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LANDER'S

VETERINARY
TOXICOLOGY
REVISED BY

.]. A. NICHOLSON, M.A., PH.D., M.R.C.V.S.


PROFESSOR OF PHYSIOLOGY AND BIOCHEMISTRY, THE VETERINARY
COLLEGE OF IRELAND, B.(I.LL'S BRIDGE, DUBLIN

THIRD EDI7'lON

LONDON
BAILLIERE, TINDALL & COX
7 & 8, HENRIETTA STREET, COVENT GARDEN, W.C. z
1945
B.L. No. 64.
Imperial Veterinary Research Institj..\te
Library, 6 \ =:J L'AN.
5.
MUKTESWAR.
Class.~~.
Register No. 4,S';1. Room No.
Inward No. 3/19. \ Shelf No.
l

Received. 2-' - 0~ftf Book No.

MGIPC-S2-rII-6-2!iIPD\-6-6-38-250.
First Edition
Second Edition-
Third Edition -

BOOK
PRODUCTION
WAR ECONOMY
STANDARD

THIS BOOK IS PRODUCED IN


COMPLETE CONFORMITY WITH
THE AUTHORIZED ECONOMY STANDARD

Printed in Great EJritain


PREFACE
IN preparing a new edition of Lander's" Veterinary Toxicology':."
the main difficulty has been to present, without overburdening

the book, the many new facts of toxicological importance which
have come to light during the eighteen years which have elapsed
since the .previous edition was published. The present writer,
however, was fortunate enough to have discussed this problem
with th. late Professor Lander on sev~ral occasions and has
attempt~ to carry out his ideas as far as possible.
It was leit that the form of the book should remain unaltered
but that, although primarily intended for veterinary practitioners
and students, its usefulness to the practising toxicologist and to
the research worker should be increased. This has been attempted
not only by a revision of the whole text and the inclusion of new
material, but also by rearrangement of the references, which are
intended to form a convenient starting point for further research.
Whilst the difficulty of pleasing many masters is fully appreciated,
it is hoped that some measure of success has been achieved ..
My thanks are due to Mr. B. G. Fagan, F.r.C., Public Analyst
to the City of Dublin, and also to my colleague Professor A. F.
O'Dea for much helpful advice and encouragement. The publishers,
Messrs. Bailliere, Tindall and Cox, also deserve much credit for
undertaking the production of the work under such difficult
circul}1stances.
]. A. N.
THE VETERINARY COLLEGE OF IRELAND,
BALL'S BRIDGE,
DUBLIN,
December, 1944.

iii
TABLE OF CONTENTS
pAGE
INTRODUCTION I
Definition of a Poison 2
General Chemistry of Poisons 4
Conditions Governing the Action of Poisons 6
Variations of Action due to Species 15
Variations of Action due to the Individual 15
Classification 16
Common Causes of Poisoning 18
Kinds of Poisoning 20
Diagnosis of Poisoning 20
Treatment 21
Post-mortem 25
Chemical Analysis 25
MINERAL OR INORGANIC PO&ONS 28
vJ\rsenic 28
Antimony 41
Lead 44
Mercury - 52
Copper 56
Zinc 60
Silver 63
Thallium 65
Barium 67
Chromium 69
Iron 71
Phosphorus 71
Ammonia 75
Strong Acids and Alkalis 78
Sodium 80
Nitrates - 87
Sulphur - 89
Selenium - 91
Molybdenum 94
ifalogen Elements and their Compounds 95
.fFluorine - ~ 99
Carbon Monoxide 102
ORGANIC POISONS AND DRUGS 10 4
Hydrocyanic or Prussic Acid 10 4
Carbolic Acid and Allied Preparations 112
Strychnine II8
Morphine and Opium 12 4
Cocaine 129
Eserine or Physostigmine 13 0
Pilocarpine 13 2
Ipecacuanha and Emetine 133
Gelsemium 134
Veratrine I35
Curarine - 13 6
Yohimbine I37
Coccu]us Indicus 13 8
Canabis Indica, or Indian Hemp 13 8
Santonin and Wormwood i 139
"
VI TABLE OF CONTENTS
ORGANIC POISONS AND DRUGS-Continued PACE
Turpentine, Camphor and Essential Oils 14 0
Oil of Choenopodium -' -
144-
Oxalic Acid 145
Alcohol - 147
Cantharides
Carbon Tetrachloride 149
15 1
Phenothiazine 154
POISONOUS PLANTS
157
Conifer<e - 159
Arace<e 163
lridace<e - 164
Amaryllidace<e 166
Dioscoridace<e 16 7
Liliace<e - 16&
Gramin<e - 174
Eq uisetace<e 178
Poisoning due to Diseased Forage 180
Ranunculace<e 18 5
Papaverace<e 201
Crucifer<e 20 4
Violace<e ~ 20 7
Caryophyllace<e - 20 7
H ypericace<e 210
Meliace<e 212
Celastrace<e 212
Rhamnace<e 214
Leguminose<e 21 4
Rosace<e - 224
Cucurbitace<e 224
Crassulace<e 226
Umbellifer<e 227
Araliace<e 23 6
Caprifoliace<e ' 23 6
Valerianace<e 23 6
Dipsace<e 23 6
Composit<e 237
Campanulace<e 24 1
Ericace<e 24 2
Oleace<e - 244
Primulacere 245
Apocynacere 245
Asclepiadace<e 249
Convolvulace<e 249
Solanace<e 25 1
Scrophulariace<e - 265
Phytolaccace<e 27 1
Polygonace<e 27 1
Aristolochiace<e - 27 2
Thymelacere 273
Euphorbiace<e 276
Plants and Food Reputed to be Poisonous 28 4
EMICAL TOXICOLOGY 292
)EX
3 IB
VETERINARY TOXICOLOGY

INTRODUCTION
TOXICOLOGY embraces the general study of the origin, properties
and effects of poisons upon the animal body and has the practical
object of t~le diagnosis and treatment of poisoning together with
a study of the post~mortem indications and the chemical detection
of poisons.
Since most drugs are also poisons, it follows that the art of
toxicology is closely allied to that of pharmacology, which deals
with the description and explanation of the symptoms induced by
chemical substances entering the animal organism. Therefore, in
so far'!ts toxicology is concerned with the study of the mechanism
of the absorption, action and elimination of a drug, it is a branch
of the science of pharmacology. .
A complete scientific and practical development of the subject
manifestly demands the joint contributions of the botanist,
chemist, physiologist, pathologist, and clinician, and in propor-
tion as there is increase in exactness in our knowledge of th~se
subjects, so do toxicology and the wider domain of pharmacology
assume greater precision and efficiency.
The nefarious and often lucrative practice of malicious poison-
ing is as old as man, and a moment's reflection on the state of
knowledge of the exact sciences among the ancients and during
the Middle Ages-indeed, until the nineteenth century-will
satisfy us that poisoning must have been most extensively
practised, and enjoyed remarkable immunity from detection and
punishment.
The ancients, besides being aware of many poisonous herbs,
were acquainted with certain mineral and other poisons. Thus,
arsenic was known to the Greeks, and the Egyptian priests knew
how to prepare (and use) hydrocyanic acid from the peach kernel.
The Dark Ages were in these, as in most matters, Tar less well
informed. Fiction and romance have invested the malpractices of
medieval Italy-of such expert poisoners' as the Borgias-with an
air of subtlety, suggesting that recondite poisons of extreme
violence, now no longer known, were used. There seems, however,
I
2 VETERINARY TOXICOLOGY
little doubt that arsenious oxide was their chief agent. True
subtlety and an empirical prevision of profound pathological fact
are found rather in the East and among the gipsies, in the use
by those peoples of vegetable toxins-e.g., abrin-and dangerous
moulds and fungi as poisonous agents:
The foundations of chemical toxicology were laid in the earlier
decades of the nineteenth century by the distinguished French
physiologist Orfila. He first showed that many poisons (notably
arsenic) could be separated and identified in the ingesta and
tissues of a poisoned subject, and he also did much towards
<

elucidating the manner of absorption and distribution of a poison


in the system. -
Since the time of Orfila knowledge has extended, .the active
principles of very many poisonous plants have been separated
and characterised, chemical methods of separation of poisons from
plants and from tissues have gained in accuracy, and characteristic
tests for many important poisons have reached an extraordinary
pitch of delicacy. In illustration it may be remarked that arsenic
can be detected in such minute quantities as the five-hundredth of
a milligramme-i .e., the thirty-thousandth of a grain-and
recently it has been shown that hydrocyanic acid can be recog-
nised in the same small proportion. Such examples render it
abundantly clear that with ordinary care it is impossible to fail to
detect these poisons; indeed, the difficulty is often felt in the
laboratory that some of our tests are almost too delicate to be
diagnostic of poisoning. Indeed, it very often happens that a sub-
stance is found which, on inquiry, proves to have been given as
an ordinary and legitimate medicinal dose.

DEFINITION OF A POISON.
A poison may be defined as a substance which, when introduced
into the body in relatively small amount, a.cts deleteriously, and
may cause death.
It is at once evident that a hard-and-iast deiinition, here as in
most things, is almost impossible. Restrictions-many based on
scientific grounds, but most on those of common sense-at 'once
suggest themselves. The. forcible introduction of a bullet, or a
knife-blade, or the mechanical lesions of powdered glass, cause
death. Though not scientifIcally called a poison, the latter sub-
stance would be held equivalent in the eyes of the law. The great
INTRODUCTION 3
majority of the poisons are also drugs, and, as Cushny (I94I) well
expresses it, "some bodies may, in fact, be remedies, foods, or
poisons, according to the quantity ingested and the mode of
application. "
The following important restrictions and limitations to the fore-
going definition are accordingly suggested:
I. A poison in sublethal quantities exercises a specific effect on
the organism, interfering with the normal action of some one or
more particular group of cells.
This distinction appears necessary, for it is desirable to with-
draw from the category of poisons, properly so understood,
certain (possibly all) foods. It is -distressing to hear that, on the
strength of the bad results of injudicious feeding, or over-feeding,
certain foodstuffs are given the grave designation of "poisonous."
Yet we know that bad dieting, and especially the irrational use
of a new food, may earn it an evil, but often undeserved, reputa-
tion.
2. A poison differs from a bacterial toxin in that a poison, as
here understood, never gives rise on long-continued sublethal
dosage to the formation of antibodies in the blood stream, although
a resistance or tolerance to it may be developed. This distinction
seems quite sharp in spite of the fact that bacterial toxins-e.g.,
diphtheria or tetanus toxins-may correctly be said to be
poisonous. In this connection it should be mentioned that some
highly toxic albumins found in plants (phytotoxins) and snake
venoms (zootoxins) are usually classified as' poisons, although
they resemble ba:cterial toxins in that they can pro<;luce immunity
reactions. They differ from other poisons, however, by the fact
that whilst minute doses will produce harmful effects when
injected into the canimal body, large amounts must be taken by
the mouth before symptoms of poisoning set in, since the protein
is in large part destroyed by the digestive enzymes .
. In practice, by common consent, certain inorganic and organic
compounds, and certain plants and plant products, irrespective
of any possible therapeutic action or dietetic value, are held to
be poisonous. In most, but unfortunately by no means in all,
cases of .plants, the essential cause or active principle has been
separated in a more or less pure form, capable of recognition.
4 VETERINARY TOXICOLOGY

GENERAL CHEMISTRY OF POISONS.


An attempt may be made to give an outline of the various
classes of substances falling under the above heading, and re-
sponsible for poisoning. But it must clearly be understood that
such an outline can have no pretensions to completeness.
I. Inorganic or Mineral Poisons.
(a) Certain elements-e.g., phosphorus, sulphur.
(b) Simple gases-e.g., carbon monoxide, oxides of nitrogen,
ammonia, sulphuretted hydrogen.
(c) Acids and alkalis.
(d) Metalloids, or elements, which chemically form the border-
line between non-metal and metal-e.g., arsenic and antimony
compounds.
(e) Metals and their salts-e.g., lead, mercury, copper, barium,
zinc, chromium, iron, etc. '
2. Organic Poisons.-By organic is understood any compound,
necessarily containing carbon, other than the oxides of carbon
and the carbonates, often of animal or vegetable origin, but often
synthetic-i.e., capable of being made from its elements. Apart
from artificial drugs this great division includes the active prin-
ciples of poisonous plants.
(a) Alkaloids, distinguished by being bases-i.e., forming salts
with acids. A most numerous class represented by, e.g., strychnine,
atropine, coniine, taxine, etc.
(b) Glycosides, compounds which, by the action of dilute acids
or enzymes, take up the elements of water, and are resolved,
giving, along with other compounds, always sugars--e.g., digi-
talin, helleborin, amygdalin, etc.
(c) Acrid juices or resins, amorphous, faintly acid, irritant sub-
stances, commonly contained in saps-e.g., of euphorbia and
ranuncullJs.
(d) Indefinite pr.inciples, neutral in chemical respects-e.g.,
anemonin, cicutoxin, picrotoxin.
(e) Essential oils-e.g., turpentines (savin), tana~etone (tansy),
camphor, mustard oil.
(j) Toxins-e.g., ricin, abrin, veiioms.
(g) Cyanides, hydrocyanic acid produced in plants from glyco-
sides, but also prepared in other ways, and its salts.
(h) Phenols, hydroxy derivatives -of the aromatic or benzene
hydrocarbons, sometimes found in. plants-e.g., tannin-but
INTRODUCTION 5
mainly encountered in the tar of coal and wood distillation-e.g.,
carbolic acid, cresols.
The extraordinary range and variety of chemical types covered
by this incomplete scheme serves to accentuate the extreme
difficulty of correlation of chemical nature and physiological or
toxic activity. Some of the effects of poisons are undoubtedly due
to definite chemical reactions-e.g., the formation of insoluble
calcium salts in the presence of oxalates-but in most cases the
reactions are probably extremely complicated. There is no doubt
that the action of some poisons depends, at least in part, on
physical considerations such as solubility, the formation of
adsorption compounds, changes in osmotic pressure, and alteration
of the surface tension of the cells. In some cases, however, there
does appear to be a direct relationship between activity and
chemical constitution, thus:
1. Antimony, closely allied chemically to arsenic, resembles
it in its effect on the organisms.
2. In general the condition known to chemists as un saturation
(i.e., the possession of unsatisfied or uncombined valencies by a
molecule, rendering it able to combine directly with other sub-
stances), in comparision with saturation, (i.e., when all the valen-
cies are actually in combination), is accompanied by greater.
physiological activity. In illustration, arsenic acid is saturated and
is less poisonous than 'arsenious acid, which is unsaturated, and
Ehrlich's (I9I2) researches tend to prove that a reduction from the
pentavalent arsenic to the triv,?-lent arsenious stage is a necessary
precursor to toxicity of the arsenic compounds; the unsaturated
hydrocarbon acetylene in distinction to the saturated ethane is
poisonous; hydrocyanic acid is more unsaturated and more toxic
than the sulphocyanides; the alcoholic compound betaine is far
less toxic than the unsaturated and more reactive but similarly
constituted aldehyde muscarine.
3. Among organic compounds similarity of type commonly
denotes similarity of effects, which, however, grow less as com-
plexity increases in a series of compounds. Thus the alcohols
resemble one" another, the lower being more active than the
higher, and similarly phenols show general likeness to one another.
But there are anomalies-e.g., sulphonals containing only ethyl
groups lack the hypnotic effect of those containing the analogous
methyl group.
6 VETERINARY TOXICOLOGY

CONDITIONS GOVERNING THE ACTION OF POISONS.


