Produced by Richard Tonsing, Chris Curnow, and the Online
Distributed Proofreading Team at https://www.pgdp.net (This
file was produced from images generously made available
by The Internet Archive)









                   CAMBRIDGE AGRICULTURAL MONOGRAPHS


                          PLANTS POISONOUS TO
                               LIVE STOCK




                       CAMBRIDGE UNIVERSITY PRESS
                          C. F. CLAY, MANAGER
                       London: FETTER LANE, E.C.
                     Edinburgh: 100 PRINCES STREET

[Illustration]

       London: H. K. LEWIS AND CO. LTD., 136, GOWER STREET, W.C.
        London: WILLIAM WESLEY AND SON, 28, ESSEX STREET, STRAND
                     New York: G. P. PUTNAM’S SONS
          Bombay, Calcutta and Madras: MACMILLAN AND CO., LTD.
                   Toronto: J. M. DENT AND SONS, LTD.
                  Tokyo: THE MARUZEN-KABUSHIKI-KAISHA


                         _All rights reserved_

[Illustration: _a_ Reddish-brown to reddish-purple “Java” Beans
(_Phaseolus lunatus_); _b_ “Red Rangoon” Beans (_P. lunatus_); _c_
“Large White” Beans (_P. lunatus_); _d_ Castor Oil Beans (_Ricinus
communis_); _e_ “Indian Peas” (_Lathyrus sativus_), from Bombay; _f_
Ergot (_Claviceps purpurea_), from Spain. All natural size.]




                     PLANTS POISONOUS TO LIVE STOCK


                                   BY

                     HAROLD C. LONG, B.Sc. (Edin.)

               of the Board of Agriculture and Fisheries

            Author of _Common Weeds of the Farm and Garden_


                               Cambridge:
                        at the University Press
                                  1917




                                PREFACE


As in the case of a previous volume, _Common Weeds of the Farm and
Garden_, the preparation of this handbook was undertaken because of the
great lack of readily available and reliable information on the subject
in English scientific literature. Many of the facts were known to a few
interested persons, but many others were so scattered here and there in
technical reports and journals that they were scarcely known even to
expert chemists and botanists. The bringing of this information together
in some sort of order has involved considerable labour extending over
several years, but if the volume be found helpful to those for whose use
it has been prepared I shall feel more than gratified.

That the subject is of importance is fully realised by farmers and
veterinary surgeons alike, for the annual loss of stock due to poisonous
plants, though not ascertainable, is undoubtedly considerable. It was
felt that notes on mechanical injury caused by plants and on the
influence of plants on milk might usefully be included, as in some
degree related to poisoning; this has therefore been done. On the other
hand, a number of cultivated plants (_e.g._ _Rhus_, _Wistaria_) which
are poisonous have not been included because exotic and hardly likely to
be eaten by stock. Fungi generally also find no place in the volume, as
they are sufficiently extensive to deserve a volume to themselves, and
are far less readily identified than flowering plants.

The dividing line between plants which are actually poisonous and those
which are only suspected is far from clear, but a division was
considered desirable for the convenience of the reader, and an endeavour
has been made to give a sound but brief statement as to the present
information on plants poisonous to live stock in the United Kingdom,
with symptoms, toxic principles, and a list of the more important
references to the bibliography in relation to each plant included in
Chapters II to VI (the numbers corresponding with the numbers in the
Bibliography).

Regarding symptoms it is to be regretted that in many cases they appear
to be the result of injections of the toxic extracts, and not
observations made after natural poisoning by ingestion of the plants.
Further, there may frequently be doubt as to the identification of the
plant suspected of causing poisoning; indeed, in some cases it is
possible that the identification rests on the veterinary surgeon or the
stockman _thinking_ a certain plant is the cause. The most complete and
systematic account of European poisonous plants is that of Cornevin
(1887), and references to poisonous plants in the ordinary literature
are heavily indebted to him. In so far as the toxic principles of the
plants are concerned, however, his book is in many instances no longer
reliable.

The chemical formulae, quoted for the use of students and research
workers, have been checked by consulting works by the following authors,
the reference to the bibliography being given in brackets: Henry (128),
Dunstan (76), Allen (4), Haas and Hill (114), Thorpe (240), Van Rijn
(252), Kobert (161), Esser (81), and Beilstein (16).

Apart from the literature consulted I desire to acknowledge my great
indebtedness to the Board of Agriculture and Fisheries for kind
permission to make use of official records; to Mr F. W. Garnett,
M.R.C.V.S., for kindly reading the proofs from the veterinary
standpoint; to very many Experiment Stations, State Departments of
Agriculture, and other authorities in Australasia, America and the
Continent of Europe, for assistance given and literature sent; to Sir
David Prain and members of the staff at Kew for much friendly advice,
and aid in consulting the Kew library; to Sir James Dobbie for
permission to spend some time at the Government Laboratories to consult
certain volumes; to Mr T. H. Middleton, C.B., Dr. E. J. Russell,
Professor W. Somerville, Sir Stewart Stockman, Professor T. B. Wood, and
others, for information and many helpful suggestions; to my friend Mr W.
A. Whatmough, B.Sc. (Lond.), for many suggestions and kindly reading the
proofs; and to my colleague Mr W. R. Black for invaluable help in
preparing notes, checking data and reading proofs. To all these, and
many others who are not mentioned by name, I tender my sincere thanks.

For any shortcomings I crave the indulgence of my readers, only
requesting that they be friendly enough to spare a moment to call my
attention thereto.

                                                             H. C. LONG.

  SURBITON,
      _October_, 1916.




                                CONTENTS


 CHAP.                                                              PAGE
    I. INTRODUCTION                                                    1

       What is a Poisonous Plant? Harm done by Poisonous
       Plants. Circumstances in which Poisoning occurs.
       Effect of Soil, Climate and Cultivation on the
       Toxic Properties of Plants. Variation in the
       Poisonous Parts of Plants. Eradication of
       Poisonous Plants. Treatment of Poisoned Animals.
       Tests with Suspected Plants. Legal Aspect of Plant
       Poisoning. The Toxic Principles of Plants.

   II. RANUNCULACEÆ. PAPAVERACEÆ. CRUCIFERÆ.
         CARYOPHYLLACEÆ. HYPERICINEÆ. GERANIACEÆ                       9

  III. CELASTRACEÆ. RHAMNACEÆ. PAPILIONACEÆ. ROSACEÆ.
         CUCURBITACEÆ. UMBELLIFERÆ                                    24

   IV. ARALIACEÆ. CAPRIFOLIACEÆ. COMPOSITÆ. ERICACEÆ.
         PRIMULACEÆ. OLEACEÆ. CONVOLVULACEÆ. SOLANACEÆ                43

    V. SCROPHULARINEÆ. POLYGONACEÆ. THYMELACEÆ.
         EUPHORBIACEÆ. AMENTACEÆ. CONIFERÆ. AROIDEÆ                   61

   VI. DIOSCORIDEÆ. LILIACEÆ. GRAMINEÆ. EQUISETACEÆ.
         FILICES. FUNGI                                               78

  VII. PLANTS SUSPECTED OF BEING POISONOUS                            92

 VIII. THE EFFECTS OF PLANTS ON MILK. PLANTS WHICH CAUSE
         MECHANICAL INJURY                                            99

   IX. CLASSIFICATION OF POISONS                                     103

       BIBLIOGRAPHY                                                  106

       INDEX                                                         114


       Photograph of three varieties of _Phaseolus_
         beans, of Castor Oil Beans, Indian Peas, and
         Ergot                                            _Frontispiece_




                               CHAPTER I
                             INTRODUCTION.


=What is a Poisonous Plant?= As will be shown later, so-called
“poisonous” plants differ widely in “degree of harmfulness,” and it is
highly probable that under ordinary conditions many of the plants
commonly reputed to be poisonous are really almost or quite harmless. It
is possible, however, that a plant usually unsuspected may on occasion
prove noxious—for example, _Nepeta Glechoma_ (p. 96), included as
suspected of poisoning horses. For these reasons, no line of demarcation
can be drawn to separate actually poisonous plants from those which are
suspected or are almost certainly quite harmless; and a large number of
species is included in Chapter VII as suspected, many of them, however,
being almost certainly more or less poisonous in certain circumstances.
In many cases it is practically impossible to come to any conclusion as
to the degree of toxicity of a plant, owing to the want of exact
information. Many plants are quite harmless except when affected by
fungi, moulds, etc.

A really poisonous plant may be defined as one a small quantity of which
when eaten induces some form of indisposition with irritant, narcotic,
or nervous symptoms, with serious or even fatal consequences either
immediately or by reason of cumulative action of the toxic property.

=Harm done by Poisonous Plants.= A perusal of the following pages will
afford convincing proof that the question of the general “wholesomeness”
of wild plants is worthy of serious consideration by all who are
interested in the practice of agriculture. Still more important is a
satisfactory knowledge of the extent to which plants are actually
_poisonous_—that is, sufficiently injurious when eaten in small or large
quantities to induce more or less severe indisposition, illness or
death, with the consequent losses which such bring in their train—loss
of milk and meat production in the case of cattle, of meat and wool
production in sheep, of power in the horse, of expenditure in attendance
and veterinary treatment generally, and possibly total loss by death of
the animals concerned.

The losses due to Poisonous Plants in Great Britain happily afford no
comparison whatever with the immense losses sustained in some other
countries, such as the cases of lupine poisoning mentioned at p. 29, but
deaths are sufficiently numerous to make it certain that financial
losses are in the aggregate very heavy. In this connection it may
suffice to refer to the many cases of yew poisoning, the losses due to
Umbellifers (pp. 36–42), and the instance reported in the _Staffordshire
Weekly Sentinel_ in relation to meadow saffron and water hemlock (p.
80). Further, it appears to be extremely likely that many losses due to
unascertained causes are really due to plant poisoning. For this reason
veterinary surgeons will be well advised always to consider this
possibility and, if need be, to obtain the services of a trained
botanist to survey the farm or field involved, with the object of
deciding whether poisonous plants are present.

=Circumstances in which Poisoning occurs.= It may be assumed that many
plants are to a considerable extent protected from animals by the fact
that they have an unpleasant odour, are acrid or bitter to the taste, or
are actually toxic in character, just as others assume such protective
devices as spines. In a state of nature animals appear to avoid
instinctively such plants as are toxic or “unwholesome,” and to be less
readily poisoned than are domesticated animals living under artificial
conditions. Indeed, it has been remarked that farm stock reared in a
locality where certain poisonous plants abound are much less likely to
be injured by these plants than animals imported from a district where
they do not occur.

The individuality of stock is also a factor which may be responsible for
poisoning, some animals having what may be described as a depraved
appetite for unusual and unappetising food plants. It would appear that
animals are often tempted to eat dark-green plants of luxuriant growth
which are soft and succulent. This is especially true when the plants
are young and tender, particularly as regards sheep, which, however,
usually avoid tall, old rank-growing and coarse herbage—unless
absolutely pressed by hunger. Cattle, however, are not so particular,
and will commonly eat large coarse-growing plants.

Sheep have been observed to be particularly variable in their choice of
food plants, not only individually in the flock, but from day to day.
Chesnut and Wilcox remark[1] that “there seems to be no way of
accounting for the appetite or taste of stock. This statement is perhaps
especially true of sheep. We have often observed sheep eating greedily
on one day plants which they could scarcely be persuaded to eat on the
following day on the same range.” In the case of one flock of sheep on a
foothill range at an altitude of 4,600 ft. “a few of the sheep were
observed eating large quantities of wild sunflower (_Balsamorhiza
sagittata_), a few ate freely of false lupine (_Thermopsis
rhombifolia_), some confined their attention largely to the wild
geranium, while others ate false esparcet (_Astragalus bisulcatus_)
almost exclusively. Two sheep were seen eating the leaves of lupine, and
about fifty ate a greater or less quantity of _Zygadenus venenosus_,
while the majority of sheep in the band fed exclusively upon the native
grasses on the range.”

Footnote 1:

  “The Stock-Poisoning Plants of Montana,” V. K. Chesnut and E. V.
  Wilcox. _Bul. No. 26. U.S. Dept. Agric., Div. Bot._, 1901.

Horses also have been known to acquire in America a depraved appetite
for horsetail and loco-weed.

The different species of live stock are often quite differently affected
by poisonous plants, some being very susceptible to a given plant while
others may be little or not at all susceptible. One species (_e.g._ the
pig) may readily vomit the poison of a plant which is emetic, while
another (_e.g._ the horse) may be unable to do so and hence be the more
seriously injured. The variability of the different classes of live
stock in this respect is frequently brought out in Chapters II to VI.
Poisonous effects may also vary with the individuality and age of
animals of the same species.

At certain periods of the year—_e.g._ in early spring, and during dry
summers,—there may be a scarcity of green herbage, and this may induce
animals to eat any green plants which are especially early, including
poisonous ones, which they would otherwise refuse.

In some cases poisonous plants which do not lose their toxic properties
on drying (_e.g._ meadow saffron) may be included in hay, and hence find
their way to stock in such a form that they may not be distinguished. It
has been found, however, that some poisonous plants or parts of them are
refused by stock when mixed with good herbage in hay. Care should be
exercised that poisonous plants are not included with hay or green
fodder, and in cases of poisoning all forage should be examined.

Animals may also be poisoned by certain toxic seeds (_e.g._ corn cockle)
fed to them with cereal grains, in feeding stuffs generally, or in the
refuse seeds from the sources mentioned. Here again judgment is
necessary, and it is probably advisable on all counts to burn the weed
seeds and similar refuse from the sources mentioned. Poisonous seeds may
occur in low quality feeding stuffs, and poisonous seeds of foreign
origin are occasionally sold for food purposes owing to the mistaken
idea that they are a valuable addition to the ration (_e.g._ the
poisonous “Java” beans). In any case in which an animal is believed to
have been poisoned purchased feeding stuffs should always be considered
as a possible source of injury and be submitted to examination.

Clippings and trimmings from gardens and shrubberies have proved a more
or less common cause of live stock poisoning, such material being too
often carelessly thrown out for animals to pick over. In such
circumstances it may quite easily happen that the animals get yew,
daphne, privet, rhododendron, azalea, solanums, and other plants of a
poisonous character. For this reason it is better to destroy such
trimmings, etc., by burning them, or by adding them to the compost heap
as the case may be.

A further source of poisoning must be noted here—fleshy and parasitic
fungi (toadstools, rust fungi), moulds and similar organisms. Many
toadstools are directly poisonous when eaten, but the microscopic
organisms are probably in themselves harmless, though taken with food
which they are responsible for injuring (bad hay, cakes, etc.), the
poisoning being due to the changed and damaged feeding stuffs, or
possibly to poisonous principles directly elaborated by the microscopic
fungi. Fungi and related organisms cannot be dealt with in this volume,
but it may at least be said that the use of mouldy hay and similarly
affected feeding stuffs is attended with some danger, which is not yet
very clearly defined.

=Effect of Soil, Climate and Cultivation on the Toxic Properties of
Plants.= In general, wild poisonous plants are richer in either
alkaloids or glucosides than the same species when cultivated, though
there are exceptions. In many cases it is found that plants vary
considerably in toxicity, or the percentage content of the poisonous
principle, according to soil, light, moisture, etc. Solanaceous plants
in particular vary in this way, and one or two instances may be given as
examples. _Solanum nigrum_ varies so much that it has been regarded as
harmless in one country and quite poisonous in another (p. 52).

Experiments conducted at the Arlington Experimental Farm, Virginia,
showed that in 24 first-year plants of _Atropa Belladonna_ grown in 1910
the alkaloid contents of the leaves varied from 0·334 to 0·700 per
cent., and averaged 0·547 per cent. In 1911 the alkaloid contents
(usually the average of five pickings) of the leaves of 59 plants varied
from 0·306 to 0·766 per cent., and averaged 0·532 per cent. In 1912 the
alkaloid contents (commonly the average of 5 pickings) of the leaves of
57 plants varied from 0·352 to 0·768 per cent., and averaged 0·545 per
cent. In individual plants at a single picking the highest alkaloid
content in 1911 was 0·925 and the lowest 0·200, and in 1912 the highest
was 0·882 and the lowest 0·292. (_Jour. Agric. Res._, I. 2, Nov., 1913.)

The variation in the percentage of poisonous principle was well shown in
several papers read at the International Congress of Applied Chemistry
held at Washington and New York in 1912 (see _Chemist and Druggist_
reports). For example, Carr stated that at the Wellcome Materia Medica
Farm, Dartford, Kent, the effect of manuring on medicinal plants has
been tested for some years, and the effect of the more common
fertilisers on _Atropa Belladonna_ was shown by the following table:—

 ────────────────────────────────────┬──────────────────────────────────
                                     │Percentage of Alkaloid in Dry Stem
                                     │             and Leaf
 ──────────────┬───────────┬─────────┼──────┬──────┬──────┬──────┬──────
               │           │         │ 1906 │ 1907 │ 1910 │ 1911 │ 1912
   Fertiliser  │  Time of  │Per acre │ 3rd  │ 4th  │ 1st  │ 2nd  │ 3rd
               │Application│         │year’s│year’s│year’s│year’s│year’s
               │           │         │plants│plants│plants│plants│plants
 ──────────────┼───────────┼─────────┼──────┼──────┼──────┼──────┼──────
 Main crop     │           │         │ 0·54 │ 0·34 │ 0·61 │ 0·59 │ 0·68
 Farmyard      │   March   │50 loads │ 0·54 │ 0·34 │ 0·61 │ 0·53 │ 0·71
 manure        │           │         │      │      │      │      │
 Nitrate       │  March &  │ 2 cwt.  │ 0·52 │ 0·23 │ 0·54 │ 0·46 │ 0·64
               │   April   │         │      │      │      │      │
 Calcium       │    Do.    │ 1 cwt.  │      │      │ 0·69 │ 0·49 │ 0·75
 cyanamide     │           │         │      │      │      │      │
 Basic slag    │    Do.    │ 2 cwt.  │ 0·61 │      │ 0·65 │ 0·56 │ 0·84
 Superphosphate│    Do.    │ 5 cwt.  │ 0·46 │      │ 0·81 │ 0·49 │ 0·76
 Potash        │    Do.    │ 5 cwt.  │ 0·61 │ 0·40 │ 0·75 │ 0·53 │ 0·69
 ──────────────┴───────────┴─────────┴──────┴──────┴──────┴──────┴──────

In considering these results it must be remembered that the soil is
naturally suited to the plant, and the percentage of alkaloid obtained
without added fertilisers is already high. The low figures obtained in
1907 were probably due to the seasonal conditions. Atmospheric
conditions have a modifying influence.

It was also shown that the Belladonna root of commerce varies greatly in
alkaloid strength. “In a number of analyses made of commercial roots,
variations from 0·27 to 0·69 per cent. have occurred. The average of
twenty-one analyses of German and Austrian commercial roots was 0·40 per
cent. Other observers have recorded similar results. Chevalier (_Compt.
Rend._, 1910, 150, 344) gives the following figures for Continental
roots: French, 0·300 to 0·450 per cent.; Austrian, 0·251 to 0·372 per
cent.; Italian, 0·107 to 0·187 per cent. Henderson has shown the average
of thirty samples of foreign root to be 0·3 per cent. It is interesting
to observe that the average of nine samples of root grown at Darenth is
0·54 per cent. In order to determine whether this variation was due to
collecting at different times of the year, roots from the same plot,
derived from second year’s plants, which were sown at the same time,
were dug up at intervals and dried. The following is a record of the
analysis of these samples:—

                     March, 1911    0·56 per cent.
                     May, 1911      0·59   „   „
                     June, 1911     0·53   „   „
                     August, 1911   0·50   „   „
                     December, 1911 0·59   „   „

“The amount of variation throughout the year is thus seen to be very
small.”

Dunstan (_Bul. Imp. Inst., 1905_) has shown that _Hyoscyamus muticus_
grown in India yielded 0·3 to 0·4 per cent. of hyoscyamine, but that the
same species grown in Egypt produced 0·6 to 1·2 per cent.

According to Esser no coniine is found in _Conium maculatum_ growing in
the far north. The same authority says that the root of _Hyoscyamus
niger_ is quite free from toxic properties in winter.

=Variation in the Poisonous Parts of Plants.= As will be shown in
succeeding chapters, many plants (_e.g._ meadow saffron) are poisonous
in all their parts, though the amount of the toxic substance may differ
according as to whether the seeds, leaves, stem or roots are severally
considered. In other cases one part of the plant alone is toxic (_e.g._
the seeds, as in corn cockle). Further, some species vary in the
percentage of the toxic substance in the leaves before and after
flowering. Frequently the root is the most toxic portion of the plant.
This point may be usefully recollected in relation to poisoning of live
stock, which are in general affected by the foliage or ripe seeds.

=Eradication of Poisonous Plants.= Wherever poisonous plants are found,
particularly in quantity, where they are liable to be eaten by live
stock, an attempt should be made to eradicate them. They may be simply
dealt with as weeds as may be necessary according to the species
concerned. When any difficulty is experienced in regard either to
determination of the species or to methods of eradication the advice of
the Board of Agriculture and Fisheries (Whitehall Place, London, S.W.)
should be requested. Stock should at once be removed from a suspected
pasture, which should be immediately and thoroughly examined by a
competent botanist. Harmful plants should be eradicated and their place
filled by better herbage.

=Treatment of Poisoned Animals.= This volume makes no pretensions to
deal with the veterinary treatment of cases of plant poisoning. Whenever
poisoning is suspected the services of a veterinary surgeon should be
sought without delay; the text books at his disposal will aid him in the
treatment of any case which presents unusual difficulties. The symptoms
indicated in the following pages, together with the possible discovery
of a suspected plant, may be utilised in diagnosis.

=Tests with Suspected Plants.= The action of plants on animals may be
ascertained (1) by observing the effects in cases in which it has been
established that the plants have been eaten, or (2) by direct
experimental feeding of animals with the plant. In the first case the
results may be accurate and satisfactory if observations have been made
from the outset.

As regards (2) the results may or may not be satisfactory according as
the plan pursued is sound or otherwise. For example, it cannot be
considered altogether reasonable and satisfactory to extract the
principles present in the plant, inject them into the blood stream, and
conclude from any ill effects that the animal may exhibit that the plant
is poisonous, since the substance extracted may be poisonous under such
conditions but little or not at all harmful when the plant is eaten in
the small quantities commonly taken by animals. Again, it cannot be held
satisfactory to feed an animal on a heavy and exclusive diet of the
suspected plant for a considerable period. The real test would, in
general, consist in a feeding trial in which the suspected plant
occupied a place in the ration in reasonable quantity—such a quantity as
might well be taken in natural circumstances, in view of its relative
abundance in regard to other food available; and if considered likely
that the plant would be eaten daily it may be fed regularly for some
days. Should such a test prove negative it may generally be held that
the plant is not poisonous, or only so in exceptional circumstances.

=Legal Aspect of Plant Poisoning.= There is clearly some legal liability
in regard to poisonous plants which may, by hanging over a boundary,
cause injury to a neighbour’s stock. The only cases known to the author
are in relation to the yew. In the case of _Crowhurst v. Amersham Burial
Board_ (48 L. J., Ex. 109; 4 Ex. D., 5) a Burial Board was held liable
for the loss of a horse poisoned by eating leaves of a yew tree planted
in the cemetery owned by the Board, the tree having grown through and
over their fence and projected on to the meadow occupied by the
plaintiff. In _Ponting_ v. _Noakes_ (63 L. J. B. 549; (1894) 2 Q.B.,
281) the defendant was not held liable for the death of a horse which
ate off the branches of a yew tree, because the tree did not extend up
to or over the plaintiff’s boundary, though it overhung a ditch, the
edge of which was the boundary, and was hence accessible to the
plaintiff’s stock.

=The Toxic Principles of Plants.= The poisonous substances in plants may
be grouped either (1) according to their physiological effects on
certain organs; (2) according to the principal outward and perceptible
symptoms caused; or (3) in accordance with their chemical relationships.

In regard to (1) the poisons may be nerve, heart, blood-poisons, etc.
(2) The poisons may be acrid, narcotic, or both. _Acrid poisons_ are
those which cause irritation or inflammation of the digestive tract
(_Euphorbia_, _Ranunculus_, _Daphne_, _etc._); _narcotic poisons_ affect
only or chiefly the brain (_Agrostemma_, _Papaver_, _Atropa_) or chiefly
the spinal cord (_Claviceps purpurea_, _Lolium temulentum_);
_acrid-narcotic poisons_ induce to a greater or less extent the symptoms
of both the foregoing groups (_Taxus_, _Colchicum_, _Cicuta_, _Solanum_,
_etc._).

(3) As the accounts of the individual plants will show, the toxic
principles of many plants are not yet well understood, either as regards
chemical constitution or symptoms caused. Many poisons may be driven off
by heat (boiling, drying), and some plants may thus be rendered
harmless.

Most of the toxic principles of our native poisonous plants are
Alkaloids or Glucosides. The former all contain nitrogen, differ
considerably in molecular constitution, and are usually combined with
widely distributed organic acids. In the pure state they are colourless
and usually stable, crystalline or amorphous solids, or readily volatile
liquids; they usually have a burning taste. In general the same base is
confined to species of the same order—_e.g._ Solanine to the
_Solanaceæ_. The alkaloids include the most powerful poisons.

The term “Glucoside” indicates a group of substances which by the action
of an acid or enzyme are split up into a sugar (grape sugar, galactose
or rhamnose) and other substances (alcohol, aldehydes, acids). They have
a bitter taste and are generally readily soluble in water. Related to
the glucosides are also the Saponins, remarkable for the fact that they
induce an exceedingly frothy condition in water; the prussic acid
yielding compounds or cyanogenetic glucosides (_e.g._ Amygdalin and
Phaseolunatin) also belong to this group. Other substances will be
mentioned in the succeeding chapters.




                               CHAPTER II
                             RANUNCULACEÆ.


=Traveller’s Joy= (_Clematis Vitalba_ L.). The extent to which this
species is poisonous is not clear, though all parts are stated to be
poisonous, acrid and narcotic, while the juice tends to blister the
skin. It is remarked by Cornevin that it is less poisonous in spring,
when the ass and goat browse on it to a considerable extent without
serious trouble, than later, when it cannot be eaten without danger.

_Toxic Principle._ Traveller’s Joy appears to contain strongly poisonous
substances which have not been closely investigated. Greshoff found a
_Saponin_ in the leaves[2]. The poison is dissipated by heat.

Footnote 2:

  Kobert states that various species of _Clematis_, _Ranunculus_,
  _Anemone_, and also _Caltha palustris_ and _Trollius europæus_,
  contain _Anemonal_ or _Pulsatilla-camphor_, which causes strong local
  irritation, burning and swelling in the mouth, vomiting, intestinal
  inflammation, etc.

_Symptoms._ When eaten in quantity the young shoots are diuretic,
violently purgative, causing dysentery, and in rare cases death. Applied
to the exterior it is irritating and even vesicatory. (Cornevin.)

                              REFERENCES.

                      63, 81, 101, 130, 161, 233.

=Anemone= (_Anemone_ sp.). Both our native species of Anemone appear to
be more or less poisonous in character: the Wood Anemone or Wind Flower
(_A. nemorosa_ L.), and also the Pasque Flower (_A. Pulsatilla_ L.).
These plants, the former of which grows in woods and damp shady spots in
fields, and the latter on chalk downs and limestone pastures, may on
occasion be taken by stock in early spring, when green herbage is not
too plentiful, but deaths appear to be rare, even if they have occurred.
All parts of the plants contain a toxic principle, which is volatile and
destroyed by drying.

_Toxic Principle._ The toxic substance is stated to be _Anemone-camphor_
(oil of Anemone) which imparts a bitter taste to the plants, and itself
gives rise in the plant to _Anemonic acid_ and _Anemonin_
(C_{10}H_{8}O_{4}), a very poisonous, narcotic substance, stated to be
neither a glucoside, nor an alkaloid, but a ring ketone with the
properties of an acid anhydride.

_Symptoms._—The symptoms recorded by Cornevin in the poisoning of
animals by the fresh plants are nausea, coughing, vomiting (if
possible), stupefaction, muscular tremors, and violent colic,
accompanied at times by hæmaturia and always by diarrhœa and dysentery.
There are pronounced respiratory and heart troubles.

Pott confirms the symptoms of hæmaturia, diarrhœa, and inflammation of
the stomach and intestines in the case of _A. Pulsatilla_ when fed in
the green condition. According to Esser, the plant poison affects the
spinal cord and the brain, the symptoms being similar to those produced
by _Aconitum Napellus_.

                              REFERENCES.

               16, 63, 81, 191, 197, 198, 213, 233, 240.

=Buttercups= (_Ranunculus_ sp.). A number of species of _Ranunculus_ are
acrid, irritant or severely poisonous, as the case may be. There are
variations in the poisonous character according to the season, and some
parts of the plant are more toxic than others. At the time the young
shoots develop in the spring but little of the poisonous principle is
present, and some (_e.g._ _R. Ficaria_) are not then poisonous, but a
larger quantity of the poisonous principle forms later, and some species
are especially dangerous at the time of flowering, after which the
toxicity decreases with the maturity and state of dryness of the plant.
The flowers are the most poisonous, and then the leaves and stem. It
does not seem to have been demonstrated that the seeds of any species
are dangerous, though Henslow states that the fruits of some species,
when green, appear to be most intensely acrid.

Some species of _Ranunculus_ are especially harmful (_R. sceleratus_,
_R. Flammula_, and _R. bulbosus_), while others are less so (_R.
lingua_, _R. Ficaria_, _R. acris_). The toxic principle is volatile, and
buttercups are easily rendered innocuous by drying or boiling—so much so
that when dried in hay they may be regarded as a nourishing food for
stock, and are readily eaten. Indeed, _R. repens_ is scarcely, if at
all, injurious even when green, though a case of fatal poisoning to
sheep said to be due to this species was reported in the _Veterinarian_
in 1844. Fresh _R. aquatilis_ is held to be quite harmless, and has been
used as a fodder. “Along the banks of the Hampshire Avon, and other
places in the same neighbourhood, it is used by the peasantry as fodder.
They collect it in boats and give it to their cows and horses, allowing
the former about twenty to thirty pounds a day. One man is said to have
kept five cows and a horse, with little other food but what they could
pick up on the heath, using no hay but when the river was frozen. Hogs
eat it and will live upon it alone until put up to fatten.” (Johnson and
Sowerby—_Useful Plants of Great Britain_.)

_R. sceleratus_ L., or Celery-leaved Buttercup, is probably the most
toxic species, and it is stated that in man a single flower may cause
poisonous symptoms resembling those due to _Anemone_ and _Colchicum_. It
is considered especially dangerous to cattle, and has caused many
losses: among its French names are _Mort aux Vaches_, and _Herbe
sardonique_. Poor people have been known to eat the young shoots when
boiled, heat dispelling the poison.

_R. Flammula_ L., the Lesser Spearwort, has repeatedly proved fatal to
horses and cattle.

_R. bulbosus_ L., the Bulbous Buttercup, is somewhat variable in
toxicity, and is least dangerous after the flowers have dropped their
corolla, and the bulb-like rootstock is most harmful in autumn and
winter. The flowers are the most dangerous part.

_R. Ficaria_ L., Lesser Celandine, varies in toxicity with locality and
season, being most harmful at the flowering period. It is stated that
wood-pigeons eat the roots with avidity, and that the young shoots have
been eaten as a salad in Germany, as they are not toxic. An English
veterinary surgeon (Flower) recorded that three heifers were poisoned by
it (_Vide_ Cornevin).

_R. acris_ L., Acrid Buttercup or Tall Crowfoot, is a frequent cause of
poisoning in cattle, and Cornevin says it is perhaps the species which
causes the most accidents.

_Toxic Principle._ The buttercups contain an acrid and bitter juice, the
chemical properties and composition of which are not well known, but it
is believed that the substance is identical with the _Anemonin_ of the
_Anemone_ sp. (_q.v._). Beckurts isolated _Anemonin_ and _Anemonic acid_
from _R. acer_. Pott, however, states that the poisonous species contain
the two alkaloids _Aconitine_ and _Delphinine_.

_Symptoms._ The buttercups are acrid, burning and narcotic, causing
irritation of the mucous membrane, with inflammation of the intestinal
tract.

Cornevin shows that _R. sceleratus_ induces gastro-enteritis, colic,
diarrhœa with excretion of black foul-smelling fæces, vomiting when
possible, falling-off in milk yield in cows, nervous symptoms, reduction
in pulse, and stertorous respiration, dilation of the pupils, enfeebled
condition, difficult mastication, spasmodic movements of the ears, lips,
etc.,—followed in serious cases by convulsions, sinking of the eye in
its socket, possibly stoppage, and death in 6 to 12 hours after
convulsions first appeared.

In the _horse_ symptoms substantially similar to the above have been
recorded (Lander).

In _cows_, Pott records hæmaturia, and reddish or bitter milk.

_Sheep_ after eating _R. repens_ have been noticed to fall suddenly in
the field; their eyes rolled, and some animals showed dizziness, and
died with the head inclined over the left flank (Lander).

                              REFERENCES.

   47, 63, 81, 112, 130, 140, 145, 170, 203, 204, 205, 213, 233, 235.

=Marsh Marigold= or =King-Cup= (_Caltha palustris_ L.). Like the species
of _Ranunculus_, the Marsh Marigold is to some extent poisonous in
character, and both animals and man have suffered. Cattle have died from
eating it, and Müller records the poisoning of many horses, one of which
died. In general, animals refuse it, but may possibly eat it when
pressed with hunger in times of scarcity of green herbage. Cornevin
states that it has little or no acrid properties when very young, but
that it is toxic by the time of flowering—acridity increasing with age.

_Toxic Principle._ The toxic character of the Marsh Marigold has not
been fully investigated, though the presence of an alkaloid has been
determined, and A. B. Smith states that the toxic properties are due to
the alkaloid _Jervine_ (C_{26}H_{37}O_{3}N2H_{2}O) and the glucoside
_Helleborin_ (C_{36}H_{42}O_{6}). On drying—_e.g._ in hay—the plant
becomes harmless, as in the case of most species of _Ranunculus_.

_Symptoms._ Cornevin records that _cattle_ have died from inflammation
of the digestive tract, and gives the symptoms as those of _Ranunculus_
poisoning. There seem to be digestive troubles, diarrhœa, and loss of
milk production, even (according to Rusby) when fed with hay. In the
_horse_, there is colic, bloating, and inflammation of the bladder,
while the urine is dark red. According to Cornevin, the symptoms are
similar to those produced by _Ranunculus_ sp. Pammel quotes Friedberger
and Fröhner as stating that the plant causes hæmaturia. Five persons who
ate it as a herb were “seized with violent sickness and pain in the
abdomen, followed by diarrhœa and general œdematous swelling over the
whole body,” but they recovered (Johnson and Sowerby).

                              REFERENCES.

                    63, 81, 140, 190, 203, 213, 233.

=Hellebores= (_Helleborus_ sp.). Two poisonous species of hellebore may
on occasion be taken by live stock, though rarely—Stinking Hellebore
(_H. fœtidus_ L.) and Green Hellebore (_H. viridis_ L.). The much
esteemed Christmas Rose (_H. niger_) is also toxic, but unlikely to be
eaten by stock. In no case should trimmings of these plants from
shrubberies, etc., be thrown to stock—cows have died from eating such
trimmings. The two species first mentioned are equally toxic, all parts
are poisonous, and drying does not render them innocuous. Cornevin
records that animals have been killed by _H. fœtidus_, and says that 9½
oz. of the fresh root or 2½ oz. of the dried root are poisonous doses to
the horse, while 120 to 150 grains are fatal to sheep. It was recorded
in 1847 (_Veterinarian_) by Mayer that a horse was fatally poisoned
through eating five half-pints of the chopped-up leaves of this species
in two days in a bran mash. In regard to this species also Johnson and
Sowerby write: “The Bear’s-Foot has been used as a vermifuge ever since
the days of Hippocrates, notwithstanding its dangerous qualities. Every
part of the plant is a violent cathartic, but far too uncertain in the
degree of its action to be safely administered.”

_Toxic Principle._ Both species contain the poisonous glucosides
_Helleborin_ (C_{36}H_{42}O_{6}), a highly narcotic and powerful poison;
_Helleborein_ (C_{26}H_{44}O_{15}); and the alkaloid _Jervine_
(C_{26}H_{37}O_{3}N2H_{2}O).

_Symptoms._ The Hellebores are cathartic, narcotic, and drastically
purgative. Stupor is followed by death with spasms in the case of _H.
viridis_ (Pammel). In general there is in the horse and ox bloody
purgation, salivation, attempts to vomit, and excessive urination,
according to Lander, who cites Mayer as noting violent straining and the
discharge of frothy mucus, but no effort to vomit, the heart action
resembling that observed in Digitalis poisoning, showing periodic
intervals of arrest in systole.

Müller gives the symptoms in cattle and sheep after eating the leaves as
loss of appetite, nausea, and even vomiting, salivation, grinding of
teeth, wind, colic, bloody diarrhœa, decrepitude, giddiness, loss of
sensation, convulsions, and not seldom death.

