, and the whole aspect is
that of collapse and sinking. These cases may die from shock or tympany
in a few hours, or they may survive 24 or even as long as 48 hours but
rarely longer. In case of rupture of the stomach there may be the usual
feature of eructation or vomiting. Resolution may occur but non-fatal
cases are liable to become chronic with ascites.

_Diagnosis._ Apart from traumatism, the evidence of some previous
intestinal or gastric lesion, or abscess, succeeded by continuous dull
colicy pains, the arching of the back and drawing together of the limbs,
the tender abdomen, the careful decubitus and lying on the side, the
tympany, obstinate constipation, and pale conjunctiva, the pleuritic
ridge and breathing without the friction sounds or intercostal
tenderness of pleurisy, the high temperature, the weak rapid pulse and
rapidly advancing weakness, prostration and collapse furnish a
combination which is very characteristic.

_Lesions._ In rapidly fatal cases there may appear to be little more
than general peritoneal congestion and ecchymosis. In such cases,
however, there is usually a mixture of the ingesta with the intestinal
convolutions and omentum.

In cases that have survived twelve hours, false membranes are found, in
the form of fine filamentous shreds on the surface of the congested
serosa, which has become dull, opaque, and thickened. In twenty-four to
thirty hours these have increased in thickness and solidity, binding
together the convolutions of the intestines or floating free as shreds
or membranous layers in the exuded liquid. At first yellowish white,
these become gray, red, and finally white as they become organized into
fibrous tissue. They may cover any of the abdominal organs and bind
these together more or less firmly.

The liquid effusion collecting at the lower part of the abdomen, may be
blood red, serosanguinolent, or straw colored, and contains a
considerable amount of albumen, fibrine, granules and cells as well as
the bacteria. It may attain to as much as 25 or 30 quarts. When purulent
or septic the liquid is comparatively limited in amount and is usually
connected with a ruptured abscess or external wound or intestinal
perforation. The presence of alimentary matters, the fœtid odor, and
gaseous emanations are marked features in this last condition.

The intestines are usually distended with gas, and have thin walls
infiltrated, pale and thickened, and often bound to other convolutions
or to adjacent organs by false membranes. The liver and spleen are
pallid, and their capsules swollen, thick and opaque, with more or less
membranous exudate.

In case the patient survives, the effusion and neoplasm are slowly
absorbed, but the false membranes only imperfectly, and they may be
found later as organized bands attaching the intestines or other organs
to adjacent parts, and limiting their motions or constricting and
strangling them. Hence there is left a predisposition to relapse or to
other disease of the abdomen. Röll has noticed degeneration and
softening of the false membranes, which extended to the wall of the
bowel beneath and led to perforation.

_Prevention._ In solipeds especially this affection is so fatal that
every precaution should be adopted to prevent its occurrence. In this
class of animal the tendency to suppuration in wounds and inflammations
of all kinds greatly exceeds what we see in other animals. A wound that
in man will heal kindly by first intention will almost certainly
suppurate in the horse, and an abdominal wound which in man, ruminant,
or pachyderm might be viewed with confidence, must be treated as a very
serious matter in the horse. But though thus differing in degree, all
abdominal wounds must be considered as serious lesions. The peritoneal
sac is, like other serous sacs, a dependency of the great lymphatic
system of vessels, and the liquid present in it in health is, like the
lymph, the most favorable culture medium of the body for microbian life,
the greater the amount of such peritoneal fluid (as in inflammatory or
other exudate) the more favorable it becomes to its growth and
diffusion, and finally the enclosed intestine is teeming with
micro-organisms, which, though held in check by the healthy mucosa, are
ready when any congestion, inflammation or other morbid process gives
occasion, to traverse these thin walls and start their deadly career in
the peritoneum.

In every animal, therefore, but in solipeds above all, every precaution
should be taken against the infliction of accidental wounds of the
abdominal walls, and to remedy any serious derangement of the digestive
organs. Above all, operations that involve the peritoneal cavity should
be made only under careful surgical precautions. The introduction of
pyogenic, septic or potentially septic material from hands, head, beard,
floating dust, unboiled water, or surgical appliance of any kind, is a
direct bid for a fatal peritonitis. Next to this the greatest care must
be exercised to prevent unnecessary injury to the peritoneum or any
abdominal organ, which would in any way impair its vital properties and
resisting power. Again, to leave blood or exudate of any kind in the
wounded peritoneum is a direct bid for the propagation of
micro-organisms. These should be removed by means of aseptic agents.
Finally, in case of enteric disease and abdominal wounds the patient
should be guarded against chill, which would lower the vital and
resisting powers and lay the system open to microbian invasion.

_Treatment._ The therapeutics of peritonitis furnishes a striking
example of the transforming influence of bacteriological discovery.
Systematic medical and veterinary works enjoin the time-honored method
of treatment by opium to check intestinal peristalsis and the painful
friction of inflamed surfaces on each other, and to keep the organs
quiescent until nature shall have time to subdue the inflammation. The
still older treatment by calomel and opium has essentially the same
foundation. To the bacteriologist the latter has the recommendation of
being to some extent antiseptic and of tending to secure depletion from
the intestinal mucosa. Another cardinal principle of the old
practitioner was to hail the liquid exudate as tending to separate the
inflamed and painful surfaces, and as allowing them to move past each
other without aggravating the suffering and inflammation. In short, the
practitioner of the past had an especial dread of mechanical injury, and
treated all other measures as secondary to this though by no means
unessential.

Bacteriological considerations direct attention rather to the vital
properties of the causative bacteria and seek to check the disease by
checking this its most effective cause.

In simple local peritonitis, as in the infection following castration,
the washing out of the infected wound with boiled water and application
of an antiseptic (iodoform, iodoform or carbolic acid guaze), and the
free use of carbolic acid solution (1:50) to the skin is of great value.
If the sheath or inguinal region is swollen to any extent, puncturing it
at intervals with a lancet to the depth of half an inch so as to drain
it speedily and thus reduce the swelling and culture fluid, and to
restore the vitality of the parts, and the frequent bathing with the
carbolic acid lotion, will usually succeed in bringing about a healthy
action.

The question of medical treatment comes forward mainly in cases that
have invaded the abdominal peritoneum, and which are not already
completely generalized, nor the result of extensive escape of gastric
nor intestinal contents. In such forms and above all in the early stages
of surgical cases sulphate of soda given to the extent of causing free
purgation has been found to be incomparably more effective than the
opium treatment. The explanation of its action may rest in part (1) on
the expulsion from the bowel of a large proportion of the dangerous
microbes which are simply waiting for that opportunity to pass into the
peritoneum, which will be furnished by the inflammation of the
intestinal walls; (2). On the elimination from the blood and system of
much of the deleterious ptomaines and toxins which have already been
absorbed from the inflamed surface and the presence of which robs the
tissues of their vitality and resisting power; (3). On the active
depletion from the intestinal mucosa and (through the common capillary
plexus) from the congested peritoneal coat, counteracting alike the
effusion into the peritoneum which forms the culture fluid for the
invading bacteria, and the infiltration of the serous and subserous
tissues which beside tearing apart the tissue-elements, and robbing
their leucocytes of their power of phagocytosis, furnishes within the
invaded tissue itself the most favorable of culture media; and (4) on
preserving a better tone of the nervous system and, locally, of the
tissues the cells of which, can struggle more successfully against the
small body of invading bacteria advancing slowly along the surface of
the peritoneum, than with the countless myriads produced in and washed
everywhere by the abundant liquid exudate.

Along with the soda sulphate may be given antiseptics, like sodium
salicylate, or chloral hydrate. The latter serves to mitigate the pain
without checking the secretion or peristalsis.

When the suffering is very acute, opium may still be resorted to, but
preferably subcutem, in the form of morphia sulphate so as to lock up
the poisons as little as possible.

Enemata are in order to facilitate the operation of the bowels, and may
be made laxative and antiseptic. The danger of tympanitis speaks
forcibly for a judicious use of antiferments, both by the mouth and
anus.

Hot fomentations have long been in use but require persistent
application and this is often difficult to secure. Recently cold
applications to the abdomen in the form of ice or snow, or in the
absence of these of cold water applied on a light rug, kept against the
abdominal walls by elastic circingles, have been found of great service.
This can be persistently applied, as all that is requisite is to keep
the rug constantly wet.

When pus forms in the peritoneum or when extensive effusion has taken
place, it should certainly be evacuated, as it is but a centre for the
development of the deadly bacteria. It can be drawn off through the
already existing traumatic orifice, or, if necessary, a new opening can
be made by cannula and trochar, or by direct incision under suitable
antiseptic precautions. The opening having been made, and the liquid
having escaped, the peritoneum may be profitably washed out with a
normal salt solution which has been recently boiled and which is used at
near the body temperature (80° to 90°).

Blisters are sometimes of use in the advanced stages of the disease, in
stimulating resolution and reabsorption, but hot or cold applications
are preferable in the early acute stages.

Laparotomy in cases due to rupture of stomach or bowel, or of extensive
perforation, has not been attempted in solipeds, and it could hardly be
expected to succeed, yet in such cases, which are otherwise inevitably
fatal, any measure giving even a remote hope of success is allowable.

When tympany sets in it may be met by using a fine cannula and trochar,
and as soon as the gas has escaped, antiseptics like chloral hydrate,
salicylate of soda, salicylic acid, or glycerine, can be injected into
the fermenting mass by attaching a caouchouc tube and funnel to the
cannula.


                    CHRONIC PERITONITIS IN SOLIPEDS.

  Secondary: after acute, or with disease of liver, spleen, kidney,
  rheumatism, melanosis, lymphadenoma, epithelioma, carcinoma, or
  sarcoma. Gastric ulcer, infected punctures. Symptoms: poor health,
  tender abdomen, irregular bowels, slight colic, tense, fluctuating
  belly, pallid mucosæ, dropsy of sheath, limbs, etc., slight fever.
  Treatment: remove primary disease: saline laxatives, diuretics,
  drainage, antiseptic irrigation (boric acid, etc.), abdominal bandage,
  tonics, derivatives.

_Causes._ Chronic peritonitis is always a secondary disease, succeeding
the acute, or dependent on some other affection of the abdominal organs,
as chronic congestion of the liver, or spleen, Bright’s disease,
rheumatism, melanosis, lymphadenoma, epithelioma, carcinoma, or sarcoma.
Tuberculosis and actinomycosis, so common in cattle, are rare in
solipeds. Chronic ulcers of stomach or bowels and injuries and
infections from punctures are exceptional causes.

_Symptoms._ The manifestations of the disease are indefinite, the acute
form may have subsided so that the patient is supposed to have
completely recovered, a moderate appetite and a certain capacity for
work may be present, yet he is easily fatigued, there is some tenderness
of the abdomen to pressure, some irregularity of the bowels—constipation
and diarrhœa alternating—and occasional slight colics. Some weeks later
may be noticed abdominal tension and tympany, with perhaps fluctuation
in the lower parts, increasing pallor of the mucosæ, and œdematous
swelling of the sheath, mammæ, abdominal walls or hind limbs. To detect
fluctuation it is sometimes necessary to introduce one hand into the
rectum. When present hyperthermia is slight, but assists in diagnosis
from ascites.

_Treatment_ should be directed to the primary disease. As that is too
often irremediable the peritonitis will resist all other treatment.

In cases that supervene on the acute form, paracentesis, saline
laxatives and diuretics with antiseptics, tonics, and counter-irritants
will sometimes succeed. As in the acute form of the disease the removal
of the effusion is the removal of the culture fluid, and may be followed
by irrigation of the peritoneum with a normal salt solution, or with an
antiseptic solution (boric acid or potassium permanganate), 1:20 warm
water; Aluminum acetate, 1:2000. Sulphate of soda given to keep up a
moderately laxative action, tends to counteract the contraction of the
intestine by false membranes, and operates with diuretics in reducing
the tendency to exudation or in causing its reabsorption. After removal
of the liquid, support by a close (or elastic) abdominal bandage is
often of value in preventing further effusion. As tonics, gentian, nux
vomica and the iron salts may be profitably employed, and as antiseptics
salicylate of soda and iodide of potassium. As counter-irritants mustard
and cantharides may be named.




                       PERITONITIS IN RUMINANTS.

  Causes: infection, chill, blows, wounds, debility, ill health,
  Chauveau’s experiment with castration, dystokia, abdominal congestion
  and inflammation, bile or urine in absence of sepsis, gastric or
  intestinal ulcer or perforation, foreign bodies, abscesses, surgical
  wounds. Spoilt marc of beet sugar factories. Symptoms: fever,
  stiffness, dragging hind limbs, knuckling, arched back, shifting feet,
  moving tail, tense belly, pendent, fluctuating below, friction sounds,
  diarrhœa, later constipation, weakness, emaciation, death fourth to
  twentieth day. Recovery, often partial. After dystokia putrid vaginal
  discharge, and nervous depression, resembling parturition fever.
  Infection in ewes through shepherd’s hands, œdematous swellings of
  vulva, perineum and abdomen. Lesions: as in solipeds, with abundant
  false membranes, fœtid pus metritis, with putrid contents of womb.
  Treatment: saline laxatives, diuretics, demulcents, enemata, morphia,
  antiseptics, cold to abdomen. After dystokia, antiseptic irrigation of
  womb, elevation of head, with ice, strychnia, acetanilid. Tubercular
  peritonitis.


_Causes._ As in solipeds infection of the peritoneum and the increase of
susceptibility by exposure to cold, blows, wounds, poor feeding or
stabling, disease and other causes of ill health, operate together in
inducing peritonitis.

The effect of debility or predisposition of the tissues is well shown in
Chauveau’s experiments with _bistournage_ in rams. Healthy rams
subjected to bistournage showed no infection, and rams subjected to
intravenous injection of pus microbes without _bistournage_ showed no
infection, whereas if the rams were first subjected to injection of pus
microbes, and then to _bistournage_, peritonitis set in. In the same way
chills occurring after dystokia, when the womb is charged with microbes
and more or less congested, may determine peritonitis, and congestions,
impactions, tympanies, and other injuries of the gastro-intestinal
viscera coöperate with cold to the same end. Rupture of the gall or
urinary bladder does not usually cause prompt peritonitis, yet it
irritates the serosa and lays it open to infection if the germs should
reach it through the circulation. Otherwise the animal suffers only from
uræmia or biliary poisoning and may survive one or two weeks. Ruptures
of stomach or intestine, or ulceration or the perforation of their walls
by hard, pointed or other metallic bodies are causes of peritonitis. The
rupture of abscesses into the peritoneum and the escape of germs from
the womb in case of rupture of the womb in difficult parturition, or in
metritis, are additional causes. Surgical wounds as in castration of the
male or female, and punctures and incisions of the rumen are occasional
causes, but there is by no means the tendency to extension of such
peritonitis that we see in solipeds. The self-protective power of the
tissues is incomparably greater in the ruminant.

Nocard, Butel and others have recorded a gastro-entero-peritonitis of
septic nature, occurring in cattle and above all in sheep, fed on the
fermented refuse of beet sugar factories, which had been kept in silos
through the winter. On the third and fourth days of this feeding many
were attacked.

_Symptoms._ Beside the general systemic disorder and a very variable
amount of hyperthermia (102° to 107°), there are the special indications
of abdominal inflammation, stiff movement and dragging of the hind
limbs, or if standing the back is arched, the head drooping and the legs
drawn together and slightly bent, with uneasy shifting of the hind feet,
and lateral movements of the tail. The walls of the abdomen are usually
tense, often bulging laterally below, though fallen in beneath the
lumbar transverse processes (pot-bellied); they are tender to pressure,
and may be drum like to percussion above, while flat, dull, and
fluctuating below. The tenderness is slightest below, where liquid
effusion has settled, but is quite marked in the upper and resonant
parts, where pressure will cause wincing and trembling. In this upper
part on the left side may be heard friction sounds after the fourth or
sixth day. This is especially observable in tuberculous peritonitis over
the parts covered by tubercular growths. There may be at first diarrhœa
which usually soon gives place to constipation, and weakness and
emaciation advances rapidly, and death may take place from the fourth to
eighth day, or may be deferred for some weeks.

In favorable cases the acute symptoms subside, the liquid effusion is
absorbed, appetite and rumination are in great part restored, and a
partial recovery is made. It is, however, very liable to merge into the
chronic form, and inevitably so in tuberculous cases.

In cases following on difficult parturition there are redness of the
vaginal mucosa, with mucopurulent or putrid discharges, and swelling of
the lower part of the abdomen, with liquid effusion and fluctuation, and
tenderness of the right flank. The further symptoms are largely nervous,
approximating somewhat to those of parturition fever. Temperature may
rise to 104° or 106°, blindness, stupor, incoördination of muscular
movement, staggering gait, if down she may lie on the side or sternum
unable to rise, has frequent afterpains, tympany, sour eructations, and
grinding of the teeth. The case may culminate in loss of vision, in
stupor and coma, or improvement may set in and go on to a rapid
recovery. This is a more common affection in ewes than in cows and is
very destructive, the infection being carried by the hands of the
shepherd. The most fatal cases are those in which the infection becomes
generalized, and œdematous swellings appear round the vulva, between the
thighs and beneath the abdomen.

In traumatic cases the external wounds can usually be found with active
inflammation and surrounding tumefaction.

_Lesions._ The peritoneum, as in solipeds, shows the symptoms of
congestion, exudation of a fine fibrinous network or shreds, of thicker
and more extended false membranes in patches, of effusions more or less
sanguineous, of formation of pus, usually fœtid, or the presence of
decomposing ingesta which has escaped through a lesion of stomach or
bowels. The peritoneal and subserous tissue are infiltrated with liquid,
and the other gastric and intestinal organs are more or less tympanitic,
and the mucosa of the latter is thickened, ecchymosed, or eroded, with
black, fœtid bloodstained contents. In parturient cases, the uterine
mucosa is congested, reddened and softened, the cotyledons swollen,
perhaps gangrenous, and the membranes, if still present, float in a
dark, putrid offensive liquid.

_Treatment._ As in the horse, morphia has been used to relieve pain and
check peristalsis. The addition of saline laxatives, and diuretics, will
assist in elimination and depletion, and in the removal of intestinal
bacteria which become a source of danger. A laxative dose should be
followed by frequent drinks of pure water or mucilaginous liquids, and
sulphate of soda may also be given freely in enema. As diuretics,
saltpeter or digitalis may be resorted to. Antiferments (salicylate of
soda, bisulphite of soda) should not be forgotten nor cold applications
to the abdomen. When effusion or suppuration has taken place evacuation
by puncture may be followed by antiseptic irrigation.

If with septic metritis, antiseptic injections of the vagina and womb
are the first consideration. With boiled water at a tepid heat the womb
should be thoroughly washed out, followed by a solution of mercuric
chloride (1:2000), or permanganate of potash (1:1000), or boric acid
(1:25) until the liquid returns clear and odorless. This may be repeated
several times a day. The symptoms of brain congestion, may be met by
tying, or packing up the patient with straw so that the head will be
somewhat elevated, and bags of ice or snow, or simple cold water may be
kept applied to the upper part of the head and neck. When there is no
great nervous excitement the nervous functions may be roused by nux
vomica in enema, or strychnia subcutem. If on the other hand the
temperature runs very high acetanilid may be tried with caution, or
resort may be had to wet compresses.

In case of perforation or rupture, if the animal cannot be at once
sacrificed for beef or mutton before inflammation has set in, the only
hope lies in laparotomy, followed by the cleansing, disinfection and
suturing of the wound.

In tubercular peritonitis which constitutes a very large proportion of
bovine cases, treatment is undesirable, and the animal is unfit for
consumption.


                       PERITONITIS IN CARNIVORA.

  Causes: gastro-intestinal inflammations, metritis, trauma to walls of
  abdomen, pyæmia, septicæmia, tuberculosis, cancer, tumors, parasites.
  Symptoms: dullness, hiding away, movements tardy, painful, arched
  back, retracted abdomen, tense and tender, drags hind limbs, vomits,
  yawns, bloats, hopeless look, snappish, death in 2 to 8 days.
  Treatment: anodynes, saline laxatives by mouth and rectum, damp
  compress, warm bath, antiseptics, diuretics, in effusion, puncture,
  antiseptic irrigation, laparotomy.

_Causes._ All inflammatory and other serious affections of the stomach
and bowels may be associated with peritonitis. Metritis and injuries to
the womb, and all injuries to the walls of the abdomen (kicks, blows,
penetrating and castration wounds), may have a similar complication.
Pyæmia and septicæmia may also have localization in the peritoneum. It
must be borne in mind, however, that purulent and septic infection are
less likely to occur in the dog than in cattle, the leucocytes of the
dog having much more resisting power. On the other hand the dog, and,
still more so, the cat has a fair measure of susceptibility to
tuberculosis, cancer and various forms of tumors, which show a strong
tendency to localization in the abdomen. Parasites also penetrate and
irritate the peritoneum.

_Symptoms._ The animal becomes dull, retiring, and inclined to lie in a
quiet place, though his suffering may lead to frequent change of bed, he
moves slowly, painfully, with arched back, retracted abdomen, and
drooping head, and dragging his hind limbs stiffly. The abdomen is tense
and firm, hot and very tender, drawing forth whines and yelps when it is
handled. There are hyperthermia (104°), small, weak, accelerated pulse,
hurried, catching breathing, vomiting, yawning, tympany and
constipation. The face has a hopeless, stupid look and the eyes are
sunken and at times glazed. Some patients become ill natured and
snappish. The animal gradually sinks into a condition of prostration and
finally of collapse and dies in two to eight days.

_Treatment_ does not differ materially from that given for larger
animals. Pain may be moderated by belladonna, hyoscyamus, chloral, or
even opium, while the sulphate of soda is employed by both mouth and
rectum. The abdomen may be enveloped in a damp compress, or a warm bath
may be given. Diuretics will be in order and above all antiferments, the
latter by enema as well. Distension of the abdomen with fluid may be
relieved by puncture, followed by antiseptic irrigation. If there is
good ground to suspect a gastric or intestinal lesion or tumors,
laparotomy is a much more hopeful resort than in the larger animals.




                         PERITONITIS IN BIRDS.

  From caponizing, accidental traumas, ruptured oviduct, perforations of
  bowels by foreign bodies or worms, pyogenic susceptibility slight.
  Symptoms: inappetence, drooping head, wings, tail, erect plumage,
  stiffness, straining, tense, tender, pendent belly. Treatment: unload
  cloaca, puncture and irrigate abdomen, laxatives. Prophylaxis, by
  laxative food, expulsion of worms, antisepsis in operations, unloading
  cloaca, etc.


_Causes._ Male birds contract peritonitis from caponizing, and other
penetrating wounds of the abdomen, from rupture of the oviduct impacted
with egg matter, from perforations of the intestines by foreign bodies,
and from perforations by worms.

The danger from ordinary pyogenic germs is, however, at its minimum,
since birds stand at the opposite extreme from the horse, and their
wounds rarely suppurate.

_Symptoms._ The bird loses appetite, droops head, wings and tail,
ruffles its feathers, walks stiffly and heavily, and expels fæces with
much effort and even with cries. When caught the abdomen is found to be
full, tense and pendent and very tender to the touch. There is more or
less hyperthermia (108° and upward), and the subject becomes more and
more dull, stupid and feeble until death.

_Treatment._ In certain cases relief may be had by the unloading of the
cloaca, or the evacuation of peritoneal fluid, followed by antiseptic,
irrigation of the cavity. Laxatives may also be resorted to. The most
important measures are however prophylactic, and run in the direction of
careful manipulation and antisepsis in caponizing, the unloading of
impacted cloaca, before it has developed serious disease, the
maintenance of a suitably laxative diet, and the prevention and
treatment of worms. In case of tumors causing chronic peritonitis,
laparotomy can be resorted to with great confidence.




                          ASCITES IN SOLIPEDS.

  Causes: follows peritonitis, obstruction of portal vein, tumors,
  hepatic diseases, pressure on posterior cava, dilated right heart,
  heaves, ovarian disease, nephritis or kidney degeneration, hydroæmia.
  Symptoms: slow advance, pot-bellied, with fluctuation, hollow above,
  dropsy in limbs, sheath and under belly, percussion sound flat below,
  weakness, debility, no fever. Diagnosis: Absence of fever, and of
  fibrine, cells and granules in effusion. Lesions: those of primary
  disease, amount and composition of effusion. Treatment: treat primary
  disease glandular swelling or actinomycosis, iodide of potassium,
  remove diseased ovary or tumor, draw off fluid, compress abdomen,
  saline laxatives, diuretics, iodides, pilocarpin, electricity,
  bitters.


_Causes._ Ascites may be a remnant of a pre-existing chronic
peritonitis, or it may occur from any obstruction of the portal
vein, such as compression by organized false membranes, thrombus, in
the vessel, or pressure by lympadenoma in the portal fissure,
melanosis, sarcoma and other tumors. It results from cirrhosis and
other diseases of the liver which retard its circulation, from
pressure on the posterior vena cava, from insufficiency of the right
auriculo-ventricular valves, from dilatation of the right heart, and
from heaves or other obstruction in the pulmonic circulation. Other
causes are cystic or other disease of the ovary, diseases of the
kidney and hydroæmia, the latter two tending to general œdema as
well as ascites.

_Symptoms._ The disease comes on slowly and insidiously and at first it
usually passes unnoticed. When more fully developed the abdomen is
distended but somewhat pendent (pot-bellied), fluctuating below, with
falling in beneath the lumbar transverse processes. Later the whole
abdomen may be full, rounded, smooth and tense, and the hind limbs
œdematous to above the fetlocks or hocks. There may be œdema of the
sheath or lower wall of the abdomen. Fluctuation can still be felt as a
shock when an assistant makes sudden concussion with the fist on the
opposite side from that on which the hand is pressed. This may be felt
even more distinctly by the hand introduced into the rectum. Percussion
gives a flat sound below and more or less resonant above. The pulse is
small, weak, and accelerated, heart beats irritable (sometimes
palpitating), and respiration labored and with lifting of the flank.
From first to last there is no hyperthermia.

If the cause is irremediable the issue is necessarily fatal sooner or
later.

_Diagnosis_ from peritonitis depends largely on the absence of
hyperthermia, and of abdominal tenderness, and on the nature of the
ascitic fluid which is incoagulable, and comparatively destitute of
leucocytes cells and granules.

_Lesions._ The quantity of effused liquid is often enormous (50 qts.
Reynal, 80 qts. Woodger, 150 qts. Friedberger and Fröhner). It is very
watery and poor in salts and albuminoids, of a density near 1012,
neutral or slightly alkaline, does not coagulate spontaneously, and is
not associated with false membranes. The peritoneum shows no congestion,
but is pale, and, like the abdominal walls, infiltrated. Tumors, cysts
and venous obstructions referred to under causes may be found.

_Treatment._ When ascites depends on actinomycosis or glandular
enlargement a course of iodide of potassium may remove the cause. In
other cases an operation may remove the offending tumor or ovary. Too
often, however, the cause is beyond remedy and palliative treatment only
is available. The most urgent indication is the removal of the
accumulated fluid, and paracentesis under proper antiseptic precautions
is the readiest means to this end. Compression by a tight bandage is
necessary to prevent the sensation of vacuity and tendency to fainting
which come from the removal of the fluid and to counteract the
disposition to the instant effusion of more. Even with the compress it
is judicious not to draw off all of the fluid at once in bad cases, but
to make two or three operations and allow the patient to become
accustomed to the change in the intervals. These may be repeated as
circumstances demand. Saline purgatives, or diuretics (saltpetre 1 oz.,
digitalis 25 grs., squill 3 ozs., iodide of potassium 2 drs.), are
useful, and pilocarpin is the most efficient agent of this kind, but
also dangerous by reason of the extreme depletion which it causes.
Electricity has been employed with alleged advantage, also poultices of
digitalis applied over the loins.

Cholagogues are also recommended especially in cases of liver disease.
Bitters may prove useful.




                         ASCITES IN RUMINANTS.

  Causes: as in horse, tuberculosis, in sheep distomatosis, chills when
  heated and fatigued. Symptoms: pot-belly, fluctuating on percussion,
  gives flat sound, debility, pallid mucosæ, sunken eyes, superficial
  dropsies on belly, in limbs, and under jaw, in distomatosis, great
  emaciation, weakness, paperskin, ova of distoma in fæces. Diagnosis:
  from ruptured bladder by passage of urine, and perhaps by sex, and
  absence of urinous odor in liquid, from hydrometra by fluctuation over
  whole belly. Lesions: those of solipeds, also tubercles or enlarged
  gall ducts with distomata. Treatment: as for solipeds. Tuberculosis
  demands separation or destruction, distomatosis, prevention.


_Causes._ These are in the main those which operate in the horse and
need not be repeated. In cattle, however, the affection is to a large
extent the result of abdominal tuberculosis, while in sheep it is a
constant result of advanced distomatosis. Gellé says it is common in
working oxen, which are turned out, hot and perspiring, to pass the
night in cold and wet.

_Symptoms._ The belly is enlarged and pendent, bulging out back of the
ribs, with fluctuation and dullness on percussion. The animal is in very
low condition, the mucosæ pale or yellowish white, the eyes dull and
sunken, panting and palpitations may be roused on the least exertion,
and swellings often appear along the lower aspect of the body and
between the branches of the lower jaw. In distomatosis it is common to
find dropsy of the chest, pallor and attenuation of the skin, complete
absence of the subcutaneous fat (paperskin), and great emaciation and
weakness. Ova of the distoma can be found in the fæces. (See
distomatosis). By turning the sheep on its back or setting it up on its
croup the percussion dullness will be made to shift, always to the
dependent part of the abdomen.

_Diagnosis._ From rupture of the bladder it is distinguished, by its
occurrence in females as well as males, by the absence of fever, and of
the complete suppression of urine and emptiness and tenderness of the
bladder which characterize the latter. Liquid drawn from the abdomen has
no urinous odor. From hydrometra, pyometra, and hydramnios it is
distinguished by the fact that the water accumulates in the lower part
of the abdomen, and is not confined to the womb. On rectal exploration
the outline of the empty womb is made out.

_Lesions._ Besides the lesions described for solipeds, one finds in
cattle, tuberculosis of the liver, spleen, and lymph glands, and
extensive clusters of tubercles on the peritoneum. In sheep the white
branching lines on the back of the liver may indicate the distension of
gall ducts infested by distomata.

_Treatment_ does not differ from that recommended for solipeds. In
tuberculous cases, sanitary considerations demand the destruction of the
animal and disinfection of the carcass. In distomatosis treatment must
be preventive, as the distomata are difficult to reach with vermifuges.


                         ASCITES IN CARNIVORA.

  Causes: obstructed flow of blood in hepatic, portal or renal veins, or
  in vena cava, renal, heart, liver or splenic diseases, pulmonary
  congestion, asthma, tuberculosis. Symptoms: pot-belly, hollow above,
  drooping back and loins, flat percussion sound and fluctuation, change
  of position changes area of flatness, anæmia, debility, scanty urine,
  diarrhœa, no fever. Diagnosis: absence of fever, general fluctuation
  changing its seat by turning the patient, not confined to a given
  organ like the bladder or womb. Lesions: quantity and composition of
  liquid, lesions of primary diseases. Treatment: Correct if possible
  the primary disease, evacuate the liquid, compress on abdomen, iodine
  solution for irrigation, saline purgatives, diuretics, pilocarpine,
  bitters, iron, sunshine.

_Causes._ Ascites is generally the result of some obstruction to the
return of blood from some abdominal organ, but may also come from renal
disease, or hydroæmia in which general dropsy is likely to occur. The
dog is specially subject to heart disease, and disease of the right
heart (tricuspid insufficiency, dilatation, hydro-pericarditis, fatty
degeneration, etc.) throws the blood back on the whole venous system and
the extensive and dilatable portal veins are especially liable to
suffer. Diseases of the liver, so common in pampered house dogs, still
more directly block the portal circulation and induce ascites. Tumors in
the liver or spleen or in the lymph glands of the porta act in this way,
also cirrhosis, tuberculosis, cancer, hepatic congestion, and
degeneration. Constrictions of the vena portæ by false membranes the
result of former peritonitis must also be recognized. As more distant
causes, must be named obstruction to the pulmonary circulation, as in
congestion, asthma, tuberculosis and diseases of the left heart.
Seventy-eight cases were traced as follows: to diseases of the heart and
pericardium, 10; to tuberculosis, 8; to pleurisy, 4; to malignant tumors
of the liver and lung, 2; to hepatic disease without heart lesion, 3; to
cancer of the liver, 1; (Cadiot).

_Symptoms._ Enlargement of the belly is marked and peculiar, the liquid
accumulating below, pushing outward the lower ends of the ribs, and
making the lower part of the abdomen baggy while the upper part, under
the lumbar transverse processes, is flattened or hollow. The back and
loins droop forming a concavity superiorly, so that the belly may almost
drag on the ground. On palpation this pendent abdominal sac gives the
sensation of a mobile fluid without the usual firm outlines of the
intestinal masses, and when percussed it gives out a flat, dull sound
and produces a fluctuation or shock at the opposite side of the abdomen.
In the upper part of the abdomen over the hollow flank more or less
resonance is found. If the animal is made to stand on his hind limbs the
saccular dilatation and flatness on percussion are in the region
adjoining the pelvis; if held up by its hind limbs they are transferred
to the epigastric and hypochondriac regions and the respiration is
seriously interfered with; if turned upon his back, the resonance is
obtained on the linea alba and at each side, while the percussion
dullness is next to the vertebræ. The clearness of the fluctuation is in
ratio with the amount of liquid present.

As in other animals, there are anæmia, pale mucosæ, poor condition,
thin, dry, unhealthy skin, weak pulse, irritable heart and interference
with respiration proportionate to the amount of liquid. The urine is
scanty, and there may be diarrhœa.

_Diagnosis._ From advanced or chronic peritonitis it is distinguished by
the history or evidence of diseased liver, heart, or kidney, the absence
of hyperthermia or abdominal tenderness, and the absence in the ascitic
fluid, extracted with a hypodermic needle, of blood globules, or
leucocytes in numbers, of false membranes, of excess of salts, or of a
tendency to coagulate firmly.

From overdistended bladder it is diagnosed by its slow, and gradual
development, and the change of fluctuation to the most dependent part no
matter what position is given to the patient, whereas the tense bladder
can be felt through the abdominal walls, extending forward from the
pelvis under all circumstances.

From ruptured bladder there is the same distinguishing feature of slow
development, the absence of symptoms of uræmic poisoning, of tenderness
of the bladder, and of suppression of urine, and also of the urinous
odor in the ascitic liquid obtained with the hypodermic needle.

From advanced gestation the differentiation is found in the general
diffusion of the swelling and fluctuation, which is not confined as in
gestation to the mobile uterine horns, with a series of enlargements
each containing a solid nodular fœtus.

From hydrometra and pyometra there are the same pathognomonic
differential features of the general diffusion of the swelling among the
intestines, and its accumulation in one fluctuating mass at the most
dependent part of the abdomen.

Tympany of the bowels causes uniform drumlike resonance, and the
swelling does not sag and fluctuate in the lower part of the abdomen.

Abdominal obesity in old dogs gives the rounded swollen abdomen, but
there is an entire absence of the pendulous and fluctuating features,
and when punctured with the hypodermic needle it furnishes no fluid.

From tuberculosis it is distinguished by the absence of nasal discharge,
or of tubercle bacilli in such discharge, or in the ascitic fluid, and
the latter inoculated on guinea pigs or rabbits does not cause
tuberculosis. The tuberculin test may also be resorted to.

_Lesions._ The liquid exudate has been found to amount to 30 or 40
quarts in large dogs (Hordt). It is often clear and translucent, of
amber tint, though in some cases it is slightly opaque, or reddish
yellow. It may remain fluid after extraction or again it may form a
loose jelly. It may be red in case of soft tumors or other neoplasms.
The liquid is very watery but may contain a considerable amount of fatty
globules or granules, and a few epithelial cells and leucocytes. The
peritoneum is pale or in advanced cases dull white from fatty
degeneration of the epithelium.

_Treatment._ The first consideration is the removal of the cause. If
this is a mere vicious action of the peritoneum, or the presence of a
thrombus, or of operable tumor, or even of curable disease of the liver
or kidneys, success may be hoped for, while in dilatation of the heart,
insufficiency of the cardiac valves, irremediable disease of the lungs,
liver or kidney, or malignant or inoperable tumor no such result can be
hoped for.

Apart from the removal of the cause the first indication is to evacuate
the liquid and this may be done with a large hypodermic needle or small
cannula and trochar inserted by preference on or near the linea alba
while the animal is in a standing position. Skin and instrument should
be rendered thoroughly aseptic, and a bandage should be wrapped round
the abdomen and gradually tightened as the liquid escapes. This to a
large extent obviates the tendency to faint, or to cerebral anæmia which
has caused sudden death in a number of cases. It also to some extent
counteracts the sudden effusion of blood in the abdomen, which is at
times determined by the sense of vacuity.

Injection of a solution of iodine (tincture of iodine 1 pt., iodide of
potassium 1 pt., boiled water 20 pts.) has been employed sometimes with
success, but in other cases it has roused a fatal inflammation. It is
best adapted to a simple morbid, relaxed state of the peritoneum.

Saline purgatives (sulphate of soda or magnesia) are especially useful
in constipated cases and should be pushed in continuous action, as far
as the strength of the animal will warrant. By depletion from the portal
system they oppose the tendency to mechanical transudation, while by
rendering the portal blood more dense they strongly solicit endosmosis
from the adjacent peritoneum.

Diuretics have been used extensively and with benefit. They may prove
injurious in a kidney that is already the seat of irritation and yet
after all be the least of two evils. In some cases instead, the
resulting dilution of a dense and irritating urine is directly soothing
to the tender kidney. Saltpeter (10 to 15 grs.), acetate of soda (15 to
30 grs.), squills (1 to 2 scr.), may be repeated so as to keep up a free
action. Pilocarpine (subcutem) (¹⁄₁₀₆ to ¹⁄₃₀ gr. daily), has removed
the ascitic fluid in 14 days (Zahn), but its action is always to be
dreaded in a weak system, or with a diseased heart, or lungs.

A supporting bandage on the abdomen is always useful as counteracting
the tendency to vacuity and further transudation.

A course of bitters and iron, and a supporting diet, and out door life
(sunshine) are important elements in treatment.


                         DISEASES OF THE LIVER.

In veterinary and medical works the diseases of the liver have been
accorded a minor place, ill in keeping with the great physiological
importance of the organ. If the function of the liver were circumscribed
by the mere secretion of bile there would be some excuse for the
apparent neglect, as the gland is so deeply situated and so much
enveloped in surrounding organs that physical exploration is difficult
and somewhat unsatisfactory, and the one symptom of jaundice was long
relied on as indicating hepatic disorder.

Taking into account all the varied functions of the liver we realize the
wide-reaching nature of its physiological influence and the extensive
and varied effect of its disorders. We can also deduce, with greater or
lesser certainty, the existence of hepatic disorders from the morbid
conditions of the blood or of organs, the functions of which are
inter-dependent with those of the liver. To elucidate the subject it is
well to trace some of the most prominent functions of the liver; the
following considerations are submitted.




                      SANGUIFICATION IN THE LIVER.

  Glycogenic function. Glycogen derived through glucose and laevulose
  from starch, glycerine, milk and cane sugars. Less from proteids.
  Peptones as a source. Its use in cell growth and heat production, in
  white blood cells, in contracting muscle, becoming lactic acid. Excess
  dissolves red globules, setting free hæmoglobin. Ammonia carbonate and
  asparagin increases it. Arsenic, phosphorus or antimony arrests
  glycogenesis. Liver increases leucocytes, and reduces size of red
  globules. Reduction of proteids. Fibrine formers reduced, urea formed;
  liver inactivity means less of soluble urea, and more of less soluble
  and more dangerous products. Urea increases with hepatic circulation.
  Hepatic disorder and suppression of urine dangerous. Red globules
  probably destroyed. Bile: Amount, uses, oil solvent, helps endosmosis,
  deodorant, stimulates glycogenesis, excretory. Source of bile
  pigments, tests. Bile acids, dissolve blood globules, antiseptic,
  tests. Bile increased by; bile absorbed from bowel, olive oil, salol,
  salicylates, benzoic acid and benzoates, turpentine, terpene,
  terpinol, euonymus, alkalies, arsenic, ether. Agents lessening biliary
  secretion, starvation, excess of fat, alkaline iodides, atropia,
  strychnia, hepatic diseases, septic duodenal fermentation. Arrest in
  liver of copper, iron, iodides, bromides, nicotine, quinine, morphia,
  curare, toxic bile products, ptomaines, toxins. Reduces toxicity of
  peptones, casein, ammonia salts, indol, phenol.


The liver is the goal to which most of the products of gastric and
intestinal digestion are carried by the portal vein. In the hepatic
cells large quantities of _glycogen_, 6 (C_{6}H_{10}O_{5}) + H_{2}O, are
stored up after each meal. This is believed to be derived largely from
the transformation of glucose, (C_{6}H_{12}O_{6}) and laevulose
(C_{6}H_{12}O_{6}) which have been produced from starch in the
alimentary canal and conveyed by the portal vein to the liver. By the
liberal use of starch, glycerine, or the sugars of milk, fruit or cane,
(but not mannite, or glycol, or inosite) the glycogen is very greatly
increased (to 12 per cent. in the fowl), but it is diminished on a
purely albuminous diet. Yet it can be produced from albuminous food, as
it is always increased in the dog after a meal of flesh, and is largely
present in the livers of carnivorous animals that have been fed for a
month on flesh only (Landois). The peptones are therefore decomposed in
the liver with the production of glycogen and such waste products as
leucin and tyrosin, which are finally resolved into urea. A purely fatty
diet diminishes it enormously and during prolonged abstinence it
practically disappears. It passes, not into the bile, but into the
hepatic veins, and the general circulation, where it serves in its
decomposition to generate heat, and probably to hasten cell growth. In
the vegetable and animal world, in the germinating seed, and in
cartilage, muscle and epidermis of the fœtus and in the amnios, glycogen
and glucose are found in abundance. The liver, too, the great center for
the production of glycogen, is relatively much larger in the young and
growing animal, and also in the adult animal which has great power of
assimilation.

Glycogen is always present in the white blood globules so long as they
maintain their vitality and amœboid movements, but when they die, it is
replaced by sugar (Hoppe-Seyler). The red blood globules give up a
ferment which rapidly transforms glycogen into sugar.

Glycogen and sugar are evidently of use in muscular contraction as they
are always diminished in the vessels of contracting muscles (Sanderson),
being converted into lactic acid (Bernard).

Forced muscular movements soon expel glycogen from the dog’s liver,
passing it into the blood, and there the excess of glycogen dissolves
the red blood globules. If glycogen is injected into the blood,
achrodextrin and hæmaglobin appear in the urine (Landois).

Ammonia carbonate and asparagin, or glycin, with a carbhydrate diet
produced in rabbits a considerable increase of glycogen (Rohmann).

Poisoning by arsenic, phosphorus or antimony destroys the glycogenic
function of the liver, which then fails to respond even to diabetic
puncture of the medulla.

There are important changes effected in the blood globules in passing
through the liver. The _leucocytes_ are increased, the hepatic veins
containing 5 or even 10 times as many as the portal vein (Bernard,
Lehmann, McDonald). Their ratio to the red globules is in the portal
vein 1:524 and in the hepatic veins 1:136 (Hirt). The _red globules_
undergo marked changes, having, in the hepatic veins, a smaller size,
sharper outlines, less flattening in the disc, a habit of massing
together irregularly in place of adhering in rouleaux, and they dissolve
less readily in water.




                       REDUCTION OF ALBUMINOIDS.


A large proportion of the fibrine formers are changed in passing through
the liver (Lehmann, Bernard), in man as much as 2,690 grammes daily
(Brown Sequard), a fact which goes to account for the increase of
fibrine in inflammation when the liver is inactive. The change consists
mainly in deoxidation and reduction into simpler compounds which can be
more readily dissolved and eliminated. Arrest of the liver functions in
fever is therefore liable to throw into the blood, products that are
little soluble and often poisonous. The end product is largely urea, and
this Cyon always found in excess in the hepatic veins of dogs (in the
portal veins 0.08 grammes, and in the hepatic veins 0.14 to 0.17
grammes). In man hepatic disorder is at once marked by the lessening or
disappearance of urea from the urine, and the increase of the less
oxidized uric acid (Parkes). In acute atrophy of the liver, urea
disappears from the urine, being replaced by the less oxidized leucin
and tyrosin (Frerichs, Murchison). In birds urea is replaced by uric
acid and this is always found in the liver.

The increase of urea and allied products bears a direct relation to the
activity of the hepatic circulation. Stimulation of the liver by
electric current sent through the abdominal walls largely increased the
secretion of urea (Sigrist, Stolnikow, Schröder and Salomon). Murchison,
Perrin and Bruardel had a great increase of urea by stimulating the
circulation in the liver. Certain agents ingested are transformed into
urea, among which may be named glycocolle, brucin, asparagin, sarcine,
alanine, and ammonia muriate.

Any degeneration of the hepatic cells which impairs or arrests their
functions lessens the production of urea. In fevers therefore and in
hepatic degenerations the extent of the functional or structural
derangement may be to a large extent gauged by the diminution of urea. A
simple hyperæmia, without as yet any serious impairment of structure or
function, may be attended by a marked increase of urea, whereas any
destruction of the liver cells, or any serious modification which
interferes with the normal function, brings about a decided decrease. A
hepatic disorder accompanied by suppression of urine is always a grave
disorder. On the contrary a free secretion of urine during liver disease
is a favorable symptom.

There is reason to believe that red blood globules are destroyed in the
healthy liver, producing bilirubin and urea (Landois). In diseased
states this becomes excessive, and the resulting coloring matter is
often modified, giving the strong tints, seen in the urine in fever and
certain hepatic disorders.


                           SECRETION OF BILE.

The secretion of bile is but a small part of the function of the liver,
and that is by no means a purely eliminating process. Man secretes in
twenty-four hours about 10 parts per 1,000 of body weight, the dog 14 to
15, the cat 15 to 20, the sheep 25, the rabbit 130, the Guinea-pig 170,
the goose 12 (Cadeac), the horse 12 (Colin). But the amount varies
largely; Scott found that a dog yielded 21, and Kölliker that another
yielded 36 per 1,000 of the body weight.

Only about one-fourth of the biliary acids (Bischoff, Voigt), and
one-eighth of the sulphur (Bidder and Schmidt) of the bile can be found
in the fæces. Most of the bile is re-absorbed from the intestine and
secreted anew, so that, in the course of twenty-four hours, the material
secreted serves the same purpose again and again. During this repetition
of secretion and absorption, it becomes little by little metamorphosed
into other products, which are eliminated by the lungs and kidneys
(Parkes, Murchison).

The functions of the bile so far as known are:

_a._ The solution of alimentary matters, and especially of fat, in the
intestine, and the hastening of endosmosis, of fats and peptones;

_b._ The stimulation of peristalsis in the bowel;

_c._ Antisepsis and deodorization of the contents of the bowels;

_d._ The determination of the formation of glycogen;

_e._ The excretion of bile coloring matter, bile acids and cholesterine.

In regard to the glycogenic action it may be said that in cats, the bile
ducts of which have been tied, no glycogen was formed, even when the
diabetic puncture of the brain was made (Legg). Clinical observation
seems to throw some doubt on the formation of bile coloring matter apart
from the liver. In diseased liver with suspended secretion of bile (waxy
and fatty degeneration, cancer, cirrhosis) the bile pigment was found in
neither blood nor urine (Frerichs, Murchison, Haspell, Budd). Even after
extirpation of the liver in frogs, neither biliary acid nor pigment
could be found in the blood (Müller, Lehmann, Moleschott). These results
must, however, be qualified by the observations of Hammersten who found
bilirubin as a normal constituent of blood serum in the horse, and by
Virchow’s discovery that hæmatoidin (now held to be identical with
bilirubin) is constantly found in old blood extravasations into the
tissues.