A very large number of factors determine the action of a poison
in a given case, of which the more important are: Absorption, dis-
tribution and acc1tmulation in the organs, and elimination. Minor
factors arc the species, age and idiosyncrasy of the subject. A
manifest condition precedent to all is the administration ~f a
sufficient quantity, the toxic or lethal dose.
Absorption.-The absorption of a poison depends:
1. On the physical nature of the poison.
2. On the channel of absorption.
1. Before absorption, which requires the formation of a solu-
tion, can occur, it is necessary that the poison be in a soluble and
absorbable form when given, or that it becomes modified so as to
fulfil these conditions after administration.
The gaseous state represents the most easily absorbable of all
forms, when the gas enters the lungs. The very rapid action 01
gases, such as hydrocyanic acid, carbon monoxide, sulphuretted
hydrogen, and volatile anresthetics-e.g., chloroform, ether, and
nitrous oxide-illustrates this point.
Solids insoluble in water, in dilute acids, or in dilute alkalis
in general are not poisonous by the alimentary tract. Thus, the
soluble salts 9f barium are very poisonous, but barium sulphate
is insoluble and non-toxic. With lead sulphate the insolubility i~
not so pronounced, and therefore it has a definite though slow
toxic action. Perhaps the best instance is that of arsenious oxide.
When the coarsely powdered vitreous substance is freed from im-
palpable particles, large quantities may be given to-dogs without
bad effect.
Solutions or solids soluble in the body fluids are easily absorbed
from the alimentary tract, provided that they are not precipi-
tated-e.g., by acid, or alkali, or albumin-and that they arE
diffusible by osmosis-i.e., can permeate animal membranes
Thus, a solution of arsenious oxide, or of an alkaloid, is a readil)
absorbable and diffusible substance, but a dilute solution of silvel
nitrate is mainly precipitated as the insoluble silver chloride b)
the hydrochloric acid of gastric juice. The absorption of an alka
lo~d is retarded by the formation of the-insoluble tannate wher
tannin is employed as a remedial agent, and most of the heav~
metal salts give precipitates ~f insoluble albuminate~ whereb~
INTRODUCTION 7
absorption is retarded. Toxins (except ricin and crotin) are not,
or only very slowly, diffusible, and therefore not absorbed by the
intact membranes. They are thus not toxic by the alimentary
tract, or, like ricin, act far less intensely in this way. Another
example of a soluble poison which is not' easily absorbed is
afforded by the alkaloid curarine. Moreover, the living cell wall
is impermeable to certain dissolved substances-thus- to the mag-
nesium radicle, or ion, in solution-so that metal is not absorbed
from the stomach or intestines.
2. The channel of absorption or administration is of great
practical. importance in determining the effects of a poison. The'
channels are-(a) By the respiratory membranes, (b) by the skin,
(c) by the alimentary tract, (d) by subcutaneous or intravenous
injection.
(a) The very extensive highly vascular pulmonary mucous mem-
brane offer& an excellent channel of absorption not only for gases,
of which it is the natural medium, but also of liquids. Large
quantities of water are speedily absorbed after injection into the
trachea, and intrathoracic injection is the most rapid method of
giving hydrocyanic acid. The vapours of amesthetics, of alcohol,
and of turpentine, rapidly display their effects on inhalation.
All soluble poisons are quickly absorbed in this way, and even
fats in small quantities._
(b) The intact skin in general is not a good channel of absorp-
tion, but the conditions under which absorption may occur are
of extreme importance on account of the frequent application to
the skin of poisonous materials, in mange dressings, dips, and the'
like. Gases are certainly slowly absorbed, but any such absorption
has little significance in veterinary toxicology.
Water, and saline solutions, such as solutions ,of potassium
iodide, potassium ferrocyanide, and strychnine sulphate, are
gradually absorbed, but prolonged contact is required, and the
method has no practical importance in toxicology.
Powders are not e~sily absorbed, and not at all unless they are
soluble in the cutaneous secretions. The skin has a naturally oily
secretion, the sebaceous glands are open to the surface, and.there-
fore substances in ointments of animal or vegetable fat are fairly
easily absorbed, as, for example, mercury, iodides and alkaloids.
But mineral oil, such as vaseline, does not promote absorption,
and a remote action, due to a drug in vaseline excipient, need not
be seriously feared.
8 VETERINARY TOXICOLOGY
In conformity with the fatty nature of the normal secretion of
the skin, it follows that media capable of dissolving fat are
penetrant-such as alcohol, benzene, turpenti;nes, phenols and
alkaline liquids. The latter point is important. An alkali saponifies
a fat and emulsifies-it, and thus alkaline solutions of phenols, and
of arsenic, such as are used in dips, may penetrate and cause
danger if the solution is too strong, or if it is left too long in con-
tact. Very little arsenic would be absorbed from a solution of
equivalent strength in an acid liquid.
Absorption from the broken skin or from a wound is naturally
far more rapid than from the intact surface, and, varying with the
nature 'of the wound, approximates to subcutaneous injection.
The difference is well illustrated by Kaufmann's (1901) figures for
the toxic doses of powdered .arsenious oxide for the sheep, which
are by the mouth 75 grains, and by application to a wound
3 grains.
(c) The alimentary tract offers a more suitable mucous surface,
external to the body, than the skin, forming a very extensive,
moist surface, covered by a delicate epithelium, and is the most
usual channel of absorption of a poison. In contradistinction to
the stomach and intestine, the membranes of the mouth and
gullet are thicker, and swallowed materials do not rest in contact
with them for very long, so that absorption by this channel is of
less importance than from the stomach and intestines.
Among carnivores the stomach offers an acid medium to the
ingested materials, thus favouring the solution of substances
. sparingly soluble in water, but yielding soluble salts with hydro-
chloric acid. Such are the majority of alkaloids, and many metallic
oxides-e.g., those of lead, barium, zinc and mercury. Absorption
takes p1ace freely -from the stomach of a carnivore. Thus, Taylor
(1934) quotes results obtained by giving strychnine wrapped in
paper to cats and dogs. In the case of a dog, death resulted after
some considerable period-longer than three hours-and ! grain
of a dose of 2 grains had been dissolved.
In the horse absorption from the stomach is not so rapid or
complete as in the carnivores. Thus, Smith (1921) draws attention
to the lack of absorption of strychnine therefrom, after ligature of
the pylorus. It cannot, however, be $afely laid down that no ab-
sorption takes place, for traces of potassium ferrocyanide, given
by injection into this viscus after ligature of the pylorus, have been
found in the urine.
INTRODUCTION 9
The first stomachs of the ruminants are not adapted to absorp-
tion, which is active from the fourth or digestive stomach. Bouley
and Colin (I87I) injected a solution of alcoholic extract of nux
vomica in water into the abomasum of a bullock after pyloric
ligature, and observed symptoms after five, and death after seven,
hours. Craig (I9II) gave a goat IO grains strychnine in water
coloured by magenta, and obtained symptoms in twenty minutes,
when, on slaughter and post-mortem, coloration extended over the
rumen, reticulum and omasum, and just entered the abomasum.
The small intestine, crecum, colon, and rectum all absorb
rapidly and quicker than the stomachs. Thus, strychnine injected
into the small intestine may produce its results in a few minutes.
The general condition of the organs has naturally an influence
on the rate of absorption. In all cases this is more. rapid when the
stomach is empty than when it is full. The magnitude of the dose,
as well as the nature of the substance, is also clearly an important
factor. It is evident that many variable conditions unite in making
it impossible to answer the highly important medico-legal ques-
tion, "How long after dosage would symptoms set in?" with any-
thing more than very approximate accuracy.
(d) SUbC1ttalteoUs or intravenous injection is a method of intro-
duction of poisons rarely, if ever, likely to give rise to poisoning.
but of immense value in studying the toxic effects of drugs, and in
medicinal treatment. The possibility of loss by vomition or other-
wise is obviated, and, moreover, the ge~eral effects of the drug are
more fully disclosed. Absorption in this way is rapid; thus, Colin
(I87I) showed that potassium ferrocyanide or iodide injected
under the skin of the face of a horse could be found after eight
minutes in the urine ..
The Mechanism of Absorption.-The underlying physical prin-
ciple governing absorption is that of osmosis.
By osmosis is understood the passage of a dissolved substance
through a membrane, such as parchment or the protoplasmic cell
wall" of the living cell, or the epithelial layers of the alimentary
tract. In general, only relatively simple, soluble, and crystalline
substances, such as salts, sugars and urea, diffuse at all easily
through such a membrane. They are called crystalloids. Sub-
stances which are of greater complexity, which are not crystalline,
and which tend to form viscous or mucilaginous solutions, or sus-
pensions in water, do not osmose, or, at any rate, o:rily do so very
slowly. Typical of this class are starch, proteins including enzymes,
10 VETERINARY TOXICOLOGY
and glue. They are called colloids. Amongst inorganic compounds,
silicic acid forms a typical colloidal solution. In the light of tbese
facts one understands why proteins and starGhes must be resolved
into simpler crystalloids-peptones and sugars-before absorp-
tion, and why toxins-e.g., ricin and snake venom-are not
absorbed, or only very slowly, by the alimentary mucosa.
But the epithelium is not only capable of separating, by the
process ot osmosis, the crystalloid from the colloid, it is also senti-
permeable-that is, will allow osmosis of certain substances and
not of others. This may be illustrated by reference to salts. In
water solution a salt (in part and to an extent dependent on the
strength of the solution and temperature) is split up or dissociated
into ions, which are held to be the carriers of electric charges, and
which do not possess the ordinary properties of the atoms or
groups of which they are composed. In illustration, sodium
chloride splits into ions N a + and CI- not possessing the ordinary
qualities of sodium and chlorine, existing independently of one
another, and bearing charges of electricity, positive on the metal,
and negative on the acid ion respectively.
Too great emphasis cannot be laid on the essential point that
the ions do not possess tile ordinary properties of their com-
ponents. It is only when the ions are discharged, as in electrolysis,
or in the course of a chemical reaction, that the ordinary pro-
perties of the element or group are displayed. To suppose, for
instance, that the existence of the sulphate ion S04 - in a solution
of magnesium sulphate in the least degree confers the properties
of ordinary sulphuric acid on the solution may prove most mis-
leading.
The existence of S04 ions in a solution, together with metal ions,
such as those otmagnesium, zinc and sodium, means that we have
to do with a salt solution. In ordinary sulphuric acid solution we
have whole molecules of H 2S0 4 and ions of S04 and hydrogen, all
in proportions determined by the concentration. Similarly with
other acids, such as nitric and hydrochloric, in solutions of which
we have ions of hydrogen, and of N0 3 and chlorine, respectively.
The existence of hydrogen ions in a solution means the possession
of acid properties. Alka js, such as caustic potash, KOH, ionise
into K ion and OH ion and similarly with other alkalis, and the
existence of alkalinity in a solution is a fact parallel with the
existence of OR or hydroxyl ions in it.
The simple physical laws'" of osmosis, in accordance with which
INTRODUCTION II

a dissolved crystalloid tends to permeate the membrane, passing


from the more to the less concentrated solution, adequately
accounts for the absorption of dissolved alkaloids and organic
poisons, which do not exercise local chemical reactions. If on the
one side we have a solution of strychnine, and on the other a
liquid free of that substance, the alkaloid will traverse the mem-
brane. If the solution into which it pa~ses is not removed, equi-
librium will be established when the solutions on both sides are of
the same strength, but if, as in the digestive system, this solution
is continually removed, the osmosis will go on to completion.
The intestinal epithelium is semi-permeable to some salts, and,
for example, will not allow of the passage of the magnesium ion.
This metal is, therefore, not ;;tbsorbed from the alimentary tract,
and consequently exercises different effects when given by the
mouth than when injected. Similarly, zinc is not at all readily
absorbed.
The case of the action of the heavy metal salts is, however,
more complex, and attempts have been made to account for their
general irritant effect in the light of the theory of ionic dissociation.
When the salts of tha heavy metals-e.g., lead, silver, mercury,
copper, zinc-come into contact with the proteins of the cells and
cell walls, for the most part they form an albuminate of the metal,
which is insoluble, or soluble only in excess of albumin.
The general reaction for an albumin of feebly acid character
would be, taking the case of a sulphate:
Metal, S04+H2 alb. == Metal-albuminate+2H+ +504;
i.e., there would be formed metal-albuminate and sulphuric acid,
more or less completely ionised according to concentration, the
whole being a reversible reaction, since the albuminate is decom-
posed by excess of acid. The irritant effect is ascribed to the acid
thus liberated.
Irritant effects cannot be held to be solely due to the degree of
ionic dissociation. Were this alone responsible, the greater the
ionisation the greater the irritation, in accordance wherewith the
alkali nitrates, chlorides, and sulphates ought to be more irritant
than the corresponding salts of copper, which is not the case,
although ionic dissociation is more complete with the former than
the latter.
A possible explanation of some value is to be found in the fact
that, with the heavy metal salts as a class, a different type of dis-
12 VETERINARY TOXICOLOGY
sociation occurs. That is hydrolytic dissociation, which means that
water decomposes the salt into oxide and acid, as may be illus-
trated by reference to zinc chloride; thus-
ZnC1 2+2H 20 === Zn(OH)2+ 2HCl.
The extent or degrees of hydrolytic dissociation is generally
small, and the, reaction is reversible-i.e., for every concentra-
tion and temperature there will be a given proportionality be-
tween the four components of the system. Hydrolytic dissociation
of the type shown is indicated by the marked acidity of the solu-
tion to litmus and other indicators.
The kinds of salt liable to suffer hydrolytic dissociation are:
(1) Salts of weak bases and strong p.cids showing acid reaction-
e.g., heavy metal chlorides, nitrates and sulphates; (2) salts of
strong bases with weak acids, showing alkaline reaction-e.g.,
carbonates of the alkali metals; (3) salts of weak bases with weak
acids-e.g:, the organic acid salts of the heavy metals, such' as
zinc and lead acetates. The reaction of such heavy metal acetates
is feebly acid.
It seems not unreasonable to associate irritant effect with
hydrolytic dissociation. A solution of zinc chloride contains a
fair proportion of free hydrochloric acid, and, similarly, the
sulphates contain free sulphuric acid. In support may be adduced
the well-known fact that the double alkali chlorides and sul-
phates-e.g., potassium zinc sulphate, potassium copper sulphate,
potassium zinc chloride-are less irritant and are also less hydro-
lysed than the normal sulphates. On the other hand, mercuric
salts are feebly hydrolysed and also feebly ionised', yet they are
irritant, or eVen corrosive, a fact which well illustrates the danger
of ascribing to anyone property an effect which is jointly due to
several factors, the chief of which, in the case of. mercury, appears
to be the facility with which itjorms compounds with proteins.
But considerations of this kind help us to understand why the
double salts-the salts of the weak organic acids and the metal
albuminates-are more or less devoid of irritant properties.
The formation of albuminates and their degree of solubility in
excess of protein, or in salt solutiop, are very important factors
as regulating the penetration of metals into the cells and tissues,
and the speed of their absQrption into the circulation.
By whatever chemical . .and physical processes the liberation of
free acid from an irritant saH takes place, the modern standpoint
INTRODUCTION 13
..
of physiology enables one to conceive of the mechanism hf its
action. Brought into a normally alkaline medium, the acid
stimulates the cells to increased alkali secretion in order to
counteract the acidity. Similar considerations hold for the intro-
duction of alkali into a normally acid medium. This requires in-
creased circulation of blood and increased cell activity, and
whilst tonic when small quantities of acid are concerned, the effect
becomes toxic with larger quantities.
Distribution and Accumulation.-It may now be regarded as
fully established that all poisons, -save those which act by the
formation of gross lesions resultant upon the destruction of the
cells (strong acids and alkalis), causing death by shock, exercise
their effects only after entrance into the general, and in particular
the arterial, circulation. In a few cases, such as those of arsenic
and hydrocyanic acid, tnese poisons may actually be detected in
the blood after administration. The fact that most poisons cannot
so be detected is merely due to the lack of sufficiently . refined
chemical methods of separation and recognition. Thus, atropine
produces its remote mydriatic effect, though it could not be
chemically detected in the blood or nervous tissue. For this reason
a characteristic physiological effect often constitutes a better test
than a chemical reaction.
Before the poison absorbed by the above-mentioned channels
can reach the capillary system and cells of the body it must
traverse the liver and lungs, which thus play a protective role.
Sulphuretted hydrogen may be introduced by the rectum, in
doses considerably greater than those which prove fatal on res-
piration. After such administration the blood, arriving at the
pulmonary 'mucosa, and carrying the dissolved gas, abandons it
to the exhaled air, in which it may be detected by the smell, and
by blackening a paper soaked in lead acetate solution.
The liver arrests most metals, phosphorus, and many alkaloids,
so that on arriving thereat in the portal system, after absorption
from the alimentary tract, the whole or a great part, depending
on the quantity, may be held back from the blood stream. The
activity of the liver in this r.espect appears to be proportional to
its glycogen content, for when this is reduced the liver no longer
arrests the drug, and a very much smaller dose than the normal
may be toxic. Some substances-e.g., salts of sodium and potas-
sium, alcohol and digitalis-are not arrested by the liver. Metals
are stored in an, unknown condition, possibly as albuminates, in
VETERINARY TOXICOLOGY
the liver, and many unstable poisons are modified-e.g., ammonia
is converted into urea, and some alkaloids oxidised, so that the
liver does not exercise a merely passive function in its protective
capacity. The condition as to health or disease of this organ is
thus of importance, since when the glycogenic function is low,
little arrest of a poison will occur. It is chiefly in the liver that
accuntttlation takes place. Besides metals a few organic poisons,
notably digitalin, helleborein and strychnine, are cumulative,
although not necessarily stored in the liver. To designate a poison
as cumulative does not endow it with exceptional properties.
The only difference between such and ordinary drugs is that
elimination is slower in the former than in the latter, though both
may be stored. The difference is of degree, not kind, although
important from the practical standpoint. The sudden display of
symptoms, after more or less prolonged dosage, means, then, that
elimination has not kept pace with absorption, or that absorption
has through some cause become more active, or elimination less so.
Elimination.-Poisons may be divided roughly into those which
are slowly (cumulative) and those which are rapidly eliminated.
In the first category we have, as the most important examples,
the metals, which are arrested chiefly by the liver. From that
organ they pass off in part .by the blood but mostly by the bile.
From the bile a portion may pass into the fceces, and a portion
be reabsorbed and carried back to the liver, thus establishing a
gastro-hepatic circulation.
Most of the poisons, however, do not accumulate, and elimina-
tion starts immediately after absorption. This is especially true
for volatile poisons like hydrocyanic acid, alcohol, and the like,
which are eliminated in great proportion by the lungs.
All the excretory channels are concerned in elimination, .but the
most important in this respect are the kidneys. The milk is a less
important channel of elimination. The skin also plays a part, and
the beneficial effects of drugs-are in many cases attributable to
their local excretion-e.g., of balsams through the lungs and of
arsenic through the skin.
The time taken in elimination varies very greatly, is most rapid
with volatile agents, and generally is quicker after injection than
after ingestion. ./
An instructive and important example regarding arsenic is given
by Tay~or (I934). The maximum of arsenic in the liver was attai!led
in fifteen hours after ine:estion-viz .. 2 e:rains to q};. Dounds: after
'DUCTION IS
fourteen days the proportion was 017; and after seventeen days
nil. Valuable as such data are, they must on no account be
taken to be general and .precise. They only serve to illustrate
the relative speed of elimination, which, in a given case, will be
modifIed by such factors as dosage, condition of the subject,
and other circumstances.