Affected cows are stated to give bitter milk which has purgative effects
(Pott).

The poisoning of two cows by _H. viridis_ came under the notice of
Cornevin. There was observed loss of appetite, diarrhœa, tenesmus,
violent attempts to evacuate, which after 5 or 6 days resulted only in
the expulsion of glareous blackish matter; to the end the pulse was slow
and intermittent. The heart beats were weak, and after 5 or 6 beats
there was a stop equal in duration to at least a beat and a half. A
remarkable fact was the very gradual loss of condition, while the milk
secretion was maintained until the last day. In one case death occurred
after 12 days and in the other after 28 days.

                              REFERENCES.

          63, 81, 130, 140, 170, 190, 203, 205, 213, 233, 254.

=Larkspur= (_Delphinium Ajacis_ Reich.). In the United States of America
certain species of Larkspur are exceedingly harmful to live stock, and
it has been said that “with the exception of the Loco weeds there is
probably no poisonous plant on the cattle ranges of the West that has
caused such heavy losses to stockmen as has larkspur” (_Far. Bul. 53, U.
S. Dept. Agric._). _D. Ajacis_ is the only British species, occurring in
cornfields in Cambridgeshire, Sussex and elsewhere, and, like the
Continental species _D. Consolida_, must be regarded as poisonous and
fatal to cattle, while horses and sheep may also suffer. Sheep and
goats, however, appear to resist the poison unless taken in considerable
quantity. Wilcox fatally poisoned a yearling lamb within an hour of
administering per os the extract from less than 1 oz. of the dried
leaves of an American species. The seeds are the most dangerous part of
the Larkspur, and should never be ground up with wheat should the two
plants grow together. The seeds of _D. Staphisagria_ are used in
medicine.

_Toxic Principle._ The species _D. Ajacis_ has been little studied, but
_D. Consolida_ and _D. Staphisagria_ contain the alkaloids _Delphinine_
(C_{31}H_{49}O_{7}N), very poisonous and having a bitter taste;
_Delphisine_ (C_{31}H_{49}O_{7}N), which is extremely poisonous;
_Delphinoidine_ (C_{42}H_{68}N_{2}O_{7}), which is poisonous; and
_Staphisagrine_.

_Symptoms._ The seeds are stated to be emetic and purgative, and _D.
Consolida_ is stated by Pott to be an acute narcotic poison to horses
and cattle. In general the symptoms appear to resemble those produced by
_Aconitum_ (p. 15). There is salivation, vomiting, colic, convulsions,
and general paralysis (Müller).

                              REFERENCES.

          16, 63, 93, 128, 130, 190, 203, 204, 205, 213, 233.

=Monkshood= (_Aconitum Napellus_ L.). The extremely poisonous character
of this plant has been recognised since ancient times, and it is
mentioned by Pliny, Dioscorides, etc. It is not common in the wild state
in Britain—chiefly occurring in some Welsh and one or two West of
England counties—and is not very liable to cause poisoning of live stock
in Britain. Cases of poisoning of horses, cattle, sheep and pigs have
been recorded on the Continent, however (Cornevin), and cows died in
Victoria. Linnæus says that it is fatal to cows and goats when they eat
it fresh, but that when dried it does no harm to horses. Medical works
record many cases of human poisoning, particularly in cases where the
root has been mistaken for horse radish—from which, however, it markedly
differs. The leaves at first taste insipid and then sharply burning; the
root when fresh smells like the radish and has a slightly sweetish
taste, which is succeeded by characteristic tingling of the tongue and a
sensation of numbness in the mouth.

_Toxic Principle._ Monkshood is very poisonous, and though all parts are
toxic the root is the most dangerous, and next the seeds and leaves. The
plant seems to vary in toxicity with age and climate, being but slightly
active when very young, most active just before flowering, and at the
minimum of activity when the seeds ripen. The cultivated form is stated
to be much less poisonous than the wild one. Drying removes a part of
the toxic substance, and boiling removes most of it. The plant contains
the toxic alkaloid _Aconitine_ (C_{34}H_{45}NO_{11}), and also Aconine
(C_{25}H_{39}NO_{9}). The root contains 0·17 to 0·28 per cent. of
_Aconitine_, but the leaves and flowers less.

_Symptoms._ The chief symptoms are those of depression, and are
manifested through the nervous system and the circulatory and
respiratory organs. Tetanic symptoms are also present. There is loss of
appetite, salivation, inflammation of the mucous membrane of the mouth
and jaws, grinding of teeth, nausea and vomiting, great restlessness and
colic; the animal groans and walks with an uncertain gait owing to
bodily weakness, giddiness and paralysis of hind feet or of all limbs;
there is also a notable slackening in the pulse, breathing becomes
difficult, consciousness is lost and the pupils are dilated. Death
ensues in most cases within a few hours, and after convulsions.

Kaufmann (quoted by Cornevin) observed in the _horse_ champing of the
jaws, salivation, fibrillous contraction of the muscles of the
olecranon, then of the buttocks, then of the whole body. The intestinal
pains were shown by the blows of the animal’s hind feet under and at the
back of the belly. There was also observed an intense and painful
contraction of the muscles in the inferior cervical region, the hyoid
and the abdomen; an increased sensibility; repeated evacuations; at
first congestion, then great paleness of the mucous membranes;
diminution in the volume of the arteries; faint whinnyings at the moment
of the contraction of the muscles of the neck, shoulders and stomach;
muscular rigidity of the posterior limbs; uncertain gait; laboured
breathing; and finally paralysis of motion, respiration and senses.

Lander in giving similar symptoms for the horse notices also choking
movements of the œsophagus, eructation of frothy matter, dilatation of
pupils and low temperature.

Kaufmann gives the poisonous doses of powdered root for the horse and
dog as 13 to 14 oz. and ⅙ oz. respectively.

                              REFERENCES.

    4, 16, 63, 78, 81, 128, 130, 153, 161, 170, 203, 205, 213, 233.


                              PAPAVERACEÆ.

=Poppies= (_Papaver_ sp.). Poisoning by the two common poppies (_P.
Rhoeas_ L. and _P. dubium_ L.) is not common, but Cornevin says that the
former is poisonous in all its parts, and sufficiently so to cause
accidents every year. Animals may be affected by eating the plant when
mixed with green fodder, or by ingesting the seeds and capsules with
waste material after the winnowing and grading of cereals. Stock,
however, will most likely reject the plants, owing to their unpleasant
odour and taste, but cattle have been poisoned by eating unripe heads of
_P. Rhoeas_ when the plant was mixed with clover and sainfoin. _P.
dubium_ has caused poisoning of horses, cattle and pigs.

_Toxic Principle._ Both species contain the alkaloids _Morphine_
(C_{17}H_{19}NO_{3}) and _Rheadine_ (C_{21}H_{21}NO_{6}), which are
present in the milky juice of the plant. The latter, which was isolated
by Hesse, is believed to have no narcotic effects. The toxic principle
is not destroyed by heating, and the plant is therefore poisonous both
in the green state and when dried in hay.

_Symptoms._ It is remarked by Cornevin that cattle poisoned by _P.
Rhoeas_ at first exhibit symptoms of excitement, shown by continual
movement, by pawing of the soil or litter, increased respiration and
more rapid pulse; this is followed by stoppage of the digestive
functions, sometimes a little swelling of the eyelids, and coma, one
affected animal appearing to sleep while standing, remaining motionless,
and if forced to move walking in an unsteady manner. Finally, the animal
falls, and if a fatal result is likely (which is unusual) it remains
stretched on the ground; respiration becomes slower, the temperature
falls, and after a few convulsive movements death occurs owing to
asphyxia.

Müller notes excitement, wildness of look, dilatation of pupil,
convulsions; then coma, loss of sensation and symptoms of depression
replace those of excitement. There is salivation, bloating,
constipation, and in many cases also bloody diarrhoea. Death, however,
is rare.

Pott gives stupidity, retention of urine, colic, with sickness and
diarrhœa, convulsions, and epileptic symptoms, the animals falling over
and rolling.

                              REFERENCES.

                  4, 16, 63, 128, 190, 205, 213, 262.

=Greater Celandine= (_Chelidonium majus_ L.). This common plant exhales
an unpleasant odour, and when bruised or broken shows the presence of a
yellowish acrid juice, which becomes red immediately on exposure to the
air. It is an old medicinal drug plant, but is dangerous, being emetic
and purgative, with a strongly irritating effect on the digestive tract.
Animals are but rarely likely to take it, and no record of the death of
domesticated animals has been found.

_Toxic Principle._ Among the substances contained in the Greater
Celandine may be mentioned the bitter alkaloid _Chelidonine_
(C_{20}H_{19}NO_{5} + H_{2}O), which, especially occurring in the root,
does not appear to be poisonous, or is of feeble activity; the alkaloid
_Chelerythrine_ (C_{21}H_{17}NO_{4}), which is poisonous; and
_Protopine_ (C_{20}H_{19}NO_{5}). It is stated by Cornevin that the
toxic substance is not removed on drying, but Pott (1907) remarks that
the dried plant is harmless to animals, the poisonous alkaloid being
volatile and disappearing on drying.

_Symptoms._ The action of this plant is acrid, irritant and narcotic,
emetic and purgative. Esser remarks that when Chelerythrine is
introduced on the nasal mucous membrane it causes violent sneezing, and
taken internally causes vomiting. Müller says that poisoning of
domesticated animals is not recorded, but that according to old accounts
500 grammes (about 1 lb.) of the fresh plant eaten by the horse will at
most cause slight diabetes.

                              REFERENCES.

               16, 63, 81, 128, 141, 190, 203, 205, 213.


                               CRUCIFERÆ.

=Charlock= (_Brassica Sinapistrum_ Boiss.), also known as _B. Sinapis_
Visiani and _Sinapis arvensis_ L., may be regarded as harmless in the
young state, but liable to cause injury after flowering, when the seeds
have formed, when it may occasion serious accidents if eaten by live
stock. A case in which rape cake containing the seeds of charlock caused
poisoning was recorded in 1875 (_Jour. Roy. Agric. Soc._). The seeds
only are dangerous.

_Toxic Principle._ The seeds contain minute quantities of volatile _Oil
of Mustard_ or _Allyl-isothiocyanate_ (C_{3}H_{5}NCS), the alkaloid
_Sinapine_ (C_{16}H_{23}NO_{5}), and the alkaloidal glucoside
_Sinalbin_.

_Symptoms._ Ingestion of the seeds may cause inflammation of the stomach
and intestines (with loss of appetite, wind, colic, and diarrhœa);
inflammation of kidneys (difficult, excessive or bloody urination); and
nervous symptoms, with great exhaustion, uncertain gait, paralysis of
limbs and in isolated cases convulsions (Müller).

Pott also records increased salivation.

In the _horse_ Cornevin records great depression, difficult and
accelerated respiration, yellowish mucus and convulsive cough. A
characteristic symptom is the emission of frothy liquid through the
nostrils (as much as 10 litres in one hour). Death often occurs from
asphyxia in a fit of coughing.

In _cattle_, cake containing the seeds caused inflammation of the
intestines, exhausting diarrhœa, and unquenchable thirst.

The cultivated Mustards may induce similar effects, and Lander records
the following symptoms as caused by _Brassica nigra_:—In the _horse_,
bronchial symptoms, marked by difficulty in breathing and the discharge
of great quantities of yellowish frothy matter from the nose; in
_cattle_, uneasiness, restlessness and intense colic, with frantic
rushing about and mania, ending in exhaustion, falling, struggles and
collapse; in a recent case there were dullness, coldness, some tympany,
laboured respiration, staggering and falling, and in fatal cases,
immobility and a semi-comatose condition.

                              REFERENCES.

              4, 16, 63, 76, 127, 170, 190, 205, 213, 219.

=Wild Radish= (_Raphanus Raphanistrum_ L.). As in the case of charlock,
the seeds of wild radish are very acrid, and susceptible of introducing
intestinal troubles if eaten by animals when mixed with cereals.

=Garlic Mustard= (_Alliaria officinalis_ Andrz.) and =Treacle Mustard=
(_Erysimum cheiranthoides_ L.). The seeds are stated to have properties
similar to _Brassica Sinapistrum_ (p. 18) owing to a pungent oil; and
when eaten in quantity to induce poisoning, inflammation of the
digestive tract and of the kidneys, as well as nervous symptoms
(Müller).


                            CARYOPHYLLACEÆ.

=Soapwort= (_Saponaria officinalis_ L.). This plant is more or less
poisonous, but is rarely, if ever, eaten by stock, and no recorded case
of the poisoning of stock has been met with.

_Toxic Principle._ The whole plant, especially the root, contains the
poisonous glucosidal _Saponin_ (C_{18}H_{28}O_{10})_{4}, a peculiar
substance which causes intense frothing when stirred in water.

_Symptoms._ No symptoms of animal poisoning by the plant are recorded,
but the action of Saponin in the blood stream is to induce dissolution
of the red cells, with stupefaction and paralysis, as in the killing of
fish by poisoning. It also causes vomiting and purging. Taken by the
mouth it causes inflammation of the alimentary tract, the contents of
which are fœtid and mixed with blood.

                              REFERENCES.

                       16, 63, 76, 81, 203, 235.

=Corn Cockle= (_Agrostemma Githago_ L.). This well-known plant of
cornfields must be regarded as poisonous, though experiments and reports
as to its effects on the different classes of live stock vary widely.
Though a poisonous principle is found in nearly all parts of the plant,
the plant in the green state appears to be innocuous, and is in any case
rarely likely to be eaten fresh by stock, which probably refuse it on
account of its hairy character. The seeds, however, are by no means
harmless. They are rather large, and somewhat troublesome to separate
from cereal grains. When ground up with wheat they both discolour the
flour and impart a grey tint and disagreeable odour to bread made from
it. Further, flour containing a considerable quantity of cockle must,
owing to the poisonous character of the latter, be held to be unfit for
consumption. Fatal results have followed the use of bread containing
Corn Cockle. The toxic principle therefore is not destroyed by heating,
even in an oven in baking.

As regards domestic animals, Corn Cockle seeds have frequently been
mixed with feeding stuffs and have caused many deaths. Cornevin’s
experiments in feeding calves, pigs and fowls led to fatal results. He
was able to say that the amounts of cockle flour necessary to cause
death were:—

                 Calf 0·25 lb.│per 100 lb. live weight.
                 Pig  0·10  „ │           „
                 Dog  0·90  „ │           „
                 Fowl 0·25  „ │           „

Among other cases, Kornauth and Arche found that in their feeding trials
pigs were not killed, but albuminoid metabolism was diminished and fat
production increased. In 1893 pigs died in Germany with symptoms of
acute poisoning, when fed on tailings containing six per cent. of
cockle. In 1903–4 experiments showed that with the cow, sheep, pig and
goat, cockle is not poisonous when fed in amounts usually found in
feeding stuffs. Millspaugh gives a case in which two calves died on
being fed with two lots of 14½ oz. each of wheat flour containing 30 per
cent. and 45 per cent. of cockle seeds. About 1892 Nevinny concluded
that six grammes of cockle seed consumed in 1200 grammes of bread were
beyond doubt poisonous in effect, and that the sale of grain or flour
containing it should be forbidden. Kobert held that the sale of feeding
stuffs containing cockle should be forbidden by law. An extensive study
of this question was made by Pesch, who concluded that “Under certain
conditions Corn Cockle is injurious to domestic animals. The amount of
the poisonous substance in the seed is variable, depending probably upon
the season and the soil. Animals become accustomed to it, so that
amounts of seed which at first cause sickness, later have no injurious
effect. The susceptibility of animals to the poison varies both with the
species and the individual. Young animals are more readily affected than
older ones. It is believed that rodents and sheep are not susceptible,
and, as far as is known, grown cattle are only slightly or not at all
affected by the poison. Calves, swine, horses, and especially dogs, are
more or less susceptible. Concerning birds and fowls there is some
doubt.”

Though animals are reputed to become tolerant of the poison if the
cockle is only taken in small regular doses, yet there appears to be a
chronic form of poisoning due to this cause and termed _Githagism_,
while there is an acute poisoning due to the ingestion of large
quantities of the seeds which may cause death in 24 hours or less.

It is clear that the evidence is quite sufficient to warrant the
statement that the ingestion of more than a very small quantity of
cockle seed is dangerous, and the consumption of even small quantities
should be avoided. Thus care should be taken to remove the seeds from
cereal grains.

_Toxic Principle._ The dangerous substance contained in cockle seeds
is the glucoside variously known as _Githagin_, _Saponin_,
_Agrostemmin_, _Sapotoxin_, _Agrostemma-Sapotoxin_, or _Smilacin_
(C_{17}H_{26}O_{10})_{2}. This principle appears to occur chiefly in
the seeds, which contain up to 6·56 per cent., but it has been found
in small quantities in other parts of the plant. It is very freely
soluble in water, in which it froths like soap when shaken up, and it
has a sharp taste and no odour.

_Symptoms._ A sufficient quantity of the toxic substance may cause
nervous debility and dysentery—according to Chesnut “intense irritation
of the digestive tract, vomiting, headache, nausea, vertigo, diarrhœa,
hot skin, sharp pains in the spine, difficult locomotion, and depressed
breathing. Coma is sometimes present and may be followed by death. In
animals chronic diarrhœa and gradual depression.”

The chronic form, which occurs when small doses are repeated over a long
period (practically the only form found in human beings, but never in
animals, except perhaps in the pig) is characterized by gradual wasting
away, loss of breath, loss of strength, chronic diarrhœa, and nerve
troubles, death taking place in marasmus and decline. The active
principle acts as an irritant on the digestive tract, causing colic,
diarrhœa and enterorrhagia.

Cornevin describes the symptoms in the acute form of the poisoning in
the case of horses, cattle, pigs and dogs.

In the _horse_, if a small quantity only is taken, there is yawning,
heavy colic, stamping and evacuation of rather soft fæces. If larger
quantities are taken, the symptoms, which commence in about an hour, are
salivation, frequent yawning and turning of the head, colic, pale mucus,
hurried and weak pulse, rise in temperature and accelerated respiration.
Some time later there are muscular tremors succeeded by pronounced
rigidity, and the fæces are diarrhœic and fœtid. The animal lies down,
and getting up is painful; it falls into a kind of coma, stretches
itself to the utmost, and death takes place without convulsions.

In _cattle_, the symptoms observed one hour after eating are
restlessness, salivation, and grinding of the teeth. Excitement and
colic are followed sometimes by coughing, this state lasting from five
to eight hours. There is then a period of coma, characterized by
permanent decubitus, repeated fœtid diarrhœa, hurried and plaintive
respiration, accelerated and gradually weakening pulse, a gradual loss
of motor and sensory powers, and a progressive decline in temperature.
Death occurs in twenty-four hours.

In the case of _pigs_, the animal grunts, lies down and remains thus
with its snout embedded in the straw. There is vomiting, more or less
violent colic and diarrhœa, the evacuation consisting of bad-smelling,
spumous fæcal matter. At times there are clonic contractions. Young pigs
are most susceptible.

Pott cites cases in which abortion was a feature of the poisoning, both
in cows and pigs. The results of numerous experiments which he quotes
(among others some carried out for the Prussian Ministry of Agriculture)
are very contradictory, a small quantity causing death in some animals,
while others of the same species were left unharmed by large quantities.
He ascribes this to the very variable proportions of the poison present
in the seeds.

                              REFERENCES.

  4, 16, 28, 46, 52, 53, 63, 76, 81, 82, 144, 161, 172, 184, 190, 203,
                             205, 213, 249.


                              HYPERICINEÆ.

=St. John’s Wort= (_Hypericum perforatum_ L.). There appears to be no
record of poisoning of live stock by this plant in Britain, but Cornevin
records that it injured breeding mares fed on lucerne containing it in
large proportion. Drying in converting into hay did not render it
innocuous. It is only poisonous if eaten in considerable quantity, and
in general animals are not likely to eat much of it voluntarily, owing
to its resinous odour when crushed, and a bitter and slightly saline
taste.

_Toxic Principle._ The poisonous properties of St. John’s Wort have not
been fully investigated, but it is stated to contain an oil and an acrid
bitter resin. Ewart says that it “contains an oil whose medicinal value
was formerly highly esteemed; but this oil, and the woody nature of the
plant, render it somewhat injurious in fodder.” Summers says (_Journ.
Agric. S. Australia_, Sept. 1911, p. 144) that “it is reported to be
decidedly injurious, causing horses who eat it to break out in sores,
while milk cows have a tendency to dry off owing to its effect on the
system.”

_Symptoms._ In mares, dullness, sinking of head, loss of appetite,
slackening of pulse and respiration, dilatation of pupils, defective
sight, and lips purple (Müller).

                              REFERENCES.

                         63, 82, 117, 190, 203.


                              GERANIACEÆ.

=Wood Sorrel= (_Oxalis Acetosella_ L.). Though rarely likely to be eaten
by stock this plant must be mentioned here, as it is considered
dangerous on account of its high content of oxalates, which may cause
serious illness and diarrhœa, and in the case of sheep even be fatal.
Pott says that the milk of cows eating it is with difficulty converted
into butter.

                               REFERENCE.

                                  213.




                              CHAPTER III
                              CELASTRACEÆ.


=Spindle Tree= (_Euonymus europæus_ L.). According to Cornevin the
spindle tree is poisonous in all its parts, especially the fruits, which
are emetic and strongly purgative. Sheep and goats have been injured
from eating the leaves, and children have suffered from eating the
fruits.

_Toxic Principle._ This plant does not appear to have been closely
studied from the toxicological point of view; contrary to the statements
generally made in the literature Van Rijn remarks that this species does
not contain the doubtfully classed _Euonymin_.

_Symptoms._ Ingestion of the plant induces symptoms and lesions such as
are due to violent vegetable purgatives.

                              REFERENCES.

                           63, 81, 205, 252.


                               RHAMNACEÆ.

=Buckthorn= (_Rhamnus Catharticus_ L.) and (_R. Frangula_ L.). The
berries of both species are toxic and purgative, but both are uncommon
and rarely eaten by stock.

_Toxic Principle._ The berries and bark contain the glucosides
_Frangulin_ (C_{21}H_{20}O_{9}) and _Rhamnetin_ (C_{16}H_{12}O_{7}).

_Symptoms._ The berries are purgative, and there is some danger from
large quantities, which may induce superpurgation. The leaves are
astringent and may arrest milk secretion (Cornevin). Müller states that
the inflammation of the stomach and intestines may terminate fatally.

                              REFERENCES.

                          4, 63, 76, 190, 203.


                             PAPILIONACEÆ.

=Laburnum= (_Cytisus Laburnum_ L.). The well-known and much admired
Laburnum must be regarded as one of the most poisonous species of
British plants. By numerous experimental researches Cornevin proved that
all parts of the plant are poisonous—root, wood, bark, leaves, flowers,
and seeds, especially the seeds. In his experiments the horse, ass,
sheep, goat, dog, cat, fowl, duck and pigeon, were utilized, seeds being
given. He found that 80 centigrammes per kilogramme live weight would be
necessary to kill a horse (say 1 lb. for an animal of 1200 lb. live
weight), 60 centigrammes per kilogramme live weight to kill an ass (say
6 oz. for an ass weighing 600 lb.); and 6 grammes in the case of a fowl
(say 0·4 oz. for a fowl weighing 4½ lb.). The sheep and goat he was not
able to kill, as they refused the food after a certain point; the dog
and cat he was not able to kill because they so readily vomited; and the
duck and pigeon vomited with extreme facility.

Many cases of the poisoning of children have occurred through the
ingestion of the flowers and seeds. In 1908 a case was recorded by the
Board of Agriculture and Fisheries, in which two horses were alleged to
have been poisoned in North Wales by laburnum seeds, a very small
quantity of which was found in their stomachs after death.

Müller states that in Dalmatia goats which had eaten _Cytisus Weldeni_,
though themselves uninjured, produced milk which was poisonous to man.

_Toxic Principle._ All parts contain the toxic alkaloid _Cytisine_
(C_{11}H_{14}N_{2}O), said by Moer and Partheil to be identical with
Ulexine; it is found in the seeds to the extent of 1·5 per cent.
Cornevin states that the root, wood and bark are nearly constant in
toxicity, but that the leaves and pods present remarkable seasonal
variations owing to the migration of the poison into the seeds. The
toxic property is not destroyed by drying of the plant.

_Symptoms._ Laburnum poisoning is of the acrid, narcotic type, with, in
man, nervous symptoms, abdominal pain, vomiting, purging, tetanic spasms
and convulsions.

Cornevin’s observations show that the symptoms occur in three
consecutive stages,—(1) excitement, (2) coma and incoordination of
movement, and (3) convulsions. The order of the appearance, their
duration, and the association of each with the others depend upon the
susceptibility of the animal and the quantity ingested. Thus the
symptoms of excitement may be present alone if only a small quantity is
eaten; the duration of the symptoms in this case is never considerable,
and the normal is gradually regained. In general, however, the symptoms
are associated in pairs; thus when an average quantity is fed there is
excitement and coma but _no_ convulsions; when large quantities are fed
the first stage is suppressed or is so short as to be almost
imperceptible, the coma and convulsions being present simultaneously. As
regards temperature, there is, in stage (1) a rise, in stage (2) a drop,
and in stage (3) a rise again near death. In stages (2) and (3) there is
a slackening of respiration, the arterial tension is raised, there is an
increase in the number of pulsations and a modification of the rhythm.
In stage (3) near death there is a lowering of the arterial tension, and
the pulsations become gradually less perceptible, but with a uniform
rhythm; there is a slackening in respiration, and by the time this
finally ceases the heart beats have become imperceptible.

When _horses_, _asses_ or _mules_ have eaten a small quantity of the
seeds or leaves, there is simply yawning and uncertain gait, these
symptoms lasting for two hours, and the normal being regained after
urination. Considerable (but not fatal) quantities cause unsuccessful
attempts at vomiting, sometimes opisthotonos in asses, sweating,
muscular tremors, and then a deep coma which may last 15 hours. Fatal
quantities cause yawning, sexual excitement, accelerated and noisy
respiration, wheezing, muscular tremors followed by contractions which
commence in the posterior limbs and spread to the anterior limbs, facial
contractions, staggering and copious sweating. A rapid fall in
temperature follows, but there is a slight rise during the period of
convulsions; the pulse is at first quicker and stronger, but the number
of beats rapidly comes back to the normal, to rise again shortly before
death; the rhythm of the pulse is at first regular (in groups of 2, 3 or
4) but becomes irregular again just before death. The animal at length
falls, and cannot get up, the nostrils are distended, the mouth is wide
open, respiration becomes gradually slower, and death takes place in
great agony.

In cases of poisoning of horses and asses noticed by Pott animals that
could not vomit died very quickly. The symptoms were excitement, nausea,
coma, slower breathing, convulsions, paralysis of the motor nerves, and
finally cessation of the action of lungs and heart.

_Ruminants_ are much less susceptible than horses. Cornevin’s attempts
at poisoning failed through their refusal of the plant. Müller observed
in a case of cattle poisoning, bloating, paralysis of the limbs
(especially fore limbs), sleepiness, dilatation of pupils, and later
salivation, nausea, coma and occasional convulsive movements of the
muscles of the extremities. These symptoms persisted through several
days and then disappeared.

                              REFERENCES.

            4, 16, 63, 64, 81, 128, 144, 161, 190, 205, 213.

=Broom= (_Cytisus Scoparius_ Link.). This very plentiful and widely
distributed plant is undoubtedly to some extent poisonous, though
perhaps only feebly so in the quantities likely to be eaten by domestic
animals. Blyth records 400 cases of poisoning from it, however. Very
hungry animals might eat too much of it, and hence show symptoms of
poisoning.

_Toxic Principle._ The plant contains the alkaloid _Cytisine_
(C_{11}H_{14}N_{2}O); also the volatile alkaloid _Sparteine_
(C_{15}H_{26}N_{2}), a single drop of which, according to Blyth, killed
a rabbit, which showed symptoms similar to those of nicotine poisoning.

_Symptoms._ Taken in sufficient quantity broom induces narcotic
poisoning, with symptoms resembling those caused by Coniine, with
central nervous paralysis.

Cornevin gives the symptoms as similar to those due to _C. Laburnum_.

                              REFERENCES.

                          4, 16, 82, 128, 203.

=Indian Peas= (_Lathyrus sativus_ L.). A type of poisoning that deserves
attention here is that known as _Lathyrism_, since it is due to the
consumption of peas of the genus _Lathyrus_, the most dangerous being
the “Indian Pea,” _L. sativus_. The peas of this plant (see
Frontispiece) are small and dark-coloured, and are imported largely from
India and other countries under the general name of Mutter peas, a name
which they share with the ordinary pea _Pisum sativum_. In addition to
the seeds of this species the seeds of two South European and North
African species—_L. Cicera_ and _L. Clymenum_—have commonly caused
poisoning both in man and in animals, not infrequently leading to fatal
results. Horses, cattle, sheep and pigs have been affected—horses
particularly so—and many cases have been recorded in the veterinary
journals since 1885. Very heavy losses have occasionally resulted from
the use of the raw peas as a food for stock. For example, in 1884
Messrs. Leather of Liverpool had 35 out of 74 cart horses ill through
eating Indian peas at the rate of 3 to 4 lb. per head per day. Of the 35
no less than 19 died, and 2 were slaughtered, while 14 recovered. In the
famous Bristol Tramways case (1894) 123 out of 800 horses became ill
owing to being fed on the peas of _L. sativus_, and many died. There are
few records of harm to cattle, sheep and pigs, and Watt quotes Don to
the effect that pigeons lose their power of flight by feeding on the
peas. Very large quantities of the peas are used for feeding purposes,
and the fact that the losses are not larger is probably because the peas
only comprise a small proportion of the ration or are cooked before use.

After boiling or roasting the peas appear to be less harmful, as they
are eaten in India when cooked, or ground into flour and converted into
bread—though Cornevin states that drying and cooking does not destroy
the toxicity, while boiling for some time showed that at any rate part
of the toxic substance passed into the water, which became toxic and
caused death, the boiled seeds losing the greater part of their
poisonous property and not causing accidents when the water was
rejected. MacDougall states that as far as experimental evidence was
available (1894) it seemed to show that boiling the seeds before use
renders them innocuous.

Lathyrism usually only supervenes when the use of the peas for food is
prolonged, and the peas are taken in considerable quantity, but it is
possible that there is wide variation in the toxicity of different
samples, owing to differences in soil, climate, and other factors. In
man, Lathyrism is stated to be common in Spain, Italy, Russia and India,
owing to continued use of bread from flour of the three species of
_Lathyrus_ mentioned above. It is said especially to affect males.

_Toxic Principle._ Nothing certain as to the poisonous properties is
known, attempts to isolate the toxic substance having failed (Kobert),
though Smith gives it as prussic acid, apparently indicating a
cyanogenetic glucoside. This, however, can hardly be so, as the poison
is cumulative, and may not show its effects for weeks or months, or, in
man, even years—according to the quantity of peas eaten.

_Symptoms._ Lathyrism is only produced when the ration consists largely
of the pea for a considerable period (see above); in the horse fed
exclusively on the pea, the tenth day; but when one or two quarts are
given daily, only towards about the 80th day. Moreover, the malady may
declare itself as long as fifty days after the cessation of the pea
feeding (Lander).

In general Lathyrism is marked by paralysis of the lower extremities in
man and the hind limbs in animals, owing to the degeneration of the
muscle fibres, and possibly to affection of the nerves. In _horses_
there is paralysis of the hind limbs, dyspnœa and roaring—with paralysis
of the recurrent laryngeal nerve, and transverse myelitis. The horse
thus shows weakness of the hind quarters, staggering in the effort to
stand, difficulty in breathing, abnormally fast and irregular pulse,
open mouth, distended nostrils. Tracheotomy often gives almost immediate
relief.

Lander mentions in cart horses grinding of teeth, and convulsive
movements of the eyes, recalling epilepsy. In one outbreak there was
thick wind, staggering gait, weakness of hind quarters, and general
signs of intoxication; and sudden violent attacks of laryngeal paralysis
and dyspnœa during which there was palpitation, frothing, tongue
protruded, eyes staring, bluish tint of buccal membranes, and
palpitation. Paroxysms sometimes proved fatal.

An attack among 125 _lambs_ is mentioned by Cornevin. The lambs could
not stand on their fore legs and were obliged to go down on their knees.
On setting them up again, they were only able to keep up while
motionless or moving slowly. There was loss of sensibility in the front
members. In spite of this the eye was alert, they were attentive to
everything that went on around them, and were easily frightened.

In _pigs_ paralysis of posterior members has been observed.

In _cattle_ there was staggering, blindness, and stiffness of the lower
joints. In _sheep_ and _pigs_ there was also paralysis of the hind
limbs.

                              REFERENCES.

                 63, 82, 137, 170, 179, 190, 203, 205.

=Yellow Vetchling= (_Lathyrus Aphaca_ L.). To what extent this vetchling
is poisonous to stock is not clearly known, but it is cultivated in
India as a fodder for cattle. The seeds, however, are not altogether
safe when ripe, and MacDougall says “The seeds and pods have been known
to be used in soup in their young state and without harm resulting, but
the ripe seeds are narcotic and cause sickness and headache.”

=Lupines= (_Lupinus_ sp.). Different species of _Lupinus_ have been
found to cause poisoning of live stock, more particularly sheep, which,
when fed largely on lupines, develop a chronic type of poisoning known
as _Lupinosis_, or poisoning may be acute and rapid in its effects, as
in the United States. Records of large numbers of sheep being affected
at a time date from 1872, in various parts of the German empire. In
Europe by far the most harmful species is the Yellow Lupine (_L.
luteus_), which has been the cause of heavy losses of sheep, though
horses, cattle and goats may also be affected. The Blue Lupine (_L.
angustifolius_) and White Lupine (_L. albus_) may also be toxic. _L.
luteus_ has caused lupinosis in Germany since 1860, and Cornevin states
that in 1880 no less than 14,138 out of 240,000 sheep fed upon it (or
5·89 per cent.) died. Of 44 horses affected 11 died.

It must not be thought that all crops of lupine are poisonous, as
lupines are extensively grown on the Continent for fodder purposes and
are usually harmless. Even where Lupinosis occurs, considerable
quantities of the lupine must be ingested to cause poisoning. The
toxicity appears to vary according to soil and certain indefinite
conditions, and sometimes even a kilogramme (2·2 lb.) of the plant would
suffice to kill a sheep. Poisonous symptoms may sometimes be observed
after a single meal. Desiccation does not render the plant innocuous,
the seeds and hay being poisonous.

In the United States species of _Lupinus_ have caused great loss. In
1898 no fewer than 1,150 of a flock of 2,500 sheep died from eating one
species; one sheep farmer lost 700 sheep from the same cause; and 1,900
out of 3,000 sheep died from Lupine poisoning in Montana in 1900. Lupine
hay is found to be less harmful to horses and cattle, and Chesnut and
Wilcox suggest that this is possibly because as a rule they avoid the
pods, while sheep eat them. Lupines in America are very rapid in their
action on sheep, which may often die in one-half to three-quarters of an
hour after eating a quantity of the pods. Further, there is evidence
that sheep may gradually become immune to the poison by eating Lupines
regularly, since sheep fed regularly on hay nearly half lupine were
unaffected, but others eating the same hay for the first time died in
considerable numbers. The lupines are certainly far the most dangerous
when they bear ripe seeds—cut and made into hay before the pods form
they are much less dangerous.

In regard to _L. luteus_ Lander says: “According to the German
authorities a daily ration of 1 pound of the whole plant, ⅗ pound of
empty pods, or 1⅕ pound of seeds, will produce poisoning.”

Various means have been tried to render Lupines harmless, and success is
stated to follow heating with steam under a pressure of 2 to 2½
atmospheres.

_Toxic Principle._ A very full account of Lupine poisoning is given by
Pott, and from this a brief summary may be made. Siewert and Wildt
(1879) found two substances very like the alkaloids of _Conium
maculatum_—one like Coniine and the other like Conhydrine, the former
only being proved to be very poisonous. Baumert states that in _L.
luteus_ there are only two bitter alkaloids, _Lupinine_ (C_{10}H_{19}ON)
and _Lupinidine_ = _Sparteine_ (C_{15}H_{26}N_{2}). Many investigators
(_e.g._ Kühn at Halle) held that lupinosis was not identified with the
presence of lupine alkaloids. Then, in 1883, Arnold and Schneidemühl
caused the disease (lupinosis) in sheep with lupines freed from all
alkaloids, and they isolated from the seeds a substance they named
_Lupinotoxin_, which they found to be poisonous. The nature of the
poison cannot yet be said to be fully understood. The Lupine does not
always appear to be poisonous—only under certain conditions which are
not too well defined. One farmer had Lupines on the same soil for twelve
years without ill effects when fed to sheep, and then of 450 sheep 120
were severely ill, and 80 died; they had had unthrashed Lupine, not
quite ripe, to the extent of one-fourth of the ration. It is held to be
definitely established that the presence of this poison is due in turn
to the presence of a saprophytic fungus; when the fungus is absent or
only present in small quantity the lupine is not at all or only slightly
poisonous.