The origin of the bile coloring matters may be traced in part to
destruction of red globules in the liver. Quincke has shown that in the
hepatic capillaries in post-embryonic life the leucocytes englobe and
destroy the old and worn out red blood corpuscles which thus become a
source of bile coloring matter. Such destruction is specially likely to
occur in badly maintained conditions of the blood, and in hepatitis or
other liver disease in which the white cells accumulate in the hepatic
capillaries, and when the blood current is retarded. Hence the liability
to jaundice in such conditions. The formation of new red blood
corpuscles has been observed in the protoplasmic cells of the liver in
the embryo, but this has not been established for post-embryonic life
(Neumann, Lowit).

The two common coloring matters of the bile are =bilirubin= which
colors the yellow bile of man, omnivora, and carnivora and
=biliverdin= which tints the dark green bile of herbivora. =Bilirubin=
(C_{32}H_{36}N_{4}O_{6}) forms transparent fox red clinorhombic
prisms. It is insoluble in water but soluble in chloroform, and may
thus be separated from the biliverdin which is insoluble in
chloroform. United as a second basic acid with alkalies it is soluble
in water. It is easily obtained from the red gall-stones of man or ox,
and is chemically identical with hæmatoidin. =Biliverdin=
(C_{32}H_{36}N_{4}O_{8}) is an oxidized derivative of bilirubin and is
insoluble in chloroform, slightly soluble in ether and freely soluble
in water. In addition to its presence in bile it has been found in the
placenta of the bitch. The =test= for bile coloring matter is made by
placing a drop of the suspected liquid on a white porcelain plate and
adding a drop of impure, brown, nitric acid (nitric and nitrous
acids). If bile is present there is produced a beautiful play of
colors passing from the green of biliverdin, through blue, violet,
red, and ending in yellow.

With regard to the formation of bile pigments in morbid conditions it
may be noted, that agents which dissolve the red blood globules (such as
bile acids or water), when injected into the veins determine the
appearance of bile pigment in the urine (Frerichs, Kuhne). When we
consider that an animal (dog) secretes ¹⁄₅₀ of its body weight daily of
bile, and that nearly all of this is re-absorbed from the intestines, we
can realize this as an important source of bile and urinary pigments.

Of the =bile acids=, =taurocholic= is the most abundant in the bile of
man, birds, and of many mammals and amphibians, while =glycocholic acid=
is the more plentiful in the ox and pig. It is absent in sucklings. The
taurocholic acid has been found to prove most destructive to red blood
corpuscles, and in strong solution is distinctly antiseptic, checking
the development of bacteria, of the alcoholic and lactic fermentations
and of the tryptic and diastatic action of pancreatic juice.

These are conjugate acids, formed by the union of cholic acid with
taurin and glycin respectively, and they are found almost exclusively,
in combination with soda in the bile. They are found in the liver and do
not accumulate in the blood when the liver has been removed. They
increase under an albuminous diet.

The =test for bile acid=, is to take the suspected liquid from which all
albumen has been precipitated, add a few drops of solution of cane
sugar, shake into a froth, and pour sulphuric acid, drop by drop, down
the side of the test tube. A _reddish purple_ color appears in the
froth, and shows two absorption bands at E and F. Any albumen left in
the liquid will give the same color, but only one absorption band.

The =secretion of bile= is more abundant on animal than on vegetable
food, and on albuminous than fatty. It ceases during hunger, but is
increased by ingestion of water. Its solids are most abundant one hour
after feeding. It increases under a copious and rapid blood supply, but
is arrested by diminished blood flow, even under increased pressure (in
ligature of the vena cava in front of the diaphragm). Vigorous exertion,
drawing off blood to the muscles of the trunk, diminishes the secretion
of bile, while transfusion of blood, up to a given grade of blood
pressure increases it. Nervous conditions, which cause contraction of
the portal vessels, increase the secretion by forcing more blood through
the liver. Such are strychnia or other stimulation of the valve of
Vieussens, of the inferior cervical ganglion, of the hepatic or
splanchnic nerves, or of the spinal cord. Fever causes its arrest.

The =secretion of bile= is further stimulated by the following :

_a._ The ingestion of bile into the stomach and abdomen. This being
absorbed and carried to the liver greatly increases the biliary
secretion. It is not necessary that the bile shall be a product of the
same genus of animal, the bile of the ox is an active stimulant of the
liver of the dog.

_b._ Of medicinal agents the following increase and liquefy the bile:
olive oil in large doses, phosphate of soda, salol, and salicylate of
soda.

_c._ The following not only increase the bile, but through their
purgative operation, expel it from the bowels: calomel, mercuric
chloride, colocynth, aloes, jalap, rhubarb, podophyllin, and cold rectal
injections. These accordingly lessen the secretion later, by removing
the stimulus of the absorbed bile.

_d._ The following are comparatively mild biliary stimulants: benzoic
acid, benzoate of soda, oil of turpentine, terpene, terpinol, and
euonymus, and still less active are alkaline bicarbonates, bromides,
sulphates and chlorides, arsenic and ether.

=Secretion of bile is lessened= by: starvation, a too fatty dietary,
alkaline iodides, atropia, strychina, hepatic degenerations, (fatty,
cirrhosis), catarrh of the bile ducts, diseases of the liver, gall duct,
or duodenum which interfere with the discharge of bile, the antisepsis
of the bowels, or the reabsorption of bile. This work virtually moves in
a vicious circle, as the action of septic ferments in the duodenum
hinders the reabsorption of bile and of the food products which go to
the production of bile, and in its turn the withholding of bile from the
intestine removes the normal antiseptic (the bile acids) and favors
septic fermentation and the inhibition of duodenal digestion and
absorption. Another factor is found in the ptomaines and toxins absorbed
from the alimentary canal and arrested in the liver. These debilitate
the liver cells, impair the liver functions and lay the gland open to
bacteridian infection. The bile in such a case is transformed into a
pale or yellow, viscid liquid, with more or less dark colored granular
debris, and this proves a favorable culture ground for bacteria
especially the _golden staphylococcus_ and the _bacterium coli commune_.
With septic condition of the liver the usual result of ligature of the
bile duct is a peri- and intralobular sclerosis and the formation of
minute biliary abscesses. In the absence of sepsis, ligature of the
biliary duct, produces—not abscess but—necrobiosis, preceded by
interlobular connective tissue hyperplasia, and granular or fatty
degeneration of the hepatic cells. (Charcot, Legg, Lahousse, Dupre).


          THE LIVER AS A DESTINATION AND DESTROYER OF POISONS.

The liver in the mature animal, being the one destination of the blood
carried in the portal vein, necessarily becomes the recipient of all
medicinal and poisonous agents absorbed by the capillaries and venous
radicals of the stomach and intestines. This organ retains and lays up
for a time the heavier metals, such as the salts of copper and iron, the
iodides and bromides, the vegetable alkaloids such as nicotine, quinine,
morphia, and curare, the toxic elements of the bile, the ptomaines and
toxins produced by gastric and intestinal fermentations, indol, phenol,
etc. Some agents it transforms, as peptones (which it renders
non-poisonous), casein, the carbonate of ammonia and its salts with
vegetable acids, also indol and phenol, which it combines with sulphuric
acid as indyxol and phenyl sulphate, thus rendering them much less
toxic. The destructions or new combinations established in the cases of
the ptomaines and toxins may explain why such agents are usually much
less poisonous when taken by the stomach than when generated in tissues
or blood, or when injected hypodermically. Another interesting fact in
connection with the ingestion of these bacteridian products (ptomaines
and albumoses) is that, when the liver functions are normal as evidenced
by the production of glycogen, the toxins are largely destroyed, and
they fail to produce poisoning, whereas with a functionally deranged
liver and no production of glycogen, they retain their potency, almost
as if injected subcutem.


                   FUNCTIONAL DISORDERS OF THE LIVER.

MELLITURIA, GLYCOSURIA, DIABETES MELLITUS, SACCHARINE URINE.

  Source of glucose in food. Glycogen: Its use: Enlarged liver means
  more glycogen. Glycosuric centre in medulla. Other glycosuric nerve
  centres. Reflex action, action of drugs and poisons, phlorizin.
  Disease of lungs or pancreas. Removal of pancreas in dogs. Removal of
  thyroid. Diseased, liver, fatty, fibroid, hypertrophy, congestion.
  Extreme fatty change arrests glycogenesis. In solipeds: 3 cases with
  liver hypertrophy; 1 case with adenitis; 6 cases with emaciation; 2
  cases with hæmoglobinuria. Symptoms: Emaciation, debility, langor,
  fatigue, breathlessness, hollow flanks, unthrifty skin, ardent thirst,
  polyuria, urine saccharine, of high density. Diagnosis by analysis of
  urine, sweet taste, Fehling’s test, Trommer’s test, fermentation test.
  Prognosis: Grave, diet being carbonaceous, when functional resulting
  from curable disease is hopeful. Treatment: In poisoning cases,
  antidotes and eliminants, in curable disorders treat these, in more
  inveterate cholagogues, antiseptics, codeine, opium, croton chloral,
  strychnia, phosphoric acid, iodoform, ergot, skim milk or buttermilk,
  good hygiene, open air, shelter, carminatives, bitters, mineral acids,
  treat complications.

Grape sugar (glucose, C_{6}H_{12}O_{6}) is undoubtedly formed in the
stomach and intestines by the action of saliva and pancreatic juice
on starch (C_{6}H_{10}O_{5}), and glucose and laevulose
(C_{6}H_{12}O_{6}) are also derived from the transformation of cane
sugar (C_{12}H_{12}O_{11}). These sugars are absorbed, transformed
into glycogen in the liver and passed into the circulation, where
they serve to maintain animal heat through their decomposition into
carbonic acid and water. They further assist in nutrition and
growth, and if their metamorphosis is imperfect they pass out of the
system in the urine, producing a temporary glycosuria. As shown
above glycogen is produced in the liver cells, and stored up there,
in greatest abundance during digestion of starchy and saccharine
food, but it is also formed in animals kept on a purely albuminous
diet, (flesh), and in the fœtal calf and unhatched chick to which
neither starch nor sugar has been furnished as food. It is produced
during the decomposition of albuminoids, along with the other end
products, leucin, tyrosin and urea. None of these last three is
found in the portal vein nor bile ducts, but all four are found in
the liver cells, and in the hepatic veins.

In health a physiological balance is maintained by the oxidation of the
glucose, mainly in the lungs, so that in the blood of the pulmonary
veins no sugar is found. There is an exception to this observable after
a full meal, rich in starch and sugar, which produces such an excess of
glycogen that a portion is carried to the kidneys and expelled by them
causing temporary glycosuria.

A small amount of glycogen is also produced habitually by the white
blood cells and stored up in them, but this is insufficient to determine
its appreciable elimination by the kidneys.

In cases of persistent glycosuria the fault may be held to consist in
one of three functional derangements:

1st. The failure of the liver to transform the alimentary sugar into
glycogen.

or 2d. The excessive production of glycogen in the liver.

or 3d. The arrest of the destructive oxidation of sugar in the lungs and
tissues.

In a diabetic patient who died suddenly of apoplexy Bernard found that
the liver was enlarged, comparing with the average as 25:14 while the
contained sugar bore the ratio of 37.5:22. This enlargement coming from
malaria or other poison, such as alcohol, ether (Harley), arsenic,
quinia (Aitken), ammonia, chloroform, or phosphoric acid (Murchison), is
an established condition of glycosuria. A rich and abundant food
(starchy and saccharine especially), or an unusually active hepatic
circulation acts in the same way.

Bernard as early as 1849 showed that the glycogenic function of the
liver was greatly increased and glycosuria determined by pricking the
floor of the fourth ventricle in the median line just in front of the
calamus scriptorius and near the root of the vagus nerve, or a few
millimeters in front of this.

It follows that irritation of this part of the medulla however produced,
whether from local disease, or by reflex action from some distant organ
in a state of irritation, may serve as the starting point of diabetes in
particular instances. That the cause may be a reflex stimulus is shown
by the suspension of the glycogenic function after section of the vagus
nerves, and its reappearance when the central end of the cut vagus is
galvanized, or, the floor of the fourth ventricle is irritated, the
direct or efferent excitation being transmitted through the sympathetic
nerve (Bernard). I can cite a case of glycosuria in a man supervening on
a severe blow on the head from a falling ledger. Brain injuries which
suspend animal functions, but not the nutritive ones, such as apoplexy,
concussion of the brain or curare poisoning are liable to induce
diabetes.

Traumatic injuries to other parts of the nervous system induce
glycosuria. Thus traumatism of the optic thalami; of the cerebral lobes
or peduncles; of the pons; of the cerebellum or of its middle or
posterior peduncles; transverse section of the medulla or of the spinal
cord opposite the second dorsal vertebra; traumatism of the superior or
inferior cervical ganglion or the first thoracic (Eckhard); of the
sympathetic twig which accompanies the vertebral artery (Pavy); of the
brachial plexus; of the solar plexus (Munck, Klebs); or of the sciatic
nerve (Schiff).

The explanation of these facts may be sought in a reflex action
established by the conveyances of irritation to the true glycogenic
centres in the brain and the transference of the efferent nervous
impulse through the sympathetic nerve to the liver. It will be borne in
mind that in the case of section of the vagus nerve electric stimulation
of its detached peripheral part has no glycogenic effect on the liver,
while galvanizing the central portion determines glycosuria.

In the case of glycosuria through stimulation of the sympathetic nerve
or its ganglia the action may be concluded to be direct. Strangely
enough, irritation of the sympathetic between the tenth and twelfth ribs
or the splanchnic nerves fails to produce glycosuria, though the hepatic
branches of the sympathetic pass through them.

In ordinary cases of reflex glycosuria it may be assumed that the
existence of irritation at the peripheral ends of the vagus and of some
other nerves, leads to an apparent glycogenic influence passing through
these to the brain, and of the distribution of the efferent impulse
through the upper portion of the spinal cord, as far as the fourth
dorsal vertebra in the rabbit (Cyon, Aladoff, Schiff), and through the
sympathetic nerve to the liver. This may account for the appearance of
the disorder as a sequel of disease in any part to which the vagus in
particular is distributed, and notably in the lungs. A number of poisons
(malarial, alcoholic, ether, carbon monoxide, amyl nitrate, curare, or
the nitro-propionic acid, methyl delphinin, morphia, chloral hydrate,
arsenic, quinia, ammonia, chloroform, phosphoric acid, and phlorizin)
produce glycosuria.

The intravenous injection of dilute saline solutions, or frequent blood
letting materially increases the sugar, probably by causing solution of
the red globules. Phlorizin is the most potent of all these agents.
Whether given hypodermically or by the stomach it causes in three hours
a marked production of glucose which continues to be eliminated for a
period of thirty-six hours. The urine may become charged with glucose to
the extent of from 6 to 13 per cent., and without any rise in the body
temperature. This artificial glycosuria may be kept up indefinitely by
the continued administration of phlorizin, and even in the fasting
animal, or one on an exclusively albuminous diet, as well as in those on
an aliment rich in saccharine or hydro-carbonaceous matter. In the frog
it produces diabetes even after the extirpation of the liver showing
that it stimulates other sources of sugar production beside the hepatic
or that it inhibits the transformation of sugar derived from the
alimentary canal and other sources.

Another suggestive source of mellituria is disease of the lungs, or any
condition which interferes with the due æration of the blood and
oxidation of the alimentary or hepatic sugar. But it cannot be assumed
that the rôle is altogether or mainly chemical. The thoracic organs
being supplied by branches of the vagus and sympathetic nerves there is
the obvious suggestion of a reflex action through the diabetic centers
in the brain. The frequent complication of diabetes with lung diseases
(inflammatory, tubercular, syphilitic, and otherwise) is abundantly
proved, whether it is to be explained on the above hypothesis or through
other unknown changes in the blood.

Diabetes has been repeatedly found in connection with disease of the
pancreas, and the complete extirpation of the pancreas in dogs gives
rise to glycosuria (Mering and Minkowski, Thiroloix, Lancereaux,
Lepine). If a small portion of the pancreas remains glycosuria does not
supervene. It has been suggested that the pancreas has a double
function, and beside its secretion, produces a glycolytic ferment which
passing into the portal blood determines the formation of glycogen in
the liver. Arrest of the pancreatic secretions does not cause
glycosuria, so it has been suggested that the glycogenic enzyme is a
product of the connective tissue cells of the pancreas. Functional as
well as structural disease of the pancreas can be conceived of as
inhibiting the production of this ferment and the consequent elaboration
of glycogen. Chauveau and Kauffmann deduce from their observations that
the action is a reflex one established through the glycogenic centres in
the medulla. Pancreatic glycosuria is especially fatal (Harley).

Finally extirpation of the thyroid body in dogs has been followed by
glycosuria (Falkenberg). This suggests a systematic examination of the
urine in all cases of goitre, with extensive glandular changes.

Apart from experimental cases diabetes in the lower animals has been
observed to be nearly always associated with diseased liver. Fatty
degeneration has been the most frequent lesion, but cirrhosis,
hypertrophy and congestion were present in other cases. In a number of
cases as the fatty degeneration reached an extreme degree, the sugar
disappeared from the urine, the hepatic cells being no longer
functionally active, and death speedily followed. The same has been
observed in the fatty degeneration attendant on poisoning by arsenic or
phosphorus.




                        GLYCOSURIA IN SOLIPEDS.


Heiss records two cases of this disease in heavy Belgian horses ten and
eleven years old, the urine of which showed a percentage of 3.75 of
grape sugar, and which died in two months in a state of marasmus. The
liver was enlarged and of a clay yellow color. Dieckerhoff reports one
fatal case in which there were also yellow discoloration, congestion and
hypertrophy of the liver. No lesion could be found in the pancreas nor
nervous system. Perosino records a case in a horse suffering from
contagious adenitis, which may be supposed to have been connected with
the action of the toxins or the imperfectly oxidized albuminoids on the
nerve centres or liver. Delprato relates six cases in the same stable in
overworked, half starved and emaciated horses. Rueff and Mouquet each
contributes a case occurring in paraplegia attendant on hæmoglobinuria
and in which the amounts of sugar were respectively 5.85 and 1.01 per
cent. These latter cases are manifestly complicated ones in which the
reflex irritation (or inhibition of glycogenesis) is transmitted from
the diseased or poisoned brain to the already disordered liver.

_Symptoms._ There is a profound interference with nutrition, a rapid
loss of flesh and weight, of spirit and energy and an extreme muscular
weakness in spite of an excessive appetite. The subject is fatigued and
breathless under the slightest exertion, the flanks are retracted and
hollow, and the hair dry, rigid and lifeless. Appetite is poor and
fastidious, but an intense and consuming thirst is usually present, the
animal drinking deeply at every opportunity, and passing urine with
corresponding frequency and abundance. The urine is clear, yellow,
neutral, and saccharine, the sugar varying from 1 to 12 per cent. (3.6
on an average). Notwithstanding the amount passed (55 litres per day,
Cadeac) the density usually exceeds the normal (1052 and upward), normal
being 1040 to 1050. There may or may not be hyperthermia, and in
exceptional cases appetite has been retained to the last. Cataract and
corneal ulceration are sometimes observed as in man.

_Diagnosis._ Presumption may arise from the above mentioned symptoms,
and especially the bulimia, the polydipsia, the polyuria, the rapidly
advancing emaciation, weakness, and prostration and the ocular troubles,
but conclusive evidence is only found in the presence of glucose
permanently in the urine.

_Tests for Sugar in the Urine._ For one who can go through it the
touching of the tip of the tongue with a drop of the suspected urine
will give a prompt and reliable test.

_Fehling’s_ cupric test is the next best for simplicity and
availability. Dissolve 34.639 grammes (1⅕ oz.) pure cupric sulphate in
200 cubic centimeters of distilled water: 173 grammes (6 ozs.) of pure
neutral sodio-potassic tartrate and 80 grammes of potassium hydrate in
500 cubic centimetres of distilled water. Add the copper solution slowly
to the potassium one and dilute the clear mixture to one litre. One
cubic centimeter of this fluid will be discolorized by 0.005 gramme of
sugar; or 200 grains will be discolorized by 1 grain of sugar.

_Trommer’s_ test is even simpler for a mere qualitative test. Pour the
suspected urine, freed from albumen, into a test tube and add a solution
of caustic potassa or soda until distinctly alkaline. Should this throw
down earthy phosphates or carbonates filter these out. Then add drop by
drop a solution of pure cupric sulphate in distilled water (3.5:100) so
long as it throws down a yellowish red precipitate of oxide of copper.
When the supernatent liquid remains clear and assumes a distinctly
bluish tint, the sugar has all been precipitated. The amount of
precipitate is a criterion of the quantity of sugar, which may be
otherwise estimated by the amount of copper salt used.

_The fermentation test_ is made by adding a teaspoonful of liquid yeast
to four ounces of the suspected urine, stopping the flask lightly and
placing it in a temperature of 60° to 80° F. for 12 to 24 hours when the
sugar will have been converted into alcohol and dioxide of carbon. The
loss of weight will indicate the amount of sugar, as also will the
lowering of the specific gravity. If before testing the urine was 1060,
and after 1035, it contained 15 grains of sugar to the fluid ounce.

_Prognosis._ This is always rendered more grave in the horse than in
man, because of the impossibility of putting him on a purely albuminous
diet. The great tendency is to a rapidly fatal issue, especially in
cases of irremediable structural lesions in the brain and liver. Where
the disorder is largely functional, as in connection with hæmoglobinuria
or as the result of poisons ingested the prospect of recovery is often
good.

_Treatment._ In cases due to poisoning the use of antidotes and
eliminating agents will be effectual, and in transient and curable
diseases like pulmonary disorder, hæmoglobinuria and paralysis the
appropriate treatment will restore. In the more inveterate or
constitutional cases all treatment is liable to prove ineffectual. At
the outset some apparent amelioration may be obtained from salicylic
acid, salicylate of soda, bicarbonate, acetate, citrate, sulphate or
chloride of soda, nitro-muriatic acid and other cholagogues. Blisters to
the perichondrium may also be employed. Later, when degeneration of the
liver has reached an extreme point, these will be of no avail. Cadeac
recommends acetanilid, antipyrine, and benzo-naphthol largely on their
antiseptic merits, and Jong claims a recovery in a horse under daily
doses of 12 grains of codeine. Opium has long been employed in man with
partially good results, and croton chloral, strychnia, phosphoric acid,
iodoform and ergot are recommended in different cases.

One of the most beneficial agents is skim milk or buttermilk as an
exclusive diet, and this may be to a large extent adopted for the horse.
Under its use the sugar may entirely disappear, and though rheumatoid
pains in the joints may be brought on, these usually subside on
withdrawing the source of lactic acid. They may further be met by the
use of salicylates. The greatest care should be taken of the general
health, an open air life, with protection against colds and storms, and
a healthy condition of bowels, kidneys and skin being particularly
important.

The impaired digestion and assimilation usually demand carminatives,
stomachics, bitters, and mineral acids, particularly the nitro-muriatic.
With the same intent a fair amount of exercise short of absolute fatigue
should be secured. But each case will require a special study and
treatment consonant to its special attendant lesions, its causative
functional disorders, and its stage. One case may demand attention to
bacteridian poisoning, one to a better regimen and diet, one to liver
disease, and one to disease of the brain, etc. After this treatment
specially directed to the abnormal function or structure, would come the
more specific treatment for mellituria which would be more or less
applicable to the general glycolytic disorder.




                         GLYCOSURIA IN CATTLE.

  Accompaniment of parturition fever and apoplexy. Essential glycosuria.
  Dense saccharine urine, passed often, congested mucosæ, emaciation.
  Lesions uncertain. In parturition fever and apoplexy the congested
  medulla is the reasonable starting point. Toxic glycosuria. Treatment:
  addressed to the primary disease or poison; otherwise treat as in the
  horse.


In cattle this has been observed as a symptomatic affection in
connection with parturition fever or apoplexy (Nocard, St. Cyr, Violet).
One case of essential mellituria has been recorded by Darbas.

_Symptoms._ In the last mentioned case in a work ox, the animal, when at
work, would stop every five or ten minutes to urinate, passing a small
quantity of amber colored urine of a high density and containing a large
amount of glucose. The conjunctiva was pink, the animal considerably
emaciated, and rest and generous feeding brought about no improvement,
so that the subject was finally sent to the butcher to anticipate a
natural death.

The lesions in this case are altogether hypothetical. The red eyes might
imply congestion of the encephalon (medulla), but the redness might be
caused by active disease in the liver, pancreas or kidney. The failure
to notice jaundice does not indicate a healthy liver, as some of the
most fatal diseases of that organ are unattended by icterus. The
frequent emission of urine in small amounts would imply irritation in
kidneys or bladder, from which the glycogenic stimulus may have started.
In the absence of any more definite evidence of disease in other organs
it is, however, more probable that the fundamental disorder resided in
the liver, the great glycogenic factor of the body.

In parturition fever, the presumption is in favor of considering the
congested medulla as the starting point of the disease, yet in view of
the manifest paralysis of stomach and bowels, it is not improbable that
the vascular congestion and paralysis of the chylopoietic viscera
constituted the initial step in the morbid process, while the
glycogenesis was the result of a reflex operation on the liver.

Toxic mellituria would occur in cattle under the same conditions as in
the horse.

_Treatment_ is only hopeful in the sympathetic and toxic forms. These
must be treated according to the nature of the primary disease or the
poison. To these the general principles of treatment as recommended for
the horse should be superadded. For essential diabetes an exclusively
milk diet and any one of the agents that have given good results in man
or horse can be tried, but with an animal in fair condition it will be
better as a rule to turn him over to the butcher.


                         GLYCOSURIA IN THE DOG.

  More common than in horses and cattle. Causes: pampered in diet,
  sweets, liver, disease of pituitary body, or mostly of the liver.
  Removal of pancreas. Brain and nervous lesions and reflex action.
  Symptoms: pampered asthmatic subject, with dysuria and lameness,
  dense, saccharine urine, bulimia, loss of weight, corneal ulcers,
  cataracts, palsy, coma. Duration: 4 to 8 months, sugar may disappear
  with complete liver degeneration. Diagnosis: by pampered condition,
  asthma, thirst, diuresis, later by loss of weight, troubles of vision,
  saccharine urine. Lesions: usually hypertrophied, fatty or caseated
  liver, thickened capsule, disease of thyroid, heart and eye.
  Treatment: skim or butter milk as sole diet, restricted diet of lean
  meat clear of fat, warmth, dryness, pure air, sunshine, gentle
  exercise only, cholagogues, sodium sulphate, or chloride, or
  carbonate, or salicylate, salol, nitro-muriatic acid, antithermics,
  ergot, codeine, bitters, mineral acids, derivatives.

Among domestic animals the dog has furnished the greatest number of
cases, yet even in this animal the disease appears to be far from
common.

_Causes._ The relative frequency of diabetes in the dog is probably
dependent on his life in human dwellings and on gourmandizing on dishes
prepared for man. Friedberger and Fröhner have produced the disease
artificially by feeding a great quantity of sugar and W. Williams has
met the disease in dogs fed exclusively and generously on liver.
Thiernesse records one case complicated by atrophy and steatosis of the
pituitary body, but in all other instances the appreciable lesions were
confined to the liver. In one case, reported by St. Cyr, the liver was
hypertrophied, yellow, mottled, marked by irregular elevations of
congested and hypertrophied hepatic tissue, and showing extensive
degeneration—mucous, caseous and fatty. Thiernesse found the liver of a
yellowish white color, and the seat of fatty degeneration implicating
the hepatic cells. Franzenberg in one case found fatty degeneration of
the liver, and Fröhner and Schindelki, in four cases, met with extensive
hepatic disease. The macroscopic lesions of the disease in dogs as in
horses appear to be mainly hepatic.

On the other hand the complete removal of the pancreas in the dog by
Mering, Minkowski, Thiroloix, Lancereaux and others was invariably
followed by mellituria, so that even in the absence of clinical
examples, we must recognize pancreatic lesions and functional disorders
as possible primary causative factors in glycosuria. In the light of
experimental medicine we must similarly recognize brain and nervous
lesions and reflex actions as possible causes, even if as yet
unsupported by clinical facts observed in the dog.

_Symptoms._ The disease usually appears in an old, fat, pampered dog,
affected with dyspnœa or asthma, with dysuria and lameness. The urine is
high colored, viscid, and of a high density (1055 to 1060, the normal
canine urine being about 1020), and charged with glucose. The subject
may have an enormous appetite but fails to gain in weight, and after a
time loses flesh and becomes badly emaciated. The pulse is small and
frequent, and the temperature which at the outset may reach 102°, falls
to the normal as the end approaches. Watering eyes, corneal ulcers, and
cataracts as well as hemiplegia and diabetic coma may precede death. The
amount of sugar has been found to vary in different cases from 3.2 to 12
per cent. of the urine.

_Course._ _Duration._ The dog may live from four to eight months and, as
in the horse, sugar may finally entirely disappear from the urine, in
connection with the progressive degeneration of the liver. If the
patient is unable to take exercise, the case reaches a more speedily
fatal issue.

_Diagnosis_ is deduced from the bulimia, pampered condition,
breathlessness, thirst, and diuresis, the subsequent loss of condition,
ocular troubles, and dropsy or coma, the whole being confirmed by the
dense, high colored, viscous, saccharine urine.

_Lesions._ As already noticed the most constant lesion is hypertrophy of
the liver, which is swollen unevenly, has thickened borders, is yellow
or red, very friable and often fatty, or caseated. The capsule of
Glisson is thickened and fibrous. Hypertrophy and fatty degeneration of
the thyroid have been found in different cases and in one instance
insufficiency of the mitral valve with systemic venous congestion.
Ocular troubles are constant.

_Treatment._ Put the patient on an exclusive diet of skim or butter milk
or if this is impossible it may be conjoined with lean meat—raw or
cooked—keep warm and dry, but give plenty of open air and sunshine.
Avoid fatigue and over exertion. Restricted diet is of great importance.
During the siege of Paris the short rations led to the disappearance of
glycosuria from many human patients.

Among medicinal agents, cholagogues come first, sulphate of soda with
chloride of sodium, bicarbonate of soda, salicylate of soda, salol,
nitro-muriatic acid, may be named. For the febrile condition,
antipyrine, acetanilid, or phenacetin may be employed, and iodoform,
ergot or codeine may be tried when other measures fail. Bitter tonics
and mineral acids may be beneficial, and lastly blisters to the region
of the liver may prove of service.


                        OBESITY AND EMACIATION.

  Sugar essential to growth. Ratio of liver to active increase in
  weight. Obesity and fatty degeneration. Small inactive liver and
  stunted growth, or loss of weight. Biliary fistula, death in 12
  months. Influence of pancreas. Nitrogenous food for obesity, outdoor
  life, exercise, cholagogues, salines. Saccharine and starchy food for
  emaciation, hepatic, and pancreatic stimulants. Mild laxatives and
  cholagogues, pure air, green, succulent food, pure water, bitters,
  tonics, moderate exercise.

There is reason to believe that both of these occur as results of
hepatic disorder. The generation of sugar in connection with rapid cell
growth in germinating seeds and growing plants, and also in rapidly
growing animal tissues as in the body of the fœtus and fœtal membranes,
and finally in the inflammatory products of pneumonia and in leucocytes,
seems to imply that it is essential to such cell growth (Murchison). In
keeping with this is the fact that the liver is of relatively much
greater size in the fœtus and in the young and rapidly growing animal,
and also in meat producing animals which have been selected and bred
through many generations for early maturity and rapid fattening. The
enormous development of adipose tissue and of lipomata in such animals
is essentially abnormal, though it is a deviation from the natural that
is esteemed as evidence of excellence, and a necessary condition of
success in the meat producing industry. While other conditions are
necessary to the production of such obesity, such as abundance of rest,
slow, shallow breathing, a genial climate, and a generous
hydro-carbonaceous food, yet all of these would prove ineffective
without a large liver, working under high pressure in producing a large
output of sugar. The mere obesity in the meat producing animal is not
considered as disease and it is only when the tendency to fat production
culminates in an adipose degeneration of the muscles and other tissues
that actual disease is conceded.

_Emaciation_ in certain cases is traceable to the opposite condition. A
small or inactive liver with a diminished production of sugar and fat
will ensure loss of weight, which is still further aggravated by
decreased secretion of bile and insufficient absorption of peptones.
Experimentally this condition has been repeatedly brought about by
making a biliary fistula, and cutting off all bile from the intestine.
Death preceded by extreme emaciation ensues in 12 months (Murchison).
This being the case with the escape of all the bile secreted, a slower
but no less certain emaciation must follow on a structural or functional
disorder of the liver which is attended with a greatly lessened
production of bile. This, indeed, is the condition met with in advanced
glycosuria, when the liver is the seat of general fatty degeneration.

From the experiment of the removal of the pancreas we may infer that
diseases of this organ which pervert or destroy its normal functions,
will check glycogenesis in the liver by withholding the supposed
pancreatic ferment, and by so doing will conduce to emaciation and
marasmus.

So far as obesity and emaciation are dependent on diet they may be
checked by subjecting the patient to the dietary which will favor a more
healthy liver function. For excessive _obesity_ a strictly nitrogenous
food in restricted amount will tend to lessen the glycolytic action of
the liver and secure the formation of muscle rather than fat. An outdoor
life, and an active though not exhaustive use of the muscles will
greatly favor this result. For the carnivora or omnivora a diet of lean
meat or skim milk might be employed, while for the herbivora, wheat
bran, cotton seed hulls, beans, peas, vetches, or cotton seed would
measureably meet the demand. Cholagogues and saline laxatives, by
eliminating from the liver and intestine, will contribute to the same
end.

If _emaciation_ depends on a deficiency of sugar, that may be freely fed
along with richly amylaceous food, and the liver may be stimulated to
increased glycogenesis, by stimulants such as chloroform, ammonia, or
ether, and by a moderate use of carbonate of soda or other alkalies.
Ether has in addition a stimulating effect on the pancreas and will tend
to increase that ferment which stimulates the liver to its glycogenic
work. Mild laxatives and cholagogues will second this, such as small
doses of podophyllin, taraxacum, nitro-muriatic acid, chloride or
bromide of ammonium, plenty of pure air, abundance of green or aqueous
food, and plenty of pure drinking water. Finally moderate exercise, by
increasing the aspiratory action of the chest and thereby accelerating
the hepatic circulation is a material stimulant of the glycolytic
function. Bitter and other tonics are contributions to the same object
and should not be neglected.




             SECONDARY OR REMOTE RESULTS OF LIVER DISEASE.

  In gout: Arrest of oxidation of proteids into urea. Deposits of
  biurate of lime on joints, and other disorders. Urinary calculi
  containing urates, cystine, xanthine, etc., also from imperfect
  oxidation of albuminoids. Oxalic acid represents a similar arrest.
  Kidney degenerations from irritating urates and oxalates. Fatty kidney
  from excessive glycogenesis. Digestive disorders from excess or
  deficiency of bile or torpid liver. Nervous disorders, dullness,
  lameness, vertigo, spasms, irritability from hepatic inactivity and
  resulting poisons. Sore throat and bronchitis from hepatic
  derangement. Skin eruptions in tardy or imperfect action of the liver.
  Treatment: Abundant water, succulent vegetables, ensilage, fresh
  grains, balanced ration, in carnivora and omnivora oat meal,
  buttermilk, clear meat juice, avoid sweets, gravies, spiced animal
  food. Dangers for pampered horses, dogs, and old improved meat
  producing animals. Open air exercise. Laxatives with alkalies,
  salines, mercurous and mercuric chloride, pilocarpin, chlorides,
  iodides, bromides, nitro-muriatic acid, ipecacuan, euonymus, bitters.


Among the many secondary results of hepatic disorder, and which are
habitually described as affections of other organs a few may be
mentioned as indicating the wide range of influence exercised by the
liver in disease as well as in health.

_Gout_ as it appears in fowls and omnivora is directly due to the arrest
of the transformation of the albuminoids into urea. Circulating in the
system in the form of the less perfectly oxidized and less soluble uric
acid, it determines deposits of biurate of lime around the joints, with
local inflammations, and disorders of circulation and innervation, and
altered spirit, temper, etc.

_Urinary calculi_ in the same animals, are composed largely of urate of
lime, cystine, xanthine and other nitrogenous products representing
various stages of oxidation short of the final transition into urea and
ammonia. Recognizing the active rôle which the urinary bacteria fill in
this respect we must still acknowledge the great importance, as
causative agents, of an excess in the urine of these comparatively
insoluble products.

The oxalic acid found in certain calculi points in the same direction,
as this acid, both in the body and in the laboratory, is found to result
from the oxidation of uric acid (Wohler, Schenck, Hutchinson).

_Degenerations of the Kidneys_ are to be largely traced to the same
hepatic source. The uric acid diathesis, and the oxalic acid diathesis,
both the result of imperfect liver function, are among the most frequent
causes of irritation of the kidneys, by which channel they are
eliminated from the body. Hence acute and chronic nephritis, as well as
nephritic calculi result from morbid conditions which have their
starting point in the imperfect function of the liver. Again fatty
degeneration of the kidney is very liable to result from derangement of
the glycogenic function of the liver, the tendency to the formation of
fat and the constant irritation caused by the passage of the sugar
contributing to the tissue degradation. In such cases albuminuria is a
not uncommon accompaniment.

_Derangements of the Digestive Organs_ may be said to be a necessary
result of hepatic disorder. Excessive secretion of bile stimulates
peristalsis and may induce diarrhœa, while diminished secretion tends to
constipation, light colored, fœtid stools, intestinal fermentations and
poisoning by the irritant products. A torpid hepatic circulation means
congestion of the whole portal system, indigestions, colics, chronic
muco-enteritis, intestinal hemorrhages, hemorrhoids, etc.

_Derangements of the Nervous System._ In this connection may be named
the lameness of the right shoulder which accompanies certain disorders
of the liver, the extreme dullness and depression that attends on
others, the sluggish pulse that appears in certain types, the
unsteadiness of gait (giddiness) in others, the muscular cramps, and
irritability in still others. These appear to be due in some instances
to the nervous sympathy of one part with another, whilst at other times
they as manifestly depend on the circulation in the blood of partially
oxidized and other morbid products of hepatic disorder which prove
direct poisons to the nervous system.

Derangements of the circulation, like extreme rapidity, or slowness of
the pulse, irregularities in rhythm and intermissions, may be charged
more directly on the nervous affection, though primarily determined by
hepatic disorder.

On the part of the _Respiratory Organs_, affections of a chronic type,
like sore throat and bronchitis may often be traced to hepatic torpor or
disorder.

_Skin Diseases_ are notoriously liable to come from inactive or
disordered liver, the irritant products circulating in the skin or
sweating out through it, giving rise to more or less irritation. The
result may be a simple pruritus, an urticaria, an eruption of papules,
vesicles or even pustules. In any such cases it is proper to look for
other indications of liver disease,—pale color and offensive odor of the
fæces, muco-enteritis, indigestion, icterus or yellow patches on the
mucous membranes, tenderness on percussion over the asternal ribs,
muscular neuralgia, nervous disorder, the passage of bile, hæmoglobin,
albumen, sugar or other abnormal elements in the urine, etc.


      TREATMENT OF SECONDARY AND FUNCTIONAL DISEASES OF THE LIVER.

_Diet._ Many hepatic disorders, and especially those that are
exclusively or mainly functional may be corrected by diet alone.
Prominent among dietary influences is the abundant supply of water. The
succulent grasses of spring and early summer constitute the ideal diet,
hastening and increasing elimination, and lessening the density of the
bile, even to the extent of dissolving biliary calculi and concretions.
Upon dry winter feeding such calculi are common especially in ruminants,
whereas after a month or two at pasture they are extremely rare. In
winter the same good may be arrived at by the use of ensilage, brewer’s
grains, roots, fruits, or even scalded hay or bran. The two extremes of
highly albuminous and highly carbonaceous or saccharine food are to be
avoided or used only in limited amounts. In the one class are clover,
alfalfa, sainfoin, vetches, cowpea, lespedeza, especially in the form of
hay, beans, peas, cotton seed, gluten-meal, rape and linseed cake. In
the other are wheat, buckwheat, Indian corn, sorghum, sweet-corn and
cornstalks. Some agents like beets which are rich in saccharine matter
may be actually beneficial by reason of their laxative and cholagogue
action. In the carnivora the food should be largely of simple mush of
oatmeal, wheat seconds, or barley meal, skimmilk or buttermilk. If it is
needful to tempt the appetite in a fleshfed animal this should not be
done by rich, fat gravies, highly spiced animal food, or rich saccharine
puddings, but rather by the addition of a little pure juice of lean
meat, or some well skimmed beef tea.

It is as important to regulate the quantity as the quality of the food
as the heavy feeder will over-charge the liver as much by an excess of
otherwise wholesome food, as will the ordinary animal by the
indigestible and unwholesome articles. As a rule the improved breeds of
meat producing animals, have acquired such facility in fat production
that much of the surplus is largely and profitably disposed of in this
way, and in their short lives little obvious evil comes of the
overfeeding, but in cases in which this outlet proves insufficient, as
in horses and dogs that are highly fed on stimulating or saccharine
diet, and which are kept for the natural term of their lives, with
little exercise, the evil tends to reach a point of danger. Nursing
mothers and dairy cows find a measure of safety in the free flow of milk
and the yield of butter, but breeding cows that have been improved till
they have no longer a capacity for milking, but must have their calves
raised on the milk of other and milking strains are correspondingly
liable to suffer.

_Exercise in the Open Air._ As enforced idleness, on a full diet and in
a warm and moist environment is a main cause of hepatic disorder, so
abundant exercise in the open air and especially in a cool season is
beneficial in a marked degree. Beside the bracing effect on the
digestive organs and the improvement of the general tone of the system,
the action of the muscles in hastening the circulation greatly favors
the removal and elimination of waste matters. Still more advantageous is
the increased activity of the respiration and the aspiratory power of
the chest in at once unloading the portal system and the liver by
hastening the progress of the hepatic blood into the vena cava and right
heart, and in furnishing an abundant supply of oxygen for the
disintegration of the albuminoids and amylaceous products. Such exercise
must of course be adapted to the condition of the animal and its power
of sustaining muscular work, but judiciously employed, it is one of the
most effective agencies in correcting and improving hepatic disorder or
hepatic torpor. Idle horses, the victims of obstinate habits of
constipation, muco-enteric irritation, indigestion, nervous, urinary or
cutaneous disorders will often be greatly benefited or entirely restored
by systematic exercise. This is one of the great advantages of a run at
pasture, as the subject secures at once the laxative cholagogue diet, an
abundant supply of oxygen, a better tone of the muscular and general
system, and a more perfect disintegration of albuminoids. Sea air with
its abundance of ozone is especially advantageous.

In the carnivora while we cannot send them to grass, much can be done in
the way of systematic exercise, and in the case of city dogs a change to
the country, where they can live out of doors and will be tempted to
constant exercise and play, will go far to correct a faulty liver.

_Laxatives._ _Cholagogues._ When a free action of bowels and liver
cannot be secured by succulent food and exercise, we can fall back on
medicinal laxatives. These are advantageous in various ways. Some
laxatives like podophyllin, aloes, colocynth, rhubarb, senna, jalap, and
taraxacum act directly on the liver in increasing the secretion of bile.
These may be used for a length of time in small doses and in combination
with the alkalies. Other aperients act directly on the bowel carrying
away the excess of bile, the albuminoids and saccharine matter that
would otherwise be absorbed, and by a secretion from the portal veins,
abstracting nitrogenous and saccharine elements which would otherwise
overtax the liver to transform them. Thus indirectly these also act as
cholagogues by withholding the excess of material on which it has to
operate, and by rousing its functions sympathetically with those of the
bowels. Thus sulphates of magnesia and soda, and tartrates and citrates
of the same bases, given in the morning fasting, dissolved in a large
quantity of warm water and conjoined with sodium chloride, ammonium
chloride, sodium carbonate or other alkaline salts, or with one or more
of the vegetable cholagogues above mentioned, may be continued for a
length of time until the normal functions have been re-established, and
will maintain themselves irrespective of this stimulus.

Calomel (and even mercuric chloride in small doses), though it is not
experimentally proved to be a direct cholagogue, is one of the very best
correctives of impaired hepatic function. It expels the bile from the
duodenum and bowels generally, thereby preventing its reabsorption; it
proves antiseptic to the ingesta; it eliminates much of the peptone,
saccharine and fatty matter from the intestines and portal system thus
relieving the liver materially; and it is supposed further to modify the
other liver functions by a direct action on the hepatic cells, and by
reducing the cohesion of fibrine, and promoting the disintegration of
albumen. Certain it is that calomel gives most substantial relief in
many torpid and other disorders of the liver and as it is not in itself
an active liver stimulant but has rather a soothing action on that gland
it can be safely resorted to in states of hepatic irritation in which
the more direct cholagogues would prove more or less hurtful.

In some forms of hepatic disorder where a speedy and abundant secretion
is demanded, pilocarpin may be employed, with great caution so as not to
reduce the strength unduly by the attendant diaphoresis, diuresis,
salivation or diarrhœa.

_Alkalies_ have long been recognized as of great clinical value in
hepatic disorders. Though carbonate of soda decreases the secretion of
bile, (Nasse, Röhrig), yet the alkalies generally appear to promote
oxidation, and to hasten the disintegration of albumen and the
albuminoids. They increase the disintegration of sulphur compounds
materially adding to the sulphates and urea in the urine. They further
tend to increase the hippuric acid, carbonate of soda (2 drs.) even
determining the abundant excretion of this acid in man (Nasse). It may
be concluded that the acknowledged value of alkalies in these diseases,
is largely due to their hastening of the metabolic processes in
albuminoids. Small doses of sodium carbonate further stimulate the
gastric secretion and may thus benefit by rendering the process of
digestion more complete and satisfactory.

_Chlorine, Iodine, Bromine and their Salts._ These halogens are of great
value in many hepatic disorders. The universal craving for sodium
chloride indicates the need of its elements in the animal body, and
whether this is mainly the supply of chlorine for the hydrochloric acid
of the gastric juice, or to fulfill its uses in favoring the oxidation
and disintegration of the nitrogenous matters in the blood and tissues,
or for other more or less obscure uses, it is well to recognize and act
upon the indication. The various mineral waters which are held in high
esteem in liver affections contain a large proportion of sodium
chloride. As a medicinal agent ammonium chloride maintains an equally
high position. Large doses thrice a day, so as to induce diaphoresis and
diuresis greatly relieve hepatic congestions. This agent determines a
great increase in the urea eliminated so that it is even more effective
in the same direction, than sodium chloride. Free chlorine is also
effective in hepatic torpor and congestion, and to this in part may be
attributed the great value of nitro-muriatic acid.

Bromide and iodide of potassium have been found to be effective in
reducing hepatic enlargement and thus in conducing to a more healthy
activity of the liver.

_Ipecacuanha, Euonymus, etc._ These agents are more or less hepatic
stimulants and may be found beneficial as combined with the laxative or
alkaline agents in securing a better functional activity in cases of
torpor or deranged function.

_Tonics, Bitters._ Tonics are often useful when the health has been
undermined by long continued hepatic disorder. The iron tonics are as a
rule contraindicated as tending to check secretion of bile, unless they
can be given with alkalies. Iron sulphate or chloride, combined with
sodium or potassium carbonate so as to establish a mutual decomposition
will obviate this objection. The vegetable bitters (gentian, cascarilla,
calumba, salicin, serpentaria, aloes, nux vomica) combined with alkalies
are often of great value. Quinia, like opium, checks secretion and is to
be avoided or used with judgment and in combination with cholagogues.