VARIATIONS OF ACTION DUE TO SPECIES.


Wide differences in reaction towards a given poison are noticed
in comparing the various species with one another. In part these
variations are explicable on anatomical and physiological grounds,
though by no means always. The differences in the digestive
apparatus and in the nervous system serve to account for some
variations. In ruminants ingested poison is immensely diluted in
the rumen, is distributed evenly on rumination, and in general
is absorbed more slowly than in the horse or carnivore. This
affords greater opportnnity for elimination, and accounts partially
for the usually high degree of resistance of the ox and goat.
The relative stage of development of the nervous system greatly
affects the dosage and action of many drugs. In illustration, the
dog is more susceptible to morphine than the rabbit and less so
tban man. Morphine acts as an hypnotic on man and the dog, but
as an excitant and convulsive on the cat, goat, pig, ox and horse.
But some variations cannot easily be explained on such con-
siderations. Thus, the ox is considerably more sensitive to mercury
and lead than the horse; the rabbit is insensitive to atropine; birds
withstand large doses of strychnine.

VARIATIONS OF ACTION DUE TO THE INDIVIDUAL.


Age.-As a rule, young animals are more sensitive than adults,
but the young cat is less susceptible to morphine than the old,
and young animals are less affected by strychnine than older ones.
On the other hand, according to Frohner (1927), whilst a dog of
ten years can resist r7 grammes of santonine per kilogramme,
02 gramme per kilogramme will kill a dog of a few weeks old.
Idiosyncrasy.-Subjects apparently similar in all respects often
display great diversity in relation to a drug. Thus, strychnine
sometimes is dangerous in ordinary medicinal doses on dogs, on
account of which, as also by reason of the accumulation due to
tardy elimination, dosage of tills drug ought .to be kept down.
r6 VETERINARY TOXICOLOG},~

In poisoning, where a large overdose is almost always t5lVl::ll,


there is not so much room for the display of idiosyncrasy as in
therapeutic treatment.
Other factors of tolerance and habituation do not playa sig-
nificant part in toxicology on the same grounds of the large dose
commonly. given. Habituation is displayed towards nervous
poisons in man-e.g., opium, nicotine, alcohol, and probably also
towards arsenic, of which the mountaineers of Styria eat rela-
tively large quantities. The question as regards animals assumes
interest in view of the fact that cases of poisoning by the local
, poisonous plants do not often occur amongst animals bred in a
particular locality. But it is almost certain that it is due to their
a voidance of the dangerous herb. When fresh stock is put on the
land, the animals eat indiscriminately, and poisoning occurs.

CLASSIFICATION.
The rational basis of classification is that of physiological action,
but unfortunately no satisfactory scheme is available. In many
cases the action is complex; thus there may be local effects and
general effects, as with ammonia and aconitine. There may be
much overlapping as regards the centres acted upon, making it
difficult to assign a particular poison to a particular class. The
course of poisoning by a plant is always complex. In the majority
of cases poisonous plants owe their activity to alkaloids, which act
after absorption. At the same time, on account of other com-
ponents (acrid juices, oils, and the like), they exercise irritant
effects. The effects of a large poisonous dose are not necessarily
similar to those exercised by moderate therapeutic administra-
tions.
A useful, if broad, distinction may be made between-{I) corro-
sives, (2) irritants, (3) non-irritant nervous poisons.
Corrosives owe their action to their concentration, and are
represented by the strong miner~al acids and alkalis, phenols,
and very concentrated solutions of many salts. A poison acting as
a corrosive in a concentrated form may have an entirely different
action in a diluted condition. Actual destruction by water abstrac-
tion, by decomposition, and solution of fats and proteins in the
living cell mark the effect of a corrosive.
Irritants so modify the cell as to disturb its normal course of
metabolism, ultimately causing inflammation. The irritant effect
INTRODUCTION I7
is general, not being limited to special cells of the organism, and
poisons having a wide range of activity are the protoplasmic
poisons, such as mercuric chloride, phenol and hydrocyanic acid.
Among irritants are included typically the salts of the heavy
metals, but it will be remembered that to an irritant effect may
often be added nervous effects, leading to the designation of
narcoto-irritant applied in practice to so' many vegetable poisons.
And similarly wi th the metals there must be distinguished the local
irritant effects and the general effects produced after absorption.
N01t-irritant nervous poisons may be distinguished according to
the centre acted upon. Local effects are not significant, and only
after absorption do symptoms set in.
A fairly complete survey of poisons according to their physio-
logical effect is:
Acting on blood corpuscles: cyanides, carbon monoxide, etc.
blood plasms : silver, etc.
" blood vessels: ergot, nitrites, etc.
" heart: digitalis, etc.
" brain: chloroform, opium, chloral, etc.
" spinal cord: strychnine, etc.
" peripheral nerves: curare, aconitine, etc.
" muscle: ver.atrine, etc. .
" liver: phosphorus, etc.
kidney: cantharides, etc.
The chemical classification depends oh the most convenient
routine followed in an analysis.
For analytical purposes we class poisons as follows:
(a) Volatile poisons-i.~., those which may be distilled either
from an alkaline or acid solution, comprising phos-
phorus, hydrocyanic acid, carbolic acid and its allies,
essential oils, alcohol, chloroform, ammonia, coniine,
and nicotine.
(b) Metals and metalloids: Lead, mercury, arsenic, antimony,
copper, zinc, chromium.
(c) Fixed, or non-volatile, bases and acids: Caustic alkalis,
mineral acids, oxalic acid.
(d) Fixed, or non-volatile, organic poisons: The alkaloids and
glycosides.
Further details regarding this subject will be given in a later
section.
2
18 VETERINARY TOXICOLOGY

COMMON CAUSES OF POISONING.


It will be advantageous to refer at this point.to some of the more
usual causes of poisoning, although further details will be given.
for each particular poison later.
Poison is nearly always conveyed in food or water. Poisoning
by subcutaneous injection, though more certain and less easily
proved by analysis, is very rare as a malicious practice, and when
it happens is usually the result of an accident in treatmenL
Malicious poisoning is generally done by means of poisoned
food, and affects chiefly dogs, foxhounds and foxes. The agent
is almost always an accessible poison, such as a rat paste or
powder, and in the majority of cases strychnine. It should be re-
membered as regards foxes, for which a common bait is a poisoned
rabbit, that it is no offence to kill a fox, but that the exposure of
poison above ground constitutes an offence.
The malicious poisoning of the larger animals is fortunately rare.
Of accidental poisoning the ox is the most frequent victim; this
no doubt on account of its feeding habits. This animal is an indis-
criminate feeder in comparison with the horse and sheep. All our
experience tends to the conviction that the greater number of
cases of poisoning of cattle are the result either of gross careless-
ness or culpable ignorance.
Sheep dips either in powder or solution, and weed-killers, are
too often left exposed where animals can get t_hem; troughs of
solution, or water-carts, are left for weeks overlooked or forgotten.
Very ~ften a l~ng and painstaking search after the event discloses
such a cause open to all observers. The same remarks apply to
paint, which is eagerly eaten by cattle, and generally contains
lead, though green copper arsenite is often used. Paint tins 'are
left in fields. Paint splashes are not removed. Refuse is frequently
thrown over the fence. A case of lead poisoning occurred recently
due to old tarpaulin, crusted with oil paint, stripped from a roof
and thrown into a field.
Bullet splashes have caused lead poisoning, and the impregna-
tion of herbage with lead and other metals on account of smelting
and similar operations lead$ to chronic poisoning.
Water is less often the ...vehicle. In spite of the considerable
solubility of lead and zinc in rain water, it is not likely that a very
large quantity of p_oison would be taken in this way, so that acute
INTRODUCTION 19
poisoning from this cause is rare. On the other hand, chronic
poisoning may happen.
Another prolific source of troublc is the inveterate habit of
dosing the animals common to so many attendants and even
owners, who might be presumed to pos~ess more jUdgment. Whole-
sale administration of condition powders and salts always does
more harm than good, and often destroys life.
Vegetable poisons are more likely to be eaten by animals in the
spring and early summer, when the tcnder green food is especially
tempting after the winter fodder, or in a dry season, when herbage
is scarce (cJ. the acorn poisoning of 19II). Fortunately many
poisonous plants contain less poison in the young than in the
mature state, but this rule is not general. For instance, certain
cyanide-producing plants are more poisonous in" the earlier than
the later stages of growth.
Poisonous plants in general display great variation of the
proportion of poison. Two conditions of significance both
tend to modify the poison content. They are latitude and culti-
vation. .
In higher latitudes plants of the same species are often less
poisonous than in lower and warmer situations; for example, the
aconite and cherry laurel. The rule is not absolute; thus rhodo-
dendron, veratrum and the hellebores are flourishing and dan-
gerous in Alpine districts. A scrutiny of the distribution of
poisonous plants in Great Britain, however, soon satisfies one that
they are less numerous in Scotland than in England, and in the
latter country more often found in the south than in the north.
Poisonous plants are particularly common in rocky and arid
districts, especially near the sea. One is struck by the profusion
of Solanum d'ulcamara and nigrum, of hyoscyamus, and of the
horned or sea poppy in the more sandy coast localities of the
South of England.
As regards warmer latitudes, poisonous plants are both more
numerous and usually more virulent. .
As to cultivation, this is well known to lead to a diminution in
the generation of poison by a plant. Since the presence of poison
is no doubt a measure of natural protection, one understands how
this occurs; for Nature never wastes energy, and when the pre-
servation of a species is assured, there is no need to elaborate
poison. An excellent instance is the Phaseohts, or French bean,
which is harmless, whilst the uncultivated variety, PhaseoZ,u.s
20 VETERINARY TOXICOLOGY
l1matus, contains a cyanogenetic glucoside. Aconite is l:mother
species whose poisonous properti~s diminish on cultivation.
The hemlocks are often eaten .by cattle, and both cattle and
horses frequently crop overhanging growths of yew, rhododendron,
aconitum, and other plants. The throwing of garden clippings over
the fence is a common cause of disaster. Those responsible ought
to remember that common garden shrubs and flowering plants
comprise many poisonous species, and it would be a safe rule to
regard all as dangerous.

KINDS OF POISONING.
The course of poisoning follows three types-acute, subacute,
and chronic-dependent on the dosage.
Awte poisoning manifests the intense symptoms, and rapid
denouement and termination consequent on the taking of a large
dose. Thus, with irritant poisons, there may be burning sensa-
tions, nausea, vomiting (when possible), abdominal pain, diarrhcea,
vertigo, and evidences of collapse; with nerve poisons, unrest,
excitement, delirium, tremors, convulsions, difficult respiration,
cyanosis, paralysis, coma, ang the like.
Subacute poisoning results from smaller doses, and displays the
same train of symptoms, less rapidly developed, less violent,
and more protracted, extending over days or even weeks with
eventual recovery or death.
Chronic poisoning resulting from the accumulated effect of
repeated small goses, each inadequate to the production of serious
symptoms, is not common among animals. Great differences may
appear with one and the same poison as between the acute and
chronic forms, as, for instance, in phosphorus poisoning in man.
Chronic lead poisoning in animals is marked by persistent colic
and constipation, and sometimes the formation of a blue "lead
line" on the gum.s; nervous symptoms are paralysis, convulsions,
coma, and muscular wasting, and general debility and emaciation.