_Symptoms._ The disease is either acute or chronic according to the
amount of poison ingested. Most writers describe the disease in sheep,
but symptoms given vary somewhat.

In the acute form sheep become ill suddenly. There is loss of appetite,
dyspnœa, intense fever, hæmaturia, circulatory and digestive troubles,
grinding of teeth and trembling, which may pass into spasmodic
contractions. Vertigo is sometimes present. Jaundice then appears and is
evidenced by the yellow colour of the mucous membranes. Tumefaction of
the eyelids, lips and ears is common, but not invariably present.
Micturition is frequent, but not abundant, and the urine contains
albumen; the excrements are few and dry. There is collapse, and loss of
condition progresses rapidly, death occurring on the fourth to the sixth
day after the commencement of the illness.

In the chronic form the interstitial hepatitis predominates. Tumefaction
of the head may also appear as in the acute form. Digestive troubles
indicate chronic gastro-enteritis. This condition lasts for from 15 to
20 days, during which the cephalic œdemæ are eliminated by gangrene and
the animals remain listless and without appetite. The illness in sheep
is grave, and affected animals are rarely completely cured. The
mortality in other species does not seem to be less than in sheep.
(Cornevin.)

In describing the acute form of lupinosis Pammel adds that the initial
temperature may be as high as 104° to 106° F., but that it is
intermittent and gradually falls just before death. The pulse may reach
130 per minute and the respirations 100. A bloody froth may issue from
the nostrils. Animals apparently prefer the recumbent position, extend
the head on the ground, and seem entirely oblivious to all surroundings.
At first there is constipation, but later diarrhœa may set in and the
excreta be tinged with blood. In the chronic form the symptoms are not
so violent. Jaundice may be entirely absent, and emaciation and anæmia
may be the chief signs.

Chesnut and Wilcox record a case in which two sheep were each given 150
medium-sized pods of a native lupine, and seemed to like them. In 45
minutes, however, they became frenzied and died an hour later. They give
the symptoms as practically the same as those caused by European species
of _Lupinus_; acute cerebral congestion, with great mental excitement,
the sheep rushing about and butting into things; following is a stage
characterized by irregularity of movement, violent spasms, and falling
fits; in most cases collapse and death occur within half-an-hour to an
hour and a half; the pulse is strong and regular; the convulsions
resemble to some extent those caused by strychnine; the excretion of the
kidneys is much increased and sometimes bloody. In post-mortem
examination the kidneys are found affected, the lungs slightly
congested, the cerebral membranes in all cases congested, and in violent
cases small blood vessels are ruptured in different parts of the body.

                              REFERENCES.

  4, 16, 20, 21, 42, 57, 63, 69, 82, 93, 128, 161, 166, 170, 190, 203,
                                  213.

=“Java” Beans= (_Phaseolus lunatus_). Though not native to Great
Britain, the so-called Java Beans have been imported in considerable
quantities for stock feeding, and in the past nine years have caused the
death of a large number of animals. For example, in March, 1906, the
Board of Agriculture and Fisheries published an account of the poisoning
of animals by these beans at eight centres; at six of the centres 133
cattle were involved and 43 died. The beans are of varying origin, and
pass under the name of Java beans, Rangoon beans, Burma beans, Lima
beans, and Paigya beans. They are considerably different in colour
according to origin, the _Java_ beans being pale brown to almost black;
_Rangoon_, _Burma_ or _Paigya_ beans smaller, plumper, and lighter in
colour (“red Rangoon beans” are pinkish with small purple splotches, and
“white Rangoon beans” are pale cream); and _Lima_ beans are much larger
than the last-named and pale cream or white in colour (see
Frontispiece).

It has long been known that beans of certain forms of _Phaseolus
lunatus_ are poisonous, and the fact is noted by Church (_Food Grains of
India_, 1886), and by Watt (_Dictionary of the Economic Products of
India_, 1889–96). The coloured forms, and particularly the wild forms,
are the most dangerous, the white types being in general safe for stock
feeding. Some forms have a general similarity to butter beans and
haricots, and have hence been favourably regarded by farmers, but it is
a sound plan to purchase under a guarantee beans with such names as
those given.

_Toxic Principle._ It was shown in 1903 (_Proc. Roy. Soc._, Vol. 72)
that the seeds of _P. lunatus_, uncultivated in Mauritius, contained a
cyanogenetic glucoside, _Phaseolunatin_ (C_{10}H_{17}O_{6}N). This
glucoside, under favourable conditions, such as are present when the
beans are moist, masticated and ingested at the temperature of the
animal body, gives rise to prussic acid, which is the direct cause of
poisoning. The seeds of the wild forms yield, like bitter almond seeds,
considerable quantities of prussic acid, while the cultivated forms
resemble sweet almonds in yielding only traces of the acid, or none at
all. Determinations of the yield of prussic acid by various
investigators show percentages of from 0·027 to 0·137 in _Java_ beans,
and 0·004 to 0·02 in _Burma_ beans. The largest proportion therefore
occurs in the coloured beans, while the white forms contain much less or
none at all, and may be generally regarded as safe for stock.

_Symptoms._—The symptoms given by Damman and Behrens (_Veterinary
Journal_, 1906) were vertigo, tympany, and falling, with death in most
cases. Mosselmann (_Vet. Jour._, 1908) observed the symptoms due to the
ingestion of a small quantity of the beans by six head of cattle. They
were: great excitement, salivation, swelling, slight diarrhœa, quick
pulse and respiration, muscular spasms, and paralysis of the hind
quarters in one instance; all recovered rapidly.

                              REFERENCES.

              5, 38, 76, 77, 107, 109, 125, 129, 144, 255.

=Castor Oil Plant= (_Ricinus communis_ L.). The beans (see Frontispiece)
of this exotic are toxic, and poisoning is only likely to occur if they
are sold in error as a feeding stuff, or from the use for feeding
purposes of the press-cake after the extraction of the well-known castor
oil, a purgative commonly used medicinally, of which the beans contain
about 50 per cent. According to Cornevin four seeds suffice to cause
accidents in man, eight lead to very grave results, and beyond that
number death may ensue. Pigs and poultry have been poisoned by the
seeds, and M. Audibert (near Beaucaire) reported the death of 80 sheep
from eating the press-cake, which is stated to have more pronounced
properties than the oil. It has been found as an impurity in linseed
cake and maize meal. (_Jour. Roy. Agric. Soc._, 1892.)

_Toxic Principle._ The toxic properties of the bean are due to _Ricin_,
a toxin which is similar to bacterial toxins, and the activity of which
is destroyed by heating to 100° C. The beans also contain the alkaloid
_Ricinine_ (C_{8}H_{8}O_{2}N_{2}), the toxic properties of which are
regarded as doubtful. (See Deane and Finnemore, _Yearbook of Pharmacy_,
1905, p. 473.)

_Symptoms._ These usually appear some days after the ingestion of the
beans or press-cake. There is generally purging. Broad observed in an
affected horse loss of appetite, shivering, cold extremities, dejection,
abdominal pain, constipation, temperature 103° F., pulse 70, and death
in about three days.

                              REFERENCES.

                        4, 16, 66, 73, 128, 205.


                                ROSACEÆ.

=Cherry Laurel= (_Prunus laurocerasus_ L.). This exceedingly common
ornamental shrub has caused the poisoning of numerous cattle and sheep
on the Continent, but is apparently less harmful in Great Britain—and in
any case animals are not much given to eating the foliage of this shrub,
the strong smell of the leaves when bruised affording a warning of its
unwholesome character. Gerlach recorded the intoxication of 25 sheep.
Bibbey also records the poisoning of 15 sheep by laurel, some of them
dying (_Farmer and Stockbreeder_, Jan. 29, 1912). On the other hand,
Henslow wrote of his cows that they “completely ruined a long laurel
hedge adjoining the field in which they lived; but this abnormal food
did no harm either to themselves or the milk they produced.”

_Toxic Principle._ So long ago as 1803 Schrader showed that the cherry
laurel contains a substance yielding prussic acid. The leaves contain
the cyanogenetic glucoside _Prulaurasin_ (C_{14}H_{17}O_{6}N), and an
enzyme-emulsin which, by its action on the cyanogenetic glucoside,
induces the formation of prussic acid, which is the actual cause of
poisoning. The percentage of the glucoside appears to be greatest about
July and August. By a microchemical examination Peche has clearly
localised hydrocyanic acid compounds in the leaf parenchyma.

_Symptoms._ In poisoning by Cherry Laurel there is bloating, inability
to rise, loss of sensation, difficult breathing, convulsions and
dilatation of pupils, and the results may be fatal if unattended to,
prussic acid being formed.

In the case of poisoning of ewes Aggio observed (_Veterinary Journal_,
1907) loss of appetite, vomiting, and inability to rise, followed by
several deaths. In 1871 Adsetts described (_Veterinarian_, 1871)
symptoms of poisoning in the horse: indistinct and feeble pulse;
congested mucous membranes, difficult respiration, uneasiness,
prostration, coldness of the extremities, loss of appetite,
constipation, diminished urination, and acute pain, eventuating in death
in three days. In sheep Bibbey observed salivation, grinding of teeth,
brain symptoms, paralysis in the back, coma, and death.

                              REFERENCES.

    4, 16, 73, 76, 81, 128, 129, 130, 132, 170, 205, 232, 254, 255.


                             CUCURBITACEÆ.

=Bryony= (_Bryonia dioica_ L.). This widely distributed hedge climber,
which produces large quantities of scarlet berries, is a highly irritant
plant, with an unpleasant odour and a nauseous juice. The large fleshy
tuberous rootstocks have caused the poisoning of whole families who have
eaten them in mistake for turnips and parsnips. The berries may tempt
children, and cases of poisoning have occurred. Cornevin estimated that
15 berries would cause the death of a child and 40 that of an adult. No
deaths of domestic animals have been observed in searching the
literature, but animals may possibly eat it along the hedgerows at times
when grass is scarce. Pigs might possibly eat sufficient of the
rootstock, or poultry of the berries, to cause poisoning.

_Toxic Principle._ The plant contains the bitter and poisonous glucoside
_Bryonin_ (C_{34}H_{48}O_{9}).

_Symptoms._ The symptoms are those resulting from inflammation of the
stomach and intestines, together with convulsions. According to Cornevin
consumption of the plant promotes sweating, and causes a livid hue,
nausea, diuresis and abundant painless, watery defæcation, to which are
added in cases of poisoning nervous symptoms of stupor and tetanic
convulsions. There may be superpurgation or a suppression of defæcation.

Lander states that 2 lb. of fresh or 6 to 8 oz. of dried root given to
_horses_ did not cause purging, but there was abdominal pain, loss of
appetite, accelerated breathing, fever, dullness and copious urination.

Cases may end fatally.

                              REFERENCES.

                       73, 76, 81, 141, 170, 233.


                              UMBELLIFERÆ.

=Cowbane= or =Water Hemlock= (_Cicuta virosa_ L.). This plant is
undoubtedly exceedingly poisonous, and fatal cases have occurred in both
man and farm live stock. It has been mistaken by man for parsley, celery
or parsnip, with fatal results, many persons having succumbed to it. The
rootstock is attractive to children on account of its sweetish taste.
Pott says that either fresh or dry it is poisonous to all animals when
only a small quantity is eaten, and often causes rapid death. Sheep and
goats appear to be less readily affected than other domestic animals,
and cattle to be most sensitive. The loss of eleven animals in Brittany
was noted in the _Veterinarian_ in 1877, and a number of cattle died in
Ireland (_Veterinary News_, 1911), death in both cases being due to
Cowbane. It is clearly dangerous to grazing animals which have easy
access to it, especially if ordinary herbage is scarce. Hedrick (Canada)
is quoted as stating that a piece of the root about the size of a walnut
is sufficient to kill a cow in about fifteen minutes; and Müller says
that the quantity of dried plant sufficient to kill a horse appears to
be about 1 lb. According to Kanngiesser the mortality in human poisoning
due to this plant amounts to 45 per cent. of the cases.

_Toxic Principle._ The poisonous character of Cowbane has not been fully
investigated, and the toxic principles are given as the alkaloid
_Cicutine, with Oil of Cicuta_, and _Cicutoxine_. The last is a bitter
resinous substance classed by Cushny in the picrotoxin group; it occurs
in the dry root to the extent of 3·5 per cent. The toxicity is stated to
vary with season and climate; the rootstock is most poisonous in spring.

_Symptoms._ In man the yellow poisonous juice in the rhizome induces
epileptic convulsions, followed by death. The cicutoxine gives acrid
narcotic symptoms quickly followed by fatal results. The symptoms
usually appear within two hours, and death ensues in half-an-hour to
several hours. The symptoms which appear in an hour or so are given as
loss of appetite, salivation, vomiting (in swine), nausea, colic (in
horse), bloating (in cattle), diarrhœa, irregular pulse and heart,
dilatation of pupils, rolling of eyeballs, vertigo, reeling in circles,
twisting of neck, falling down, automatic movement of limbs, opening and
shutting of mouth, and death, usually with convulsions, in from half an
hour to an hour after first manifestation of symptoms.

For _cattle_, Lander gives hurried respiration, collection of froth at
the mouth and nostrils, and tympanites. The limbs are extended and
alternately stiffened and relaxed.

In his description of the symptoms Esser states that swallowing is
difficult, the tongue is stiffened, there is salivation, and death takes
place after loss of consciousness and convulsions.

                              REFERENCES.

     31, 73, 81, 123, 141, 151, 170, 190, 203, 205, 213, 233, 238.

=Water Parsnip= (_Sium latifolium_ L.). The leaves and especially the
root of this species are regarded as poisonous, and the plant is
described as “poisonous” by Strasburger.

According to Müller the symptoms resemble those produced by
_Chaerophyllum_ (p. 40). After eating the roots _cows_ showed symptoms
of excitement, leading, in some instances, very quickly to death. The
milk, according to Cornevin, is of a disagreeable flavour.

The related _S. angustifolium_ has also been mentioned as objectionable.
As regards the toxic principle these plants have not been closely
studied, and it is not possible to give detailed symptoms.

                              REFERENCES.

                           73, 81, 190, 235.

=Water Dropwort= (_Oenanthe crocata_ L.). This weed of marshes, ditches,
and similar wet spots, has been a frequent cause of loss of stock. Cases
of fatal human poisoning have also occurred, owing to the leaves having
been mistaken for celery and the rootstock for parsnips. Several cases
of the poisoning of cattle have been recorded in the veterinary
journals, and sheep and cattle died on a farm near Bristol (_Jour. Roy.
Agric. Soc._, 1898). Horses have also been poisoned. Johnson and Sowerby
(1861) record the poisoning of 17 convicts near Woolwich, the leaves and
roots being eaten in mistake for celery and parsnips respectively. Nine
suffered from convulsions and became insensible; one died in five
minutes, a second in a quarter of an hour, a third in an hour, and a
fourth a few minutes later, while two more died during the next few
days.

Cornevin says that this plant causes the poisoning of animals every
year—they eat it willingly, showing an enfeebled instinct owing to
domestication. The plant is poisonous in all its parts, the root being
the most toxic, and drying does not destroy the toxic property. Cornevin
gives the following quantities of the fresh root as necessary to poison
various animals:—

               Horse  0·100 per cent. of the live weight.
               Ox     0·125       „       „       „
               Sheep  0·200       „       „       „
               Pig    0·150       „       „       „
               Rabbit 2·000       „       „       „

Holmes described _Oenanthe crocata_ as the most dangerous and virulently
poisonous of all our native plants (_Pharm. Jour._, 1902).

Other species of _Oenanthe_ are also poisonous in a less degree—_e.g._
_O. fistulosa_ L., and _O. Phellandrium_ Lamk.

_Toxic Principle._ Poehl (1895) obtained from the root of this species
an amorphous neutral product which he designated _Oenanthotoxin_. The
latest investigation is that by Tutin, who examined entire dried plants
collected in early spring, and the experiments confirmed the conclusion
arrived at by Poehl, that the toxic principle is a neutral resin. A
dark-coloured, viscid resin, insoluble in water, and equal to 3 per
cent. of the weight of the plant, was extracted, and it is stated that
the neutral portions of the petroleum and ether extracts of this resin
represent the toxic principle of the plant. As there is no evidence of
the homogeneity of this product, and it is probably complex in
character, it was given no name or formula. The fact that it has
poisonous properties was ascertained by administering the various
products to guinea pigs _per os_.

_Symptoms._ In poisoning by _O. crocata_ the symptoms generally appear
very quickly, and in serious cases death may follow in from one hour to
a few hours. In Tutin’s experiments on guinea pigs the extracts referred
to above rendered the animal hypersensitive in two to four hours, while
marked convulsions, with trismus soon appeared; the heart-beat became
very noticeably slow and the convulsions persisted until death ensued.
There is great restlessness, difficult breathing, convulsions, loss of
sensation, blindness and stupefaction (Müller); Lander says the symptoms
recall hemlock poisoning, with the addition of green fœtid diarrhœa.

In _cattle_, one hour after eating, there is depression and accelerated
respiration; the conjunctivæ are injected, the eye turns in its orbit,
the pulse is weak but rapid, and there is foaming. Later, there is
colic, and spasmodic contractions of limbs and jaws. If the quantity
ingested is sufficient to cause death, the animal falls, but still moves
its limbs. There is bellowing, contraction of pupils, insensibility, and
death in convulsions—or, if not fatal, cattle may remain paralysed.

In the _horse_, the appearance of the symptoms and the course of the
illness are much more rapid and the nervous symptoms are accentuated.

If the _pig_ has consumed only a small quantity it soon gets rid of the
poison by vomiting; but if the quantity is considerable there is no
vomiting and death is as rapid as with cyanide poisoning (Cornevin).

                              REFERENCES.

      10, 14, 73, 81, 141, 146, 170, 190, 205, 209, 213, 235, 246.

=Fool’s Parsley= (_Aethusa Cynapium_, L.). Much has been written about
the toxic properties of this weed of cultivated fields, principally
because, owing to the fact that the foliage has often been mistaken or
misused for parsley and the roots for radishes (!), it has been the
cause of human poisoning, though it seems to be one of the least active
of the poisonous Umbellifers. Its poisonous character is undoubted, but
it is unlikely to cause the poisoning of stock, which seem to refuse it.
Some authors regard it as strongly poisonous, but others as more or less
harmless. Johnson and Sowerby cite a case in which a child of five years
old died within an hour after eating the root, and a second death (in
Germany) within twenty-four hours from the use of the leaves in soup.

The most complete account of this plant is that by Power and Tutin,
issued from the Wellcome Chemical Research Laboratories in 1905. Many
authors since 1807 are cited as writing of its poisonous properties, and
of cases of poisoning, two of which terminated fatally. Miller (1807)
says that “most cattle eat it, but it is said to be noxious to geese.”
Bentley and Trimen write that “in all recorded experiments with it on
animals, it has had poisonous effects.” Dr. John Harley (1876 and 1880),
after experiments on a child and adults, concluded that the plant was
absolutely free from the noxious properties attributed to it. In 1904,
however, a case of severe poisoning by it was recorded (_Brit. Med.
Jour._, July 16, 1904, p. 124).

_Toxic Principle._ This has for many years been stated to be the
alkaloid _Cynapine_. For their investigation Messrs. Power and Tutin
collected the plant round London in July and August, with the fruits
still green, and after thorough chemical examination found 0·015 per
cent. of an _essential oil_ of rather unpleasant odour; 0·8 per cent. of
_resinous substances_; and an exceedingly small amount of a _volatile
alkaloid_ having the peculiar characteristic odour of _Coniine_. The
amount of hydrochloride of the alkaloid obtained showed that if the base
were Coniine it would correspond to only 0·00023 per cent. of Coniine in
the plant. In a degree this confirms the statement by Walz (1859) that
the fruit “contains a volatile base, very similar in odour and chemical
behaviour to Coniine, and probably identical with it.” The investigators
suggest that the alkaloid is Coniine, and the small amount would justify
the opinion, but there may be variation in toxic property according to
stage of development and climate. The authors conclude that “it cannot
be considered improbable that under favourable conditions of growth, the
proportion of alkaloid may be increased to such an extent as to impart
to the plant the poisonous properties ascribed to it.”

_Symptoms._ In a child which died, there were abdominal pain, a feeling
of sickness, and a tendency to lockjaw, and death supervened within an
hour; and in a German case, vomiting, diarrhœa, lockjaw, and death in 24
hours. (Johnson and Sowerby.) The plant causes convulsions and stupor,
with nausea and vomiting (Henslow).

The symptoms observed in _cows_ are loss of appetite, salivation, fever,
uncertain gait, and paralysis of hind limbs (Müller).

Pott refers to a case which occurred in Guernsey among _horses_. Animals
with white muzzles and feet had diarrhœa, while other horses remained
healthy. All white places on the body were badly inflamed. Pammel states
that the plant causes stupor, paralysis and convulsions in domestic
animals.

                              REFERENCES.

             45, 73, 81, 121, 130, 141, 190, 203, 213, 214.

=Chervils= (_Chaerophyllum_ sp.). No investigation of these plants
appears to have been undertaken, but _C. sylvestre_ L., though eaten by
some animals, including the ass and the rabbit, is stated by a German
observer (_vide_ Cornevin) to have caused the death of pigs. Müller
states that according to the literature both cows and pigs have been
poisoned, even fatally, by _C. temulum_ L. The plants have a strong
odour and acrid taste.

_Toxic Principle._ This, if any, appears to be unknown, though Müller
(1897) says that _C. temulum_ contains in all its parts the little known
_Chaerophyllin_ (? alk.).

_Symptoms._ The pigs referred to above as having died were said to show
paralysis, dilated pupils, and enteritis, and to refuse food. Postmortem
examination showed acute gastro-intestinal inflammation. In the case of
cows there are similar symptoms.

                              REFERENCES.

                                73, 190.

=Hemlock= (_Conium maculatum_ L.). This plant, famous from ancient times
as extremely poisonous, has a fœtid, disagreeable odour—a mousy
smell—especially noticeable when the plant is bruised. It has caused
human poisoning in three ways: the seeds have been eaten in error for
anise, the leaves for parsley, and the roots for parsnips.

Animals rarely appear to eat this plant, but cases have been recorded.
It is stated that in the United States many domestic animals have been
killed by it; and Ewart says that it is responsible for poisoning a
number of cows in Victoria. Goats are believed to be largely immune to
the poison, or are less harmed than other animals, and sheep are stated
to eat the plant with impunity, though cases of poisoning are recorded.
Johnson and Sowerby state that horses have occasionally swallowed
considerable quantities without apparent effect, while Cornevin remarks
that to cause death a horse would need to eat 4 to 5½ lb. of the fresh
plant, or a cow 8¾ to 11 lb.

Hemlock is probably most dangerous to live stock in the spring, when
green herbage is least plentiful and the young shoots of hemlock are
fresh and short. Chesnut says that the root is nearly harmless in March,
April and May, but dangerous later, especially in the first year of
growth; but Esser states that it is only poisonous in the spring. The
foliage is more poisonous before flowering than after, when the
poisonous principle passes to the fruits, which are more poisonous
before ripening (three quarters ripe) than afterwards. Pott remarks that
after eating hemlock cows give milk with a bad taste.

_Toxic Principle._ Early in summer the toxic principle appears to be
chiefly contained in the foliage, but later in the fruit, particularly
when still green. Among the substances contained in hemlock are the
toxic alkaloid _Coniine_ (C_{8}H_{17}N), the poisonous _Coniceine_
(C_{8}H_{15}N), _Conhydrine_ (C_{8}H_{17}NO), the alkaloid
_Methylconiine_ (C_{9}H_{19}N), _Pseudoconhydrine_ (C_{8}H_{17}ON).
Coniine may be described as an oily, colourless, quite volatile liquid,
quickly turning brown on exposure to the air, and giving a mousy odour
to the whole plant. The amount of Coniine in the fresh leaves is given
(Pammel) as 0·095 per cent., but in the ripe seeds 0·7 per cent. English
fruits contain much more of the total alkaloids than imported fruits.
Owing to the volatile character of the poisons hemlock largely loses its
toxicity when dried in hay, and is therefore the less likely to prove
injurious to domestic animals.

_Symptoms._ Hemlock is a dangerous narcotic plant. Even the smallest
quantities may cause inflammation of the digestive organs, paralysis and
death. The general symptoms are salivation, bloating, dilatation of
pupils, rolling of eyes; laboured respiration, diminished frequency of
breathing, irregular heart action; loss of sensation, convulsions,
uncertain gait, falling, and at the end complete paralysis. Death occurs
after a few hours. The poison acts on the motor nerve endings, causing
paralysis, dyspnœa resulting from paralysis of the pectoral nerves, and
acceleration of the heart from that of the inhibitory fibres of the
pneumogastric.

Small quantities cause in the _horse_ a little prostration, yawning,
acceleration of pulse, dilatation of pupils and sometimes muscular
spasms of the neck and shoulders. Large quantities cause nausea,
unsuccessful attempts to vomit, gritting of teeth, accelerated
respiration and dyspnœa, and muscular tremors commencing in posterior
members and spreading to anterior members and spine. There is next
difficulty of locomotion, sweating (but not continual), falling,
paraplegia, then paralysis, loss of feeling, lowering of temperature,
rapid pulse, increasingly difficult respiration, and death from stoppage
of respiration.

With _cattle_ there is ptyalism, cessation of digestion, bloating,
constipation, weakness and stupor. Pregnant cows have been observed to
abort; the milk of cows has an unpleasant flavour. There are bloody
evacuations in some instances in the case of the ox. In cows Chesnut
says that there was “loss of appetite, salivation, bloating, much bodily
pain, loss of muscular power, and rapid, feeble pulse.”

In _sheep_ the abdomen is tucked up, the animal has a dazed appearance,
there is dilatation of pupils, unsteady gait, the hind limbs being
dragged, coldness, and death after a few convulsive movements.

In the _pig_ there is prostration and inability to move, coldness, slow
breathing, livid mucous membranes, imperceptible pulse, paralysis,
particularly of the posterior members, and no convulsions.

                              REFERENCES.

   4, 16, 52, 53, 73, 81, 82, 91, 128, 141, 161, 203, 205, 213, 238.




                               CHAPTER IV
                               ARALIACEÆ.


=Ivy= (_Hedera Helix_ L.). The berries of the Ivy are said to be largely
eaten by certain birds (_e.g._ blackbirds, thrushes, wood-pigeons), but
have poisoned children. The plant has long been said to be poisonous,
but no definite case of poisoning of live stock has been discovered;
possibly farm live stock would need to eat a considerable quantity for
serious effects to be induced. Indeed, when keep is short, it is quite
common in some districts to see Ivy strewed on the fields for cattle and
sheep to eat, and it is very frequently given to sick animals by country
people (Garnett).

_Toxic Principle._ This has not been closely studied, but ivy contains a
bitter principle which is strongly cathartic, emetic and purgative. Ivy
contains a poisonous glucoside _Hederin_ (C_{64}H_{104}O_{19}) and a
resin (_Gummi hederæ_).

_Symptoms._ As suggested above, it is doubtful whether animals have been
poisoned by Ivy. Symptoms given appear to refer to children, and consist
in sickness, diarrhœa, nervous symptoms, excitement at first, then
convulsions and paralysis (Müller). Sickness and purgation (Esser).

Cornevin states that the symptoms are complex, emeto-purgative effects
being present, with nervous symptoms resembling those of intoxication,
viz. excitement, then coma, convulsions, uncertain gait, and stertorous
respiration.

                              REFERENCES.

                       73, 76, 81, 130, 208, 240.


                             CAPRIFOLIACEÆ.

=Common Elder= (_Sambucus nigra_ L.) and =Dwarf Elder= (_S. Ebulus_ L.).
These two plants are usually avoided by stock, no doubt in view of their
odour, more particularly in the case of the latter species. The bark,
leaves and berries of both species were noticed by Cornevin as having
pronounced purgative properties, and the berries of _S. Ebulus_ as
having poisoned turkeys. Esser remarks that the use of _S. Ebulus_ by
country folk as a purgative has caused fatal poisoning. The leaves of
_S. nigra_ have caused severe irritant poisoning in a child.

_Toxic Principle._ Some doubt exists as to the poisonous principle
of the Elders, the leaves of which contain _Sambunigrin_
(C_{14}H_{17}O_{6}N), a cyanogenetic glucoside; the alkaloid
_Sambucine_; and a purgative principle. According to Cornevin drying
reduces the toxicity but does not destroy it.

_Symptoms._ The symptoms are not very definite, but small quantities
cause purgation, while large quantities induce depression and violent
emetic and cathartic effects, with diarrhœa, abundant diuresis and
acceleration of pulse. The leaves of _S. Ebulus_ have caused vomiting,
obstinate constipation and enteritis in a boy, and in the case of
another boy the flowers caused vertigo and headache.

                              REFERENCES.

                          4, 73, 81, 203, 233.


                               COMPOSITÆ.

=Tansy= (_Tanacetum vulgare_ L.). Live stock are most unlikely to eat
this plant, as it is bitter and acrid. Cattle appear to have been
poisoned by it in Germany, Kobert’s opinion being that death had
resulted from tansy. There have also been many serious cases of human
poisoning.

_Toxic Principle._ Tansy contains the bitter, volatile and poisonous
_Oil of Tansy_.

_Symptoms._ Tansy Oil has been employed as an abortifacient, and
produces convulsions, violent spasms, frequent and feeble pulse, and
paralysis of the heart and lungs, inducing a condition similar to that
observed in rabies.

Pammel cites cases of the action of the oil from the plant on _dogs_.
According to Pott the tansy imparts a bitter taste to the milk of cows
which eat it.

                              REFERENCES.

                          161, 203, 204, 213.

=Ragwort= (_Senecio Jacobœa_ L.). No suspicion appears to have been
focussed on Ragwort in Britain, but it must be recorded here as the
cause in Canada of the Pictou cattle disease, or hepatic cirrhosis, a
somewhat fatal disease which has caused much loss during the last few
years. In New Zealand also the same disease has been experienced, and
has caused considerable mortality among sheep. In one case sheep were
closely pastured on about 4000 acres with the object of eradicating the
too prevalent weed, but after a year losses ensued. Gilruth concluded
that if the weed does not monopolise the ground, sheep may, with few
exceptions, eat it daily without suffering ill effects. Cattle and
horses avoided it when possible.

It may be remarked that in Britain feeding the young shoots off with
sheep, which seem to like the plant, is regarded as the best plan of
reducing Ragwort in grass land. So far there seems to be no record of
injury from this cause.

In South Africa cirrhosis of the liver in cattle (locally termed Molteno
cattle sickness) has been traced to _S. latifolius_, 8 to 10 lb. of
which in daily feeds of 2 to 6 oz. caused death in about six weeks.
Another species, _S. Burchellii_, is similarly poisonous, ½ lb. daily
for four days having killed an ox on the fifth day; at Molteno half the
quantity proved fatal. Both species are fatal to cattle and horses.

_Toxic Principle._ As regards _S. Jacobœa_ nothing appears to be known
as to any toxic principles, though an alkaloid has been isolated by Watt
(1911), but not fully described. The South African _S. latifolius_,
however, was examined at the Imperial Institute, and two new crystalline
alkaloids were isolated—_Senecifoline_ (C_{18}H_{27}O_{8}N) and
_Senecifolidine_ (C_{18}H_{25}O_{7}N)—1·20 per cent. being present in
the plant before flowering and 0·49 per cent. after flowering.

_Symptoms._ As they may to some extent serve as a guide in relation to
possible Ragwort poisoning in Britain the symptoms observed from
poisoning by the South African species may be given: Severe and strained
purging: fæces yellowish to dark brown; cows cease to give milk;
abdominal pain, groaning; animal may go mad and charge anyone
approaching, or lie with outstretched head, drooping ears, staring coat,
and dull glaring eyes; death usual within three days from commencement
of purging. The post-mortem shows an inflamed fourth stomach; hardened
condition of the liver, often dull grey with spots in the interior;
expanded gall bladder, with dull yellow viscid bile.

                              REFERENCES.

                           43, 128, 195, 260.

=Wild Lettuce= (_Lactuca_ sp.). Just how far the two species _L.
scariola_ L. and _L. virosa_ L. are really poisonous is not clearly
known, and it is probable that to be seriously harmful to farm live
stock they would need to be ingested in considerable quantity, and this
they never seem to be. They are certainly not actively poisonous, though
Bailey and Gordon say that “we have been informed that this European
plant—now a national pest—is sometimes eaten by cattle, on whom it has
been observed to have had an injurious effect.”

_Toxic Principle._ Authorities differ as to the substances to which the
toxic property, if any, is to be attributed. According to Ludwig the
milky juice, known as _Lactucarium_, includes _Lactucone_, _Lactucin_,
and _Lactucic Acid_, the second of these being the narcotic substance.
Nearly half the weight of _Lactucarium_ (a form of dried juice) consists
of the tasteless inodorous _Lactucone_ or _Lactucerin_ (C_{14}H_{22}O),
and the bitter taste is due to _Lactupicrine_, Lactucin and Lactucic
Acid. In the leaves of _L. virosa_, Dymond found traces of _Hyoscyamine_
or a similar substance (_Jour. Chem. Soc._, 1892, Vol. 61, p. 90).

_Symptoms._ Intoxication is produced similar to that caused by poppy
heads; the narcotic effects are dominant (Cornevin).

                              REFERENCES.

                       11, 73, 81, 130, 213, 240.


                               ERICACEÆ.

=Rhododendron= (_Rhododendron_ sp.). The literature points to there
being no doubt as to the poisonous character of a number of species of
_Rhododendron_, and indeed most species are suspected. Animals do not
appear to eat Rhododendrons very extensively, but both English and
Belgian veterinary surgeons have published records of poisoning of sheep
and goats by _R. ponticum_. Suspected cases were recorded in the
_Journal of the Board of Agriculture_ (1907 and 1914); three cases of
cattle poisoning in the _Veterinary Record_ (1900, 1906, and 1907); one
of calves in the _Veterinarian_ (1859); and three of sheep-poisoning—one
in the _Veterinary Journal_ (1906), and two in the _Veterinarian_
(1865); but these cases were not all fatal. The death of 19 out of 21
cross-bred Scotch lambs due to eating _R. ponticum_ was reported by C.
T. Baines in the _Journal of the Land Agents Society_ (Aug. 1914, p.
373). The plant was eaten after a heavy fall of snow. Chesnut includes
_R. maximum_ as one of the thirty most poisonous plants of the United
States. According to Cornevin, _R. ferrugineum_ causes frequent
poisoning of animals which graze on the plateaux where it
grows—especially sheep and goats, the latter providing the most victims,
as they willingly browse the young shoots and leaves. _R. californicum_
is said to be poisonous to sheep in Oregon. _R. Chrysanthum_, the leaves
of which have been used in Russia and Germany for rheumatism, has caused
poisoning in man. _R. punctatum_ and _R. hirsutum_ appear to be not less
poisonous.

Both leaves and flowers are narcotic, and even the honey in the flowers
is regarded with suspicion. The following quotations are not without
interest:—

“In these regions (Tungu) many of my goats and kids had died foaming at
the mouth and grinding their teeth, and I have discovered the cause to
arise from their eating the leaves of _Rhododendron cinnabarinum_ (“Kema
Kechoong,” Lepcha; Kema signifying Rhododendron); this species alone is
said to be poisonous, and when used as a fuel it causes the face to
swell and the eyes to inflame, of which I observed several instances.”
(Hooker, _Himalayan Journals_, ii. p. 150).

“_Rhododendron arboreum_ becomes plentiful at 5000 to 6000 feet (East
Nepal), forming a large tree on dry clayey slopes.... In the contracted
parts of the valley the mountains often dip to the riverbed in
precipices of gneiss under the ledges of which wild bees build pendulous
nests looking like huge bats suspended by their wings; they are two or
three feet long and as broad at the top whence they taper downwards; the
honey is much sought for except in spring, when it is said to be
poisoned by Rhododendron flowers just as that eaten by the soldiers in
the retreat of the Ten Thousand was by the flowers of _R. ponticum_.”
(_l.c._ i. p. 200).

_Toxic Principle._ The leaves and flowers contain a bitter poisonous
glucoside, _Andromedotoxin_ (C_{31}H_{50}O_{10}), which has been
regarded as more poisonous than Aconitine. Other glucosides found in
Rhododendrons are _Ericolin_ (C_{34}H_{56}O_{21}), _Arbutin_
(C_{12}H_{16}O_{7}), and _Rhododendrin_ (C_{16}H_{22}O_{7}), but it is
not clearly shown whether these are poisonous when ingested; Kobert,
however, includes the two former among cerebro-spinal poisons.

_Symptoms._ In the case of goats Cornevin records intense pain,
diarrhœa, discomfort, gritting of teeth, salivation, and frequently
vomiting; while there is reduced lactation, trembling, spasms, vertigo,
loss of power, and death. Lander notes similar symptoms in cattle and
sheep.

According to Eve (_Veterinary Record_, 1907), a reddish colour was
observed in the milk of a cow poisoned by Rhododendron.

                               REFERENCES.

 4, 16, 53, 63, 73, 76, 81, 144, 161, 170, 203, 205, 211, 212, 213, 231,
                                252, 264.