    HÆMOGLOBINÆMIA. AZOTÆMIA. AZOTURIA. HÆMOGLOBINURIA. TOXÆMIA FROM
                      IMPERFECT HEPATIC FUNCTION.

  Definition. Theories, of hysteria, uræmia, spinal myelitis,
  myelo-renal congestion, rheumatic lumbago, myosito-myelo-nephritis,
  rheumatic chill with destruction of muscle albuminoids. Yet it occurs
  in our semi-tropical midsummer with a temperature of 80 or 90, in
  spring and autumn, and rarely even in the cold, damp stable in
  midwinter in the absence of exercise. Constant conditions: One or more
  days absolute rest, preceding steady work, a strongly nitrogenous
  ration, continued during the rest, sudden active exertion accelerated
  breathing and unloading of peptones and proteids from portal vein and
  liver into the general circulation. Sanguineous albuminuria from
  excess of albuminous food, free ingestion of water, suppressed milk
  secretion, forced marches. Transfusion of blood. Excess of albumen
  dangerous, excess of red globules not dangerous. The blood
  concentration of diuresis or diaphoresis is not dangerous. Continuous
  muscle decomposition from work bars the disease. Stable miasm
  untenable. Poison may be drawn suddenly from the enormous mass of
  blood in the liver, spleen and portal system. The absence of icterus
  antagonizes the bile theory. Benzoic acid, unaltered peptones, and
  glycogen are examples of elements destructive to blood. Normal
  destruction of red globules in liver, spleen and bone marrow. Sudden
  access of resulting hæmoglobin to the blood. Other products of
  disintegrated globules. Poisons from food, and antitoxic action of
  liver in presence of glycogen. Carbon dioxide favors solution of red
  globules. Theories of hæmoglobinæmia in man. Lesions: Blood black,
  diffluent, iridescent, has no avidity for oxygen, with excess of urea
  and extractives, serum of clot red, globules, small, pale, distorted,
  not sticky, extravasations, liver, enlarged, congested, blood gorged,
  spleen congested, swollen: Lumbar or gluteal muscles pale,
  infiltrated, with loss of striation; bone marrow congested,
  hemorrhagic; kidneys congested infarcted; urine dark brown or red,
  with excess of urea and hæmoglobin. End of spinal cord has congestion
  or infiltration. Symptoms: History of high condition, constant work,
  high feeding, a day’s rest, then exercise and attack. To full life,
  follows flagging, droops, moves one or both hind limbs stiffly,
  knuckles, drags toes, crouches, trembles, perspires, breathes rapidly,
  is tender on back, loins, croup or thigh, muscles firm, paretic, and
  drops unable to rise. Urine retained, brown, red or black, sometimes
  glairy, later may have casts. Appetite may return. In mild cases,
  stiffness, lameness, with or without visible muscular lesions or
  tremors. Urine glairy, dense, with excess of urea and nitrogenous
  products. Recover under careful feeding and exercise, and relapse
  under original causes. Progress: May recover under rest. In bad cases
  accelerated breathing and recumbency forbid rest and recovery.
  Recovery in a few hours or after a week. Urinary casts with renal
  epithelium, imply nephritis and grave conditions. In persistent
  paresis, muscles waste. Modes of death. Mortality 20 per cent.
  Diagnosis, by history of onset, etc. Prevention: When highly fed and
  hard worked, give daily exercise, with comparative rest, reduce
  ration, and give laxative or diuretic. Plenty of water. Treatment:
  Rest, sling, diffusible stimulants, bleeding, bromides, water ad
  libitum, fomentations, unload liver and portal vein, purgative,
  eserine, barium chloride, enemata, diuretics, for remaining paresis,
  derivatives, strychnia, diet, laxative, non-stimulating, restore to
  work gradually.


_Definition._ An acute auto-poisoning occurring in plethoric horse on
being subjected to active exertion after a period of idleness, and
manifested by great nervous excitement and prostration, paresis
commencing with the hind limbs and the passage of hæmoglobin in the
urine.

_Nature and Causes._ The most varied conclusions as to the nature of
this disease have been put forward by different authors. In England,
Haycock called it hysteria, mistakenly supposing that it was confined to
mares, and Williams attributed it to uræmic poisoning, conveniently
ignoring the fact that the sudden manifestation of the most extreme
symptoms in an animal which just before was in the highest apparent
health and spirits contradicted the conclusion. In France (Trasbot) and
Southern Europe (Csokor) it has been looked on as a spinal myelitis, a
conclusion based on the disturbed innervation of the posterior
extremities in the great majority of cases, but which is not always
sustained by the pathological anatomy of the cord. In Germany
veterinarians have viewed the disease from widely different standpoints.
Haubner calls it myelo-renal-congestion (Nièren-Rückenmarks): Weinmann,
a rheumatic lumbago; Dieckerhoff defines it as an acute general disease
of horses, manifested by a severe parenchymatous inflammation of the
skeleton muscles, with a bloody infiltration of the bone marrow,
especially of the femur, and with acute nephritis and hæmoglobinuria. He
attributes the attack to exposure to cold. If this were the real cause
the attack would be far more common in very cold weather when the horse
is suddenly exposed to cold drafts between open doors and windows, than
when he is harnessed and driven so as to generate and diffuse animal
heat. Yet attacks in the stable are virtually unknown, and in almost
every instance the onset occurs during a short drive. Friedberger and
Fröhner say that the epithet rheumatismal may be correctly applied to
almost all cases that we meet in practice. They quote Goring as having
produced the disease experimentally by exposure to cold, and go on to
explain that rest in the stable before the attack causes the extreme
sensitiveness to cold that is generated by a warm environment. The
implication of the lumbar, pelvic and femoral muscles they explain by
the stimulation of the nutritive metamorphosis by the action of cold on
the sensitive nerves of the skin. The effect of this cutaneous
irritation is exaggerated by the heat of the stable to which they have
been previously subjected. The products of the destruction of the
albuminoids of the muscles, pass into the blood as hæmoglobin, and
produce the ulterior phenomena. The muscles of the hind quarters
especially suffer because of their greater exposure and because they are
subjected to the hardest work in propelling the animal machine. In this
connection they quote the experiments of Lassar and Nassaroff in which
sudden exposure to cold determines parenchymatous degeneration of
muscles; also the cases of paroxysmal or winter hæmoglobinuria in
certain susceptible men whenever they are exposed to an extremely low
temperature.

There are serious objections to the acceptance of this as the essential
cause, among which the following may be named:

1st. The disease is not confined to the cold season but occurs also at
midsummer when the outdoor temperature is even higher than it is in the
stable.

2d. In our Northern States it appears to be more common in spring and
autumn or early winter, when the extreme colds have either already
passed, or have not yet set in, but when the abrupt changes of weather
(rain-storms, etc.) are liable to shut up the animal indoors for a day
or more at a time.

3d. The popular names quoted with approval by these authors—Monday
disease, Easter disease, Whitsuntide disease—indicate the prevalence in
Europe also, of the malady in the milder, or more temperate seasons
rather than during the prevalence of extreme cold.

4th. The fact that the disease rarely or never occurs in the stable, no
matter how cold the season, how open the wooden walls or floor, nor how
strong the draft between doors or windows, shows that the theory of cold
as the sole or main cause must be discarded.

It is not necessary to ignore the action of cold as a concurrent factor
in certain cases, or as a stimulant to reflex vaso-motor paresis, to
muscular metamorphosis and the increase of hæmoglobin in the blood. It
is only necessary that this should be held as subordinate and
non-essential to the final result. Several other factors that are
accorded a subordinate place by these writers, are so constant and so
manifestly essential that they must be allotted a much more important
position in the list of causes.

A =period of rest= is a constant precursor of an attack. The more
extended the inquiry the more certain we become that a short rest is a
prerequisite to equine hæmoglobinæmia. The horse that is kept at daily
steady work may be said to be practically exempt. Even the
non-professional observer recognizes the fact and names the disease
after the weekly or yearly holiday or rest day which was the occasion of
it. To him it is the Monday morning disease, the disease of the day
following Thanksgiving, Christmas, New Year, or Fourth of July. It is
the disease of wet weather, of heavy snowfalls, of the blizzard, or of
the owner’s absence from home, of any time that entails one or two days
of absolute inactivity in the stall.

But again the affection does not appear in the horse that is absolutely
idle for a length of time. It is the =short period of rest in an
interval of otherwise continuous work= that determines it. In short the
subject must be in good muscular condition and with a hearty, vigorous
appetite and good digestion. The short unwonted rest interrupts the
disposal of the rich products of a vigorous digestion, and tends to
overload the portal veins, the liver, the blood and tissues with an
excess of proteids. The condition of the animal is so far one of
plethora.

Another feature that bears this out is that the attack comes only in the
animal that is =heavily fed on a strongly nitrogenous ration=. It is not
the disease of the horse kept on straw, or hay, or which receives a
limited amount only of grain. It does not occur in the animal which has
its grain suspended or materially reduced during the one or two days of
idleness. It does not select the horse that has had a laxative either in
the form of food or medicine. This last may increase the sensitiveness
to cold, but it certainly lessens the tendency to hæmoglobinæmia. The
most rational explanation appears to be that it affords this protection
by interfering with the thoroughness of digestion and absorption, by
securing elimination from the portal veins and liver, and by reducing
the amount of albuminoids in the blood.

A blood abnormally rich in albuminoids, as it is in the transient
plethora induced by a short period of rest, in the well-conditioned
working horse, without any restriction of his diet, may therefore be set
down as one of the most important factors in producing hæmoglobinæmia.
Nor is this without approximate examples in human pathology. Von
Bamberger has shown that “hæmatogenous albuminuria” will occur in
healthy individuals when there is an excess of albumen in the
blood-plasma, as after a too free use of albuminous food, or after
suppression of the milk secretion (Landois). A similar result comes from
increase of blood pressure, as after drinking freely, or when, under
emotion or violent exertion, the heart’s action is increased in force
and the blood is thrown with greater impetus into the large renal
arteries. Senator has found albuminous urine to attend and follow, for
several days, upon forced marches made by young recruits. Here the
muscular work is added to the increased blood tension superinduced by
the more active contractions of the heart.

In this connection it is interesting to trace the changes in the blood
after transfusion. The dilatability of the capillaries enables the
system to accommodate itself to a very great increase in the volume of
blood An increase of 83 per cent. may be borne without serious results,
but above this limit there is increasing risk and an increase of 150 per
cent. entails immediate danger to life. In the restoration of the blood
to its normal condition, the secretion of water sets in promptly leaving
an excess of albuminoids and blood globules. The next change is in the
albuminoids which in two days are almost entirely transformed into urea.
This leaves the blood abnormally rich in globules (Panum, Lesser,
Worm-Müller), the red globules break up much more slowly and may still
be in excess after the lapse of a month (Tscherjew).

In this light, temporary plethora cannot of itself be accepted as the
main or essential cause of the disease. It must be admitted to be a more
constant and important factor than the mere exposure to cold, but of
itself it is inadequate to the production of hæmoglobinæmia. In the
absence of exertion the general plethora fails to produce the specific
disease; again, after transfusion a plethora of albumen lasts for one or
two days, but hæmoglobinæmia sets in only in the first few minutes after
the animal starts out from the stable, (never after an hour or two at
work): once more, excess of globules may last for a month, but with
steady work there is no danger of this disease, after the first mile or
two has been traversed, on the first day of the resumption of labor.

A similar plethora of albuminoids and globules may be induced in a
plethoric animal by a profuse diarrhœa, diuresis or perspiration, the
blood having been robbed of its watery constituents, and concentrated
especially as regards its globules and albuminoids, but hæmoglobinæmia
never occurs as the result of such an artificial concentration. On the
contrary a free secretion by the bowels or kidneys is of the greatest
value in cutting short its progress after it has set in.

The doctrine of poisoning by hæmoglobin produced by excessive work and
disintegration of the muscles is equally insufficient to account for an
attack. Excess of muscular work and of muscle-decomposition-products,
would not reach its maximum within the first few minutes after the
animal has started from the stable, but, other things being equal, would
increase with the continuance of work and the accumulation in the blood
of a constantly increasing amount of these products. The sharp line of
restriction by which the attack is limited to the initial period of
work, while it is never seen after hard work continued for hours in
succession, rules out this from the list of essential causes. It may be
that the products of muscular decomposition aggravate the attack, but to
set them down as the cause of the attack is to beg the whole question
and to contradict the truth that continuous and severe muscular work
with its consequent increase of waste products is a direct bar to the
development of the disease. It should be noted in this connection that
the increase in the waste of nitrogenous bodies, as shown by the
increase of urea, is dependent far more on the amount of nitrogenous
matters ingested than on the muscle work or decomposition. In eleven
hours just before ascending the Faulhorn, Fick passed 21.686 grs. of
urea per hour; in eight hours ascending the hill, 12.43 grs. per hour;
and in six hours after the ascent he passed 13.39 grs. per hour.

A general survey of the field shows that it is not the simple increase
of any normal waste product in the blood which determines
hæmoglobinæmia, and on the other hand the suddenness and severity of the
attack bears all the marks of a profound poisoning. The nature of the
poison has not yet been definitely ascertained, yet one or two
hypothesis may be hazarded, as furnishing a working theory, in
anticipation of the actual demonstration which may be expected in the
early future.

The action of a _stable miasm_ as claimed by some writers is
contradicted by the fact that the disease does not develop so long as
the animal is left to inhale that _miasm_, and on leaving the stable,
the life and vigor are usually remarkable.

The morbific agent must be sought in some source from which it can be
supplied with great rapidity under the stimulus of a short but active
exertion. The chylopoietic viscera furnish such a source. The healthy
liver contains one-fourth of the entire mass of the blood. The torpid
congested liver of the vigorous high conditioned horse, after a short
period of idleness, on full, rich feeding, must hold much more than this
normal ratio. The spleen, the natural store-house or safety valve of the
portal veins, is also gorged with this liquid in the high fed, idle
animal. This organ which is always turgescent after meals, is especially
so in the over-fed horse, which for twenty-four hours has been denied
the opportunity of working off by exercise, the superfluous products of
an active digestion and absorption. Then the whole of the portal veins
and the capillaries in which they originate are surcharged with rich
blood which cannot make its way with the necessary dispatch through the
inactive liver.

In this condition there is incomparably more than a quarter of the
entire mass of blood, enriched to the highest degree in proteids, ready
to be discharged through the liver and hepatic veins into the general
circulation. Under the action of the hurried breathing and circulation,
caused by the sudden and active exertion, this whole mass of rich blood
is speedily unloaded on the right heart, the lungs and the systemic
circulation. One can hardly conceive of a more effective method of
inducing a sudden plethora, with an excess of both globules and
albuminoids.

The presence of actual poisons in such blood is not so easily certified.

The absorption of _bile_ elements and especially of taurocholic acid,
which is a solvent of the red blood globules, and would set free their
globulin might account for the characteristic condition of the blood.
The powerful aspiratory action of the chest, would speedily empty the
whole of the liver blood vessels, and lessening their tension below that
of the biliary radicals would determine an active absorption of bile or
of the more diffusible of the bile elements. A manifest objection to
this view is the absence of an icteric tint in the mucous membranes of
the affected animals. The visible mucosæ are of a brownish red hue, such
as might come from hæmoglobin dissolved in the blood serum, rather than
the yellow tint which might be expected from bile pigment. The theory of
poisoning by bile acids therefore, would require an explanation of
concurrent suppression or decomposition of the bile pigments.

Other sources, however, offer solvents for hæmoglobin, benzoic acid,
which is derived from a cellulose in the fodders, and forms the source
of hippuric acid, dissolves red globules (Landois). In the over-fed
horse with active digestion, but inactive body and liver, this must
accumulate in the liver, spleen and portal system, and when suddenly
drawn into the blood without time for oxidation in the liver it will
contribute to the condition of hæmoglobinæmia.

Peptones, being very diffusible, are very rapidly absorbed, but they are
not found, in healthy conditions, in the portal vein (Neumeister). These
are manifestly transformed into albumen in the intestinal mucosa
(Salvioli), or taken up by the very numerous leucocytes and transformed
or carried elsewhere (Hoffmeister). But peptones injected into the blood
of the dog render it incoagulable, and in large quantity are fatal
(Landois). An excess of glycogen dissolves the red globules, and the
conditions of heavy feeding and torpid liver, are calculated to produce
this in great excess and to store it in the liver cells.

Under the extra vigorous aspiratory force of the chest, these highly
diffusible agents, present in great excess, are likely to be drawn on
through the mucosa, into the portal vein, liver, and cava, without an
opportunity for complete transformation by leucocytes or liver cells.
These would tend to rob the blood globules of their normal physiological
vigor, would unfit them for maintaining the healthy functions of lungs,
kidneys, brain or muscle, and would unfit the globules for successful
resistance to solvents and other inimical influences.

Again it is an important function of the liver, spleen and red bone
marrow to disintegrate worn out or abnormal red globules. These are
taken up by the white blood corpuscles of the hepatic capillaries, by
the cells of the spleen and the bone marrow and are stored up chiefly in
the _capillaries of the liver_, in the _spleen_, and in the marrow of
bone. They are transformed, partly into colored and partly into
colorless proteids, and are either deposited in the granular form, or
are dissolved (Landois). Quincke says: “That the normal red blood
globules and other particles suspended in the blood stream are not taken
up in this way, may be due to their being smooth and polished. As the
corpuscles grow older and become more rigid, they, as it were, are
caught by the amœboid cells. As cells containing blood corpuscles are
very rarely found in the general circulation, one may assume that the
occurrence of these cells within the spleen, liver, and marrow of bone,
is favored by the slowness of the circulation in these organs.” From
this chain of normal processes of blood disintegration, we may
reasonably infer, a greatly exaggerated work of blood destruction when,
in connection with an increased density of the plasma, and the presence
in the portal blood of poisonous products of digestion, the red globules
have been altered in density, in outline and in vitality, so that they
become ready victims of the amœboid cells of blood and tissues. Then the
stagnant condition of this altered blood in the compulsorily idle animal
favors the greatest excess of this destruction and the storing up of an
increased quantity of hæmoglobin and other products, to be poured
suddenly into the general circulation as soon as the movement of the
blood is quickened by exercise.

This destruction of the red blood globules by disintegration contributes
to the formation of numerous decomposition-products, like succinic,
formic, acetic, butyric and lactic acids, inosite, leucin, xanthine,
hypoxanthin, and uric acid, some of which are strongly toxic. The
tendency will be to lower the vitality of the red globules and thus to
render them the easier victims of the leucocytes and of the liver,
spleen and marrow cells. Even the freed hæmoglobin appears to exert a
solvent action on the red blood globules. These are, of course, most
concentrated and effective in the seat of their production, yet when
drawn suddenly in large amount, into the general circulation, by the
vigorous aspiratory action of the chest, they may prove seriously
detrimental to the blood at large.

Again a variety of toxic matters are introduced into the system in the
food and others are developed from the food in the stomach and
intestine. Brieger found in the gastric peptones a potent alkaloid
having the effect of urari, and which in excess would determine muscular
paralysis. The alkaloidal and other poisons produced by fermentations in
the intestines have to be safely disposed of. The ptomaines, if not too
abundant, are arrested or even decomposed in the liver which thus stands
as a guardian, at the outlet of the portal system, to protect the body
at large. But this antitoxic function of the liver is only exercised in
the presence of glycogen (Rogers, Landois), and forced muscular movement
soon removes all glycogen from the liver of the dog (Landois). Again
glycogenesis in the liver is now believed to be dependent on a ferment
produced by the pancreas. If therefore, the sudden active exercise and
the aspiratory action of the chest freed the liver of its glycogen, and
hurried the alkaloidal and other poisons through its capillaries too
rapidly to allow of the protective action of the liver cells, or if the
pancreas as well as the liver had become torpid and had failed to
produce the requisite amount of glycogen-ferment for the liver, the
poisoning of the blood and system at large would be imminent.

Not to mention the other toxic products which come from imperfect
metamorphosis in the liver, it may be noted that a venous condition of
the blood or an excess of carbon dioxide contributes greatly to the
solubility of the red blood globules. It also tends greatly to modify
the fibrinogenous elements. Thus the blood of a suffocated animal fails
to coagulate or coagulates loosely, and the blood of the portal vein of
a suffocated horse is strongly toxic (Sauson). Now the conditions
attendant on the onset of equine hæmoglobinæmia are such as to give free
scope to both of these inimical influences. The great mass of blood in
the portal vein, spleen and liver is venous blood strongly charged with
carbon dioxide, and by the sudden, active exertion this is forced
rapidly through the liver and lungs without time for full æration, so
that the whole mass of the circulating blood is speedily reduced below
par, and laid specially open to the action of blood solvents. By the
same action the systemic blood is charged with poisons, direct from the
food, and fermenting ingesta, and from the overworked spleen and liver
whose functions are profoundly impaired, and later from other important
organs, the healthy functional activity of which can no longer be
maintained by the deteriorated blood supplied to them.

Hæmoglobinæmia in dogs has been produced experimentally by the injection
of water into the veins the mere dilution of the plasma dissolving out
the coloring matter from the red globules (Hayem); also by the
inhalation of arseniureted hydrogen (Naunyn and Stadelman); by the
ingestion of toluylendiamine, or phosphorus (Afanassiew, Stadelman); by
snake venom, septicæmia, influenza, contagious pneumonia, petechial
fever, anthrax, etc. These cannot be looked on as causes of the acute
hæmoglobinæmia in the horse, but they serve as illustrations of changes
in the plasma, and poisons in the blood determining the escape of
hæmoglobin from the cells.

Ralfe recognizes two forms of hæmoglobinæmia in man:

1st. That in which the hæmoglobin is simply dissolved out of the blood
globules, the solution taking place chiefly in parts exposed to cold.

2d. A more severe form in which the dissolution is general and probably
attended by some destruction of red globules in the liver, spleen and
even in the kidneys. The general opinion appears to be that the attacks
are due to some nervous disturbance, which causes vaso-motor disorder
and it is supposed that there is an exaggerated sensibility of the
reflex nervous system. It has been suggested that peripheral irritation
causes irritation of the vaso-motor centre, and in turn this causes
local asphyxia in the part stimulated, under which conditions the red
globules part with their hæmoglobin (Roberts).

Murri holds that the disease depends on an increased irritability of the
vaso-motor reflex centre, and the formation, owing to the disorder of
the blood forming organs, of corpuscles unable to withstand exposure to
cold or carbon dioxide.

While it is not assumed to point out the actual poisons of
hæmoglobinæmia in the horse the above suggestions may offer valuable
hints as to the lines of inquiry that may be followed with the best hope
of reaching definite results.

_Lesions._ These are especially found in the blood, liver, spleen,
muscles, bone marrow and kidneys. The spinal cord and nerve trunks are
occasionally affected.

The _blood_ is charged with carbon dioxide and is black, tarry,
comparatively incoagulable remaining in the veins and showing an
iridescent reflection. It does not absorb oxygen readily though exposed
to the air, and thus bears a strong general resemblance to the blood of
anthrax. It contains an abnormal proportion of urea and allied
extractive matters which greatly increase its density, and interfere
with the healthy exercise of the different cell organisms and functions.
These are not due to excessive muscular activity as stated by
Friedberger and Fröhner, but are derived mainly from the abundant
products of digestion. When the shed blood coagulates it forms a soft
clot without buff and the expressed serum is reddish from the presence
of hæmoglobin, and of hæmatoidin crystals. The uncoagulated blood drawn
over a sheet of white paper stains it deeply by reason of the same
coloring matters in solution. The red corpuscles may be paler than
natural, some even entirely colorless, and they are often notched or
broken up in various irregular forms. They have lost the natural
tendency of the shed equine blood to stick together, to collect in
rouleaux and precipitate to the bottom of the vessel, so that no buffy
coat is formed, should the blood coagulate. The white corpuscles are
relatively increased. Finally the coloring matters contained in the
plasma are imbibed by the different tissues and give a brown or reddish
tinge to such as are naturally white. Limited blood extravasations are
not uncommon especially in the more vascular organs like the muscles,
liver, spleen and kidneys.

The _liver_ is more or less congested and enlarged, friable, yellow, or
mottled yellow and red and exudes black blood freely when incised. The
bile is thick, viscid and dark green, as in cases of experimental
intravenous injection of hæmoglobin.

The _spleen_ is also swollen and congested with blood, and the pulp is
very high colored from the excess of hæmoglobin and other products of
blood destruction. The _muscles of the croup_ are usually the seat of
visible lesions. There may be pallor, œdema and swelling, but not
unfrequently there are blood extravasations varying in size from a pin’s
head upward and giving a dark red aspect to the affected tissues. Under
the microscope the affected fibres are seen to have lost their
transverse striation and to have assumed a more or less granular or
hyaline appearance. Next to the gluteal muscles, these changes are
frequently found, in the muscles of the thigh (especially the rectus
femoris, and triceps extensor cruris), and in those of the loins (psoas,
ilio-spinalis, and longissimus dorsi). Exceptionally the pectoral
muscles are involved or even the abdominal muscles. A considerable
straw-colored œdema may be found in the intermuscular connective tissue.

The _red bone marrow_ primarily of the large bones of the limbs (femur,
tibia, humerus, radius,) and less frequently of other bones, even of the
vertebræ, is often the seat of intense vascular congestion and even of
hemorrhage. The medullary matter is of a deep red or black color, and
there is an abnormal accumulation of red globules in various conditions
of growth and destruction (red nucleated corpuscles, fragments of
corpuscles, colored granules). Dieckerhoff considers the condition one
of osteomyelitis, but it seems to be rather a sudden, extraordinary
exaggeration of the processes of blood metamorphosis. Neumann found that
when the blood regeneration process is very active even the yellow
marrow may be changed into red, and this throughout all the bones of the
extremities.

The _kidneys_ are usually the seat of congestion, and black spots of
infarction, when the disease has lasted for twenty-four hours. In
rapidly fatal cases they may appear normal. There may be enlargement of
the kidneys with softening and granular degeneration of the renal
epithelium in cases that survive for some days.

The _bladder_ contains dark brown or red glairy urine of a high density
and loaded with urea, hæmoglobin, etc.

The _terminal portion of the spinal cord_ and the lumbo-sacral plexus,
or some of its branches, are sometimes blood stained, or the seat of an
exudate or surrounded by one.

_Symptoms._ In the regular type of hæmoglobinæmia in the horse the
history of the attack is highly significant. The subject is in good
working condition, he may be fat, or lean, but in either case the
muscles are firm and well developed, diet has been liberal, embracing a
large proportion of albuminoids, work has been constant up to within a
day or two preceding the attack, when the animal has been left
absolutely idle in the stall without any reduction of feed. Then finally
it has been suddenly subjected to active exertion which demands vigorous
muscular movement, and above all activity of the respiratory muscles and
the heart. This exertion usually consists in riding under the saddle or
going in harness, but may attend on casting in the stall, lounging in a
ring, or in a playful run when suddenly set at liberty.

=Severe Cases.= The attack comes on early in the course of such
exercise. The patient may not have gone more than one hundred yards from
the stable or he may have traveled for half an hour or an hour, but the
disease rarely shows itself after a longer period of work.

The horse which left the stable full of life and spirit, suddenly flags
and hangs on the bit, the ears or head may drop, and one or more limbs
usually the hind ones, are moved stiffly and awkwardly, or even stagger.
He knuckles over at the fetlocks, drags the toes on the ground, flexes
the joints imperfectly, the muscles appearing to be rigid and
uncontrollable, or he crouches, the joints remaining semiflexed the
animal in vain attempting to extend them. The patient trembles
violently, sweats profusely, breathes deeply and rapidly and assumes a
pinched, anxious, agonized expression of countenance. The heart beats
tumultuously, the pulse (in 84 per cent. Friedberger and Fröhner) is
accelerated to a variable degree, and the temperature is still normal
(in 80 per cent. Friedberger and Fröhner), or rarely exceeds 101.5°F.
There is often tenderness on percussion and sometimes even on
manipulation over the loins, short ribs, and the croup, and pinching of
the loins may cause wincing. The affected muscle or muscles (lumbar,
gluteal, crural) are usually firm, hard and tender, they may be the seat
of spasm or of œdema and paresis. These parts may, however, have their
sensitiveness lessened and even punctures or electric currents may have
little effect on them.

Soon the increasing muscular weakness is incompatible with the
maintenance of the standing position, the bending of the limbs and
crouching become extreme, the animal makes vain efforts to control the
muscles and extend the joints, and helplessly drops to the ground. When
down he moves his legs convulsively, but is unable to coördinate the
muscular movements and all efforts to rise are unavailing.

The spasms and paresis may attack other parts of the body such as the
pectoral region the shoulders and even the abdomen, but the earliest and
most persistent disorder is usually in the divisions of the lumbo-sacral
plexus affecting the supra or sublumbar muscles, the gluteals, the
patellar (triceps,) the adductors and the abductors. The caudal muscles
are exceptionally involved. In a series of ten cases Bouley noticed that
the left hind limb was always the first paralyzed (evidently a simple
coincidence).

Urine may be passed freely or the bladder may be paretic so that it must
be emptied with the catheter. In severe cases the urine is of a high
density and of a dirty brownish gray, red or almost black color. It
contains no blood clots, nor blood globules, but granular hæmoglobin,
tyrosin and other waste products contribute to produce the reddish
color. In some instances there is an abundant _metalbumen_ which renders
the liquid glairy, causing it to fall in fine threads or films. Urea is
usually present in great excess. Hippuric and even uric acid are usually
present but not in excess. When the disease has advanced to nephritis
the albuminuria is complicated by the presence of casts of the
uriniferous tubes, renal epithelium, white and even red blood globules.

During the violence of the attack there is no disposition nor leisure to
eat, but when the more violent symptoms abate appetite is usually
manifested. There may be more or less paresis of both bowels and
bladder, so that neither fæces nor urine is passed yet in other cases
both are discharged spontaneously.

The senses are preserved, excepting in the case of the affected muscles
and the integument which covers them. There may, however, be more or
less dullness and stupor in certain cases from poisoning of the cerebral
centres by the poisons circulating in the blood.

=Mild Cases.= In the mildest cases there is stiffness and lameness in
one, or less frequently in both hind limbs, coming on when put to work
after a period of idleness, and not associated with any appreciable
lesion of the limb in question. There may or may not be hardness and
swelling of the gluteal or other muscles of the quarter or loins. This
has the appearance of rigidity or spasm but may be primarily due to
œdema or exudation into the substance of the muscle. In some instances
the muscles of the breast, shoulder, or forearm are the seat of the
trouble. Muscular trembling and perspiration may be present and if the
urine is examined, it is often found to be glairy, or charged with urea,
and allied nitrogenous products. These cases are not benefited by local
applications, but they recover (temporarily) under rest and above all
under active eliminating treatment. Under gentle and progressive
exercise too they improve and get well. They recur, however, with great
readiness under a rich nitrogenous diet and a temporary rest followed by
sudden exertion.

Between the mildest and gravest cases there are infinite gradations of
severity, one-third to one-half of the worst cases usually terminating
fatally, whereas the mildest are always amenable to treatment.

_Progress._ The course of the disease depends on the severity of the
attack but also, in no small degree, on the good judgment of the driver.
Cases that develop with great suddenness, and apparently with extreme
severity may subside spontaneously if the animal is placed in a
condition of absolute rest. If, however, we can secure rest of the
muscles of progression only, while the breathing remains rapid and
labored, improvement is unlikely, as the system continues to receive
large accessions of the toxic products. When the patient is down and
unable to rise, the enforced rest may be beneficial, but too commonly,
the greater effort with which breathing is carried on in the recumbent
position, and the frequent ineffectual struggles of the limbs prevent
the requisite muscular quietude.

In some cases, and especially in the mildest, recovery may seem to have
been effected in a few hours, and in others it will be seen in
twenty-four or forty-eight hours, while in still others the paresis and
helplessness may continue for a week and yet be followed by recovery. In
these cases appetite may be retained in greater or less degree, but the
intestinal peristalsis is usually weak and imperfect, the fæces small in
quantity and dry, and the bladder atonic so that the urine may have to
be drawn off with the catheter. It usually retains the deep red color,
or improvement may be heralded by a change to a dirty grayish hue. If,
however, it shows an excess of albumen, cylindroid casts entangling
renal epithelium and white or red globules it will indicate the access
of diffuse nephritis and a prolonged or even a fatal illness.

When control of the limbs is not restored at the end of a week, the
paretic muscles usually undergo marked and rapid wasting, which may last
for months or years. This is especially common in the case of the
patellar muscles (muscle of the fascia lata, triceps extensor cruris) in
which the atrophy may become so extreme that the skin covering the inner
and outer sides of the thigh may be brought virtually in contact in
front of the femur. This entails an almost complete inability to sustain
the body on the hind limbs. When atrophy is less extreme, there is only
a weakness, stiffness, or swaying or staggering on the hind limbs in
progression.

In fatal cases death may occur early in connection with the violent
struggles, the excited breathing, pulmonary hypostasis and congestion, a
cyanotic hue of the visible mucous membranes and a gradual increase of
stupor. Though delayed for several days, there is a continuation of the
muscular struggles, and the labored breathing; the red or glairy
character of the urine persists or is exaggerated; the nervous
irritability increases, with muscular trembling; and cyanosis, or stupor
increases until death.

The _mortality_ is always high in the severe forms of the disease, the
deaths ranging from 20 per cent. upward.

After a first attack there is a strong predisposition to a second under
similar exciting conditions.

_Diagnosis._ The peculiar symptoms of this disease and the circumstances
attending its onset, are usually sufficient to distinguish it from all
others. There may be danger of confounding certain cases with thrombosis
of the posterior aorta, or of the iliac arteries or their branches, but
the absence, in such cases, of the special history of the attack and of
the morbid state of the urine, and the absence of pulsation in the
arteries distal to the thrombosis will serve to prevent confusion.
Spinal myelitis will be distinguished by the gradual nature of the
onset, by the absence of the conditions attending on the attack of
hæmoglobinæmia, and usually by the absence of hæmoglobin, urea and other
nitrogenous products in excess in the urine.

_Prevention._ The hard worked or systematically exercised horse, which
is at the same time heavily fed must not be left in a state of absolute
rest in his stall for twenty-four hours. A fair amount of exercise must
be given on every day in the week, and at the same time, the food should
be restricted in ratio with the restriction of exercise. Turning for an
hour or two daily into a yard may be a sufficient precaution. When from
any cause, rest is imperative, the diet must be materially reduced and
given in part in a laxative form (bran, roots), or a slight laxative
(Glauber salts) or diuretic (saltpeter) may be added. Cleanliness and a
free ventilation of the stable, are also of value in obviating at once
auto-intoxication and the admission of poison through the lungs. In the
same way a free allowance of drinking water is beneficial as favoring a
general elimination from the various emunctories, and a dilution of the
plethoric blood.

These precautionary measures are especially important in the case of
horses which have passed through a first attack and which are in
consequence strongly predisposed to a second. Horses fed liberally on
highly nitrogenous food (oats, beans, peas, cotton seed meal), will also
require specially careful oversight when at rest for a day or two only.

_Treatment._ The first and perhaps the most important consideration is
absolute rest. If the subject is stopped instantly on the appearance of
the first symptoms, the disease may be often aborted. It is better to
avoid the exercise of walking to a stable until such time as the
severity of the attack has somewhat moderated and then to move the
subject only in the slowest and quietest possible way. If the patient is
already down and unable to rise, he may be carried to the nearest stable
in an ambulance or on a stone-boat, and there helped to his feet and
supported in slings. Though he may be unable to continue in the standing
position without the sling, yet if he can use his limbs at all for
support, and is prevented from lying down, the breathing will be
rendered so much more free and quiet, that it may greatly lessen the
transfer of the poisonous elements into the general circulation and
materially contribute to recovery. If, however, he cannot stand on his
limbs at all, but must settle in the slings, the compression of the
chest will so excite the breathing that it will induce dyspnœa,
pulmonary congestion and a rapidly fatal result. In such a case a good
bed must be provided and the patient made as comfortable as possible in
the recumbent position.

In some cases in the earliest stages a full dose of sweet spirits of
nitre or even half a pint of whiskey has seemed to assist in aborting
the disease though the urine was already of a deep red color. It
probably acted by supporting the already oppressed heart, and securing a
prompt elimination by the kidneys.

Friedberger and Fröhner strongly recommend bleeding in all cases of
dyspnœa and excited heart action, and considering the plethoric
condition of the animal it would equally commend itself in other cases
as well. This is the most prompt sedative of the nervous and vascular
excitement, and the most speedy and certain means of removing much of
the poisons accumulated in the blood, and of diluting what remains by
reason of the absorption of liquids from every available source. This
will more than counterbalance any temporary increase of poisons drawn
from the portal system to fill up the vacuum in the systemic veins
caused by the emission of blood. When the thick tarry condition of the
blood seriously hinders a speedy abstraction both jugulars may be opened
at once.

In some cases of great nervous excitement bromides may be useful in
moderating circulatory and respiratory movement, but on the whole the
advantage is greater from an immediate resort to eliminating agents.

One of the most effective agents is water. If the patient is thirsty he
should have all he will drink, and if not, it may even be given from a
bottle, or thrown into the rectum. A still more effective resort would
be to introduce water intravenously in the form of a normal saline
solution, or even to pass it into the trachea through a small cannula or
large hypodermic needle. This serves to dilute the over dense blood, to
stimulate the kidneys and other emunctories to active secretion, and to
retain in solution the hæmoglobin, urea and other products which would
otherwise cause greater irritation. This would be especially applicable
after the blood tension had been diminished by phlebotomy.

Warm fomentations to the loins or croup are not without their influence.
They tend to soothe the irritated parts and to solicit the action of the
kidneys more particularly. The old resort of a fresh sheep skin, with
the fleshy side in, may be used as a substitute.

Perhaps the most important indication is to secure depletion from the
overloaded portal system and liver. Where nothing better offers, a pint
or quart of castor oil, or a pound of Glauber salts, or a half drachm of
podophyllin and four drachms of aloes may be given. If available 1 to 1½
grains of eserine, or 7 grains of barium chloride may be given
hypodermically in distilled water or that which has been raised to the
boiling point. This may be supplemented by frequent injections of hot
soap suds or even of laxative saline solutions. If the bowels can be
roused to free secretion the removal of toxic matters from the portal
blood and the delay in the progress of similar matters through the liver
will go far toward securing a favorable result. When free purgation has
been secured recovery can usually be counted on.

The action on the bowels must be followed up by diuretics to eliminate
the offensive matters from the general system. Colchicum has been
recommended because of its action in increasing the solids of the urine,
and this may be combined with saltpeter or other diuretic, or the latter
may be used alone and repeated twice a day. If, however, the patient
can, by the free use of common salt or otherwise, be induced to drink
freely of water, the elimination through the kidneys will be
sufficiently secured.

The muscular weakness and paralysis that remain after the acute symptoms
have subsided must be met by stimulating liniments and even blisters to
the loins or affected muscles, by the internal use of strychnia (2 grs.
twice daily) until the jerking of the muscles indicates that its
physiological action has been secured, and by an electric current daily
for ten minutes at a time through the affected nerves and muscles.
Animals that have been helpless for weeks have, in our hands, recovered
under such treatment, and even cases of several months’ standing, with
the most extensive atrophy of the triceps, and in which the animal could
barely stand, have made a satisfactory recovery.

Any remaining nephritis must be treated according to its indications.

During recovery and in the convalescent animal the diet should be
laxative and non-stimulating. Bran mashes, turnips, beets, carrots,
green fodder, ensilage and scalded hay may be allowed. Oats, corn,
beans, peas, vetches, etc., must be carefully avoided. If the food fails
to maintain the bowels in a gently relaxed condition one, two or more
ounces of sulphate of soda may be added daily.

In the mild cases a good dose of purgative medicine succeeded by a
course of diuretics will serve a good purpose.

In all cases alike work must be resumed very gradually. At first the
animal may be walked a few hundred yards, and the pace or load and
duration of exercise may be increased day by day until full work can be
safely endured. In an animal that has once suffered the same gradual
inuring to labor should be followed, after any short period of rest on a
fairly good ration.


                    JAUNDICE, ICTERUS, THE YELLOWS.

  Symptomatic. Causes: Mechanical obstruction of bile duct, gall-stones,
  hydatids, distomata, extraneous bodies, inflammation, stricture,
  obliteration, absence, ulceration, spasm, tumor, enlarged lymph
  glands, gastric tumors, pancreatic, kidney or omental tumor, aneurism,
  fæcal accumulation, pregnancy, ovarian tumor: Without mechanical
  obstruction, ptomaines and toxins, animal venoms, mineral poisons,
  hepatic atrophy, fear, other emotions, cerebral concussion, imperfect
  oxidation, excess of bile, hepatic inflammation, constipation and
  reabsorption of bile, experimental jaundice, balance of tension in
  gall ducts and blood vessels, duodenitis, compression of aorta,
  hæmatoidin and bilirubin, destruction of blood globules by hydroæmia,
  taurocholate of soda, chloroform, ether, freezing, heat, electricity,
  alkalies, nitrites. Hæmoglobin: Its solubility in horse. Bile acids
  and blood pigment. Summary of causes. Gravity of icterus. Symptoms:
  Coloration, yellow, orange, brown, of tissues and secretions: Tests,
  staining white paper, Gmelin’s test, nitric and sulphuric acids,
  rainbow hues: Pettenkofer’s test for bile acids, syrup and sulphuric
  acid, dark violet: Stranburg’s test syrupy paper and sulphuric acid,
  dark violet; clay colored fœtid stools; gravity.

The terms icterus and jaundice are applied to a yellowness of the
mucosæ, urine, skin and tissues caused by the presence in them of the
coloring matters of bile. The condition is a symptom of many different
affections rather than a disease _per se_, yet the phenomenon is so
characteristic that it has been hitherto accorded a special place and
article in systematic works.

Jaundice is either associated with _mechanical obstruction of the bile
duct_ or ducts, or it is _independent of such obstruction_. The
following enumeration of its causes slightly modified from Murchison, is
equally applicable to the lower animals as to man:

A. Jaundice From Mechanical Obstruction of the Bile Duct.

_I. Obstruction by foreign bodies within the duct_:

   1. Gall stones and inspissated bile.

   2. Hydatids and distomata.

   3. Foreign bodies from the intestines.

_II. Obstruction by inflammatory tumefaction of the duodenum or of the
lining membrane of the bile duct with exudation into its interior._

_III. Obstruction by stricture or obliteration of the duct._

   1. Congenital deficiency of the duct.

   2. Stricture from perihepatitis.

   3. Closure of the orifice of the duct in consequence of ulcer of the
        duodenum.

   4. Stricture from cicatrization of ulcers in the bile duct.

   5. Spasmodic stricture.

_IV. Obstruction by tumors closing the orifice of the duct or growing in
its interior._

V. Obstruction by pressure on the duct from within, by:

   1. Tumors projecting from the liver itself.

   2. Enlarged glands in the fissure of the liver.

   3. Tumor of the stomach.

   4. Tumor of the pancreas.

   5. Tumor of the kidney.

   6. Post peritoneal or omental tumor.

   7. An abdominal aneurism.

   8. Accumulation of fæces in the bowels.

   9. A pregnant uterus.

  10. Ovarian and uterine tumors.

B. Jaundice Independent of Mechanical Obstruction of the Bile Ducts.

_I. Poisons in the blood interfering with the normal metamorphosis of
bile._

  1. The poisons of the various specific fevers (Anthrax, Texas fever,
  Hog cholera, Swineplague, Petechial fever, Pyæmia, Septicæmia, etc.).

  2. Animal poisons: snake poison.

  3. Mineral poisons: phosphorus, mercury, copper, antimony, etc.

  4. Chloroform, ether, etc.

  5. Acute atrophy of the liver.

II. Impaired or deranged innervation interfering with the normal
metamorphosis of bile.

  1. Severe mental emotions: fright, anxiety, etc.

  2. Concussion of the brain.

III. Deficient oxygenation of blood interfering with the normal
metamorphosis of bile.

IV. Excessive secretion of bile, more of which is absorbed than can
undergo the normal metamorphosis.

  Congestion of the liver: _a._ Mechanical, _b._ Active, _c._ Passive.

V. Undue absorption of bile into the blood from habitual or protracted
constipation.

Mechanical obstruction, by tying the bile ducts in a dog, caused in two
hours yellow coloration of the contents of the hepatic lymphatics and
thoracic duct, and also of the blood in the hepatic veins (Saunders).
That this jaundice is due to reabsorption and not to suppressed
secretion of bile, already present in the blood, may be fairly inferred,
from the complete absence of icterus, where, from general disease of the
liver, the secretion of bile has been entirely suspended, and in which
the gall ducts and bladder contain only a little gray mucus (Haspell,
Frerichs, Budd, Murchison), also from the fact that after complete
extirpation of the liver in frogs not a trace of biliary acids nor
pigment can be detected in the blood, urine, or muscular tissue (Müller,
Runde, Lehmann, Moleschott). Bile acids and bile pigment are formed in
the liver by disintegration of blood globules, and when present in
excess in the blood it is by virtue of reabsorption.

This reabsorption will take place under the slightest favoring
influence. The obstructions in the bile duct, above referred to, cause
the tension in these ducts to exceed that of the blood in the
capillaries of the liver and at once osmosis of bile into the blood
vessels sets in. This may occur from so slight a cause as the congestion
and swelling of the duodenal mucosa around the opening of the bile duct.
Again reabsorption of bile may be determined by a lessening of the
normal fullness and tension of the hepatic capillaries as when the aorta
is mechanically compressed by abscess, neoplasm, ingesta, or otherwise,
just behind the diaphragm (Heidenham, Brunton). The cause is the same in
both cases, namely, the want of balance between the fullness and tension
of the bile ducts, and the hepatic blood vessels. There is increased
fullness of the hepatic biliary ducts, or decreased plenitude of the
hepatic capillaries and lymphatics.

It must be added, however, that the coloring matter of the bile is
apparently produced, in the liver, from that of the blood, and that the
pigment (hæmatoidin), found in old extravasations of blood, is probably
identical with bilirubin, and that any agent or condition which causes
liberation of the coloring matter of the red blood globules, will cause
a staining of the tissues, like that of jaundice. The following agents
are known to have this effect on the blood globules: water, in hydroæmic
states of the blood (Hermann); taurocholate of soda from absorption of
bile (Frerichs, Kuhne, Feltz, Ritter); chloroform (Chaumont); ether
(Burdon-Sanderson); freezing (Rollet); a high temperature +60° C.
(Schultze); frictional and induction currents of electricity
(Burdon-Sanderson); the alkalies (ammonia, potash and soda) and nitrites
when present in excess.

The injection of hæmoglobin into the veins of dogs has been followed by
the appearance of bile pigment in the urine, but Naumyn, Wolff, Legg and
Brunton failed to obtain the same result in rabbits.

It is noticeable that the hæmoglobin of horses’ blood is very soluble at
all temperatures and that of dogs very slightly so (Burdon-Sanderson).
This may serve to explain the great prevalence among solipeds of
diseases, associated with dusky brown or yellow discoloration of the
mucosæ, with petechiæ, and with the passage of blood pigments in the
urine. It may further explain the usually benignant course of jaundice
in the horse and its extreme gravity in the dog.

There is further reason to believe that the bile acids, when in excess,
may be transformed into bile pigment in certain conditions of the blood,
as occurs under the action of sulphuric acid out of the body (Stœdler,
Meukomen, Folwarcyny, Röhrig). Moreover, in the healthy state, the
greater part of the bile secreted, including acids and pigment, is
re-absorbed from the intestinal canal, but is oxidized and decomposed in
the blood so that it cannot be detected, in blood or urine. But let the
transformation be interrupted, as in certain diseases of the lungs, with
imperfect oxidation, and the bile circulates in the blood, stains
tissues and urine, and in short causes jaundice.