DIAGNOSIS OF POISONING.
Any ca~e of sudden illne~i or death, especially following on a
meal, or after dipping; is commonly held to be one of poisoning.
This idea is not ly any means invariably right. It can only be
verified by a full .post-mortem inquiry, observation of the
INTRODUCTION 2I

symptoms and history of the case, and chemical analysis of the


organs. But when one or two animals are suddenly seized with
violent symptoms, the presumption of poisoning has sufficient
justice to make a post-mortem. and analysis desirable. This is,
perhaps, even more true when each of several animals known (as
so commonly occurs) to move about and feed together are equally
affected.
It is manifestly quite impossible to state general symptoms by
means of which a case may be diagnosed as one of poisoning.
Nevertheless, certain observations on the chief symptoms .pro-
duced by common poisons may be of value.
(a) Alimentary symptoms comprise-Salivation, foaming, colic,
retching, vomition, purgation (which may be bloody), bloody
extravasation of the mouth, tongue, jaws, and fauces.
(b) Circulatory symptoms comprise-Accelerated or retarded
throbbing or feeble heart-beat; hard, imperceptible or weak,
irregular pulse; cold or hot dry skin; sweating.
(c) Respirat01y symptoms comprise-Accelerated, retarded,
intermittent breathing, with groaning, rattling, or gasping.
(d) ~.Motor symptoms comprise-Trembling, quivering, cramp,
stiffness or twisting of the neck, locking of jaws, epileptiform or
convulsive seizures, paralysis of the hind or all the limbs, loss of
feel1ng or great irritability of the skin.
(e) Ce'rebral symptoms comprise-Fear; shrinking on disturb-
ance; frenzy and delirium, or dejection; hanging of the head;
drowsiness; loss of sensibility and coma.
(f) Other symptoms are contraction or dilatation of the pupil,
the eye being protruded or retracted in orbit; a fixed, anxious
look; staring coat; suspension of lactation; repression or incon-
tinence of urine, which may contain blood, albumin, bile or
excreted substances, such as phenol derivatives in carbolic
poisoning. The breath also may contain recognisable traces of
volatile substances, especially hydrocyanic acid, and the mucous
membrane of the mouth may show characteristic staining or
erosion.
TREATMENT,
In any case of suspected poisoning it is essential to institute
treatment at the earliest possible moment. Since, however, the
particular poison involved is probably unknown, specific treat-
ment may have to be delayed until further information is available,
22 VETERINARY TOXICOLOGY
and treatment of the symptoms as they arise is all that can usually
be attempted to begin with. The aim should be to assist. the
maintenance of respiration and the cardiovascular system, to
relieve pain, and to control convulsions or coma should they
develop. A careful note should be: made of the symptoms not
only because they may be a valuable guide as to the nature of the
poison, but also because an exact record of them may be required
in case of future litigation.
Symptomatically poisons may be classified into three mam
groups:
I. Irritants which by acting locally on the alimentary canal
cause vomition, diarrhrea, collapse and coma. They include the
corrosive poisons which, in addition, cause intense destruction of
the tissues. This may produce a condition of shock similar to that
seen after extensive burns to the surface of the body.
2. Nerve poisons which by acting on the neuromuscular
structures may cause cardiovascular disturbance, paralysis of
respiration, convulsions, etc.
3. Poisons which destroy the red blood corpuscles or hremo-
globin, giving rise to cyanosis.
In almost all cases of 'poisoning death is due to failure of
respiration, and' is therefore preceded by cyanosis.
The general principles to be adopted when dealing with a case
of poisoning are: , , '
I. Prevent more poison being taken. The affected animal and
others liable to the same source of poison ought to be put in a safe
place and the food changed. Only food arid water (ad lib.) of
proved purity should be offered. Samples of suspected food or
water should be taken for future analysis. As -far as possible keep
the patient quiet and undisturbed.
2. Prevent absorption and render inert any poison present. The
measures to be adopted will of course depend on the mode of
application of the poison.
(a) Any skin application such as an ointment or dip must be
washed off, using plenty of water, as it helps to dilute the poison.
If the poison is an acid, soap, sodium bicarbonate, lime water or
borax should be added to the water. If an alkali, vinegar or
lemon juice should be used, soap being contra-indicated. If the
poison is insoluble in water-e.g., phenol-alcohol may be used.
(b) If the poison has been taken by the mouth, the stomach
should be well washed out by means of the stomach-tube, again
INTRODUCTION 23
using plenty of water, but taking care not to over-distend the
stomach. To avoid this, the stomach should be washed repeatedly
with small quantities of water:, and it is advisable to keep the
first washings, as they may be of value for analysis. The washing
should continue until the water returns clear and free from
stomach contents. The use of a stomach-tube is contra-indicated
in cases of corrosive poisoning, as there is a danger of perforating
the stomach, and also in cases of strychnine poisoning, as the
operative procedures may cause convulsions.
Gastric lavage is preferable to the use of emetics, as the stomach
may be emptied more completely and fine particles of undissolved
poison more thoroughly removed; in addition, it may be possible
to add the correct antidote to the water-e.g., I : 2,000 potassium
permanganate if the poison is phosphorus or an organic substance,
but in this connection care must be taken to see that all the
potassium permanganate crystals are dissolved before adminis-
tration. Moreover, with depressant poisons the vomiting centre
may be paralysed, so that emetics will have little effect, and
certainly in cases of poisoning due to irritants they should be
avoided, as most of them are themselves irritants. Emetics, how-
ever, are often convenient to use, and may be more readily
available than the stomach-tube. Useful emetics are: a strong
salt solution (not advised for the pig); mustard and water (a
dessertspoon in 4 to 6 ounces); zinc sulphate (dog, grs. v. to x.;
pig, grs. x. to xv.); pulv. ipecac. (dog, grs. x. to xxx.; pig, grs.
xv. to 3i.); apomorphine hydrochloride hypodermically (dog,
grs'Tlr to}; cat, gr.lTf to io)' Tartar emetic and copper sulphate
should be avoided.
To hinder the further absorption of the poison, precipitants
should be administered. The most useful are tannic acid (horse,
3ii.; ox, 3iv.), the action of which is increased by the addition
of sodium bicarbonate, which precipitates metals, alkaloids, and
other organic poisons; raw eggs, which precipitate metals, es-
pecially mercury; copper sulphate, which forms an insoluble
coating of metallic copper on phosphorus; lime water, chalk or
whiting, which precipitates oxalates; and sulphf,Ltes, which pre-
cipitate barium. In addition to attempting to precipitate the
poison, absorption may be hindered by the administration of
adsorbents such as animal charcoal (bone-black) and demulsants
such as 'raw eggs, boiled starch flour, oatmeal, petroleum emul-
sion, carron oil, olive oil or castor oil. Demulsants hinder absorp-
24 VETERINARY TOXICOLOGY
tion less effectively than animal charcoal, but are of value as they
help to overcome local irritation.
3. Neutralise the effects of the poison taken. Against irritants
and corrosives use demulsants and relieve abdominal pain by the
administration of tincture of opium, morphia hypodermically
or chloral hydrate. It must be remembered, however, that many
vegetable irritants exert narcotic effects after absorption, so that
care must be taken when using sedatives that a fatal depression
is not produced ..
Against narcotics, paralysants and depressants such as opium,
hemlock, etc., stimulants are indicated such as draughts of strong
tea, inhalations of ammonia, ether subcutaneously or per rectum.
It is essential to maintain the respiration, as not only is it usually
the first function to fail, but if it does so any possible oxidation of
the absorbed poison is prevented, and also the convulsions and
later paralysis due to asphyxia endanger the life of the patient
still further. Reflex stimulation of the respiratory centres may be
attempted by means of the inhalation of ammonia or direct
stimulation by the inhalation of carbon dioxide or the injection
of lobeline. In small animals artificial respiration should be
applied, but this must not be too vigorous, as there is the danger
of removing so much carbon dioxiqe from the blood that the
respiratory centres are no longer stimulated. If the animal has
become drowsy or comatose, it must be kept moving and awake
by douches of cold water or even by use of the whip. The applica-
tion of a liniment of ammonia and turpentine in oil may also be
useful for this purpose in horses and cattle.
Against. convulsants such as strychnine use sedatives such as
opium, morpbIne, chloral hydrate per rectum or anresthetics
(chloroform for the horse;. nembutal intravenously for small
animals). - -
4. Promote excretion. Unabsorbed material may be expelled
by oily purgatives such as linseed oil or castor oil. Enemata
promote peristalsis and excretion. The elimination of certain
poisons is hastened by particular drugs; thus potassium iodide
is held to facilitate the elimination of lead and mercury.
The best advice to owners is to do-as little as possible, keep the
patient quiet, summon professional assistance at once, and inform
the vetex:inarian of all the circumstances and the measures already
taken.
INTRODUCTION 25

POST-MORTEM.
The post-mortem of a suspected poison case should be made
with extreme care, particularly in view of possible legaJ action.
Full notes of all circumstances relating to the surroundings of
the subject, feeding, accessibility to sources of poisoning, or of
persons likely to have malicious intent, and of the symptoms,
should be made, verified, and preserved. Careful search may reveal
recognisable or suspicious traces of poison, or of a poisonous plant.
Any such material should be preserved and verified by ex parte
evidence, which, while satisfactory in all cases, is almost essential
in litigious cases.
The lesions are rarely-perhaps never-very characteristic, and
the most common observation is of more or: less acute gastro-
enteritis. Such pathological changes as yellow atrophy of the liver
in phosphorus and arsenic poisoning may be absent in very acute
cases. In general pure alkaloid or other vegetable poisons do not
produce irritation, but most mineral poisons and plants do so.
Search of the alimentary contents often discloses the cause.
Hydrocyanic acid imparts its faint smell to all parts of a poisoned
subject; similarly carbolic acid, chloroform, alcohol, and essential
oils may be found. Phosphorus betrays its presence by its garlic
odour and luminescence, but only when free, and it is hardly ever
thus encountered in the dog.
Certain poisons impart colour; thus, copper salts give a greenish-
blue, chromic compounds a yellow to orange or green, nitric acid
and picric acid a yellow colour. The blue (indigo, ultramarine or
Prussian blue) or black (soot) pigments of vermin powders arc
rarely detectable, because of the small quantity of the poison
ingested.
CHEMICAL ANALYSIS.
Some details as to chemical toxicology are reserved for a later
treatment in this volume. At this place, however, a few points
of value to the clinician and chemist may be indicated. The
analyst is at the mercy of the pathologist, who has it in his hands
to render an analysis decisive, for or against, or to nullify the
value of a laborious search. .
The following suggestions are therefore made:
I. General details of the symptoms should be given, and par-
ticular note of the drugs administered in treatment. In a stomach
the analysfmay find a trace of an active drug, such as strychnine.
26 VETERINARY TOXICOLOGY
Without knowledge of the treatment, he is confronted with the
problem, Is this a residu~ of an original poisonous dose, or is it an
unabsorbed fraction of a legitimate medicinal dose? With nothing
before him save a jar of contents, and a card desiring an analysis,
it is impossible to answer this question.
This particular case is not uncommon. In other instances, both
lead and morphine have similarly been found, their presence
being the result of legitimate medicinal dosage.
2. In the majority of cases the best material for research is
contents of the stomach or intestines, not from the scientific, but
from the practical point of view. In poisoning there is almost
invariably a large overdose, and the unabsorbed excess can be
separat~d and detected with facility from contents. In spite of the
consensus of textbook opinion, our repeated experience, both in
practice and experimental work, is that alkaloids cannot be
satisfactorily separated from liver, kidney or even urine. The case
is different with metals and such poisons as cyanide~, where very
delicate tests are available along with simple and quantitative
methods of separation. It is, therefore, desirable to reserve con-
tents, carefully selected, sealed, and labelled, or with a small
animal the entire organs. A piece of stomach wall, carefully washed
with water, is not a promising material.
3. Besides contents, portions of liver, kidney, blood and urine
ought to be taken and separately sealed. To take a case in point.
Arsenic is found in contents. The liver and kidney are then tested
with positive results, thus giving satisfactory evidence of the giving
of arsenic and its absorption. Or, if strychnine or an alkaloid is
found in a stomach, and the other organs or urine can be shown
to give evidence, in itself not conclusive so far as a clear chemical
reaction is concerned, a satisfactory' proof 1S afforded.
4. It is undesirable to add any preservative, such as carbolic
acid, alcohol, glycerine, formalin, or the like. Practically all the
ordinary poisons are stable, many quite permanent, for a sufficient
length of time, and advanced decomposition does not affect the
processes of extraction.
5. The proper sealing, labelling, witnessing, and transit of
parts is expedient, as otherwise in contentious cases a large and
expensive host of witnesses through whose hands the package has
passed may be required in court.
6. If autopsy is not deemed necessary, the despatch of the
uncut body or unopened stomach is most satisfactory.
INTRODUCTION 27
It cannot be too strongly emphasised that the results of analysis
are in the majority of cases of value only as confirmatory evidence.
They confirm the suspicions aroused by the train of symptoms and
lesions observed by the clinician and pathologist. The mere dis-
covery of the presence of a poisonous substance in organs does not
necessarily mean that damage has been caused. Most analysts are
unfortunately prone to use the term "trace," and the veterinarian
or lawyer may be misled. It should be taken that in general a
trace (commonly the least quantity a particular chemist is able
to d~tect) is negligible from the medico-legal aspect. Not always;
for much depends-e.g., in such cases as hydrocyanic acid or
alkaloids-on the substance and on the ~part of the organism in
which the trace. is detected. Thus the detection of a trace of
hydrocyanic acid in the brain would have far more significance
than it? detection in the stomach.
The veterinarian will be interested to know that a chemist's
"trace" may be anything from the three-hundred thousandth
to the one-hundredth part of a grain, a remark which serves
further to confirm the dictum that chemical analysis is cor-.
roborative and not diagnostic.
REFERENCES.
Colin, G. (1871), Traite de physiologie Comparee des Animaux, 3rd ed.
Craig, J: F. (1911), Vet. Rec., 24, 10 3.
Cushny, A. R. (1941), Pharmacology and Therapeutics, 12th ed.
Ehrlich, P. (1912), Abhandlungen tiber Salvarsan.
Fr6hner, E. (1927), Lehrbuch der Toxikologie, 5th ed.
Kaufmann, M. (1901), Therapeutique et Matiere Medicale Veterinaire,
3rd ed.
Smith, F. (1921), Veterinary Physiology, 5th ed.
Taylor, A. S. (1934), Principles and Practice of Medical Jurisprudence,
9th ed.
MINERAL OR INORGANIC POISONS

ARSENIC.
Forms and Occurrence.-Arsenic is extremely widely diffused
in nature, the chief sources being the yellow sulphides, orpiment
(As ZS 3) and realgar (AszS z). It also occurs in most patural
metallic sulphides such as iron pyrites (FeSz) and zinc-bien de
(ZnS) , where a part of the sulphur is replaced by arsenic-e.g.,
arsenical pyrites (FeAsS). When such ores are roasted or smelted,
the contained arsenic becomes oxidised to arsenic trioxide (As Z0 3),
which collects as a dust in the flues and so may be carried into the
air and on to the soil, herbage and water in the neighbourhood of
the workings. It may also be found in chemicals prepared from
arsenical ores, and so find its way into a variety of substances,
particularly sulphuric acid manufactured from arsenical pyrites;
thus, the extensive outbreak of arsenical poisoning in Manchester
in 1900 was traced to beer, in the manufacture of which glucose
prepared with contaminated sulphuric acid had been used. In
addition, arsenic enters into the composition of many everyday
substances such as pigments, sheep-dips, weed-killers, rat
poisons, fiy-papers, sprays for fruit trees, insect poisons, etc.
Trivalent arsenic (arsenites) has been shown to be much more
toxic for lower forms of life such as protozoa and bacteria than
pentavalent arsenic (arsenates), and it is generally held that when
pentavalent arsenic is taken by higher animals its toxicity depends
upon the reduction of the arsenic to the trivalent form in the
tissues. The most poisonous compound of arsenic is arsine or
arseniuretted hydrogen (AsH3)' which is produced in the form of
a gas when zinc arsenide is treated with dilute hydrochloric acid.
Poisoning from this cause is unlikely, except perhaps in labora-
tories, where fatal accidents have occurred from inhalafion of the
gas. By far the commonest compound of .arsenic in general use
is the trioxide, arsenious acid anhydride (As Z0 3), which is obtained
by subliming the dust which collects in the flues during the roast-.
ing of arsenical ores. It occurs as an amorphous or crystalline,
tasteless, white powder, sparingly soluble in water, volatile on
heating, and forming characteristic, glistening, octahedral crystals
on sublimation. It is usually referred to as white arsenic or simply
arsenic and is widely used in commerce. Accidents have occurred
28
MINERAL OR INORGANIC POISONS 29
from its likeness to flour when powdered, and it is often mixed
with barium carbonate, flour and blue to form a rat poi!>on.
Arsenious. acid (HaAsOa), which has a faint sweetish taste,
readily loses water with the formation of the anhydride and: to-
gether with its salts, is extremely poisonous. The metallic arsenites
commonly met with are copper arsenite (CuHAsO a) and a double
copper acetate and arsenite compound Cu(C 2H a0 2) 2, Cua(AsO a) 2'
These are known under such names as Scheel's gr.een, emerald
green, mineral green, Brunswick green, Vienna green, Schwein-
furt's green, or Paris green, and were formerly extensively used
as cheap pigments for colouring wallpapers, artificial flowers, etc.;
but since they contain up to 60 per cent. arsenic trioxide and may
give rise to arsenical dust, which has been responsible for causing
cases of poisoning in the human subject, their use has been more
or less discontinued. On the other hand, sodium, potassium, and
thioarsenites are extensively used as weed-killers, dressings for
grain, insect poisons, and sheep-dips, and form perhaps the main
source of arsenic availabl~ to animals. Weed-killers are usually
solutions of sodium arsenite (NaaAsOa) and may contain from I4
to 40 per cent. of arsenif as As 20 a. Arsenical sheep-dips are
usually combined with sulphur and contain about 20 per cent.
of soluble arsenic and 3 per cent. of insoluble arsenious sulphide.
After solution for use, the strength of soluble arsenic lies between
0'25 to 0'5 per cent. The arsenites are the most toxic of the
ordinary arsenical preparations.
The sulphides of arsenic, orpiment, and realgar are insoluble
when pure and so are non-toxic, but since they nearly always
contain arsenious acid they must be considered dangerous.
Arsenic acid (H 2As 20 6 ), its oxide (As 20 5 ) and salts are less com-
monly met with and are less toxic, their action probably depend-
ing on their reduction frqm the pentavalent to the trivalent ,form.
Sodium arsenate (NaAs0 4 ) is sometimes used as the poison on fly-
papers, and lead arsenate [Pb a(As0 4 hJ is extensively used as spray
for fruit trees.
The common medicinal forms of arsenic are liquor acidi arsenosi,
which contains r per cent. arsenious acid acidulated with hydro-
chloric acid; liquor arsenicalis or Fowler's solution, which con-
tains I per cent. arsenious trioxide either in neutral solution or
made alkaline with potassium bicarbonate; and liquor arseni et
hydrargyri or Donovan's solution, which contains I per cent. of
arsenic iodide and I per cent. red mercuric iodide. To these
30 VETERINARY TOXICOLOGY
must now be added the numerous organic derivatives of arsenic
which have been introduced because of their trypanocidal action.
The earlier substances employed, such as sodium cacodylate
[(CRa)2AsO.ONa]; atoxyl:
C-AsOONa.OH
HC.f'''''-CH