=Azalea= (_Azalea_ sp.). A suspected case of poisoning was recorded in
the _Journal of the Board of Agriculture_ in 1907. No British record of
poisoning has been found. Various species of Azalea (_A. pontica_, _A.
indica_, _A. arborescens_, _A. nudiflora_, etc.) are stated to be very
poisonous to all animals which browse on them in the East. Cuttings
should never be thrown down where they can be eaten by stock.

_Toxic Principle._ Little work has been done on these plants, but they
are believed to contain _Ericolin_, _Arbutin_, and _Andromedotoxin_ as
in the case of rhododendrons (p. 47).

_Symptoms._ Azaleas appear to be narcotic, and to produce symptoms
resembling those caused by _Lolium temulentum_ (Cornevin).

                              REFERENCES.

                           73, 144, 190, 205.


                              PRIMULACEÆ.

=Scarlet Pimpernel= (_Anagallis arvensis_ L.). Unless it occurs in very
considerable quantity this little plant is unlikely to be eaten to an
extent sufficient to cause definite poisonous symptoms, as it is a
cornfield weed. It may be taken, however, if animals are allowed to run
over stubble. Sheep are said to refuse it in general, but have died from
eating it (see below).

There seems to be no doubt that if eaten in sufficient quantity it has a
poisonous action, having an irritant action on the digestive tract—the
intestines—as well as producing narcotic effects. Strasburger notes it
as “slightly poisonous”; Bailey says “a dog is stated to have been
destroyed by making it swallow three drachms of the extract,” while
according to Hyams the fluid extract in 4 drachm doses is fatal to dogs
(the size of the dog is not mentioned!); at the Veterinary School at
Lyons horses were intentionally killed by administering a decoction of
the plant; in America Chesnut notes it as suspected of killing a horse;
Ewart says it “has been reported to render the chaff from oat crops
infested by the weed unpalatable to stock”; and Gilruth states that a
year or two ago it was responsible for the death of a large number of
sheep in Victoria, apparently acting as a narcotic poison (_Amer. Vet.
Rev._, July, 1913, p. 383.). On the Pacific coast the plant is known as
“Poison Weed.” Grognier and Orfila are stated to have put its poisonous
properties beyond doubt.

_Toxic Principle._ The plant contains the glucoside _Cyclamin_
(C_{20}H_{34}O_{10}), and a saponin-like substance (Pammel). Van Rijn
says it contains two glucosides.

_Symptoms._ The plant has an irritating effect on the intestines and a
stupefying effect on the nervous system. Cornevin states that it is
never taken by the larger domestic animals in quantity sufficient to
cause poisoning.

                              REFERENCES.

                    10, 73, 82, 190, 203, 235, 252.


                                OLEACEÆ.

=Privet= (_Ligustrum vulgare_ L.). The facts as to the poisonous
character of Privet are by no means clear, but Taylor records a case in
which three children who ate the berries were attacked by violent
purging, and a boy and girl died. Turner observed a case in which horses
died after eating Privet.

_Toxic Principle._ The Privet is stated to contain the poisonous
glucosides _Ligustrin_ and _Ligustron_, not mentioned by Van Rijn,
who says it contains _Syringin_ (C_{17}H_{24}O_{9}), while Pammel
(1911) adds the bitter glucosidal principle _Syringopicrin_
(C_{26}H_{24}O_{17}).

_Symptoms._ In horses Turner observed loss of power in the hind limbs,
with a pulse of 50, temperature 102° F., slightly injected mucous
membranes, and dilated pupils, with death in 36 to 48 hours. The berries
are stated by Müller to cause sickness and diarrhœa.

                              REFERENCES.

                        130, 190, 203, 233, 252.


                             CONVOLVULACEÆ.

=Bindweeds= (_Convolvulus sepium_ L. and _C. arvensis_ L.). The creeping
rootstocks and foliage, as well as the seeds, are held to be more or
less poisonous if eaten in quantity, and as long ago as 1872 Olver
recorded (_Veterinarian_, 1872) that pigs which ate freely of
_Convolvulus_ died. These species, when eaten in considerable quantity,
appear to be cathartic and purgative, causing symptoms resembling those
due to jalap.

                              REFERENCES.

                        82, 141, 190, 203, 254.


                               SOLANACEÆ.

=Thorn Apple= (_Datura Stramonium_ L.). This species is an escape from
cultivation, but on occasion occurs plentifully in gardens, and if
allowed to seed may escape to arable fields and find its way to stock,
though it does not appear to have done so in Britain. Several species of
_Datura_ are recognized as virulent poisons in North America, where they
are known as Jimson Weeds. All parts are poisonous, especially the
seeds, which have a somewhat sweetish taste, and have frequently caused
accidents to children who have eaten them. Cases are recorded in the
United States in which cattle have been poisoned by eating the leaves of
young plants in hay. Live stock, however, usually avoid the plant, which
has an unpleasant odour and taste, while the seeds are enclosed in
thorny capsules. Walsh states that the seeds are very fatal to young
ostriches. Drying does not destroy the toxicity.

_Toxic Principle._ The Thorn Apple is usually stated to contain the
highly poisonous narcotic alkaloid _Daturine_, but this appears to be a
mixture of the two alkaloids _Hyoscyamine_ (C_{17}H_{23}O_{3}N) and
_Atropine_ (C_{17}H_{23}O_{3}N), which, together with the alkaloid
_Scopolamine_, or _Hyoscine_ (C_{17}H_{21}O_{4}N), have been found in
the plant, the principal constituent being Hyoscyamine. In some analyses
as much as 0·33 per cent. of Atropine has been found in the seeds, and
0·2 per cent. in the leaves (Pammel). The three alkaloids occur together
to the extent of 0·48 to 3·33 per cent. in the leaves, 0·43 per cent. in
the flowers, and 0·1 per cent. in the root, Hyoscyamine predominating
(Esser). An investigation conducted at the Imperial Institute (_Bul.
Imp. Inst._, 1911) showed the amount of alkaloids in European specimens
to be:—

                     Seeds  0·21 to 0·48 per cent.
                     Leaves up to 0·4        „
                     Stems  average 0·22     „
                     Roots  average 0·17     „

_Symptoms._ The general effect of _Datura_ poisoning appears to resemble
that of _Atropa Belladonna_, but is by some considered more rapidly
effective. There is paralysis, dilatation of the pupils, suspension of
secretion and of the inhibitory fibres of the vagus, leading to rapid
action of the heart (Lander). Poisoning may terminate fatally. Pammel
quotes Winslow as stating that two grains of Atropine produce mild toxic
symptoms in the horse; cattle are as susceptible as horses, though
herbivora are not so easily influenced as carnivora. Chesnut gives the
following symptoms: “Headache, vertigo, nausea, extreme thirst, dry,
burning skin, and general nervous confusion, with dilated pupils, loss
of sight and of voluntary motion, and sometimes mania, convulsions, and
death.” Walsh gives the toxic symptoms in ostriches as staggering gait,
spasmodic jerking of the neck, stupor, and death in a comatose state.

                              REFERENCES.

    4, 10, 16, 39, 52, 53, 73, 81, 92, 128, 141, 170, 203, 213, 260.

=Henbane= (_Hyoscyamus niger_ L.). The poisonous character of Henbane is
well known, but the plant is by no means common (except in Ireland),
though found in parts of England, Scotland, and Wales. Poisoning of live
stock may occasionally occur, but the disagreeable odour is likely to
prevent all but abnormal or very hungry animals from touching it. The
seeds are eaten by birds, apparently without injury, but poisoned
chickens which ate the ripe seeds in Montana. Cornevin records that cows
have been poisoned by eating the plant when given mixed with other
herbage. There are numbers of cases of children having been poisoned by
eating the seeds. The root has also caused accidents by being taken for
other herbs, and the young shoots and leaves have been used in error as
a vegetable. A case was reported in the press in 1910 in which 25 men
and women visitors at a Davos pension suffered from the effects of
eating the root of Henbane given in error for horse-radish, or mixed
with it. All suffered from strange hallucinations, but with prompt and
careful treatment all had recovered in twelve hours. Kanngiesser says
that poisoning by this plant very seldom terminates fatally.

Welsby records a case in which animals were poisoned in a field in which
Henbane was grown for medicinal use some years before (_Veterinary
Record_, 1903). According to Rodet and Baillet (_vide_ Cornevin) small
quantities of the seeds are in some countries mixed with the food of
fattening stock; if true that fattening is promoted, it is probably due
to the inducement to quiet and repose caused by the narcotic properties
of the seeds.

_Toxic Principle._ Poisoning by Henbane is due to the alkaloids
_Hyoscyamine_ (C_{17}H_{23}NO_{3}) and the closely related _Hyoscine_,
or _Scopolamine_ (C_{17}H_{21}O_{4}N). The glucoside _Hyoscypicrin_ is
also found in Henbane. The poisonous property is not eradicated by
drying or boiling. The leaves of Henbane grown in Europe contain from
0·04 to 0·08 per cent. of total alkaloid, and the seeds 0·06 to 0·10 per
cent. (_Bul. Imp. Inst._, 1911).

_Symptoms._ Henbane is an anodyne, and hypnotic. The symptoms resemble
those caused by _Atropa Belladonna_ (p. 58). The important differences
(Cornevin) are that there is here abundant salivation and no dryness of
the mouth as in _Atropa_. There is dilatation of the pupils; and
mydriasis, which is dissipated more slowly than in Belladonna poisoning.

Further differences in the action of the two poisons are given by
Winslow (_via_ Pammel): The tetanic stage succeeding spinal paralysis
observed in Atropine poisoning does not ensue with Hyoscine. The latter
alkaloid slightly depresses and slows the heart and does not paralyse
the vagus terminations, nor depress the motor and sensory nerves or
muscles. The circulation is but slightly influenced, and vasomotor
depression only occurs in the later stage of lethal poisoning. Death
occurs from paralysis of the respiratory centres. Poisoning in animals
is exhibited by loss of muscular power, slowing and failure of
respiration, stupor, and asphyxia. The pulse may be infrequent, the
pupils are dilated, and the skin is moist rather than dry.

The following symptoms in animals are given by Welsby: Nervo-muscular
exaltation, eyelids and irides much dilated, eyes amaurotic and very
bright, pulse full, temperature normal, respiration difficult and
hurried, profuse salivation, muscles of neck and extremities in a state
of tetanic rigidity, considerable abdominal distension, stercoraceous
and renal emunctories entirely suspended, death.

In a _cow_ there was observed, two hours after eating, dilatation of
pupils, the conjunctivæ were injected, and the carotids beat violently.
There were general convulsions, loud respiration, salivation, and
purgation. According to Pott the milk of affected cows is of an
unpleasant taste.

                               REFERENCES.

 4, 16, 39, 57, 68, 73, 81, 128, 141, 151, 157, 161, 190, 203, 205, 213,
                                   257.

=Garden Nightshade= (_Solanum nigrum_ L.). This species is described as
“one of the widest spread weeds over every part of the globe, except the
extreme north and south; varying so much in warmer regions as to have
been described under more than forty names” (Bentham and Hooker). In the
same way there can be no doubt that, though it must always be regarded
as poisonous, this plant varies considerably in toxicity according to
soil, climate, and general condition of growth. For this reason the
plant may sometimes be eaten in considerable quantities without ill
effects, while in other cases it will undoubtedly prove poisonous.

Children have been poisoned by the berries, but may on occasion eat them
with no other ill effect than a stomach ache, or, if eaten in excess,
sickness and purging. The berries “have even been used instead of
raisins for plum puddings with no effects out of the ordinary” (Ewart).
The plant has also been used in Queensland and elsewhere as a substitute
for spinach. In several cases the plant has proved fatal. Gohier gave 3
kilogrammes (6½ lb.) of the green plant to a horse and observed no
serious symptoms. Cases of poisoning are recorded for calves, sheep,
goats and pigs (Chesnut and Wilcox). According to Lehmann, Schraber and
Haller, the berries are poisonous to ducks and chickens. Over thirty
years ago the death of a number of cattle in Victoria was recorded as
being due to poisoning by this weed.

Though cases of poisoning of stock are rare, partly perhaps because the
plant is a weed of arable land and partly because animals are likely to
avoid it unless starved, _Solanum nigrum_ must be regarded as a
poisonous plant, any examples of which may prove toxic. The downy and
more prostrate form has been considered the most poisonous.

The “Wonderberry,” said to be a hybrid between _Solanum guineense_ and
_S. villosum_, which are probably varieties of _S. nigrum_, cannot in
England be distinguished from the last named, the fruits of which appear
to be edible in some countries and poisonous in others. Greshoff found
that fruits of the “Wonderberry” contained more Solanine than the wild
English _S. nigrum_ or the Canadian form known as the “Huckleberry,” and
hence they should not be eaten.

_Toxic Principle._ The Garden Nightshade, in particular the berries,
contains the alkaloidal glucoside _Solanine_, of which the formula is
considered doubtful. Solanine is readily converted into sugar and the
poisonous _Solanidine_. It was isolated from the berries in 1821, and
though decidedly active in sufficient quantity is not a violent poison.
A small quantity of _Solanine_ is present in the stem and berries, but
these are probably less poisonous than green potatoes (p. 54).

_Symptoms._ The symptoms of poisoning are apparently much the same in
man and animals: “Stupefaction; staggering; loss of speech, feeling, and
consciousness; cramps and sometimes convulsions. The pupil is generally
dilated.”

                               REFERENCES.

 4, 10, 11, 16, 17, 52, 53, 57, 73, 81, 82, 128, 141, 161, 203, 235, 240.

=Bittersweet= (_Solanum Dulcamara_ L.). Some doubt exists in regard to
the toxic character of this common denizen of the hedge-row, some
persons regarding the berries as harmless and others as poisonous.
Possibly the plant varies in toxicity. Floyer states that 30 berries
killed a dog. Though stock rarely touch the plant there seems to be no
doubt that it is poisonous, stem, leaves, and berries containing the
toxic alkaloid found in _S. nigrum_ and the potato (_q.v._), and it is
especially possible that poisoning may follow the ingestion of the
berries. Johnson and Sowerby (1861) say that the leaves are narcotic,
causing nausea and giddiness, and that the fruit is equally harmful,
though no fatal cases then seemed to be recorded. Gillam records (_Vet.
Record_, 1906) a case of poisoning of sheep. An anonymous writer in the
_Mark Lane Express_ (July 24, 1911) states emphatically that this plant
is very poisonous, and that he has known 14 per cent. of the sheep on a
farm to be killed by it in a year, while his veterinary surgeon had had
40 cases that season, some proving fatal.

_Toxic Principle._ Like _S. nigrum_, the stems, leaves, and berries of
Bittersweet contain _Solanine_. The berries are stated by Esser to
contain 0·3 to 0·7 per cent. of Solanine. The stems also contain the
glucoside _Dulcamarin_ (C_{22}H_{34}O_{10}), which imparts a bitter
taste to the plant, but which has not been fully studied.

_Symptoms._ In the case recorded by Gillam (see above) the symptoms
observed in sheep were small intermittent pulse, temperature 104° F.,
quickened respiration, staggering gait, dilated pupil, and greenish
diarrhœa. The symptoms appear to be the same in the case of cattle
(_Farmer and Stockbreeder_, July 10, 1911).

                              REFERENCES.

          4, 16, 40, 50, 52, 73, 81, 141, 147, 203, 213, 257.

=The Potato= (_Solanum tuberosum_ L.). Though potato haulm is more or
less commonly utilised on the Continent as a green fodder, and has been
so used in England, yet there are good grounds for the general belief
that it is not a suitable food for stock. The tubers may in general be
eaten with impunity, but, under certain conditions, cannot be regarded
as blameless, since they have caused serious injury. There are certainly
records of injury to man from eating Potatoes, and accidents with
animals have occurred more commonly. “Greened” tubers, and tubers with
young shoots appear to be the chief cause of accidents, and, as regards
live stock, usually when fed raw.

Cornevin knew of no case of poisoning in man, and considered that this
was probably because man (1) eats only the part poorest in the toxic
principle (see below), (2) does not eat the skin, (3) always cooks the
tubers, and (4) rarely subsists only on potatoes for a considerable
time. He found accidents among _animals_, however, not rare. In fact,
eliminating cases possibly due to changes caused by weather, cryptogams,
and ferments, he found poisonings every year unquestionably due to
Solanine, chiefly among cattle. Cows will eat the haulm without trouble
in times of scarcity of green fodder, but to the detriment of their
health if such feeding is prolonged.

Macfadyen showed some time since that old sprouted Potatoes, even after
boiling, are poisonous to horses. In 1896 eleven horses died from eating
in most instances small quantities of spoiled and somewhat sprouted
Potatoes, and two test-horses fed on the Potatoes died. In this case,
however, it was conjectured that the poison was probably some organic
substance generated by the bacteria or fungi growing on the Potatoes.

Chesnut and Wilcox (1901) recorded the death of six pigs due to eating
sprouted uncooked Potatoes; after cooking the potatoes did not cause
poisoning. With sufficient boiling most of the poison appears to remain
behind in the water and might be thrown away.

Cases of poisoning of stock by Potatoes appear to have occurred more or
less frequently in Germany. Two such cases were noted in the _Berliner
Tierärztliche Wochenschrift_ in 1909, in one of which 64 cows developed
symptoms of poisoning after being fed on a large quantity of raw tubers,
while in the other instance two cows became ill after eating Potato
parings—which, as shown below, contain more Solanine than the “flesh.”

In the case of two children who died, F. W. Stoddart, Public Analyst of
Bristol, after a post-mortem in one case, gave a very guarded opinion
that death was probably due to Solanine poisoning, due to eating raw
Potato peel, but was not confident. A most interesting case of severe
but not fatal poisoning is described in _The Lancet_ (1899). No less
than 56 soldiers in Berlin were badly affected, until the supply of
Potatoes was stopped, but the men recovered.

Pammel (1911) states that some persons cannot eat Potatoes because
poisonous to them, but such persons must be extremely rare, and
hypersensitive to minimum quantities of Solanine, which is almost if not
quite absent in the “flesh” of Potatoes.

_Toxic Principle._ The Potato plant, like the other species of _Solanum_
mentioned above, contains _Solanine_, which occurs not only in the
haulm, but in the flowers and fruits, and in the peel of the tubers.
_Solanidine_ also occurs ready-formed in the young sprouts of potatoes
to the extent of 1·5 per cent. (Allen). In the case of the soldiers
poisoned in Berlin analysis demonstrated the presence of Solanine to the
extent of 0·038 per cent. in boiled tubers and 0·024 per cent. in raw
tubers, and on an average every man who fell ill had 0·3 gramme of the
alkaloid, a sufficient quantity to produce toxic results. Esser (1910)
states that in midsummer the haulm contains 0·0925 per cent. of Solanine
but late in summer only 0·0374 per cent. In the tubers the alkaloid
occurs in the inner layers of the peel to the extent of 0·0124 per
cent., red or pink varieties containing rather more than yellow sorts.
The same authority says that damp soils tend to a higher percentage of
Solanine than dry soils[3], and that nitrogenous manuring as compared
with potash tends to an increase of Solanine. In fresh spring shoots 1·5
per cent. of the alkaloid has been found, and the percentage is
especially high in tubers which have been “greened” by long exposure to
light. As already stated it is the greened tubers which appear to be the
chief cause of accidents. Tubers with young shoots are richer in
poisonous alkaloids than those which have not yet been sprouted; such
tubers when fed raw to stock may on occasion induce poisoning, unless
fed only in small quantities.

Footnote 3:

  On the other hand, potatoes grown in a dry sandy soil are stated to
  contain more Solanine than those grown in other soils.

Writing in 1887 Cornevin remarked that Solanine, though neither very
active nor very abundant in Potatoes, nevertheless causes accidents, as
it is cumulative, or, to be more exact, is eliminated slowly.

_Symptoms._ In poisoning by potato _haulm_, Cornevin records
constipation, loss of appetite, rise in temperature, accelerated
circulation, normal respiration, salivation, tumefaction of eyelids,
eyes watery, conjunctivæ injected, and hair erect. The skin is covered
with scabs which exude matter, the skin being cracked. These scabs are
found especially on the scrotum of male cattle and the udder of female
cattle, but also in the caudal region and round the anus. An examination
of the mouth shows places on the upper jaw which are devoid of mucus and
are purulent at the centre, the mucus round the edges being swollen. The
posterior members are similarly but not so badly affected. Movement of
these members seems to cause the animal much pain. Defecation is
frequent, the fæces being liquid and dark in colour. The animals are
recumbent for a considerable time with the posterior members stretched
out. In the worst cases there is pronounced emaciation.

According to Friedberger and Fröhner (_vide_ Pammel) animals affected by
potato tops show symptoms resembling those of foot-and-mouth disease.

According to Pott the _berries_ cause colic and foul smelling diarrhœa
in _cattle_. A German veterinary surgeon after feeding the green plant
observed symptoms of delirium, paralysis, and flatulence. In other cases
trembling and uncertain gait, with paralysis of the spinal cord, have
been observed in _cows_.

In poisoning by _tubers_ there is depression, loss of appetite,
cessation of lactation, gritting of teeth, profound prostration, with a
remarkable somnolence, but no dilatation of the pupils. The animals
remain recumbent, with closed eyes, and refuse to get up. Respiration is
somewhat retarded, and the pulse is small and accelerated. There are
digestive disturbances, tympanitis, diarrhœa succeeds constipation, and
there is vomiting (where possible). The poisoning is usually fatal.

Where a large quantity of sprouted Potatoes has been fed the prostration
becomes paraplegia, with loss of sensibility, stupefaction, and death.
Where there is prolonged ingestion of a large quantity of unsprouted
tubers there is prostration, intestinal irritation, rapid emaciation and
death in marasmus after an illness of from one to three weeks
(Cornevin).

Pott states that potatoes diseased with wet rot, when fed raw, cause
digestive troubles, bloating, diarrhœa, abortion, and decrease in milk
yield, with fatal results in some cases. Potatoes diseased with dry rot
cause constipation in sucking pigs, and a “fishy” butter from cow’s
milk.

Lander notices two cases of poisoning of _horses_ by tubers. In the
first case the symptoms were a small and weak pulse, normal temperature
and loss of coordination in movements; complete loss of appetite,
excessive thirst, but inability to drink; mydriasis, stertorous
breathing, suspension of peristalsis, and slight tremors over the crural
muscles. In the second case there was a rapid and feeble pulse,
temperature 103° F., intense congestion of the mucous membranes, and
very fœtid diarrhœa, terminating fatally.

In poisoning of _horses_ after receiving large quantities of raw
Potatoes, Pott records boil-like swellings on the skin, loss of hair,
diarrhœa, inflammation of the stomach and intestines, skin irritation,
and swollen fetlocks and hocks.

In reference to the horses mentioned above (p. 55) it is stated that an
affected animal seems dull, and dies within twelve hours after being
first observed, without evincing any sign of pain. The first symptoms in
ten cases were weakness and loss of power over the limbs.

In _cows_ the symptoms (Müller) are loss of appetite, bloating,
diarrhœa, staggering, dilatation of pupils, convulsions, loss of
sensation and paralysis. In many cases, however, these symptoms do not
appear, but instead there are outbreaks on the skin of the hind legs
similar to those in foot-and-mouth disease. Pott mentions abortion as a
symptom. After the ingestion of green Potato parings by dairy cows he
remarks catarrh of the stomach and intestines, and bad milk and cheese;
consumption of diseased Potato parings resulted in the flow of hard
mucus from the mouth, the legs being badly swollen, and covered with
scabs, and the mouth and body covered with boils. Symptoms of paralysis
were noticed after feeding dirty Potato parings to four cows and four
bulls, and one cow died.

In the case of the cows already referred to (p. 55) as poisoned in
Germany, it was remarked as a noticeable feature in both instances that
there was the appearance of eczema on the hind limbs, causing lameness.

A case in which _pigs_ were fed on uncooked, sprouted Potatoes is
noticed by Chesnut and Wilcox; there was slowly progressing paralysis,
which became complete after about 24 hours, increased salivation, and a
regurgitation of the stomach contents. According to Pott death may
result in pigs. The symptoms given by Lander for poisoning in pigs are
loss of appetite, dullness, exhaustion, imperceptible pulse, watery
diarrhœa, low temperature and comatose condition.

In the case of the poisoned soldiers the symptoms were those of acute
gastro-enteritis; rise in temperature to 103° F.; headache, colic,
diarrhœa, general debility; in some cases vomiting, in others nausea
only; several men fainted, and one had convulsions; the majority were
drowsy and apathetic; but all recovered.

                               REFERENCES.

 4, 16, 19, 57, 73, 81, 128, 130, 141, 170, 190, 196, 203, 204, 205, 213.

=Deadly Nightshade= (_Atropa Belladonna_ L.). This plant has long been
known to be exceedingly poisonous, all parts containing a toxic
principle. Both man and domestic animals may be poisoned, though the
latter are very unlikely to touch the plant. As regards man, children
are most likely to be affected, owing to the attractive character of the
large bright black berries. Domestic animals appear to be rarely
poisoned and are less affected than man, and in any case the
susceptibility of various species—and even individuals of the same
species—is very variable. Human beings are most susceptible, followed by
the cat and dog; the horse is much less so; and the pig, goat, sheep,
and rabbit are little susceptible to poisoning, even on eating the
root—the most poisonous part (Cornevin). Gohier and others have given
over 2 lb. of the green plant to horses without ill effects, and this
repeated on three days did not cause marked pathological troubles.
Hertwig considered large ruminants to be more sensible than horses to
the action of Belladonna. It appears to be agreed that small ruminants
are very slightly susceptible to this plant. Birds are considered almost
insensitive, while rabbits may be fed for weeks on the leaves without
poisoning, as also sheep, goats, and pigs. Horses and cattle are more
sensitive but nevertheless resistant. The poison is no doubt quickly
removed by the kidneys, since ordinary injection of Belladonna causes
the usual symptoms. It is stated that the flesh of rabbits and birds
which have eaten the plant and have been slaughtered apparently healthy
is poisonous to man.

One berry can induce symptoms of human poisoning, and a child died after
eating only three berries. Mortality in human cases of poisoning by
Belladonna is given by Kanngiesser as 10 per cent.

_Toxic Principle._ Deadly Nightshade is the source of drugs widely used
in medicine, and its properties as regards man have been extensively
studied. The principal substance present is the alkaloid _Hyoscyamine_
(C_{17}H_{23}O_{3}N), readily converted into _Atropine_
(C_{17}H_{23}O_{3}N); _Scopolamine_ or _Hyoscine_ (C_{17}H_{21}O_{4}N),
and in smaller quantity _Apoatropine_, and _Belladonine_ are also
present.

All parts of the plant contain the toxic alkaloids, but in unequal
degree. The total quantity of the alkaloids is largest in the roots (0·4
to 1 per cent.), which in the fresh state contain no Atropine, but only
Hyoscyamine; the leaves and fruits contain less of the alkaloids, and
cultivated plants have been found to be poorer (0·26 per cent.) than
wild (0·4 per cent). The root has been found to be five times as toxic
as the berries. Drying does not destroy the poisonous properties.

_Symptoms._ In quantities which are not fatal the symptoms are nausea,
dilatation of pupils, muscular weakness, stumbling, falling, and rising
only to fall again. These are followed by vertigo, frenzy, and coma
(more rarely). There is a slight slackening in respiration, and an
increase in the rapidity of the heart’s action. Dysury and constipation
are observed.

In fatal quantities the symptoms are more intense and make their
appearance more rapidly. The nausea is accompanied by vomiting, and
there is almost complete loss of sight. Sensitiveness is at first
increased but later diminishes and gradually disappears; complete
incoordination of movements; increase in the heart’s action but a
gradually weakening pulse; stertorous, painful respiration; decrease in
temperature. There is repeated urination at the commencement of the
poisoning, and then dysury. At the approach of death there are muscular
trembling and clonic contractions. This phase of convulsions is short
but very clear in some cases: other cases do not leave the deep coma in
which they are plunged (Cornevin).

In regard to _cattle_, the following symptoms are given by Müller:
Injury to sight, dilatation of pupils, constipation, later bloody
evacuations, pain in hind limbs, rapid pulse, difficult breathing,
restlessness, frenzy and finally paralysis.

                              REFERENCES.

       4, 16, 61, 73, 81, 128, 138, 143, 151, 157, 161, 190, 205.




                               CHAPTER V
                             SCROPHULARINEÆ


=Foxglove= (_Digitalis purpurea_ L.). The Foxglove has been recognized
as poisonous for centuries, and one of its trivial names is Dead Men’s
Bells—a name suggestive of the consequences of taking it. It is the
source of the well-known drug; and cases of human poisoning have been
very common, though by no means always fatal—indeed, Esser says “seldom
resulting in death.” Animals are not known to touch this plant, but it
may possibly be included in rough meadow hay, though only one case, in
which two cows and a horse became ill after eating hay containing dry
foxgloves, has come to notice (_Veterinary Record_, 1906). Cornevin,
however, experimented on animals, and found the following amounts of
fresh leaves capable of causing death in the animals specified:—

                 Horse 120–140 grammes (4 to 5 oz.)
                 Ox    160–180    „    (5·5 to 6·5 oz.)
                 Sheep  25– 30    „    (0·88 to 1 oz.)
                 Pig    15– 20    „    (0·5 to 0·7 oz.)

The weight of dried leaves would be only one-fourth of these figures.

All parts of the foxglove are poisonous, but especially the seeds, and
the leaves are more active before than after the flowering period.
Cultivated varieties are stated to be less toxic than the wild species.
The effects of poisoning may terminate fatally in a few hours, or if
small quantities are taken regularly the poison may be cumulative and
induce chronic poisoning.

_Toxic Principle._ The foxglove contains several poisonous glucosides,
investigated by Kiliani, Schmiedeberg, Cloette, Bourquelot, Herzig, and
others. The following substances are toxic: _Digitalin_
(C_{35}H_{56}O_{14} or C_{36}H_{58}O_{14}) in the seeds and leaves;
_Digitonin_ (C_{54}H_{92}O_{28} or C_{55}H_{94}O_{28}) in the seeds;
_Digitalein_, only in small quantity; _Digitoxin_ (C_{34}H_{54}O_{11})
in the leaves; and _Digitin_. The toxic property of the foxglove is not
lost on drying or boiling.

_Symptoms._ Digitalis is an active heart poison, and causes nausea,
pressure in the region of the stomach, with diminished pulse, darkening
of the field of vision, dizziness, buzzing in the ears, and usually
dilated pupils.

According to Pammel the symptoms in animals are dullness, lassitude,
loss of appetite, nausea, flatulence, diarrhœa; infrequent, full pulse
(reduced 6–10 beats in the horse); and contracted pupils. In fatal cases
these symptoms are followed by severe colic and tympanites; rapid,
feeble, dicrotic, irregular or intermittent pulse (120–140 in horses),
while the heart may be heard and felt beating wildly and strongly, and a
systolic blowing murmur can frequently be detected. This is due to
mitral or tricuspid regurgitation caused by irregular contraction of the
columnæ carnæ. The pulse is imperceptible because of the failure of the
heart to fill the vessels. The extremities are cold, the eye is
protruding, and salivation occurs. Bloody diarrhœa is very often present
and the urine may be suppressed. The breathing finally becomes difficult
and death ensues within a few hours, or as late as several days.

The following account of the symptoms of poisoning in various animals is
collected by Lander:—

Horses. On the first day sleepiness, swollen eyelids, dilated pupils,
injected conjunctivæ, considerable swelling in submaxillary space;
respiration normal, temperature 103·5° F.; pulse full, between 65 and
75, very intermittent, being occasionally normal; the second heart sound
frequently obliterated. On the next day laboured breathing, head
immensely swollen, tongue greatly enlarged and protruding, pulse 80 and
most erratic, temperature very slightly up, great restlessness.
Respiration became more difficult and stertorous, tongue and buccal
membranes livid, jugular standing out.

A mare experimentally poisoned showed on the _third day_ dullness and
loss of appetite; _fourth day_ nauseated; nose, mouth, and ears cold;
abdomen blown, with colicky pain, and occasional pawing; pupil somewhat
contracted, pulse firm at axilla and heart, but not perceptible at jaw;
at 4.30 p.m. she was down, much pained, and attempting to roll; pulse
82, but unequal; _fifth day_, pulse, imperceptible at jaw, about 120;
respiration 25, and very much laboured: lips retracted and saliva
dripping from the mouth; enormous abdominal tympanites, and much pain;
rapid sinking: died _sixth day_.

Cows. Fed erratically, breathed hard, lay down after feeding. Pulse
almost imperceptible, contracted pupil, and excessive urination.

Pigs. Languid and sleepy: refused to eat or drink, attempting to vomit
and repeatedly passing small quantities of fæces. Urination was scanty
and strained.

In a case of poisoning among horses to which Müller refers the animals
had an exhausted appearance, there was loss of appetite, increasing
thirst, often also colic, and later diarrhœa, urination often in great
quantity, and staggering. Some of the animals died after a few days in
convulsions.

                               REFERENCES.

 4, 16, 73, 76, 79, 81, 161, 170, 187, 190, 203, 204, 205, 213, 229, 252,
                                   257.

=Lousewort= (_Pedicularis_, sp.). Two species of lousewort are involved,
_P. palustris_ L. and _P. sylvatica_ L., and though both are regarded as
poisonous the extent to which they are so is not well known. They have
an unpleasant smell and sharp taste, and are in general refused by all
classes of stock. _P. sylvatica_ may be eaten when young (Cornevin).
Lindley says that both plants are acrid, but are eaten by goats. _P.
palustris_ is regarded by Pott as an acutely poisonous plant, especially
for sheep. A decoction of these plants was formerly used against lice,
and hence the trivial name.

_Toxic Principle._ Very little appears to be known about the poisonous
principle, but, like _Rhinanthus_ and _Melampyrum_, they have been found
to contain the glucoside _Rhinanthin_ (see p. 96).

_Symptoms._ The plants are held to be emetic and purgative; to cause
inflammation of the digestive tract, and to cause anæmia in cattle.
Brugmann stated (_vide_ Cornevin) that if, pressed by hunger, animals
eat _P. palustris_, the first consequence is hæmaturia. Müller also
notes hæmaturia.

                              REFERENCES.

                       73, 76, 81, 190, 203, 213.


                              POLYGONACEÆ.

=Docks= (_Rumex_ sp.). In general it is probable that but little harm is
done by species of _Rumex_, but owing to the fact that Common Sorrel
(_R. Acetosa_ L.) and Sheep’s Sorrel (_R. Acetosella_ L.) contain acid
oxalates they may on occasion prove injurious. Instances have been
recorded in which children have suffered from eating the leaves of the
former species in considerable quantity, and both species have been
accused by veterinary surgeons of poisoning horses and sheep, some sheep
even dying. Pammel states that the Curled Dock (_R. crispus_ L.) induces
nausea, watery brown fæces, copious urination, dry spasmodic cough, and
perspiration; but no record of the death of animals has been found.

In regard to _R. Acetosella_ it is stated that in the _horse_ a
condition may be produced resembling drunkenness, with vacillating gait,
salivation, muscular tremors, dilatation of pupils, relaxation of
sphincters, and a feeble, slow, and intermittent pulse: then convulsive
contraction of lips, retraction of the eyeball, accelerated and
stertorous breathing, extreme dilatation of the nostrils, tetanic
contraction of the muscles of the neck, back, and limbs, abundant
sweating and falling. In bad cases after a period of extreme exhaustion,
these symptoms are repeated, and death occurs in convulsions (Cornevin).

The acid oxalates seem especially harmful to _sheep_, causing loss of
appetite, exhaustion, small and scarcely perceptible pulse, rapid
breathing, and constipation, and in many cases severe diarrhœa,
uncertain gait, and sometimes death (Müller).

The milk of affected cows is with difficulty made into butter (Pott).

                              REFERENCES.

                        73, 141, 190, 203, 233.

=Polygonum= sp. Several species of _Polygonum_ are said to have
poisonous properties. The chief among them is Buckwheat (_P.
Fagopyrum_), the grain of which is widely grown as a food for both man
and live stock. This plant, particularly the flowers, has given rise to
a well-known rash in man, cattle, sheep, and pigs, with congestion and
tumefaction—especially of the head and ears. There is also nervous
disturbance, with agitation and hallucination—sheep, for example, may
butt against objects. The affection of the nervous centres may lead to
fatal results, which have followed in cattle, sheep, and pigs. Little is
known of this so-called _Fagopyrism_, but after analytical and
spectroscopical researches on the colouring matter of the tegument Kurt
concluded that it is due to the chlorophyll.

Persicaria (_P. Persicaria_ L.) and Water-pepper (_P. hydropiper_ L.)
are also stated to be harmful, though the former has been considered a
nutritious plant and has been given to horses and cattle as a green
food.

Both species, however, are said to cause a rash, and to contain
injurious narcotic substances. Persicaria is stated by Müller to have
caused inflammation of the bladder and the digestive tract in pigs, and
Water-pepper to have caused hæmaturia; fatal results have followed. Pott
records similar symptoms. In regard to Persicaria it should be noted
that it varies considerably in general form, and may possibly vary also
in acridity. Bentham and Hooker state of _P. hydropiper_ that “the whole
plant is more or less acrid or biting to the taste.”