To sum up: it may be said that icterus is probably never due to simple
inactivity of the liver: it may, however, be caused by excessive
secretion of bile which is re-absorbed from obstructed bile ducts or
bowels:—it may result from imperfect transformation, in the blood, of
the bile which is normally re-absorbed from the intestine: or it may
possibly be caused by the formation of pigments in the blood from the
abnormal transformation of bile acids, or by solution of the hæmoglobin
of the blood corpuscles.

The gravity of jaundice varies as much as its causes. It is well known
that the system may be saturated with bile, and the tissues and urine
deeply stained without much constitutional disorder. The pigment alone
is not an active poison. But there may be much attendant suffering from
obstructed biliary ducts or bowels, from diseases of the lungs, or from
disintegration of the blood globules and imperfect nutrition, or there
may be profound nervous prostration and disorder from uræmia, or from
the presence in the blood of an excess of effete and partially oxidized
albuminoids (See Azotæmia). According to our present knowledge,
constitutional disorder, prostration and suffering in cases of jaundice,
are mainly due to the presence in the circulation of these albuminoids,
and of taurocholic acid which latter has a most destructive effect on
the blood corpuscles.

The _symptoms_, therefore, are not characteristic apart from the yellow
coloration of the tissues and urine and the chemical reactions of the
bile acids and bile pigments furnished by the latter.

The coloration of the tissues may be a simple tinge of yellow especially
noticeable in the eye (conjunctiva), or it may amount to the darkest
shades of orange and brown. It may or may not be complicated by the
presence of spots or patches of blood-staining (ecchymosis) on the
visible mucous membranes but especially in cases complicated by
poisoning with taurocholic acid or effete nitrogenous products.

The urine may be similarly colored in all shades of yellow or orange
brown, and may leave a correspondingly deep stain on white paper.

The _test_ for _bile pigments_ (Gmelin’s) is simple and beautiful. Pour
a little nitric acid into a test tube held obliquely and then add a few
drops of sulphuric acid, and finally a little urine, so slowly, that it
will remain on the surface. Soon at the point of junction appear in
succession the various colors of the rainbow: yellow, green, blue,
violet, red and lastly a dirty yellow. It is open to this objection that
the characteristic play of colors may be produced by alcohol in the
absence of bile pigments. Indican also will produce the green and yellow
with blue between but never the violet nor red, nor all in their regular
order.

A _second mode_ of applying this test is by spreading a few drops of the
urine on a white plate and letting fall a drop of nitric acid in the
centre. The play of colors is very characteristic.

The _test for bile acids_ (Pettenkofer’s) is to place a portion of the
urine in a test tube, and after adding a drop of syrup, to add
cautiously, drop by drop, two-thirds of the amount of sulphuric acid.
Shake the mixture and set aside for some minutes. If sufficient heat is
not produced by the mixing of the acid and urine warm slightly. The
mixture becomes of a dark violet color which is destroyed by a
temperature a little above 140° Fah.

A convenient application of this test (Stranburg) is to add a little
cane sugar to the urine, dip a piece of filtering paper in the mixture,
dry it thoroughly, pour a drop of sulphuric acid on the paper and allow
it to run partially off. In a quarter of a minute a beautiful violet
color is produced, best seen by holding up the paper to the light and
looking through it (Brunton).

In cases due to obstruction of the bile ducts the dung is destitute of
bile, whitish, often clayey and fœtid, while in cases due to
reabsorption without obstruction the fæces have their natural color and
odor.

It is needless to enumerate all the concomitant symptoms of jaundice
which will be better noticed under the different disorders which
determine it, for a list of which see the _causes_.

The gravity of the affection will depend on the dangerous nature of
these concurrent diseases, and the destructive changes in the liver and
blood rather than on the depth of color in the textures.


               CATARRHAL ICTERUS (JAUNDICE) OF SOLIPEDS.

  Causes: infection from duodenum through biliary duct. Suppression of
  bile favors. Musty, heated, mow burnt fodder, over feeding, irregular
  feeding, or watering, over work, worms, fatigue, damp stables,
  duodenal congestion, gall-stones, concretions, pancreatic tumor,
  ascaris in bile ducts, distoma, infection through portal vein, toxins.
  Symptoms: of duodenal catarrh, icterus, yellow, viscous, odorous
  urine, dullness, weakness, somnolence, tardy pulse and breathing,
  costiveness, or diarrhœa, pale, fœtid stools. Duration: 2 to 3 weeks
  or longer. Lesions: duodenitis, distended biliary and pancreatic
  ducts, calculi, enlarged softened liver and kidneys. Diagnosis:
  icteric symptoms in absence of fever. Prognosis: usually favorable.
  Treatment: laxative diet, pasture, soiling, ensilage, roots, fruits,
  water freely, exercise, antisepsis, elimination, laxatives,
  cholagogues, diuretics, calomel, salines, nitro-muriatic acid,
  podophyllin, castor oil, aloes, tartar emetic, bitters, sodium
  bicarbonate.

_Causes._ This may be said to be an extension of infection from the
duodenum through the bile ducts. The microbes of the intestinal canal
become acclimatized by living in the bile-charged contents of the
duodenum until they acquired the power of survival and multiplication in
the biliary ducts themselves. The well known antiseptic qualities of the
bile, constitute a powerful barrier to this, yet the power of adaptation
on the part of certain germs is greater than the defensive action of the
bile. The attack is however mostly in connection with indigestion or
muco-enteritis, and a more or less perfect suspension of biliary
secretion, so that this defensive action is reduced to its minimum and
the germs can ascend the bile ducts in the mucous secretion as a culture
medium, and by interference with the resumption of a free hepatic
secretion, they succeed in safely colonizing themselves in the mucosa
and hepatic parenchyma. Whatever, therefore, interferes with the
integrity of the duodenal functions directly contributes to the
extension of infection from bowel to liver. Old, heated, musty,
cryptogamic, dusty fodder, grains that have been badly harvested in wet
seasons, feed that has been damp and fermented, overloading of the
stomach, irregular feeding and watering, giving drink after a feed of
grain, underfeeding, overwork, worms, excessive fatigue, damp, dark
stables, etc., tend to induce indigestions and to lay the bile ducts
open to infection. Blocking of the bile duct and stasis of its contents
may be a sufficient cause. The swollen mucosa around the orifice of the
duct not only blocks the passage but favors the formation of a mucous
plug as recorded by Benjamin of an equine patient. Wolff found
obstruction of the duodenum in the horse by a mass of ingesta, and
blocking of the gall duct, with jaundice.

Gall stones and concretions are very direct causes of biliary
obstruction and jaundice. Though less common in horses than cattle,
these are not unknown in idle, pampered animals when on dry winter
feeding.

Tumors of the pancreas or adjacent organs pressing on the gall duct are
recognized as causes of equine icterus, (Megnin, Nocard).

With any obstruction to the bile a disturbance of balance of pressure
between the bile ducts and the hepatic veins is brought about by
respiratory movements. On the one hand the aspiratory power of the chest
empties the hepatic veins, lessening blood pressure, and in expiration
the contraction of diaphragm and abdominal muscles compresses the gall
ducts increasing their tension and favoring absorption of bile.

The entrance into the bile duct of the ascaris megalocephala is at once
a cause of obstruction and of the transference of duodenal microbes, and
the presence of trematodes (fasciola hepatica, or distoma lanceolatum)
will also favor obstruction. Other parasites, like the echinococcus or
actinomycosis, may press on the biliary ducts and determine jaundice.

Another mode of infection is by way of the portal vein, the microbes
entering from the intestine and becoming arrested and colonized in the
liver (Dieckerhoff).

Whether from the presence of the microbes or from the absorption of
ptomaines and toxins from the intestines, the radical biliary ducts
become inflamed, swollen, and even blocked, and the hepatic cells
degenerated or even completely devitalized, so that they fail to take an
aniline stain. In such cases the remaining sound hepatic cells go on
producing bile, but as this cannot any longer escape through the
partially obstructed interlobular biliary radicles, it is largely
absorbed and produces icterus. Cadeac mentions a case of this kind in a
mare in which the toxic matters had not only led to hepatic disease, but
also to structural changes in the eliminating organ (the kidney).

_Symptoms._ In the horse the disease is mostly attendant on subacute
duodenitis, and even when this is associated with infective catarrh of
the biliary passages the kidneys remain mostly sound and active, and
eliminate alike the bile pigments and the more toxic matters so that the
disease is not often grave. Beside the essential feature of yellow
mucosæ, and urine, the latter viscous and smelling strongly, there is
profound depression, sluggishness, weakness and somnolence. Imperfect
muscular control and even slight paresis may be present. Tardy pulse and
breathing are at times noticeable. At others these, like the
temperature, are normal. The mouth is hot and dry. The urine may be
slightly albuminous. The bowels incline to costiveness from lack of
their customary stimulus, yet this in turn may give rise to diarrhœa. In
either case, as the disease advances, the defecations lose the healthy
yellowish brown color, becoming pale and fœtid.

_Duration._ The attack may last one, two or three weeks, and generally
ends in recovery. With irremediable structural lesions, it is of course
permanent and even fatal.

_Lesions._ The most common feature is duodenitis with thickening around
the orifice of the common bile and pancreatic duct. The biliary ducts
may be distended and their contents more than usually viscid and glairy
from the presence of pus. Their mucosa may show ramified redness, or
concretions as casts or calculi. The liver is enlarged, soft and friable
giving way readily under the pressure of the finger. Enlargement of the
kidneys is usually present, the cortical substance having a brownish red
and the medullary portion a yellowish pink hue.

_Diagnosis._ The absence of hyperthermia in jaundice, serves to
distinguish it from the acute febrile affections (pneumonia, influenza,
contagious pneumonia, petechial fever, etc.,) which are marked by
yellowness of the mucosæ and skin.

_Prognosis._ The merely functional forms of icterus in solipeds usually
end in recovery.

_Treatment._ The first consideration is a laxative diet. A run at
pasture will usually meet every indication. Fresh cut grass, ensilage,
turnips, carrots, potatoes, beet, apples, or other succulent diet may be
given as substitute. Bran mashes and hay cut and moistened may be
allowed in the absence of the above. Abundance of water and especially
cool water will stimulate bowels, liver and kidneys, favor the
elimination of the bile by contraction of the biliary ducts, and hasten
the expulsion of the poisons through the kidneys. Regular exercise an
hour after meals stimulates both bowels and liver to action.

Medicinal treatment is largely directed to antisepsis of the bowels and
the arrest of the production of injurious toxins; elimination from the
bowels and incidental depletion from the portal vein and liver;
antisepsis and stimulation of the liver; and stimulation of the urinary
secretion.

The preparations of mercury fill several of these indications. Calomel 2
drs., or blue mass 1½ dr., is not only a soothing laxative and
antiseptic, but seems to operate as a calmative and antiseptic to the
liver as well. It may be continued in 5 to 10 grain doses two or three
times a day, according to the size of the animal and the condition of
the bowels, and associated with ½ dr. belladonna extract to each dose
together with a bitter (quassia, gentian, nux vomica). Or 4 or 5 ozs.
sulphate of soda may be given three times a day, with 2 drs. salicylate
of soda as an antiseptic. Or, to increase the hepatic action,
nitro-muriatic acid largely diluted may be given in sixty drop doses
thrice a day in the drinking water. These are especially valuable for
their antiseptic action, cutting off at once the source of nervous
irritation from the attendant indigestions, and duodenal congestion, and
arresting the flow of the irritant toxins and other products through the
portal system. Podophyllin, castor oil, aloes, rhubarb, often act well
by depletion from the portal vein, and expulsion of indigestible and
irritant matters from the intestines, but there is more danger of
resulting swelling of the duodenal mucosa than with the mercurials or
aqua regia. Goubaux recommends 2½ drs. of tartar emetic.

Siedamgrotzky has had good results from an electric current sent through
the region of the liver, but in the horse this is rarely demanded.

A course of bitters, with bicarbonate of soda in small doses, may be
demanded to re-establish the healthy tone of the stomach and intestines,
and a run at pasture, or at least an open air life, exercise, and a
laxative diet with abundance of good water should be secured. Any undue
costiveness should be counteracted at once by a saline laxative.


                 CATARRHAL ICTERUS (JAUNDICE) IN DOGS.

  Pampered artificial life of dogs as predisposition. Eating carrion.
  Chills especially when heated and exhausted. Infection from bowels.
  Obstruction of gall duct by inflammation, calculi, neoplasms.
  Catarrhal exudate as a protector of microbes. Toxins from intestines,
  food or water. Youth, lack of acclimation, mental shock, blocking of
  bowel, blood effusion in gall bladder, incubation. Symptoms: signs of
  gastro-enteritis, prostration with invasion of the liver and
  especially of the kidney. Icteric urine without jaundiced mucosa.
  Gravity of icterus with suppression of urine. Hypochondriac
  tenderness, arched back, dullness, irregular bowels, excited
  circulation and breathing, preliminary fever tends to subside,
  tympany, colic, trembling. Death in one or two days or more. Lesions:
  congestion, degeneration, ecchymosis, ulceration of gastro-duodenal
  mucosa, extending into liver ducts and acini, bile inspissated, liver
  enlarged, yellowish brown, softened, fatty, shrunken, distorted
  hepatic cells. Kidneys congested, ecchymosed, cortical part with
  necrotic foci; lymph glands congested. Diagnosis: by icterus of
  tissues and urine tests. Prognosis: grave in acute cases, more hopeful
  in tardy ones. Treatment: antiseptics, cholagogues, salol,
  salicylates, alkalies, carbonates, tartrates, iodides, laxatives, cold
  enemata, aloes, electricity, water freely, pilocarpin, strychnia, aqua
  regia, digitalis, bitters, muriatic acid, convalescent diet.

_Causes._ The dog is much more subject to jaundice than the horse, and
the affection is liable to be much more severe, than in solipeds. He
leads a more artificial life, especially in cities, where the lack of
open air exercise, and of the facility for attending to nature’s wants,
together with an excessive, varied, stimulating diet predisposes him to
constipation, indigestion, and disorders of the stomach, bowels and
liver. In other cases the devouring of decomposing food and foul water
proves a cause of direct microbian infection, and of poisoning by
ptomaines and toxins generated out of the body. Exposure manifestly has
something to do with the prevalence of canine icterus, which is more
common in spring and especially in autumn than at other seasons. In
hunting dogs, out of condition, the suddenly induced over-exertion and
fatigue, and the succeeding chill in cold air or water, become accessory
factors.

It appears to be most commonly the result of the transference of germs
from the intestine, either by way of the bile ducts, or with the blood
through the portal vein. The first form is usually the sequel of
muco-enteritis affecting the duodenum, with swelling of the walls of the
common bile and pancreatic duct at its orifice, or from obstruction by
gall-stones, concretions, impacted bowels or neoplasms. With the arrest
of the biliary flow the intestinal ferments gain an entrance into the
common duct and the sac of Vater, finding protection from the antiseptic
bile in the resulting catarrhal exudate, and in this way they reach the
gall-bladder, the biliary radicles and the acini. With the entrance of
bacteria or toxins by the portal vein on the other hand, there is first
a troubled condition of the acini and hepatic cells, an over-secretion
of thick bile, and blocking of the passages so that little is passed
into the intestine, the greater part being absorbed into the hepatic
veins. Fermentation microbes in the stomach and intestines, the germs of
suppuration and septicæmia, and saprophytic germs from outside the body
are held to be causative of icterus. Cadeac lays much stress on the
putrefactive germs in water, and traces different attacks to marshes and
foul ponds.

As in other infecting diseases, early age has a predisposing influence.
The older subject has presumably been already exposed to the microbe and
acquired some measure of immunity. Animals coming new to the locality
and poison, are equally susceptible with the young. Trasbot found that
14 out of 17 dogs thus attacked were between three and eighteen months.

Leblanc and Trasbot claim mental shock as a cause of icterus in the dog.
The disappointment and weariness caused by the master’s absence, the
excitement of a fiercely contested fight, and brutal punishment are
adduced as cases in point. Abuse of emetics and purgatives, in
connection with a pre-existing hepatic or duodenal disorder or as a
supposed prophylactic of canine distemper has induced jaundice.

Obstruction of the small intestine has proved a factor, partly by the
reflex irritation through the splanchnic nerves, and partly through
obstruction to the common bile and pancreatic duct.

Walley records a case of obstruction of the cystic duct by extravasation
of blood in the gall bladder.

Icterus not infrequently supervenes during canine distemper in which the
early gastric and duodenal irritation becomes an occasion of the
extension of the catarrhal infection to the common bile duct. Even apart
from this Trasbot has seen the majority of cases ushered in by a
gastro-duodenitis. In this connection it is interesting to quote the
remark of Pfuhl that 26 out of 27 persons using the foul baths of a
given establishment contracted icterus, while the soldiers bathing in
another branch of the Elbe entirely escaped.

The fact that icterus usually sets in several days after such an
exposure, whether in man or dog, indicates a period of incubation, and
thereby sustains the theory of infection.

_Symptoms._ In the majority of cases, gastro-enteritis constitutes the
first step of this affection and the early symptoms are characteristic
of that disease. Frequent vomiting, at first of food, and later of a
glairy fluid which may be discolored by bile, redness of the tongue,
especially along its margins, bloodshot, watery eyes, lying down with
the nose on the right side of the abdomen, or standing with the abdomen
tucked up and the back arched, halting movements of the limbs, wincing
if manipulation is made of the spine or the epigastrium, elevated
temperature, accelerated pulse and breathing, anorexia and perhaps
purging, mark the onset. So long as the liver is unaffected prostration
is not a marked feature.

Even when the liver is invaded, a fair measure of life and activity may
often be retained so long as the kidneys remain sound and active. The
bile pigments and salts, and the toxins generated by the invading
microbes are alike eliminated in large part in the urine, and the
profound poisoning and prostration of the nervous system are in a
measure prevented. In many cases therefore the urine is strongly
jaundiced without much or any discoloration of the mucosæ and in such
cases the prospects are usually good for an early and complete recovery.
It must not, however, be inferred that such a happy issue will always
follow, as the pigments are by no means as toxic as are other hepatic
products and fatal results may ensue with very slight jaundice of the
tissues.

As a rule, however, the jaundice of the tissues (eyes, nose, mouth,
white portions of the skin) is to be accepted as a grave manifestation,
indicating either an excessive production and absorption of bile, or a
suppressed secretion through the kidneys, or both. Then the poisoning by
biliary salts and bacterial toxins is shown in profound dullness,
prostration, muscular weakness, indisposition to rise, moving stiffly
and only when dragged by the collar, the limbs trembling and the back
arched. The tender back is arched, the right hypochondrium sensitive,
the expression dull, stupid and listless, and constipation or a fœtid
diarrhœa is liable to set in. The heart beats may be strong and
irregular, the breathing is easily disturbed and hurried. The
temperature at first 104° to 107° may descend to the normal as the
system becomes charged with the toxic products, and does not usually
exceed 99.5° after two or three days of jaundice of the tissues.

The icterus is shown in the eye or mouth, or on any white portion of the
skin, and in the urine it will be detected by the eye or by the tests
above given.

In the worst cases the urine is very scanty and of a deep yellowish
brown color, prostration is extreme, tympany, colic, obstinate
constipation or bloody diarrhœa may set in, the breathing, hurried or
not, is trembling, the pulse small, and the temperature at first high
may descend to 95° or even much lower before death.

The _course_ of the disease varies according to its gravity. If there is
complete retention of bile, and abundant production of toxins, the
animal dies in one or two days in a state of collapse. If there is
general progressive degeneration and destruction of the hepatic tissue
without at first absolute suppression of the discharge of bile into the
duodenum, the patient may last till the fourth or fifth day, or later.

_Lesions._ There are usually congestion, tumefaction, friability,
ecchymosis and even ulceration of the gastric and duodenal mucosa. The
organs are empty, but show a reddish brown exudate of a glairy
consistency, and containing red blood globules and pus corpuscles. The
same inflammatory lesions are to be traced into the common bile duct,
the cystic duct and bladder, the biliary ducts, and the acini. The mouth
of the common duct is usually blocked with a plug of tenacious mucus,
the gall bladder having been unable to expel this and the inspissated
bile into the intestine. The liver is slightly enlarged, yellowish, with
patches of brownish yellow more or less deep, and the acini contain an
abundance of oily globules, and yellowish brown granules. The acini have
no clear line of delimitation, and the contained hepatic cells are
shrunken and distorted, standing apart from each other in a dropsical or
watery medium.

The kidneys are congested and ecchymosed; the cortical substance brown,
friable, and with numerous areas of necrosis of a bluish white color,
and even abscesses. The medullary substance is yellow and the
uriniferous tubes contain an abundance of yellowish brown granules.

The lungs have a yellowish red color, with patches of ecchymosis.

The lymph glands generally are congested and many of them gorged with
blood, of a dark red color, and lacking in consistency and cohesion.

_Diagnosis._ The characteristic icterus is lacking in the early stages,
and active treatment gives good hope of success. When indigestion,
persistent vomiting and tenderness of the epigastrium, and right
hypochondrium, are associated with diarrhœa, it is highly important to
examine the urine for even slight traces of bile. When the jaundice is
due to impaction of a biliary calculus, the symptoms may increase
slowly, and yet reach a sudden climax with acute colicy pains and
tenderness of the right hypochondrium.

_Prognosis._ In acute rapidly developing cases a fatal issue is to be
expected. In those which develop more slowly, recovery may be hoped for
if early treatment is instituted.

_Treatment._ Cases due to biliary calculus must be treated for that
lesion.

In purely infective icterus attempts must be made to arrest the
intestinal and hepatic fermentation. As intestinal antiseptics,
naphthol, benzo-naphthol, naphthaline, 5 grains four to six times a day.
As hepatic antiseptics, salol 5 grains, salicylate of soda 8 grains, or
calomel 1 grain four times a day. The salol and salicylate tend to
increase biliary secretion and to render it more fluid. The same end is
attained by alkalies (carbonates of potassa, or soda or lithia,
bitartrate of soda, iodide of potassium). These are further valuable in
hastening the elimination of toxic matters by the kidneys. The expulsion
of bile, and of intestinal microbes and toxins may be sought by laxative
doses of Glauber salts, or by cold enemas of the same. Verheyen
recommends aloes in laxative doses for six days. Siedamgrotzky had good
results from induction currents of electricity, sent through the region
of the liver twice a day for ten minutes on each occasion. To assist in
elimination abundance of pure water or of watery fluids may be used. The
most effective eliminating agent is pilocarpin in ⅙ gr. dose
hypodermically, repeated daily. In weak conditions frequent small doses
of strychnia, ether, aqua regia, or digitalis may prove valuable.

In case of improvement a course of bitters is usually demanded, and
these may be combined with hydrochloric acid or small doses of sodium
bicarbonate.

Throughout the disease, gruels, beef tea, buttermilk, whey or any simple
nutritive aliment which the animal relishes may be given, but both then
and during convalescence fatty matters and indigestible materials should
be carefully withheld.


                     JAUNDICE IN CATTLE AND SHEEP.

  Usually with gall-stones or concretions, or distomata. In sheep from
  decomposing vegetation. Symptoms: anæmia, emaciation, pallor, icteric
  mucosæ. Digestive disorder and bilious stools suggest worms.
  Treatment: as in horse, or vermifuge.

Though less common than in the dog icterus in ruminants occurs, but most
commonly in connection with gall stones and concretions, or with
trematodes in the gall ducts. These forms will be noticed under these
respective headings. Verheyen describes an icterus of sheep which occurs
enzootically in damp low undrained localities, and is attributed by
shepherds to the consumption of dead and fermenting leaves. The symptoms
are those of anæmia, emaciation, and increasing weakness, with a pallor
and more or less dull yellow of the conjunctiva, and, later, of the
other mucosæ. The loss of appetite, indigestion, yellow liquid fæces,
suggest the possible presence of parasites as a cause, and the
prescribed treatment by common salt, juniper berries and tonics
strengthens the suspicion. Other forms must be treated according to
cause on the lines laid down above.


            JAUNDICE OF THE NEW-BORN. ICTERUS NOUVEAUX NÉS.

  In mules; less frequently in horses and cattle. Bacteridian.
  Predisposition from alleged miscegeneration. Offspring of lymphatic
  mares. Spoiled fodders, foul buildings, exposure, infection by
  umbilicus. From gastro-enteritis, diarrhœa, dysentery. Congenital.
  Symptoms: refuses the teat, scours, red urine, palpitation, colics,
  perspirations, inflammations, or abscesses of navel, arthritis, other
  internal disorders. Death from exhaustion or in convulsions. Or
  symptoms subside and pass in 15 days. Diagnosis: prostration,
  palpitation, icterus, and bloody urine with omphalitis. Streptococci.
  Prognosis: with hæmaturia nine-tenths fatal. Lesions: icterus, heart
  soft, flabby, lungs congested, general ecchymosis, blood black, clot
  diffluent, liver congested, enlarged, spleen, swollen, softened with
  spots of brownish yellow, meconium bloodstained, kidneys swollen,
  congested, points of infarction or necrosis, urine bloody, navel
  lesions. Treatment: for congenital cases improve hygiene for dams; for
  offspring, antiseptics to navel, shelter, warm box; aloes to dam, or
  oil to colt, antiseptics internally, demulcents, stimulants,
  derivatives, opium, water, alkalies.

This has been observed in cattle (Kitt), and in horses (Levrier,
Bernadin, Lhomme) but above all in mules (Villa-Roya, Carrere, Levriere,
Bernadin, Lhomme, Hartmann, Dieckerhoff).

The affection is a bacteridian disease, in which there is a great
destruction of red globules, and liberation of hæmatin, with hæmaturia
and yellow coloration of the tissues.

_Causes._ Carrere attributes much to a supposed congenital weakness
induced by the unnatural generation of ass with mare. Cadeac noticed
that the offspring of certain mares and horses remained sound, while the
progeny of the same animals, and asses suffered largely from icterus.
Levrier found it especially in the mules born of mares having a
lymphatic temperament or suffering from canker, grease or chronic
lymphangiectasis. Bernadin and Lhomme attribute much to bad hygiene, and
especially to poor or spoiled fodders. Lhomme, Lafosse and Trasbot find
accessory causes in cold and wet weather. Retention of the meconium is
another cause. Dieckerhoff, Hartmann, Cadeac and Bournay trace the
disease to bacterial infection as the essential cause. Many cases
originate in septic infection and inflammation of the navel and
umbilical veins. Others commence with mucous gastro-enteritis, attended
by diarrhœa or dysentery. In other cases the germs appear to have
reached the liver through the circulation as the animal is already
affected at birth.

_Symptoms._ When not congenital, symptoms are usually seen in the first
few days of life, usually before the fifth day.

In congenital cases the new born animal is unable to stand at all or for
longer than a very short time, it lies listlessly and makes no attempt
to suck even when held up to the teat. There is acceleration of pulse
and respiration, the heart beats are tumultuous, the mouth is dry, the
mucosæ of a straw yellow, the bowels are costive, and the urine, whether
discharged in life, or found in the bladder after death, is bloody.

When attacked later, the animal becomes dull, weak, and stupid, refuses
the teat, and has the bowels relaxed. The mucosæ become pale yellow, the
breathing accelerated, the heart beats violent, and the pulse rapid,
small and weak. The urine is passed slowly and with effort and has a red
hue more or less deep according to the severity of the attack. Colics
are not uncommon, causing uneasy shifting of the limbs and tail, cries,
frequent lying down and rising, and partial or general perspiration.
Complications on the part of the navel and umbilical veins are to be
looked for, in open sores, swellings, abscess, phlebitis, and in
arthritis and secondary abscesses in different organs. Death may occur
quietly, as from exhaustion, while in other cases it is preceded by
convulsions.

In case of recovery, there is an improvement of the general symptoms,
the heart and respirations become moderate, appetite is restored, the
little animal sucking the teat, there are abundant, yellow, semi-solid
defecations, the strength increases day by day, and convalescence may be
fully established by the twelfth to the fifteenth day.

_Diagnosis._ This is mainly based on the extreme weakness and
prostration, the violent heart action, the jaundiced hue of the mucous
membranes, and the bloody urine. Confirmation may be sought in the
presence of streptococci in the fresh urine, kidneys, liver and blood,
and in the artificial cultures made from them. The presence of
omphalitis is further significant.

_Prognosis._ Bernardin says that if hæmaturia is present nine out of ten
cases are fatal, while in the absence of this feature nine-tenths
recover.

_Lesions._ The jaundiced appearance of the conjunctiva and other tissues
is constant. The heart is pale, soft and flaccid, with petechial patches
of a deep red extending into the muscular substance; the lungs are
congested with similar patches of blood-staining; the blood in the heart
and larger vessels is dark, and fluid or only loosely clotted. The liver
is congested to twice or thrice its normal size (10 lbs. in place of 3
or 4 lbs.); the spleen is enlarged, softened, and shows spots of
brownish yellow. The small intestine contains a yellowish or dark red
meconium, and it may contain effusions of dark blood, while its mucosa
is inflamed, thickened, easily lacerated, and pigmented, or marked by
petechiæ. The large intestines and especially the rectum are packed with
hard dry balls.

The kidneys are enlarged, often to double their volume, and deeply
congested, with infarcts, and patches of necrosis, of a pale brownish
yellow hue. The urine in the bladder is deeply stained with blood
coloring matter.

_Treatment._ For congenital cases it is manifest that treatment must be
preventive and applied to the dam, before parturition. An open air life,
moderate exercise, sound, easily digestible and nourishing food;
grooming; in the stable, cleanliness, dryness and good ventilation; good
water, are essential.

For the offspring, antiseptics (tannin, mercuric chloride lotion,
copperas, calomel, iodoform), applied to the navel, and protection
against cold winds and rains, and damp lairs. For mules and other young
animals born in severe, winter weather a dry, warm, foaling box is
desirable, and the little animal should be rubbed dry and covered with a
warm woolen blanket. When the temperature approaches zero or the barn is
cold, the smaller animals, as soon as they are dropped, should be placed
under a box with a jar of hot water wrapped in woolen coverings, or with
hot bricks similarly wrapped, and should only be let out for food when
they are completely dried, or when the weather has moderated.

_Therapeutic treatment_ may be commenced by a dose of aloes given to the
dam, or of olive or castor oil or manna given to the offspring. As a
substitute sulphate of soda may be used. Antiseptics like salicylate of
soda, salol, or the sulphites may be added. To act as a demulcent on the
alimentary and urinary tracts, well boiled flaxseed tea is usually
recommended. Weakness may be met by warm strong coffee, salicin, quinia,
or other bitters, and more stimulating agents like camphor, angelica,
assafœtida, or even oil of turpentine may be added. Diarrhœa may be
checked by linseed tea, mustard plasters, or in obstinate cases, by
opium. Elimination should be sought by administering abundance of pure
water or watery demulcents, and even by the use of alkalies like
bicarbonates of soda or potash. A moderately free action of the bowels
must be constantly maintained.

Antiseptic treatment of the navel and umbilical veins must not be
overlooked.


  LUPINOSIS, ACUTE TOXÆMIC ICTERUS, ACUTE YELLOW ATROPHY OF THE LIVER.

  Attacks sheep, goat, ox, horse, stag; and, experimentally, dog.
  Causes: consumption of lupins, at a given stage of ripeness, from a
  given part of a field, or from centre of a stack. Lupinotoxine,
  conicine, methyl conicine, lupinine. Cryptogamic or bacterial poison.
  Weak subjects, sheep and even ewes and lambs, suffer most. Symptoms:
  Acute form: anorexia, fever, excited pulse and breathing, stupor, or
  hyperæsthesia, vertigo, swellings on head. Poisonous lupins are first
  rejected. Bloody nasal froth. In two or three days icterus. Urine may
  be bloody. Fæces at first hard, coated, bloody, later dark brown and
  often liquid. Emaciation. Death in 1 to 5 days. Chronic form,
  gastro-enteritis, emaciation, anæmia. Nasal catarrh. Facial swellings
  and sores. Lesions: hepatitis, nephritis, muco-enteritis, enlarged
  spleen, icterus, blood extravasations; hepatic tissue, infiltrated,
  cloudy, granular, fatty, later cirrhosis. Kidneys contain casts:
  Spleen tumid, blood gorged. Prognosis: grave: acute cases die, chronic
  may recover. Prevention: feed no lupins, avoid dangerous fields, wash
  off poison from lupins with a soda solution. Ensilage with acid
  producing fodder in alternate layers. Treatment: avoid alkalies, give
  acids, purgative, castor oil, water. In horse, causes anorexia,
  anæsthesia, dullness, stupor, colic, constipation, urinary irritation,
  fever, slight jaundice, vertigo, orange nasal discharge, sores on
  tongue and face, and lower part of limbs. Diagnosis. Prognosis
  hopeful. Treatment as in sheep. Icterus from other fodders.

This affection has been noticed especially in sheep, but also in the
goat, horse, ox and stag as the result of eating lupins. The dog has
contracted the disease under experiment. It has been studied especially
in Northern Germany where the lupin is largely cultivated as a fodder
crop. The yellow lupin (Lupinus Luteus) is mainly to blame for the
disease, but the Lupinus Albus and Augustifolius are also spoken of as
factors.

The disease caused by altered seeds and straw of the lupin is mainly
characterized by jaundice, fatty degeneration of the hepatic cells and
hypertrophy of the connective tissue of the liver causing acute atrophy
of the organ.

_Causes._ The essential cause of the disease appears to be the
consumption of lupins. But all lupins are not equally poisonous. Those
taken from one portion of a field are harmless, while those from another
are toxic. In stacks built in the field and weathered the upper and
outer portions are often harmless while the interior remains poisonous.
It would seem as if the poison were washed off by the rain, or deprived
of its potency by the action of the air. It successfully resists dry
heat, for three hours at boiling temperature, but is rendered harmless
by steam acting under the pressure of two atmospheres for the same
length of time. A poisonous principle (lupino-toxine) has been obtained
from the toxic lupins but it is not quite certain that this is the sole
toxic ingredient. This agent is extracted from the powdered seeds by
macerating them for two hours in a soda solution (in which it is very
soluble) at 102° F., and purified by treating the solution successively
with acetic acid, lead acetate, hyposulphuric acid and alcohol. This
agent produces the symptoms of lupinosis in the acute or chronic form
according to the doses of the agent administered. Eichhorn and
Baumstarch have isolated from lupins an alkaloid analogous to
_conicine_: Stener found an alkaloid which he believed to be
_methylconicine_: Baumert attributed the activity to another alkaloid
_lupinine_. It is not definitely known whether the poisoning is usually
effected by a simple poison or by a combination of several. Nor is it
certain whether the toxic matter is a normal product of lupins grown on
particular soils and under given conditions and harvested at a
particular stage of growth, or if it is the product of a cryptogamic or
bacterial growth. Some leguminous seeds are poisonous at a given stage
of ripening but there is as yet no proof of lupinosis being confined to
any particular stage. The common moulds often grow on lupins without
rendering them poisonous, but it does not follow that some less familiar
cryptogam is equally harmless under all circumstances. The soda extract
of the poisonous lupins was deadly though it contained no cryptogams,
but it is not shown that it was free from soluble chemical products
(toxins) of the cryptogams. The same remark applies with equal force to
the bacteria which have been invoked as the cause of the poisons. Though
not themselves present in a given deadly extract of the lupins this does
not exclude from such extract the toxic products of bacterial growth. It
is claimed that Arnold has produced lupinosis with lupins that had been
first robbed of their alkaloids. But the absence of alkaloids does not
prove the absence of nonbasic (neutral) poisons, of vegetable,
cryptogamic or bacterial origin.

That certain lupins contain a deadly poison is certified, but the
precise source of the poison remains to be demonstrated.

In estimating causes we must take into account the lessened power of
resistance of animals lacking in constitutional strength and vigor. Thus
sheep suffer far more severely than horses, oxen, or even goats. Ewes
and lambs perish in greater numbers than rams, hoggets and wethers.

_Symptoms in Sheep._ In the acute form the disease appears suddenly, as
manifested by anorexia, hyperthermia, rapid and oppressed breathing,
accelerated pulse, stupor, vertigo, and not unfrequently swellings of
lips, ears or face. Inappetence may be first manifested by the rejection
of poisonous lupins, while sound ones and especially other food are
still eaten, but soon all are refused alike. Temperature, which may
reach 104° to 106° F. on the next day after feeding on the poison, may
rise and fall day by day, and finally fall materially as a herald of
death. Respiration rises to 100 per minute and becomes labored or
panting, with, in some cases, a bloody froth in the nostrils. The pulse
rising to 130 and upwards keeps pace with the hyperthermia and general
excitement. Vertigo is shown in the staggering gait when moved, and by a
tendency to steady by resting the head on the trough, rack, fence or
ground. The recumbent position is often preferred, the head being
extended on the ground, and the animal remaining oblivious to all
efforts to raise him—even to blows. Sometimes there is stupor, and at
others hyperæsthesia, or indications of fear. There is grinding of the
teeth, and sometimes trismus (Schütz, Kotelman).

In two or three days jaundice is shown, more especially in the
conjunctiva and the urine. The latter, however, is not unfrequently
colored with blood, and contains albumen, bile acids, and renal
epithelium and casts. It is passed frequently in small quantity, so that
its condition is easily ascertained.

The fæces are at first scanty and hard with a coating of yellowish
mucus, and it may be streaks of blood. Later they are uniformly stained
of a dark brown, and diarrhœa may alternate with the constipation.
Emaciation advances with rapid strides.

Death may occur as early as one day after the attack but is usually
deferred to the fourth or fifth.

A steady amelioration of all the symptoms may be welcomed as a precursor
of recovery.

In the _chronic form_ jaundice may be entirely absent, and a subacute
gastro-enteritis may be attended by emaciation and anæmia. Roloff has
frequently found the implication of the other mucosæ especially those of
the nose and eyes which become catarrhal, and Zurn notes the implication
of the skin of the face with exudations, swellings and the formation of
sores and scabs on the eyelids, lips, ears, etc.

_Lesions in Sheep._ The prominent lesions are parenchymatous
inflammation of the liver and kidneys, muco-enteritis, enlargement of
the spleen, and icterus, with more or less blood extravasation.

The liver is the seat of acute hepatitis. It is usually swollen and
abnormally friable, with a yellowish color often as deep as citron. The
parts recently attacked exhibit albuminoid infiltration and cloudy
swelling, the older lesions show fatty or granular degeneration. These
changes exist especially in the hepatic cells, and fatty metamorphosis
bears a direct relation to the obesity of the sheep. If the patient has
survived the first few days, the liquefied products are absorbed, there
is a relative increase of the interstitial connective tissue and the
volume of the organ is materially decreased (acute yellow atrophy of the
liver, Schütz). In chronic cases, the hypertrophy of the interstitial
connective tissue is the most prominent feature, constituting a distinct
cirrhoses (fibroid induration) and the atrophy becomes very pronounced
while the surface is very irregular and uneven. The gall bladder is
distended, and its mucosa congested.

Jaundice, which may be little marked apart from the conjunctiva, is
usually shown in the subcutaneous connective tissue, the skin of the
abdomen, the omentum and mesentery, but according to Cadeac is never
shown in cartilage, bone nor tendon.

The kidneys show parenchymatous inflammation, congestion, swelling which
gives a hardness of touch through the resisting fibrous envelope, and
often a pervading shade of yellow. The epithelium of the uriniferous
tubes is cloudy, turbid and granular and the tubes themselves contain
cylindroid casts. The bladder is catarrhal and has been too irritable to
contain urine.

The spleen is tumid, soft, reddish gray, and on section shows excess of
blood, pulp, and here and there marbling by fibrinous exudate.

The heart is pale, granular, friable, with a tinge of yellow and with a
slight citron colored effusion in the pericardium. The cardiac blood is
dark and thick but coagulates and brightens in color on exposure to the
air.

There is usually some œdema of the lung, larnyx and pia mater.

There are catarrhal lesions of the abomasum and entire intestinal canal
with granular degeneration of the epithelium and spots and patches of
arborescent congestion and hæmorrhage. The icteric tint is usually
distinct.

_Prognosis_ is always grave. Acute cases are almost always fatal.
Chronic cases due to eating lupins in which the poison is relatively
weak, or a very restricted amount of the more poisonous lupins, may
recover. This mortality is very serious in the affected districts 5.8
per cent. of all the sheep of some districts in Pommerania perishing
yearly from this affection and entailing the loss of almost the same
number of lambs (Von Below-Seleske).

_Prevention._ Radical prevention can be secured by the exclusion of
lupins from the ration. Where this is undesirable the fields that
produce poisonous lupins can be ascertained and devoted to the
production of other crops. When a crop of lupins has already been
produced on a dangerous field the poison may be extracted from the
fodder or subjected to the action of an antidote. Fortunately the poison
is concentrated on the surface of the lupin and is easily washed off.

Dammann advises to leave the cut forage exposed to the rain so that the
poison may be washed off. A more prompt and effective plan would be to
put the fodder under a stream of water from a hose, and it could be fed
while still fresh and unaltered. Friedberger and Fröhner directs that
the forage be steeped for forty-eight hours in a soda solution (1:100)
to dissolve off the offensive matter, after which it may be washed and
safely fed.

Glaser would put the lupins in a silo, in alternate layers with some
material which rapidly undergoes acid fermentation (brewers grains,
maize, pulped roots). The acid renders the poison insoluble and is
directly antidotal. To develop this acid it is important to put the
materials into the silo before they have become too far matured.

The destruction of the poison by steaming the fodder under a pressure of
two atmospheres, as recommended by Kuhn and Roloff requires a too
elaborate apparatus for ordinary use.

_Therapeutic treatment._ The first desideratum is to render insoluble
any poison which has already entered the alimentary canal. Alkalies, as
solvents and distributers of the poison must be carefully avoided and
acids (acetic, nitric, hydrochloric, sulphuric) freely used. These may
be mixed with the drinking water or given from a bottle. If appetite is
still retained, they may be mixed with the food, or acid aliment (sour
ensilage, old grains, or fermented swill) may be supplied.

The next resort is a purgative to eliminate the poison from the
alimentary canal. But the cathartics usually given to the ruminants are
dangerous. Sulphate of soda undergoing decomposition, furnishes an
alkaline solvent for the poison. Castor oil is therefore to be
preferred.

An abundance of water will favor the action of both bowels and kidneys
and hasten the elimination of the poison which may have been already
absorbed into the system.

European writers recommend the use of the flesh as human food, unless
the animal had reached the last stage of the disease.

_Symptoms of Lupinosis in the Horse._ There is always the history of the
presence of lupins in the oats, or of lupin straw as a food or litter.
Though less fatal than in sheep the disease sets in with great severity,
the symptoms referring especially to gastro-enteritis, and disorders of
innervation. There is complete anorexia, impaired sensibility, dullness
and stupor, the head resting on the manger or drooping with the nose
near the ground. There is grinding of the teeth, colicy symptoms, and
constipation, the fæces being passed as a few small, hard balls covered
with mucus and fœtid. Urine is passed frequently in small amount and
albuminous. There is more or less hyperthermia (rising at times to 102°
to 103°), the respiration is hurried (36 to 40 per minute) and pulse is
rapid (60 per minute). Jaundice is usually present but less prominent
than in sheep. When moved the animal sways unsteadily or staggers.
Butzert notices, in addition to the above, a thick orange colored
discharge from the nose, and the formation of sores and scabs
(mummification) of the lingual mucous membrane, of the lips, of the
skin, of the face, and of the pastern, and swelling of the lower parts
of the limbs.

_Diagnosis._ The development of disease with the above symptoms, in the
inmates of a single stable, or in horses having a common ration, in
which the lupines are found, will make diagnosis easy and reasonably
certain.

_Prognosis_ is hopeful or confident. The disease is not fatal in the
horse.

_Treatment_ should follow the same lines as in sheep.

_Allied or identical diseases._ Friedberger and Fröhner quote a number
of outbreaks of hepatic inflammation or disorder with icterus in the
absence of lupins, but on rations that were otherwise faulty. Haubner
describes a “malignant icterus” in sheep fed on malted potatoes; Sander
records a “hepatic typhus” in the horse when fed on inundated pastures;
Reinemann and Jansen speak of a similar affection in animals fed on the
straw of peas, beans and vetches.




                        CONGESTION OF THE LIVER.

  Physiologically after a meal is hyperæmic, and may increase one-third.
  Rich feed and temporary idleness may cause morbid congestion. Other
  causes are: ptomaines and toxins in spoiled food, hepatic irritants,
  damp, hot, tropical climates, warm, damp, buildings, overfeeding,
  dilated right heart, insufficiency of tricuspid valve, pulmonary
  emphysema or congestion. Absence of valve between the right heart and
  hepatic veins, slow hepatic circulation, dilatability of hepatic
  vascular system, compression of lung by false membranes, œdema,
  hepatization, infarction, hydrothorax. In horse: special causes:
  spoiled fodders, carminatives, volatile oils, work in hot sun,
  vaso-dilatation in heat and atony, falls, kicks, goring, blows;
  passive forms from obstacles to the circulation. Lesions: Hepatic
  enlargement to 20 or 30 pounds, and dark red color, darker spots of
  extravasation, hepatic vein congestion in centre, and portal vein
  congestion in periphery of acinus, softening, granular, fatty, nuclei
  disappear from hepatic cells, nutmeg liver, cirrhosis. Symptoms:
  general febrile symptoms, great prostration, drowsiness, slight
  colics, arched loins, trembling or jerking, lies on right side,
  percussion on last ribs painful, slight icterus and increased
  urination and urea. In passive cases, less icterus and kidney trouble;
  tends to intestinal catarrh and ascites. Prevention: good hygiene,
  moderate laxative ration, cool air, exercise. Treatment: green or
  laxative foods, salines, derivatives, water at will, always before
  morning feed. In dog: overfeeding, indolence: pulmonary and
  circulatory troubles. Lesions: nutmeg liver, degeneration, cirrhosis.
  Symptoms: pampered idleness, obesity, pulmonary or cardiac disease,
  intestinal catarrh, piles, ascites, slight icterus, percussion
  tenderness of right hypochondrium, lying on right side, increase of
  percussion flatness. Treatment: saline purgatives or laxatives,
  antiseptics, restricted laxative diet, open air exercise, derivatives,
  etc.


Physiologically the liver undergoes hyperæmia in connection with an
abundant meal and active digestion. Within the limits of health it may
increase one-third in bulk and weight. When this hyperæmia attends on
temporary idleness and rich feeding it may overstep the limits of health
and become pathological. Other causes of pathological congestion are,
tainted food rich in ptomaines and toxins, food injured by cryptogams,
and food that contains principles irritating to the liver. It is
especially common in swampy regions in tropical or semi-tropical
latitudes, and where the warm air is surcharged with moisture. Hot,
close, damp stables, with overfeeding and lack of exercise in the
pampered horse or dog, or under the forcing system of feeding for
exhibition, or for the butcher, acts in a similar manner. Dilatation of
the right heart, or imperfection of the tricuspid valve is a direct
cause of mechanical congestion and emphysema, congestion or other
obstruction in the lungs has a similar effect. In short the absence of
valves between the right heart and the hepatic veins determines a
passive congestion of the liver whenever there is any serious hindrance
to the passage of blood through the right heart and lungs. The tardy
circulation through the liver (5 mm. per second) also predisposes to
congestion. The great development of the circulatory system in the
liver, and its dilatability predisposes it to such congestions in a
pre-eminent degree. For the same reason the liver suffers in the horse
that is attacked with pulmonary congestion, whether as the result of
overwork or of heat congestion. It will also suffer from compression of
the lungs by false membranes or hydrothorax, or obstruction, by œdema,
hepatization or infarction. The toxic matters produced in infectious
diseases, and especially those affecting the intestinal canal and its
connections, are arrested in the liver and contribute to hyperæmia.