'l
[-IC''\-/cH
C-NH.
and tryparsamide: C-AsO.ONa.OH
HC("'CH

HC\')CH
C-NH.CH . CONH.
although still found to be of value, have be~n largely replaced by
compounds in which the arsenic is trivalent, such as salvarsan
(arsphenamine) :
A~-C

HCII)CH
H~VC.NH2
C-OH
and neosalvarsan (neoarsphenamine):
As-C
HC/'\-CH
II .I /H
HCVCN"'CH20.S0Na
C-OH
The organic compounds of arsenic are much less toxic to animals
than the inorganic compounds, but they may give rise to symptoms
of arsenical poisoning if used injudiciously, since their effect is
probably due to the fact that trivalent arsenic is slowly liberated
in the tissues. Moreover, many are unstable and undergo decom-
position with increase of toxicity when kept for any h:ngth of
time, especially if exposed to. air. .
In view of the importance and frequency of arsenical poisoning,
the chief channels of administration may here be summarised:
(a) Administration oLthe drug lor malicious purposes; in mistake
for other drugs; or in incorrect medicinal dose. (b) As the result of
dipping or .the accidental partaking of dips, weed-killers, rat
poisons and the like. (c) By local application, as in the treatment
MINERAL OR INORGANIC POISONS 3I
of warts. (d) Administration by hors-c attendants to improve the
animal's condition and coat. (e) By contamination of water and
herbage in the neighbourhood of metal-smelting works or through
mine refuse.
Toxicity of Arsenic.-The garlic-smelling vapour of free or
metallic arsenic is toxic owing to its partial oxidation to the tri-
oxide; it is also dangerous if rubbed into the skin in a finely divided
state. However, since the toxicity of arsenic and its compounds
mainly depends on solubility, chemically pure arsenic in coarse
division is harmless when given internally. Similarly, coarsely
powdered white arsenic, which is sparingly soluble in water, can
be given in large doses without ill-effect. Thus Pocher (I9II), in
a comprehensive study of the toxicity of arsenical compounds
then in general use, found that I8 g. of white arsenic failed to kill
a dog, as did I g. per day for four months. On the other hand,
0'06 g. per kg. body weight of potassium arsenite killed a dog in
seven hours, and 0'I5 g. per kg. body weight of sodium arsenite
killed a dog in twenty-four hours when given by the mouth.
Theiler (I9IZ), in experiments to determine the safe dose of the
trioxide for sheep, found that the minimal lethal dose varied con-
siderably; thus from 0'5 to IO g. were given to individual sheep
without causing death, yet out of fifteen sheep which were given
3 g., followed immediately by watering, two died seven and eleven
days later, the post-mortem appearance being suggestive of sub-
acute arsenic poisoning. There ~s little doubt that the discrepancies
in the results can be accounted for by the fact that solid particles
of arsenic become lodged in the alimentary canal and the amount
of arsenic absorbed depends on their slow passage into solution~
It thus follows that death is more likely to occur if water is given
immediately after dosing with arsenic than if it is withheld for
twenty-four hours. Indeed, this is an extremely important point
in the dispensing of arsenic preparations, for in the case of Walton,
Purser and Corner v. Wyly, M.R.C.V.S. (I938), in which 68 out of
IOO lambs died as a result of treatment with a mixture of copper
sulphate and sodium arsenite for intestinal parasitism, the Judge
held" that the veterinary surgeon was negligent in that he did not
!:>pecificaUy warn the shepherd to prevent the lambs from having
access to water for some hours after do.sing and awarded damages
against him.
In experiments with Cooper's dip, which is an alkaline arsenite
and thioarsenite combined with sulphur, containing approximately
32 VETERINARY TOXICOLOGY
225 per cent. of arsenic as the trioxide" Theiler (1912) found that
I g. is a safe dose for sheep, but that 2 g. killed lout of 48 sheep,
3 g. killed 4 out of 30, and 4 g. killed I4 out of 15 sheep. When water
was withheld for twenty-four hours, death did not supervene for,
seven to eight days, whereas animals watered at once after dosing
died within twenty-four hours. Theiler (1912) also carried out ex-
periments with mixtures of copper sulphate and arsenious oxide
and found that a mixture containing I g. of each substance was a
safe dose. Similarly, a mixture of I g. of copper sulphate with I g. of
Cooper's dip appeared to be safe, but 2 g. of copper sulphate with
I g. of Cooper's dip proved dangerous, killing lout of 6 sheep
within twenty-four hours. The addition of equal parts of common
salt and sulphur to the mixtures increased their toxicity con-
siderably; thuS', 3 g. of equal parts of copper sulphate, Cooper's
dip, sulphur and common salt killed 5 out of 65 sheep, and a 4 g.
dose containing I g. of each substance killed 16 out of 88 sheep.
Steyn and Bekker (1938) found that 006 g. of Cooper's dip per
kg. body weight was the approximate minimal lethal dose for the
rabbit, and that the dip was two and a half times more toxic than
Cooper's double dipping powder, which contains approximately
94 per cent. of arsenic as the trioxidc. They also consider that
from 0.76 to 200 g. of sodium arsenite may be regarded as a
dangerous dose for full-grown cattle and from 024 to 0.48 g. as
dangerous for sheep. Husband and Duguid (1934) found that
grass sprayed with sodium arsenite only to the extent of 15
pounds per acre was dangerous to cattle, and Fitch, Grimmet and
Wall (1939) found that three daily doses of r367 g. of the trioxide
killed a heifer in four days.
Birds are extremely susceptible to the toxic action of arsenic,
which has been responsible for wholesale deaths amongst fowl,
pheasants and other birds. Gallagher (1919) found that 03 g. of
the trioxide killed a fowl in twenty-seven hours, and Phillipc
(1939) considers that 01 g. of atoxyl is the maximum safe dose
for fowls. The actual amount of arsenic ingested may vary con-
siderably, however, owing to the relatively large quantity which
may be stored in the crop.
H is thus evident that the toxic dose of arsenic for all species
of animals depends on numerous factors, particularly the nature
of the arsenical compound, its physical state-i.e., whether solid,
coarsely or finely powdered, or in solution;---and in addition the
condition of the digestive organs, the nature of the ingesta, and
MINERAL OR INORGANIC POISONS 33
the method of application will also affect it. In practice the most
dangerous arsenic preparations ar:e those in which the arsenic is
in a readily soluble form, as in alkali arsenite dips and weed-killers.
and to a less degree finely divided arsenious trioxide and copper
arsenite. Whilst no hard-and-fast rule can be made, the approx-
imate toxic dose of arsenic by the mouth for the different animals
is as follows:
Arsenious .Sodium
Trioxide. Arsenite.
Horse 10'00-45"0 g. 1'00-3'00 g,
Cow 14'00-45'00 g. 1'00-4'00 g,
Sheep 3 '00- 5"00 g. 0'20-0'5 0 g,
Pig .. 0'50- 1'00 g. 0'05-0 '10 g,
Dog .. 0,60- 1'50 g, 0'05-0'15 g.
Fowl 0'10- 0'30 g. 0'01-0'10 g,

Absorption.-The absorption of arsenic manifestly depends on


the form of the compound which has been taken, as solution of
the insoluble arsenic cOJ:bpounds in the digestive tract is extremely
slow. It appears possible that much of the alleged arsenic tolera-
tion in man and animals is due to the fact that the solid oxide is
taken, that absorption is very slow, and that much of the sub-
stance is excreted unchanged in the freces, whilst that portion
which is absorbed is excreted in the urine, so that no accumulation
takes place in the tissues, Thus, Clough (I929) reports that a
horse was given 645 grains (42 go) of white arsenic over a period
of sixteen days and a fortnight later 505 grains (33 go) over a
period of ten days, yet no symptoms of arsenic poisoning were
noted, and when the animal died ten weeks later from some
other cause no arsenic could be detected in the muscles, kidney
or liver, although it. was still present in the stomach contents.
There is evidence, however, that by gradually increasing the dose
of the soluble forms of arsenic a true tolerance may develop, and
there is no doubt that certain organisms such as trypanosomes
can also develop a tolerance to arsenic, but the whole question
requires further investigation.
Absorption of soluble arsenic takes place slowly through the
intact skin, but when applied to a fresh wound absorption is
extremely rapid, as is also the case from the digestive tract. Thus,
it is not unusual to find appreciable quantities of arsenic in the
stomach contents, although none may be present in the contents
of the small intestine.
Following absorption, arsenic passes to the liver, where it tends
3
34 VETERINARY TOXICOLOGY
to accumulate, probably in an insoluble form, being gradually
released into the blood stream, and so to every organ in the body.
This is well shown by the results of an analysis made on three
Jersey cows which died as a result of taking arsenical dip. In
Case I, death occurred within twenty-four hours; in Case II,
five days; and in Case III, seven days elapsed before death. The
amount of arsenic in grains per ounce were as follows:

Fourth Period oj
Rumen. Stomach. Liver. Spleen. Illness.
Case 1. . .1.
6
-.L
..0
Trace Trace Less than I day.
Case II. . _L
30 80
1
rlo - 5 days.
Case III. . 24
1
36
1
1iOO ala 7 days.