                              REFERENCES.

                       17, 19, 73, 190, 204, 213.


                              THYMELACEÆ.

=Mezereon= (_Daphne Mezereum_ L.) and =Spurge Laurel= (_D. Laureola_
L.). Both of these species are acrid and poisonous, and cases of the
death of horses due to the spurge laurel are recorded by Lander. In
general, however, animals will not eat the plants, and indeed, in one of
the cases mentioned by Lander the dried leaves were administered for
worms. Should they touch these plants most animals would probably refuse
them on account of their bitter taste. The berries are tempting to
children, and Pratt says “Death has resulted from eating but a few of
these berries (_D. Mezereum_); and Dr. Christison relates a case of a
child, in Edinburgh, who died from eating them, while another is
recorded by Linnæus of a young lady to whom twelve of the berries were
given as a medicine in intermittent fever, and who soon died in
consequence of their corrosive poison. Four berries produced thirst,
sense of heat in the mouth and throat, and also fever, in a man who ate
them; and they are proved to be poisonous to dogs and foxes.” Blyth
states that 30 grammes (1 oz.) of the powdered bark is a lethal dose for
a horse, but smaller doses of the fresh leaves may be deadly (Pammel).

_Toxic Principle._ All parts of these plants are acrid and poisonous,
especially the bark and berries. They contain the bitter, astringent,
and poisonous glucoside _Daphnin_ (C_{30}H_{34}O_{19}—or C_{15}H_{16}0_9
according to Van Rijn), an acrid resin (Mezerein), and a _vesicating
fatty oil_. (Pott remarks that Daphnin is believed to be harmless, but
that Mezerein has poisonous effects.) Drying does not destroy the
poisonous property.

_Symptoms._ The Daphnes are severely purgative, cause burning in the
mouth and throat, and in severe cases have narcotic effects and give
rise to convulsions.

Lander gives the symptoms as intense colic, constipation, followed by
dysentery and copious evacuations of fæces streaked with mucus, blood,
and intestinal epithelium. Drowsiness between the spasms.

According to Müller there is inflammation of the stomach and intestines
(with colic, vomiting, severe diarrhœa, passing of blood), inflammation
of the kidneys (with strangury, bloody urination), and in many cases
nervous symptoms (weakness, giddiness, and convulsions).

In a case observed by Lander, in the horse, there was abdominal pain,
staggering gait, anxious countenance, laboured breathing, pulse 80,
temperature 103·2° F., bowels normal. On the following day there was
excessive purgation, pulse 120, temperature 104·2° F., and death
occurred at mid-day.

                              REFERENCES.

          73, 76, 81, 130, 141, 170, 190, 203, 213, 216, 240.


                             EUPHORBIACEÆ.

=Spurges= (_Euphorbia_ sp.). Many species of Spurge must be regarded as
acrid, purgative, and poisonous. Live stock are not likely to touch
them, owing to the acrid effect of the milky juice on the mouth.

The Caper Spurge (_E. Lathyris_ L.) contains an acrid, emetic, and
highly purgative milky juice, and the fruits have commonly been employed
by country folk as a purge, and also as a pickle, though they are
dangerous and should not be so used. Pratt records a case in which five
women ate the pickled fruits with boiled mutton, and all suffered severe
pain and burning in the stomach, and showed other symptoms attendant on
irritant poisoning—and though all recovered the illness was severe. Used
in this manner, indeed, they have given rise to serious cases of human
poisoning. Only very young animals are said to eat it, but cattle in the
United States are said to be “quite resistant to its influence, but they
are sometimes overcome.” According to Chesnut goats eat this plant
extensively, and it is said that their milk then possesses all the
venomous properties.

Petty Spurge (_E. Peplus_ L.) is somewhat similar to the Caper Spurge in
poisonous properties, and fatal poisoning has occurred through a boy
eating it.

Sun Spurge (_E. Helioscopia_ L.) is similarly poisonous to the preceding
species. It has caused fatal poisoning to a boy who ate it. In Germany
cows were poisoned through pasturing in stubble in which the plant was
growing, but there were no deaths.

_Toxic Principles._ The milky juice of these spurges contains highly
acrid poisonous substances, which have not been individually and fully
investigated. Drying may reduce the toxicity but does not eliminate it.

_Symptoms._ As regards _E. Lathyris_ Chesnut says that on the skin the
juice causes redness, itching, pimples, and sometimes gangrene. The
seeds when eaten inflame the mouth and stomach, cause vomiting and
intense diarrhœa, and if the illness is serious, nervous disorders,
unconsciousness, collapse, and death.

The _Euphorbias_ have an acrid effect on the mouth, and severe poisoning
may follow their use as aperients—burning mouth, swelling tongue,
stomach pains, cold skin, vertigo, fainting or syncope, and even death
in two or three days (Esser).

Similar symptoms are given by Cornevin, who states that the Euphorbias
have an irritating effect on the mucous membrane, especially at the back
of the mouth. In from three quarters of an hour to two hours after
eating the plant, or even longer, there is painful vomiting, followed by
diarrhœic evacuations, with a lowering of the temperature. If the
quantity ingested has been sufficient there appear also nervous
symptoms, vertigo, delirium, muscular tremors, and respiratory and
circulatory troubles which disappear after abundant sweating if the
poisoning is not fatal. If it is fatal the symptoms of superpurgation
and enteritis predominate, but are accompanied by nervous symptoms and
circulatory disorders.

Müller gives in addition loss of appetite, piteous whining (in goats),
groaning, colic and tympanites; and Pott, bloating, fever, palpitation
of the heart, and loss of consciousness. Cows gave a reddish or
sharp-tasting milk. Milk of affected goats caused diarrhœa human beings.

                              REFERENCES.

            19, 52, 53, 73, 81, 82, 130, 141, 190, 213, 216.

=Dog’s Mercury= (_Mercurialis perennis_ L.) and =Annual Mercury= (_M.
annua_ L.). These two species may be taken together as they have similar
poisonous properties, and closely resemble one another, though the
former is a perennial and the latter an annual. The plants have a
somewhat unpleasant odour, and live stock are not likely to take them
unless pressed for readily available green food. The loss of one cow and
severe illness of four others was recorded by Blackhurst in the
_Veterinary Journal_ in 1896; Güssow mentioned the loss of cows in the
_Farmer and Stock Breeder Yearbook_, 1907; the loss of horses fed on
herbage cut from a hedge and containing _M. perennis_ was recorded in
the _Journal of the Royal Agricultural Society_ in 1898; the loss of
sheep was recorded by Henslow. As regards man, Ray records a case in
which a family of five persons suffered severely from eating _M. annua_
fried with bacon. Fishermen ate it with soup and all were seriously ill
an hour later, with symptoms of irritant narcotic poisoning; two
children died the next day. Cornevin saw _M. annua_ used, after boiling,
as a food for pigs, without ill consequences, in the east of France.
This is believed to be due to the poison being volatile and destroyed by
heat or boiling; hence in hay the plant is harmless, though Pott says
that even in hay stock avoid it.

_Toxic Principle._ The poisonous properties are said to be due to
_Mercurialine, Oil of Euphorbia_, a volatile toxic alkaloid. Esser
states that the stem and leaves of _M. annua_ contain _Trimethylamine_,
which may perhaps be a decomposition product of _Choline_, a poisonous
base.

_Symptoms._ Both plants are emetic and dangerously purgative, causing
irritant and narcotic symptoms. Veterinary observation has shown that
the poison is cumulative, and that it is usually after the weed has
formed part of the food for 7, 8, or 10 days that symptoms first appear.
In the case recorded by Blackhurst (see above) the cows suffered from
inflammation of the digestive tract, with severe purging and loss of
blood. The secretion of milk entirely stopped. One cow died, but three
recovered in about four days. The fifth was not convalescent for three
weeks and then had a permanently curved and injured neck, the muscles
being subsequently found rich in fibrous tissue, and the last three
joints partially anchylosed. Rabbits were tested by feeding two on the
leaves, two on the stems and roots, and two on the ground seeds mixed
with oatmeal; the first two were unaffected, but the other four died in
a few hours, showing drowsiness and suffering, while the post-mortem
showed gastritis.

The digestive and urinary tracts are affected. There is indigestion with
slight bloating, then colic of varying intensity, and at first diarrhœa
which may give place later to constipation; hæmaturia; micturition is
frequent, painful, and the urine is blackish and bloody; dullness,
weakness, loss of appetite and refusal of food; the heart beats very
strongly, the pulse is rapid, and the mucous membrane of the eye is
reddish-yellow in colour. There is no modification of respiration
(Cornevin).

According to Müller, however, the symptoms at _first_ include
constipation and _later_ severe and bloody diarrhœa.

In cattle Pott states that _M. annua_ causes inflammation of the stomach
and intestines, bloody urine, paralysis of bladder, fœtid diarrhœa,
abortion, and bluish coloured milk deficient in fat. Müller states that
there is occasionally blood in the milk. According to Lander there is in
cows excessive bloody purgation, cessation of lactation, temperature
105° F., pulse 90, and increased respiration. The illness is protracted
over several weeks, the animals being comatose after the first symptoms.

                              REFERENCES.

            73, 81, 112, 130, 146, 170, 190, 205, 213, 255.

=Box= (_Buxus sempervirens_ L.). Farm live-stock may occasionally have
the opportunity of browsing on box, or clippings may be thrown to them
with other green herbage from gardens. Care should be taken that
clippings are otherwise disposed of. All parts of the plant are bitter
and have been proved to be poisonous. The bitter taste tends to prevent
animals eating sufficient of the plant to cause serious injury. Pigs
have died a day after eating the leaves. Horses also were killed by
eating 750 grammes (1·6 lb.) of the foliage.

_Toxic Principles._ Fauré found in the bark and leaves of box the toxic
alkaloid _Buxine_, but it was believed that there were other toxic
substances, since analysis showed the leaves to be less rich in Buxine
than the bark, while they are three times as active. Other substances
occurring in box are _Parabuxine_, _Buxinidine_, and _Parabuxinidine_.

_Symptoms._ Small amounts have an emetic and purgative action; with
average amounts, there are, in addition, nervous symptoms, lameness,
muscular tremors, vertigo, then a period of coma. Large amounts cause
death with intense abdominal pains, dysenteric flux, tenesmus,
convulsions, respiratory and circulatory troubles.

Pigs are chiefly affected after eating the leaves, exhibiting great
thirst, uncertain gait and delirium, while death occurs within
twenty-four hours.

Pott gives the general symptoms as sickness, diarrhœa, giddiness,
stupefaction, convulsive movements, and colic.

                              REFERENCES.

                  4, 16, 73, 128, 190, 205, 213, 235.


                               AMENTACEÆ.

=The Oak= (_Quercus_ sp.). Injury to stock from the Oak has been due in
the first place to the leaves, and in the second to the acorns. In
regard to the leaves no injury appears to have been recorded in Britain,
but Cornevin devotes attention only to poisoning by the leaves, which in
special circumstances have caused serious accidents to animals which
have eaten them. In France, cattle taken to the forests for grazing
purposes browse on the young shoots and leaves of the oak, and after
some days there arises a trouble long known as _Mal de Brou_ or _Maladie
des Bois_, which may end fatally, sometimes even in 24 hours (see
_Symptoms_ below). A case was also reported from Nebraska in 1903, ten
head of cattle having apparently died from eating oak leaves, the
trimmings from trees. The stomachs were full of the leaves, and the
intestines had the appearance of being burned in places. There was no
evidence of impaction. When the cut branches were removed no more cattle
were lost.

Serious losses have been caused through the ingestion of acorns by young
cattle not over about two years old, the years 1808, 1870, 1884, and
1900 being especially noteworthy in this respect. Cattle over three
years old have seldom been affected, while sheep and pigs, if not immune
to “acorn poisoning,” are but slightly affected. Müller, however, states
that horses, cattle, sheep, and goats are affected; 9 quarts (10 litres)
taken in four days were sufficient to cause poisoning in the case of a
bullock. It is believed by some observers that half-ripe acorns—_e.g._
acorns which may drop owing to drought—are more injurious than
thoroughly ripened acorns.

Some authorities appear to be of the opinion that “acorn poisoning” is
not actually poisoning, but a serious form of indigestion. If this be so
the symptoms must be regarded as exceedingly severe. There is no doubt
that “acorn poisoning” is not well understood, but a great deal has been
observed and written on the subject, and there is clear evidence that
acorns may reasonably be held to be poisonous. It must be pointed out,
however, that the poisoning does not usually follow on the consumption
of acorns in small quantities, but is commonly due to full meals of
acorns taken in periods when there is a dearth of herbage. By proper
preparation and storage acorns have been converted into a most useful
food for horses, cattle and sheep (_Jour. Bd. Agric._, Sept. 1914 and
Feb. 1916, and Leaflet No. 291 of the Bd. Agric., _The Food Value of
Acorns, Horse-Chestnuts and Beech Mast_). In Germany it has been found
that acorns fed to fowls caused diminished egg-laying, which finally
ceased, while the yolks of eggs laid were discoloured a dirty brown
(_Jour. Bd. Agric._, Dec. 1915, p. 902).

_Toxic Principle._ The facts as to acorn poisoning and oak-leaf
poisoning are not clearly known, and the actual toxic substance is
similarly not certainly known. It is probable, however, that it consists
of _Tannin_, or substances which give rise to Tannin.

_Symptoms._ In relation to _Maladie des Bois_ due to leaves, Cornevin
gives the symptoms as loss of appetite; less (and more difficult)
rumination; constipation, which increases; lying down, animals looking
at their flank as in colic, followed by rising and attempts to urinate,
with passing of rosy-coloured liquid in jets; loss of milk production,
which may drop to nothing; fever, trembling, enfeebled condition.

Three or four days after the commencement of illness rumination is
completely suspended; there is stamping of the feet, colic, retracted
stomach, pulse hard, heart agitated, accelerated respiration, violent
muscular shocks, and frequent urination. The urine is always dark in
colour, but varies from clear red to dark black, nut-brown being usual.
Cases are only serious when a fœtid, frothy, and abundant dysentery
succeeds constipation, in which case there is rapid emaciation and
death.

Usually the course of the illness is not rapid; but occasionally there
is immediate and bloody urination with violent colic and sometimes
intestinal hæmorrhage, death occurring in 24 hours.

In poisoning by _acorns_ there is progressive wasting, entire loss of
appetite, diarrhœa, discharge of an excessive quantity of pale urine,
sore places inside the mouth, discharge from the nostrils, and also from
the eyes, which are always sunken, giving the animal a peculiar haggard
expression. There is no fever; on the contrary, the temperature is
commonly below normal, though in some cases stated to be above normal.

Müller remarks on the severe constipation, followed by dysenteric
diarrhœa, caused by acorns, especially when eaten in the half-ripe
condition, horses, cattle, sheep, and goats being affected.

The experimental poisoning of a young steer and a young sheep by fully
ripe acorns was described in 1871 (_Jour. R.A.S.E._, 1871). In the steer
the symptoms were a semi-conscious condition, weak pulse, pallid
membranes, cold surface of body, torpid bowels, slow breathing,
twitchings of muscles, and a disposition to maintain a recumbent
position. Inflammation was entirely absent. The symptoms increased in
severity day by day; there ensued a copious flow of colourless urine; a
mucopurulent discharge from the eyes and nostrils. No impairment of
health followed the feeding of acorns to the sheep.

Thorburn (_Veterinary Journal_, Feb., 1902) mentions loss of appetite,
grunting, disinclination to move, prostration, icy coldness of
extremities, very rapid emaciation (this sometimes was particularly
noticeable), pulse very small and weak (in some cases almost
imperceptible), temperature high (105° to 107° F.,) and constipation
succeeded by watery diarrhœa.

Brookes and Yeomans described (_Veterinary Journal_, 1912) an instance
in which 30 animals were affected and 9 died. The chief symptoms were a
dull and depressed appearance, entire absence of appetite and
rumination, a weak feeble pulse, subnormal temperature and
disinclination to move. Three cases showed a mucous and blood-tinged
discharge from the nostrils and anus, and these all died, one eight days
after being seen and the other two the day afterwards. Obstinate
stoppage was noticeable in all cases, and the fæces were inky black,
stinking and very thick. Yeomans observed similar symptoms of acute
digestive disturbance; later the eyes had a sunken appearance, diarrhœa
set in, the fæces being dark coloured, offensive and bloodstained. The
temperature was at first normal and later subnormal, and in fatal cases
death took place in from 3 to 7 days.

                              REFERENCES.

          4, 13, 20, 26, 29, 70, 73, 130, 144, 190, 240, 255.


                               CONIFERÆ.

The only Conifer which commonly causes poisoning of live-stock is the
Yew, but injury might more frequently occur were it not for the fact
that Conifers generally are unpleasant to the taste, and are hence
avoided by stock. Many species, however, contain _Tannin_, _Resins_ and
_Gums_, _Volatile Oils_, and an acrid substance which may cause
inflammation of the digestive and urinary tracts, while Tanret found in
the young shoots of _Picea_ the bitter glucoside _Picein_
(C_{14}H_{18}O_{7}H_{2}O); Kawalier and Thal found the intensely bitter
glucoside _Pinipicrin_ (C_{22}H_{36}O_{11}) in _Pinus sylvestris_,
_Thuja occidentalis_ and _Juniperus Sabina_; and Kubel isolated
_Coniferin_ or _Abietin_ (C_{16}H_{22}O_{8}), a slightly bitter
glucoside found in _Abies excelsa_, _A. pectinata_, _Pinus strobus_,
_Larix europæa_ and other conifers. It is not clear, however, whether
these substances are at all poisonous. It is quite possible that if
eaten in quantity the foliage of some Conifers may induce poisonous
symptoms and even death in the animals concerned. It is noteworthy,
however, that according to Pott the needles of _Picea excelsa_, _Abies
pectinata_, _Larix europæa_, and _Pinus_ sp. are, in the mountainous
districts of Steiermark, Kärnten, and Tyrol, extensively fed to cattle
and sheep, usually as a supplementary food, either fresh or dried and
ground up—chiefly perhaps as an appetiser, and in small quantities as a
dietetic; _Juniperus_ sp. are similarly utilised in some districts. It
is not known to what extent the foliage may be fed without harmful
consequences, but Pott states that large quantities can cause hæmaturia
and similar effects, and hence only small quantities should be used, and
even so may impart a bad flavour to the milk of cows. All green needles
frequently cause digestive troubles.

A case has recently (January, 1916) been reported to the author in which
a Douglas Fir was cut down and a small branch about 4 ft. long was flung
over into a field. Two sheep nipped off the bark and nearly died, but
both vomited and recovered. The farmer reporting this experience recalls
that over 30 years ago, after a gale, a lot of trees were blown down in
a small plantation, and in severe weather the sheep ate the bark to such
an extent that 80 of them aborted, while of the ewes which did not eat
the bark none aborted, so that it would appear that the bark of Scotch
Fir and Spruce was to blame for the loss.

The foliage of the Yew (_see_ below) is well known to be dangerously
poisonous to stock, and has caused many losses.

In regard to _Cupressus_ the only cases of poisoning which have been
traced are recorded in _The Journal of the Board of Agriculture_
(October, 1905). These cases were reported as follows:—

“Two instances have recently come before the Board in which the death of
cattle has been attributed to the poisonous effects of _Cupressus
macrocarpa_ and _C. nootkatensis_. In one case four bullocks died, and
on the internal organs being forwarded by the owner to the Royal
Veterinary College, Professor McFadyean reported that from the inflamed
condition of the fourth stomach and from the description of the symptoms
he had little doubt that the cause of death was irritant poison. Some
pieces of _Cupressus macrocarpa_ were found in their stomachs, and in
default of any other explanation it was suggested that this plant might
have some poisonous properties.

“In another case three heifers are stated to have suffered from irritant
poison; one of them died, but the other two recovered on removal to
another field. The veterinary surgeon in this case also attributed the
death to a Cupressus (_C. nootkatensis_) growing by the side of the
field.

“The Board have no information as to the poisonous properties of these
two species, nor can any record be found of any similar case which would
tend to confirm the suspicion that they are poisonous to cattle.”

                              REFERENCES.

                       4, 16, 76, 144, 213, 252.

=Yew= (_Taxus baccata_ L.). As stated above, the Yew is the only British
conifer that is likely to prove seriously poisonous to live stock. It
has unfortunately caused the death of many horses and cattle, while
asses, mules, deer, pigs, rabbits, and pheasants have also been
poisoned. Many cases of fatal human poisoning have also occurred. For
example, the poisoning of a horse, and of cattle, horses, and deer were
mentioned respectively in 1885 and 1893 (_Jour. Roy. Agric. Soc._).
“Through eating the poisonous leaves of a Yew tree, four cross-bred
cattle were found dead in a shrubbery at Elmswell, near Driffield”
(_Daily Mail_, 13th Dec., 1913). Many cases of poisoning and death of
animals due to eating the foliage direct from the trees have been
recorded in the veterinary journals—e.g. the death of 15 cattle in _The
Veterinary News_, 7th Dec., 1912. Tegetmeier recorded the death of
pheasants due to Yew leaves and seeds (_The Field_, 11th Nov., 1893). On
the other hand many cases have been recorded in which fatal results have
not followed the ingestion of the leaves, and it appears that the lower
branches of Yew trees in parks are constantly cropped by cattle without
ill effects. (_Trans. Chem. Soc._, 1902; _Jour. Bd. Agric._, 1903).

The bark, leaves, and seeds are all poisonous, the leaves usually being
the parts eaten. Henslow states that of 32 cases of Yew poisoning 9 were
due to the berries and the remainder to the leaves, while 20 of the 32
cases were fatal. In 1879 R. Modlen published a circumstantial account
of children poisoned at Oxford by the fruits, and demonstrated that the
arillus or scarlet mucilaginous cup surrounding the ripe seed is not
poisonous, but that the seeds are so. Apart from idiosyncrasy of
appetite stock are perhaps more likely to eat the dark green foliage of
the Yew in winter or during scarcity of green fodder than at other
times. The old leaves or shoots are the most poisonous parts.

By experiments with autumn and winter leaves Cornevin found that the
following quantities would be necessary to kill various animals:—

            Horse         0·2  lb. per 100 lb. live weight.
            Ass and Mule  0·16 lb.      „            „
            Cow and Sheep 1·0  lb.      „            „
            Goat          1·2  lb.      „            „
            Pig           0·3  lb.      „            „
            Rabbit        2·0  lb.      „            „

Other authorities, however, quote much lower quantities as necessary to
kill the horse and ox, and Pott says that in the case of horses 150 to
180 grammes (0·33 to 0·4 lb.) is sufficient to cause death in
one-quarter to one-half an hour, without previous symptoms. Eaten by an
animal on a full stomach a small quantity of Yew may cause little or no
dangerous results.

_Toxic Principle._ The researches of Marmé pointed to the alkaloid
_Taxine_ (C_{37}H_{52}NO_{10}) as the toxic substance. Later
investigations of Thorpe and Stubbs confirmed this view, and it is
generally agreed that this substance is the toxic principle, though
doubts as to its being the only poison have been expressed. Taxine has a
bitter taste, is a heart depressant, and may cause death from
suffocation. The yew also contains a considerable quantity of _Formic
Acid_, and the acrid, irritant volatile _Oil of Yew_.

Thorpe and Stubbs (_Trans. Chem. Soc._, 1902) found in the fresh leaves
of the common Yew from 0·1 to 0·18 per cent. of Taxine. In an
investigation of the Irish Yew (_T. baccata_ var. _fastigiata_) Moss
found Taxine present as follows:—

             Leaves from female tree, fresh 0·596 per cent.
             Leaves from female tree, fresh 0·623     „
             Seeds from fruit of same tree  0·079     „
             Another female tree—leaves     0·323     „
             Another female tree—seeds      0·082     „

In the leaves of the male common Yew Moss found 0·082 per cent. of
Taxine, or less than one-half the quantity found by Thorpe and Stubbs.

_Symptoms._ The Yew is irritant and narcotic, and the poison is not
cumulative, but on the other hand rapidly effective, so that animals may
die apparently suddenly, no previous symptoms having been observed.

When small quantities only have been taken the closest attention is
necessary to discern the symptoms, which simply consist in a little
excitement with a slight rise in temperature.

With larger (but not fatal) quantities the first symptom, excitement, is
more pronounced and is followed by nausea, and (where possible)
vomiting. There is a pronounced slackening of respiration and
circulation, the pulse being small, slow, and difficult to perceive, and
the movement of the flanks very slow; sensibility is diminished. There
is a fall in temperature, the skin and extremities being cold. The head
is lowered, the eyes are closed and there is decubitus. In some cases
pregnant animals have aborted. In the _horse_ there are muscular tremors
and frequent urination. In _cattle_ and _sheep_ rumination is suspended
and there is more or less pronounced tympanites, with eructation,
nausea, and sometimes vomiting. _Pigs_ bury the head in the litter and
sleep, their sleep being interrupted from time to time by nausea and
groaning; or the animals rise, stagger about, and lie down again.

With fatal quantities the foregoing symptoms may be followed by coma,
with death in two hours or more after the poisoning, but more generally
and usually in horses, asses, and mules (but also in cattle) there is no
period of coma, the excitement is less pronounced and often unobserved,
and death appears very sudden. The animals stop, shake their heads,
respiration is modified, there is falling, and death (sometimes with
convulsions) results from cessation of the heart’s action (Cornevin).

The symptoms given by Müller are roaring, torpidity, stupefaction,
laboured breathing, convulsions and death in from ten minutes to an hour
in the worst cases; or where the course of poisoning is slower, there is
salivation, nausea, vomiting, bloating, retardation of pulse and
respiration, great giddiness and stupefaction, diabetes and hæmaturia.

The rapidity of the poisoning is confirmed by cases noted in the
veterinary journals. Lander shows that the effects often only appear in
cattle when chewing the cud; whilst quietly chewing, they drop as if
shot. In some examples the animal died while eating the plant, or was
found to have fallen and died suddenly and without evidence of a
struggle. The animal in some cases will stop suddenly whilst working,
start blowing and trembling, stagger, fall on its haunches, then on its
side, and die quietly. Death occurs in about five minutes with symptoms
resembling apoplexy. A colt died after 16 or 17 hours; the plant was
taken on a full stomach, but paralysis of the alimentary system with
stoppage of digestion immediately ensued.

In the case of pheasants there was acute inflammation of the small
intestines (Tegetmeier).

                              REFERENCES.

          4, 16, 49, 73, 81, 84, 100, 128, 130, 141, 144, 161,
                170, 189, 190, 205, 213, 239, 240, 256.


                                AROIDEÆ.

=Cuckoo Pint= (_Arum maculatum_ L.). The well-known Cuckoo Pint, or
Lords and Ladies, is to be regarded as highly poisonous, and children
have died from eating the berries. Animals have exceptionally eaten the
plant, but no record of death has been found, as it does not appear to
be taken in sufficient quantity. Cornevin records that pigs have eaten
the roots, and suffered in consequence, though the results were not
fatal. All parts of the plant are poisonous, though the virulence is
lost on drying. The plant is acrid, and emits a disagreeable smell when
bruised. In Gerarde’s _Herball_ the following passage occurs: “The most
pure and white starch is made from the rootes of the Cuckowpint; but
most hurtfull for the hands of the laundresse that hath the handling of
it, for it choppeth, blistereth, and maketh the hands rough and rugged,
and withall smarting.” In Dorset the tuber-like corms have been
macerated in water, dried and powdered, and eaten under the name
Portland Sago or Portland Arrowroot, the poisonous property being
dissipated.

_Toxic Principle._ The Cuckoo Pint does not seem to have received much
attention in this connection, but the poisonous principle is believed to
be a _Saponin_.

_Symptoms._ The juice acts as an irritant when in contact with the
mucous membrane. When a _pig_ has eaten several roots rich in sap, the
mouth and tongue redden and tumefy, there is salivation, and swallowing
is difficult on account of the inflammation at the back of the mouth.
Introduced in small quantity into the digestive tract it acts as an
irritant and purgative, and sometimes causes vomiting. Severe intestinal
pains, excitement, some muscular contraction of the limbs, rocking of
the head, and superpurgation with tenesmus are also symptoms which have
been observed. The intestinal pains continue for some days and the
appetite is small. Cornevin states that animals never take a sufficient
quantity to cause _fatal_ poisoning, but according to Lander, if a
dangerous quantity is taken, convulsions, exhaustion, and death from
shock may possibly follow the foregoing symptoms.

A case in which a _horse_ was poisoned through a wound being washed with
a decoction of arum leaves is cited by Müller. There was much local
swelling, trembling, and rapid breathing, and the heart beat strongly;
the animal died on the third day.

                              REFERENCES.

                      73, 81, 130, 141, 170, 190.




                               CHAPTER VI
                              DIOSCORIDEÆ.


=Black Bryony= (_Tamus communis_ L.). The stem and foliage of Black
Bryony are apparently harmless, being browsed by sheep and goats with
impunity, but the scarlet fruits are decidedly poisonous and the starchy
root is acrid and purgative.

_Toxic Principle._ This is probably the glucoside _Bryonin_, which
occurs in _Bryonia dioica_ (p. 35).

_Symptoms._ Cornevin, in citing experiments on animals, states that
small quantities of the fruits cause uneasiness, somnolence, and
difficult locomotion. Larger quantities cause vomiting, intestinal
pains, and paralysis of hind quarters. Death is rapid. Müller, however,
remarks that paralysis of the hind quarters and convulsions may result
from small quantities, large quantities causing in addition inflammation
of the stomach and intestines.

                              REFERENCES.

                                73, 190.


                               LILIACEÆ.

=Herb Paris= (_Paris quadrifolia_ L.). Owing to its habitat—damp
woods—it is unlikely that stock will eat this plant, but it may be
possible where fields border open woods in which it grows. No records of
stock poisoning have been met with, but cases of poisoning in man are
recorded, one due to eating a considerable number (30 to 40) of the
berries, and symptoms of poisoning in a child four years of age who had
eaten a few berries. In smaller quantities they are very poisonous to
poultry. All parts are stated to be poisonous, especially the berries.
Fatal poisonings are nil, or very rare if recorded.

_Toxic Principle._ Walz isolated the glucoside _Paridin_; and Esser
states that the toxic property is due to a Saponin,—the bitter irritant
glucoside _Paristyphnin_ (C_{38}H_{64}O_{18}), which is convertible into
Paridin (C_{16}H_{28}O_{7} + 2H_{2}O) and sugar.

_Symptoms._ The plant is emetic, purgative, intensely acrid, and
narcotic. Poisoning up to the present only appears to have been recorded
in fowls, the symptoms being intense local inflammation, narcotic
effects, vomiting, colic, diarrhœa, stupefaction, convulsions, and
paralysis (Müller).

                              REFERENCES.

                   4, 16, 73, 76, 81, 130, 141, 190.

=Lily-of-the-Valley= (_Convallaria majalis_, L.). This beautiful plant
is only likely to induce poisoning of domestic animals at very rare
intervals, as it occurs wild in only a few woods from Moray southwards,
being, however, abundant in some districts. All parts are stated to be
poisonous, especially the flowers. It has an acrid, bitter taste. Few
cases of poisoning are recorded. Sheep and goats are believed to eat the
leaves with impunity. The extract is so poisonous that four drops
injected into the blood stream sufficed to kill a dog in ten minutes
(Cornevin). The leaves have been known to kill geese and fowls.

_Toxic Principle._ All parts of the plant contain the bitter poisonous
glucoside _Convallamarin_ (C_{23}H_{44}O_{12}), the glucoside _Paridin_
(C_{16}H_{28}O_{7} + 2H_{2}O), and the glucoside _Convallarin_
(C_{34}H_{62}O_{11})—the first a dangerous purgative, and the last a
cardiac poison resembling Digitalis. Convallamarin is a very poisonous
crystalline substance, with at first a bitter and afterwards a sweetish
taste.

_Symptoms._ The action of this plant on the animal organism is not yet
clearly known, but it is stated to have marked emetic and purgative
action. Taken in moderate quantities a period of retardation of the
heart and lung action is followed by a period in which the heart action
is intermittent, and there are stoppages in respiration, and vomiting.
Taken in large quantities, the first of these periods is extremely
short, the pulse soon becomes rapid and small, respiration is quickened,
and the heart action ceases (Cornevin).

Pott observes that the leaves cause stupefaction, convulsions, and death
after a few hours in the case of _geese_. He cites a case in which ten
_fowls_ ate the leaves and nine died.

                              REFERENCES.

                  52, 73, 76, 81, 190, 203, 205, 213.

=Meadow Saffron= (_Colchicum autumnale_ L.). The Meadow Saffron, Autumn
Crocus, or Naked Ladies, as it is variously named, occurs in meadows in
many districts in England and Wales. All parts are poisonous, both in
the green state and when dried, as it possibly may be, in hay. It has
caused extensive losses of live stock, and the greatest care should be
taken to eradicate it from grass land. The leaves and seed-vessels are
produced in spring, and the flowers from August to October—and it is at
these two periods that cases of poisoning by this plant are most
frequent, though, as stated, it may be included in hay. Many horses,
cattle, and pigs have been killed by Meadow Saffron, though cattle
commonly avoid it. Sheep and goats are believed to be very slightly
affected. Children and fowls died at Schorren (Canton Berne) from eating
the seeds, and there have been many cases of human poisoning due both to
eating the seeds and the bulbs. In Staffordshire, Mr J. C. Rushton
reported some years ago[4] that in one year a farmer lost seventeen
milking cows; in 1908 he lost seven calves; and in 1909 he lost a number
of sheep and cows. It was then discovered that the field in which the
animals grazed contained “any quantity of Meadow Saffron and Water
Hemlock,” and this was the cause of the losses. Horses and cattle are
more commonly poisoned than other domesticated animals. Johnson and
Sowerby record the case of a woman who ate the corms in mistake for
onions at Covent Garden, and died; and state that deer and cattle have
been killed by the leaves. Kanngiesser notes that this species is the
most toxic of German plants, and that in cases of human poisoning the
mortality is 90 per cent., children being chiefly affected. Cornevin’s
experiments showed that 8 to 10 grammes of green leaves per kilogramme
of live weight—say 3 to 5 lb. for an average cow—was sufficient to kill
ruminants; while 30 centigrammes of corms per kilogramme of live weight
sufficed to kill pigs—say 4½ oz. for a pig of 200 lb. live weight.
Barret and Remlinger (_Veterinary Journal_, 1912, p. 306) record the
sudden illness of 31 out of 51 cattle, and 5 of them died.

Footnote 4:

  _Staffordshire Weekly Sentinel_, Aug. 21st, 1909.

The toxic principle is cumulative, that is, small quantities of the
plant eaten regularly may result in poisoning, owing to the poison being
slowly eliminated by the kidneys. Indeed, cases have been recorded in
which the poison has been secreted and eliminated in the milk of cows
and so has caused poisoning of both calves and infants.

_Toxic Principle._ Meadow Saffron contains in all parts the acrid,
poisonous alkaloid _Colchicine_ (C_{22}H_{25}NO_{6}) stated by Esser to
occur to the extent of 0·2 per cent. in the corms, 0·4 to 0·6 per cent.
in the seed coats, but only traces in the leaves. Hertel obtained 0·38
to 0·41 per cent. of alkaloid from the _seeds_, Farr and Wright from
0·46 to 0·95 per cent., and Carr and Reynolds 0·12 to 0·57 per cent.;
the U.S. Pharmacopœia, 1905, required a Colchicine content of 0·45 per
cent. in the _seeds_, and 0·35 per cent. in the _corms_ (Allen).

_Symptoms._ After small, but not fatal doses there is loss of appetite,
suppression of rumination, salivation, light colic, diarrhœa and voiding
of small quantities of urine. Blood has been observed in the milk of
affected cows. Larger and fatal quantities cause total loss of appetite
and sensation, stupefaction, loss of consciousness, dilatation of
pupils, unsteady gait, and even paralysis of limbs, sweating, severe
colic, and bloody diarrhœa, strangury and bloody urination; rapid,
small, and finally imperceptible pulse, laboured breathing; and death in
from one to three days. Where recovery takes place it is very slow (12
to 14 days according to Cornevin).

Cornevin draws attention to the fact that, as the symptoms do not occur
until several hours after ingestion, by which time the poison must be
partly distributed, the poison is very dangerous and difficult to
combat, attempts at vomiting or evacuation, whether spontaneous or
caused therapeutically, having little chance of ridding the organism of
the poison. Cornevin’s account of the symptoms shows that at first there
is abundant salivation, with constriction of the throat, and dysphagia;
then nausea with vomiting; colic; abundant, repeated and diarrhœic
evacuations, which at the end become dysenteric with painful tenesmus;
abundant urination; short, accelerated and difficult respiration, with
incoordination in the thoracic and abdominal movements. The circulatory
functions are modified only in fatal cases, when the pulse is small and
intermittent towards the end. There is finally a notable drop in
temperature, shown by the coldness of the skin. Death occurs in from 16
hours to 6 days after ingestion. During the last few hours the animals
are stretched at full length and are incapable of getting up. There may
be prolapsus of the rectum; the eye is deeply sunk; sensibility is
deadened and death is due to stoppage of respiration.