                 CONGESTION OF THE LIVER IN THE HORSE.

_Causes._ Beside the general causes above mentioned, may be specially
named, musty, decomposed, and irritant fodders: those which like green
legumes, are easily fermented; and those which contain stimulating
volatile oils or carminative principles. They are also especially
exposed to such causes as severe and prolonged work under a hot sun, the
nervous atony which causes vaso-dilatation in a hot climate, and such
traumatisms as come from falls, kicks, goring, and blows by shafts,
poles and clubs. These especially induce _active congestion_. The
_passive_ forms come mainly from obstruction in the lungs, or heart
(dilatation, right valvular insufficiency, pericarditis,
hydropericardium, myocarditis, fatty degeneration, endocarditis), or in
the posterior vena cava.

_Lesions._ The congested liver is enlarged and deeply colored with
blood. The weight of twenty to thirty pounds is often attained. While
the color is of a deep red throughout, there are spots of a still darker
hue indicating the seat of subcapsular or deeper seated hemorrhages. The
color varies according as the congestion is passive or active. In the
former the coloration is deeper in the centre of the acinus (nutmeg
liver) indicating congestion of the hepatic veins, while in the latter
the periphery of the acinus may be most deeply stained implying
congestion of the portal vein. The consistency of the organ is
diminished, and the more acute the attack the greater the friability. In
such cases there is a parboiled appearance indicating granular and
commencing fatty degeneration. Under the microscope the relative
distension of the intralobular, and interlobular veins and the hepatic
capillaries becomes more distinctly marked and the presence of pigment
and fatty granules and the lack of protoplasm and nuclei in the hepatic
cells indicate their progressive changes. When the peripheral cells are
pale from fatty granules the contrast between the light margin and dark
centre of the acinus, makes the mottled or nutmeg aspect of the liver
much more pronounced.

In old standing cases of passive congestion the liver may be the seat of
fibroid degeneration, extending from the capsule inward in bands or
trabeculæ, and giving to the organ a firm resistant character
(sclerosis, cirrhosis).

_Symptoms._ The symptoms are general and suggestive rather than
pathognomonic. There are dullness, prostration, unsteady walk, pendent
head, with occasional jerking, semi-closed eyes, redness of the
conjunctiva, slight colicy pains, arching of the loins, muscular
tremblings and decubitus on the left side rather than the right. The
more definite symptoms are tenderness on percussion with the closed fist
over the last ribs (the liver) especially on the right side, increase of
the area of hepatic percussion dullness (which may be rendered valueless
by a loaded colon), the presence of a slight icterus in the conjunctiva
and urine, and an increase of the urine secreted and an excess of the
contained urea.

In _passive_ cases however the obstruction to the escape of blood from
the liver prevents the development of icteric symptoms, of uræmia and of
polyuria. In all such cases however there follows a general congestion
of the portal system and if it persists for any length of time
gastro-intestinal congestion and catarrh and even ascites may develop.

In all cases alike the history of the attack will help towards a
satisfactory diagnosis.

_Prevention._ A rational hygiene embracing daily work or exercise,
moderate laxative diet, green food in its season, pure cool air are
important precautions.

_Treatment._ A moderate supply of green or laxative food, the
withholding for the time of grain, and especially of maize, wheat or
buckwheat, saline laxatives daily, and a stimulating embrocation or
blister to the tender hypochondrium are the most important measures.
Exercise in a box stall, or still better in a yard or paddock in the
intervals between more systematic work forms an important adjunct to
medicine. As a laxative sulphate of soda is to be preferred at first in
a full cathartic dose and later in a daily amount sufficient to relax
the bowels. Given in a bucket of water every morning before the first
meal a very small dose will be effective.


                  CONGESTION OF THE LIVER IN THE DOG.

_Active_ congestion is very rare excepting in over-fed and indolent
family pets. _Passive_ congestion induced by diseases of the lungs and
heart is however far from uncommon.

_Lesions._ True to their origin these usually appear as the spotted
nutmeg liver with the deep congestion in the centre of the acini. For
the same reason the fibroid degenerations shown in chronic cases, show
the firm fibroid neoplasm chiefly around the hepatic veins. Granular,
fatty and pigmentary degeneration of the cells are found as in the
solipeds.

_Symptoms._ These are as obscure as in the horse. There is always a
history of a sluggish, gourmandizing life, and in the early stages, a
manifestation of embonpoint which suggests a torpid liver. Further
suggestions may also be obtained from coexisting diseases of the lungs,
or heart, from gastro-intestinal catarrh, from piles, or ascites. Then
there is at times a slight icterus of the conjunctiva and urine. Finally
tenderness on percussion on the right hypochondrium, decubitus on the
left side, and an increased area of dullness on percussion may afford
useful hints for diagnosis.

_Treatment._ In the rare cases due to infection from the intestine, an
active saline purgative followed by antiseptics (salol, naphthalin,
naphthol, etc.,) daily will be of value. It is also desirable to keep up
the action of the bowels by morning doses of salines. In cases
consequent on chest disease attention must be given to such primary
trouble. In all cases a restricted laxative diet, and graduated but
increasing exercise in the open air are demanded.


                     HEPATIC HÆMORRHAGE OR RUPTURE.

  Causes: Mechanical injuries, falls, blows, kicks, degenerations,
  amyloid, fatty, granular, congestion, neoplasms, glanders,
  tuberculous, myomatous, microbian infection. In the horse, disease of
  liver, heart, lungs, hepatic artery, portal vein, degenerations
  following overfeeding, idleness, foreign bodies, arsenic, phosphorus,
  parasites, violent movements in colic, running, draught, leaping. In
  the dog, pampering and traumatism. In cattle forced feeding,
  emaciation, microbian infection. In birds, tubercle, tæniasis,
  microbian infection. Lesions: extravasation, intracapsular, or through
  capsule into the peritoneal cavity. The extravasation bulges of a deep
  black, covering a dark softened, pulpy, hepatic tissue, with light
  colored fatty tissue around. Clots may be stratified from successive
  bleedings. Liver usually enlarged. Symptoms: onset sudden, or preceded
  by stiffness, soreness and other signs of hepatic trouble. Extensive
  rupture, entails weakness, unsteady gait, perspiration, pallor of
  mucosæ, small weak rapid pulse, palpitations, dilated pupils, rolling
  eyes, amaurosis, tremors, convulsion in case of survival, coldness,
  œdemas. Death in five hours to five days. Risk of relapse in
  recovering cases. Treatment: rather hopeless, rest, laxative, ergot,
  ferric chloride, tannic acid, witch hazel, cold water, snow or ice to
  right side. In meat producing animals fatten.

_Causes._ Hemorrhage and rupture of the liver are closely correlated to
each other, the accumulation of extravasated blood in the parenchyma in
the one case leading to over distension of the capsule, and the
laceration of this capsule and of the adjacent substance of the liver
occurring in the other as a mere extension of the first. They usually
occur as the direct result of mechanical injury (falls, blows, kicks)
acting on a liver already softened and friable through disease. These
predisposing degenerations may be amyloid (Caparini, Johne, Rabe), fatty
(Julien, Gowing, Adam, Siedamgrotzky), granular softening, hepatitis or
congestion (Zundel), glander neoplasms (Mathis), tubercles, angiomata
(Trasbot), microbian infection (Stubbe), tumors (Brückmüller).

In the horse predisposing conditions may be found in diseases of the
liver, heart or lungs, in embolism of the hepatic artery (Wright), in
obstruction of the portal vein (Pierre), in infarction of the liver, in
degeneration with softening, in sarcomatous, melanotic, glanderous or
cancerous deposits in its substance, in degenerations consequent on over
feeding, idleness, congestions, on the penetration of husks of grains
into the liver substance, on arsenical or phosphorus poisoning. The
presence of flukes, echinococci and other parasites may also cause
congestion and softening. To the _immediate_ or _traumatic_ causes above
named may be added the violent movements attendant on a severe attack of
colic, and violent exertions in running, draught, leaping, etc.
(Friend).

In the =dog= we must recognize all the pampering conditions which
predispose to congestion and degeneration, together with more direct
operation of kicks, blows, falls, fights, over exertion, etc.

In =cattle= a forcing regimen is especially predisposing, and yet the
loss of vigor resulting from a diametrically opposite treatment, must be
accepted as an occasional cause. Stubbe found in emaciated cows miliary
hemorrhagic infarcts of a dark red color which gradually extended to an
inch or more in diameter. These he traced to microbian infection coming
by way of the chronic intestinal lesions which are common in old cows.
The final result of such infarctions was loss of hepatic substance and
the formation of cicatricial tissue with a marked depression on the
surface of the organ.

In =birds= fatal hepatic hemorrhages occur in connection with local
tubercle (Cadiot), tæniasis of the liver, or microbian infection.

_Lesions._ The hemorrhage may take place into the substance of the liver
only, or the capsule may be lacerated so that the blood escapes into the
peritoneal cavity in considerable quantity.

In the _horse_ it usually occurs in the right or middle lobe, rarely in
the left. There may be one or more hemorrhagic effusions varying in size
from a cherry to a duck’s egg, or even an infants’ head (Lorge). This
projects from the surface of the organ and its deep black contrasts
strongly with the white of the adjacent capsule. When laid open the
hepatic tissue is seen to be softened and pulpy, and its dark color
forms a striking contrast with any surrounding fatty liver. Any form of
degeneration may be revealed on microscopic or chemical examination. Not
unfrequently small clots of blood form under the capsule raising it in
the form of little sacs. Such clots are usually stratified indicating a
succession of small hemorrhages.

When the capsule is torn, the lesion may extend from one surface of the
organ to the other, and the edges, smooth, uneven or fringed, are united
together by a blood clot.

In case of hemorrhagic infarcts the lesion usually has a distinctly
conical outline corresponding to the vascular distribution. These are
especially characteristic of cases supervening on heart disease.

The volume of the liver is usually increased and the weight may reach 30
lbs. (Schmeltz), 34 lbs. (Lorge), or even 66 lbs. (Trasbot).

In _other domestic animals_ analogous lesions are found modified largely
according to the size of the subject.

_Symptoms._ These may develop instantaneously without any marked
premonitory indication. In other cases tenderness on percussion over the
liver, stiffness or groaning under sudden movements or turning, arching
of the back, hanging of the head, slowness in rising, costiveness,
slight transient colics, and even icterus may have been detected on
close observation. The symptoms of actual rupture are essentially those
of internal hemorrhage. The animal becomes weak, or unsteady upon its
limbs, perspires, arches the back, and shows a marked pallor of the
visible mucosæ. The pulse is small, thready, weak and accelerated, and
the heart beats violent or palpitating. The percussion dullness over the
liver is extended (Weber), the loins become insensible to pinching, and
there may be some distension of the abdomen. Dilatation of the pupils,
retraction or rolling of the eyes, amaurosis, tremors of the muscles of
the neck, lying down, or falling, and general convulsions may precede
death. This may occur in a few hours or it may be delayed if the lesions
are restricted. In case of survival, coldness and œdema of the
extremities and sheath have been observed. The lesser hemorrhages may
terminate in recovery if there is no attendant incurable disease. In
anthrax, glanders, cancer, tuberculosis, septicæmia, etc., a favorable
issue is not to be looked for.

_Duration. Termination._ In severe cases a fatal issue may be expected
in from five hours to five days. In the milder cases which make a
temporary recovery there is great danger of a second hemorrhage from the
new vessels in the tissue undergoing organization or from the adjacent
degenerate liver tissue. The course of the affection may be altered by
such complications as arthritis (Dieckerhoff), pneumonia, pulmonary
thrombosis (Leblanc), enteritis or peritonitis (Cadeac).

_Treatment_ is usually of no avail. Rest, and the administration of
laxatives and hæmostatics, have been especially recommended. Of the
latter, ergot by the mouth or ergotin subcutem, tends to contraction of
the blood-vessels and to check the flow. Ferric chloride is also used,
though apt to interfere with hepatic function. Tannic acid, hamamelis,
and other astringents may be used instead. Cold water, snow or ice
applied to the right hypochondrium may act as a check to the hemorrhage.
Unless in purely traumatic cases in an otherwise healthy liver, a
recovery is at best temporary, and the already degenerate liver is
liable to relapse at any moment. In horses and dogs, therefore, recovery
is by no means an unmixed good. Meat producing animals that recover
should be prepared for the butcher.


                               HEPATITIS.

  Forms of hepatitis: Parenchymatous hepatitis. Definition: Degeneration
  of hepatic cells. Relation to enteritis and nephritis. In
  horse—causes:—as in congestion, pampering, spoiled fodder, malt,
  inundated meadows, chill, overfeeding, hot moist climate,
  hæmoglobinæmia, infection. In cattle—causes:—forcing ration, hot
  weather, overwork, infection. In dog—causes:—infection from alimentary
  canal. Lesions: Enlarged, softened liver, round edges, a week later
  yellow atrophy, granular on section, bloodless. Acini with indefinite
  margins, cells granular, nuclei lost. In dog centres of softening.
  Symptoms:—in horse: Attack sudden, rigor, fever, dullness,
  prostration, yellowish red mucosæ, unsteady gait, slight colic,
  anorexia, urine decreased, glairy, brownish red, groaning in
  defecation, excited circulation and breathing, increased icterus by
  third day, fœtid, colorless diarrhœa. Diagnosis: Coincidence of fever,
  prostration, icterus, painful defecation, fœtid diarrhœa, light color
  of stools, tenderness and flatness on percussing hepatic area. From
  influenza by absence of watering eyes and contagion. Prognosis in
  horse: Very grave unless urine is free. Treatment in horse: Portal
  depletion, calomel, ipecacuan, salines, diuretics, fomentation of
  loins, antiseptics, derivatives, mineral acids, bitters. Careful
  laxative diet in convalescence. Symptoms in cattle: Slower onset,
  anorexia, dullness, depression, drivelling saliva, grinding teeth,
  icterus, constipation, later fœtid diarrhœa, pale colored stools,
  recumbency, groans on rising, arching back, tender right
  hypochondrium, fever. Prognosis grave. Death in five to six days.
  Treatment as in horse: Only saline laxatives. Symptoms in dog:
  Muscular tremors, staring coat, hyperthermia, icterus, fœtid breath,
  ventral decubitus, extreme prostration, anorexia, tender right
  hypochondrium, diminished urine, death in two or three days. Treatment
  in dog: Calomel and jalap, diuretics, laxatives, derivatives,
  germicides, in convalescence, mineral acids, bitters, careful diet.

The different forms of inflammation of the liver are distinguished
according as they affect, especially the hepatic cells and tissue of the
acini (parenchymatous), as they result in suppuration (suppurative,
catarrhal, abscess), as they cause necrobiosis in nodular masses
(infectious or necrotic), as they lead to fibroid thickening under the
peritoneum and proper capsule (perihepatitis); or as they cause general
fibroid induration of the organ by increase of its connective tissue
(cirrhosis).


      PARENCHYMATOUS HEPATITIS, ACUTE YELLOW ATROPHY OE THE LIVER.

The characteristic morbid lesion in this disease is the degeneration of
the liver cells, loss of their protoplasm and nuclei and of their normal
functions. It may be circumscribed to limited areas, or may affect the
liver, generally. As the hepatic functions, are so intimately related to
those of the bowels and kidney, the affection is usually accompanied by
inflammations of these organs as well.

_Causes in horses._ The same general causes which produce congestion,
may also determine the further morbid stage of inflammation. Cadeac
mentions a case which developed in a horse kept alone and idle in the
stable. He makes no mention of condition, food, cleanliness nor
ventilation. Haubner and Franzen have traced it to a diet of malt or of
hay harvested from inundated meadows. Zundel records a case following
exposure to extreme cold. More commonly the disease is secondary to the
overtaxing of the liver, by heavy feeding in warm moist climates, or in
hæmoglobinæmia, or to the arrest of the micro-organisms of the food, or
of infectious diseases.

_Causes in Cattle._ These suffer rarely, but from essentially the same
conditions. It has followed aphthous fever (Eletti), and arisen under a
forcing ration, in hot weather (Callot, Cruzel), or under overwork
(Cruzel).

_Causes in Dogs._ Most cases result from infection by way of the stomach
and intestines, or by the transfer to the liver of the ptomaines and
toxins of such infections. It is thus related in its origin to catarrhal
jaundice and hyperæmia.

_Lesions._ In the earliest stage with albuminoid exudation into its
substance the liver may be greatly enlarged, its sharp edges rounded,
and its consistency softened. After a week’s illness atrophy may have
set in and the organ appears shrunken and of ocherous yellow. In the
early stages there may be sanguineous engorgement, the cut surface may
bleed freely, and small extravasations may show throughout the liver
substance, later the clay yellow hue, the granular aspect and the
absence of blood on the cut surface are characteristic. The margins of
the adjacent acini are indefinite or lost, and under the microscope the
hepatic cells are charged with granules (albuminoid, fatty and
pigmentary), while the nuclei are no longer demonstrable.

In _cattle_ the liver may be double the normal size and at first of a
deep purple red, which may change later to the earthy yellow.

In _dogs_ the liver is tumid and yellow, and marked by small pea-like
centres of softening. There is marked softening and the microscope
reveals the characteristic degeneration of the hepatic cells.

_Symptoms in the Horse._ These resemble those of congestion rendered
more intense and therefore somewhat less obscure. The attack is usually
sudden, there may be rigor followed by hyperthermia, dullness, pendent
head, drooping eyelids, injected conjunctiva with a yellowish tinge,
unsteady gait and slight indications of colic. There is anorexia,
partial suppression of urine, and what is passed is thick, glairy and
brownish red, fæces are passed with pain, and groaning, probably from
compression of the liver, the heart beats violently, while the pulse is
small, breathing accelerated and perspiration abundant. The temperature
rises (101° to 106°) and remains high throughout unless lowered through
biliary intoxication. Percussion over the liver and especially on the
right side shows increased area of dullness and marked tenderness. On
the second or third day the icterus usually increases, and a slight
fœtid diarrhœa may set in with marked fœtor of the pale or colorless
discharges. The jaundice is not, however, a criterion of the danger, as
it may become less marked or entirely disappear because of the extensive
degeneration of the hepatic cells and the arrest of the formation of
bile.

_Diagnosis in the horse._ The disease is recognized by the coincidence
of fever, with great depression, icterus, painful defecation,
constipation followed by a fœtid diarrhœa with lack of color in the
stools and by increased area of dullness and tenderness in the region of
the liver and especially on the right side. From influenza which it
resembles in many respects, it is distinguished by the absence of watery
discharge from the eyes, and by the entire absence of all indication of
contagion. The cases occur one at a time.

_Prognosis in the horse._ The disease is exceedingly fatal. When the
kidneys remain active, the poisons are eliminated and there may be hope
of recovery, but when urine is suppressed an early death by poisoning is
to be expected.

_Treatment in the horse._ A most important indication is to secure
depletion from the portal system. Calomel 1 dr., aloes 4 drs., ipecacuan
1 dr. may be given in bolus, and followed by small daily doses of
sulphate and nitrate of soda with bitters, with or without the
ipecacuan. Action on the kidneys is essential to secure elimination of
the poisons which threaten a fatal poisoning if retained. To favor the
same action fomentations may be applied to the loins. The frequent
presence of pathogenic microörganisms either in the bowels or liver
suggests the use of germicides (salol, salicylic acid, salicylate of
soda, naphthalin, naphthol, beta-naphthol, etc.) as in catarrhal
jaundice. Sinapisms or blisters applied to the right side of the chest
and over the short ribs may be useful, and after the subsidence of the
more violent symptoms, dilute mineral acids and especially
nitro-muriatic acid may be resorted to in combination with diuretics and
bitters.

When appetite returns succulent, laxative, non-stimulating food in small
quantity should be given. Wheat bran mashes, carrots, turnips, potatoes,
apples, fresh grass, ensilage may be adduced as examples. Throughout the
disease the ingestion of an abundance of pure water should be
encouraged.

_Symptoms in the ox._ These may appear more tardily than in the horse,
loss of appetite, staring coat, dullness, pendent head and ears,
unsteady movements, rigors, drivelling of saliva from the mouth and
grinding the teeth are usually noted. To these are added the more
diagnostic symptoms of slight (or severe) jaundice, constipation
followed by a fœtid light colored diarrhœa, a strong disposition to
remain recumbent, marked suffering attendant on rising, arching of the
back when up, and tenderness on percussion over the right hypochondrium.
The temperature gradually rises, though more slowly than in the horse,
and may again descend under a profound poisoning.

_Course._ The disease reaches its acme in four to six days, and
generally has a fatal issue.

_Treatment_, is on the same lines as for the horse only as a purgative,
sulphate of soda may advantageously replace the aloes.

_Symptoms in the dog._ The symptoms are those of congestion in an
exaggerated form. There are muscular tremors, erection of the hair,
followed by rising temperature up to 105° or 106°, an icteric hue of the
mucosæ, the pulse is accelerated, strong, irregular, respiration rapid,
panting, fœtid breath, ventral decubitus, and prostration extreme.
Appetite is completely lost, the bowels become relaxed, the stools
fœtid, the right hypochondrium painful on pressure or percussion, and
the urine greatly reduced and icteric or suppressed. This feature of
urinary suppression, determines a rapid poisoning and death in two or
three days.

_Treatment_ must follow the same lines as in other animals, a purgative
of calomel and jalap, followed by diuretics, laxatives, derivatives, and
above all germicides. In case of survival mineral acids, aqua regia,
bitters, and a carefully regulated diet will be in order.


                SUPPURATIVE HEPATITIS. HEPATIC ABSCESS.

  Causes in horse: pyæmia, omphalitis, thrombosis, infection, biliary
  calculi, concretions or parasites, foreign bodies, hot, damp climates,
  strangles, brustseuche, glanders, endocarditis. Lesions in horse: from
  parasites and mechanical irritants, pea-like or hazelnut; embolic
  abscess, pin head to hen’s egg; infection from strangles, foreign
  bodies, etc., may be of large size, and burst into adjacent organs,
  the peritoneum or externally. Symptoms in horse: of pre-existent
  malady, remitting fever, successive chills, intermittent icterus,
  hypochondriac tenderness. Spontaneous recovery, aspiration, opening,
  antiseptics locally and generally. Lesions in ruminants; secondary
  multiple abscesses, bean-like or (with foreign body) very large, may
  extend into adjacent parts. Symptoms in cattle: fever, chills,
  jaundice, tympany, diarrhœa, dysentery, wasting, tender right
  hypochondrium. Treatment: as in horse. Causes in dog: foreign bodies,
  tumors, infections, blows, traumas. Lesions: traumatic abscesses,
  single, large, infectious abscesses multiple, small. Former fœtid.
  Symptoms in dog: hepatic congestion or colic, then chills,
  prostration, irritability, tenderness of right hypochondrium, nausea,
  vomiting. Treatment in dog: antiseptic aspiration, laparotomy.

_Causes in the Horse._ Hepatic abscess arises from a great many primary
morbid conditions. As a secondary abscess it is seen in the different
forms of pyæmia and especially in suppurative omphalitis in young
animals. It may start in thrombosis determined by clots or septic
matters carried from a distance through the portal vein or hepatic
artery, in biliary calculi or concretions, in parasites introduced from
the duodenum, in barbs or husks of the cereals that have penetrated
through the biliary ducts, or in bacteria or their toxins which have
been carried from the bowels, spleen or pancreas. The government
veterinarians have found it a comparatively common lesion in the hot
damp climate of Hindoostan, and a similar frequency has been noticed in
west Africa. Among general affections it is liable to occur in
strangles, contagious pneumonia, glanders, endocarditis of the left
heart and phlebitis with the formation of thrombi in the lungs. In the
two last named disorders, the affection takes place by the simple
transference of detached clots to the liver to block its arteries or
capillaries. Or it may be that micro-organisms are transferred in the
same way. With modern views of suppuration the presence of the pyogenic
organisms must be conceded.

_Lesions in the horse._ Cadeac distinguishes the different types of
hepatic abscess as: _1st biliary abscess_ in which suppuration commences
in the interior of the biliary ducts and usually from parasites or
mechanical irritants introduced or from calculi or concretions formed
within them: these rare abscesses contain biliary salts, pigments, and
epithelium and acquire the size of a pea or hazelnut: _2d Metastatic
abscesses_ which start in the arterial, portal, or capillary vessels, by
the arrest of infecting clots, which determine a further clotting, the
obstruction of the vessel, the accumulation of leucocytes and the
formation of abscess of the size of a pin head or larger up to a hen’s
egg, surrounded by a hæmorrhagic infarct softening in the centre: these
are numerously disseminated through the liver: _3d Mechanical Abscess_
due to the penetration of foreign bodies or parasites: 4th Infection as
in strangles. These may attain a large size, cause adhesion to adjacent
organs, and rupture into the chest, the colon, stomach or peritoneum.
The pus may even escape externally through the right hypochondrium.

_Symptoms in the horse._ These are always obscure and vary much with the
source of the malady. If there has been a pre-existing hepatic malady
the symptoms of that will be in evidence; if an omphalitis its existence
may still be recognizable; if pulmonary or cardiac disease, that may be
detected; if parasites, evidence of their existence may perchance be
found; if gall stone, a previous violent hepatic colic with icterus may
have occurred; and if intestinal septic disorder, there may be the
testimony of intestinal troubles. The more diagnostic symptoms are a
fever of a remittent type, one or several violent shivering fits, a
marked jaundice which like the fever shows exacerbations, and a similar
irregularity of the condition of the urine which may be successively of
a dark brown, a deep yellow, and a transparent amber color. Tenderness
and grunting on percussion of the right hypochondrium would be an
additional aid in diagnosis.

_Treatment._ Death has been hitherto considered as the inevitable
result, yet recoveries may ensue after rupture into the colon or through
the abdominal walls. If the seat of the abscess can be ascertained its
evacuation through an aspirator and the subsequent injection of an
antiseptic would be appropriate. The concurrent use of antisuppurants
like hyposulphite of soda, or sulphide of calcium would also be in
order.

_Causes in Cattle._ Hepatic abscess is much more frequent in cattle, and
is commonly a result of perforation by sharp pointed bodies (needles,
pins, nails, wires, etc.) from the reticulum and rumen, or of parasites,
or biliary calculi. Other cases are occasioned by the presence of
tubercles, actinomycosis, or omphalitis.

_Lesions in Cattle and Sheep._ Secondary abscesses are usually multiple
and disseminated through the organ, though Cadeac says they are more
common in the left half. They vary in size from a bean to a pigeon’s
egg, project often from the surface, and contain a viscid, creamy,
yellowish or greenish pus. Abscesses dependent on foreign bodies often
attain a great size, so as to contain a pint or quart of pus (Landel).
They may make their way through the diaphragm, rumen, or abdominal wall
leaving a thick cicatrix in the liver, or they may become slowly
absorbed and dry up into a putty-like or cretaceous mass. Brusaferro
found hepatic abscesses in lambs twenty to thirty days old—probably of
omphalic origin.

_Symptoms in Cattle_ are usually very obscure. Fever, shivering fits,
jaundice, indigestion, diarrhœa or dysentery, emaciation, colics, tender
right hypochondrium, and peritonitis may all be in evidence but the
diagnosis is little better than a guess.

_Treatment_ when possible at all would be on the same lines as for the
horse.

_Causes in the dog._ According to Cadeac these are mostly foreign bodies
(needles, pins, etc.) which have been swallowed, tumors of the liver or
adjacent organs, phlebitis and thrombosis of the portal vein, pyæmia,
septicæmia, and external injuries (kicks, blows, contusions, falls,
etc.)

_Lesions in the dog._ As in the other animals _traumatic_ abscess is
usually solitary and large, _secondary_ abscess multiple and small. The
pus developed around a foreign body is reddish, greenish and fœtid, that
of the metastatic abscess is usually whitish or yellowish and with a
sweet odor.

_Symptoms in the dog_ are those of hepatic congestion, or violent gall
stone colic, followed by severe rigor, great depression, or
irritability, and tenderness over the right hypochondrium. Nausea and
vomiting is a marked symptom though not a diagnostic one.

_Treatment._ If the flaccid abdominal walls will allow of the locating
of the abscess it should be treated by aspiration and antiseptic
injections. It would even be admissible to perform laparotomy, stitch
the wall of the abscess to the external wound, and empty it under due
antiseptic precautions.


         INFECTED HEPATITIS. NODULAR NECROBIOSIS OF THE LIVER.

  In ox, sheep, pig, dog, horse. Necrotic areas projecting on surface of
  liver. Causes: bacteria, toxins, from bowels, womb, navel. Lesions: In
  cattle dirty gray nodules in brownish red liver, nodules firm,
  granular, necrotic, elements do not stain, later leucocytes and
  fibro-plastic growth in periphery. In lambs the nodules are white,
  common to the lungs and pleura, pathogenic to rabbit. In pigs nutmeg
  liver, cells without nuclei, fatty, granular, pathogenic to rabbits,
  guinea pigs, rats and young pigs. In dog, nutmeg liver, with violet
  areas, and white spots, 1–2 lines, having granular, fatty cells
  without nuclei. Symptoms: fever, constant lying, tarry fæces, icterus,
  tender right hypochondrium, and those of the primary disease.
  Treatment: antisepsis of primary seat, and bowels, elimination by
  kidneys, general antisepsis, stimulants, etc. Case usually hopeless.
  Prevention.

This has been observed particularly in cattle, but also in sheep, pig,
dog and horse. It is characterized by the formation of circumscribed
areas of gangrene, becoming hard, dry, yellowish and usually slightly
projecting beyond the adjacent surface. Its infected character is shown
by the presence in the lesion and adjacent parts of the hepatic tissue
of an abundance of bacteria, which, from the varied description, appear
to differ in different cases. The cause may however be safely stated as
one of the bacteria of gangrene. It is alleged with some show of reason,
that the lesion may be determined by the action of toxins and ptomaines
produced by bacteria in the alimentary canal and carried to the liver
with the portal blood (Cadeac). The bacteria themselves commonly come
from the same source, (Stubbe), but also from the uterus (Berndt), the
mammæ (LeBlanc), and above all from the suppurating or septic umbilicus.
McFadyean in five cases found a long slender bacillus, Hamilton in a
single case in the horse found cocci, Rivolta in an infectious hepatitis
in sheep found _bacterium subtilis agnorum_, and Semmer found the same
condition in young pigs from micrococci introduced through the diseased
umbilicus.

_Lesions._ In _cattle_ the liver has a general brownish red, or greenish
white color, and shows projecting, hard nodules of a dirty gray color
more or less tinged with yellowish brown. The margins of these hard
nodules are very sharply defined, and on section show a homogeneous
granular surface, devoid of areas of softening or of connective tissue,
and formed of the hepatic parenchyma in a state of necrobiosis. The
granules and nuclear elements do not stain like those of healthy liver.
As the disease advances the periphery of the nodule may be invaded by
leucocytes and become the seat of a fibro-plastic hypertrophy
(McFadyean) with the ultimate formation of cicatricial tissue (Stubbe).

In _lambs_ Rivolta found the necrosed nodules standing out as white
patches under the capsule of the liver, but similar lesions were met
with in the lungs and pleuræ, an observation which has been confirmed by
Hanbold. The affection was conveyed by inoculation to the rabbit.

In _pigs_ Semmer found nutmeg liver, deep red or grayish yellow,
hypertrophied, the hepatic cells swollen and divested of nuclei but
containing fatty and pigmentary granules. It was inoculable on rabbits,
guinea pigs, white rats and on young pigs.

In the _dog_, Courmont and Doyon found congested liver (portal
congestion) with projecting patches of a deep violet color and sharply
defined borders, and one to two lines in diameter, also salient white
spots with distinct outlines. In the white spots the hepatic cells had
lost their nuclei and were charged with fatty granules.

_Symptoms._ These are indications of hepatic disease. In _parturient
cows_, Berndt noted fever (102° to 104°), anorexia, stiffness, cough,
labored breathing, intense thirst, constant decubitus, and constipation
followed by lowering temperature, tarry fæces and icterus. The region of
the liver was very sensitive to pressure or percussion. In the other
animals the symptoms appear to be largely over-shadowed by those of the
primary disease, but the same general indications of jaundice, hepatic
tenderness and digestive disorder are superadded.

_Treatment_ when it can be intelligently adopted, consists largely in
evacuation and antisepsis of the seat of primary infection, and of the
_prima viœ_, and in maintaining elimination by the kidneys. In this way,
as in congestion and hepatitis, the concentration of the poison is as
far as possible counteracted, and an opportunity may sometimes be
furnished for the recuperation of the liver cells. As a rule, however,
the case is hopeless, and thus preventive measures, by cleanliness,
disinfection and antisepsis of the ascertained sources of the infection
are indicated.


                             PERIHEPATITIS.

  Inflammation of capsule of liver (external and Glisson’s). Causes:
  Traumas, infective diseases, phlebitis of the portal vein, chill,
  distomatosis. Lesions: Peritonitis and inflammation of the capsule in
  patches, yellowish gray exudate, fibroid thickening or pus. Adhesions
  to adjacent objects. Thickening of trabeculæ. Symptoms, tardy
  respiration and circulation, tender hypochondrium, colics, diarrhœa,
  painful defecation, moan with expiration. Slight cases recover.
  Sequelæ: compression of portal vein or bile duct, gastric catarrh,
  piles, etc. Treatment: Salines, alkaline diuretics, mineral tonics,
  bitters.

This is inflammation of the external capsule of the liver and Glisson’s
capsule. It may arise from direct mechanical injury, or by extension of
inflammation from adjacent structures, such as the peritoneum. It may
also complicate contagious pneumonia in the horse, tuberculosis in the
ox, pneumoenteritis in pigs, and also phlebitis of the vena portæ
(Cadeac, Morot). It may follow a chill, or distomatosis.

_Lesions._ These are essentially peritonitis circumscribed by the liver,
and extending to the proper capsule, and its vaginal investments of the
hepatic vessels. It is usually limited to certain spots which become the
seats of a yellowish gray exudation, with a tendency to fibroid
development and thickening, but sometimes degenerating into pus. The
deposits on the outer side of the hepatic peritoneum may develop false
membranes and fibrous adhesions to surrounding objects, the diaphragm,
omentum, stomach or intestine. The deposits under the peritoneum lead to
similar fibrous development with hypertrophy or thickening of the
capsule, the trabeculæ extending thence into the liver and the vaginal
sheaths of the vessels. Such areas of thickening are revealed as
depressed spots or patches of a white color, and showing a firm fibrous,
pearly appearance when incised. Such lesions are not uncommon in the
livers of horses, cattle and swine. In the pig they may have a violet,
or brownish red color, but with spots of other colors—grayish or
brownish (Kitt).

_Symptoms._ Dopheïde, who has studied the disease in cows and to a less
extent in horses, found a reduction in pulsations (26 per minute) and
respirations (6 per minute) in connection with a mild peritonitis,
intestinal catarrh, colicy pains and diarrhœa. The conjunctiva is pale,
the pulse compressible, the respirations unequal and accompanied by a
moan, and the appetite impaired or lost.

If confined to mere spots on the liver, a restoration to apparently
vigorous health may take place, but if extensive it may lead to
compression and obstruction of the portal vein or bile duct, or to
compression and atrophy of the liver, with corresponding symptoms.

_Treatment._ As in other congestions of the liver, the use of salines to
deplete the portal system, and of alkaline diuretics are especially
indicated, to be followed by bitters and mineral acids. Sinapisms and
other counter-irritants to the region of the liver are of great service.
If not complicated with abscess, or microbian infection, cases of this
kind will often do well.




             CIRRHOSIS OF THE LIVER. FIBROID DEGENERATION.

  Definition. Increase of connective tissue, decrease of gland
  parenchyma. Causes: in man, alcoholism; in animals, chronic heart
  disease, chronic recurrent perihepatitis, biliary obstruction, toxins.
  In horses: age, emphysema, unwholesome fodders, vegetable alkaloids,
  infection. Symptoms: prostration, hebetude, impaired appetite, colics,
  constipation, later diarrhœa, unthriftiness, emaciation, dropsy,
  icterus, ascites, intestinal catarrh, tender hypochondrium, early
  fatigue. Lesions: increase of connective tissue, compression and
  absorption of parenchymatous tissue, greatest around portal vessels,
  thickening of fibrous stroma between capillaries of acini, shrunken,
  granular, pigmented liver cells. Treatment: salines, Glauber salts,
  diuretics, sodium carbonate, or iodide, or salicylate, derivatives,
  mineral acids, bitters, open air, laxative food, pure water. In
  cattle: obstruction to circulation or the flow of bile; advances from
  the vessels, causes absorption, caseated foci, adhesions, enlarged
  liver. Symptoms: jaundice, yellow, red, albuminous urine, chronic
  indigestion, tends to fatal though slow advance. Treatment: green
  food, open air life, saline laxatives, alkalies. In dog: common
  following heart disease, parasites, bacteria. Lesions: Congested
  brownish red liver, fibroid increase from Glisson’s capsule,
  compression of acini, their elevation above surface, fatty and
  pigmentary degeneration of hepatic cells, increasing sclerosis.
  Symptoms: as in parenchymatous hepatitis with slower advance, in time
  tender loins, brownish or reddish urine, ascites, intestinal catarrh,
  it may be icterus. Treatment: Correct cardiac troubles, digitalis,
  strophanthus, and intestinal, careful diet, mineral acids, bitters,
  pure water, saline laxatives, antiseptics, alkaline diuretics.
  Potassium iodide. Derivatives. Draw off liquid. Laxative
  non-stimulating diet.


_Definition._ An interstitial inflammation of the liver characterized by
a great increase of the connective tissue and compression, atrophy and
degeneration of the glandular elements.

The same final result may undoubtedly originate in various different
primary morbid processes.

In man cirrhosis is looked upon as almost always the result of abuse of
alcohol. In animals this cannot be the case, apart from a few kept in
connection with breweries or distilleries.

In heart disease a long continued mechanical congestion of the liver
causes compression and degeneration of the secreting cells in the centre
of the acini (around the intralobular veins), while the peripheral
portions undergo cell proliferation and increase of connective tissue.

In chronic or recurrent perihepatitis, a whole lobe may be compressed by
the hyperplasia of the investing connective tissue, and the hepatic
cells are degenerated and absorbed.

Overdistension of the biliary ducts from obstruction to the flow of bile
(gall stone, catarrhal inflammation, constipation), leads to
proliferation and hyperplasia in the walls of the biliary radicals
throughout the entire liver.

The presence in the liver of toxic agents, ingested, or generated from
microbian fermentation in the intestinal canal or liver is another
recognized cause of connective tissue hyperplasia.


                        CIRRHOSIS IN THE HORSE.

Cirrhosis of venous origin has been observed mainly in old horses, while
hypertrophic cirrhosis from biliary obstruction occurs rather in the
young (Cadeac). Bruckmüller records a case of the first kind in a horse
with extreme pulmonary emphysema. Walley gives a bad condition of
fodders as the main cause, virtually implying, in many cases, infective
catarrh and obstruction of the biliary ducts.

A form of the disease prevails at Schweinsberg in Hesse, and has been
variously attributed to spoiled fodders (Nicklas), to vegetable
alkaloids and other poisons in the food (Friedberger and Fröhner), to
clover, to telluric poisons (Redner), to infection (Meminger), and to
heredity (Neidhardt). It is a suggestive fact that it is confined to the
valleys of the Ohm, Glon, and Zusam where the land is peaty or swampy
and subject to inundations, while it is unknown on the dry table lands
(Friedberger and Fröhner). This strongly suggests intoxication with
microbes or their deleterious products. The gastric catarrh that
frequently attends the disease may point in the same direction.

_Symptoms._ These are too often general rather than diagnostic.
Dullness, prostration, hebetude, yawning, hot, sticky mouth, lost,
irregular or depraved appetite, colics, constipation or diarrhœa, dry,
harsh coat, emaciation, weakness, œdema of the limbs, vertigo and
drowsiness may be among the symptoms. More characteristic are icterus,
abdominal distension from ascites, or congestion of the liver, yellow or
high colored urine, intestinal catarrh, indigestion, and tenderness in
the region of the liver. The mucosæ are usually pale at first and not
always icteric later. On exertion the horse shows early fatigue,
tumultuous heart beats and oppressed breathing.

The Schweinsberg disease often lasts for months, with alternate
improvements and exacerbations, but almost invariably ends in death, and
sometimes completely depopulates a stable.

_Lesions._ These consist primarily in the great increase of the
connective tissue and the relative decrease of the hepatic tissue. This
is usually mostly around the divisions of the portal vein and the
periphery of the acini, but also in the end around the hepatic veins as
well. When it has formed around the biliary canals there is a great
increase of the liver (often doubled) and its edges have become rounded.
Within the acini the increase of the fibrous stroma is seen between the
radiating capillaries, and the hepatic cells are contracted, granular,
pigmented, and comparatively destitute of protoplasm around the still
persistent nucleus.

_Treatment._ Glauber salts to clear the bowels of offensive matter, and
deplete from liver and portal vein, bicarbonate of soda or iodide of
potassium to eliminate the poisons through the kidneys and to lessen the
induration, and finally salicylate of soda as a liver stimulant and
intestinal antiseptic are suggestive of the line of treatment that may
be pursued. The saline laxatives and diuretics, and antiseptics may be
changed for others according to special indications, and bitters and
mineral acids may be resorted to. Counter-irritants to the right
hypochondrium should not be neglected in case of local tenderness. In
the otherwise fatal Schweinsberg disease, Imminger, Künke and Stenert
had a remarkable success from the free use of potassium iodide, which
suggests a cryptogamic origin, as this agent is so valuable in polyuria
which results from musty fodder. In all cases, gentle exercise in the
open air and a moderate ration of laxative food (green) are of great
value. Above all the old suspected diet should be carefully avoided,
also any impure water supply.




                          CIRRHOSIS IN CATTLE.


This has been recorded by different observers and usually as the result
of some obstacle to the circulation, or of catarrh and obstruction of
the biliary passages. Morot saw it in young calves, which showed greatly
enlarged liver (in one case 24 lbs.) and kidneys, the former containing
numerous cysts and marked sclerous thickening around the vessels. This
advancing thickening of the connective tissue, causes increasing
firmness of the liver and absorption, distortion and diminution of the
lobules. Albrecht describes a chronic interstitial hepatitis with
caseated centres (nontuberculous) many of them an inch in diameter. The
liver is brown or grayish with whiter callosities which extend into its
substance and make points of attachment to the diaphragm or other
adjacent organ. The contrast between the fibrous layers and the hepatic
tissue has been likened to a checker board (Höhmann). The enlarged liver
may weigh 30 lbs.; in one remarkable case it weighed 300 lbs. (Adam).
The bile is of a light color and mixed with mucus.

_Symptoms._ The symptoms are indefinite: a gradually increasing
jaundice, the passage of yellowish red urine becoming more and more red
and albuminous, and finally coagulating on the walls of the urethra or
on the litter, chronic indigestion, salivation (Schäffer), weakness,
breathlessness and more or less fever may give indications of the
disorder. Höhmann failed to find tenderness of the right hypochondrium.
The disease is liable to go on to a fatal issue, so that it is often
sought to prepare the animal for the butcher.

_Treatment_ will follow the same line as in the horse. Green food,
pasturage, open air life, saline laxatives, and alkalies with a free use
of potassium iodide to check the sclerosis will be indicated.




                         CIRRHOSIS IN THE DOG.


In the dog, cirrhosis is much more common than in the larger animals, in
connection with idle pampered habits, the frequency of diseased heart
and consequent disturbance of the circulation, and the presence of
parasites in the liver or biliary ducts. Bacteria intoxication and
infection are also common.

_Lesions._ The liver is at first tumefied, with hard consistency and
rounded edges, and a deep brownish red color, but this is modified by
the grayish fibroid hyperplasia which is especially abundant in and
around the vaginal sheaths of the capsule of Glisson. In cases arising
from diseased right heart or lungs the induration is rather concentrated
around the hepatic veins. The contraction and shrinking of the fibroid
hyperplasia as the disease advances causes the projection of the hepatic
tissue in minute rounded elevations which give a peculiar uneven
appearance to the surface of the organ. The fibroid growth gives a
remarkable hardness to the liver which resists even the edge of a knife.
The hepatic cells are the seat of fatty and pigmentary degeneration.
Inflammation and tumefaction of the kidneys, and ascites are common
features of the malady.

_Symptoms._ The general symptoms are as in parenchymatous hepatitis with
a more tardy development. There are impaired or irregular appetite,
dullness, sluggishness, in an obese animal short-windedness or
palpitations on slight exertion, symptoms of disease of the heart, lungs
or digestive organs, a spasmodic cough, constipation followed by
relaxation of the bowels, nausea and vomiting. As the disease advances
tenderness of the loins, the passage of brownish or reddish, albuminous
urine, the formation of ascites and of gastro-intestinal catarrh may be
noticed. Icterus may be entirely absent, but, with a flaccid abdomen,
enlarged liver and spleen may be detected.

_Treatment._ The indications are to first combat the causes.
Irregularities in the heart’s action may be met by digitalis or
strophanthus; gastro-intestinal catarrh by a carefully regulated diet,
with mineral acids and bitters; portal congestion by a free use of water
and other diluents and by saline laxatives; intestinal fermentations by
antiferments (salol, naphthol) and toxic matters in the blood by
alkaline diuretics. For the liver hyperplasia, potassium iodide may be
freely used. Blisters to the right side will occasionally prove useful.
The ascitic fluid must be drawn off when it accumulates. A diet of milk,
bread and milk, buttermilk and mush, or one in which albuminoid elements
are in minimum amount and the action of which is laxative is to be
preferred. Out door exercise is desirable.


                     CHRONIC ATROPHY OF THE LIVER.

  _Chronic Atrophy_: In _old horses_: in right and spigelian lobes;
  others show hypertrophy. In _ruminants_, omnivora and carnivora: in
  areas compressed by tumors or parasites. Perihepatitis. Sclerosis.
  Remedy causes if possible. _Fatty Degeneration_: Oil globules in liver
  cells, pathological when they destroy the protoplasm. In ducks and
  geese on forced feeding. Causes: poisoning by phosphorus, arsenic,
  antimony, lead, phenol, iodoform, alcohol; excess of fat in food,
  spoiled fodders, colchicum autumnale, yellow lupins, bacteria,
  hemorrhages, inflammations, tumors, parasites; improved meat producing
  breeds, old animals, hot stables. Lesions: liver enlarged, pale,
  yellow, bloodless, knife in cutting is smeared with fat, oily stain on
  paper, liver cells enlarged, protoplasm replaced by fat or oil; may be
  circumscribed. Symptoms: obesity, over-fed in fats and starches, of
  fattening breed, kept in confinement, in hot moist environment, if fed
  certain poisons, with costiveness and indigestion, no endurance, short
  winded, slight icterus, scanty urine, little urea, later, emaciation,
  palpation of enlarged liver. Treatment: send to butcher, pampered
  horses, cows from swill stable, a run at grass, with shade trees, a
  poor pasture, salines, cholagogues, mineral acids, bitters, iron with
  alkalies, currying, massage, douches.

Acute yellow atrophy has been referred to under parenchymatous hepatitis
but a chronic atrophy is also met with in all domestic animals.

In _old horses_ it affects, by preference the right and spigelian lobes,
the portal circulation of which is less direct because of the veins of
supply leaving the parent trunk at right angles (Leblanc), and because
these lobes are more exposed to compression by solid accumulations in
the double colon (Kitt). In such cases a compensatory hypertrophy of the
left and middle lobes is often observed.

In _ruminants_ the lesion is often circumscribed to the areas that have
undergone compression by tumors or parasites (echinococcus,
actinomycosis), and there may be compensatory increase elsewhere in the
organ.