In chronic cases of poisoning there is a tendency for the arsenic to


be stored in the bones, skin and keratin tissues such as hair and
hoof, and to disappear from the soft tissu~s.
Elimination of arsenic is, however, rapid and it may be detected
in the urine five to six hours after administration. It is also ex-
creted in the milk, sweat, bile, mucous and other secretions, and
elimination is probably complete within two to three days after
a single dose, with the possible .exception of the keratin tissues,
especially the hair, in which the arsenic may persist for several
weeks.
Diagnosis.-The sudden appearance of violent symptoms of
colic, thirst, straining and purgation, and perhaps vomiting, will
arouse the suspicion that irritant poisoning, probably by arsenic,
has occurred.
Symptoms.-The general symptomatology of arsenic poisoning
has now been fairly well established, and cases may be classified
as peracute when death takes place very shortly after the taking
of the poison, acute and subacute when death does not occur for
several days, and chronic when the patient may live for many
months before death supervenes. Arsenic is_an irritant poison,
although it differs from the heavy metals in that it does not pre-
cipitate albumin, so that in general it will give rise to local irrita-
tion as well as systemic effects.
It may be mentioned here that arseniuretted hydrogen, unlike
other arsenical compounds, combines directly with hremoglobin
and causes a severe hremolysis and hremoglobinuria, death in
this case being due to sudden heart failure.
MINERAL OR INORGANIC POISONS 35
In peracute cases death may ensue SQ rapidly that the animal
is never observed to be ill. The chief symptoms are intense
abdominal pain, staggering gait, collapse, paralysis and death.
In acute and subacute cases the most prominent symptoms are
salivation, thirst, vomition where possible, violent colic, watery
diarrhcea sometimes ha:morrhagic, exhaustion, collapse and death.
In those cases which live for some days there may be, in addition,
depression, loss of appetite, staggering gait, apparent paralysis
of the hind quarters, trembling, stupor, convulsions, coldness of
the extremities and subnormal temperature. Albuminuria and
ha:maturia may also occur. In chronic cases, which"are less frequent
and less well marked than in man, the most characteristic symp-
toms are indigestion, thirst, great wasting, and general appearance
of unthriftiness, with a dry staring coat and brick-red coloration
of the visible mucous membranes; the pulse is weak and irregular,
but the temperature is normal. Such cases OCCur in areas near
smelting works, mines, etc., as a result of contamination of the
herbage with arsenic, and it is usual to find the grass and other
vegetation showing brown patches from its destruction by the
arsenic in the smoke or effluent from the works.
Arsenical dermatitis is not so commonly observed in animals
as it is in man, but it does occur following the ingestion of arsenic,
especially in pigs, and may be readily set up as a result of repeated
application of arsenic to the intact skin. Thlis, Clough (1929)
records that an arsenical dermatitis occurred in a number of pit
ponies where the skin was in contact with the collar and saddle,
owing to the fact that arsenic was present in the flannel lining
of the harness. Most authorities, however, are agreed that there
is little danger of the absorption of arsenic in toxic doses from
dips through the unbroken skin provided proper precautions are
taken. In dipping, the solution should not contain more than 5
pounds of arsenic per 100 gallons, each sheep being immersed for
from forty to sixty seconds and requiring I gallon. The solution
must be as completely squeezed out of the fleeces as possible, and
the animals turned out, if possible, on to a dry road or large yard
free of hay, litter, vetches, or green food. Accidents arise chiefly
from the licking of the fleeces when the sheep are overcrowded,
and from the drippings on to grass or fodder, which then become
vehicles of poisoning.
Although no damage isto be anticipated from the proper use of
arsenical sheep dips, it may be found that in double dipping
VETERINARY TOXICOLOGY
within a period of fourteen days it is desirable to reduce the
strength for the second dip. It, however, remains an indisputable
fact that damage to all classes of stock is very often caused by
lack of care in disposing of waste dip liquors, and by leaving
powder in exposed situations. Manifestly the same remarks apply
to all other poisonous preparations, such as coal-tar and nicotine
dips, arsenical weed-killer, lead arsenate spray, vermin-killers, etc.
As regards dips, lime-sulphur or soda-sulphur dips containing
about 8 pounds of dissolved sulphur, chiefly as polysulphide, per
100 gallons of actual dip, have the advantage of being non-
poisonous. They are cheap, easily made at home by a man of
average ability, and do not injure the fleece. Very dilute mono-
and hydrosulphide of soda do definitely injure wool, but neither
of these nor caustic soda is present in the properly made dip, the
pentasulphide, which is the main component, being without
action on wool. These dips are widely used and favoured in the
Union of South Africa.
, Post - Mortem Appearances. - The characteristic lesions of
arsenical poisoning are an intense rose-red inflammation of the
alimentary tract, particularly the stomach, with ecchymoses and
extravasation of blood. The mucous membrane appears swollen,
and the epithelium readily comes away when gently rubbed. The
inflammatory changes are probably due to dilation of the blood-
vessels, with swelling, congestion and transudation of fluid, which
accounts for the watery diarrhrea associated with arsenical
poisoning, but in addition there is ~ direct action on the epithelial
cells, which show cloudy swelling and fatty degeneration. These
latter changes are also seen in the liver, kidneys and heart, and
these organs may a]so show ecchymoses and small h;:emorrhages. In
cattle, inflammation of the fourth stomach is usually pronounced,
although in cases where only small amounts of arsenic have been
taken, inflammatory changes may not be very noticeable, but
this is the exception. In pigs, inflammation of the mouth and
fauces with extravasation of fluid may be severe and extend to
the mucOus membrane of the larynx~and trachea, thus causing
asphyxia. In fowls, the characteristic lesions are an intense
inflammation of the proventriculus and gizzard, the horny epi-
thelial layer of the gizzard being separated from the underlying
muscles by a gelatinous exudate. Other portions of the alimentary
tract may show few if any lesions, with the possible exception of
a slight reddening of the crop and the duodenal mucosa. The liver
MINERAL OR INORGANIC POISONS 37
is usually pale, friable, and shows evidence of fatty degenera-
. tion.
Treatment.-This should consist of repeated stomach lavage,
if possible; fajJing this, the administration of emetics followed
by demulcents and purgatives. Useful demulcents are milk, egg-
white, oil, lime-water or linseed tea. As specific antidotes, freshly
precipitated ferric oxide in warm water should be given ad lib.
This may be readily prepared by dissolving I ounce of sodium
carbonate in 12 ounces of water, adding the sodium carbonate
to a solution of 3 ounces liquor ferri perchlor. in 10 ounces of
water, filtering, and administering at once. Dialysed iron, l to
I ounce for dogs and 6 to IS ounces for horses and cattle, may also
be used. In addition, calcined magnesia or charcoal should be
given to allay gastric inflammation.
Revaut (1920), Semon (1924) and others have suggested that
the intravenous injection of a '10 per cent. solution of sodium
thiosulphate ("hypo") should be used in the treatment of metallic
pois,oning, as the drug appears to stimulate the excretion of metals.
In human medicine this treatment has been employed with success
in cases of arsenical poisoning, particularly in the treatment of
dermatitis resulting from the administration of organic arsenical
preparations, and Steyn (1939) recommends that in protracted
cases of arsenical poisoning in animals, cattle and horses should
be given 8 to 10 g. of a 10 to 20 per cent. solution intravenously
and 20 to 30 g. orally in about 300 ml. of water; sheep and goats
receive a quarter of these doses.
As a result of a study of the ~ction of arsenic on cell metabolism,
Voegtlin (1925) concludes that the arsenic interferes with tissue
oxidations and that the rational treatment of cases of poisoning
would be the administration of, reduced glutathione, since it is this
system wh,ich appears to be disturbed. However, there are as yet
no reports as to the value of such treatment in veterinary medicine.
Chemical Diagnosis.-More attention has probably been paid
to methods of detecting traces of arsenic than has been devoted
to any other analytical process. The epidemic of arsenical poison-
ing through beer led to the establishment of refined standard
methods, and laid new emphasis on the extremely wide distribu-
tion of this element and the need for caution against its presence
in laboratory re.agents. The reagents used should be of guaranteed
purity, and in addition it is necessary to prove by blank experi-
ments that the apparatus and chemicals are free from arsenic.
VETERINARY TOXICOLOGY
The first procedure is to carry out a Reinsch test, which is
sufficiently delicate to' detect as little as 0'05 mg. of arsenic in
IOO g. of material. The presence of arsenic must be verified by
heating the coated copper in a dry ignition tube, when the cooler
parts of the tube should become covered with a glistening, white
crust showing characteristic octahedral crystals of arsenious
oxide when examined under the lower power of the microscope.
Numerous methods are available for the quantitive estimation
of arsenic. All require the previous destruction of organic matter
and depend on the reductiqn of the arsenic to arsine, which is
readily accomplished in the presence of nascent hydrogen. De-
struction of organic matter may be accomplished in a variety of
ways. The method of Babo and Fresenius may be used, but in
this case there is a risk of loss of arsenic by volatilisation; to over-
come this, Allcroft and Green (I935) recommend either a wet
combustion process using perchloric and nitric acids or a dry
combustion with magnesium nitrate. The procedure to adopt
using perch,loric acid, which must be free from arsenic, is to add
20 ml. of the acid to IO g. of finely divided wet tissue in a 300 ml.
Kjeldahl flask containing glass beads and boil until white, per-
chloric fumes are visible at the neck of the flask. The flask is then
transferred to a cork ring and nitric acid added from a drQPping
pipette until there is no further reaction. The mixture is then
heated again, when it should become pale yellow or almost colour-
less; if it remains dark brown, further addition of nitric acid is
necessary. The method of dry ashing, which is especially recom-
mended for rumenal contents, consists of thoroughly mixing 40 ml.
of a 20 per cent. solution of magnesium nitrate with every 10 g. of
material taken, evaporating the mixture. to dryness on a water-
bath and ashing in a muffle furnace. The ash so obtained can be
dissolved in sulphuric acid.,
The classical method for the estimation of arsenic is Berzelius'
modification of the Marsh test, and depends on the fact that when
free arsine is burnt in a current of hydrogen, the element is
deposited on coming into contact with a cold surface. The amount
of such deposit or mirror can then be fairly accurately assessed by
comparison with the mirror formed by a known quantity. of
arsenic.
The hydrogen is generated either by means of an electrolytic
cell or by means of zinc and dilute sulphuric acid. If the latter
method be used, the reagents must be free from arsenic and the
MINERAL OR INORGANIC POISONS 39
pure zinc activated by the addition of a few millilitres of cadmium
chloride. The zinc is placed in a generating flask provided with a
tightly fitting ground-glass stopper having two openings; a
dropping funnel passes through one of the openings and a drying
tube containing calcium chloride is connected to the other. A
Marsh tube is securely attached to the other end of the drying
tube and provision is made for heating one portion of the Marsh
tube by means of a Bunsen burner provided with a fish-tail. The
exit portion of the Marsh tube is drawn out into a thin jet through
which the hydrogen escapes, and this portion of the tube is kept
cool by means of pads of cotton-wool dipped in iced water. The zinc
is covered with water, a few millilitres of cadmium chloride added,
and dilute sulphuric acid allowed to run into the generating flask
at a rate sufficient to produce a brisk but not too vigorous evolu-
tion of hydrogen. The reaction is allowed to proceed until all the
air has been expelled from the apparatus, when the hydrogen
escaping from the jet can be safely ignited. The Marsh tube, with
the exception of the portion nearest the jet, is then heated as
strongly as possible, and if, after fifteen minutes or so, no dark
stain is visible on the cool part of the tube when examined against
a white background, the apparatus and reagents may be con-
sidered as being free from arsenic. A known quantity of the fluid
to be tested is then added to the dropping funnel and a little at a
time allowed to enter the generating flask until a deposit is formed
on the sides of the Marsh tube which roughly corresponds to one
of the previously prepared, standard mirrors. When this occurs,
no more of the test fluid is added to the generating flask, but the
r~action is allowed to continue for a further twenty minutes after
washing down the dropping funnel with dilute sulphuric acid.
The mirror obtained in this way is then carefully matched with one
of the standard mirrors, when it becomes a simple matter to
calculate the amount of arsenic in the unknown material, since
the amount of fluid added to the generating flask is accurately
known. Standard mirrors are best prepared from solutions con-
taining from 002 to 005 mg. of arsenious oxide. This should be
carefullyresublimed and dissolved in pure dilute sodium carbonate,
so that 10 m!. of the solution contains the required amount of
arsenious oxide. If antimony is present in the material under
examination, it also will be deposited on the sides of the Marsh
tube, but it may be distinguished from arsenic by the fact that it
is insoluble in a solution of bleaching powder.
40 VETERINARY TOXICOLOGY
The Gutzeit test is also a useful test for arsenic, which may
be used either quantitatively or simply as a qualitative test. It
depends on the fact that arsine decomposes silver nitrate with the
formation of a double compound of silver nitrate and silver
arsenide, and the yellow colour ot the latter substance may easily
be compared with stains made from known quantities of arsenic.
Filter paper is impregnated with a I in I silver nitrate solution,
allowed to dry and cut into convenient strips. Arsine is set free
in a Marsh apparatus from a known amount of the test fluid,
iodine being first added to the generating flask until the contents
are distinctly yellow in order .to remove S02 and H 2S,. which may
arise from the reduction of the sulphuric acid. The generating
flask is connected to a drying tube as before, but to this is attached
a glass tube containing a strip of the silver nitrate paper instead
of a Marsh tube. The reaction is allowed to proceed as in the
Marsh test, and if arsenic be present in the test fluid a yellow
stain will appear on the silver nitrate paper. The intensity of this
stain can then be compared with stains made by known quantities
of arsenic, and so the amount of arsenic in the material under
examination can be calculated. The standard papers should be
freshly prepared from known amounts of arsenious oxide dis-
solved in dilute hydrochloric acid. As little as 0'003 mg. of arsenic
may be dete'cted by means of this test.
The titrimetric method of AllcrOft and Green (1935) is ba;;ed on
the Gutzeit test, but to overcome the error which is liable to arise
with colorimetric comparisons the liberated arsenious acid is
titrated with iodine in the presence of potassium iodide. The
arsine is generated in a Marsh or other su~table apparatus from a
known quantity of the test fluid, using stannous chloride and
concentrated sulphuric acid for the generation of hydrogen from
pure zinc, and is then led through ~our absorption tubes, the
current of hydrogen being as fast as possible. The first absorption
tube contains I per cent. lead acetate to remove any traces of
hydrogen sulphide, and the remaining tubes contain N /50 or
N /100 silver nitrate. After. the_ reaction has proceeded for twenty
minutes the tubes containing the silver nitrate are disconnected,
their contents bulked, 0'1 g. sodium bicarbonate and about 2 g.
potassium iodide added, and microtitration with standard iodine
solution performed, using 0'5 ml. of a I per cent. starch solution
as indicator, which gives a sharp violent end-point. A N /495
solution of ;iodine is a convenient strength to use, since I ml. =
MINERAL OR INORGANIC POISONS 41
0'1 mg. of arsenious oxide. This method permits of the rapid
estimation of arsenic, since several determinations may be carried
out simultaneously, and is eminently suitable for the estimation
of small amounts of arsenic in biological fluids such as blood or
urine.
REFERENCES.
Allcroft, R, and Green, H. H. (1935), Biochenz. I., 29, 824.
Clough, G. W. (I929), Vet. Rec., 9, 992.
Fitch, L. W. N., Grimett, R E. R, and Wall, E. M. (1939), New Zealand
I. Sci. and Tech., 21, 146A.
Gallagher (1919), I. A mer. Vet. Med. Ass., 7,337.
Husband, A. B., and Duguid, J. F. (1934), Rhodesia Agric. I., 31, 25.
PhilJipe (1939), Bull. Servo zootech. Epiz. A.O.F., 2,8.
Pocher, C. (19Il), Rev. gen. Med. vet., 17, 193.
Revaut, P. (1920), Presse Med., 28, 73.
Semon, H. C. (1924), Brit. Med. I., April I2, 662.
Steyn, D. G. (1939), J. S. Afr. Vet. Med. Ass., 10, 151.
Steyn, D. G., and Bekker, P. M. (1938), Onde1'stepoort J. vet. Sci., 11,247.
Theiler, A. (1912), South Afr. Agric. J., 3, 321.
Voegtlin, C. (1925), J. Pharmacol. and Exp. Therap., 25, 168.
Walton, T. W., et al., and Wyly, E. H. (1938), Vet. Rec., 50,308.

ANTIMONY.
Forms and Occurrence.-Antimony is found in the form of the
oxide and sulphide, and, like arsenic, occurs as an impurity in
mineral ores. It forms trivalent or pentavalent compounds, the
most common being the trisulphide or black' antimony, Sb 2 Sa.
Black antimony purified by fusion and digestion with ammonia
to free it from arsenic is still extensively used in the manufacture
of so-called "condition powders,," which contain 18 per cent. of
antimony sulphide together with potassium nitrate, sulphur and
a spice-e.g., aniseed or fenugreek. The old-fashioned Kermes
mineral is a mixture of t.he sulphide and oxide, but otherwise
the compounds of antimony do not find much use in modern
medicine.
The oxide Sb 20 a is colourless and insoluble, but, 'like arsenious
oxide, is volatile and combines with alkalis to form soluble salts.
The chief compound is antimony-potassium ta1'trate or tartar
emetic, z(KSbOC4 H 4 0 a)H 20, which is formed when the trioxide
is heated with a solution of potassium bitartrate. This compound
occurs as a white, crystalline powder and has been mistaken for
tartaric acid, sodium carbonate, or even cream of tartar. Formerly,
butter of antimony, prepared by boiling the sulphide with hydro-
42 VETERINARY TOXICOLOGY
chloric acid to form the chloride SbC13 , evaporating and then
distilling, leaving a hard, white crystalline solid, was used as a
caustic dressing for canker of the foot of the horse or fOT foot-rot
in sheep.
Actions of Antimony.-The sulphides and oxides are slowly dis-
solved by the digestive juices, and thus exercise similar, but less
intense, effects to those of the soluble preparations. The soluble
compounds act as gastro-intestinal irritants, causing, in carnivora,
vomition, and in large doses also violent purging, weakness,
collapse, and death.
According to Kaufmann (Igor), dogs are poisoned by 3 to
6 grains.
The antimony compounds do not appear to owe their emetic
properties to an action upon the centres of vomition, but to their
local gastro-intestinal effect; for, on injection, very large doses
are required to produce emesis, and it is found that the antimony
is excreted into the alimentary tract.
Like arsenic, antimony causes fatty degeneration of the liver,
and the oxide is therefore given to geese to produce fatty liver for
the preparation of joie grasse.
Ruminants are able to withstand very large doses, and some
doubt has been expressed as to whether poisoning can possibly be
produced by antimony; but extreme nausea, colic, and death have
been observed in the horse, whilst actual vomition in the cow,
following the administration of Kermes mineral, is on record.
Dun (I9IO) quotes valuable experiments on horses with tartar
emetic. They show that such large quantities as 10 ounces of the
drug given over a period of ten to eighteen days do not exercise
any noticeable physiological effect. But a healthy horse, given
10 ounces of tartar emetic in solution in one dose, showed nausea,
uneasiness, and pain, and died within about six hours.
Concerning the toxic effect of antimony on carnivora there can
be no question, and as regards the herbivora, there is sufficient
evidence to warrant the opinion that the habitual use of anti-
monial medicines is objectionable, and may,_particularly with
young and delicate thoroughbred animals, cause poisoning. In
consideration of the large quantities of antimonial condition
powders which are administered empirically as a matter of weekly
routine by persons in charge of stock, this is a very important
point, worthy of close attention. .
Armitage (r865) quoted a case of the death of pigs. They were
MINERAL OR INORGANIC POISONS 43
stated to have had the usual foog, exhibited severe abdomi,gal
pain, and made unsuccessful efforts to vomit, but there was no
purgation.
On post-mortem the stomachs were gorged, and the mucous
membrane showed intense inflammation, extending to the whole
of the small intestine. The large intestine was not inflamed. In the
stomach was found a deposit of black grains of antimony sulphide,
and the opinion was formed that death had resulted from an
antimony, nitre, and sulphur condition powder.
In I909 a case was investigated in which a six months blood
filly, apparently well overnight, was suddenly seized with violent
scouring, and died very quickly. On post-mortem acute inflamma-
tion of the stomach and bowels was observed, the other organs
appearing normal. Antimony was found in the viscera-it was
admitted that the animal had been dosed with a condition powder
-and no other cause of poisoning or death was discernible.
In another case investigated in I905, doping heavily with anti-
mony prior to a sale appeared the only explanation of the sudden
death of a mare.
Treatment.-Antimonial poisoning is treated by removal of the
cause by evacuation of the stomach and oily purgatives with
demulcents.
Tannic acid precipitates tartar emetic, and is used as a chemical
antidote.
Morphine against pain, and stimulants are to be used as
required.
Chemical Diagnosis.-This is best accomplished by means of a
Reinsch test, the deposit on the copper being distinguished from
arsenic by yielding an amorphous sublimate, and further by a
Marsh test, in which a black stain which is insoluble in a solution
of bleaching powder may be taken as confirmatory evidence of
antimony.
For the quantitative estimation of antimony Bamford (I94o)
recommends the production of the characteristic orange-coloured
sulphide for colorimetric comparison with sulphide formed from
a known amount of tartar emetic.
REFERENCES.
Armitage, G. (1865), Veterinarian, 11,337.
Bamford, H. F. (1940), Poisons, their Isolation and Identification.
Dun, F. (19IO), Veterinary Medicines, 12th ed.
Kaufmann, M. (1901), Therapeutique et Matiere Medicale Veterinaire,
3rd ed.
44 VETERINARY TOXICOLOGY