In the _horse_, there are spasmodic movements of the hind-quarters and
excessive excitement of the urinary genital organs. In _cattle_ there is
cessation of rumination, grinding of teeth, dryness of muzzle, ptyalism,
groaning, painful colic, dysentery, deeply sunken and watery eyes, anus
wide open, and evacuation of very fœtid, blackish, glareous matter round
the excrement. In _cows_ there may be suppression of milk, and abortion.
In the _pig_ there is abundant salivation and vomiting, and the animal
keeps its snout buried in the litter. There is also extremely fœtid
diarrhœa, with dysentery.

                              REFERENCES.

              4, 16, 27, 73, 81, 128, 130, 141, 148, 151,
                        190, 192, 203, 217, 255.


                               GRAMINEÆ.

=Darnel= (_Lolium temulentum_ L.). The grass known as Darnel, of the
same genus as rye-grass, has been recognized for centuries as a harmful
species, and it is considered by some authorities that it is really the
tares of Scripture which the enemy sowed among the wheat. Its effect on
eyesight was known to the ancients[5], and its objectionable character
was noted by Shakespeare:—

Footnote 5:

  E.g. Ovid says “Let the fields be clear of darnel that weakens the
  eyes.” In Plautus’ comedy, _The Braggart Soldier_, one servant says to
  another, “’Tis a wonder that you are in the habit of feeding on darnel
  with wheat at so low a price.” “Why so?” “Because you are so dim of
  sight.” [_Agric. Jour. Union of S. Africa_, Jan. 1914, p. 82.]

                             “Want ye corn for bread?
         I think the Duke of Burgundy will fast
         Before he’ll buy again at such a rate:
         ’Twas full of darnel: Do you like the taste?”
                                 —I _Henry_ VI, Act III, Sc. 2.

Its effect when mixed with flour was also referred to by Gerarde (1597):
“The new bread wherein Darnell is, eaten hot, causeth drunkenness; in
like manner doth beere or ale wherein the seede is fallen, or put into
the mault.”

Before the seeding stage is reached Darnel seems to be quite suitable as
a food for stock, only the seed or grain being poisonous, and this not
invariably so. The chief danger perhaps is that the grain may not be
thoroughly removed from cereal grains, and may thus find its way into
bread or cereal stock foods. Though it has caused many cases of human
poisoning, fatal results seem to be rare: Dr. Taylor could record no
fatal case up to 1859. Darnel mixed with barley caused the poisoning of
pigs (_Veterinarian_, 1842). Johnson and Sowerby (1861) state that
Darnel has in several cases proved fatal to horses and sheep. The same
authorities quote a case in which 80 inmates of Sheffield Workhouse were
attacked by violent vomiting and purging from the use of oatmeal
containing Darnel. At the Veterinary School at Lyons a horse was killed
by giving it 2 kilogrammes (4·4 lb.) of Darnel. Cornevin concluded that
the amounts of Darnel necessary to kill certain animals would be as
follows:—

           Horse     0·7 lb. per 100 lb. live weight.
           Ruminants 1·5 to 1·8 lb.  per 100 lb. live weight.
           Poultry   1·5 to 1·8 lb.       „           „
           Dog       1·8 lb.              „           „

He found pigs very little affected. As regards man 30 grammes (1 oz.) of
the flour appear to be about the most that can be taken without showing
dangerous symptoms.

The presence of Darnel flour in flour of the cereal grains may be
determined by an examination of the starch granules, which are given by
Cornevin as only 5 to 8µ; in diameter (compared with 25 to 4µ for rye),
simple in general, but sometimes in groups of 2 to even 5, polyhedral or
partly rounded, with a nucleus or fusiform nucleal cavity, and readily
coloured blue with iodine; they resemble those of maize but are only
about one-eighth the size.

_Toxic Principle._ The grains only are harmful, and contain the narcotic
alkaloid _Temuline_ (C_{7}H_{12}N_{2}O), which Hofmeister showed to be a
strong nerve poison, and which is said to occur to the extent of 0·08
per cent. in the seeds. Other authorities impute the toxic property to
_Loliine_, while Smith states that the toxic principle is _Picrotoxin_.
In relation to the grain fungal hyphæ have usually been found, though
not invariably, 20 to 30 per cent. of the plants sometimes being free
from it. The fungus (_Endoconidium temulentum_) is propagated
vegetatively by means of mycelium. It appears to live symbiotically in
the maturing grain, and perhaps to a slight extent renders possible the
assimilation of nitrogen from the atmosphere; but Freeman observed that
though generally stimulating to the Darnel, it is occasionally injurious
to it. Esser sums it up by saying that according to most authorities who
have investigated Darnel the fungus alone contains the toxic
substance—the Temuline—and hence the grains in which the fungus does not
occur should be harmless. The fungus is found in Darnel grain in all
countries—Chile, Brazil, S. Africa, Persia, Spain, France, Sweden,
Germany, etc. So far as can be ascertained there have been no feeding
experiments to determine the difference in toxic character between
fungus-infested and fungus-free grains. The dangerous properties are
said to be most pronounced in wet seasons.

_Symptoms._ In France Darnel is called _Ivraie_, because, when brewed
with barley, it acts as a narcotic intoxicant.

Darnel poisoning induces giddiness, drowsiness, uncertain gait, and
stupefaction (Müller), and, in the older animals, vomiting, convulsions,
loss of sensation and death (Pott).

The symptoms in the _horse_ are dilatation of pupils, vertigo, uncertain
gait, and trembling. The animal falls, the body is cold and the
extremities are stiff, respiration is laboured, the pulse is slow and
small, and there are convulsive movements of the head and limbs. There
is rapid enfeeblement, and death may occur within thirty hours.

In _pigs_, foaming, convulsions and paralysis have been observed; the
stomach and intestines were inflamed and the lungs congested.

                              REFERENCES.

           4, 16, 73, 81, 106, 128, 130, 141, 190, 203, 204,
                        205, 213, 233, 235, 254.


                              EQUISETACEÆ.

=Horsetails= (_Equisetum_ sp.). A very great deal has been written on
the subject of Equisetosis or _Equisetum_ poisoning, and even at the
present day opinion is divided as to which species are poisonous and to
what extent. From the time of Linnæus there has been uncertainty as to
the species, which has generally been given as _E. arvense_. Two German
papers, by Weber and Lohmann respectively, published by the German
Agricultural Society in 1903 and 1904, have done much to remove doubt on
the matter, but cannot be said to have settled the question absolutely.
These two papers seem to have been overlooked by some recent writers on
the subject, but Lohmann’s appears to be the most authoritative paper
yet written. Both are referred to below.

It seems to be definitely proved that certain species of _Equisetum_
really are poisonous, hesitating statements notwithstanding. Chesnut and
Wilcox state that there are cases of poisoning of both horses and sheep
by _E. arvense_ in the United States, though they are not common, and
the opinion is expressed that “the plant, if deleterious, is evidently
so only on account of its harsh scouring action in the mouth and
intestinal tract.” On the other hand Rich and Jones record poisoning of
horses by _E. arvense_ in hay, but while adding that horses seem to
develop a depraved appetite for the weed, they state that they have no
evidence that horses grazing upon _the green plant_ are poisoned.
Güssow’s experience has been that cattle do not suffer any inconvenience
at all from this species, or only very slight disturbance of the
digestive organs, but that horses are conspicuously subject to fatal
poisoning by it. Examination of hay on which a considerable number of
poisoned horses were fed revealed in every case the presence of _E.
arvense_. When the food was changed, horses, if not too seriously
affected, made rapid recovery. (Treatment suggested is to change to
easily digested food, give a sharp purgative, and follow by small doses
of nux vomica three times a day.) Pammel says that in recent years a
disease of horses in Vermont has been attributed to hay and fodder
containing the weed; that it is proved by experiment that when ingested
in sufficient quantity _E. arvense_ is capable of causing fatal
poisoning in horses, and is at times the cause of extensive losses; and
that young horses are most susceptible, while grain-fed horses are less
susceptible than others. He adds that sheep are supposed to be slightly
affected, but cattle eat hay in which it occurs in large proportion with
impunity.

Coming to the two German reports, it is stated by Weber (1903) that _E.
palustre_ contains a specific poison for cattle and other ruminants, but
sheep and goats are able, owing to their fine muzzles, to separate it in
fodder, and hence suffer less. Horses and pigs, he says, seem to suffer
very little. Young animals and stock, from districts where the species
does not occur, suffer more than those from places where it occurs—the
latter appearing to learn early to avoid it.

Lohmann conducted feeding experiments with guinea-pigs with _E.
arvense_, _E. palustre_, _E. pratense_, _E. sylvaticum_, _E. maximum_,
and _E. heleocharis_ (not British). He also fed _E. arvense_ and _E.
palustre_ to horses, cattle, sheep, pigs, and geese in considerable
quantities for many days on end; and made experiments with aconitic acid
on guinea-pigs and horses. The feeding experiments with guinea-pigs
showed that of the species named only _E. palustre_ and to a less extent
_E. sylvaticum_ are poisonous plants (to guinea-pigs). With the large
domestic animals the experiments showed _E. arvense_ to be a harmless
plant, and _E. palustre_ to be really injurious to cattle but avoided by
other stock. Lohmann considers that the many statements in the
literature agree in part with this result, and that the divergent
observations may be traced to various causes, among which perhaps an
abnormal chemical composition of the weed fed plays a principal part.

In this connection, however, the American results must be carefully
borne in mind, and _E. arvense_ must not too hastily be regarded as
blameless.

_Toxic Principle._ It was for some years believed that the apparent
toxic symptoms induced by Horsetails were due to Silica or to Aconitic
acid—the latter a substance found by Matz and Ludwig. The conclusion
come to by Weber, however, was that the poisoning by _E. palustre_ is of
an organic character, not due to silica. The young shoots, which contain
little silica, were found in general to be much more poisonous than the
old plants, which contain much silica. It was long since found by
Wiggers that dried plants of _E. palustre_ contained 8·88 per cent. of
silica, but all species contain this substance in greater or less
degree, and it varies considerably in amount, even in the same species.
The feeding experiments conducted by Lohmann, with certain species of
_Equisetum_, and the observed symptoms of illness after the consumption
of some of them, particularly _E. palustre_, serve to show that the ill
effects are neither to be attributed to greater or less digestibility,
nor to the silica present. Neither are the aconitic acid and other
organic substances, in part found in previous investigations,
responsible for the poisoning. However, an active compound named
_Equisetine_, a substance belonging to the alkaloid group, was isolated;
this occurs usually, perhaps only, in _E. palustre_, at any rate in
sufficient quantity to be dangerous to animals. Lohmann then, following
up the investigations of Paucerzynski, Matz, Meyer, Weber and others,
ascertained definitely that _E. palustre_ contains an alkaloidal nerve
poison, to which the name _Equisetine_ was given, and the experiments
were held to decide that this is the poisonous substance in this
species. (As stated above, _E. arvense_ was held to be harmless.)

_Symptoms._ At first, excitement and anxiety, followed by uncertainty of
movement, reeling and staggering; paralysis of hind limbs at least,
falling, possibly general paralysis, insensibility to external
irritants, unconsciousness, and coma. Pulse accelerated, appetite at
first normal, but in course of time great disturbance of nutrition;
sugar in the urine. Course sometimes very acute, death occurring in a
few hours, but sometimes protracted (two to eight days), and at times
even chronic (one to several weeks).

In _cattle_, after excessive eating, continuous diarrhœa is
characteristic, with paralysis; while, if the food be persisted with,
cachexia and hydræmia combined with weakness bordering on paralysis make
their appearance (Friedberger and Fröhner, _via_ Pammel). In addition to
cachexia, Pott also mentions colic, stoppage, bloody urination,
abortion, and loss of teeth.

Young animals appear to succumb sooner than older ones, while grain-fed
animals are more resistant than others. Referring to _E. arvense_ Pammel
says it produces paralysis of the rear extremities, and when death
occurs spasms are noted. In relation to the poisoning of _horses_ by the
same species in hay Rich and Jones note unthriftiness, the animal
appearing thin and the muscles wasted. In from two to five weeks,
according to the age of the horse and the manner of feeding, the animal
begins to lose control of the muscles, and there is swaying and
staggering, though the eye is bright and the appetite good. If the plant
is regularly ingested the horse loses the power of standing, becomes
nervous, struggles to rise, the legs become more or less rigid, and at
times all the muscles of the body seem convulsed. Even in this condition
one well-nursed patient lived two weeks. The horses are generally
willing to eat, although unable to rise, but become sore and tired from
struggling, finally dying from exhaustion. Life is much prolonged by
turning from side to side three or four times in twenty-four hours, thus
preventing congestion. The pulse is slow till near the end, when it is
rapid and weak; the temperature is below normal at first, but when the
animal is down there is fever; the extremities are usually cold; and the
lining membrane of the mouth, nose, and eye becomes pale.

Of _Equisetum_ sp. Stebler and Schroeter say that they induce diarrhœa
in cattle, which become poor, and in cows the milk yield is checked or
ceases. Weber also refers to the effect on milk yield of _E. palustre_,
which he says causes the milk of affected cows to become watery, poor in
fat, and gives rise to a greasy, unappetising butter, while the yield
may soon quite fail.

                              REFERENCES.

   2, 20, 57, 111, 176, 203, 204, 213, 220, 221, 222, 237, 260, 261.


                                FILICES.

=Bracken= (_Pteris aquilina_ L.). The Bracken, Brake Fern, or “Fern” is
of very considerable importance to farmers for four reasons: (1) It is a
most pernicious weed; (2) it forms an excellent litter for stock and
treads down into good manure; (3) it is said to have been successfully
converted into silage; but (4) it has been accused of poisoning cattle.

In regard to possible poisonous properties, it must be said that the
facts are at present somewhat uncertain, but a number of authorities
clearly regard the Bracken as poisonous. (_a_) Müller (1897) records the
poisoning of horses which ate it for some weeks with chaff—and some
died. (_b_) Chesnut and Wilcox (1901) say that cases of poisoning of
horses and cattle have been reported from England and a few localities
in the United States. (_c_) Pott states that when eaten in quantity by
cattle Bracken causes hæmaturia, and in horses nervous symptoms (brain
trouble), sometimes with fatal effects. (_d_) Pammel also remarks on the
believed poisonous character of this plant. (_e_) In view of its
suspected poisonous character feeding experiments were conducted by the
Board of Agriculture and Fisheries with a large quantity of Bracken, but
the results were negative, yielding no experimental proof of the plant
being poisonous. One animal—a heifer—consumed 60 lb. of Bracken between
Aug. 14 and Aug. 20, and after two meals containing about 30 lb. of
Bracken showed only symptoms of indigestion. After the 60 lb. there were
no symptoms of illness. It has been thought possible that the so-called
Bracken poisoning is due to _Potentilla Tormentilla_ (_q.v._).

In 1893 Storrar dealt with the question and expressed the view that any
disorder due to Bracken was probably not a toxic effect but a digestive
trouble simply (_Jour. Comp. Path._, 1893).

_Toxic Principle._ Continental authorities say that Bracken contains the
poisonous _Pteritannic acid_, which is identical with the _Filicic acid_
of the Male Fern (_Aspidium filix-mas_).

_Symptoms._ In the cases of horses which died Müller gives the symptoms
as timidity, slower movement or action, loss of balance, dilated pupils,
reddening followed by yellowing of the conjunctivæ, and slowing of the
pulse.

Pammel notes Bracken as an astringent and anthelmintic, and also says it
causes enteritis, spasms, and paralysis.

                              REFERENCES.

                    10, 25, 57, 190, 203, 204, 213.


                               FUNGI[6].

=Ergot= (_Claviceps purpurea_). This fungus, parasitic on rye and a
number of grasses, has long been known to induce distinct poisonous
effects on man and domestic animals when ingested in sufficient
quantity.

Footnote 6:

  Poisonous parasitic fungi generally are not dealt with in this volume,
  but ergot is included because it is widely distributed and perhaps the
  best known, while its effects have been fully studied.

Ergot must be regarded as a cause of abortion in cows, though somewhat
divergent views have been expressed as to the facts, some authorities
considering the belief well founded, while others consider that there is
little ground for it. It is quite clear, however, that when taken in
sufficient quantity Ergot induces serious poisoning of domestic animals.
Horses have died in two or three days from eating ergoted hay and wild
rye. Extensive outbreaks of ergotism have occurred in the United States,
and serious losses have been recorded in the Central and Western States.
Ewart remarks that “a comparatively small number of fresh Ergot grains
suffice to injure or kill a horse, cow, or sheep.” The effects of the
poisoning of animals will be found under _Symptoms_ below.

_Toxic Principle._ Ergot of rye is used in medicine. It contains 0·20 to
0·25 per cent. of _Ergotinine_. In the British Pharmaceutical Codex,
1911, the grains (sclerotia) of Ergot (see Frontispiece) are described
as longitudinally furrowed, 1 to 4 cm. long, slender, curved, tapering
to both ends; they break with a short fracture, and are somewhat
triangular in transverse section; they have a characteristic and
disagreeable odour and taste, are dark violet to black in colour, and
whitish within. Ergot contains the physiologically active alkaloid
_Ergotoxine_ or _Hydroergotinine_ (C_{35}H_{41}O_{6}N_{5}), also known
as _amorphous Ergotinine_, and, when formerly obtained in an impure
state, as _Cornutine_ and _Ecboline_. It is the hydrate of the
crystalline base Ergotinine (C_{35}H_{39}O_{5}N_{5}). There are also
other physiologically active constituents derived from amino-acids.

_Symptoms._ In man Ergot has induced two types of epidemic ergotism,
caused by the prolonged use of ergoted rye bread. The two forms are
rarely or never found together. One is a gangrenous form characterized
by agonizing pain in the extremities, followed by dry gangrene of the
peripheral parts of the body. The second type of ergotism is much more
rare—a nervous epidemic characterized by paroxysmal epileptiform
convulsions.

Owing to the fact that at the outset ergotism causes irritation in the
hands and feet it is termed “Kribbelkrankheit” in Germany.

The three substances noted above as isolated by Kobert are stated to
cause poisoning—the first producing inflammation of the serous and
mucous membranes, disintegration of the red blood cells, and widespread
ecchymoses; the second excites the central nervous system and causes
general convulsions; and the last induces gangrene.

In one case a horse ate ergoted hay: next day the left hind leg was
stiff, and moist with cold sweat; on the second day it was badly swollen
and gangrene of all the tissues became apparent, and after the skin of
the leg and a considerable part of the muscular tissue had sloughed off
the animal died on the third day. In other cases horses showed symptoms
twenty-four hours after eating ergoted hay: fatigue, indisposition to
work, cold sweat, particularly on the neck, paralysis of the tongue and
muscles concerned in swallowing, and then generalized paralysis, very
slow and deep respiration, subnormal temperature, normal pulse at first
and then weaker till scarcely distinguishable, death in six or eight
hours (Chesnut and Wilcox).

According to Pammel ergotism manifests itself among animals chiefly in
the chronic form, the poison being acquired in small amounts and
accumulation taking place slowly. Two distinct forms of the disease are
recognized, the spasmodic and gangrenous. “Symptoms referable to the
digestive tract, such as nausea, vomiting, colic, diarrhœa, or
constipation occur in both forms. Pregnant animals very frequently
abort.”

“In the spasmodic type of the disease, symptoms due to overstimulation
of the central nervous system appear. These are tonic contraction of the
flexor tendons of the limbs, anæsthesia of the extremities, muscular
trembling, general tetanic spasms, convulsions and delirium. Death
usually occurs from secondary causes.”

“Gangrenous ergotism is characterised by coldness and anæsthesia of the
extremities, followed ultimately by dry gangrene of these parts. The
effects of this dry gangrene are often very serious and amount to
sloughing of the feet, tips of the ears, tip of the tail, shedding of
the hair, teeth, etc. Death takes place from exhaustion.

“Acute poisoning is characterized by vomiting (in dogs), profuse
salivation, dilatation of the pupils, rapid breathing and frequent
pulse. The animal cries out, has convulsive twitchings, staggering gait,
paraplegia, intense thirst and coma, terminating in death.”

In an extensive outbreak of ergotism in the United States in 1884 Law
and Salmon reported as a prominent symptom ulceration of the mucous
membrane of the tongue and mouth cavity, this and lesions on the
extremities giving the appearance of foot-and-mouth disease. Affected
animals showed weakness, dullness, and paralytic conditions of certain
groups of muscles. When in pregnant animals the uterus is acted upon,
labour pains occur, and the fœtus is expelled. The straining in those
cases is often very painful and may be so severe that prolapsus of the
uterus or even the rectum is the result. When Ergot produces gangrene,
it usually affects the extremities, like the lower parts of the legs,
the ears, tail or teats in cattle, and the comb, wattles, toes, wings or
tongue of poultry. It is preceded by redness, coldness, and painful
swelling of the parts affected. After a while sensibility of the dying
region is lost and the line of demarcation between it and the living
tissue becomes manifest. The dead portion commonly dies and is cast off.
In some cases the gangrene is accompanied by symptoms of a septic
nature.

“The possible result of the poisoning depends largely on the amount of
Ergot taken and on the severity of the symptoms produced thereby. When
small amounts are taken and only a slight dullness or digestive
disturbance results the outlook may be quite favourable. Even Ergot
abortion with rather severe symptoms usually is followed by recovery,
but in the gangrenous cases, fatal terminations are common. The animals
which through this cause have lost one or more parts are not only
crippled, but septic or embolic complications may lead to a fatal
termination. Paralytic cases do not permit of a favourable prognosis,
especially if muscle groups containing important functions are
involved.” (_N. Dakota Exp. Sta. Rept._)

                              REFERENCES.

      1, 4, 13, 16, 35, 57, 81, 82, 128, 154, 161, 203, 242, 251.




                              CHAPTER VII
                  PLANTS SUSPECTED OF BEING POISONOUS.


A very large number of plants have at various times been suspected of
possessing poisonous properties and causing harm to live stock. Of these
it is quite probable that many are in practice entirely harmless, but
some must be included as possibly deleterious, complaints having been
made which vary in gravity from a slight irritation to causing death.

=Purging Flax= (_Linum catharticum_ L.). It is perhaps doubtful whether
this plant is really poisonous unless taken in considerable quantity by
animals—as it is quite unlikely to be. It may, however, be included
here, as it is stated to contain a glucoside which is purgative and
which on fermentation yields prussic acid.

=Furze= or =Gorse= (_Ulex europæus_ L.). In view of the fact that
Gerrard isolated from the seeds of Gorse the alkaloid _Ulexine_, which
is identical with _Cytisine_ (p. 27) and that the alkaloid is also
contained in less quantity in the bark of young shoots, this plant has
been suspected of possessing toxic properties. Experiments (179)[7] with
the alkaloid definitely showed it to be a nerve and muscle poison, 3
milligrammes having killed a chloroformed cat with convulsions in three
minutes, though the animal could be kept alive as long as artificial
respiration was kept up. As, however, Gorse has long been used very
widely and in considerable quantities as a fodder the percentage content
of the alkaloid must in general be exceedingly small, and no harmful
effects need be feared from the consumption of the cut and bruised
plant. Possibly the seeds might prove injurious if eaten in quantity.

Footnote 7:

  Reference to Bibliography.

=Melilot= (_Melilotus_ sp.) may at times cause injury. Ewart (82)
writes: “All the species contain Cumarin, a volatile odoriferous
principle, which in excess produces a disinclination to locomotion,
paralysis and ultimately fatal symptoms. No harm is to be apprehended if
the amount present does not exceed 10 per cent. of the herbage.”

=Silver Weed= (_Potentilla Anserina_ L.). This well-known and elegant
little weed is scarcely likely to be eaten to any extent by farm stock,
though it may possibly be taken occasionally on roadsides. It has not
been proved to be poisonous, but Pott states that it has a strongly
constipating effect (213).

=Tormentil= (_Potentilla Tormentilla_ L.). In relation to supposed
bracken poisoning (see p. 87) in regard to which experiments were
conducted by the Board of Agriculture and Fisheries, Tormentil occurred
in several instances with the bracken in localities where this plant was
reported to cause poisoning. Two feeding experiments in which the weed
was fed to heifers gave negative results. In a further case, however, 4
or 5 lb. were collected from a field where sick animals were grazing,
and fed to a heifer; it appeared to be the cause of rise of temperature
(to 106° F.), diarrhœa, and the passing of a considerable quantity of
blood in the fæces for three days, after which the animal improved. It
was, however, slaughtered, and lesions were found similar to those found
in animals dying in the field from so-called bracken poisoning. Though
the plant was suspected, results generally were not held to prove that
it was the cause of poisoning (25). According to Van Rijn the root of
Tormentil contains a considerable quantity of _Chinovic acid_
(C_{32}H_{48}O_{6}?).

=Wall-Pepper= (_Sedum acre_ L.) is regarded as emetic and purgative, but
to lose the harmful properties on drying.

=Sundews= (_Drosera_ sp.) are reputed to be poisonous to sheep, but no
evidence has been found.

=White-Rot= or =Marsh Penny-Wort= (_Hydrocotyle vulgaris_ L.) is stated
to have caused inflammation of the digestive tract, and hæmaturia; and
to contain a toxic substance _Vellarin_ (213).

=Wild Parsnip= (_Pastinaca sativa_ L.). This plant has often been
supposed to be poisonous, but Pammel shows that in Iowa the plant is
quite harmless, as it appears to be in Britain.

=Devil’s-Bit= (_Scabiosa succisa_ L.) is stated by Moir to have caused
injury to cattle in one instance (_Vet. Record_, 1899), causing
salivation, gritting of the teeth, twitching of facial muscles, and
slightly protruded, abraded, swollen and sensitive tongue. An experiment
on cattle showed the plant to induce violent inflammation of the mouth
and tongue.

=All-Heal= (_Valeriana officinalis_ L.) is not likely to be eaten by
stock in sufficient quantity to cause poisonous symptoms, though it is
stated to contain the poisonous _Valerianic acid_ and _Oil of Valerian_.
According to Chevalier (_vide_ Henry) this plant contains an alkaloid
not yet fully characterised.

=Canadian Erigeron= (_Erigeron canadensis_ L.), sporadic in England, is
suspected in America. It contains an oil, chiefly a _terpene_
(C_{10}H_{16}). It has an acrid taste, causes smarting of the eyes,
soreness of throat, aching of extremities, and colic; and irritation to
people handling it (203).

=Mayweeds= (_Anthemis_ sp.). It is not at all clear whether these plants
are more than irritant in character, and they are so very common and
widely distributed that there would probably be more evidence if they
were poisonous. _A. Cotula_ is regarded as suspected by Smith and
Halsted, while Ewart says that it is obnoxious to stock on account of
its unpleasant flavour, and if eaten by them in time of scarcity is apt
to give their flesh, milk, or butter an unpleasant flavour. Güssow
states that this species blisters the mouth and nostrils of animals. In
his investigations at Kew, Greshoff found that the seeds of _A. Cotula_
and _A. arvensis_ contain much hydrocyanic acid. (He further found that
the cyanogenetic glucoside from _A. aetnensis_ Schouw. and _A. chia_ L.
belongs to the amygdalin type, giving off hydrocyanic acid and
benzaldehyde on hydrolysis. “The strong odour of benzaldehyde may even
be observed on grinding the seeds with water. Species of _Anthemis_
contained from 0·15 down to 0·03 per cent. of hydrocyanic acid.”)

=Cat’s-Ear= (_Hypochæris radicata_ L.). No record of poisoning of Cat’s
Ear has been found, but it may be mentioned here, since Ewart says of
it: “It contains a bitter, milky sap, which makes it unpalatable though
not entirely poisonous.... An exclusive diet of this weed could not help
but injure stock eventually.”

=Dodders= (_Cuscuta_ sp.), when parasitic on clovers and fed as fodder
or hay, have been suspected of causing digestive troubles in horses and
cattle in the United States. Müller records a case of poisoning of young
pigs by _C. europæa_, with inflammation of the intestines and nervous
symptoms. Barbey determined the presence of the glucoside _Cuscutin_ in
_C. Epithymum_.

=Viper’s Bugloss= (_Echium vulgare_ L.) is suspected of being poisonous;
according to Friedberger and Fröhner it causes slavering (see also
_Cynoglossum_).

=Hound’s Tongue= (_Cynoglossum officinale_ L.). To what extent this
plant is actually poisonous is not clear, but with some other members of
the order (_Echium vulgare_, _Anchusa officinalis_), it contains the two
alkaloids _Consolidine_ and _Cynoglossine_—the former of which paralyses
the central nervous system and the latter the peripheral nerves.
(Greimer, 1900: _vide_ Henry).

According to Hooker, Hound’s Tongue is narcotic and astringent, and
Smith includes it as a simple vegetable irritant, causing nausea and
purging. No records of actual poisoning of animals have been found.

=Broom-rape= (_Orobanche minor_ Sutt.) has been suspected, and according
to Boitel is liable to cause violent colic when it occurs in
considerable proportion in clover and is ingested with it (73). On the
other hand, in a case noted by Stapledon, in which Broom-rape (_O.
minor_) had completely overrun the aftermath on a farm near Fishguard,
two-year-old cattle devoured the plant with apparent relish and cleared
off most of it in a few days after being turned in. The farmer stated
that he saw no trace of colic or other ill effects. (_Jour. Bd. Agric._,
September, 1916.)

=Great Mullein= (_Verbascum Thapsus_ L.). Though it does not appear to
be touched by farm live-stock the Great Mullein must be mentioned here.
The leaves and flowers have been used medicinally as an emollient and
pectoral, while the seeds possess narcotic properties and serve to
stupefy fish (73). Pammel states that the plant causes irritation, but
is probably not very poisonous to stock.

=Toadflax= (_Linaria vulgaris_ Mill.). Cornevin describes Toadflax as
acrid and poisonous, but says that stock reject it, and he could record
no accidents to animals. In his full and excellent account of this weed,
Kraus says it is regarded as poisonous, or suspected of being so, but
that according to most accounts it is not harmful to cattle (168).
Leunis regards it as suspicious on account of its acridity. Some German
authorities say it is willingly eaten by cattle, but it is generally
believed to be avoided, and owing to its disagreeable odour and acrid
taste this view is probably correct. The plant has not been exhaustively
studied, and while Smith gives the toxic principle as _Oil of
Snapdragon_ and the resin _Gratiolin_, it may be observed that Toadflax
contains the glucoside _Linarin_ (C_{64}H_{56}O_{40}).

=Figworts= (_Scrophularia nodosa_ L. and _S. aquatica_ L.). These plants
are not likely to be eaten by animals, but Cornevin states that the
former is strongly emetic and purgative, and that in excess it may cause
superpurgation ending in death. Müller says that the two species have
respectively caused poisonous symptoms in a cow and a sheep; in the case
of the cow there were loss of appetite and symptoms of paralysis. From
_S. nodosa_ Walz extracted a bitter, crystalline substance,
_Scrophularine_.

=Yellow Rattle= (_Rhinanthus Crista-galli_ L.). When grass land is put
under the plough Yellow Rattle present may re-appear in a cereal crop as
a semi-parasite, and its seeds may later be ground up with the grain,
imparting a reddish or violet-brown colour and an unpleasant taste to
the flour and even bread made from it. It is strongly suspected of being
poisonous, like _Pedicularis_ and _Melampyrum_, but it is by no means
clear how far it may prove harmful to stock. It is believed by some
people to impart a bad taste to the butter made from the milk of cows
grazing on infested pastures. Lehmann ate without harm 35 grammes (about
1¼ oz.) of the seeds made into a cake and cooked; and during four days
he gave a rabbit 1238 grammes (2·7 lb.) of the fresh plant with
half-ripe seeds, without apparent injury (73).

In some poor pastures it occurs in excessive quantity, and would appear
to be only very slightly poisonous, or would have attracted wider
attention. It is possibly only poisonous after being eaten for a
prolonged period, as in the case of _Lolium temulentum_, and _Lathyrus
sativus_. The seeds contain the bitter-sweet glucoside _Rhinanthin_
(C_{29}H_{52}O_{20}), which is suspected of having poisonous properties.

=Cow-Wheat= (_Melampyrum arvense_ L.). It seems clear that Cow-Wheat is
at least not poisonous unless eaten in very considerable
quantities—amounts in fact which in practice are most unlikely to be
eaten. The seeds may occur in cereal grains, and hence be ground up into
meal. As they are said to contain a glucoside analogous to _Rhinanthin_,
have a bitter taste and peculiar odour, and impart a violet coloration
to flour, their presence in cornfields is most undesirable. According to
Pammel this plant induces sleepiness and colic.

=Ground Ivy= (_Nepeta Glechoma_ Benth.) is, according to Schaffner,
poisonous to horses. It contains a volatile oil and bitter principle, as
also does Catmint (_N. Cataria_). In a case which came before the Board
of Agriculture and Fisheries in 1906 three horses became ill with
symptoms of poisoning, and the only weed found in the lucerne they were
getting was Ground Ivy, and this was suspected but not proved to be the
cause. In a further case, reported in 1909, eleven horses were believed
to have been poisoned by this weed, and in one of the dead horses
scarcely any food but Ground Ivy was found, and to it the veterinary
surgeon in attendance attributed death. During preceding years several
horses had died in the locality (Ely), owing, it was believed, to
poisoning by the same weed. The losses, however, were not _proved_ to be
due to this plant.

In the _Veterinary Journal_ (October, 1914, p. 515) poisoning of horses
by this weed was noted (after Ferenczhazsy in the _Recueil de Médecine
Vétérinaire_). The author observed nine cases of intoxication due to the
weed, though it is stated that it “has occasioned no trouble in cattle
and sheep that consumed it.” The symptoms in horses were “anxious look,
dyspnœa, salivation, sweating, dilatation of the pupils, cyanosis, signs
of pulmonary œdema.” Two horses died. In 1913 similar cases were
observed by other owners, and terminated fatally.

Hooker states that _N. Glechoma_ is “bitter and aromatic, formerly used
for beer, occasionally for tea.”

=Orache= (_Atriplex_ sp.). So far as known these plants are not
poisonous, but it may be stated that Greshoff found the seeds of five
species, and the leaves of two species, to contain a _Saponin_.

=Nettles= (_Urtica_ sp.). Nettles are not generally regarded as
poisonous otherwise than as causing painful nettle rash on the bare
skin, but _Urtica dioica_ L. is stated to have caused the death of dogs
(_Berliner Tierärztliche Wochenschrift_, 1909).

=Yellow Flag= (_Iris Pseud-acorus_ L.). The wild Flag was noted by
Linnæus as dangerous to cattle, but no case of actual poisoning has been
found in the literature. The plant is stated to have marked emetic and
purgative properties, and Cornevin remarks that in Belgium intense
gastro-enteritis is attributed to it. It contains the glucoside _Iridin_
(C_{24}H_{26}O_{13}).

=Narcissus= sp. Various Narcissi (_e.g._ _N. pseudo-narcissus_, _N.
poeticus_, and others) have been regarded as irritant to the hands.
They would rarely if ever be eaten by live-stock in Britain, but it
is stated that on the Continent many poisonings of cattle, goats,
and pigs have been recorded, not infrequently ending in death after
two or three days. The Narcissi are strongly narcotic, emetic, and
purgative, and cause dilated pupils. Pott states that they cause
inflammation of the digestive tract, and convulsions, sometimes with
fatal results; and according to Pammel _N. poeticus_ induces intense
gastro-enteritis. _N. pseudo-narcissus_ contains the alkaloid
_Narcissine_ (C_{16}H_{17}O_{4}N), which with cats causes nausea and
purgation (Henry).

=Common Fritillary= (_Fritillaria Meleagris_ L.). The Fritillary or
Snake’s Head occurs only in a few places in England, and truly wild
perhaps only rarely in southern and eastern counties—not in Scotland or
Ireland. No definite case of poisoning has been found in the literature,
but the plant is stated to be poisonous. It contains the bitter alkaloid
_Imperialine_ (C_{35}H_{60}NO_{4}), which is a heart poison.

=Bog Asphodel= (_Narthecium ossifragum_ Huds.) has by some been regarded
as a poisonous plant, and Müller says that the poisoning of cows has
been recorded, and also that a cat died after drinking the milk of an
affected cow. The toxic property is believed to be the glucoside
_Narthecin_.

=Molinia caerulea=, _Moench_. A short account by Pott shows that when
forming the principal part of moorland pasture grasses, and hence
extensively eaten, this grass causes brittleness of the bones of stock,
and in sheep chlorosis and wool eating. It also induces hæmaturia, but
if free from parasitic fungi (_e.g._ _Claviceps microcephala_) and not
covered with microscopic, sharp crystals, is quite harmless if only
eaten as a secondary or incidental fodder. This grass seems to be very
poor in lime (Immendorf, 1898), and Schulze and Castoro found the
internodes of the stem to contain a considerable quantity of a pentosan
(Xylan). It is poor in nutritive constituents. The harm done is due
perhaps in part to this fact, and in part to more or less accidental or
occasional constituents (as 0·046 per cent. of lead oxide in a case of
the var. _altissima_ near some lead works). Plants said to be
occasionally similarly harmful are _Juncus_ sp., _Nepeta Glechoma_, and
_Hieracium Pilosella_.