In _swine_, _dogs_ and _cats_ the same conditions are operative. In all
alike perihepatitis may be a causative factor, and sclerosis
(cirrhosis), with contraction of the fibrous hyperplasia may also
operate.

_Symptoms_ are very obscure and _treatment_ unsatisfactory unless the
active causes can be recognized and arrested.


          HEPATIC STEATOSIS. FATTY LIVER. FATTY DEGENERATION.

The presence of oil globules in the liver cells is normal and
physiological, the liver acting to a certain extent as a store-house for
fat. This is always a marked feature, in healthy animals on high
rations, and taking little or no work, but so long as the protoplasm and
nuclei of the cells retain the normal characters and functions the
condition is not a morbid one. It may, however, become excessive, with
great enlargement of the liver, and with the substitution of fatty
granules for the protoplasm of the cells as in ducks and geese subjected
to forced feeding, and the condition becomes a distinctly pathological
one.

In true fatty degeneration the protoplasm of the hepatic cells is
destroyed and replaced by fatty granules, the resulting condition being
a permanent destruction of the cell for physiological uses.

_Causes._ The liver cells undergo fatty degeneration under the action of
certain poisons like phosphorus, arsenic, antimony, lead, phenol,
iodoform and alcohol. According to Neyraud oxide of antimony is given
daily to fattening geese to hasten the development of fatty liver.

An excess of fatty elements in the food leads to the same result as
shown first by Majendie in dogs, in which not only did the liver undergo
this degeneration but the sebaceous glands of the skin secreted an
excess of volatile fatty acids.

The cryptogams and their products on musty fodders determine a
gastro-enteritis in herbivora, accompanied by fatty degeneration of the
liver.

Colchicum Autumnale, and poisonous yellow lupin both determine this
degeneration.

The products of a number of pathogenic bacteria have a similar effect.
This has been noticed in the cat with bacillus pyocyaneus (Charrin), the
cholera spirillum, pyæmic and septicæmic infection, contagious pneumonia
of the horse, strangles, and ulcerative endocarditis. It has been long
noticed to be a complication of pulmonary tuberculosis, the result in
this as in other affections of the lungs having been attributed to
lessened oxidation in the tissues. It occurs also in hæmorrhages,
ruptures and inflammations of the liver and in passive congestions of
the organ, the impairment of the normal functions (in the altered
conditions of nutrition, or under the influence of poisons,) proving an
important factor in the process. The same remark may apply to the fatty
degeneration which complicates most other liver diseases, cirrhosis,
catarrh of the bile ducts, distomatosis, echinococcus, carcinoma, and
epithelioma.

Certain other factors must be taken into account. The inherited
disposition to the production of fat which characterizes the improved
breeds of butcher animals, and particular individuals of all breeds,
mature age which predisposes to the deposit of fat in internal organs,
old age which lessens the vitality of the cells, and hot, damp climates
or stables, all operate more or less in determining the fatty change.

_Lesions._ In fatty degeneration the liver is enlarged, pale, bloodless,
yellowish, its cut surface exudes an oily fluid which smears the knife,
and it is so light that it floats on water. If scraped and the material
drawn across a sheet of paper it forms a transparent oily stain. Under
the microscope the liver cells are seen to be enlarged and to have their
protoplasm and nuclei replaced by fat or oil. If due to obstruction in
the heart or lungs the degeneration is greatest toward the centre of the
acinus, if due to an infectious disease it is usually greatest towards
its periphery. In infectious diseases too the liver is not pale yellow,
but usually of a deep brownish or yellowish red. The degeneration may be
local or general. McFadyean found a circumscribed lesion in an ox’s
liver, of a bright ochreous color, and the cells completely transformed
into fat cells, while the rest of the liver was sound. In the dog fatty
areas, up to an inch in diameter, are not uncommon. The swollen cells
pressing on the adjacent vessels, account for the bloodless condition,
and favor the degenerative process.

Neyraud records a fatty liver of 28 ℔s. weight from the horse, and Kitt
one of 10 ℔s. from the pig.

_Symptoms._ Like as in most chronic liver diseases the indications are
uncertain. The conditions may, however, suggest fatty degeneration; if
the patient is very obese; if it has had an abundant food, rich in
hydrocarbons and carbohydrates, and little exercise; if it has received
in food or water continuous doses of phosphorus, arsenic or antimony; if
it has lived in a hot moist climate or stable; if there has been a
tendency to costiveness and indigestion; if the patient is weak, easily
fatigued and short-winded; if there is a slightly yellowish red tinge of
the conjunctiva and if the urine is scanty and contains little urea. If
the disease is more advanced and the animal emaciated, it may be
possible in the smaller animals at least to manipulate the liver to make
out its increase, its smooth surface, and its absence of tenderness.

_Treatment._ When met with in meat producing animals the best resort is
to turn these over to the butcher. When in an animal which is mainly
valuable for breeding purposes, or in horses or carnivora, something may
be done to check the progress of the malady, and maintain at least the
present condition. The value of this will of course depend on how far
the disease has already progressed. Cows that have spent a winter in a
hot swill stable are of little use afterward for breeding or dairy uses
and advanced cases of fatty degeneration in the horse or dog hold out
little hope of a satisfactory issue. For cases in the earlier stages,
nothing can be better than a run at grass, where there is opportunity
for shelter from the noonday sun. If the pasture is short and the animal
has to exercise to secure a living, so much the better. If kept indoors
the patient should have a clean, roomy airy box stall, with a moderate
allowance of easily digested food, and laxatives and cholagogues daily
such as Glauber salts, aloes, calomel, podophyllin or cream of tartar.
Mineral acids, especially nitro-muriatic acid, and bitters may also be
given. The preparations of iron are sometimes useful in maintaining the
tone of the digestive organs and counteracting anæmia but they must be
conjoined with diuretic doses of bicarbonate of soda.

There is great advantage in stimulating the skin, and active brushing,
currying, hand-rubbing, and even cold douches may be resorted to.


                   AMYLOID DEGENERATION OF THE LIVER.

  Degeneration of basement substance of connective tissue, swollen,
  transparent, homogeneous, colored mahogany brown by iodide. In wasting
  diseases, tubercle, cancer, malaria, dysentery, leukæmia, suppuration,
  ulceration, pleurisy, pericarditis, peritonitis, chronic catarrh,
  broncho-pneumonia, orchitis, biliary calculi, nephritis. Chronic.
  Lesions: Affected part swollen, sinks in water, bloodless, clear,
  smooth, homogeneous, yellowish or reddish gray, under compound
  solution of iodine becomes mahogany brown, under sulphuric acid dark
  violet. Extends from vessel walls to adjacent connective tissue.
  Symptoms: Of wasting diseases, but not diagnostic. Treatment:
  Unsatisfactory, directed to causative disease.

This is a condition in which the basement substance of the connective
tissue, and especially of the walls of the vessels, becomes swollen and
composed of a transparent, homogeneous substance, albuminous in
character, and which stains of a deep mahogany brown on the application
of a solution of iodine. The degeneration is usually associated with
severe wasting diseases, in the human being with tuberculosis, syphilis,
malignant tumors, malarial infection, dysentery, leukæmia, and chronic
suppuration or ulceration, especially of the bones.

In the _lower animals_ (horse, dog, ox, sheep, rabbit, poultry) it has
been seen to attend or follow on similar cachectic conditions. In the
_horse_ it has been seen in connection with the effusions of pleurisy,
pericarditis and peritonitis (Rabe), in chronic bronchial catarrh
(Fischkin), in chronic broncho-pneumonia, and dilated right heart
(Trasbot), in orchitis, phlebitis and cachectic states (Caparini), and
in calculous obstruction of the biliary duct (Burgoin). In _cattle_ it
has accompanied chronic nephritis (Brückmüller), tuberculosis, leukæmia,
etc. In _lambs_ kept in confined stables, though well feed on oats
(Werner). In long standing suppurations and in animals fed on distillery
swill it has been observed.

It may last for months or years, and predispose to other disorders,
functional and structural. It does not, however, interrupt secretion as
bile continues to be formed.

_Lesions._ The affected part of the liver is enlarged, the entire organ
in the horse may amount to 32 lbs. It is smooth and even, though thick
and rounded at its inferior border, yet occasionally on the posterior
aspect there may be hyperplasia and a rough irregular surface. The
diseased liver is heavy and sinks in water, unlike the fatty liver. In
the horse it is soft and friable or even pasty whereas in man it is firm
and resistant. The cut surface is bloodless, smooth, clear, homogeneous
and grayish, yellowish or reddish gray. When treated with a solution of
iodine and potassium iodide it changes to a deep mahogany brown; if
dilute sulphuric acid is then used it changes to a deep violet, almost
black color. If the iodine solution is brushed over the smooth cut
surface the mahogany color of the amyloid stands out in marked contrast
with the bright yellow of the healthy hepatic tissue. The amyloid
commences in the walls of the smallest arteries, in the media and
intermediary layers of the intima, and thickens the walls so as to
obstruct their lumen more or less completely and render the part
comparatively exsanguine. It may extend to the connective tissue of the
organ, but it is not certain that the hepatic cells are involved in the
process. The cells are, however, pressed upon by the diseased vessels
and stroma and undergo consequent fatty degeneration. The amyloid may be
confined to but a small part of the liver or to its smaller
blood-vessels or it may extend to the whole. In fowls it is always in
multiple centres (Leisering). It may be found in other important organs,
kidneys, spleen, lymphatic glands, intestinal mucosa, etc.

_Symptoms_ are not diagnostic. If with an old standing, exhausting
disease, paresis, weakness, emaciation and unfitness for work, there is
loss of appetite, dryness of the mouth, congestion of the rectal mucosa,
yellowish, whitish, or dark tarry fæces, and a slightly brownish or
yellowish tinge of the visible mucous membranes (Rexante) it may be
suspected. In fowls Leisering noticed, weakness, lameness, ruffling of
the feathers and attacks of vertigo. Icterus, ascites and tenderness
over the region of the liver may all be absent. In the absence of
ascites, tympany, or an excess of fat in the smaller animals,
manipulation may detect the considerable enlargement of the liver, and
the characteristic smoothness, of its surface. In other cases some
indication may, at times, be had from the increased area of dullness on
percussion.

_Treatment_ is essentially unsatisfactory even if a correct diagnosis
can be made. The most hopeful course would be to correct the
debilitating disease in which the amyloid seems to have originated.
Diseased bones, ulcers, chronic suppurations, and catarrhs may be done
away with, and at least any further advance of the degeneration
arrested. Open air exercise and a green or otherwise laxative diet would
be indicated. The amyloid in lambs fed on oats was corrected by a change
of diet (Werner). As medication the alteratives, potassium iodide and
potassium arseniate have been mainly resorted to. Bitters and iron may
also be of use to build up the strength. The latter should be given with
potassium bicarbonate.


        BLACK PIGMENTATION OF THE HEPATIC CELLS. BROWN ATROPHY.

  _In horse._ With melanoma and atrophy, or without, pigment granules
  fill hepatic cells, liver becomes brown or black. In calves. In sheep.
  Apart from melanosis, the real cause unknown.

The accumulation of granules of black pigment in the hepatic cells has
been noticed in old and worn out horses (Louis Blanc, Cadeac,
Bruckmüller), in calves (Degive, Cadeac), and in sheep (Siedamgrotzky,
Barrier). In _horses_ it has been found in connection with atrophy, or
in other cases, with melanotic tumors in other parts. In atrophic cases
the liver is small, puckered, brown and dull, with a leathery appearance
on section, and with the hepatic cells charged with pigment granules so
that each acinus has a stellate appearance from the radiating lines of
cells. This constitutes _brown atrophy_.

The second form which may be called _melanotic liver_, is not associated
with atrophy, but is characterized by the crowding of the hepatic cells
with black pigment granules, which fill up the protoplasm and crowd the
still pale nucleus to one side. The affected portions become of a deep
black.

In _calves_ the pigmentation may be confined to the superficial portion
of the liver (Degive).

In _sheep_ pigmentation may be in the peripheral cells only of the
acinus (Cadeac) but is about equally distributed on the surface, and
throughout the interior of the liver, and may extend to the stroma of
the gland (Siedamgrotzky).

Apart from the general causes of melanosis, benignant or malignant, no
definite reason for this pigmentation has been assigned. The development
of melanæmia and tissue pigmentation in man from malarious
microörganisms suggests that other germs and their products may have a
similar effect in the lower animals but nothing certain is known as to
the true cause.

Apart from melanosis, it is not known that this pigmentation of the
hepatic cells is of any essential pathological importance. It is
important however for the veterinarian to be acquainted with the
condition, that he may intelligently deal with such lesions whether seen
in ordinary post mortem examinations, or in the course of meat
inspection.


             DILATATION OF THE GALL BLADDER AND BILE DUCTS.

  Causes: obstruction of common bile duct, distoma, round worms, tæmiæ,
  gall stones, encrustations, inflammations, tumors, cicatrices,
  hydatids. Congenital absence. Ducts stand out on liver. Symptoms of
  colic, icterus, bile poisoning, marasmus. Treat the causative
  conditions.

This may occur in all our domestic animals except solipeds in which
latter there is no gall bladder.

_Causes._ Any serious obstruction to the discharge of the bile into the
duodenum may cause it. The presence of trematodes, nematodes, or even
tæniæ in the ducts, gall stones, incrustations, occlusion of the ducts
by inflammatory swelling, tumors of the liver or adjacent parts,
echinococcus, cysticercus, or cicatrices may be cited. Cadeac mentions a
case of congenital atresia of the bile duct in the calf. Vigney records
a case in the cow in which the greatly dilated gall bladder formed a
hernial mass in the epigastric region which was, however, easily reduced
by manipulation.

In all such cases the distended bile ducts stand out as white branching
lines on the back of the liver converging toward the portal fissure. The
walls of the ducts may be attenuated or thickened and it is alleged
calcified. They are usually lined by a deposit of cretaceous consistency
precipitated from the retained bile. The contents of the distended ducts
and bladder are variable. They may have the color (yellow, green) and
consistency of bile; they may be thick, dense and albuminous; they may
be thin and serous from inflammatory or dropsical exudation; they may be
granular, or purulent.

Though there is no gall bladder, in the soliped, a similar condition of
the biliary ducts may be produced in the same way.

According to the degree of obstruction there may be more or less acute
symptoms of biliary colic, icterus, marasmus, poisoning by bile acids,
etc.

_Treatment_ must be directed toward the removal of the special cause of
dilatation.


                          DOUBLE GALL-BLADDER.

As a congenital formation the gall bladder is sometimes divided into two
at its fundus, and in other cases the division extends throughout,
forming two complete sacs. This has been found in the sheep, cat, ox
(Gurlt, Goubaux) and pig (Goubaux). Such a redundancy does not interfere
with normal functions.




             CHOLELITHIASIS. BILIARY CALCULI. GALL STONES.

  In ruminants, omnivora, and carnivora, less often in horse, 1 to 1000,
  or more, biliary sand to marble or more, casts; nucleus, bile pigment,
  blood mucus, etc., with concentric layers of cholesterine, pigment,
  salts and lime. Causes: idleness, overfeeding, dry feeding, thickening
  of bile, colloids, bacteria, wintering in stable. Colloids induce
  globular deposits. Parasites. Inflamed biliary epithelium secretes
  excess of cholesterine and lime. Age. Acid bile, constipation.
  Diseased liver. Lack of bile salts. In _solipeds_: all sizes and
  numbers, green, brown, yellow or white. Liver disease. Symptoms: colic
  with depression, prostration, yellow or red urine, icterus, sudden
  recovery. Treatment: sulphate of soda, olive oil, antispasmodics, warm
  drinks, fomentations, salicylate of soda, chloroform, pasture, or
  succulent food, and open air exercise. In _cattle_: musk odor; calculi
  dark green, yellowish green, whitish or orange, dry red, all sizes and
  numbers. Causes: dry winter feeding, etc. Lesions: dilated biliary
  ducts and bladder. catarrh, thickening, rupture, septic peritonitis.
  Symptoms: relapsing colic, with icterus, prostration, and tender right
  hypochondrium, in stalled animal on dry feeding. Suggestive: not
  pathognomonic. Treatment: as in horse: succulent spring pasturage. In
  _sheep_: rare, musky odor; concretions and casts common in
  distomatosis. Hypertrophied ducts. Symptoms of distomatosis.
  Treatment: for distomatosis and calculi. In _swine_: rare: circular.
  In _carnivora_: round, dark green, pin’s head to hazel nut. Symptoms:
  colics, constipation, emesis, icterus, tender right hypochondrium,
  concurrent catarrh of bowels, heart disease, dyspnœa, sudden relief.
  Mode of relief. Treatment: olive oil, bile, sodium sulphate, or
  salicylate, antispasmodics, alkalies, enemata, fomentations. Laxative
  food, exercise, open air.


Gall stones are most frequent in animals having a gall bladder. Some
medical writers say they are formed in the gall bladder only, but the
soliped which has no gall bladder has in particular instances furnished
hundreds of gall stones. Yet the ox, dog, sheep and pig are the common
victims of biliary calculi among our domestic animals. In these the
calculi appear to be mostly deposited from the stagnant bile in the gall
bladder, yet concretions on the biliary ducts and hollow casts inside
the ducts are by no means uncommon.

A gall stone may be single, or they may be multiple up to hundreds or
even thousands, and when very numerous they are individually small,
perhaps no larger than a pin’s head. They may, however, attain the size
of a marble or more, and by mutual pressure and wear they assume various
polygonal forms. If they lie apart in the gall ducts or bladder they are
regularly rounded. They are sometimes mulberry shaped as if
conglomerate. In other cases the solid masses are so small as to have
secured them the name of biliary sand. Casts and incrustations in the
ducts are not necessarily made up of smaller globular masses.

On section a calculus shows a nucleus, composed of bile pigment, blood,
mucus, with the debris of parasites or bacteria. Around this nucleus the
calculus is deposited in concentric layers, of a hard material
consisting largely of cholesterine, but containing also bile coloring
matter, bile salts, and lime, in short all the constituents of bile.

_Causes._ Various conditions contribute to the precipitation of biliary
solids in the form of calculi or encrustations. The most prominent
causes are: lack of exercise, overfeeding, dry feeding, concentration of
the bile, the presence of colloids and bacterian infection.

_Idleness_ is especially operative in cattle, which are quite subject to
biliary calculi and concretions, when shut up in the stall on _abundant,
dry feeding_ for a long winter. They are not noticed in stalled animals,
that are fed watery or succulent rations, such as green fodder,
distiller’s or brewer’s swill, ensilage, brewer’s grains, mashes, roots,
potatoes, apples, pumpkins, and in case a tendency to their formation is
developed on the dry feeding of winter, the concretions may be
re-dissolved and entirely removed by the succulent spring grass. A
similar influence is noticed in the human family, as the female sex
living mostly indoors, and males pursuing sedentary occupations furnish
the greatest number of gall stones.

_Concentration of bile_ results in part from muscular inactivity and
hepatic torpor, but also from overfeeding which loads the portal blood
and indirectly the bile with an excess of solids, and from dry feeding
which lessening the secretion of water leaves the bile more dense and
predisposed to precipitate its solids. The density of the liquid,
however, developed from a rich and dry ration and a prolonged
inactivity, may continue for a length of time, without the occurrence of
actual precipitation. It usually requires some additional factor to make
this predisposition a direct cause.

=Presence of Colloids.= This may be found in the presence of solid or
semi-solid particles. Just as the introduction of a thread into a
concentrated solution of sugar or salt will induce an instant
crystallization on the filament so the presence of solid bodies
determines a similar condensation in solid form of the solids of the
bile. But this tendency is increased materially if the solid body is
itself of a colloid or non-crystallizable material. Rainey and Ord have
shown experimentally that colloid bodies like mucus, albumen, pus,
blood, epithelial cells, not only determine the precipitation of
crystallizable salts from a strong solution, but that they cause the
precipitate to assume the form of globular or spherical particles, which
by gradual accretions on their surfaces tend to grow into calculi. They
found that salts which are deposited by mere chemical reaction, without
the intervention of colloids, appear in the form of sharply defined
angular crystals. The very fact that a precipitate assumes a spherical
form suggests the presence of colloids as an active factor in the
precipitation. Heat appears to intensify this action, though probably
the normal body temperature operates mainly through the more active
proliferation of bacteria.

_Bacteridian infection._ In connection with the action of colloids it
has been observed that when such bodies are in a condition of
fermentation they are much more potent as precipitants than if inactive
and sterile. But as all fermentations are the work of microörganisms we
are at once brought to the conclusion that bacterial infection is one of
the most potent causes of calculous formations. The invading microbes
operate upon the dissolved solids, causing changes in their condition
which reduce their solubility, and thus determine the separation of
calculi and concretions in a manner allied to the precipitation of
nitrates in the soils.

But the same microbes operate in producing the colloids which coöperate
so effectively in the formation of calculi. The catarrhal biliary ducts,
or bladder, shed their epithelium, and transude white and red globules,
and form pus and an excess of mucus, all tending to the separation of
the biliary solids or forming nuclei on which these solids may condense.
The calculi and concretions tend in their turn to maintain and advance
the inflammation.

The access of the microbes to the biliary duct or bladder may be
effected through the blood of the portal vein or hepatic artery, or in
the new-born, through the umbilical vein from an infected navel. As
other modes of access may be named, a gradual advance from the duodenum
through the common bile duct, or more speedily on or in the bodies of
parasites (ascaris, strongylus, stephanurus, tænia, echinococcus,
distoma, fasciola, coccidia), etc.

_Changes in the chemical composition of the bile_ have been invoked as a
cause of gall-stones, and Naunyn has found that the inflamed biliary
epithelium secretes an excess of cholesterine and salts of lime. Thomas
has also observed a great increase of cholesterine in connection with a
catarrhal angiocholitis in the dog.

Among other alleged causes of biliary calculi are _advanced age_ (Rigot,
Hering), _acidity of the bile_ (Zundel), _constipation_, and any
_organic disease of the liver and bile ducts which interferes with
excretion of bile_.

Age is supposed to act by inactivity, lessened secretion, hepatic
torpor, and the greater presumption of liver disease, acidity by the
precipitation of cholesterine and the dissolving of lime present in the
tissues, and constipation through hepatic inactivity, obstruction of the
flow of bile, and the tendency to infection through intestinal
fermentations.

It may be added that any diminution of glycocholate or taurocholate of
soda or potash, decreases the solubility of cholesterine and bile acids
and favors their precipitation.


                        GALL STONES IN SOLIPEDS.

_Characters._ The biliary calculi of solipeds are of all sizes and
shapes. When numerous they are mostly the size of a pin’s head (Lucet).
Birnbaum found in one animal 400 like peas. Dieckerhoff has repeatedly
found four or five of the size of a hazelnut. Verheyen found one as
large as an apple and says one exists at the Berlin Veterinary College
which weighs several pounds. Rigot found 90 in the biliary ducts of an
old horse, and Zundel records the death of a stallion of twenty-six
years from multiple gall stones.

The calculi may be little larger than grains of coarse sand. When larger
and solitary they are mostly globular or mulberry shaped; if many are
together they have become polygonal by friction. In other cases notably
with distomata they form hollow tubular incrustations on the bile ducts,
and contain a thick grumous bile. They are usually of a green color, but
may be yellowish brown, yellow, or whitish. When cut across they present
a nucleus enclosed in successive layers, each successive one often
differing from the last in color. Their specific gravity is low, some
will even float in water when taken from the ducts, and all float when
dried. Their composition is variable but chiefly cholesterine, bile
acids, resin and pigments, an albumoid matter, with lime salts, etc. The
nucleus may be the remains of a dead parasite, epithelial cells, blood,
pus, mucus, etc. The outer layers are usually the hardest.

There may be attendant hypertrophy of the liver, cirrhosis, amyloid and
other degenerations, catarrh of the biliary ducts, and distension or
(according to Birnbaum) rupture of the portal vein.

_Symptoms._ There are no reliable diagnostic symptoms apart from the
colics which accompany the obstruction of a bile duct by a passing
calculus. These in the main resemble the colic of ordinary indigestion,
but they may be complicated by unusual depression and nervous
prostration. There may be drooping of the head, ears and eyelids, watery
eyes, resting the head on the manger or pushing it against the wall. The
urine is liable to be red or reddish (Jobelot), and if it or the mucosæ
show a yellowish tinge it is strongly suggestive. There may be
constipation or diarrhœa. The colics are severe and may last for several
days (Seaman, Lucet, Burgoin) without fever and recover abruptly when
the stone passes into the duodenum. They recur, however, with the
impaction of another stone, and this intermittent feature, with the
marked prostration, and the access of slight jaundice with each colic
furnishes the best means of diagnosis.

_Treatment._ During the access of colic give a full dose (1 to 2 lbs.)
sulphate of soda in warm water along with some active antispasmodic
(belladonna, lobelia, chloroform, ether), and foment the loins and
hypochondriac regions. Olive oil in large doses (1 to 2 quarts) has been
found effective. Salicylate of soda in full doses is beneficial in
stimulating the biliary secretion, diluting the bile, and securing some
measure of antisepsis in both bowels and liver.

In the intervals between the colics, sodium salicylate, sodium or
potassium carbonate, or olive oil in continuous doses may assist in
disintegrating the calculi or passing them on. Chloroform tends to break
them up by dissolving the cholesterin. But any such treatment must be
accompanied by the abundant ingestion of water, and this is often best
secured by a run in a rich green pasture. In the absence of pasturage,
succulent fruits, and roots, ensilage, mashes, and gruels may be
advantageously substituted, and conjoined with systematic exercise in
the open air.


                         GALL STONES IN CATTLE.

_Characters._ The biliary calculi of cattle are characterized by a faint
odor of musk, which becomes stronger on the addition of potassa and the
consequent disengagement of ammonia.

They are distinguished according to their color as dark green, yellowish
green, and orange, brownish or white. There are also the sedimentary
deposits (biliary sand).

The _dark green calculi_ are the most frequent, and being found in the
gall bladder and larger bile ducts, they attain a larger size than the
others. Those in the gall bladder may be pear-shaped, and those in the
ducts, round, ovoid or cylindroid. They are often rough and uneven on
the surface with deep cracks and holes penetrating deeply into their
substance and often filled with cholesterin. The pigments may change to
a blood red when dried. The consistency of these calculi varies, some
being hard, resistant and heavy, while others are soft and friable. All
are composed of concentric layers around a central nucleus as in those
of the horse. They vary in weight up to seven ounces in exceptional
cases. They contain cholesterin, fat, resin, pigments, and lime and
magnesia salts.

The _yellowish green calculi_ are usually spherical unless moulded into
polygonal shapes by mutual contact. In the last case they have flattened
surfaces. These have a firm consistency and are composed of successive
layers of nearly equal color and density surrounding the central
nucleus. They are on an average smaller than the dark green variety but
individual calculi have been found of three ounces.

The _whitish or orange calculi_ are usually in the form of hollow casts
of the bile ducts having a dull white color externally and a yellowish
brown internally. They are usually thin, fragile and crystalline and
contain relatively more earthy salts than the two first named varieties.
From this cause also they have a higher specific gravity. One specimen
weighed 8 ounces.

The _biliary sand or pulp_, is made up of granules of a yellowish, dark
green or black color, forming with the bile a pultaceous mass but drying
into a consistent mass. It may be firmly adherent to the mucosa of the
gall bladder and require to be scraped off. These granules may be looked
on as the first step in the formation of calculi or encrustations.

The _causes_ of biliary calculi in cattle are mainly close confinement,
dry feeding, abundant rations, the presence of trematodes in the bile
ducts and finally microbian infection.

_Lesions_ vary. With obstruction of the common bile duct or cystic duct,
there are usually dilatation of the bile ducts with fibrous thickening
of their walls so that they stand out as white branching lines on the
back of the liver. In extreme cases the common duct may acquire the
calibre of the small intestine. The gall bladder may participate in this
thickening (Chassaing) or may even rupture (Proger, Shaw).

In connection with obstruction microbian infection extends upward into
the liver, and in rupture of the bladder an acute, diffuse septic
peritonitis follows (Chassaing). This only follows on infective
inflammation of the gall bladder. Aseptic bile causes little or no
irritation.

_Symptoms._ As in the horse, general symptoms of ill health or hepatic
disorder are not pathognomonic. The presence of intermittent attacks of
constipation, and colic, with icterus, tympanies and violent efforts at
expulsion are the diagnostic symptoms of an acute attack. Pulsation and
respiration are accelerated, and the urine dense, high colored, oily and
slightly yellow. Reboul has noticed that symptoms are aggravated on
exposure to cold; there are great prostration and dullness, frequent
moaning and marked indications of tenderness when the right
hypochondrium is percussed. Charlot has observed that the only symptoms
may be persistent jaundice with scanty, high colored urine, containing
some sediment.

_Treatment_ is essentially the same as in the horse. Vanswieten and
Verheyen draw special attention to the fact that whereas biliary calculi
are very common in cattle during winter, they are rarely found in
animals that have been for even a short period on the spring grass.
Spring pasture is therefore the best therapeutic agent. During paroxysms
of colic, Glauber salts, or olive oil, antispasmodics and fomentations
over the liver are to be tried. In the intervals salicylate of soda,
sodium and potassium carbonate, olive oil, chloroform, and ether may be
used. Abundance of water and aqueous rations are essential.


                         GALL STONES IN SHEEP.

Calculi are very rare. One described by Morton had a brownish yellow
color on its surface, and a white color spotted with green internally;
it had a bitter taste, colored saliva yellow, and melted when heated,
diffusing the odor of musk. It weighed twelve grains and contained 70
per cent. of cholesterin, calcic phosphate and carbonate and the usual
biliary elements.

But if spherical calculi are rare, concretions and casts of the bile
ducts are common, especially in distomatosis. These are of a yellowish,
reddish, greenish or blackish brown, and form granular plates, or
veritable cylindroid casts often firmly adherent to the mucous membrane
of the duct.

In such cases the walls of the encrusted ducts are hypertrophied and
stand out on the back of the liver as white bands diverging from the
portal fissure.

Apart from the usual _symptoms_ of distomatosis no special indications
have been observed.

_Treatment_ is primarily that for distomatosis, to which the general
measures advised for calculi may be added.




                         GALL STONES IN SWINE.


_Characters._ The calculi are spherical, rough or on their opposed
surfaces flat, clear and glistening where they have become polished by
friction. They are found as a fine sand or as calculi the largest of
which have been 75 grains, and of a high density (1303 to 1484).
Bruckmüller found that they contained carbonate of lime and biliary
mucus. Verheyen found biliary resin, mucus, pigment, and a little fat.
They are rare in fat hogs in America. No diagnostic _symptoms_ have been
observed.


                      GALL STONES IN DOG AND CAT.

These are more or less spherical, dark brownish green, and usually found
in the gall bladder or larger bile ducts. They may vary in size from a
pea to a hazel nut. Their chemical analysis is wanting.

_Symptoms._ There may be evidence of biliary obstruction and if this
occurs intermittently and is associated with colic, it becomes somewhat
characteristic. Constipation, emesis, icterus, and sometimes tenderness
of the right hypochondrium would indicate the source of the colic. A
pre-existing and concurrent catarrh of the bowels corroborates these
indications.

Cadeac explains that the obstructing calculus is called on to resist the
impulse of the bile forced upon it by the spasmodic contraction of the
bile ducts, which distends the bile duct immediately back of the stone
to perhaps ten times its normal size. Then under a suspension of the
spasm or even an antiperistaltic contraction of the duct, the calculus
is forced back into the dilated portion or even into the gall-bladder,
and the attack is relieved. Under repeated irritations of this kind the
inflammation of the bile ducts extends into the liver and determines
cirrhosis. The irritation further through the sympathetic produces a
reflex constriction of the pulmonary capillaries, with the natural
results of increasing tension of the pulmonary artery and right heart,
and dilatation and degeneration of the walls of the latter even in the
best nourished animals. Thus dyspnœa and modified heart sounds (murmurs)
may be symptoms of biliary calculi.

_Treatment._ Three or four ounces of olive oil were found to greatly
increase the quantity and fluidity of the bile in from thirty to
forty-five minutes. Bile, sulphate of soda and salicylate of soda are
excellent cholagogues, and the latter at the same time an antiseptic.
Anti-spasmodics are especially indicated to relieve the colics, but they
must be used in relatively smaller doses than in the herbivora. Potassic
and sodic carbonates or tartrates (Vichy) may be used as enemas if they
cannot be administered by the mouth. Fomentations may be resorted to.
The food must be laxative and aqueous, and exercise must be imposed as
far as the animal can bear it.


                      FOREIGN BODIES IN THE LIVER.

  In _horse_: spikes of leguminosæ, barley awns. Symptoms: of internal
  hemorrhage, pallor, weakness, vertigo, death; jaundice, prostration,
  stupor, weakness, crossing of fore limbs, tender right hypochondrium.
  In _cattle_: bodies passing from rumen. In _swine_, sand. In _dog_,
  sharp bodies from stomach. Treatment: laparotomy.

Foreign bodies are rare in the liver in our domestic animals. _Horse._
St. Cyr has found the spikes of leguminosæ and Megnin the beards of
barley. St. Cyr believed that he traced the passage followed by the
stalk through the walls of the duodenum, and portal vein where it
divided to be distributed through the liver. At the point of supposed
entrance the walls of the vena portæ were thickened and its lumen filled
with clots. The further course of the portal vein and its branches
showed similar thickening and clots, and on the branch leading to the
right lobe was a large abscess containing 4 decilitres of pus. Clots
extended into the splenic, omental and mesenteric veins, and between the
folds of the mesentery of the small intestine were a number of minute
ruptures and blood extravasations.

Megnin found traces of the passage of the barley beards through the
gastric walls and into the substance of the liver close to the portal
fissure. Around the centre where the barbs were implanted there was an
irregular hæmorrhagic extravasation in the liver, and in the abdominal
cavity an effusion of 8 or 10 quarts of blood.

_Symptoms._ In such a case the only definite symptoms are those of
internal hemorrhage, pallor of the mucous membranes, gradually
increasing weakness, vertigo, unsteady gait, and an early death. In more
protracted cases slight jaundice, dullness, prostration, stupor,
drooping of head, ears and eyelids, resting it on the manger or walls,
muscular weakness, crossing of the front limbs, and it may be tenderness
on percussion on the right side of the chest posteriorly. It resembles
the _coma_ or _immobility_ of the horse but the patient backs more
easily.

_Cattle._ In ruminants sharp pointed bodies passing from the rumen will
occasionally penetrate the liver, and give rise to symptoms of hepatic
disorder. Augenheister found in a cow dilatation of the larger bile
ducts, which contained about 10 quarts of sand, that had apparently
entered from the duodenum by the common bile duct which had an orifice
of an inch in diameter.

_Pig._ The gall ducts of a pig’s liver, in the Veterinary College of
Berlin contains a large amount of sand (Gurlt).

_Dog._ The liver is exceptionally perforated by sharp pointed bodies
coming from the stomach. Cadeac and Blanc report three cases of needle
in the liver. Blanc’s case had been killed because of old age; one of
Cadeac’s showed symptoms resembling rabies.

_Treatment_ of these cases would be very hopeless as nothing short of
laparotomy and the removal of the foreign body would promise success.




                    TUMORS OF THE LIVER. NEW GROWTH.

  Largely secondary, from stomach, intestine, lymph glands, spleen,
  pancreas; the hepatic tumor may be disproportionately large. In
  _horse_: sarcoma rapidly growing soft, succulent, slow-growing,
  fibrous, tough, stroma with round or spindle shaped cells and nuclei.
  Symptoms: emaciation, icterus, enlarged liver, rounded tumors on
  rectal examination. Melanoma, in old gray or white horses, with
  similar formations elsewhere; not always malignant. Lymphadenoma.
  Angioma. Carcinoma. Epithelioma, lesions, nodular masses, white or
  grayish on section, and having firm stroma with alveoli filled with
  varied cells with refrangent, deeply staining, large, multiple nuclei,
  cancerous cachexia and variable hepatic disorder. In _cattle_:
  sarcoma, adenoma, angioma, cystoma, carcinoma, epithelioma. In
  _sheep_: adenoma, carcinoma. In _dog_: lipoma, sarcoma, encephaloid,
  carcinoma, epithelioma. Wasting and emaciation, yellowish pallor,
  temporal atrophy, ascites, liver enlargement, tender right
  hypochondrium, dyspepsia, symptoms of primary deposits elsewhere.


The great quantity of blood which passes through the liver lays it open,
in a very decided way, to the implantation of germs and biological
morbid products. Hence tumors of the liver are largely secondary, the
primary ones being found mostly in the stomach, intestine, abdominal
lymph glands, spleen and pancreas. The primary neoplasm is often
comparatively small, while the hepatic one supplied with a great excess
of blood may be by far the most striking morbid lesion. The hepatic
tumors are mostly of the nature of angioma, sarcoma, melanoma, adenoma,
lipoma, cystoma, carcinoma, and epithelioma.


                       NEOPLASMS IN HORSES LIVER.

_Sarcoma._ This is usually a secondary formation from the primary tumors
in the spleen and peritoneum, and it occurs as multiple masses
throughout the substance of the gland. The liver is greatly increased in
size, extending far beyond the last rib on the right side, and weighing
when removed as high as 70 ℔s. (Mason), or even 88 ℔s. (Cadeac), in
extreme cases.

The whole surface of the liver may show bulging, rounded masses, and the
morbid growth may have involved the capsule and caused adhesion to the
back of the diaphragm (Bächstädt). The cut surface of the neoplasm is
smooth, elastic, yellowish and circular or oval in outline. It may have
a variable consistency—friable or tough, according to the activity of
growth and the relative abundance of cells and stroma. The portal glands
are hypertrophied and thrombosis of the portal vein is not uncommon.

Microscopic examination of the dark red scrapings shows numerous blood
globules, intermixed with the round or spindle shaped cells and nuclei
of the tumor. Sections of the tumor show these cells surrounded by a
comparatively sparse fibrillated stroma. The round cells may vary
from .005 to .05 m.m. They contain one or more rather large nuclei and a
number of refrangent nucleoli. The nuclei are often set free by the
bursting of the cells in the scrapings. They become much more clearly
defined when treated with a weak solution of acetic acid. Small grayish
areas in the mass of the tumor represent the original structure of the
liver, the cells of which have become swollen and fatty.

A liquid effusion more or less deeply tinged with red is usually found
in the abdominal cavity.

_Symptoms_ are those of a wasting disease, with some icterus, sometimes
digestive disorder, and a marked enlargement of the liver. The last
feature can be easily diagnosed by palpation and percussion. If an
examination through the rectum detects the enlargement and irregular
rounded swellings of the surface of the liver or spleen, or the
existence of rounded tumors in the mesentery or sublumbar region, this
will be corroborative. The precise nature of the neoplasms can only be
ascertained after death.

_Melanoma._ Melanosis of the liver is comparatively frequent, especially
in gray horses, and above all when they are aging and passing from dark
gray to white. In many cases a more certain diagnosis can be made than
in sarcoma for the reason that primary melanotic neoplasms are
especially likely to occur on or near the naturally dark portions of the
skin, as beneath the tail, around the anus or vulva, in the perineum,
sheath, eyelids, axilla, etc. The extent of the disease is likely to be
striking, the liver, next to the spleen, being the greatest internal
centre for melanosis. The whole organ may be infiltrated so that in the
end its outer surface is completely hidden by melanotic deposit. The
surface deposits tend to project in more or less rounded, smooth masses
of varying size according to the age of the deposit and the rapidity of
its growth. Individual deposits may vary in size from a pea to a mass of
40 or 50 lbs. They are moderately firm, and resistant, and maintain a
globular or ovoid outline. The color of the melanotic deposits is a deep
black with a violet or bluish tint. If the pigmentary deposit is in its
early stage it may be of a dark gray. The deposits are firmer than the
intervening liver tissue and rarely soften or suppurate.

Melanosis in the horse is not always the malignant disease that it shows
itself to be in man, and extensive deposits may take place externally
and considerable formations in the liver and other internal organs
without serious impairment of the general health. It is only in very
advanced conditions of melanosis of the liver that appreciable hepatic
disorder is observed. If, however, there is marked enlargement of the
liver, in a white or gray horse, which shows melanotic tumors on the
surface, hepatic melanosis may be inferred.

_Lymphadenoma. Adenoid Tumor._ Lienaux describes cases of this kind in
which the liver was mottled by white points which presented the
microscopical character of adenoid tissue, cells enclosing a follicle
and a rich investing network of capillaries.

_Angioma._ These are rare in the horse’s liver, but have been described
by Blanc and Trasbot as multiple, spongy tumors on the anterior of the
middle lobe, and to a less extent in the right and left, of a blackish
brown color, soft and fluctuating. The largest mass was the size of an
apple, and on section they were found to be composed of vascular or
erectile tissue. The tendency is to rupture and extensive extravasation
of blood (30 to 40 lbs.) into the peritoneum.

_Carcinoma. Epithelioma._ These forms of malignant disease are not
uncommon in the liver as secondary deposits, the primary lesions being
found in the spleen, stomach, intestine, or pancreas, or more distant
still, in the lungs. The grafting or colonization of the cancer in the
liver depends on the transmission of its elements through the vena portæ
in the one case, and through the pulmonary veins, the left heart and
hepatic artery in the other.

_Lesions._ The liver may be greatly enlarged, weighing twenty-seven
pounds (Benjamin) to forty-three pounds (Chauveau), hard, firm, and
studded with firm nodules of varying sizes. These stand out from the
surface, giving an irregular nodular appearance, and are scattered
through its substance where, on section, they appear as gray or white
fibrous, resistant, spheroidal masses shading off to a reddish tinge in
their outer layers. Microscopically these consist of a more or less
abundant fibrous stroma, enclosing, communicating alveoli filled with
cells of various shapes and sizes, with large nuclei (often multiple)
which stain deeply in pigments. The relative amount of fibrous stroma
and cells determines the consistency of the mass, and whether it
approximates to the hard cancer or the soft. In the horse’s liver they
are usually hard, and, on scraping off the cut surface, yield only a
limited quantity of cancer juice. In the epithelial form, which embraces
nearly all that have originated from primary malignant growth in the
walls of the intestine, the epithelioid cells, flattened, cubical,
polyhedral, etc., are arranged in spheroidal masses or cylindrical
extensions, which infiltrate the tissues more or less. These seem in
some cases to commence in the radical bile ducts (Martin), and in others
in the minor coats of the larger biliary ducts.

As the disease advances a brownish liquid effusion is found in the
abdomen, and nodular masses formed on the surface of the peritoneum.

_Symptoms._ As in other tumors of the liver these are obscure. As the
disease advances there may be œdema of the legs and sheath, indications
of ascites, stiff movements, icterus, occasional colics, tympanies, and
diarrhœa. Nervous symptoms may also appear, such as dullness, stupor,
coma, vertigo and spasms. Emaciation goes on rapidly and death soon
supervenes.




                     TUMORS OF THE LIVER IN CATTLE.


_Sarcoma._ Round or spindle shaped celled sarcomata have been described
by Sodero and Cadeac, leading in one case to perforation of the vena
portæ and death by hæmorrhage into the peritoneum.

_Adenoma._ Martin records a case of a hepatic tumor formed of adenoid
tissue which had extended into the vena portæ, and microscopically
presented a cylindroid character. In the advanced stages it caused some
jaundice, digestive disorder, obstinate constipation, progressive and
extreme emaciation, and weakness which kept the animal constantly in a
recumbent position.

_Angioma._ These are rarely seen in the young but are comparatively
common in old cows as they are in aged men. They form masses of a dark
red color and very variable size, and have a limiting sac of connective
tissue or merge into the adjacent hepatic structure. Microscopically
they consist of a series of irregular lacunæ filled with liquid blood,
blood clots, or leucocytes, and communicating with small blood vessels
in the walls and partitions. They are believed to be formed by
dilatation of the liver capillaries with subsequent thickening of their
distended walls, and atrophy of the nearest liver cells. Cases of the
kind have been recorded by Kitt, Martin, McFadyean, Saake, Van der
Sluys, Korevaar and others. Though often seen in abattoirs, they seem to
have little effect on the general health, and no special symptoms have
been noted as indicating their existence.

_Congenital Cysts._ These are found on the anterior surface or lower
border of the liver in young calves. They have no connection with the
blood vessels, nor biliary canals, contain no head of larval tænia, and
do not constantly show the presence of any particular bacterium. These
walls are thin and their contents alkaline, with sometimes slight blood
extravasation, or a yellowish deposit in which cocci have been found.
Unless connected with cirrhosis or other serious disease of the hepatic
tissue, their presence seems to have no pathological significance.

_Carcinoma._ This has been recorded in the liver of cattle by Gurlt,
Brückmüller, Kitt and others. From the walls of the gall bladder it
grows in pyriform masses, and on the surface and in the interior of the
liver, it may appear as hard, cancerous masses of all sizes.

_Epithelioma._ This has been described by Kitt, Martin, Blanc, Leblanc,
Morot, Cadeac, and Besnoit. It appears in masses varying in size from a
millet seed up, bulging from the surface of the organ or deeply hidden
in its substance, and stained yellow or green with bile. The liver is
usually enlarged, amounting to even 34 pounds (Cadeac). The formation
commencing in the acini invades all surrounding parts causing
compression and atrophy of the liver cells, and the formation of nests
of epithelioid cells often with multiple nuclei and nucleoli. Cirrhosis
is not uncommon, and fatty and other degenerations. Microbic invasion
and necrobiosis are also common.


                    NEOPLASMS IN THE SHEEP’S LIVER.

_Adenoma_ has been met with by McFadyean, Johne, Kitt and Bollinger.
They hung as pediculated tumors from the surface of the liver, and were
in part wedged into its substance displacing the hepatic tissue and
vessels. In general they consisted of a dense fibrous stroma with
cylindroid and biliary cells in great abundance, sometimes arranged in
tubular form. Specimens described by Kitt and Bollinger attained to the
size of a man’s head and were stained of a deep green color.

_Carcinoma._ Casper reports a case of hepatic cancer in the sheep
secondary to cancer of the mesentery.




                     NEOPLASMS IN THE DOG’S LIVER.


_Lipoma._ Trasbot describes two fatty tumors in the liver of a bitch,
one of them as large as an infant’s head. It had a yellowish white
color, and had taken the place of the proper hepatic tissue.

_Malignant Tumors._ These are rather common. _Sarcomatous_ masses with
round and fusiform cells in a fibrous stroma; _encephaloid_ with a
delicate stroma and large alveoli filled with cells, and having a soft
brainlike consistency; _carcinoma_ with dense and thick fibrous stroma
and nests of cells in comparatively small numbers; and _epithelioma_
with flattened, cylindroid or other epithelial cells in masses often
affecting a tubular aggregation, are seen in different cases. Sometimes
apparently primary, they can more commonly be traced to pre-existing
centres of the same formation on the course of the portal vein or
elsewhere.

_Symptoms._ A gradual wasting and emaciation with a yellowish pallor of
the mucous membranes are characteristic. Trasbot gives the excessive
atrophy of the temporal and masseter muscles as pathognomonic. Ascites
is a usual complication. Enlargement of the liver, as shown by
percussion of the right hypochondrium, and, in case of flaccid abdomen,
by manipulation, and attendant signs of tenderness are corroborative.
Variability or loss of appetite, and vomiting is not uncommon, and in
case of primary or secondary deposits in other organs in the abdomen,
thorax or elsewhere, the symptoms resulting from functional derangement
of such organ may be found. Treatment is hopeless.




           CALCAREOUS NODULES AND DEGENERATIONS OF THE LIVER.

  Calcified roundish nodules, in groups, under capsule. Mostly in
  solipeds. Theories of origin: parasites, microbes, emboli, omphalitis,
  intestinal disease, biliary obstructions. Calcification of liver with
  large abdominal aneurisms. Cszoker’s case, Diagnosis and specific
  treatment impossible.