LEAD.
Forms and Occurrence.-The common preparations of lead
likely to give rise to poisoning are: the oxides litharge and red
lead, the latter being used as a paint and in plumbing; lead acetate,
or sugar of lead, and the basic acetate-Goulard's solution: white
lead, a basic carbonate, the common pigment, and the most usual
vehicle of poisoning, also used in the manufacture of oilcloth and
linoleum*; the sttlphate, less frequently used as a pigment. Lead
arsenate is a very common material for the spraying of fruit trees,
and may also cause acute poisoning. Metallic lead, in the form of
bullet splashing, has been observed to give rise to poisoning, but
only after prolonged lodgment in the digestive system, during
which the metal is corroded and absorbed. Metallic lead, through
solu'tion in water under certain conditions, may also be the cause
of chronic lead poisoning, or plumbism. The conditions governing
the solution of lead by water are: that the water is soft-that is,
free of lime and magnesia salts-and aerated. It must contain
dissolved oxygen and carbon dioxide, and the presence of nitrates
further facilitates solution. The extent of solution may be gathered
from the following figures of Roscoe and Schlorlemmer (I897),
which show the number of milligrammes of lead dissolved by
500 C.c. of water from a bright surface of 5,600 square millimetres:
Twenty-jour Forty-eight Seventy-two
Hours. Hours. Hours.
Distilled water 2'0 2'0 3'0
Distilled water + 0'02 gramme
ammonium nitrate per litre .. 3I'0

Suchconditions are fulfilled by rain water, but ordinary hard


water is without perceptibl~ solvent action. The lead is at first
dissolved by soft water, but eventually separates in the form of
white flakes of basic carbonate. .
Acute lead poisoning of cattle almost always results from eating
white paint or red lead or chewing old painted canvas and the like,
and of dogs by licking wet paint, or by licking lotions applied
externally.
Absorption and Elimination.-With the exception of the acetate,
or sUBar of lead, and the basic acetate, ~he preparations named
>I< 'Vhite lead substitutes, such as "lithopone," which do not contain
lead, are corning into increasing vogue.
MINERAL OR INORGANIC POISONS 45
above are insoluble in water, the oxides and carbonate dissolving
easily in dilute hydrochloric acid, * the sulphate less readily, in
conformity wherewith it has the least toxicity, and its formation
by the exhibition of dilute sulphuric acid, or a soluble sulphate
(Epsom or Glauber salt), is an antidotal measure.
It is particularly,necessary, in connection with the study of the
physiological effects of all drugs, to be careful in the use of the
term insoluble. The compounds of lead form a good case in point.
When a chemist speaks of insoluble he means insoluble in water,
but at closer grips he will admit that he cannot postulate absolute
insolubility. Perhaps sand and sulphate of barium approach the
ideal. What is of far greater importance is that insolubility in
water does not necessarily imply insolubility in acid or alkaline
media, such as the body fluids. Thus lead sulphide (galena), lead
sulphate, lead arsenate, white lead, and the lead oxides are all
definitely soluble in the digestive juices. When one remembers
that the ratio of poison to juices is small-e.g., when an ounce is
churned in the alimentary tract of an ox-it is clear that a very
moderate solubility, expressed as a percentage, may mean a
sufficient absorption to cause grave damage. Lead sulphate and
barium sulphate offer a good illustration. Each is "insoluble," but
whereas the salt of lead is sparingly soluble in digestive juices,
that of barium is not. Although soluble compounds of barium are
fully as ,toxic as those of lead, it results that barium. sulphate is
harmless, whereas lead sulphate is dangerous. To take another
illustration, lead arsen,ate is spoken of as insoluble, But it ought
to be definitely known' that firstly lead arsenate is actually de-
composed by water into soluble arsenic acid and "insoluble" lead
oxide, and secondly that "insoluble" lead oxide is soluble in
digestive juices. '
A very clear and careful qualification of the word "insoluble"
is highly important, especially in the witness box.
It has been held that lead is absorbed as the chloride formed
by the action of the gastric juices. Lead salts, however, 'pre-
cipitate albumins, and absorption as lead albuminate is more
probable.
The relative insolubility of the lead salts and of the albuminate
accounts for the fact that lead is one of the least corrosive metallic
poisons. The question of poisoning by metallic lead has been the
subject of some controversy, but is now held to be established.
* 1t will be rememl?ered that lead chloride is sparingly soluble.
VETERINARY TOXICOLOGY
The exposure of bullet splashes to weather leads to super-
ficial oxidation or rusting, whereby a coating soluble in acid
will be formed. In like manner, effluvia: from lead-works may
eventually impregnate herbage, and lead from the refuse of old
disused workings gradually finds its way into the neighbouring
streams, soils, and herbage. Thus, in a case brought under the
author's notice by Dunstan of Liskeard, the water of a stream was
proved to contain both lead and arsenic-the latter being ad-
sorbed by suspended iron oxide.
The mining of lead is not now carried on in this country to the
extent of bygone times, but the contamination or "bellanding" of
land in mining districts is still a matter of grave medico-legal
concern. The formation of dumps is an obvious possible cause of
trouble. Even the stable galena (lead sulphide) is distinctly
attacked by the alimentary juices, and is also liable to weathering
with formation of the more easily absorbed oxide and sulphate.
The fume from a lead-smelting hearth contains oxide and sulphate
of lead in such an extraordinary fine state of subdivision as almost
to possess the properties of a heavy gas. Like the finely divided
volcanic dust of a big eruption, this fume may travel miles.
Contrary to first thoughts, the close vicinity of the shafts receives
less deposit than localities at greater distances. Indeed, it has been
stated that in some works innocence of pollution is suggested by
drawing attention to thriving flower beds at the shaft foot. In
any case, it is well known that the lands in smelting districts are
contaminated, and it is even likely that in an industrial country
refined micro-analysis will reveal lead (and other metals such as
zinc, arsenic, etc.) in samples of soil taken anywhere in the land.
Manifestly in the great majority of cases these amounts are of no
practical significance.
Lead is retained -by the organs for a long time: The blue line
on the gums, supposed to be caused by a deposition of lead
sulphide, only disappears very slowly after withdrawal of the
cause. The liver, kidneys, bones, nervous tissue, and muscle retain
lead in the relative order given. According to Ellenberger, the
percentages of lead found in those organs of a sheep which
during four months had received I64 grammes of lead acetate
were:
/"
Liver 06 Nervous ti:;sue
Kidneys 0.
0475 'I Muscle
Bones 0.3 2
MINERAL OR INORGANIC POISONS 47
Elimination is slowly effected by way of the bile, urine, salivary,
mucous, and cutaneous excretions, and is stated to be hastened by
the administration of potassium oxide.
Toxic Dose.-This cannot be regarded as satisfactorily estab-
lished. Very usually a large excess of lead remains in the alimentary
tract, cows frequently eating lead paint refuse by the pound. The
dose is also determined by the nature of the preparation given,
the general corrdition, idiosyncrasy, and species of the subject.
The following provisional figures may be quoted for minimum
toxic doses of acetate of lead:
Ox .. 720 grains
Horse _, 7.500
Sheep 450
The relative tolerance displayed by the horse is a remarkable
point, and is on a parallel with the comparative rarity of acute
cases among these animals, the usual victims being in order-
cattle, pigs, sheep, dogs. Birds are readily susceptible to the effects
of lead, and cases of poisoning are by no means rare from lead shot
picked up in the food, the ingestion of about six pellets being
sufficient to cause death. The minimal lethal dose of absorbed lead
for birds lies between 0r6 and 06 g. per kg. body weight, death
occurring in two to three weeks.
Symptoms.-Lead is perhaps the most frequent cause of acci-
dental mineral poisoning in domestic animals, especially cattle,
and numerous well-authenticated cases are on record. Cases may
be classified as acute, subacute or chronic, depending on the
.
amount of lead ingested, the rate of absorption, and the length of
time over which it has been taken.
In acute cases, which occur most frequently in cattle and which
may be mistaken for vegetable poisoning or lactation tetany owing
to the nervous symptoms, the chief signs are blindness, gastro-
enteritis, colic, convulsions, coma and death. There may be, in
addition, intense abdominal pain, grinding of the teeth, nasal
discharge, salivation, pallid mucous membranes, constipation
with the passage of hard, black freces or sometimes diarrhcea,
muscular tremors and coma. The pulse is hard and thready,
breathing accelerated, and temperature normal or slightly sub-
normal, whilst the extremities are cold. In cattle, delirium alter-
nating with a semi-comatose condition in which the animal may
assume an unnatural posture, making no attempt to alter it, is
not uncommonly seen. In some cases no marked symptoms are
VETERINARY TOXICOLOGY
shown. Illness usually lasts several days, but death may super-
vene within forty-eight hours. This point seems well established,
although in the case of Brown v. Caivert, as recorded by Clough
(1925), it was stated by Professor Dixon that acute lead poisoning
could not occur owing to the slow absorption of lead. Following
this statement, numerous cases were reported in which the time
between the ingestion of lead and death could be accurately
stated; thus, Watkins (I925) records the death of a cow within
twenty-four hours of its having been seen to eat lead paint just
left by a workman near a gate; Sti~son (I925) observed the
poisoning of a bullock by lead arsenate within twenty-four hours;
and Waters (I925) the death of a heifer forty to sixty hours after
swallowing about a pint of white paint. There is therefore con-
clusive evidence that acute lead poisoning can and does occur at
any rate in cattle.
In subacute cases, symptoms set in gradually, but after forty-
eight hours or so, during which time the animal only shows in-
appetence and listlessness, marked symptoms of acute lead
poisoning usually appear. On the other hand, no definite symp-
toms may be shown; thus Bywater (I937) records the deaths of a
number of pigs in which the only symptoms were impaired
appetite with the passage of black, rather firm freces, together
with a little blood, and abortion among the pregnant sows. Illness
may last from several days to two or three weeks. or longer. In a
typical case Robb and Campbell (I940) record the poisoning of
eight heifers from eating the remains of green paint-lead
chromate-which had been used to paint a fence about a month
before the ~nimals became affected. Five of the heifers died in
the course of three days after showing symptoms of poisoning,
and it was not until six weeks later that the re~aining three
heifers recovered completely. Taylor (I9I5) records an interesting
case of lead poisoning in the pig. The subject was a three months'
pregnant sow which was known by direct observation to have
eaten white lead paint from a tin containing about 2 pounds. In
two to three days the animal went off its feed andpassed greyish-
white freces, and professional advice was sought on the eleventh
day. After iodide and sulphate treatment the case appeared more
hopeful, but on the sixteenth day blindness" violent frenzy and
all the symptoms of acute lead poisoning set in, with a fatal end.
Abortion did not occur in this case. Gregg (I924) observed a case
of acute lead poisoning in a mare attributed to mining con-
MINERriL OR INORGANIC POISONS 49
tamination. In addition to respiratory symptoms, partial paralysis
of the hind extremities was noted. "The hind legs gave one the
impression that they were too short for the body, due to flexion
of the joints. Left undisturbed, the mare stood as if rooted to the
ground in front, but kept constantly paddling behind" and when
forced to move, control of the fore parts seemed normal, but great
difficulty in getting the hind legs forwards was manifested, and
the hind quarters swayed from side to side." Abdominal pain
seemed subacute. Death in convulsions occurred.
ChronicPoisoning.-The blue line on the gums only appears in
chronic poisoning, which is a rarer event in practice than the
acute. In chronic poisoning, so common formerly among workers
in lead, are to be noted the general digestive derangements, colic,
constipation alternating with diarrhcea, a~d thirst; the nervous
symptoms of paralysis, convulsions, and coma observed in the
acute form; the general symptoms of wasting, emaciation, de-
bility, and the like. Rumination and lactation cease, and con-
vulsions, coma, and paralysis precede death.
Some excellent examples of chronic or slow lead poisoning in
cows, due to bullet splashes, were recorded by Tuson and Broad
(I86S). In these cases the period intervening between the inges-
tion of the lead splashes and illness was prolonged, amounting
to as much as fifty-eight weeks. The symptoms observed were:
abdomen tucked up, staring eyes, dull look, staggering, groan-
ing; lactation ceased, -appetite good, constipation alternated by
diarrhcea; gradual wasting and prostration preceded death. The
blue line was absent. The viscera generally were pale, the intes-
tinal walls having a peculiar blue colour, and the abdominal
cavity contained about 3 gallons of straw-coloured fluid. Metallic
lead was found in the reticulum, and Tuson (I86S) observed that
this had been corroded by the digestive juices. These cases are
further remarkable in illustration of the lodgment of the solid
matter so permanently in the digestive system.
The Veterinarian, I8SS, p. 609, records an interesting legal
action, with comments, arising from the chronic poisoning of
stock, due to lead-smelting operations in the Mendips. There were
observed stunted growth; leanness; shortness of breath; paralysis,
especially of hind extremities; swelling at knees; but no constipa-
tion or colic. It was adduced by Herapath, in evidence, that the
blue line on the gums gave,_ on dissection and blowpipe reduction,
-"'visible beads of metallic lead.
4
50 VETERINARY TOXICOLOGY
Plumbism is remarkable from the length of illness, which may
be protracted over weeks or even months. In horses lead causes
roaring and dyspnrea by acting on the vagus nerve. Cases in point
are given by the German authorities, and have also been observed
by Shenton (r86r) in this country.
Among more recent observations useful information on chronic
lead poisoning of stock is contained in articles by Morgan (r924)
and by Edwards (r924). They serve particularly to emphasise the
"roaring" symptoms in working horses which have so long been
associated with chronic lead poisoning, and also the brain or
"stagger" symptoms so commonly observed in cattle.
Post - Mortem Appearances. - Inflammation of the fourth
stomach and intestines is a common, but not invariable, condi-
tion. Particles of lead, sometimes amounting to several pounds,
as in a case recorded by Nash (r894), may be found in the retic-
ulum. It is usual to find pieces of lead paint of the size of beans,
blackened externally, friable, and white internally. Where such
pieces have been in contact with mucous membrane, the latter is
also blackened and easily detachable, revealing inflammatory
patches. Acute peritonitis, with formation of greyish-yellow false
membrane, has been observed.
In a case observed by Lawson (r884) the mucous membrane
was detachable; no inflammation; liver bloodless and yellow;
lungs engorged with black blood, inflamed and emphysematous;
trachea and bronchi filled with a frothy spume.
In some cases the liver has been found engorged, and in others
the organs have been found healthy. The production of inflamma-
tion depends on the nature of the preparation given. It is not
shown when the dose is small or in the presence of an excess of
acid; in the form of albuminate dissolved in acetic acid death is
.rapid and inflammation absent; but with solid carbonate dark
red inflammation is to be anticipated.
Treatment.-Removal of the cause by emetics, by the pump,
and by means of saline urges; as chemiCal antidotes, dilute
sulphuric acid; or soluble sulphates, such as Epsom or Glauber
salts; casein, given as milk, is recommended, in order to precipitate
lead albuminate; tannic acid, as tea or coffee; and stimulants-
e.g., digitalis or ammonium acetate-have been used. In chronic
plumbism the exhibition of potassium iodide is claimed to facilitate
elimination. Kety and Letonof{ (r94r) report that the oral ad-
min~stration of sodium citrate rapidly relieved the symptoms of
AIINERAL Ul(. INORGANIC POISONS 51
lead poisoning in the human subject, so that this drug may prove
to be of value in the treatment of lead poisoning in animals.
Chemical Diagnosis.-The separation of lead from organic
matter is conveniently carried out by the method of Babo and
Fresenius. The lead will be in the form of the chloride, so that the
final filtration must be carried out whilst the solution is hot, as
lead chloride is insoluble in the cold. The filtrate so obtained is
neutralised with ammonia and the lead precipitated as lead
sulphide by means of hydrogen sulphide bubbled through the
solution. The lead sulphide is filtered off, dissolved in a little
warm, dilute nitric acid, the solution evaporated to dryness, and
the residue of lead nitrate used for further tests for which the
nitrate may be dissolved in a little wate_r. The addition of potas-
sium iodide to the solution produces in the cold the precipitation
of bright yellow lead oxide crystals which are soluble in sodium
hydroxide. The addition of dilute sulphuric acid or any soluble
sulphate produces a precipitate of white lead sulphate which is
soluble in caustic alkalis. The addition of potassium or sodium
hydroxides also give a white precipitate of lead hydroxide which
is soluble in excess of the reage,nts.
For the estimation of lead, the residue of lead nitrate is dis-
solved in dilute sulphuric acid and allowed to stand f~r twenty-
four hours, when a precipitate of lead sulphate forms. This is
filtered off by means of a Gooch crucible, washed, dried and
weighed, I g. of the filtrate corresponding to 0.6832 g. of metallic
lead. For the estimation of small amounts of lead in organs,
Lynch (1934) recommends the colorimetric estimation of lead as
the sulphide in colloidal suspension.
As is to be expected, the quantities found in alimentary con-
tents show very wide variation, as much-as 2l per <;ent. of red
lead having been found, and, on the other hand', as little as '2'Jo
grain per 2 ounces in well-authenticated cases. The detection of
lead in the liver or kidneys, even in small quantities, affords
better medico-legal evidence, representing absorbed lead, whereas
medicinal doses-e.g., lead acetate-might easily be recognised
in visceral contents, but not in the organs.
REFERENCES.
Broad, ]. M. (1865), Veterinarian, 11,222.
Bywater, H. E. (1937), Vet. Rec., 49,549.
Clough, G. W. (1925), Vet. Rec., 5, 115.
Edwards, ]. E. (1924), Vet. I., 80,81.
52 VETERINARY TOXICOLOGY
Gregg, R. (1924), Vet. ]., 80, 76.
Kety, S. S., and Letonoff, T. V. (1941), P"OC. Soc. expo BioI., N. Y., 46,476.
Lawson, A. W. (1884), Veterinarian, 30, 447.
Lynch, R. (1934), Analyst, 59, 787.
Morgan (1924), Vet. J., 80,2.
Nash, G. E. (1894), Vet. Ree., 7, 398.
Robb, W., and Campbell, D. (1940)' Vet. Ree., 52,29.
Roscoe and Schorlemmer (1897), Treatise on Chemistry.
Shenton (1816). See Dun, F., Veterinary Medicines, 12th ecl.
Stinson, O. (1925), Vet. Rec., 5, 160.
Taylor, H. (1915), Vet. Ree., 28,97.
Tuson (1865), Veterinarian, 11,217.
Waters, W. (1925), Vet. Rec., 5,160.
Watkins, G. (1925), Vet. ]., 81, 407.