                              CHAPTER VIII
                     THE EFFECTS OF PLANTS ON MILK.


A number of poisonous plants have a considerable influence on the milk
yield of animals which eat them, reducing it in volume or in fat
content, or imparting to it an unpleasant flavour which renders it unfit
for human consumption, and even affecting the butter made from it. Other
plants not actually poisonous also affect milk by “tainting” it, and
must therefore be considered harmful otherwise than as mere weeds. Still
others affect milk by causing it to be stained with blood, and in some
cases the toxic principle of the plant concerned is even stated to have
rendered the milk poisonous. It will be useful to give here a brief
account of milk-affecting plants, though it is probable that there may
be others which are not mentioned.

The plants best known in this connection are the Garlics (_Allium
oleraceum_ L., _A. ursinum_ L., _A. vineale_ L., and others), which
impart to milk a strong “oniony” flavour. These plants also seriously
affect the flesh of animals which eat them, even rendering it unfit for
consumption. A case came before the author several years ago in which a
considerable number of sheep had eaten a quantity of _Allium ursinum_,
which was growing in a field in which they had been grazing for some
days. The meat was so strongly tainted that, as the owner (a butcher)
stated, it was quite unfit for sale. The only thing to be done was to
pasture the sheep elsewhere for a time.

Pott notes that species of _Ranunculus_ give rise to reddish or bitter
milk (_Mölkereizeitung_, 1897), while _Caltha palustris_ causes loss of
milk production in cows.

_Ranunculus repens_ imparts a strong unpleasant flavour to the milk of
cows that have eaten it, and the butter made from such milk is
distinctly bitter in taste (Güssow).

_Ranunculus sceleratus_ causes a falling-off in milk-yield. (Cornevin.)

_Alliaria officinalis_ Andrz, imparts an oniony flavour to milk.

_Achillea Millefolium_ L. is stated to impart its bitter taste and
strong odour to dairy products when eaten by cows. It contains an
alkaloid, _Achilleine_ (C_{20}H_{38}O_{15}N_{2}) having a peculiar odour
and bitter taste.

_Chrysanthemum Leucanthemum_ has also been suspected of imparting a bad
flavour to butter.

According to Pott the milk of cows eating _Oxalis Acetosella_ is with
difficulty converted into butter.

The poisonous principle of _Colchicum autumnale_ is stated to find its
way into the milk of animals consuming it, and Müller states that the
milk of goats which have eaten it has caused the poisoning of infants.

Müller states that a cat died after drinking the milk of a cow suffering
from poisoning by _Narthecium ossifragum_.

_Mercurialis annua_ is said to cause milk to be thin, “blue,” and poor
in fat; while in a case already mentioned (p. 68) _M. perennis_ entirely
stopped the secretion of milk.

According to Chesnut, goats may eat quantities of _Euphorbia Lathyris_,
and it is said that their milk then possesses the poisonous properties
of the plants. Ingestion of other Euphorbias appears to have the same
effect.

Cornevin remarks that _Melampyrum arvense_ is considered to influence
cows to produce more milk.

According to some authorities species of _Equisetum_ check milk
production or cause it to cease, and _E. palustre_ is stated by Weber to
cause the milk of affected cows to become watery, poor in fat, and give
rise to a greasy and unappetising butter, while the yield may soon quite
fail.

The ingestion of the foliage of the oak (_Quercus_ sp.) is stated by
Cornevin to induce _Maladie des Bois_, with reduction or entire loss of
milk production (see p. 69). Acorns have also affected milk production,
and a case is recorded (_The Dairy_, 1913) in which it is stated that
cheese made from the milk of cows which had fed on acorns developed a
sharp acid flavour when about four weeks old, though the texture was
good. It is not clear, however, how it was proved to be due to the
acorns.

In one case recorded a reddish tinge was observed in the milk of a cow
suffering from Rhododendron poisoning (p. 46), and in general reduced
milk production appears to occur.

In addition to the foregoing, there is good authority for saying that
the following plants may impart a disagreeable flavour to milk, and in
many cases the butter made from it:—

             _Anthemis arvensis_L.      (Corn Chamomile).
             _Anthemis Cotula_L.        (Stinking Mayweed).
             _Artemisia Absinthium_ L.  (Wormwood).
             _Conium maculatum_ L.      (Hemlock).
             _Hyoscyamus niger_ L.      (Henbane).
             _Matricaria Chamomilla_ L. (Wild Chamomile).
             _Pinguicula vulgaris_ L.   (Butterwort).
             _Senebiera didyma_ Pers.   (Lesser Wartcress).
             _Sium angustifolium_ L.    (Lesser Sium).
             _Sium latifolium_ L.       (Water Parsnip).
             _Tanacetum vulgare_ L.     (Tansy).
             _Thlaspi arvense_ L.       (Penny Cress).

           (See also Index “Milk, plants affecting,” p. 117.)


                 PLANTS WHICH CAUSE MECHANICAL INJURY.

There are a number of plants which, while not necessarily physiological
poisons, may induce injuries of a severe character when taken by
animals, and by causing festering may bring about septic poisoning. For
example the sharp pointed fruits of _Stipa pinnata_ and _Nardus stricta_
may cause injury to the skin and mouth, piercing the palate and causing
inflammation, and when eaten may even perforate the wall of the
intestine and cause death; and the awned glumes of species of _Bromus_
or the spikelets of Hordeum may injure the gums, causing inflammation,
ulceration, sores, the formation of pus, and loss of teeth. The _Bromus_
and _Hordeum_, also, together with over-matured “heads” of _Trifolium
incarnatum_, may give rise to Phytobezoars or balls in the stomach of
horses and cattle (60, 119). The sharp pointed fruits of _Erodium
cicutarium_ may cause local irritation by working into the wool of
sheep. _Aira caespitosa_ may also cause injury to the mouth of stock.

A case is recorded in New South Wales in which cattle and horses ate
Shepherd’s Purse (_Capsella Bursa-pastoris_). The cattle were
unaffected, but the horses scoured, though most of them soon recovered
when removed from the cultivated paddock containing the weed. Two young
horses, however, showed signs of colic, became bloated, and died. It was
then found that they contained balls of fibrous material (one weighed 1
lb. 9½ oz.) which consisted to the extent of nearly 50 per cent. of
fibres from Shepherd’s Purse, and death was due to simple mechanical
obstruction of the bowel (155).

Chickweed (_Stellaria media_) has been found to cause digestive disorder
in lambs and sheep when eaten in large quantities (48), and has caused
the death of many a lamb. It would appear to be due entirely to the
formation of large lumps of the weed in the stomach, and subsequent
fermentation (_Farmer and Stockbreeder_, Mar. 16, 1908).

According to Cornevin, Black Bindweed (_P. Convolvulus_ L.) may prove
injurious, owing to the occurrence of the hard, trigonous, and pointed
“seeds” in cereal grains. Galtier published facts which show that oats
which contain too many of the “seeds” may, by prolonged use, occasion a
more or less serious enteritis, which is sometimes fatal, particularly
when the grain is fed to greedy horses which scarcely grind their food
(73). The fruits or “seeds” of Knot-weed (_Polygonum Aviculare_ L.) may
similarly prove injurious, and probably the seeds of other plants.




                               CHAPTER IX
                       CLASSIFICATION OF POISONS.


The classification of poisonous plants according to their effects is a
somewhat difficult process, since more than one prominent symptom may be
produced by the same plant. Two classifications, however, may be given
as examples, the first that of Blyth, and the second that of A. B.
Smith. These must be regarded as essentially applicable to human beings,
though serving more or less as a guide in case of poisoning of farm
live-stock.


                 Blyth’s Classification (after Pammel).

  =A.—Poisons causing death immediately or in a few minutes=: Prussic
  acid, cyanides, oxalic acid, and occasionally strychnine.

  =B.—Irritant Poisons=, with symptoms chiefly pain, vomiting, and
  purging: Ergot, digitalis, colchicum, yew, laburnum.

  =C.—Irritant and Narcotic Poisons=, with symptoms of an irritant
  nature, with more or less cerebral indications: Oxalic acid or
  oxalates.

  =D.—Poisons more especially affecting the Nervous System=:

  1. NARCOTICS.—Symptoms: insensibility, which may be preceded by more
  or less cerebral excitement. Opium.

  2. DELIRIANTS.—Delirium, for the most part, a prominent symptom:
  Belladonna, hyoscyamus, stramonium, and other _Solanaceæ_, Lolium
  temulentum, Oenanthe crocata, poisonous fungi.

  3. CONVULSIVES.—Almost every poison has been known to produce
  convulsive effects, but the only true convulsive poisons are the
  alkaloids of the strychnine class.

  4. COMPLEX NERVOUS PHENOMENA.—Aconite, digitalis.


                  A. Bernhard Smith’s Classification.

=A.—Poisons acting on the Brain.=

  1. NARCOTICS.—_Symptoms_: Giddiness; dimness of sight; contracted
  pupils; headache; noises in the ears; confusion of ideas, and
  drowsiness, passing into insensibility.

  _British Plants included_: Papaver somniferum.

2. DELIRIANTS.—_Symptoms_: Spectral illusions; delirium; dilated pupils;
thirst and dryness of the mouth; incoordination. Occasionally, though
rarely, there are paralysis and tetanoid spasms.

_British Plants included_: Datura Stramonium, Hyoscyamus niger, Solanum
Dulcamara, Solanum nigrum, Atropa Belladonna, Lolium temulentum.

3. INEBRIANTS.—_Symptoms_: Excitement of cerebral functions and of the
circulation; loss of power of coordination and of muscular movements,
with double vision; leading to profound sleep and deep coma.

_British Plants included_: Pinus pinaster, Pinus larix, Artemisia
maritima, Artemisia Absinthium.

=B.=—=Poisons acting on the Spinal Cord.=

CONVULSIVES.—_Symptoms_: Clonic (intermittent) spasms, extending from
above downwards. Opisthotonos very violent; but trismus (lockjaw) rare.
Swallowing spasmodic. Death, usually, in less than three hours, or rapid
recovery.

_British Plants included_: none.

=C.=—=Poisons acting on the Heart.=

1. DEPRESSANTS.—_Symptoms_: Vertigo; vomiting; abdominal pain; confused
vision; convulsions; occasional delirium; paralysis; syncope; sometimes
asphyxia.

_British Plants included_: Conium maculatum, Cytisus Scoparius.

2. ASTHENICS.—_Symptoms_: Numbness, and tingling in the mouth; abdominal
pain; vertigo; vomiting; purging; tremor; occasional delirium;
paralysis; dyspnœa, ending in syncope.

_British Plants included_: Prunus laurocerasus, (Phaseolus
lunatus—imported cattle food), Lathyrus aphaca, Rumex Acetosa, Aconitum
Napellus, Actaea spicata, Delphinium consolida, Digitalis purpurea,
Convallaria majalis, Colchicum autumnale.

=D.=—=Vegetable Irritants.=

1. PURGATIVES.—_Symptoms_: Abdominal pain; vomiting and purging; cramps;
strangury and tenesmus, followed by collapse, and sometimes accompanied
by drowsiness, and slight nervous symptoms.

_British Plants included_: Sambucus nigra, Sambucus Ebulus, Helleborus
viridis, Helleborus fœtidus, Caltha palustris, Linum catharticum.

2. ABORTIVES.—_Symptoms_: Nausea; vomiting; stupor; polyuria; sometimes
tenesmus. Abortion may or may not occur; coma.

_British Plants included_: Juniperus Sabina (cultiv. in Britain),
Claviceps purpurea; Ruta graveolens (cultiv. in Britain).

3. IRRITANTS WITH NERVOUS SYMPTOMS.—_Symptoms_: Abdominal pain; vomiting
and purging; dilated pupils; headache; tetanic spasms; occasional
convulsions; sometimes rapid coma.

_British Plants included_: Oenanthe crocata, Oenanthe Phellandrium,
Oenanthe fluviatilis, Cicuta virosa, Aethusa Cynapium, Sium
angustifolium, Taxus baccata, Cytisus Laburnum, Paris quadrifolia,
Mercurialis perennis.

4. SIMPLE IRRITANTS.—_Symptoms_: Burning pain in the throat and stomach;
thirst; nausea; vomiting; tenesmus; purging; dysuria; dyspnœa and cough
occasionally. Death through shock; convulsions; exhaustion; or
starvation due to injury to throat or stomach.

_British Plants included_: Arum maculatum, Daphne Laureola, Daphne
Mezereum, Narcissus moschatus, Narcissus poeticus, Scilla bifolia,
Galanthus nivalis, Hyacinthus nonscriptus, Fritillaria meleagris,
Clematis Vitalba, Anemone nemorosa, Anemone appenina, Ranunculus
aquatilis, R. Flammula, R. Ficaria, R. auricomus, R. sceleratus, R.
acris, R. bulbosus, Aquilegia vulgaris, Bryonia dioica, Ligustrum
vulgare, Asarum europæum, Saponaria officinalis, Valeriana officinalis,
Agrostemma Githago, Doronicum Pardalianches, Impatiens noli-me-tangere,
Erysimum cheiranthoides, Cynoglossum officinale, Arctostaphylos
Uva-ursi, Tamus communis, Euonymus europæus, Rhamnus catharticus,
Glaucium luteum, Roemeria hybrida, Papaver Rhoeas, Chelidonium majus,
Sedum acre, Sedum album, Drosera rotundifolia, Linaria vulgaris, Iris
Pseud-acorus, Iris foetidissima, Buxus sempervirens, Crocus sativus,
Euphorbia Peplis, E. pilosa, E. Helioscopia, E. platyphylla, E. hiberna,
E. portlandica, E. Paralias, E. Peplus, E. exigua, E. Lathyris, E.
amygdaloides, Urtica dioica, U. urens, U. pilulifera, Viscum album,
Lepidium latifolium.

5. SIMPLE IRRITANTS WHEN TAKEN IN LARGE QUANTITIES.—_Symptoms_: Burning
pain in throat and stomach, vomiting; purging; difficulty in swallowing.
Recovery usual.

_British Plants included_: Sinapis alba, and S. nigra.




                              BIBLIOGRAPHY


   1. ADERHOLD, R. Über das Mutterkorn des Getreides und seine Verhütung
        Kais. Biol. Anst. f. Land. und Forstw., Flugblatt No. 21.

   2. AGRICULTURAL JOURNAL, Union of S. Africa, July, 1913.

   3. AGRICULTURAL GAZETTE of New S. Wales, Oct. 2, 1913.

   4. ALLEN’S Commercial Organic Analysis. Vols. vi. and vii, 1913.

   5. ANALYST, August, 1906.

   6. ARMATAGE, G. The Sheep Doctor, 1895.

   7. ATKINSON, V. T. Action of Poisons. Special Report, Diseases of
        Cattle and on Cattle Feeding. U.S. Dept. Agric., Bur. An. Ind.,
        1896.

   8. —— Poisons and Poisoning. Special Report, Diseases of Cattle, rev.
        by L. Pearson. U S. Dept. Agric., Bur. An. Ind., 1908.

   9. AULD, S. J. M. (See DUNSTAN, W. R.)

  10. BAILEY, F. M. Weeds and Suspected Poisonous Plants of Queensland,
        1906.

  11. —— and GORDON, P. R. Plants reputed Poisonous and Injurious to
        Stock, 1887.

  12. BANG, B. Cases of Poisoning from Rape-seed Cakes. Ugeskr. Landm.,
        1897. Abs. in Exp. Sta. Rec., 9, p. 994.

  13. BARGER, G., and CARR, F. H. Note on Ergot-Alkaloids. Phar. Jour.,
        23, p. 257.

  14. BAUME, M. Poisoning by Oenanthe crocata. Archiv, des Mal.
        Mentales, 1881, No. 3. Abs. in Ed. Vet. Rev., 4, p. 704.

  15. BECKER, T. C. (See WITTHAUS, R. A.)

  16. BEILSTEIN, F. Handbuch der Organischen Chemie. 3 Bd. Hamburg and
        Leipzig, 1897.

  17. BENTHAM AND HOOKER. British Flora, 1908.

  18. BERGE, FR., and RIECKE, V. A. Giftpflanzenbuch, 1845.

  19. BERLINER TIERÄRZTLICHE WOCHENSCHRIFT. Var. issues.

  20. BESSEY, C. E. Poisonous Weeds. Rept. Nebraska Agr. Exp. Sta., 16,
        pp. 14–62.

  21. BLANKINSHIP, J. W. The Loco and other Poisonous Plants in Montana.
        Agric. Coll. Exp. Sta., Montana, Bul. 45, 1903.

  22. BLYTH, A. W. Poisons: Their Effects and Detection. 4th Ed., 1906.

  23. —— Old and Modern Poison Lore, 1884.

  24. —— and BLYTH, M. W. Poisons. Rev. Edn., 1906.

  25. BOARD OF AGRIC. AND FISHERIES. Ann. Rept. Proc. Dis. Anim. Acts
        for 1910 (Cd. 5606, 1911).

  26. —— Leaflet, No. 13. Acorn Poisoning.

  27. —— „ No. 222. Meadow Saffron.

  28. —— „ No. 251. Some Common Weeds (Corn Cockle).

  29. —— „ No. 291. Food Value of Acorns, Horse-Chestnuts and Beech
        Mast.

  30. BOECK, H. VON. (See BÖHM, R.)

  31. BOEHM. Cicutoxin. Archiv. f. exp. Path. u. Pharmakol., 5, 279–310.

  32. BÖHM, R., NAUNYN, B., and BOECK, H. VON. Handbuch der
        Intoxicationen. Ed. 15 of the German Ed. of Ziemssen’s Cyclop.

  33. BRANDT, J. F., and RATZEBURG, J. F. C. Deutschlands phan.
        Giftgewächse in Abbildungen u. Beschreibungen, 1838.

  34. BRETEAU. (See CAZENEUVE.)

  35. BRITISH PHARMACEUTICAL CODEX, quoted in Pharm. Jour., Aug. 29,
        1911.

  36. BRÜHL, J. W., in col. with E. HJELT and O. ASCHAN. Die Pflanzen
        Alkaloide. Braunschweig, 1900.

  37. BRÜNNICH, J. C. Hydrocyanic Acid in Fodder Plants. Jour. Chem.
        Soc., 1903, 788–796.

  38. BULLETIN OF THE IMPERIAL INSTITUTE, 1903, 1905, 1906.

  39. —— 1911, (Datura, Hyoscyamus).

  40. BULL. AGRIC. INTELLIGENCE AND PLANT DISEASES. Inter. Instit.
        Agric. Aug.-Oct., 1911, p. 2099 (Solanum Dulcamara).

  41. BULLIARD, P. Histoire des Plantes vénéneuses et suspectes de la
        France, 1798, Ed. 2.

  42. CALLSEN, J. Ueber die Alkaloide der Samen von Lupinus
        angustifolius und von Lupinus perennis, var. polyphyllus.
        Archiv. der Phar., 237, 566–595.

  43. CANADIAN DEPT. AGRIC., OTTAWA. Farm Weeds of Canada. 2nd Ed.,
        1909.

  44. CARR, F. H. (See BARGER, G.)

  45. CARRUTHERS, WM. Aethusa Cynapium. Jour. Roy. Agric. Soc., England,
        63:280.

  46. —— Lychnis Githago. Id., 63:279.

  47. —— Ranunculus bulbosus. Id., 63:279.

  48. —— Stellaria media: Is it Poisonous? Id., 64:308.

  49. —— and Others. Yew Poisoning. Id., Ser. iii, 3:698.

  50. CAZENEUVE, P., and BRETEAU, P. Sur la Solanine. Compt. Rend., tome
        128, 1899, p. 887.

  51. CHEMIST AND DRUGGIST. Var. issues.

  52. CHESNUT, V. K. Principal Poisonous Plants of the United States.
        U.S. Dept. Agric., Div. Bot., Bull. 20, 1898.

  53. —— Thirty Poisonous Plants of the United States. U.S. Dept. Agric.
        Farmers’ Bull. 86, 1898.

  54. —— Preliminary Catalogue of Plants Poisonous to Stock. Ann. Rept.
        Bur. An. Ind., U. S. Dept. Agr., 15: 387–420.

  55. —— Some Common Poisonous Plants. Year Book, U.S. Dept. Agr., 1896.

  56. —— Some Poisonous Plants of Northern Stock Ranges. Id., 1900.

  57. —— and WILCOX, E. V. Stock Poisoning Plants of Montana. U.S. Dept.
        Agr., Div. Bot. Bull. 26, 1901.

  58. COALE, R. D. (See REMSEN, I.)

  59. COLLIN, EUG. Traité de Toxicologie végétale, 1907.

  60. COLVILLE, F. V. Crimson Clover Hair Balls. Cire. U.S. Dept. Agr.,
        Div. Bot., 8:4.

  61. COMPTES RENDUS. No. 147, 1906; 150, 1910; &c.

  62. COOKE, M. C. Seven Sisters of Sleep. London, 1860.

  63. CORNEVIN, CH. Des Plantes Vénéneuses, 1887.

  64. —— Sur l’empoisonnement par quelques espèces de Cytisus. Compt.
        Rend., 1886.

  65. CUSHNY, A. R. Pharmacology, 1898.

  66. —— Ueber das Ricinusgift: Arch. f. exper. Path. u. Pharm., 1898.

  67. CZAPEK, F. Biochemie der Pflanzen, 1905.

  68. DAILY MIRROR, Dec. 13, 1910 (Hyoscyamus poisoning).

  69. DIE FUTTERMITTEL DES HANDELS, 1906.

  70. DIE LANDWIRTSCHAFTLICHE VERSUCHS-STATIONEN, LXXXII, 1 and 2, p.
        93.

  71. DIETRICH, D. N. F. Deutschlands Giftpflanzen, 1826.

  73. DIXON, W. E. Manual of Pharmacology. 4th Ed., 1915.

  74. DOELTZ, J. C. Neue Versuche und Erfahrung der einige
        Pflanzengifte, 1892.

  75. DUCHESNE, E. A. Répertoire des Plantes Utiles et des Plantes
        Vénéneuses du Globe. Brussels, 1846.

  76. DUNSTAN, W. R. Glucosides, 1913.

  77. —— HENRY, T. A., and AULD, S. J. M. Cyanogenesis in Plants, Proc.
        Roy. Soc., Vol. 72, 1903; B. Vol. 79, 1906; B. Vol. 79, 1907.

  78. —— and UMNEY, C. I, Contributions to Our Knowledge of the Aconite
        Alkaloids; II, The Alkaloids of the true Aconitum Napellus; III,
        Formation and Properties of Aconine and its Conversion into
        Aconitine. Jour. Chem. Soc., 1892.

  79. EDEN, R. T. Digitalis and its Cumulative Action. Ther. Gaz., 6:89.

  80. ERDMANN, K. G. Sammlung und Beschreibung der Giftpflanzen.
        Dresden, 1797.

  81. ESSER, P. Die Giftpflanzen Deutschlands, 1910.

  82. EWART, J. Weeds, Poison Plants and Naturalized Aliens of Victoria,
        1909.

  83. FALCK, F. A. Lehrbuch der praktischen Toxikologie, 1880.

  84. FIELD, THE. Var. issues.

  85. FLÜCKIGER, F. A. Pharmakognosie der Pflanzenreiche, 1881–2.

  86. —— and HANBURY, D. Pharmacographia, 1879.

  87. FRIEDBERGER, F., and FRÖHNER, E. Veterinary Pathology. Ed. 6.
        1:731; 2:702.

  88. FRÖHNER, EUGEN. Lehrbuch der Toxicologie für Tierärzte, 1910.

  89. —— (See FRIEDBERGER, F.)

  90. GARDENER’S CHRONICLE. Var. issues.

  91. GILMAN, J. F. Conium maculatum. Jour. belge d’homoeopathie, 1899.

  92. GIMLETTE, J. D. On Datura Poisoning. Brit. Med. Jour., 1903.

  93. GLOVER, G. H. Larkspur and Other Poisonous Plants. Agric. Exp.
        Sta., Colorado, Bull. 113, 1906.

  94. —— Poisonous Weeds. Agr. Exp. Sta., Colorado, Bull. 137, 1909.

  95. GMELIN, J. F. Abhandlung von den giftigen Gewächsen, 1775.

  96. —— Allgemeine Geschichte der Pflanzengifte, 1775.

  97. GODET, C. Les Plantes vénéneuses du Canton de Neuchâtel, 1864.

  98. GOEPPERT, H. R. Ueber die giftige Pflanzen Schlesiens, 1832.

  99. GORDON, P. R. (See BAILEY, F. M.)

 100. GRANDEAU, L. Poisoning of Cattle by Yew Tree Leaves. Jour.
        d’Agric. Prat. i, 229–230, 1894.

 101. GRESHOFF, M. Phytochemical Investigations at Kew. Bull. Misc.
        Infor. Roy. Bot. Gardens, Kew, No. 10, 1909.

 102. —— Distribution of Prussic Acid in the Vegetable Kingdom. Rept.
        Colonial Museum Haarlem, Holland, 1906.

 103. GRESSLER, F. G. L. Deutschlands Giftpflanzen, 1897.

 104. GRÖNLUND, CHR. Danske Giftplanter. Copenhagen, 1874.

 105. GUARDIA, J. Poisonous Plants and their Poisons. Bull. Pharm.,
        1893.

 106. GUERIN, P. The Probable Cause of the Poisonous Effect of the
        Darnel, Lolium temulentum. Bot. Gaz. 28.

 107. GUIGNARD, L. Le haricot à acide cyanhydrique (Phaseolus lunatus).
        Rev. Vit., 1906.

 108. —— Recherches physiologiques sur la greffe des plantes à acide
        cyanhydrique. Ann. sc. Nat., ser. 9, Bot. 6, 261–305.

 109. —— A Study of Beans yielding Hydrocyanic Acid. Rev. Vit., 26.

 110. —— Sur la greffe des plantes à acide cyanhydrique. Compt. Rend.
        Acad. Sc. Paris, 1907.

 111. GÜSSOW, H. T. Canad. Ex. Farms Rept. 1912 (Equisetum arvense).

 112. —— Cattle Poisoning by Plants. Farmer and Stockbreeder Year Book.
        1907.

 113. —— Injurious Fodder and Poisonous Plants. Jour. Roy. Agric. Soc.,
        England, 1907.

 114. HAAS, P., and HILL, T. G. The Chemistry of Plant Products, 1913.

 115. HALENKE, A., and KLING, M. Landw. Versuchs.-Stat., vol. 64.

 116. HALLE, J. S. Die deutsche Giftpflanzen, Berlin, 1784–1795.

 117. HALSTED, B. D. The Poisonous Plants of New Jersey. Rept. Bot.
        Dept., N. J. Agr. Coll. Exp. Sta., 1894 (1895), pp. 401–19.

 118. HANBURY, D. (See FLÜCKIGER, F. A.)

 119. HARSHBERGER, J. W. A Review of our Knowledge of Phytobezoars.
        Jour. Com. Med. & Vet. Arch., 19: 143.

 120. HARTMAN, G. Mechanische Vergiftungen. Berlin, 1896.

 121. HARLEY, J. _Aethusa Cynapium_, St Thomas’ Hospital Reports, n.s.
        1873.

 122. HEBERT, A. Recherches sur la présence de l’acide cyanhydrique chez
        diverses plantes. Bull. de la Soc. chim. de Paris, 1896.

 123. HEDRICK, U. P. Cicuta, a Plant that Poisons Cattle. Bull. Oreg.
        Agr. Exp. Sta., 46: 12.

 124. HEIN, HEINRICH. Deutschlands Giftpflanzen. Hamburg. 1880.

 125. HENDRICK, J. Poisonous Beans. Trans. Highland and Agric. Soc.,
        1907.

 126. HENKEL, ALICE. Weeds Used in Medicine. U.S. Dept. Agric. Farmers’
        Bull. 188, 1904.

 127. HENRY, T. A. (See DUNSTAN, W. R.)

 128. —— The Plants Alkaloids, 1913.

 129. —— On the Occurrence of Prussic Acid and its Derivatives in
        Plants. Sci. Progress, No. 1, July, 1906.

 130. HENSLOW, REV. G. Poisonous Plants in Field and Garden, 1901.

 131. —— The Uses of British Plants traced from Antiquity to the Present
        Day, 1905.

 132. HERISSEY, H. Ueber das Prulaurocerasin. Arch. der Phar.,
        245:463–469.

 133. HILGER, A. (See HUSEMAN, A.)

 134. HILL, T. G. (See HAAS, P.)

 135. HUSEMAN, A., HILGER, A., and HUSEMAN, TH. Die Pflanzenstoffe in
        chemischer, physiologischer und toxicologischer Hinsicht.
        Berlin, 1883.

 136. INDEX PHYTOCHEMICUS. I. C. Ritsema & Sack, Amsterdam, 1905.

 137. JACKSON, J. R. Poisonous Indian Peas. Phar. Jour., 76:521–22.

 138. JAHRESBERICHT ü. d. Fortschritte auf dem Gesamtgebiete der
        Agrikultur-Chemie, 3te Folge, XIV, 1911 (1912).

 139. JOHNSON, CH. British Poisonous Plants. London, 1856. [Ed. 2,
        ?1866].

 140. —— C. P., and SOWERBY, J. E. Useful Plants of Great Britain.
        London [?1865].

 141. —— CH., JOHNSON, C. H., and SOWERBY, J. E. British Poisonous
        Plants, 1861.

 142. JONES, L. R. A. (See RICH, F. A.)

 143. JOUR. AGRICULTURAL RESEARCH. Vol. 1., No. 2, Nov., 1913.

 144. JOUR. BOARD OF AGRICULTURE. Var. issues.

 145. JOUR. ROY. AGRIC. SOC., ENGLAND. Annual Rept. of Consulting
        Botanist for 1899, Poisonous Plants investigations—including
        Ranunculus acris, R. parviflorus, R. Ficaria etc., etc., 1899,
        pp. 678–688.

 146. —— Water Dropwort and Dog’s Mercury (1898), p. 561.

 147. —— Bitter Sweet or Woody Nightshade (1905), p. 164.

 148. —— Meadow Saffron (1897), p. 742.

 149. JOUR. SOC. CHEM. INDUSTRY, May 15, 1908.

 150. JUCH, K. W. Die Giftpflanzen. Augsburg, 1817.

 151. KANNGIESSER, FR. Die akuten Vergiftungen, 1911.

 152. KARSTEN, G. (See STRASBURGER, E.)

 153. KAUPP, B. F. Aconite Poisoning. Am. Vet. Rev., 30: 454–56.

 154. KEELER, D. D. Poisoning by Ergot. Am. Vet. Rev., 38: 251–2.

 155. KELLERMANN, W. A. Poisoning by Shepherd’s Purse. Bot. Gaz., 20:
        325–6.

 156. KERNER, J. S. Deutschlands Giftpflanzen. Hanover, 1798.

 157. KERNER, A., and OLIVER, F. W. Nat. History of Plants, 1902.

 158. KIONKA, H. Grundriss der Toxikologie. Leipzig, 1901.

 159. KLING, M. (See HALENKE, A.)

 160. KNOLLE, F. A. G. Plantas venenatas umbelliferas. Leipzig, 1771.

 161. KOBERT, E. R. Compendium der praktischen Toxicologie, 1912.

 162. —— Lehrbuch der Intoxicationen, 1893.

 163. —— Lehrbuch der Intoxicationen. II. Bd., 1906.

 164. KRAUS, C. Das gemeine Leinkraut. Arb. d. deut. landw. Gesell.,
        Heft 166, 1909.

 165. KREUTZER, K. J. Oesterreiches Giftgewächse, 1838.

 166. KROCKER, Dr. Zur Lupinenkrankheit der Schafe. Landw. Jahrb., 9:
        27–35.

 167. KUBINGI, A. Plantae venenosae Hungariae, 1842.

 168. KUNKEL, A. J. Handbuch der Toxicologie, Jena, 2 Vols. 1899 and
        1901.

 169. LAMBERT, L. (See NOEL, CHARLES.)

 170. LANDER, G. D. Veterinary Toxicology, 1912.

 171. LEATHER, J. W. Cyanogenesis in Plants. Ag. Jour. India, I,
        220–225.

 172. LEHMANN, K. B., and MORI, R. Ueber die Giftigkeit u. Entgiftung
        der Samen von Agrostemma Githago. Archiv. f. Hyg., 9: 257 (Bot.
        Gaz. 14: 233).

 173. LEHMANN, OTTO. Giftpflanzen mit besonderer Berücksichtigung der
        wirksamen Stoffe, 1882.

 174. LEWIN, L. Lehrbuch der Toxicologie. Ed. 2.

 175. LIAUTARD, A. Poisoning of Horses by Snow Drop. Am. Vet. Rev., 30:
        298.

 176. LOHMANN, C. E. J. Ueber die Giftigkeit der deutschen
        Schachtelhalmarten. Arb. d. deut. landw. Gesellschaft, Heft 100,
        1904.

 177. LUBENAU, Dr. On Poisoning from Foods. Centrbl. f. Bakt., 1906, I.
        Abt., Orig., XL., 433.

 178. MCCARTHY, GERALD. The Poisonous Plants of North Carolina. Bull.
        N.C. Agr. Exp. Sta. (St. Bd. Agric.), 22: 48.

 179. MACDOUGALL, R. S. On Lathyrus sativus ... and Allied Leguminous
        Plants. Jour. Bot. Soc. Edin., Dec., 1894.

 180. MAIDEN, J. H. Native Plants Poisonous to Stock. Agr. Gaz. N. S.
        Wales, 6, 57–58.

 181. —— Plants reported to be Poisonous to Stock in Australia. Id. 12,
        637–666.

 182. MARCHLEWSKI, L. (See SCHUNCK.)

 183. MARSH, C. D., and others. Larkspur or “Poison Weed.” U.S. Dept.
        Agric. Farmers’ Bull. 531, 1913.

 184. MILCH-ZEITUNG, 23 (1894), p. 6. Poisoning of Swine from feeding
        Rye Meal containing Corn Cockle Seed.

 185. MIQUEL, F. A. W. De Nord-Nederlandsche vergiftige Gewassen, 1838.

 186. MITLACHER, W. Toxicologisch oder forensisch wichtige Pflanzen,
        1904.

 187. MOELLER, J. Digitalis and Verbascum. Phar. Post., 37: 677–680.

 188. MORI, R. (See LEHMANN, K. B.)

 189. MOSS, R. J. The Taxine in Irish Yew. Sci. Proc. Roy. Dublin Soc.,
        vol. XII (N.S.), No. 10, 1909.

 190. MÜLLER, G. Landwirtschaftliche Giftlehre. 1897.

 191. MÜLLER, GEORG, and KRAUSE, C. Ueber die Giftwirkung der Anemone
        nemorosa. Archiv. für wissenschaftliche u. praktische
        Thierheilkunde, 23, 326–335.

 192. MUELLER, KARL. Colchicum autumnale. Die Natur., 44: 550.

 193. NAUNYN, B. (See BÖHM, R.)

 194. NEBRASKA. 16th Ann. Rept., Agric. Exp. Sta., Univ. Nebr., 1903,
        pp. 14–94.

 195. NEW ZEALAND DEPT. AGRIC. Ann. Repts., 1904. Ragwort Poisoning.

 196. —— Jour. of Agric., 15th Sept., 1913, 301.

 197. NOEL, CHARLES. Contributions à l’étude médicale de l’Anemone
        Pulsatilla. Nancy, 1897.

 198. —— and LAMBERT, L. Recherches expérimentales sur l’Anemone
        Pulsatilla. Arch. inter. de phar., 1897.

 199. NOLL, F. (See STRASBURGER, E.)

 200. NUNN, J. A. Veterinary Toxicology, 1907.

 201. OLIVER, F. W. (See KERNER, A.)

 202. OPWYRDA, R. J. (See PRAAG, L. VAN.)

      202_b_. ORFILA, M. J. Traité de Toxicologie, Ed. 5, 2 v. Paris,
        1852.

 203. PAMMEL, L. H. Manual of Poisonous Plants, 1911. (Contains a list
        of 1097 references to Poisonous Plant Literature.)

 204. —— Poisonous and Medical Plants of Missouri. Bul. 14, Missouri
        State Bd. Hort.

 205. PARKINSON, S. T., and RUSSELL, E. J. A List of Plants Poisonous to
        Stock. Jour. S. E. Agric. College, Wye, Kent, No. 16, 1907.

 206. PATEK, JOHANN. Die Giftpflanzen, 1866–67.

 207. PETERS, A. T. (See STURDEVANT, L. B.)

 208. PFAFF, FRANZ. Ivy Poisoning and its Treatment. Bull. Roy. Bot.
        Gardens, Kew, 1903, 15–16.

 209. PHARMACEUTICAL JOURNAL. Var. issues.

 210. PICTET, A. La Constitution chimique des Alcaloïdes Végétaux,
        2^{me} Ed., 1897.

 211. PLUGGE, P. C. Andromedotoxin-haltige Ericaceen. Arch. der Pharm.,
        229: 552–554.

 212. —— Giftiger Honig von Rhododendron ponticum. Arch. der Pharm.,
        229: 554–56.