In the domestic animals in general the liver may become the seat of
imperfectly spherical nodules of a white, yellow or brownish white
color, varying in size from a millet seed to a pea or hazel nut, and of
a gritty consistency and feeling, from the deposition of earthy salts.
These may be seen in groups under the proper capsule, the adjacent
hepatic tissue being healthy, or atrophied, sclerosed or pigmented.
These lesions have been found most abundantly in solipeds.

_Pathogenesis._ The most varied doctrines have been advanced as to the
origin of these lesions. They have been attributed to the previous
presence in the liver of linguatula, echinococcus, cœnurus, oxyurus,
distoma, and other parasites (Cadeac, Mazanti, Olt, Ostertag, Gripp,
Leuckart, Ratz), to glanders, to microbian attacks (Dieckerhoff), to
minute embolic infarcts in omphalitis in the foal, or intestinal disease
in the adult (Kitt), and to obstructions by the eggs of distomata in the
biliary ducts (Galli-Vallerio). It is not improbable that the lesion may
be due to any one of these in a specific case, and this may be
ascertained by the existence of certain definite features and
conditions. Linguatula, echinococcus and cœnurus can only be suspected
in districts where these prevail, and a careful examination of the
central mass of the nodule should reveal the presence of the
indestructible hooklets, as certified for given cases by Olt, Ostertag
and Gripp. In case of nematoid worms or distomata, the eggs may possibly
be found as in the cases of Villach and Ratz, or the embryos (Mazanti).
Or there may be traces of channels formerly hollowed out by the worms in
the vicinity of the nodules, as seen by Leuckart. Coincident tumors of
the intestinal mucosa from larval nematodes, or aneurism or emboli in
the anterior mesenteric artery would corroborate this conclusion. If
distomata had started the lesions, the distension of the gall ducts and
the thickening of their walls would be likely to indicate their former
presence. Glander nodules might be suspected from the absence of a
distinct rounded or oval outline, from the lack of a distinct, clear
line of demarcation between the nodule and the adjacent liver tissue,
and by the manifestation in the periphery of the nodule and around it of
free cell proliferation, showing the mode of progression by the invasion
of new tissue. If still active, the bacilli should be discoverable in
stained scrapings or sections. There should also be distinct indications
of the lesions of glanders in the lymph glands of the portal fissure, of
the mediastinum, of the submaxillary region and of other parts.

Heiss records an interesting case of general calcification of the
horse’s liver, with large aneurism of the abdominal aorta, mesenteric
and renal arteries. The liver was thirty-two pounds, puckered on the
surface and showed calcic degeneration of the walls of the vessels and
hepatic tissue, to such an extent that when the organ was dried it did
not add materially to its hardness. Microscopically the diseased centres
indicated minute blood clots (thrombi), with fibrinous development and
cretifaction. The lesions in this case were attributed to multiple
emboli in connection with the aneurism. It might suggest further,
microbian infection of both the aneurismal and hepatic vessels. In
another case of extensive cretifaction of the horse’s liver reported by
Cszoker, the calcified masses tended to assume rounded forms like
tubercle, and had a clear glistening surface.

These lesions are mainly interesting in a pathological sense, and unless
they are very extensive do not give rise to appreciable symptoms.

_Treatment_ could only be prophylactic and directed to the removal of
the special conditions, in which the calcification originated in a given
locality.




                      ACTINOMYCOSIS OF THE LIVER.


On damp infested soil, in cattle and swine. Round tumors, hard surface,
soft centre, fibrous sac, club-shaped cells in tufts. Symptoms of liver
disorder. Coincident external actinomycosis. Treatment: potassium
iodide.

In damp soils where actinomyces are present in the soil and vegetation,
it is not uncommon to find the characteristic growths in the liver of
cattle and swine. Rasmussen saw twenty-two cases of hepatic
actinomycosis in one year (1890) and in a number of cases he has found
the liver, spleen, peritoneum and intestine simultaneously affected.
Jensen who has also recorded hepatic cases, found tumors extending from
the liver to the diaphragm. He describes them as rounded masses, of
different sizes, enclosed in a fibrous envelope of variable thickness,
hard and resistant at the surface and somewhat softened toward the
centre. Microscopic examination detects the club-shaped cells arranged
in tufts and radiating from a common centre.

_Symptoms_ are only the general indications of hepatic disease differing
according to the size, and position of the morbid product and its
interference with normal functions. When, however, superficial
actinomycosis is found these symptoms may be fairly attributed to the
existence of similar products in the liver.

_Treatment_ consists in the administration of potassium iodide in full
doses, daily for a week, followed by a laxative, and then, after an
interval of two days, repeat the treatment for a second week, and so for
a third, fourth and fifth until the microbe has been destroyed.




                        PARASITES OF THE LIVER.


Lying as it does in the channel of the blood charged with the products
of absorption from the intestine, the liver is especially liable to
parasites. Among protozoa are: Monocercomonas hepatica (pigeon),
saccharomyces guttulatus (rabbit), eimeria falciformis (rabbit),
coccidium oviforme (rabbit, pig, dog). Among the lower cryptogams are
actinomyces (ox, pig). Of the tapeworm family are: Cysticercus
tenuicollis (ruminants, pig), c. pisiformis (rabbit), c. cellulosa (dog,
pig), echinococcus veterinorum (animals, man), tænia fimbriata (sheep,
deer), and an undetermined cœnurus (cat). Of trematodes are: Distoma
hepatica (herbivora, man), distoma lanceolatum (herbivora, man), distoma
giganteum, or Americanum (cattle), d. truncatum, d. conjunctum, d.
campanulatum (dog), amphistoma explanatum (ox). Of nematodes are:
Stephanurus dentatus, ascaris suis, oesophagostoma dentatum (pig),
sclerostoma equinum, ascaris megalocephala (horse), ascaris bovis (ox),
oesophagostoma columbiana (in ruminants), filaria hepatica, enstrongylus
gigas, ascaris marginata (dog), ollulanus tricuspis, ascaris mystax
(cat). (See Parasites).


                       DISEASES OF THE PANCREAS.

  Obscure. Shown only by digestion or hepatic disorder. Excess of fat in
  stools suggests suppression of secretion. Intestinal fermentations.
  Suspension of glycogenesis and consequent emaciation, stunting or
  poisoning. Pancreatic calculus and icterus.

Diseases of the pancreas are even more obscure than those of the liver.
Situated on the course of the duodenum, beneath the lumbar vertebræ and
their right transverse processes, and separated from the lateral walls
and floor of the abdomen by the great mass of the intestines, it is not
open to manipulation or satisfactory percussion, and its secretions
being used up in the function of digestion, so that they cannot be
perceived and tested externally like the secretions of the kidneys.
Beside the general constitutional disorder therefore, we must look
rather to the derangements of the digestive functions, to the abnormal
condition of the fæces, and to the alterations in subordinate functions
like the glycogenic action of the liver, for indications of an unhealthy
state of the pancreas. The suppression of the pancreatic secretion has
long been associated with the occurrence of fat in the stools, yet this
may result from the lack of bile which has important functions to
fulfill in emulsionizing fat, and in securing its endosmosis. On the
other hand the lack of pancreatic juice may hinder the complete
digestion of the albuminoids, and favor their fermentation and the
occurrence of tympanies, congestions, abnormal secretions, etc., which
may be easily attributed to another origin. Then again the dependence of
the liver on the pancreas for its stimulus to glycogenesis, would
suggest a series of disturbances from the abundance of the unused food
principles, from the hindrance to nutrition and growth, and perhaps from
the toxic action of the hepatic products. Once more, through the common
excretory duct, infection of the pancreas may extend to and involve the
liver, and blocking of the common duct by pancreatic parasites, or
calculi, may stop the flow of bile and cause jaundice or other icteric
disorder. And yet, it is rarely the case that pancreatic disorder is
successfully diagnosed, and it is too often only at the post mortem
examination that the actual lesions are revealed.


                        CATARRHAL PANCREATITIS.

  Probable causation by parasites, calculi, irritants, microbes.
  Lesions: mucosa reddened, thickened, ducts dilated, epithelium fatty,
  granular, desquamating, pus, connective tissue indurated.
  Interdependence of pancreatitis and hepatitis in horse, sheep and
  goat. Liver lesions. Symptoms: loss of vigor, endurance, appetite, and
  condition. Icterus, costiveness, fœtid, fatty stools, percussion
  tenderness—right side. Treatment: antithermics, eliminants,
  antiseptics, derivatives, alkalies, salicylates, ether.

_Causes._ We know little of the causes of this affection, but it may be
inferred that parasites, calculi and other irritants, will produce in
this as in other mucosæ a mucopurulent inflammation. Then again the
presence of pus suggests the coöperation of pus microbes as in the
infective catarrhal icterus. The blocking of the common gall and
pancreatic duct, by gall stones or biliary products, will entail arrest
of the discharge of pancreatic juice, and a consequent pancreatitis,
just as blocking with pancreatic products will cause hepatitis and
icterus.

_Lesions._ The mucosa of the pancreatic ducts is reddened, congested and
thickened and their lumen blocked by a white, granular matter,
containing pus globules, fibrine filaments, and granular, ciliated
epithelium. The blocked ducts become dilated, and their walls thickened,
the epithelium is desquamated to a greater or less extent, and the raw
exposed surface may present ulcers or granulations. The pancreatic cells
undergo fatty degeneration and the connective tissue becomes steadily
indurated (sclerosis). These lesions were especially noted by Megnin and
Nocard in a case of pancreatitis in the horse.

In the horse, sheep and goat, which have a common outlet for the bile
and pancreatic juice, the blocking of the latter and the arrest of the
bile almost of necessity causes hepatitis, and infection in the one
gland is directly transferred to the other so that pancreatitis and
hepatitis are mutually causative of each other. In the ox, pig, dog and
cat, in which the bile and pancreatic juice are poured into the duodenum
through separate ducts and orifices, this mutual pathogenic action is
not so certain.

When the liver is implicated, there is catarrh and dilatation of the
bile ducts, fatty degeneration commencing in the centre of the acini,
pigmentation appearing at their periphery, and sclerosis of the organ
follows.

_Symptoms._ In Nocard’s equine case there was progressive loss of
spirit, energy, and endurance; appetite was poor and eating listless;
after two weeks jaundice set in, the visible mucosæ and skin showing a
yellow tinge, and the scanty urine becoming brownish yellow; the bowels
became costive the fæces being formed of small hard discolored balls,
but no excess of fatty matter is recorded. Emaciation advanced rapidly,
the most marked wasting being in the muscles of the back, loins and
croup. Death ensued at the end of two months from the commencement of
the illness. In man sudden, violent colic, with nausea, tympany and
collapse are prominent symptoms.

_Diagnosis_ is more satisfactory when with digestive disorder, tardily
developing icterus, and rapid emaciation, there is an excess of fat in
the ill-smelling fæces. Pain on percussion of the right hypochondrium
would be an additional feature.

_Treatment_ can rarely be adopted because of the uncertainty of the
diagnosis. It would proceed on general principles, antithermics,
eliminants, antiseptics, and counter-irritants being resorted to as the
conditions seem to demand. Alkaline laxatives and diuretics, salicylates
of soda or potash, and guarded doses of sulphuric ether to solicit the
action of the pancreas, might be resorted to. The disorder of the liver
would require attention along the lines indicated under catarrh of that
organ.


                       INTERSTITIAL PANCREATITIS.

  Causes: paresis, marasmus, septic infection, blood diseases. Lesions:
  connective tissue in excess—pancreas and liver; catarrhal
  complications; calcic points; congestion and petechiæ in septic
  infection. Areas of fat necrosis in the pancreas and abdominal adipose
  tissue. Stearates of lime. Calcic foci in animals. Symptoms: obscure.
  Treatment.

This is especially liable to accompany paretic and wasting diseases,
septic infection, and diseases of the blood. Radionow examined the
pancreas in animals that had suffered from chronic paralysis,
gastro-intestinal catarrh, hepatic catarrh, chronic anæmia and marasmus,
and found fatty degeneration of the epithelium, with atrophy and
pigmentary degeneration of the glandular epithelium. The fibrous tissue
of the gland was in excess in the pancreas and in the liver (sclerosis),
and mucous cysts were found.

Siedamgrotzky found a chronic interstitial pancreatitis connected with
alopecia, œdema and leucocythæmia. The pancreas was indurated, fibrous,
resisting the edge of the knife and sprinkled with gritty particles.
Much of the glandular tissue had been destroyed, and the ducts were
filled with a dense, grayish, grumous mucus.

Kirilow and Stalnikow have found interstitial pancreatitis marked by
congestion and ecchymosis, with intervening anæmic areas, in animals
injected with septic matter. There was increased secretion in the early
stages.

A marked feature of pancreatitis in man is the occurrence in the
interlobular tissue of the gland, the omentum, mesentery and abdominal
fatty tissue generally, of circumscribed areas of fat necrosis, each
varying in size from a pin’s head upward even to a hen’s egg. On section
these show a soft tallowy consistency and Langerhans has shown that they
are composed of lime and fatty acids in combination. When lime is in
excess they become gritty. According to Osler they may be dependent on
some other primary affection (Bright’s disease). The partially calcified
concretions found in the pancreatic ducts, and the yellowish white,
gritty areas, which represent the degenerate lobules in animals
(Seidamgrotzky) are suggestive of a similar morbid condition of the
pancreas or it may be of some distant organ. Of late years a number of
cases have been recorded in man and a very high mortality noted.

The _symptoms_ in the lower animals are very obscure, and an accurate
diagnosis is looked upon as almost impossible. They are essentially the
same as given above under catarrhal pancreatitis.

_Treatment_ too has the same narrow limitations.


             PANCREATIC ABSCESS, SUPPURATIVE PANCREATITIS.

  A complication of strangles or purulent infection. Symptoms: Colics,
  chill, tender right hypochondrium, emaciation, fatty stools.
  Treatment: Constitutional.

Reimers has reported several cases of pancreatic abscess, as a phase of
irregular strangles (rhinoadenitis). In one case multiple abscesses with
an aggregate capacity of 2½ quarts were found, and some of the pus had
escaped by rupture into the peritoneum and produced infective
inflammation. The abscesses had destroyed the greater portion of the
gland, only a few isolated lobules being left.

Galland found an abscess as big as a walnut in the pancreas of a horse
which had multiple tumors in the abdomen.

_Symptoms._ Colics occur from the local phlegmon, and it may be from its
pressure on the duodenum so as to obstruct it, and this appearing in the
course of strangles would indicate a forming abdominal abscess. Staring
coat or shivering may coincide. Tenderness of the abdominal walls has
been noticed by Reimers, together with a partial loss of appetite and a
characteristically rapid emaciation. Fatty stools, if present, would be
almost the only pathognomonic symptom.

_Prognosis_ is that the abscess will open into the abdomen, and cause
fatal infective peritonitis. It is only as an exceptional occurrence
that its rupture into the duodenum or colon can be hoped for, yet in
such a case recovery is possible.

_Treatment._ Little can be done. It would be well to treat the
constitutional symptoms, and await results.


                    FOREIGN BODIES IN THE PANCREAS.

Brückmüller has noticed needles and other sharp objects in the pancreas
of the dog, determining abscess and the formation of a thick, greenish
pus in the adjacent glandular follicles. Goubaux once found a fragment
of straw in the pancreatic duct of the horse. Such conditions are not
likely to be diagnosed, but if this could be done laparotomy might be
permissible in the dog for the removal of the foreign body.




                          PANCREATIC CALCULI.

  Mostly in cattle from over feeding, dry feeding, inactivity. Small.
  Multiple. Round, angular, lobulated. Nucleus. Composition. Dilated
  ducts. Atrophied or sclerosed glandular tissue. Prevention: succulent
  food, water at will, open air life, correction of local catarrh.


Pancreatic like biliary calculi have been found especially in cattle.
They appear to be predisposed by their stimulating, forcing feeding, by
their quiet life apart from all causes of excitement and especially by
the combined effect of dry feeding and prolonged confinement in the
stall through the long winter.

The calculi are usually small but numerous, Jungers having found 36
weighing 38 grammes. Bär has found a mass with an aggregate weight of 23
grammes.

The form of the calculus varies; many are angular from mutual attrition
in the large ducts; others from the smaller ducts are rounded; those
from the glandular follicles may be even lobulated, in keeping with the
divisions of the cavity. The color is white and each shows a distinct
central nucleus of epithelial, mucus, or other origin. Their specific
gravity is 2.397 (Fürstenberg), and their composition 92 per cent.
calcium carbonate, 4 per cent. magnesia, and traces of calcium phosphate
(Gurlt).

The pancreatic ducts are as a rule greatly dilated and thickened (in man
they form enormous cysts, Senn, Osler), and the glandular tissue is
atrophied, indurated (sclerosed), and of a brownish yellow color.

_Treatment_ of such cases would be unsatisfactory. By way of prevention
succulent food, abundance of pure water, and the correction of any
infective catarrhal affection of the duodenum, or of the bile or
pancreatic ducts would be specially indicated. Free exercise in the open
air would be desirable.




                     PANCREATIC NEOPLASMS. TUMORS.

  Often malignant, and secondary. Melanoma in white horse. Carcinoma in
  mare and dog. Epithelioma. Debility, icterus, abdominal swelling,
  emaciation. Treatment: laparotomy, or potassium iodide.


Tumors of the pancreas are quite frequently malignant, and show a
preference for the head of the organ. They may be primary but are more
frequently secondary.

In gray horses melanotic tumors are found, in connection with similar
formations externally, and especially as age advances. Brückmüller found
them of varying size, from a pea to a hazel nut, scattered through the
pancreas and adjacent tissues.

Gamgee records a carcinoma of the pancreas of a mare.

Carcinoma is more frequent in this organ in dogs, the neoplasm having an
irregular form, an imperfect line of delimitation from surrounding parts
and a hard, fibrous stroma enclosing caseous centers, undergoing fatty
degeneration.

Nocard reports an epithelial tumor of the head of the pancreas in a
bitch. The animal which had been ill for six weeks was debilitated,
emaciated, and icteric with a marked abdominal swelling. It died two
weeks later, and necropsy revealed a whitish sublumbar tumor, the size
of a large apple, with irregular rounded projections. This pressed on
the posterior vena cava, surrounded the vena portæ and gall duct and
completely closed the latter. Microscopic examination showed it to be an
epithelioma. The liver was undergoing cirrhosis.

_Treatment_, usually hopeless, would be by laparotomy. If actinomycosis
were present give potassium iodide.




                        DISEASES OF THE SPLEEN.

  No guidance through palpation or secretion. Leukæmia. Lymphadenoma.
  Spleen a favorite culture ground for microbes. Congestions,
  engorgements, ruptures. Safety valve to portal system and liver.
  Rhythmic splenic contractions under reflex action.


The spleen even more than the pancreas is so deeply seated and so
surrounded by other organs, that its diseases are not readily
appreciable by physical examination, while the absence of any special
secretion excludes the possibility of diagnostic deductions through this
channel. Even the relation of the condition of the organ to the number
of the leucocytes and red globules fails to afford trustworthy
indications of disease, since leucocytes originate in other tissues as
well as the spleen, and the destruction of red globules may take place
elsewhere. Yet an excess of eosinophile leucocytes in the blood suggests
hypertrophy or disease of the spleen, and an excess of leucocytes in
general is somewhat less suggestive of disease of this organ (see
Leucocythemia). If adenoma is further shown, in enlargement of lymphatic
glands elsewhere there is the stronger reason to infer disease of the
spleen.

The physiological relation of the spleen to the blood especially
predisposes it to diseases in which the blood is involved. The
termination of splenic capillaries, in the pulp cavities, so that the
blood is poured into these spaces and delayed there, opens the way, not
only for the increase of the leucocytes, and the disintegration of red
globules, but for the multiplication of microörganisms which may be
present in the blood, and for a poisoning (local and general) with their
toxins. Hence we explain the congestions, sanguineous engorgements and
ruptures of the spleen in certain microbian diseases (anthrax, Southern
cattle fever, septicæmia, etc.)

We should further bear in mind that the spleen is in a sense a safety
valve for the blood of the portal vein, when supplied in excess during
digestion. In this way it protects the liver against sudden and
dangerous engorgements, but it is itself subjected to extreme
alternations of vascular plenitude and relative deficiency. This may be
held to take place largely under the influence of the varying force of
the blood pressure in the portal vein, but according to the observations
of Roy on dogs and cats, it is also powerfully influenced by muscular
and nervous action. He found rhythmic contractions of the organ due to
the muscles contained in the capsule and trabeculæ, repeating themselves
sixty times per hour, and which might be compared to tardy pulsations.
He further found that electric stimulation of the central end of a cut
sensory nerve, of the medulla oblongata, or of the peripheral ends of
both splanchnics and both vagi caused a rapid contraction of the spleen.
The spleen may thus be looked on not only as a temporary store-house for
the rich and abundant blood of the portal system of veins during active
digestion, but also as a pulsating organ acting under the control of
nerve centres in the medulla. That the various ascertained normal
functions of this viscus may be vicariously performed by others, as
shown in animals from which it has been completely extirpated, does not
contradict the occurrence of actual disease in the organ, nor the
baleful influence of certain of its diseases on the system at large.


                         ANÆMIA OF THE SPLEEN.

  General anæmia, debility, wasting diseases, starvation, hæmorrhage,
  stimulus to formation of red globules, asphyxia, electricity, cold,
  quinine, eucalyptus, ergot. Symptoms: lack of eosinophile leucocytes
  in the blood of a debilitated subject may lead to suspicion.
  Treatment: tonic, light, sunshine, pure air, exercise, nutritive food,
  iron, bitters.

In cases of general anæmia the spleen is liable to be small, shrunken,
wrinkled, and when cut the surface is drier and lighter colored than in
the normal condition. This condition may be seen after old standing
debilitating diseases, but is common in animals that have been reduced
by starvation, just as the opposite condition of hyperæmia and
enlargement comes of abundance of rich food and an active digestion. It
may shrink temporarily as the result of profuse hemorrhage, but
Bizzozero and Salvioli found that several days after such loss of blood
it became enlarged and its parenchyma contained many red nucleated
hæmatoblasts. The result of hemorrhage is therefore to stimulate the
organ to enlargement and to the resumption of its embryonic function of
producing red blood globules. Contraction of the spleen further occurs
under asphyxia, the deoxidized blood being supposed to operate through
the medulla oblongata. As already noted the spleen shrinks under
stimulation of the central end of a sensory nerve (vagus, sciatic). An
induced current of electricity applied to the skin over the spleen
causes marked contraction (Botkin). Cold, quinine, eucalyptus, ergot and
other agents also induce contraction. In the normal condition there is
an inverse ratio between the bulk of the spleen and the liver, the
enlargement of the one entailing a diminution of the other, but in
certain diseased states, such as anthrax, ague, etc., both are liable to
enlargement at the same time.

_Symptoms_ of splenic anæmia are wanting, through a lack of eosinophile
leucocytes, in the blood of a starved or otherwise debilitated animal,
may lead to suspicion of the condition.

The _treatment_ of such a case would be addressed rather to the general
debility which induced the splenic contraction than to the contraction
itself. Light, sunshine, pure air, exercise, grooming, nourishing food
and the avoidance of all debilitating morbid conditions would indicate
the principles of therapeutic management.


                  HYPERÆMIA—CONGESTION OF THE SPLEEN.

  Four hours after full meal in splenic diastole. In well fed, high
  conditioned. From obstruction of splenic or portal vein or vena cava,
  heart, liver, or pulmonary disease, inhibition from encephalon acting
  through splanchnics or vagi, microbes, ptomaines, toxins, paresis,
  albuminoid diet. Spleen may be seven times its normal weight. Lesions:
  simple blood engorgement: proliferation of pulp cells: increased
  friability; rupture; dark color; hyperplasia of trabeculæ—hypertrophy.
  Symptoms: none; or colic; palpation in ruminants; tenderness.
  Treatment: directed against the causative disease; quinine,
  cinchonine, eucalyptus, ergot, cold douche, electricity, puncture.

Considerable hyperæmia of this organ takes place physiologically in
connection with active digestion in the first four or five hours after
an abundant meal, and especially at intervals of a minute, during what
may be called the diastole of the viscus. The supply of blood is also
much greater in the well fed animal, than in the emaciated and
impoverished one.

_Pathological hyperæmias_ of a _passive_ kind may occur as the result of
obstructions in the veins leading from the spleen, such as the splenic
veins, the posterior vena cava, or that part of the portal vein
comprised between its junction with the splenic and the liver. Diseases
of the right heart or its valves, of the lungs (emphysema), or of the
liver which hinder the onward flow of blood and increase the blood
tension in the vena cava or portal vein have a similar action. Perhaps
we should include inhibition of the nerves (splanchnic, vagi) and nerve
centres (medulla oblongata, cerebral cortex) which preside over the
contraction of the splenic vascular walls, and of the capsular and
trabecular muscles. There is reason to believe that the ptomaines and
toxins of several microbian diseases, operate through these centres,
while other such microbes and toxins operate directly on the spleen
itself.

_Active congestions_ of the spleen are most commonly associated with
microbian diseases and may be attributed partly as above stated to the
action of the toxic products on the contraction nerve centres, and on
the splenic vessels and parenchyma, but also in no small degree on the
active proliferation of the germs themselves in the splenic pulp, and of
the splenic cells. Among the most notable instances of this kind are,
_in man_, malarious, yellow and typhoid fevers, and, _in animals_,
anthrax, and Southern cattle fever. In most febrile diseases, however,
there is a tendency in this direction, which may be fairly attributed to
the paresis of the organ and the delay of the blood in its pulp channels
and spaces with the consequent local increase of microbes and toxins.
The microörganisms can usually be found abundantly in such cases, in the
liquid of the pulp, and in the interior of the leucocytes and other
cells that go to make up its solid constituents.

It has been long recognized by veterinarians that acute congestion often
arises in connection with a sudden transition from a poor or
insufficient diet to an abundant and nutritious one and especially to
one that is rich in albuminoids (beans, peas, vetches, lucerne,
sainfoin, clover, trefoil, in the fresh or preserved condition). If
these are not in themselves the direct causes of acute and fatal
engorgements of the spleen, they at least contribute in no small degree
to the overdistension of the pulp spaces, the paresis of the organ and
its successful invasion by pathogenic microbes.

The acute congestion attendant on specific microbian infection may be
estimated by the increase in weight of the spleen. In the Southern
Cattle fever this organ, which is normally 1.45 ℔., is habitually 2 to 5
℔s., and may reach 8 or 10 ℔s. and in anthrax an equal increase may be
noted.

_Lesions._ In such cases the organ may appear as if there were a simple
blood engorgement, and this is largely the case in the early stages, but
with the persistence of the disease there occurs an active proliferation
of the splenic cells and especially those of the pulp. With the
hyperæmia the consistency of the organ is diminished, and still more so
with the cell hyperplasia, so much so that in extreme cases rupture may
ensue. The color is always darker (purple or blue), but this is only in
part due to the abundance of blood and in part to the thinness of the
splenic capsule. If the condition persists a hyperplasia of the capsule
and trabeculæ ensues, and the condition becomes essentially one of
hypertrophy.

_Symptoms._ In the slighter congestions there are no appreciable
symptoms. In the more severe there may be more or less violent colic,
but this is usually marked to some extent by the profound depression
attendant on the specific fever which is the cause of the congestion.
Palpation of the spleen is impossible in the horse. In ruminants it may
sometimes be felt along the upper border of the rumen just behind the
last rib on the left side. It is soft and yielding retaining the
indentation of the finger. If manipulation produces signs of pain it is
all the more significant.

_Treatment._ As a rule this is the treatment of the fever which
determines the hyperæmia. Apart from this, laxatives, quinia other
alkaloids of cinchona bark, eucalyptus, a current of cold water directed
to the region of the spleen, or induction currents of electricity to the
same region are also decided stimulants to contraction. Ergot has been
used with alleged advantage. In cattle acupuncture of the spleen has
been put in practice in anthrax.




             CHRONIC CONGESTION OF THE SPLEEN. HYPERTROPHY.

  Hypertrophy from chronic congestion, over feeding, hepatic cirrhosis.
  In _horse_: from mechanical obstruction in heart, lungs, posterior
  cava, splenic veins, angioma, from glanders or tubercle in lungs,
  chronic splenic congestion, disease of splenic plexus. Lesions:
  increase enormous; mainly of pulp, or largely of fibrous framework.
  Special neoplasms. Symptoms: excess of leucocytes in blood,
  eosinophile cells, weakness, anæmia, emaciation, bleeding from mucosæ,
  stretching, right hypochondriac tenderness, stiff gait, ascites,
  colic, disorder of the bowels, rectal exploration. Treatment: is that
  of primary disease; not encouraging; quiniae, eucalyptus, saline
  laxatives, open air, sunshine, electricity. In _cattle_ is habitually
  enlarged in Texas fever area. In lymphadenoma increase mainly of
  fibrous framework and Paccinian bodies, and of adjacent lymph glands.
  Symptoms: leukæmia, employ palpation, percussion, rectal exploration.
  Treatment as in the horse. In _swine_: from high feeding, leukæmia,
  lymphadenoma, tuberculosis, neoplasms, liver, heart and lung disease.
  Lesions: great increase of Paccinian bodies, fibrous capsule and
  trabeculæ. In _dog_: from traumas, leukæmia and lymphadenoma. Enlarged
  Paccinian bodies and adjacent lymph glands. Symptoms: leukæmia, many
  eosinophile cells, abdominal enlargement, palpation, icterus.
  Treatment: as for large animals.


A continuation of passive congestion from the causes enumerated above,
leads to permanent increase of the fibrous reticulum and connective
tissue and increase of the splenic pulp. Even the stimulus of a rich and
abundant alimentation increases the size of the whole organ, the amount
of pulp and the number and development of the Paccinian bodies. Apart
from disease the spleens of well fed cattle or horses are always
decidedly heavier than those of the starved or debilitated. Of
mechanical causes the most potent is cirrhosis of the liver or some
other obstacle to the free passage of blood through that organ. The most
common causes are, however, the continuous operation of those specific
poisons which determine the acute hyperæmias.


                     SPLENIC HYPERTROPHY IN HORSES.

_Causes._ It occurs as the result of mechanical obstruction of the
posterior vena cava as noticed by Varnell, from obstruction in the
splenic artery or veins by Ellenberger and Schütz, as the result of an
angioma by Martin, as the result of the morbid hyperplasias in specific
diseases—glanders, tuberculosis—taking place in the spleen or lungs and
thus directly or indirectly causing chronic congestion of the spleen
(Morot, Leisering, Nocard, Varnell) and again as the result of
innervation, in disease of the splenic plexus of nerves (Varnell).

_Lesions._ The increase in size may be enormous (42 lbs. (Bouret and
Druille), 92 lbs. (Cunningham), and over 100 lbs. (Girard)). The
consistency is varied. There may be such a redundancy of blood and
splenic pulp that the capsule is distended to its utmost or even
ruptured (Peuch). In other cases the splenic veins have given way and
the blood has poured out into the abdomen with fatal result (Crafts,
Cunningham, Reis). In other cases the spleen is enlarged, unevenly
swollen and indurated by the formation of angioma (Jacob), lymphadenoma,
glander or tuberculous nodules. In still others the capsule and fibrous
framework are greatly thickened and the substance of the organ has
assumed the consistency of the hepatized lung (Rodet).

_Symptoms._ These are suggestive rather than diagnostic. Most prominent
is the condition of the blood with excess of leucocytes and especially
of the eosinophile cells. Weakness, emaciation, feebleness of pulse,
bloodlessness, bleeding from the nose or other natural passages, are
attendant symptoms. In cases of extreme hypertrophy distension of the
abdomen is marked and even the enlarged spleen may be made out by
palpation, there may be special tenderness and dullness on percussion.
Even partial sweats over the region of the spleen (Cadeac), and
stretching with the fore feet far in advance (Welsby) have been noted as
symptoms. In such conditions the animal walks stiffly, groans in
turning, or when suddenly started and is with difficulty urged beyond a
walk. There may be ascites, signs of colic, or irregularity of the
bowels. Rectal exploration may reveal the hypertrophy.

_Treatment_ is usually the treatment of the primary disease. In
glanders, tuberculosis, lymphadenoma, or leucocythemia there is little
to hope for. Nor is there much in hepatic cirrhosis, obstruction of the
vena cava or valvular disease of the heart. In simple hypertrophy we may
resort to quinia or other bitters, eucalyptus, saline laxatives,
exercise in the open air and sunshine, and local currents of
electricity.


                   SPLENIC HYPERTROPHY IN RUMINANTS.

A moderate hypertrophy is the rule in the case of cattle which have
passed through the Southern cattle fever, but have continued to live
within the area of its prevalence. Gamgee’s observations in 1868 were
very conclusive on this point. In over 1,000 western cattle the average
weight of the spleen was 1.45 ℔., in 441 Cherokee (Indian Territory)
cattle the average was 2.34 ℔s., and in 262 Texas cattle the average was
2.66 ℔s. All these animals were killed for beef, in what was considered
to be perfect health. The difference relative to the weight of the
entire animal is even greater than is indicated above, for at that date
even more than at present, the Texas steer was a small and thin animal
in comparison with the portly western bullock.

In lymphadenoma the organ may weigh 24 ℔s. (Tannenhauser); in simple
hypertrophy it has been found to weigh 37 ℔s. (Koch). There was usually
a marked increase in the size and number of the Paccinian bodies, and
hyperplasia of the fibrous reticulum, while the pulp might be deficient
and the cut surface rather dry. The adjacent lymph glands are usually
enlarged.

_Symptoms._ Unless in the case of excessive increase, no symptom is
usually observable, apart from leucocythæmia. With enormous hypertrophy
the enlarged organ may be recognized by palpation, percussion, and
perhaps rectal exploration.

_Treatment_ is unsatisfactory apart from the control and arrest of the
primary diseases. For simple hypertrophy, bitters, laxatives and
electricity may be tried.




                     SPLENIC HYPERTROPHY IN SWINE.


_Causes._ This disease appears to be rather frequent in pigs, in
connection with high feeding, and more particularly with leucocythæmia
and lymphadenoma. It is further a complication of tuberculosis and of
neoplasms located in the spleen, and of hepatic, cardiac and pulmonary
disorder.

_Lesions._ In leucocythæmia there is general enlargement of the spleen,
and especially of the Paccinian bodies which may attain the size of a
pea (Leisering, Fürstenberg, Bollinger, Siedamgrotzky, Röll, Ellinger).
The total weight of the organ may attain to 5 lbs. (Mathieu), or 13 lbs.
(Goubaux). In a remarkable case recorded by Zell, the organ measured 30
inches in its longest circumference and 20 inches in its shortest. It
had an enormous thickening of the capsule and trabeculæ which enclosed
softened contents in a state of fatty degeneration.

_Symptoms_ are wanting, as most of the observed cases were only
discovered after the animal had been killed for pork.


                    SPLENIC HYPERTROPHY IN THE DOG.

This condition has been less frequently seen in dogs, the recognizable
causes having been traumatism (Notz), and leucocythæmia (Zahn,
Forestier, La Forgue, Nocard). Lymphadenoma is another complication
(Nocard, Leblanc, Siedamgrotzky, Bruckmüller). The spleen has been found
to weigh 2 lbs., (Bollinger, Siedamgrotzky). As in other animals the
enlargement of the Paccinian bodies has been a marked feature. In other
cases the splenic lymph glands are enlarged.

The _symptoms_ are obscure as in other animals. Yet the presence of
white cell blood, with a predominance of eosinophile cells, enlargement
of the abdomen, and the detection of a large solid body in the left
hypochondrium which proves tender to the touch may prove more
satisfactory than in other animals. In certain cases it has obstructed
the biliary duct by pressure and entailed hepatic disorder and jaundice.

The _treatment_ would not differ from that of the larger animals.

Siedamgrotzky has also observed splenic hypertrophy in the cat in
connection with leucocythæmia.


                       SPLENITIS. PERISPLENITIS.

  Causes: extension from adjacent inflammations, penetrating bodies,
  contusions, lacerations, infections, over exertion, cold, damp, over
  feeding. Symptoms: those of primary disease, visible traumas, chill,
  fever, swelling, flatness of percussion sound, absence of crepitation,
  anorexia, vomiting, constipation, diarrhœa. Prognosis usually good.
  Treatment: castor oil, enemata, cold douche, electricity, phlebotomy,
  in infective cases quinine, salol, salicylates, iodides.

No accurate border line can be drawn between splenic hyperæmia and
hypertrophy on the one hand and inflammation of the spleen on the other.
It is, however, not difficult to assign to inflammatory action all cases
that tend to suppuration and abscess. Also in perisplenitis with
adhesions to adjacent parts like the liver, stomach, intestine, kidney
or abdominal wall inflammation cannot be doubted.

_Causes._ Extension from the disease of adjacent parts—perihepatitis,
perinephritis, peritonitis, enteritis—is a distinctly appreciable cause,
as are also penetration of the spleen by foreign bodies, contusions,
lacerations and infections of the organ. Cruzel, who claims an extensive
acquaintance with the disease in working oxen, attributes many cases to
violent exertions, overdriving, cold and damp weather, and an
overstimulating alimentation. As inflammation may supervene on hyperæmia
and hypertrophy we must accept the various causes of these conditions as
factors in producing inflammation.

_Symptoms._ Most observations of inflammation of the spleen and its
results have been made only post mortem, so that we must allow that the
simple forms occur and undergo resolution without obvious symptoms. In
the perisplenitis supervening on another disease also in infective cases
there will be the antecedent symptoms of such primary diseases. In those
resulting from traumatic injury, bruises, swellings or wounds, cutaneous
or subcutaneous, there will often be suggestive features. In the more
purely idiopathic cases symptoms are only shown when the lesions are
extensive and acute. In oxen, Cruzel has noted the initial chill,
followed by disturbance of the respiration, more or less hyperthermia,
and a swelling of the left flank and hypochondrium in the absence of
tympany of the rumen. The nature of this swelling is the most
characteristic feature, as it gives a flat instead of a drumlike sound
on percussion, and does not bulge outward and downward over the whole
left side of the abdomen, pit on pressure, nor crepitate uniformly all
over from fermentation, as in overloading of the stomach.

If abscess should form, chills and high febrile reaction are marked
symptoms. In vomiting animals, anorexia, nausea, vomiting, constipation,
and even diarrhœa may appear.

_Prognosis._ Unless in extreme cases and those due to traumatism or
infection, the result of splenitis is usually favorable.

_Treatment_ would consist in depletion from the portal system and spleen
by rectal injections, and laxatives which like castor oil, will operate
without extensive absorption. Cold water or ice applied to the left
flank and induction currents of electricity may also be resorted to.
General blood-letting is strongly advised by Cruzel, and Friedberger and
Fröhner. In infective cases quinia, salicylates, salol, and the
sulphites, or iodides would be indicated.


                 HÆMORRHAGIC INFARCTION OF THE SPLEEN.

  In congestive conditions. Absence of free capillary anastomosis and
  contraction, absence of valves in splenic veins. Embolism of splenic
  artery. Clots in pulp spaces. Wedge shaped infarcts, first black,
  later yellow, later caseated, or cicatrized. Abscess. Prognosis good
  in non-infective forms. Treatment as for hyperæmia, or infection, or
  both.

This condition appears in hyperæmia, hypertrophy, splenitis, and splenic
infection and largely because the structure and circulation in the organ
conduce to such trouble. The splenic arteries terminate in open vascular
spaces filled with splenic pulp and where all trace of a freely
anastomosing capillary network is lost. The splenic veins in the same
manner originate from these open vascular spaces. There is, therefore,
an absence of the free communication of capillary network, which
virtually acts as a safety valve in other vascular tissues, and the
vascular cavities connected with each terminal artery are independent of
those belonging to another, and find no way of ready relief when they
become over distended, or when there occurs obstruction (thrombosis) of
their afferent or efferent vessels. From blocking of arteries or veins
there is at once produced a wedge shaped area of stagnation which cannot
be relieved through any collateral circulation. Again the splenic veins,
being destitute of valves, offer no obstacle to the reflux of blood into
such vascular spaces whenever the further access of blood has been
arrested by the blocking of the artery. The blocking may occur in the
afferent artery through embolism by clots carried from the lungs or left
heart, or formed within the vessel by the colonization of microbes on
its walls. Even more likely is the formation of coagula in the vascular
spaces themselves as the result of the introduction of pus, or
septicæmic microbes, which are long detained and have ample time for
multiplication in these cavities. In either case the result is
obstruction to the sanguineous current, the filtering of blood backward
from the veins and the engorgement of the cavity with blood. The plugs
consist of fibrinous matter enclosing colonies of micrococci, and the
result is not only black infarction of the spleen, but a subsequent
general infection of the system at large.

The wedgeshaped infarcts are usually situated at the surface of the
organ, the base turned outward and forming a dark projection on the
surface, and the apex turned inward. The aggregation of two or three in
one group may considerably alter the outline. If recent they are of a
dark red color. Later from absorption of the coloring matter and fatty
degeneration of the mass they assume a pale yellow hue and the swelling
flattens or disappears. Later still through complete fatty degeneration
they may be transformed into caseated masses, or through organization
into fibrous tissue they may form thick white cicatrices. If pus cocci
are present suppuration and abscess may be the outcome.

The simpler forms recover like cases of simple hyperæmia while the
severe infecting forms may become the point of departure for the
formation of multiple abscesses in other organs, and of more or less
fatal general infections.

These conditions can only be discovered post mortem, and any symptoms
directing attention to the spleen could only suggest such treatment as
would be indicated in hyperæmia. Any purulent or septic disease which
might coexist would of course serve to indicate a germicide line of
treatment.


                         ABSCESS OF THE SPLEEN.

  In _Solipeds_: in infectious diseases, pyæmia, embolism. Symptoms: of
  primary disease or ill health. Involving other organs. In _cattle_:
  foreign bodies from reticulum, distomata, embolism, microbes.
  Enlargement: involving other organs: seen in left hypochondrium,
  fever, albuminuria. Treatment: aspiration, antiseptic injections,
  internal antiseptics.

=Soliped.= Abscess of the spleen in this animal is unusual and has only
been discovered post mortem. It has been found as the result of the
local colonization of pyogenic microbes, in connection with strangles,
contagious pneumonia and other infectious diseases and can then often be
traced to an infected embolus in the splenic blood vessels. The peculiar
vascular structure of the spleen is very conducive to abscess as it is
to infarction, as has been already noticed and hence this complication
of a pre-existing infection in another part is a natural pathological
sequence. Symptoms are rather the general ones of a rigor followed by
hyperthermia than any diagnostic ones of splenic disease. Bourges found
a splenic abscess in a cachectic, melanic mule but no definite splenic
symptom was observed even on rectal examination. Nottel found an abscess
as large as an infant’s head, in the base of the spleen, closely
adherent by its sac to the left kidney and containing a floating mass of
splenic tissue as large as the closed fist. Rutherford found a neoplasm
connecting the great curvature of the stomach, to the diaphragm, and
hollowed out into a series of pus cavities. Fetzner and Cadeac report
cases of extensive abscesses in the head of the spleen and intimately
connected to both stomach and diaphragm. Hahn found abscesses in
connection with the penetration of the spleen by foreign bodies. In
other cases the substance of the spleen was studded with abscesses
varying in size from a pea upward and containing necrotic tissue or
adjoining such dead tissue.

=Ruminants.= In cattle the penetration of the spleen by sharp pointed
bodies coming from the reticulum appears to be the most common cause of
abscess. Other cases depend on the penetration of distomata carrying the
pyogenic microbes, and still others are due, as in the horse, to local
infection with embolism. External traumatisms are unusual causes. There
is usually considerable enlargement of the spleen as a whole, rounded
swellings indicating the seat of the abscess, and adhesions to
surrounding parts, such as the rumen, the left kidney or the diaphragm.
When the abscess is chronic, there is emaciation, unusual flatness on
percussion of the left hypochondrium, and, at times, of the flank,
swelling and tenderness of the flank, above all, according to Imminger,
a persistent elevation of temperature (104° to 106° F.), which is not
lowered by antithermics, and albuminuria. In cattle it is sometimes
possible to diagnose the disease, and if the abscess can be definitely
located, aspiration and antiseptic injections into the sac would be
indicated, conjoined with calcium sulphide, or sodium sulphite
internally.


                     FOREIGN BODIES IN THE SPLEEN.

  In _horse_: body from intestine. In _ruminants_ bodies from reticulum.
  Laparotomy.

One such case in the =Horse= is reported by Hahn. A mare had loss of
appetite, slight colics, frequent efforts to urinate, dullness,
prostration, profuse perspirations, and tremors of the muscular walls of
the abdomen. Rectal examination detected a staff-shaped body extended
from behind forward in the direction of the stomach. The mare survived
twenty days, when it was carried off by a more violent access of colic.
At the necropsy, the spleen was found to measure 28 inches by 8; its
base was adherent to a loop of intestine, and presented a large cavity
filled with a grayish brown fœtid liquid, and a piece of oak measuring
17 inches by ½ inch.

_Ruminants._ In cattle and especially in those that are stabled,
needles, pins, nails, wires and other sharp pointed bodies, that have
been swallowed with the food, and have become entangled in the
reticulated walls of the second stomach, have been found to penetrate
the spleen and determine local abscess and fistulæ. The offending body
in such cases is found in the interior of the abscess or in its walls.
If such cases can be diagnosed the superficial position of the spleen
would seem to warrant surgical interference for the removal of the
foreign body.


                         RUPTURE OF THE SPLEEN.

  _Solipeds_: Causes: Blows, kicks, goring, leukæmia, compression of
  splenic or gastric veins, anthrax infection. Lesions: Blood may escape
  into peritoneum or remain confined under serosa. Splenic degeneration
  or pulpy condition. Fractured ribs, ecchymosis, surface swellings.
  Spontaneous arrest. Symptoms: Of internal hemorrhage. Vomiting.
  Trembling. Vertigo. Coma. Treatment: Rest, quiet, locally ice, snow,
  cold, internally iron chloride, matico, astringents, anodynes.
  _Cattle_: Blows, crowding, leukæmia, youth, anthrax, Texas fever,
  microbes. Symptoms: Persistent lying down, advancing bloodlessness,
  surface coldness, stiffness, local tenderness, fluctuation. Treatment
  as in horse.

_Horse._ This is not a frequent lesion in solipeds, yet the number of
cicatrices of the spleen which are found post mortem in old horses would
indicate a considerable number of slight and non-fatal cases. The most
common cause appears to be external violence and especially kicks or
blows with horns on the left hypochondriac region. Horses running at
large in pastures, or in yards, or standing side by side in short stalls
or tied with too long halters are the usual victims. Cadeac refers to
cases reported by Tausch, Millot, Berndt, Humbert and Pont, and one case
occurring in a three year old colt came under the notice of the author.
The subject stood in a stall to the right of an irritable mare, and
though the kick left no noticeable skin lesion the colt died in three
hours with symptoms of internal hemorrhage. At the necropsy a laceration
of the spleen of about five inches long was disclosed, and a large
quantity of blood had accumulated in the peritoneum.

Brandis mentions a case consequent on a violent fall on the left
hypochondrium.

In other cases pre-existing disease of the spleen or its blood-vessels
have proved active factors. In the friable degenerated spleen of
leucocythæmia multiple small lacerations have been found (Peuch,
Laulanie); in engorgement of the spleen consequent on thrombosis of the
splenic vein (Wiart); in chronic indigestion with habitually loaded
stomach compressing the gastric and hepatic arteries and determining a
reflux of blood through the cæliac axis into the spleen (Mongin).

Finally, though less frequently than in the ox, the engorgement of the
spleen with blood in cases of anthrax may be a cause of rupture.