 213. POTT, EMIL. Handbuch der tierischen Ernährung und
        landwirtschaftlichen Futtermittel, II. Bd., 1907.

 214. POWER, F. B., and TUTIN, F. Chemical Examination of Aethusa
        Cynapium. Wellcome Chem. Res. Laboratories, No. 58, 1905.

 215. PRAAG, L. VAN, and OPWYRDA, R. J. Leerbuch voor practische
        giftleer, 1871.

 216. PRATT, ANNE. The Poisonous, Noxious and Suspected Plants of our
        Fields and Woods [?1887].

 217. RATTI, Professor. On Colchicum Poisoning. Phar. Jour. and Trans.,
        iii, 6: 47 (abstr. from _Lancet_).

 218. RATZEBURG, J. F. C. (See BRANDT, J. F.)

 219. REMSEN, I., and COALE, R. D. Am. Chem. Jour., vi, 1884, p. 50.

 220. RICE, W. S. Equisetum Poisoning. Am. Vet. Rev., 26: 944–951.

 221. RICH, F. A. Poisonous Equisetum. Proc. Am. Vet. Assoc., 1902.

 222. —— and JONES, L. R. A. Poisonous Plant: the Common Horsetail.
        Bull. Vt. Agr. Exp. Sta., 95: 187–192.

 223. RICHET, C. Les poisons convulsivants. Arch. inter. de phar., 4:
        293–309.

 224. RIECKE, V. A. (See BERGE, Fr.)

 225. ROTHERA, A. C. H. Reputed Poison Plants. Jour. Dept. Agr.
        Victoria, Nov., 1910.

 226. RUSSELL, E. J. (See PARKINSON, S. T.)

 227. SCHENCK, H. (See STRASBURGER, E.)

 228. SCHIMPFKY, RICHARD. Deutschlands wichtigste Giftgewächse in Wort
        und Bild, nebst einer Abhandlung über Pflanzengift, 1893.

 229. SCHMIEDEBERG, O. On Digitalin. Archiv. Exp. Path., 16: 149.

 230. SCHÜNEMANN, H. Die Pflanzenvergiftungen, 1891.

 231. SCHUNCK, E., and MARCHLEWSKI, L. Ann. d. Chem., 278, 354.

 232. SITZBERICHT K. ACAD. WISS. (VIENNA), Math. Naturw. Kl., 121 (1912)
        i, No. 1–3.—Abs. Exp. Sta. Record, XXIX, p. 133.

 233. SMITH, A. B. Poisonous Plants of All Countries, 1905.

 234. SOWERBY, J. E. (See JOHNSON.)

 235. STRASBURGER, E., NOLL, F., SCHENCK, H., and KARSTEN, G. Text Book
        of Botany. 3rd Eng. Ed. Rev. by W. H. LANG. 1908.

 236. STUBBS, G. (See THORPE, T. E.)

 237. STURDEVANT, L. B., and PETERS, A. T. The Poisoning of Horses by
        the Common Horse-tail Weed. Rept. Neb. Agr. Exp. Sta., 19:
        111–115.

 238. TASMANIA, AGRIC. AND STOCK DEPT. Hemlock. Bull. No. 22, 1911.

 239. THORPE, T. E., and STUBBS, G. Yew Poisoning, Trans. Chem. Soc., 81
        (1902).

 240. THORPE, T. E. A Dictionary of Applied Chemistry, 1912.

 241. TRANS. CHEM. SOC., 1902.

 242. —— 1907, p. 337.

 243. TREUB, M. Nouvelles recherches sur le rôle de l’acide cyanhydrique
        dans les plantes vertes. Ann. Jardin bot., Buitzenborg, Ser. ii,
        6: 79–106.

 244. TUCZEK, F. Behandlung der Vergiftungen mit Pflanzenstoffen. Handb.
        d. Spec. Therap. innerer Krankh. 2: 234–334, 1894.

 245. TUTIN, F. Chemical Examination of Oenanthe crocata. Wellcome Chem.
        Res. Laboratories, No. 132, 1911.

 246. —— (See POWER, F. B.)

 247. UMNEY, C. (See DUNSTAN, W. R.)

 248. U.S. DEPT. AGRIC. Experiment Station Record. Var. issues.

 249. —— See (7), (8), (52–57), (60), (126), and (183).

 250. VAN ES, L., and WALDRON, L. R. Some Stock Poisoning Plants of
        North Dakota. N. Dak. Agr. Coll. Exp. Sta., Bull. 58, 1903.

 251. VAN RIJN, J. J. L. Die Glykoside, 1900.

 252. VERSCHAFFELT, E. Bepaling der werking van vergiften op planten,
        Afd. d. k. Akad. v. Welensch. Amst. 12: 855–9, 1903–4.

 253. VETERINARIAN. Var. issues.

 254. VETERINARY JOURNAL. Var. issues.

 255. VETERINARY NEWS. Var. issues.

 256. VETERINARY RECORD. Var. issues.

 257. VICAT, P. R. Histoire des Plantes vénéneuses de la Suisse.
        Yverdon, 1776.

 258. WALDRON, L. R. (See VAN ES, L.)

 259. WALSH, L. H. South African Poisonous Plants. 1909.

 260. WEBER, C. A. Der Duwock (Equisetum palustre). Arb. d. deut. landw.
        Gesell., Heft 72, 1902.

 261. WIEDMANN, FR. Zur chemischen Charakteristik der Familie der
        Papaveraceen. Munich, 1901.

 262. WILCOX, E. V. (See CHESNUT, V. K.)

 263. WILSON, P. Rhododendron Poisoning in a Goat. The Veterinarian, 70:
        639–640.

 264. WINSLOW, KENELM. Veterinary Materia Medica and Therapeutics. 1902.

 265. WITTHAUS, R. A., and BECKER, T. C. Medical Jurisprudence, Forensic
        Medicine and Toxicology. Vol. 4., 1896.

 266. WUNCHMANN, F. Deutschlands Giftpflanzen. 1833.

 267. ZEITSCHR. ANAL. CHEM., 1905, No. 44.

               (See also various references in the text.)




                                 INDEX


 _Abies excelsa_, 72
   — _pectinata_, 72

 Abietin, 72

 _Achillea Millefolium_, 100

 Achilleine, 100

 Aconine, 15

 Aconitic acid, 86

 Aconitine, 11, 15

 _Aconitum Napellus_, 10, 14, 15, 103, 104

 Acorns, 70–72, 100

 _Actaea spicata_, 104

 _Aethusa Cynapium_, 39, 104

 _Agrostemma Githago_, 3, 6, 8, 19, 105

 Agrostemma-Sapotoxin, 21

 Agrostemmin, 21

 _Aira caespitosa_, 101

 All-Heal, 93, 105

 _Alliaria officinalis_, 19, 100

 _Allium_ sp., 99

 Allyl-isothiocyanate, 18

 Amentaceæ, 69

 Amygdalin, 8, 94

 _Anagallis arvensis_, 48

 _Anchusa officinalis_, 94

 Andromedotoxin, 47, 48

 Anemonal, 9

 _Anemone_ sp., 9, 11
   — _appenina_, 105
   — _nemorosa_, 9, 105
   — _pulsatilla_, 9
   — Wood, 9

 Anemone-camphor (oil of anemone), 9

 Anemonic acid, 10, 11

 Anemonin, 10, 11

 Annual Mercury, 67

 _Anthemis aetnensis_, 94
   — _arvensis_, 94, 101
   — _chia_, 94,
   — _Cotula_, 94, 101

 Apoatropine, 59

 _Aquilegia vulgaris_, 105

 Araliaceæ, 43

 Arbutin, 47, 48

 _Arctostaphylos Uva-ursi_, 105

 Aroideæ, 76

 _Artemisia Absinthium_, 101, 104
   — _maritima_, 104

 _Arum maculatum_, 76, 77, 105

 _Asarum europæum_, 105

 Asphodel, Bog, 97, 101

 _Aspidium filix-mas_, 88

 _Astragalus bisulcatus_, 3

 _Atriplex_ sp., 97

 _Atropa Belladonna_, 4, 5, 8, 50, 52, 58, 103, 104

 Atropine, 50, 59

 Autumn Crocus, 2, 3, 79–82, 100, 104

 _Azalea_ sp., 4, 48
   — _arborescens_, 48
   — _indica_, 48
   — _nudiflora_, 48
   — _pontica_, 48


 _Balsamorhiza sagittata_, 3

 Beans, 4, 32, 33, 104

 Belladonine, 59

 Belladonna, _see_ Deadly Nightshade

 Bibliography, 107

 Bindweeds, 49, 102

 Bittersweet, 54, 104

 Black Bindweed, 49, 102
   — Bryony, 35, 78, 105

 Bog Asphodel, 97, 101

 Box, 69, 105

 Bracken, 87, 93

 Brake-fern, 87, 93

 _Brassica nigra_, 18
   — _Sinapistrum_, 18, 19

 _Bromus_, 101

 Broom, 27, 104

 Broom-rape, 95

 Bryogenin, 35

 _Bryonia dioica_, 35, 78, 105

 Bryonin, 35, 78

 Bryony, 35, 78, 105

 Buckthorn, 24, 105

 Buckwheat, 64

 Burma beans, 32

 Buttercups, 8, 10–12, 99, 105
   — Acrid, 10, 105
   — Bulbous, 10, 11, 105
   — Celery-leaved, 10, 11, 99, 105

 Butterwort, 101

 Buxine, 69

 Buxinidine, 69

 _Buxus sempervirens_, 69, 105


 _Caltha palustris_, 9, 12, 99, 104

 Canadian Erigeron, 93

 Caper Spurge, 66, 67, 100, 105

 Caprifoliaceæ, 43

 _Capsella Bursa-pastoris_, 101

 Caryophyllaceæ, 19

 Castor Oil Plant, 33

 Catmint, 96

 Cats-Ear, 94

 Celandine, Greater, 17, 105
   — Lesser, 10, 11, 105

 Celastraceæ, 24

 Celery-leaved Buttercup, 10, 11, 99, 105

 Chaerophyllin, 40

 _Chaerophyllum_ sp., 37, 40
   — _sylvestre_, 40
   — _temulum_, 40

 Chamomile, Corn and Wild, 101

 Charlock, 18

 Chelerythrine, 17

 Chelidonine, 17

 _Chelidonium majus_, 17, 105

 Cherry Laurel, 34

 Chervils, 40

 Chickweed, 101

 Chinovic acid, 93

 Choline, 68

 Christmas Rose, 13

 _Chrysanthemum Leucanthemum_, 100

 _Cicuta virosa_, 2, 8, 36, 104

 Cicutine, 36

 Cicutoxine, 36

 Classification of Poisons, 103

 _Claviceps microcephala_, 98
   — _purpurea_, 8, 88–91, 103, 104

 _Clematis Vitalba_, 9, 105

 Cockle, Corn, 3, 6, 8, 19, 105

 Colchicine, 80

 _Colchicum_ sp., 8, 11, 103
   — _autumnale_, 2, 3, 79–82, 100, 104

 Compositæ, 44

 Conhydrine, 30, 41

 Coniceine, 41

 Coniferæ, 72

 Coniferin, 72

 Coniine, 30, 39, 41

 _Conium maculatum_, 6, 30, 41, 101, 104

 Consolidine, 94

 Convallamarin, 79

 _Convallaria majalis_, 79, 104

 Convallarin, 79

 Convolvulaceæ, 49

 _Convolvulus_ sp., 49, 102
   — _arvensis_, 49
   — _sepium_, 49

 Corn Chamomile, 101

 Corn Cockle, 3, 6, 8, 19, 105

 Cornutine, 89

 Cowbane, 2, 8, 36, 104

 Cow-Wheat, 96, 100

 Cress, Penny, 101

 Crocus, Autumn, 2, 3, 79–82, 100, 104

 _Crocus sativus_, 105

 Crowfoot, Tall, 10, 11, 105

 Cruciferæ, 18

 Cuckoo Pint, 76, 77, 105

 Cucurbitaceæ, 35

 Cumarin, 92

 _Cupressus macrocarpa_, 73
   — _nootkatensis_, 73

 _Cuscuta_ sp., 94
   — _Epithymum_, 94
   — _europæa_, 94

 Cuscutin, 94

 Cyclamin, 49

 Cynapine, 39

 Cynoglossine, 94

 _Cynoglossum officinale_, 94, 105

 Cytisine, 25, 27, 92

 _Cytisus Laburnum_, 25, 27, 104
   — _Scoparius_, 27, 104
   — _Weldeni_, 25


 _Daphne_ sp., 4, 8
   — _Laureola_, 65, 105
   — _Mezereum_, 65, 105

 Daphnin, 65

 Darnel, 8, 48, 82–84, 96, 103, 104

 _Datura Stramonium_, 50, 103, 104

 Daturine, 50

 Deadly Nightshade, 4, 5, 8, 50, 52, 58, 103, 104

 Delphinine, 11, 14

 _Delphinium Ajacis_, 14
   — _Consolida_, 14, 104
   — _Staphisagria_, 14

 Delphinoidine, 14

 Delphisine, 14

 Devil’s-Bit, 93

 Digitalein, 61

 Digitalin, 61

 _Digitalis purpurea_, 61, 103, 104

 _Digitin_, 61

 _Digitonin_, 61

 _Digitoxin_, 61

 _Dioscorideæ_, 78

 Docks, 63, 64

 Dodders, 94

 Dog’s Mercury, 67, 68, 100, 104

 _Doronicum Pardalianches_, 105

 Dropwort, Water, 37, 103, 104

 _Drosera_ sp., 93
   — _rotundifolia_, 105

 Dulcamarin, 54

 Dwarf Elder, 43, 104


 Ecboline, 89

 _Echium vulgare_, 94

 Elder, Common, 43, 104
   — Dwarf, 43, 104

 _Endoconidium temulentum_, 83

 Equisetaceæ, 84

 Equisetine, 86

 _Equisetum_ sp., 3, 84–87, 100
   — _arvense_, 84, 85, 86, 87
   — _heleocharis_, 85
   — _maximum_, 83
   — _palustre_, 85, 100
   — _pratense_, 85
   — _sylvaticum_, 85

 Ergot, 8, 88–91, 103, 104

 Ergotinine, 89

 Ergotism, 89

 Ergotoxine, 89

 Ericaceæ, 46

 Ericolin, 47, 48

 Erigeron, Canadian, 93

 _Erigeron canadensis_, 93

 _Erodium cicutarium_, 101

 _Erysimum cheiranthoides_, 19, 105

 Esparcet, False, 3

 Euonymin, 24

 _Euonymus europæus_, 24, 105

 _Euphorbia_ sp., 8, 66, 67
   — _amygdaloides_, 105
   — _exigua_, 105
   — _Helioscopia_, 66, 105
   — _hiberna_, 105
   — _Lathyris_, 66, 67, 100, 105
   — _Paralias_, 105
   — _Peplis_, 105
   — _Peplus_, 66, 105
   — _pilosa_, 105
   — _platyphylla_, 105
   — _portlandica_, 105

 Euphorbiaceæ, 66


 Fagopyrism, 64

 Ferns, 87, 88

 Figworts, 95

 Filices, 87

 Filicic acid, 88

 Flag, Yellow, 97, 105

 Flax, Purging, 92, 104

 Fool’s Parsley, 39, 104

 Formic acid, 75

 Foxglove, 61, 103, 104

 Frangulin, 24

 _Fritillaria Meleagris_, 97, 105

 Fritillary, Common, 97, 105

 Fungi, 88

 Furze, 92


 _Galanthus nivalis_, 105

 Garden Nightshade, 4, 52, 54, 104

 Garlic Mustard, 19, 100

 Garlics, 99

 Geraniaceæ, 23

 Geranium, Wild, 3

 Githagin, 21

 Githagism, 20

 _Glaucium luteum_, 105

 Gorse, 92

 Gramineæ, 82

 Gratiolin, 95

 Great Mullein, 95

 Ground Ivy, 96

 Gummi hederæ, 43


 _Hedera Helix_, 43

 Hederin, 43

 Hellebore, Green, 13, 14, 104
   — Stinking, 13, 104

 Helleborein, 13

 Helleborin, 12, 13

 _Helleborus_ sp., 13
   — _fœtidus_, 13, 104
   — _niger_, 13
   — _viridis_, 13, 14, 104

 Hemlock (_see also_ Water Hemlock), 6, 30, 41, 101, 104

 Henbane, 6, 51, 101, 104

 Herb Paris, 78, 104

 _Hieracium Pilosella_, 98

 _Hordeum_, 101

 Horsetails, 3, 84–87, 100

 Hound’s Tongue, 94, 105

 Huckleberry, 53

 _Hyacinthus nonscriptus_, 105

 _Hydrocotyle vulgaris_, 93

 Hydroergotinine, 89

 Hyoscine, 50, 51, 59

 Hyoscyamine, 6, 46, 50, 51, 59

 _Hyoscyamus_ sp., 103
   — _muticus_, 6
   — _niger_, 6, 51, 101, 104

 Hyoscypicrin, 51

 Hypericineæ, 22

 _Hypericum perforatum_, 22

 _Hypochæris radicata_, 94


 _Impatiens noli-me-tangere_, 105

 Imperialine, 97

 Iridin, 97

 _Iris foetidissima_, 105
   — _Pseud-acorus_, 97, 105

 Ivraie, 83

 Ivy, 43
   — Ground, 96


 Java beans, 4, 32, 104

 Jervine, 12, 13

 Jimson Weed, 50

 _Juncus_ sp., 98

 _Juniperus Sabina_, 72, 104


 King-cup, 12 99, 104

 Knot-weed, 102

 Kribbelkrankheit, 89


 Laburnum, 25, 27, 103

 _Lactuca scariola_, 45
   — _virosa_, 45, 46

 Lactucarium, 46

 Lactucerin, 46

 Lactucic, acid 46

 Lactucin, 46

 Lactucone, 46

 Lactupicrine, 46

 _Larix europæa_, 72

 Larkspur, 14, 104

 Lathyrism, 27, 28

 _Lathyrus Aphaca_, 29, 104
   — _Cicera_, 27
   — _Clymenum_, 27
   — _sativus_, 27, 96

 Laurel, Cherry, 34, 104

 Laurel, Spurge, 65, 105

 _Lepidium latifolium_, 105

 Lettuce, Wild, 45

 Ligustrin, 49

 Ligustron, 49

 _Ligustrum vulgare_, 4, 49, 105

 Liliaceæ, 78

 Lily-of-the-Valley, 79, 104

 Lima beans, 32

 _Linaria vulgaris_, 95, 105

 Linarin, 95

 _Linum carthaticum_, 92, 104

 Loco-weed, 3

 Loliine, 83

 _Lolium temulentum_, 8, 48, 82–84, 96, 103, 104

 Lords and Ladies, 76, 77, 105

 Lousewort, 63, 95

 Lupines, 29
   — Blue, 29
   — False, 3
   — White, 30
   — Yellow, 29

 Lupinidine, 27, 31

 Lupinine, 31

 Lupinosis, 29–32

 Lupinotoxin, 31

 _Lupinus_ sp., 29–32
   — _albus_, 30
   — _angustifolius_, 29
 —— _luteus_, 29, 30


 Mal de Brou, 70

 Maladie des Bois, 70, 100

 Male Fern, 88

 Marsh Marigold, 12, 99, 104

 Marsh Penny-Wort, 93

 _Matricaria Chamomilla_, 101

 Mayweeds, 94, 101

 Meadow Saffron, 2, 3, 79–82, 100, 104

 Mechanical injury, plants causing, 101

 _Melampyrum_ sp., 63, 95, 96
   — _arvense_, 96, 100

 Melilot, 92

 _Melilotus_ sp., 92

 Mercurialine, 68

 _Mercurialis annua_, 67, 68, 100
   —— _perennis_, 67, 68, 100, 104

 Mercury, Dog’s and Annual, 67, 68, 100, 104

 Methylconiine, 41

 Mezerein, 65

 Mezereon, 65, 105

 Milk, plants affecting, 99, 100, 101
   — _Achillea Millefolium_, 100
   — Acorns, 100
   — _Alliaria officinalis_, 100
   — _Allium_ sp., 99
   — _Anthemis_ sp., 94, 101
   — _Artemisia Absinthium_, 101
   — _Caltha palustris_, 99
   — _Chrysanthemum Leucanthemum_, 100
   — _Colchicum autumnale_, 80, 81, 100
   — _Conium maculatum_, 42, 101
   — _Cytisus Weldeni_, 25
   — _Equisetum palustre_, 87, 100
   — _Euphorbia_ sp., 67
   — — _Lathyris_, 100
   — _Helleborus_ sp., 13, 14
   — _Hyoscyamus niger_, 52, 101
   — _Hypericum perforatum_, 22
   — _Matricaria Chamomilla_, 101
   — _Melampyrum arvense_, 100
   — _Mercurialis annua_, 68, 100
   — — _perennis_, 68, 100
   — _Narthecium ossifragum_, 97 100
   — _Oxalis Acetosella_, 23, 100
   — _Pinguicula vulgaris_, 101
   — _Quercus_ sp., 71, 100
   — _Ranunculus_ sp., 99
   — _Rhododendron_, 47, 100
   — _Rumex_ sp., 64
   — _Senebiera didyma_, 101
   — _Senecio latifolius_, 45
   — _Sium angustifolium_, 101
   — — _latifolium_, 37, 101
   — _Solanum tuberosum_, 57
   — _Tanacetum vulgare_, 44, 101
   — _Thlaspi arvense_, 101

 _Molinia caerulea_, 98

 Monkshood, 10, 14, 15, 103, 104

 Morphine, 16

 Mullein, Great, 95

 Mustard, Garlic, 19, 100
   — Treacle, 19


 Naked Ladies, 2, 3, 79–82, 100, 104

 Narcissine, 97

 _Narcissus_ sp., 97
   — _moschatus_, 105
   — _poeticus_, 97, 105
   — _pseudo-narcissus_, 97

 _Nardus stricta_, 101

 Narthecin, 97

 _Narthecium ossifragum_, 97, 100

 _Nepeta Cataria_, 96
   — _Glechoma_, 1, 96, 98

 Nettles, 97, 105

 Nightshade, _see_ Deadly Nightshade _and_
 Garden Nightshade


 Oak, 69–72, 100

 _Oenanthe crocata_, 37, 103, 104
   — _fistulosa_, 38
   — _fluviatilis_, 104
   — _Phellandrium_, 38, 104

 Oenanthotoxin, 38

 Oil of Cicuta, 36
   — Euphorbia, 68
   — Mustard, 18
   — Snapdragon, 95
   — Tansy, 44
   — Valerian, 93
   — Yew, 75

 Oleaceæ, 49

 Orache, 97

 _Orobanche minor_, 95

 _Oxalis Acetosella_, 23, 100


 Paigya beans, 32

 _Papaver_ sp., 8, 16
   — _dubium_, 16
   — _Rhoeas_, 16, 105
   — _somniferum_, 103

 Papaveraceæ, 16

 Papilionaceæ, 25

 Parabuxine, 69

 Parabuxinidine, 69

 Paridin, 78, 79

 _Paris quadrifolia_, 78, 104

 Paristyphnin, 78

 Parsnip, Water, 37, 101
   — Wild, 93

 Pasque Flower, 9

 _Pastinaca sativa_, 93

 Peas, Indian, 27, 96
   — Mutter, 27

 _Pedicularis_ sp., 63, 95
   — _palustris_, 63
   — _sylvatica_, 63

 Penny Cress, 101

 Penny-Wort, Marsh, 93

 Persicaria, 64

 Petty Spurge, 66, 105

 Phaseolunatin, 8, 33

 _Phaseolus lunatus_, 4, 32, 104

 _Picea_ sp., 72

 Picein, 72

 Picrotoxin, 36, 83

 Pimpernel, Scarlet, 48

 _Pinguicula vulgaris_, 101

 Pinipicrin, 72

 _Pinus larix_, 104
   — _pinaster_, 104
   — _strobus_, 72
   — _sylvestris_, 72

 _Pisum sativum_, 27

 Poison Weed, 48

 Polygonaceæ, 63

 _Polygonum Aviculare_, 102
   — _Convolvulus_, 102
   — _Fagopyrum_, 64
   — _hydropiper_, 64, 65
   — _Persicaria_, 64, 65

 Poppies, 8, 16, 103, 105

 Potato, 54–58

 _Potentilla Anserina_, 92
   — _tormentilla_, 88, 93

 Primulaceæ, 48

 Privet, 4, 49, 105

 Protopine, 17

 Prulaurasin, 34

 _Prunus laurocerasus_, 34, 104

 Pseudoconhydrine, 41

 _Pteris aquilina_, 87, 93

 Pteritannic acid, 88

 Pulsatilla-camphor, 9

 Purging Flax 92, 104


 _Quercus_ sp., 69–72, 100


 Radish, Wild, 18

 Ragwort, 44

 Rangoon beans, 32

 Ranunculaceæ, 9

 _Ranunculus_ sp., 8, 9, 10, 12, 99
   — _acer_, 11
   — _acris_, 10, 11, 105
   — _aquatilis_, 10, 105
   — _auricomus_, 105
   — _bulbosus_, 10, 11, 105
   — _Ficaria_, 10, 11, 105
   — _Flammula_, 10, 11, 105
   — _lingua_, 10
   — _repens_, 10, 12, 99
   — _sceleratus_, 10, 11, 99, 105

 _Raphanus Raphanistrum_, 18

 Rhamnaceæ, 24

 Rhamnetin, 24

 _Rhamnus Catharticus_, 24, 105
   — _Frangula_, 24

 Rheadine, 16

 Rhinanthin, 63, 96

 _Rhinanthus_ sp., 63
   — _Crista-galli_, 95

 Rhododendrin, 47

 _Rhododendron_ sp., 4, 46, 100
   — _arboreum_, 47
   — _californicum_, 46
   — _Chrysanthum_, 46
   — _cinnabarinum_, 47
   — _ferrugineum_, 46
   — _hirsutum_, 47
   — _maximum_, 46
   — _ponticum_, 46, 47
   — _punctatum_, 47

 Ricin, 34

 Ricinine, 34

 _Ricinus communis_, 33

 _Roemeria hybrida_, 105

 Rosaceæ, 34

 _Rumex Acetosa_, 63, 104
   — _Acetosella_, 63
   — _crispus_, 64

 _Ruta graveolens_, 104


 St John’s Wort, 22

 _Sambuca Ebulus_, 43, 104
   — _nigra_, 43, 104

 Sambucine, 44

 Sambunigrin, 44

 _Saponaria officinalis_, 19, 105

 Saponins, 8, 9, 19, 21, 77, 78, 97

 Sapotoxin, 21

 _Scabiosa succisa_, 93 93

 Scarlet Pimpernel, 48

 _Scilla bifolia_, 105

 Scopolamine, 50, 51, 59

 _Scrophularia aquatica_, 95
   — _nodosa_, 95

 Scrophularine, 95

 Scrophularineæ, 61

 _Sedum acre_, 93, 105
   —_album_, 105

 _Senebiera didyma_, 101

 Senecifolidine, 45

 Senecifoline, 45

 _Senecio Burchellii_, 45
   —_Jacobœa_, 44
   —_latifolius_, 45

 Sheep’s Sorrel, 63

 Shepherd’s Purse, 101

 Silica, 86

 Silver Weed, 92

 Sinalbin, 18

 Sinapine, 18

 _Sinapis alba_, 105
   —_arvensis_, see _Brassica sinapistrum_
   —_nigra_, 105

 _Sium angustifolium_, 37, 101, 104
   —_latifolium_, 37, 101

 Sium, Lesser, 101

 Smilacin, 21

 Snake’s Head, 97

 Soapwort, 19, 105

 Solanaceæ, 4, 8, 50, 103

 Solanidine, 53, 56

 Solanine, 8, 53, 54, 55, 56

 _Solanum Dulcamara_, 54, 104
   —_guineense_, 53
   —_nigrum_, 4, 52, 54, 104
   —_tuberosum_, 54–58
   —_villosum_, 53

 Sorrel, Common, 63, 104
   —Sheep’s, 63
   —Wood, 23, 100

 Sparteine, 27, 31

 Spearwort, Lesser, 10, 11, 105

 Spindle Tree, 24, 105

 Spurge Laurel, 65, 105

 Spurges, 66, 67, 100, 105

 Staphisagrine, 14

 _Stellaria media_, 101

 Stinking Mayweed, 101

 _Stipa pinnata_, 101

 Sundews, 93

 Sunflower, Wild, 3

 Sun Spurge, 66, 105

 Syringin, 49

 Syringopicrin, 49


 _Tamus communis_, 35, 78, 105

 _Tanacetum vulgare_, 44, 101

 Tannin, 70

 Tansy, 44, 101

 Taxine, 75

 _Taxus baccata_, 2, 4, 7, 8, 72, 73–76, 103, 104

 Temuline, 83

 Terpene, 93

 _Thermopsis rhombifolia_, 3

 _Thlaspi arvense_, 101

 Thorn Apple, 50, 103, 104

 _Thuja occidentalis_, 72

 Thymelaceæ, 65

 Toadflax, 95, 105

 Tormentil, 88, 93

 Traveller’s Joy, 9, 105

 Treacle Mustard, 19

 _Trifolium incarnatum_, 101

 Trimethylamine, 68

 _Trollius europœus_, 9


 _Ulex europœus_, 92

 Ulexine, 25, 92

 Umbelliferæ, 2, 36

 _Urtica_ sp., 97
   —_dioica_, 97, 105
   —_pilulifera_, 105
   —_urens_, 105


 _Valeriana officinalis_, 93, 105

 Valerianic acid, 93

 Vellarin, 93

 _Verbascum Thapsus_, 95

 Vetchling, Yellow, 29, 104

 Viper’s Bugloss, 94

 _Viscum album_, 105


 Wall-Pepper, 93, 105

 Wartcress, Lesser, 101

 Water Dropwort, 37, 103, 104
   —Hemlock, 2, 8, 36, 104
   —Parsnip, 37, 101
   —Pepper, 64, 65

 White-Rot, 93

 Wild Chamomile, 101
   —Geranium, 3
   —Lettuce, 45
   —Parsnip, 93
   —Radish, 18
   —Sunflower, 3

 Wind Flower, 9, 105

 Wonderberry, 53

 Wood Anemone, 9, 105
   —Sorrel, 23, 100

 Wormwood, 101


 Xylan, 98


 Yellow Flag, 97
   —Rattle, 95
   —Vetchling, 29, 104

 Yew, 2, 4, 7, 8, 72, 73–76, 103, 104


 _Zygadenus venenosus_, 3


    CAMBRIDGE: PRINTED BY J. B. PEACE, M.A., AT THE UNIVERSITY PRESS

------------------------------------------------------------------------




                       CAMBRIDGE UNIVERSITY PRESS


                   CAMBRIDGE AGRICULTURAL MONOGRAPHS

      General Editors: T. B. WOOD, M.A., and E. J. RUSSELL, D.Sc.

  =Inorganic Plant Poisons and Stimulants.= By WINIFRED E. BRENCHLEY,
    D.Sc., F.L.S., Fellow of University College, London. With 19
    illustrations. Royal 8vo. 5s net.

  =Plants Poisonous to Live Stock.= By HAROLD C. LONG, B.Sc. (Edin.), of
    the Board of Agriculture and Fisheries. Royal 8vo.


                    CAMBRIDGE FARM INSTITUTE SERIES

 General Editors: Professor T. B. WOOD, M.A., and E. J. RUSSELL, D.Sc.

  The volumes of this series are intended to meet the needs of the
  many Farm Institutes already in existence or about to be formed.
  They are intended for the average student whose object is to farm,
  rather than for the exceptional man who wishes to become an
  agricultural expert.

                              _Now ready_

  =Farm Accounts.= By C. S. ORWIN, Hon. M.A. 3s net.

  =A Student’s Book on Soils and Manures.= By E. J. RUSSELL, D.Sc. 3s 6d
    net.

  =Fungoid and Insect Pests of the Farm.= By F. R. PETHERBRIDGE, M.A.
    With 54 illustrations. 4s net.


          UNIVERSITY OF CAMBRIDGE SCHOOL OF FORESTRY BULLETINS

  =The Production and Utilisation of Pine Timber in Great Britain.= Part
    I. Production. By E. R. BURDON, M.A., Investigator in Timber, and A.
    P. LONG, B.A., Assistant Investigator.

        No. 1. Sample Plots of Scots Pine at Woburn. Demy 8vo. Paper
                covers, 1s 6d net. (Bulletin, No. 1.)

        No. 2. Sample Plot of Scots Pine at King’s Lynn. Demy 8vo. Paper
                covers, 9d net. (Bulletin, No. 2.)

                  *       *       *       *       *


                  THE JOURNAL OF AGRICULTURAL SCIENCE

                               Edited by

  R. H. BIFFEN, M.A., F.R.S., A. D. HALL, M.A., F.R.S., E. J. RUSSELL,
                      D.Sc., and T. B. WOOD, M.A.

Price per volume, consisting of four parts, 15s net in paper covers, 18s
6d net bound in buckram; to subscribers, 15s net per volume, post free,
payable in advance. The price of each part sold separately is 5s net.




 SELECTION FROM THE GENERAL CATALOGUE OF BOOKS PUBLISHED BY THE CAMBRIDGE
                             UNIVERSITY PRESS


  =Manuring for Higher Crop Production.= By E. J. RUSSELL, D.Sc.,
    Director of the Rothamsted Experimental Station. With 16
    illustrations. Demy 8vo. 3s net.

  =The Fertility of the Soil.= By E. J. RUSSELL, D.Sc. With 9
    illustrations. Royal 16mo. Cloth, is 3d net. Leather, 2s 6d net.
    Cambridge Manuals Series.

  =Agricultural Geology.= By R. H. RASTALL, M.A., late Fellow of
    Christ’s College and Demonstrator of Geology in the University of
    Cambridge. With 51 illustrations. Demy 8vo. 10s 6d net. Cambridge
    Geological Series.

  =Rubber and Rubber Planting.= By R. H LOCK, Sc.D. With 10 plates and
    22 figures. Crown 8vo. 5s net.

  =Agriculture in the Tropics. An elementary treatise.= By J. C. WILLIS,
    M.A., Sc.D. Second edition, revised. With 31 plates. Demy 8vo. 9s
    net. Cambridge Biological Series.

  =A Manual and Dictionary of the Flowering Plants and Ferns.= By J. C.
    WILLIS, M.A., Sc.D. Third edition. Crown 8vo. 10s 6d net. Cambridge
    Biological Series.

  =The Classification of Flowering Plants.= By ALFRED BARTON RENDLE,
    M.A., D.Sc., F.L.S. Vol. I. Gymnosperms and Monocotyledons. With 187
    illustrations. Demy 8vo. 10s 6d net. Cambridge Biological Series.

  =Grasses=: a Handbook for use in the Field and Laboratory. By H.
    MARSHALL WARD, Sc.D., F.R.S. With 81 figures. Crown 8vo. 6s.
    Cambridge Biological Series.

  =Trees=: a Handbook of Forest Botany for the Woodlands and the
    Laboratory. By H. MARSHALL WARD, Sc.D., F.R.S. Vol. I. _Buds and
    Twigs._ Vol. II. _Leaves._ Vol. III. _Flowers and Inflorescences._
    Vol. IV. _Fruits._ Vol. V. _Form and Habit, with an appendix on
    Seedlings._ With numerous illustrations. Crown 8vo. 4s 6d net each.
    Cambridge Biological Series.

  =Botany.= A Text-Book for Senior Students. By D. THODAY, M.A.,
    Lecturer in Physiological Botany and Assistant Director of the
    Botanical Laboratories in the University of Manchester. With 205
    illustrations. Crown 8vo. 5s 6d net.

  =Types of British Vegetation.= By members of the Central Committee for
    the Survey and Study of British Vegetation. Edited by A. G. TANSLEY,
    M.A., F.L.S. With 36 plates and 21 figures. Crown 8vo. 6s net.

                  *       *       *       *       *

  =Lessons on Soil.= By E. J. RUSSELL, D.Sc. With 58 illustrations.
    Large crown 8vo. 1s 6d net. Cambridge Nature Study Series.

  =Weeds. Simple Lessons for Children.= By ROBERT LLOYD PRAEGER. With 45
    figures and 3 plates. Large crown 8vo. 1s 6d net. Cambridge Nature
    Study Series.

                  *       *       *       *       *

                       Cambridge University Press
                Fetter Lane, London: C. F. Clay, Manager

------------------------------------------------------------------------




                          TRANSCRIBER’S NOTES


 1. Silently corrected typographical errors and variations in spelling.
 2. Archaic, non-standard, and uncertain spellings retained as printed.
 3. Enclosed italics font in _underscores_.
 4. Enclosed bold font in =equals=.
 5. Superscripts are denoted by a caret before a single superscript
      character or a series of superscripted characters enclosed in
      curly braces, e.g. M^r. or M^{ister}.
 6. Subscripts are denoted by an underscore before a series of
      subscripted characters enclosed in curly braces, e.g. H_{2}O.





End of Project Gutenberg's Plants Poisonous to Live Stock, by Harold C. Long