_Lesions._ The rupture may be on any part of the spleen and it may be
complete or incomplete; in the latter event the capsule may have
ruptured while the more elastic peritoneal covering has remained intact
enclosing a coagulum of variable size bulging above the level of the
spleen. When the peritoneal coat has given way, its laceration is
usually smaller than that in the spleen and its proper envelope. Any
degeneration of the spleen will affect the appearance of the lesion. In
one case caused by external violence the adjacent portions of the spleen
were reduced to a soft pulp. In such a case there is a slow but
continuous flow of blood in a small stream which may, however, prove
fatal (Humbert and Pont).

Again in cases caused by external violence there may be fractures of the
ribs, ecchymosis, local swellings or even wounds of the skin, but all
these may be absent. The blood effused into the peritoneum is usually
clotted. If the effusion has taken place slowly it is more or less
coagulated around the edges of the wound or even in its depth and in
this way the hemorrhage may be arrested. When the peritoneum is still
intact the pressure of the clot beneath it has served to arrest the
flow. In such cases the clot may be in part liquefied and absorbed and
in part organized into fibrous tissue, constituting the cicatrices of
the spleen found in old horses.

_Symptoms_ appear to have been varied. Colicy pains are generally noted.
Tausch has observed vomiting, Millot vertigo, and Wiart coma and
trembling. In the author’s case the animal was found down, unable to
rise, almost unconscious, pulseless, with great pallor of the visible
mucous membranes, dilated pupils, and cold extremities. A diagnosis was
made of internal hemorrhage, but its actual seat was only revealed post
mortem.

_Treatment._ The early mortality usually forbids treatment. When
opportunity is furnished keep the animal absolutely still and quiet,
apply snow, ice or other refrigerant to the left hypochondrium, give
internally tincture of muriate of iron, matico, or other astringent, and
relieve any severe suffering by anodynes (hyoscyamus, belladonna,
opium). External wounds may be treated antiseptically.

=Cattle.= The _causes_ of laceration and hemorrhage of the spleen are
similar to those acting in the horse. Blows with the horns on the left
side, crowding through a doorway or gateway, and direct blows of other
kinds are charged with its pathogenesis. The friability which attends on
leucocythæmia has been noted as a predisposing cause. Calves by reason
of their small size and the relative bulk of the spleen are especially
liable to rupture by kicks from animals or men.

Much more commonly than in solipeds, rupture of the spleen occurs as a
complication of specific microbian diseases like anthrax and Southern
cattle fever.

_Symptoms._ The mature animal assumes the recumbent position, refusing
to rise, and dies in a few hours. In calves, life may be prolonged for a
few hours longer, and there have been noticed, anorexia, watering of the
eyes, accelerated pulse and respiration, arrest of intestinal
peristalsis, cold ears, rigid limbs, and moderately full belly (Notz).
There should also be tenderness on manipulation or percussion of the
left hypochondrium, and until coagulation occurs, fluctuation in the
lower part of the abdomen, with pallid mucous membranes and other signs
of profuse internal hæmorrhage.

_Treatment_ is useless in the majority of cases. In the slighter forms
it would be the same as in the horse.




                         TUMORS OF THE SPLEEN.

  Secondary. Delay of blood favors. _Sarcoma_: horse, cattle, dog.
  _Carcinoma_: horse, dog. _Melanoma_: common and large in gray and
  white horses, rupture, external melanosis. _Angioma_: horse, ox.
  _Lymphadenoma_: horse, ox, external adenoma.


The different tumors of the spleen are usually secondary. The intimate
structure of the organ, the peculiarity of the circulation through the
pulp cavities, and the delay of the blood in the pulp spaces, predispose
it in a very especial manner to the growth of neoplasms, the germs or
bioplasts of which are carried in the blood.

=Sarcoma.= In the _horse_ sarcomata have been found in the spleen
secondary to similar tumors in the other parts of the abdominal and
thoracic cavities. They may attain to any size, from a pea to the closed
fist and, in exceptional cases, of a mass which practically fills and
distends the abdominal cavity.

In the _cow_ an encephaloid sarcoma in the spleen, weighed nine pounds
and was associated with similar formations in the lymph glands generally
of the abdomen and chest.

In the _dog_ also sarcomata are common in the spleen.

=Carcinoma.= These are found in the _horse_ in connection with similar
primary tumors, as in the case of the sarcomata. They are at times
extremely vascular and soft, and at other times they are hard and
fibrous (scirrhus).

In the _dog_ secondary cancer of the spleen is comparatively common.

=Melanoma.= Black pigment tumors are especially common in gray and white
horses. Their common seat is on the black, hairless portions of the skin
(anus, vulva, perineum, tail, sheath, mamma, eyelids, lips, etc.), and
secondarily in the lymph glands and spleen. In the latter they may grow
to an extreme size, Wehenkel having mentioned one specimen of 60 pounds.
Its surface is marked by uneven, rounded black swellings, the entire
organ, indeed, seeming to be a conglomerate of these masses. The
intimate structure is that of a sarcoma, so abundantly charged with
black pigment granules that these appear to make up the greater part of
the mass.

Rupture of these neoplasms with the escape into the abdomen of blood
highly charged with the melanic matter is not uncommon.

The _symptoms_ of the splenic deposits are not usually recognizable, but
indications of chronic abdominal disease in connection with external
melanotic formations may well lead to a reasonable suspicion.

_Angioma._ In a _horse’s_ spleen weighing 30 lbs., there were numerous
soft nodules of a deep cherry color. These were cavernous masses with
connective tissue walls and the meshes filled with blood.

Similar vascular cavernous tumors have been found in the cow.

_Lymphadenoma_ has been found in the spleen of horses and cattle in
connection with the same disease of the lymph glands.

Like the other splenic tumors this is obscure and usually only found
after death. The existence of adenoid swellings elsewhere conjoined with
excess of white globules and indications of abdominal pain would be
suggestive of splenic disease.


                  AMYLOID DEGENERATION OF THE SPLEEN.

  _Amyloid_: horse: with exhausting diseases. Waxy secretion staining
  mahogany brown with iodine. _Gangrene_: Swine. _Tubercle and glander
  nodules._

This has been occasionally detected in the spleen of the horse. It is
usually connected with longstanding suppuration especially of bones,
with advanced tuberculosis or other exhausting disease. The organ is
usually greatly enlarged and the affected parts are firm, resistant and
swollen. On section it has not the soft friable or pulpy appearance of
the spleen, but an uniform waxy looking consistency, grayish or
sometimes stained with blood. On the application of a solution of iodine
and iodide of potassium the healthy splenic tissue is colored yellow,
while the amyloid portion becomes of a deep mahogany brown.




                    GANGRENE OF THE SPLEEN IN SWINE.


Hertzen records the case of a pig in which the spleen had become
gangrenous and lay free in a surrounding fibrous capsule.


             TUBERCLES AND GLANDERS NODULES OF THE SPLEEN.

_Tubercles_ in the spleen are common in cattle, swine, guinea-pigs,
rabbits and cats, in the last largely as the result of ingestion of
tuberculous meat. In the larger mammals individual tubercles are usually
of the size of a walnut and upward, while in the smaller they show as
miliary deposits. The products are often caseated or calcified.

_Glander nodules_ are found in the spleen of the horse and other
solipeds and as the result of inoculation in that of rabbits and
guinea-pigs. In solipeds they may be of considerable size whereas in the
inoculated rodents they are usually small and numerous—like millet seed
or pins’ heads.


                        PARASITES OF THE SPLEEN.

Parasites are less common in the spleen than might be expected yet the
encysted parasites of the liver and pancreas, are also to be found in
the spleen. Thus _echinococcus_ is found in the spleen of cattle, and
headless hydatids in that of the horse; _cysticercus tenuicollis_ in the
spleen of sheep; _cysticercus cellulosa_ in that of pigs; _distomata_,
and _pentastoma denticulata_ in the spleen of cattle; _coccidia_ in the
spleen of rabbits; and _actinomyces_ in that of horses and cattle.

In addition to these the spleen is a general _rendezvous_ for the
different pathogenic organisms that can survive in the blood stream,
such as the bacilli of tubercle, glanders, septicæmia, anthrax, black
quarter, swine plague and hog cholera, and for the cocci of suppuration,
strangles, contagious pneumonia, etc. (See Parasites and Contagious
Diseases).




                                 INDEX.


 Abomasum, catarrhal inflammation of, 166.

 Abomasum, indigestion in, in sucklings, 136.

 Abomasum, indigestion of, 134.

 Abortion from ergotism, 298.

 Abscess in gullet, 93.

 Abscess in pancreas, 547.

 Abscess of bowel, 336.

 Abscess of spleen, 557.

 Abscess, supra-pharyngeal, 58.

 Acetic acid and gastro-enteritis, 266.

 Aconite poisoning, 286.

 Acorn poisoning, 286.

 Actinomycosis of lips, 7.

 Actinomycosis of liver, 536.

 Actinomycosis of omasum, 133.

 Actinomycosis of pharynx, 85.

 Actinomycosis of rumen, 123.

 Adenoma of liver, 531, 532.

 Adenosarcoma of stomach, 191.

 Albumin reduced in liver, 410.

 Alkaline caustics, causing gastro-enteritis, 264.

 Aloes poisoning, 286.

 Ammonia carbonate in gastro-enteritis, 265.

 Ammonia in gastro-enteritis, 264.

 Amphistoma conicum, 122.

 Amyloid degeneration of liver, 511.

 Amyloid of the spleen, 563.

 Anæmia of spleen, 546.

 Anemone, poisoning by, 286.

 Angioma of liver, 531.

 Angioma of the spleen, 563.

 Aqua ammonia, 264.

 Army worm, poisoning by, 288.

 Arsenical poisoning, 269.

 Arsenic, tests for, 271.

 Artichokes, poisoning by, 286.

 Arytenectomy, results of, 92.

 Ascites in carnivora, 403.

 Ascites in ruminants, 402.

 Ascites in solipeds, 400.

 Asthenia from cryptogams, 290, 297.

 Astragalus, poisoning by, 287.

 Atrophy of the liver, 507.

 Azedarach, poisoning by, 286.

 Azotæmia, 437.

 Azoturia, 437.


 Bacillus coli communis, 255.

 Bacillus diphtheriæ columbarum, 67.

 Bacillus gallinorum, 254.

 Bacillus of duck cholera, 255.

 Bacteria in gall stones, 518.

 Bacteria, poisoning by, 289, 292, 293.

 Barbs, 13.

 Barium poisoning, 279.

 Bezoars, 323.

 Bichromate of potash poisoning, 280.

 Bile acids, 413.

 Bile acids, test for, 413.

 Bile, functions of, 411.

 Bile pigments, 412.

 Bile pigments, test for, 413.

 Bile secretion, inhibitors, 414.

 Bile, secretion of, 411.

 Bile secretion, stimuli of, 414.

 Biliary calculi, 516.

 Bilirubin, 412.

 Biliverdin, 412.

 Birds, constipation in, 319.

 Birds, intestinal indigestion in, 209.

 Black pigmentation of the liver, 513.

 Bloating, 96.

 Bloating in solipeds, 150.

 Botulism, 301.

 Bowels, obstruction of in birds, 209.

 Box leaves poisoning, 284.

 Brine poisoning, 268.

 Bristle balls in stomach, 187.

 Bristle balls, Pig, 322.

 Bromine poisoning, 276.

 Bromism, 276.

 Brine poisoning, 302.

 Bryony, poisoning by, 286.

 Buccal inflammation, 8.

 Buckwheat, poisoning by, 286.

 Buxus sempervirens poisoning, 284.


 Calcareous nodules in liver, 534.

 Calculi, biliary, 516.

 Calculi, colloids as causes, 325.

 Calculi, coralline, 325.

 Calculi, diagnosis of, 327.

 Calculi, fermentation as cause, 325.

 Calves, infective gastro-enteritis in, 138.

 Calculi, intestinal, 323.

 Calculi, intestinal, sources, 324.

 Calculi in tonsils, 48.

 Calculi, pancreatic, 543.

 Calculi, pseudo, 324.

 Calculi, rate of growth of, 326.

 Calculus, salivary, 40.

 Calculi, treatment of, 327.

 Cancroid of lips, 6.

 Cantharides, poisoning by, 288.

 Carbolic acid poisoning, 281.

 Carcinoma in pancreas, 544.

 Carcinoma of intestine, 375, 378.

 Carcinoma of liver, 529, 532.

 Carcinoma of spleen, 562.

 Carnivora, cryptogamic poisoning in, 301.

 Castor oil seeds poisoning, 282.

 Catarrhal enteritis, chronic, in cattle, 239.

 Catarrhal enteritis, chronic, in solipeds, 234.

 Catarrhal enteritis in birds, 254.

 Catarrhal enteritis in cattle, 235.

 Catarrhal enteritis in dogs, 250.

 Catarrhal enteritis in sheep and goat, 246.

 Catarrhal enteritis in solipeds, 228.

 Catarrhal enteritis in swine, 247.

 Caustic acids and gastro-enteritis, 266.

 Caustic alkalies in gastro-enteritis, 264.

 Cheeks, inflammation of, 19.

 Cheilitis, 5.

 Chickweed poisoning, 286.

 Chloride of barium poisoning, 279.

 Chloride of zinc poisoning, 277.

 Cholera of birds, 254.

 Choking, injuries in, 86.

 Cholelithiasis, 516.

 Chromium poisoning, 280.

 Cicuta maculata poisoning, 285.

 Cicuta virosa poisoning, 286.

 Cirrhosis of the liver, 502.

 Cirrhosis of the liver in solipeds, 503.

 Cirrhosis of the liver in cattle, 505.

 Cleft palate, 49.

 Clematis poisoning, 286.

 Cloth in stomach, 188.

 Clover-hair balls in stomach, 187.

 Coccidian enteritis in birds, 263.

 Coccidian enteritis in cattle, 258.

 Coccidian enteritis in dogs, 261.

 Coccidian enteritis in rabbits, 262.

 Coccidiosis, intestinal, 258, 261, 262, 263.

 Coccidiosis of gullet, 93.

 Coccidium bigeminum var. canis, 261.

 Coccidium oviforme, 259, 262.

 Coccidium perforans, 259, 261, 262.

 Cockroach, poisoning by, 288.

 Colchicum poisoning, 284.

 Colic, 308.

 Colic, crapulous, 309.

 Colic cystic, 309.

 Colic from bacterial invasion, 309.

 Colic from calculi, 309.

 Colic from hernia, 309.

 Colic from impaction, 309.

 Colic from indigestion, 309.

 Colic from inflammation, 309.

 Colic from irritants, 309.

 Colic from peritonitis, 309.

 Colic from protozoa, 309.

 Colic from strangulations, 309.

 Colic, hepatic, 309.

 Colic in solipeds from verminous embolism, 210.

 Colic, lead, 309.

 Colic, nephritic, 309.

 Colic, pancreatic, 309.

 Colic, tympanitic, 309.

 Colic, uterine, 309.

 Colic, verminous, 309.

 Colloids in gall stones, 518.

 Colon bacillus, 255.

 Colon, impaction of, 197.

 Colon, impaction of, in ruminants, 203.

 Colon, impaction of, in swine, 204.

 Common salt, poisoning by, 267.

 Concretions in intestines, 324.

 Congestion of the liver, 483.

 Congestion of spleen, 547.

 Conium poisoning, 286.

 Constipation from atony, 314.

 Constipation in birds, 319.

 Constipation in dog, 205.

 Copperas poisoning, 279.

 Copper poisoning, 276.

 Corrosive sublimate poisoning, 274.

 Cotton balls in stomach, 187.

 Creosote poisoning, 282.

 Crop, impaction of, 94.

 Croton seeds poisoning, 283.

 Croupous enteritis in birds, 226.

 Croupous enteritis in cattle, 223.

 Croupous enteritis in dogs, 225.

 Croupous enteritis in sheep, 224.

 Croupous enteritis in solipeds, 221.

 Croupous pharyngitis, 60.

 Crowfoot poisoning, 284.

 Cryptogamic poisoning in carnivora, 301.

 Cryptogamic poisoning in ruminants, 295.

 Cryptogamic poisoning in solipeds, 290.

 Cryptogamic poisoning in swine, 300.

 Cryptogams, poisoning by, 292.

 Cystoma of intestine, 376, 378.


 Daffodil poisoning, 284.

 Darnel poisoning, 286.

 Delirium from cryptogams, 293, 297.

 Depraved appetite, 76.

 Diabetes mellitus, 416.

 Diarrhœa, 303.

 Diaphragmatic hernia, 359.

 Diaphragmatocele, 359.

 Digestive disorders in fever, 3.

 Digestive organs, area and capacity, 1.

 Digestive organs, food in relation to diseases of, 2.

 Digestive organs, general considerations, 1.

 Digestive organs, importance of diseases of, 1.

 Digestive organs of carnivora, herbivora and omnivora, 1.

 Digestive organs, rumination in relation to diseases of, 2.

 Digestive organs, structural diseases of, 5.

 Digitalis poisoning, 286.

 Dilation of intestine, 340.

 Dilatation of stomach, 180.

 Diphtheria in calves, 24.

 Diphtheria in chickens and pigeons, 67.

 Diphtheritic enteritis in chickens, 227.

 Dog, chronic gastritis in, 173.

 Dog, gastric indigestion in, 158.

 Dog, torsion of stomach in, 184.

 Dry murrain, 124.

 Dysentery, Amœbic, 242.

 Dysentery, catarrhal, 242.

 Dysentery, diphtheritic, 242.

 Dysentery in cats and dogs, 242.

 Dysentery in cattle, 240.


 Egagropiles, 116, 320.

 Emaciation, 427.

 Embolism, verminous, 210.

 Enteralgia, 308.

 Enteritis, catarrhal, in birds, 254.

 Enteritis, catarrhal, in cattle, 235.

 Enteritis, catarrhal, in dogs, 250.

 Enteritis, catarrhal, in sheep and goat, 246.

 Enteritis, catarrhal, in solipeds, 228.

 Enteritis, catarrhal, in swine, 247.

 Enteritis, chronic catarrhal, in cattle, 239.

 Enteritis, chronic catarrhal, in solipeds, 234.

 Enteritis, coccidian, in birds, 262.

 Enteritis, coccidian, in cattle, 258.

 Enteritis, coccidian, in dogs, 261.

 Enteritis, coccidian, in rabbits, 262.

 Enteritis, croupous, in birds, 226.

 Enteritis, croupous, in cattle, 223.

 Enteritis, croupous, in dogs, 225.

 Enteritis, croupous, in sheep, 224.

 Enteritis, croupous, in solipeds, 221.

 Enteritis from tuberculin, 254.

 Enteroliths, 323.

 Epithelioma in pancreas, 544.

 Epithelioma of intestine, 375, 379.

 Epithelioma of lips, 6.

 Epithelioma of liver, 529, 532.

 Epithelioma of the stomach, 191.

 Equisetum poisoning, 286.

 Ergot as a cause of stomatitis, 9.

 Ergotism in cattle, 296.

 Ergot, poisoning by, 289.

 Esophagitis, 86.

 Euphorbia poisoning, 283.

 Exhausted soils, 78.


 Fatty degeneration of the liver, 508.

 Fauces, injuries to, 48.

 Feathers in stomach, 188.

 Fermented marc, stomatitis from, 27.

 Fermentescible foods, 96.

 Fibroma in gullet, 93.

 Fibroma of intestine, 375, 378.

 Fibrous bands causing strangulation, 356.

 Fistula, salivary, 40.

 Foals, infective gastro-enteritis in, 138.

 Food in infective gastro-enteritis, 141.

 Food in relation to digestive disorder, 2.

 Food, unwholesome, 3.

 Foramen of Winslow, hernia through, 370.

 Foreign bodies in food, 3.

 Foreign bodies in intestines, 328.

 Foreign bodies in liver, 525.

 Foreign bodies in pancreas, 542.

 Foreign bodies in spleen, 558.

 Fourth stomach, catarrhal inflammation of, 166.

 Fourth stomach, indigestion in, 134.

 Fowl cholera, 254.

 Functional liver diseases, treatment of, 432.

 Fungi as a cause of stomatitis, 9.

 Fungi, poisoning by, 289, 291.

 Fungi, varying pathogenesis of, 9.


 Galega, poisoning by, 286.

 Gall-bladder, dilatation of, 514.

 Gall-bladder, double, 515.

 Gall ducts, dilatation of, 514.

 Gall-stones, 516.

 Gall-stones in cattle, 521.

 Gall-stones in dog and cat, 524.

 Gall-stones in sheep, 523.

 Gall-stones in solipeds, 519.

 Gall-stones in swine, 524.

 Gangrenous ergotism, 296, 298.

 Gases evolved from different foods, 100.

 Gastric catarrh in solipeds, chronic, 170.

 Gastric dilatation, 180.

 Gastric indigestion in carnivora, 158.

 Gastric indigestion in swine, 159.

 Gastric ulcer, 175.

 Gastric ulcer, perforating, 179.

 Gastritis, acute catarrhal, in horse, 160.

 Gastritis, catarrhal in swine, 168.

 Gastritis in cattle, 166.

 Gastritis in dogs, chronic, 173.

 Gastritis in ruminants, chronic, 171.

 Gastritis, toxic, in solipeds, 164.

 Gastritis, phlegmonous, in horse, 162.

 Gastro-enteritis from aqua ammonia, 264.

 Gastro-enteritis from caustic acids, 266.

 Gastro-enteritis from caustic alkalies and alkaline salts, 264.

 Gastro-enteritis, hæmorrhagic, in dogs, 452.

 Gastro-enteritis, infective, in sucklings, 138.

 Gastro-enteritis, microbes in, 144.

 Gums, inflammation of, 20.

 Giant fennel, poisoning by, 286.

 Gingivitis, 20.

 Glander nodules in spleen, 564.

 Glisson’s capsule, inflammation of, 500.

 Glossitis, 20.

 Glossoplegia, 37.

 Glycogenesis, 408.

 Glycogenic center in medulla, 417.

 Glycosuria, 416.

 Glycosuria in cattle, 424.

 Glycosuria in dogs, 425.

 Glycosuria in solipeds, 421.

 Glycosuria, reflex, 418.

 Glycosuria, tests for, 422.

 Glycosuria, toxic, 419.

 Glycosuria, pancreatic, 420.

 Glycosuria, pathological, 417.

 Glycosuria, physiological, 416.

 Gnathitis, 19.

 Gout, 430.

 Gongylonema in gullet, 93.

 Grass staggers, 124.

 Green potatoes, poisoning by, 286.

 Growth, sugar in relation to, 428.

 Gullet, inflammation of, 86.

 Gullet, spasm of, 90.

 Gut tie in ox, 357.


 Hæmoglobinæmia, 437.

 Hæmoglobinuria, 437.

 Hemorrhagic gastro-enteritis in dogs, 252.

 Hair and bristle balls, dog and pig, 322.

 Hair balls in intestines, 320.

 Hair balls in intestines, horse, 320.

 Hair balls in stomach, 187.

 Hard palate, congestion of, 19.

 Hare lip, 49.

 Harvest bug on lips, 7.

 Helebore poisoning, 285.

 Helleborus niger poisoning, 285.

 Hepatic abscess, 495.

 Hepatic congestion, 483.

 Hepatic congestion in dog, 486.

 Hepatic congestion in solipeds, 484.

 Hepatic hemorrhage, 487.

 Hepatic inflammation, 490.

 Hepatic steatosis, 508.

 Hepatitis, 490.

 Hepatitis, infective, 498.

 Hepatitis, parenchymatous, 491.

 Hepatitis, suppurative, 495.

 Hernia, 371.

 Hernia, mesenteric, 368.

 Hernia of reticulum, 367.

 Hernia, omental, 368.

 Hernia, pelvic, 357.

 Hernia, phrenic, 359.

 Hernia through foramen of Winslow, 370.

 Honey dew, poisoning by, 292.

 Horsetail poisoning, 286.

 Hydrochloric acid and gastro-enteritis, 266.


 Icterus, 457.

 Icterus, from lupin poison, 476.

 Icterus nouveaux nés, 473.

 Impacted cloaca, 209, 319.

 Impacted rumen, 108.

 Impaction of colon in solipeds, 203.

 Impaction of large intestine, soliped, 197.

 Impaction of omasum, 123.

 Indigestion, acute gastric in solipeds, 150.

 Indigestion, gastric, in carnivora, 158.

 Indigestion, gastric, in swine, 159.

 Indigestion in abomasum, 135.

 Indigestion in fourth stomach in sucklings, 136.

 Indigestion, ingluvial, 94.

 Indigestion, intestinal, 193.

 Indigestion, intestinal in birds, 209.

 Indigestion, intestinal, in solipeds, 197.

 Indigestion with impaction, in dog, 205.

 Indigestion, tympanitic, of rumen, 96.

 Ingluvial indigestion, 94.

 Intestinal atony, 314.

 Intestinal calculi, 323.

 Intestinal congestion, from verminous embolism, 210.

 Intestinal congestion in solipeds, 220.

 Intestinal indigestion in birds, 209.

 Intestinal indigestion with impaction, 197.

 Intestinal invagination, 344.

 Intestinal obstruction in birds, 209.

 Intestinal obstruction in dog, 205.

 Intestinal pain, 308.

 Intestinal strangulations, 356.

 Intestinal tympany, 193.

 Intestine, abscess of, 336.

 Intestine, dilation of, 340.

 Intestine, hyperplasia of, 378.

 Intestine, rupture of, 332.

 Intestines, foreign bodies in, 328.

 Intestines, hair balls in, 320.

 Intestines, strangulation of, by ovarian ligament, 380.

 Intestine, stricture of, 342.

 Intestine, tumors of, 374.

 Intestine, ulceration of, 338.

 Intestine, volvulus of, 351.

 Intussusception, 344.

 Invagination of bowel, 344.

 Iodine poisoning, 276.

 Iodism, 276.

 Iron, poisoning by, 279.


 Jaundice, 457

 Jaundice, catarrhal, 463.

 Jaundice, catarrhal, in dogs, 467.

 Jaundice from ferments in fodder, 476.

 Jaundice from lupins, 476.

 Jaundice from obstruction, 458.

 Jaundice from poisons, 459.

 Jaundice in cattle, 472.

 Jaundice in new born, 473.

 Jaundice without bile obstruction, 459.

 Juniperus sabina, poisoning, 286.


 Kidney, degeneration of, 431.


 Laburnum poisoning, 286.

 Laceration of intestine, 332.

 Lambs, infective gastro-enteritis in, 138.

 Lampas, 19.

 Lathyris, poisoning by, 286.

 Leather in stomach, 188.

 Lips, actinomycosis of, 7.

 Lips, epithelioma of, 6.

 Lips, indurated, 5.

 Lips, inflammation of, 5.

 Lips, polypi on, 6.

 Lips, treatment of inflammation of, 5.

 Lips, trombidiosis of, 7.

 Lips, warts on, 6.

 Lips, wounds of, 5.

 Lipoma of intestine, 374, 377.

 Lipoma of Liver, 533.

 Lipoma of stomach, 191.

 Liver abscess, 495.

 Liver, actinomycosis of, 536.

 Liver, acute yellow atrophy of, 491.

 Liver, amyloid, 511.

 Liver, brown atrophy of, 513.

 Liver and circulatory disorders, 431.

 Liver and gastro-intestinal disease, 431.

 Liver and kidney disease, 431.

 Liver and nervous disease, 431.

 Liver and respiratory disorders, 431.

 Liver and skin diseases, 432.

 Liver, as a destroyer of toxins, 415.

 Liver, calcareous nodules in, 534.

 Liver, chronic atrophy of, 507.

 Liver congestion in dog, 486.

 Liver congestion in horse, 484.

 Liver, congestion of, 483.

 Liver, cirrhosis of, 502.

 Liver disease, secondary results of, 430.

 Liver, diseases of, 407.

 Liver, effect on leucocytes, 409.

 Liver, effect on red globules, 409.

 Liver, fatty degeneration, 508.

 Liver, fibroid degeneration, 502.

 Liver, foreign bodies in, 525.

 Liver, functional diseases, treatment, 432.

 Liver, functional disorders, 416.

 Liver, infective inflammation of, 498.

 Liver, inflammation of, 490.

 Liver, metabolism in, 410.

 Liver, parasites of, 537.

 Liver, pigmentation of, 513.

 Liver, rupture of, 487.

 Liver, sanguification in, 408.

 Liver, steatosis of, 508.

 Liver, tumors in, 527.

 Liver, yellow atrophy of, 476.

 “Loco” weeds, poisoning by, 287.

 Lupinosis, 476.

 Lupinosis in solipeds, 482.

 Lymphadenoma of liver, 529.

 Lymphadenoma of the spleen, 563.


 Maize, poisoning by damaged, 289.

 Male fern poisoning, 286.

 Marsh’s test for arsenic, 271.

 Maxillitis, 44.

 May apple, poisoning by, 286.

 Meadow saffron poisoning, 284.

 Melanoma of gullet, 93.

 Melanoma of liver, 528.

 Melanoma of spleen, 562.

 Melanosis in pancreas, 544.

 Melia azedarach, poisoning by, 286.

 Melilot poisoning, 286.

 Mellituria, 416.

 Mercurialis annua poisoning, 286.

 Mercurialism, 32.

 Mercurial poisoning, 274.

 Mercurial stomatitis, 32.

 Mercury, test for, 275.

 Mesenteric hernia, 368.

 Metabolism in liver, 410.

 Meteorism, gastric, 150.

 Meteorism of the intestines, 193.

 Meteorism of rumen, 96.

 Microbes in gastro-enteritis, 144.

 Milk in infective gastro-enteritis of sucklings, 141.

 Milk of woman, and animals, 143.

 Marc, stomatitis from, 27.

 Monocercomonas gallinæ, 71.

 Moulds, poisoning by, 289, 290.

 Mouldy bread, poisoning by, 296.

 Mouth, diseases of, 4.

 Mouth, functional disorders, 4.

 Mouth, general inflammation of, 8.

 Mouth, injuries to, 4.

 Muguet, 27, 36.

 Muriatic acid and gastro-enteritis, 266.

 Mustard, poisoning by, 287.

 Musty grain, poisoning by, 290, 296.

 Myoma of intestine, 375.

 Myxoma of intestine, 375.


 Narcissus poisoning, 284.

 Nails in stomach, 188.

 Necrobiosis of liver, 498.

 Needles in stomach, 188.

 Neoplasms of intestine, 374.

 Nervous ergotism, 298.

 Neuralgic colic, 309.

 Nitrate of soda poisoning, 268.

 Nitric acid and gastro-enteritis, 266.

 Nux vomica, poisoning by, 286.


 Oat-hair balls in stomach, 187.

 Obesity, 427.

 Œnanthe crocata, poisoning by, 286.

 Œsophagean tumors, 93.

 Œsophagismus, 90.

 Œsophagus, paralysis of, 92.

 Œsophagus, spasm of, 90.

 Omasum, impaction of, 123.

 Omasum, inflammation of, 131.

 Omasum, tumors of, 133.

 Omental hernia, 368.

 Osteomalacia, 78.

 Ovarian ligament, strangulation of intestine by, 380.

 Oxalic acid and gastro-enteritis, 266.

 Oxalic acid diathesis, 430.

 Oxytropis, poisoning by, 287.


 Palatitis, 19.

 Pancreas, diseases of, 537.

 Pancreas, foreign bodies in, 542.

 Pancreatic abscess, 541.

 Pancreatic calculi, 543.

 Pancreatic tumors, 544.

 Pancreatitis, catarrhal, 538.

 Pancreatitis, interstitial, 540.

 Pancreatitis, suppurative, 541.

 Paper-ball in stomach, 188.

 Papilloma of gullet, 93.

 Papilloma of omasum, 133.

 Papilloma of stomach, 191.

 Paralysis of gullet, 92.

 Paralysis of rectum, 371.

 Paralysis of the pharynx, 83.

 Paralysis of tongue, 37.

 Parasites of liver, 537.

 Parasites of rumen and reticulum, 122.

 Parasites of spleen, 564.

 Paris green poisoning, 269.

 Parotid gland, inflammation of, 41.

 Parotitis, 41.

 Pecking feathers, 76.

 Pelvic hernia in ox, 357.

 Perforating ulcer of stomach, 179.

 Perihepatitis, 500.

 Perisplenitis, 554.

 Peritonitis, 380.

 Peritonitis, chronic, 392.

 Peritonitis, general causes, 380.

 Peritonitis in birds, 399.

 Peritonitis in carnivora, 397.

 Peritonitis, infection of, 385.

 Peritonitis in ruminants, 395.

 Peritonitis in solipeds, 383.

 Peritonitis, traumatic, 383.

 Pharyngeal abscess, 58.

 Pharyngitis, catarrhal, 49.

 Pharyngitis, chronic, 73.

 Pharyngitis, microbes in, 50, 56.

 Pharyngitis, phlegmonous, 54.

 Pharyngitis, pseudomembranous, 60.

 Pharyngitis, pseudomembranous, in birds, 67.

 Pharyngitis, pseudomembranous, in cattle, 63.

 Pharyngitis, pseudomembranous, in dogs, 66.

 Pharyngitis, pseudomembranous, in sheep, 64.

 Pharyngitis, pseudomembranous, in solipeds, 61.

 Pharynx, paralysis of, 83.

 Pharynx, tumors of, 84.

 Phenol poisoning, 281.

 Phlegmonous gastritis in horse, 162.

 Phosphatic calculi in stomach, 188.

 Phosphorus poisoning, 272.

 Phrenic hernia, 359.

 Phytolacca, poisoning by, 286.

 Pica, 76.

 Pins in stomach, 188.

 Pip in birds, 18.

 Plants, paralyzing element in, 95.

 Playthings in stomach, 188.

 Podophyllum, poisoning by, 286.

 Poisoning by acetic acid, 266.

 Poisoning by aconite, 286.

 Poisoning by acorns, 286.

 Poisoning by aloes, 286.

 Poisoning by American water hemlock, 285.

 Poisoning by ammonia, 264.

 Poisoning by anemone, 286.

 Poisoning by antimony, 273.

 Poisoning by army worm, 288.

 Poisoning by arsenic, 269, 271.

 Poisoning by artichokes, 286.

 Poisoning by astragalus, 287.

 Poisoning by azedarach, 286.

 Poisoning by bacteria, 289.

 Poisoning by barium, 279.

 Poisoning by bluestone, 276.

 Poisoning by box leaves, 284.

 Poisoning by brine, 268.

 Poisoning by bromine, 276.

 Poisoning by bryony, 286.

 Poisoning by buckwheat, 286.

 Poisoning by cantharides, 288.

 Poisoning by carbolic acid, 281.

 Poisoning by castor seeds, 282.

 Poisoning by chickweed, 286.

 Poisoning by chromium, 280.

 Poisoning by cicuta maculata, 285.

 Poisoning by cicuta virosa, 286.

 Poisoning by clematis, 286.

 Poisoning by cockroach, 288.

 Poisoning by colchicum autumnale, 285.

 Poisoning by conium maculatum, 286.

 Poisoning by copper, 276.

 Poisoning by creosote, 282.

 Poisoning by croton seeds or oil, 283.

 Poisoning by cryptogams, 290, 292.

 Poisoning by daffodils, 284.

 Poisoning by digitalis, 286.

 Poisoning by ergot, 289.

 Poisoning by euphorbia, 283.

 Poisoning by fungi, 289, 291.

 Poisoning by galega, 286.

 Poisoning by giant fennel, 286.

 Poisoning by honey dew, 292.

 Poisoning by horsetail, 286.

 Poisoning by iodine, 276.

 Poisoning by iron, 279.

 Poisoning by laburnum, 286.

 Poisoning by lathyrus, 286.

 Poisoning by lolium temulentum, 286.

 Poisoning by male fern, 286.

 Poisoning by melilot, 286.

 Poisoning by mercurialis annua, 286.

 Poisoning by mineral acids, 266.

 Poisoning by moulds, 289, 290.

 Poisoning by muriatic acid, 266.

 Poisoning by mustard, 287.

 Poisoning by nitrate of soda, 268.

 Poisoning by nitric acid, 266.

 Poisoning by nux vomica, 286.

 Poisoning by œnanthe crocata, 286.

 Poisoning by oxalic acid, 266.

 Poisoning by oxytropis, 287.

 Poisoning by Paris green, 269.

 Poisoning by phosphorus, 272.

 Poisoning by phytolacca, 286.

 Poisoning by podophyllum, 286.

 Poisoning by poppy, 286.

 Poisoning by potash, 265.

 Poisoning by potatoe beetle, 288.

 Poisoning by potatoe tops, 286.

 Poisoning by ranunculus, 284.

 Poisoning by resinous plants, 286.

 Poisoning by rhododendron, 286.

 Poisoning by ryegrass, 286.

 Poisoning by salts of mercury, 274.

 Poisoning by saltpeter, 268.

 Poisoning by savin, 286.

 Poisoning by silver, 278.

 Poisoning by smut, 289.

 Poisoning by snapdragon, 286.

 Poisoning by soda, 265.

 Poisoning by sodium chloride, 267.

 Poisoning by spoiled potatoes, 296, 300.

 Poisoning by spurge laurel, 283.

 Poisoning by spurry seeds, 286.

 Poisoning by St. John’s wort, 286.

 Poisoning by strychnia, 286.

 Poisoning by sulphur, 275.

 Poisoning by sulphuric acid, 266.

 Poisoning by tares, 286.

 Poisoning by tartar emetic, 273.

 Poisoning by tobacco, 286.

 Poisoning by toxins in food and water, 292.

 Poisoning by trefoil, 286.

 Poisoning by vetches, 286.

 Poisoning by veratrum viride, 285.

 Poisoning by white vitriol, 277.

 Poisoning by yew, 286.

 Poisoning by zinc, 277.

 Poisoning, chronic, by arsenic, 271.

 Poke root, poisoning by, 286.

 Polypi on lips, 6.

 Poppy poisoning, 286.

 Postpharyngeal abscess, 58.

 Potash and gastro-enteritis, 265.

 Potato beetle, poisoning by, 288.

 Potato tops, poisoning by, 286.

 Pseudomembranous enteritis in birds, 226.

 Pseudomembranous enteritis in cattle, 223.

 Pseudomembranous enteritis in dogs, 225.

 Pseudomembranous enteritis in sheep, 224.

 Pseudomembranous enteritis in solipeds, 221.

 Pseudomembranous pharyngitis in cattle, 62.

 Pseudomembranous pharyngitis in dogs, 66.

 Pseudomembranous pharyngitis in pigeons and chickens, 67.

 Pseudomembranous pharyngitis in sheep, 64.

 Pseudomembranous pharyngitis in solipeds, 61.

 Pseudomembranous pharyngitis in swine, 65.

 Ptomaines and toxins of brine, 268.

 Ptyalism, 39.


 Rank vegetation as a cause of stomatitis, 9.

 Rape cake, stomatitis from, 27.

 Ranunculus poisoning, 284.

 Rectum, paralysis of, 371.

 Red dysentery in cattle, 258.

 Resinous plants, poisoning by, 286.

 Rhododendron, poisoning by, 286.

 Ricinus communis poisoning, 282.

 Reticulum, hernia of, 367.

 Reticulum, tumors of, 122.

 Retropharyngeal abscess, 58.

 Rumen, actinomycosis of, 123.

 Rumen, balls of vegetable fibre in, 116.

 Rumen, foreign bodies in, 118.

 Rumen, gaseous fermentation in, 96.

 Rumen, hair balls in, 116.

 Rumen, impacted, 108.

 Rumen, inflammation of, 114.

 Ruminitis, 114.

 Rumenotomy, 113.

 Rumen, overloaded, 108.

 Rumen, parasites of, 122.

 Rumen, puncture of, 104.

 Rumen, tumors of, 122.

 Ruminants, chronic gastric catarrh in, 171.

 Ruminants, cryptogamic poisoning in, 295.

 Ruminants, impaction of colon in, 203.

 Rupture of intestine, 332.

 Rupture of stomach, solipeds, 182.

 Ryegrass poisoning, 286.


 Saccharine diabetes, 416.

 Sacculated bowel, 340.

 Saliva, excessive secretion, 39.

 Salivary calculus, 40.

 Salivary ducts, dilation of, 40.

 Salivary fistula, 40.

 Salivary glands, diseases of, 38.

 Salivary glands, surgical lesions, 46.

 Saliva, suppression of, 38.

 Salivation, 5, 39.

 Salivation, mercurial, 32.

 Saltpeter poisoning, 268.

 Sand and gravel in stomach, 188.

 Sarcoma in liver, 527, 531.

 Sarcoma of intestine, 374, 377, 379.

 Sarcoma of omasum, 133.

 Sarcoma of spleen, 562.

 Sarcoma of stomach, 191.

 Savin poisoning, 286.

 Schweinsberg disease, 503, 504.

 Sclerostoma equinum, 210.

 Scouring, 303.

 Sequestrum in spleen, 564.

 Silver salts, poisoning by, 278.

 Smut, poisoning by, 289.

 Snapdragon poisoning, 286.

 Soda in gastro-enteritis, 265.

 Sodium chloride, poisoning by, 267.

 Soft palate, injuries to, 48.

 Solipeds, acute catarrhal gastritis in, 160.

 Solipeds, chronic gastric catarrh in, 170.

 Solipeds, cryptogamic poisoning in, 290.

 Solipeds, phlegmonous gastritis in, 162.

 Solipeds, toxic gastritis in, 164.

 Spanish flies, poisoning by, 288.

 Spasm, intestinal, 308.

 Spasmodic colic, 309.

 Spirillum Metchnikowi, 256.

 Spiroptera in gullet, 93.

 Spleen, abscess of, 557.

 Spleen, amyloid degeneration of, 563.

 Spleen, anæmia of, 546.

 Spleen, chronic congestion of, 550.

 Spleen, diseases of, 545.

 Spleen, foreign bodies in, 558.

 Spleen, gangrene of, in swine, 564.

 Spleen, glander nodules in, 564.

 Spleen, hyperæmia of, 547.

 Spleen, infarction of, 555.

 Spleen, parasites of, 564.

 Spleen, rupture of, 559.

 Spleen, tubercles in, 564.

 Spleen, tumors, of, 562.

 Splenic hemorrhagic infarction, 555.

 Splenic hypertrophy, 550, 551, 552, 553.

 Splenic hypertrophy in dogs, 553.

 Splenic hypertrophy in ruminants, 552.

 Splenic hypertrophy in solipeds, 551.

 Splenic hypertrophy in swine, 553.

 Splenitis, 554.

 Spurge laurel poisoning, 283.

 Spurry seeds, poisoning by, 286.

 Staggers, 124.

 Stale fish, poisoning by, 302.

 St. John’s wort, poisoning by, 286.

 Stomach, bristle balls in, 116.

 Stomach, dilatation of, 180.

 Stomach, feather concretions in, 116.

 Stomach, foreign bodies in, 187.

 Stomach, hair balls in, 116.

 Stomach, perforating ulcer of, 179.

 Stomach, puncture of, 156.

 Stomach, rupture of, solipeds, 182.

 Stomach staggers, 124.

 Stomach, torsion of, in dog, 184.

 Stomach, tumors of, 191.

 Stomach, tympany of, 150.

 Stomach, ulceration of, 175.

 Stomatitis, aphthous, 21.

 Stomatitis, catarrhal in birds, 18.

 Stomatitis, follicular, 21.

 Stomatitis from buccal fermentation, 10.

 Stomatitis from caustics, 35.

 Stomatitis from fermented marc, 27.

 Stomatitis from rape cake, 27.

 Stomatitis, gangrenous, 22.

 Stomatitis, general catarrhal, 8.

 Stomatitis, general catarrhal in cattle, 13.

 Stomatitis, general catarrhal in dog, 15.

 Stomatitis, catarrhal, in sheep, 15.

 Stomatitis, general catarrhal in solipeds, 9.

 Stomatitis, general catarrhal in swine, 17.

 Stomatitis, local, 19.

 Stomatitis, mercurial, 32.

 Stomatitis, mycotic in birds, 36.

 Stomatitis, mycotic in calves, 36.

 Stomatitis, mycotic in foals, 36.

 Stomatitis, mycotic in young, 36.

 Stomatitis, sympathetic, 10.

 Stomatitis, ulcerative, in calves, 24.

 Stomatitis, ulcerative, in carnivora, 30.

 Stomatitis, ulcerative, in lambs and kids, 27.

 Stomatitis, ulcerative, in solipeds, 23.

 Stomatitis, ulcerative, in swine, 29.

 Stomatitis, ulcerous, 22.

 Strangulation of intestine by ovarian ligament, 380.

 Strangulations, intestinal, 356.

 Stricture of intestine, 342.

 Strongylus armatus, 210.

 Strychnia, poisoning by, 286.

 Stump sucking, 76.

 Submaxillary adenitis, 44.

 Sugar in urine, tests for, 422.

 Sulphuric acid and gastro-enteritis, 266.

 Sulphur poisoning, 275.

 Swine, catarrhal gastritis in, 168.

 Swine, gastric indigestion in, 159.

 Swine, impaction of colon, 204.


 Tartar emetic poisoning, 273.

 Third stomach, impaction in fever, 124.

 Third stomach, impaction of, 124.

 Third stomach, tumors of, 133.

 Thrush of the mouth, 36.

 Tobacco poisoning, 286.

 Tongue, inflammation of, 20.

 Tongue, paralysis of, 37.

 Tonsilitis, 46.

 Tonsils, calculi in, 48.

 Torsion of stomach in dog, 184.

 Toxæmia from imperfect hepatic function, 437.

 Toxic gastritis in solipeds, 164.

 Toxic rye, 300.

 Toxin and ptomaine poisoning, 292.

 Toxin, liver as a destroyer of, 415.

 Tracheotomy, 57.

 Trefoil poisoning, 286.

 Trichosoma contortum, 95.

 Trombidiosis of nose and lips, 7.

 Tuberculin as cause of enteritis, 254.

 Tubercle in spleen, 564.

 Tubercles in gullet, 93.

 Tumors in liver, 527.

 Tumors in liver of solipeds, 527.

 Tumors of gullet, 93.

 Tumors of intestine, 374.

 Tumors of omasum, 133.

 Tumors in pancreas, 544.

 Tumors of pharynx, 84.

 Tumors of rumen and reticulum, 122.

 Tumors of the stomach, 191.

 Twisting of intestine, 351.

 Tympanitic colic, 309.

 Tympanitic stomach in solipeds, 150.

 Tympany, chronic, of rumen, 106.

 Tympany of rumen, 96.

 Tympany of the intestines, 193.


 Ulceration, gastric, 175.

 Ulceration of intestine, follicular, 338.

 Ulceration of intestine, peptic, 338.

 Ulcer of intestine, 338.

 Ulcerous stomatitis, 22.

 Urinary calculi, 430.


 Veratrum poisoning, 284.

 Verminous embolism in solipeds, 210.

 Verminous thrombosis, 342.

 Vertigo from cryptogams, 290, 297.

 Volvulus of bowel, 351.


 Warts on lips, 6.

 Water dropwort, poisoning by, 286.

 Water hemlock poisoning, 285.

 Washing powders, poisoning by, 248.

 White scour, 138.

 Wild radish poisoning, 286.

 Wire in stomach, 188.

 Wood in stomach, 188.

 Wool balls in stomach, 187.

 Wool eating, 76.

 Worms, intestinal, 304.


 Xerostomia, 38.


 Yellows, the, 457.

 Yew poisoning, 286.


 Zinc poisoning, 277.

------------------------------------------------------------------------




                          TRANSCRIBER’S NOTES


 1. Silently corrected obvious typographical errors and variations in
      spelling.
 2. Retained archaic, non-standard, and uncertain spellings as printed.
 3. Enclosed italics font in _underscores_.
 4. Enclosed bold font in =equals=.
 5. Denoted subscripts by an underscore before a series of subscripted
      characters enclosed in curly braces, e.g. H_{2}O.