MERCURY.
Forms and Occurrence.-The most important soluble compound
of mercury is the bichloride or corrosive sublimate, one of the most
powerfully corrosive and bactericidal of the salts of the heavy
metals. It is not often the cause of accidental poisoning. The
mercurous chloride or calomel, being insoluble, is non-toxic-save
in large doses, or when elimination by purgation does not occur-
and non-irritant, and is one of the commonest medicinal forms of
mercury. M etatlic mercury, which is harmless in large globules,
is absorbed when in the finely divided form, and is thus extensively
employed in such preparations as mercury with chalk, and in
various mercurial ointments. Finely divided mercury is also some-
times incorporated with oil of tar and mineral oils in mange
dressings. The sparingly soluble red 1:odide or biniodide also finds
application as an ointment. As lotions, suspensions of the black
merC1trOUs and yellow mercuric oxides in lime water are used, and
zinc mercuric cyanide is a powerfully antiseptic, non-irritant agent.
Ammoniated mer9Hry or white precipitate, formed by acting on
mercuric chloride with ammonia, is a nori-irritant used as a
dressing, and in recent years organic mercury preparations such
as mercurochrome, a compound of mercury and fluorescein con-
taining 25 per cent. of mercury, have been introduced as non-
irritant antiseptics. Organis:: mercury preparations are also used
for seed dressings to prevent attacks by moulds, and corn so
treated has been responsible for causing mercurial poisoning.
Absorption and Elimination.-The finely'divided metal as well
as mercury compounds are readily absorbed even from the intact
skin. Thus Harvey (I93z) records a number of cases of poisoning
lvIINERAL OR INORGANIC POISONS 53
in cattle from the application of mercurial ointments to the skin
in the treatment of ringworm; the compounds responsible were
the biniodide, nitrate, yellow oxide and blue ointment, so that
such dressings should be :used with great caution. Frohner (1907)
also records a case of poisoning by blue ointment absorbed from
the skin.
When finely divided mercury has access to herbage it may be
eaten as such, or possibly may be converted into the oxide, as in
the case quoted by Lander (Ig06).
In the stomach the soluble salts of mercury come into rapid and
intimate contact with the tissues, and thus exercise the powerful
corrosive. effects due no doubt in part to the acid ion, though
chiefly to that of mercury. The mercury albuminates, being
readily soluble both in proteins and in sodium chloride, cause the
drug to penetrate deeply into the tissues, and to pass into the
circulation in the form of albuminate.
The metal thus becomes distributed throughout the body, and
is stored mainly in the kidney and liver. It is eliminated from the
organs by most of the excretory channels, chiefly through the
intestines and kidneys. The elimination is in all. cases very slow.
For the most part calomel is converted in the intestines into the
black sulphide, and excreted as such in the freces, very little of
this salt being absorbed.
The toxic doses of mercuric chloride by the mouth are given
by Kaufmann (IgOI) as:
Horse 120 grains Sheep 60 grains
Ox 120 Dog 3-5 "

Symptoms.-Recorded instances of mercurial poisoning among


animals are rare, and the data unfortunately by no means always
complete or instructive.
Acute poisoning exhibits the usual sequelre of nausea and vomit-
ing where possible, with violent diarrhcea and straining, the stools
being watery or bloody. These symptoms are followed 'by collapse,
weakness of the pulse, irregular respiration, a subnormal tem-
perature, and death by shock; or if there is survival for several
days, acute gastro-enteritis", salivation, irritation of the kidneys,
and death :from exhaustion.
Characteristic of mercurialism is salivation or ptyalism, blanch-
ing of the membranes of the mouth, and loosening of the teeth,
probably caused by the local excretion of mercury. Hoare (1924)
54 VETERINARY TOXICOLOGY
points out the danger of using too strong mercurial lotions, and
has encountered salivation and even death in dogs after the use
of white precipitate ointment. Serious local inflammation of the
mouth and eyes with formation of pustules has also been noted
by the same authority in horses, caused by rubbing against a part
dressed with the biniodide ointment.
In the case observed by Frohner (1907) a horse was dressed
over the ribs, back, and quarters with blue ointment. The symp-
toms ensued after seven days, when the patient displayed loss of
appetite, diarrhrea, profuse nasal discharge, staring coat, pulse 68
and weak, temperature I02t O F. Pustules of I inch in diameter
formed at the points of application of the ointment, diarrhrea and
discharge increased, with extreme debility, depression, and dul-
ness of sensation, followed by death on the ninth day.
In the case observed by Lander (1906) the mercury had found
its way on to the herbage as the result of a fire in an explosive
works, but three months elapsed before the cattle began to die;
so that here, no doubt, there was chronic poisoning, but, unfor-
tunately, no record was given of the symptoms'.
Examples of the toxic effect of calomel are given by Dun
(I9IO), who observed irritant and general effects in horses by 3 to
4 drachms; in cattle by 2 to 3 drachms; in sheep by 15 to 30
grains; and in dogs by 6 to 30 grains, Such doses cause colic and
copious defrecation of green, or in dogs darker, freces, and if re-
peated for three or four days fretid diarrhrea, bad breath, soreness
of mouth, loss of appetite and condition, low fever, dysentery, and
death. A donkey was killed in sixteen days by fourteen daily doses
of I drachm, having exhibited salivation, fretid breath, soreness
of the gums, and loss of appetite and general condition. After
death the teeth were found to be loose, mucous membranes of
mouth and air passages blanched, those of the stomach and
intestines softened 'and covered in parts by mucus.
Gorton (1924) has placed on record observations of the mercurial
poisoning of cats and rats in a tlrermometer factory. With the
cats the first sign was unthriftiness, succeeded by partial paralysis
of the hind limbs. Inflammation of th~ gums and looseness o(the
teeth were observed. Treatment was unsuccessful.
In addition to paralysis, the rats s~em to have suffered from
abdominal distension, even ante-mortem.
Edwards (1942) records a case in which a shire gelding died as
the result of eating oats,which had been treated with a mercurial
MINERAL OR INORGANIC POISONS 55
dressing. In this case the symptoms were anorexia, extreme de-
pression and unsteady gait, together with a rapid, weak pulse,
accelerated respirations, gangrene of the lungs, and a bloody,
muco-purulent nasal discharge.
Post-Mortem Appearances.-Those observed by Frohner (1907)
were inflammation of the mucous membranes, hremorrhagic en-
teritis, necrosis, and perforation of the crecum, peritonitis, catar-
rhal nephritis, and inflammation of the spleen, and are noteworthy
in illustration of the fact that the gastric disturbances due to
mercury are also produced when the poison has been absorbed
otherwise than by the alimentary tract.
In acute poisoning there is formation of diphtheritic false mem-
branes, particularly in the large intestine. ~
Hirst (1862) has given a somewhat imperfect account of what
was probably corrosive sublimate poisoning in the pig, in which
rupture and perforation of the stomach and ulceration of the
mucous coats were prominent effects.
Treatment.-Chemical antidotes are white of egg, which pre-
cipitates albuminate, and thus checks the corrosive action.
'Sulphur, or liver of sulphur, acts by forming the insoluble sul-
phide. Potassium chlorate tends to counteract the salivation
characteristic of chronic mercurialism, whilst potassium iodide
is thought to hasten elimination.
When the injury is due to an ointment, the skin should be
thoroughly cleansed with warm soda or soap solution.
Chemical Diagnosis.-Mercury is deposited on copper in the
well-known Reinsch test, the delicacy being about 6~O grain of
mercury in 2 ounces of organic matter. Deposition ensues even
when one has to deal with mercurial organic compounds, such as
must be formed iIi the liver, for these- are broken down by the
hydrochloric acid used. Distinct globules, which may be collected
and weighed, are obtained on heating the coated copper in a dry
tube. If only traces are present, the sublimate on heating the
copper should be treated with iodine vapour, when the formation
of mercuric iodide, yellow when freshly heated, and gradually
changing to scarlet on keeping, affords a most characteristic
reaction. Mercury is also separated as the sulphide in the nitric
acid process of extraction of organic matter. The sulphide may be
dissolved in hydrochloric acid with the addition of a scrap of
potassium chlorate, and the solution Qof mercuric chloride then
reduced to insolu'Qle calomel, and eventually to metallic mercury
VETERINARY TOXICOLOGY
by means of stannous chloride. This is also a delicate reaction,
but is less characteristic than the iodide test.
Failure to obtain a positive result with the iodide reaction must
be taken as a decisive negative to the question of the presence of
mercury.
From the medico-legal standpoint it will have to be established
that no mercurial preparation has been given. After perfectly safe
and legitimate dosage of calomel, mercury is very easily found,
especially in the alimentary contents. And it must be remembered
that it is rarely possible to ascertain the form in which the metal
was given.
REFERENCES.
Dun, F. (1910), Veterinary Medicines, 12th ed.
Edwards, C. M. (1942), Vet. Rec., 54,5.
Fr6hner, E. (1907), Vet. j., 63,448.
Gorton, B. (1924), Vet. j., 80,49.
Harvey, F. T. (1932), Vet. Rec., 12,328.
Hirst, C .. (1862), Veterinarian, 8, 143.
Hoare, E. W. (1924), Veterinary Materia Medica and Therapeutics, 4th ed.
Kaufmann, M. (1901), Therapeutique et Matiere Medicale Veterinaire,
3rd ed.
Lander, G. D. (1906), Vet. j., 62,498.

COPPER.
Forms and Occurrence.-The commonest salt of copper is the
sulphate, or blue vitriol, or bluestone, which is often used as a
dressing for grain against the depredations of birds and as a pre-
servative, and thus may give rise to poisoning._
Copper preparations, such as Bordeaux mixture, are widely
used as sprays against parasites of the vine and other fruit trees.
The effects of copper arsenite, or Scheele's green, are more
correctly referable to the arsenic than to the copper.
Copper is dissolved by liquids containing organic acids from
copper vessels, and thus is sometimes taken up from cooking
vessels. Salts of copper are further used to give a green colour to
such preserves as pickles, but could not in this way give rise to
poisoning among animals.
Copper subacetate, or verdigris, is for!lled by exposing copper
to acetic acid vapour, and is occasionally used in medicine.
The most usual sources of the poison for animals are residues
from copper sprays used in orchards, gardens, etc.; over-dosage
with copper sulphate used as an anthelmintic; c?pper dust carried
MINERAL OR INORGANIC POISONS 57
by smoke from copper-smelting works; and there is also the pos-
sibility of poisoning as a result of preparing food in dirty copper
vessels as suggested by Ogilvie (1942).
Absorption and Elimination.-Copper is not easily absorbed
through the intact skin. In the stomach the salts of copper form
albuminates, which are soluble in an excess of the albumin.
solution, and it is therefore absorbed fairly quickly, transported
by the blood to the tissues, and deposited chiefly in the liver,
lungs, and kidneys.
Elimination by the bile and urine follows very slowly, the metal
being stored for several months.
Our laboratory experience, indeed, satisfies us that copper is
normally found in the livers of the domesticated animals. Thus, in
the dog it is present to the extent of about I in 40,000.
Physiological Effects.-Concentrated solutions, especially of the
sulphate and chloride, act as irritants, more dilute solutions
exercising an astringent and antiseptic effect, contracting the
capillaries, with arrest of secretions and disinfection of the surface.
Large doses produce amongst animals loss of appetite, nausea,
colic, diarrhrea, and fatal gastro-enteritis.
Small doses continued over a long time eventuate in chronic
poisoning. Thus, Ellenberger and Hofmeistet gave sheep from 7t
to 45 grains of copper sulphate per day, and observed death in
periods of from 50 to II4 days.
Baum and Seeliger (1898) similarly experimented on sheep,
goats, dogs, and cats, to which cuprohremol (a compound of copper
with hremoglobin), copper- sulphate, copper acetate, and copper
oleate were adminsitered over extended periods. They observed
great emaciation, weakness, loss of appetite, cramp, .and death.
The injection of non-irritant copper salts-e.g., double alkali
tartrates and albuminates-induces slow and weak locomotion,
and later paralysis, in which the heart and respiration are involved.
If the animal survives, violent and bloody diarrhrea, loss of flesh
and appetite, albuminuria, icterus and anremia may ensue.
The poisonous doses quoted by Kaufmann (1901) for the horse
and ox are 300 grains each of copper sulphate. Dogs withstand
daily doses of IO to 15 grains of copper sulphate, but may
succumb under the effects of 40 to 60 grains. Fifteen grains
of the sulphate injected into the jugular vein of a dog killed in
12 seconds.
Theiler (I9I2) (see under Arsenic) found that 22 grains of copper
VETERINARY TOXICOLOGY
sulphate is a safe dose for sheep, 45 grains and upwards causing
death from acute gastro-enteritis, although Rose (I933) records
the survival of five rams, after several weeks' illness, which had
received 200 grains of copper sulphate given as an anthelmintic.
Eden (I940) found that chronic poisoning could be set up in sheep
as a result of the administration of I'5 g. of copper sulphate daily
for thirty to eighty days.
Symptoms.-In acute cases the chief symptoms are intense
thirst, vomition where possible, the vomitus having a green to
blue colour, abdominal pain, profuse diarrhcea, and all the signs
of a severe gastro-enteritis. Weak, rapid pulse, accelerated res-
pirations, convulsions, coma and death. A case of acute poisoning
is recorded by Reimers (I908) in which four six-monthsAold foals
consumed wheat dressed with copper sulphate and were estimated
to have taken about 9,000 grains. After twenty-four hours all
were ill, and one dead. The symptoms observed were sweating,
muscular spasms, difficulty in standing and unsteadiness of hind
quarters, vacant look, pulse I05 per minute, temperature I06 F.,
and dark red conjunctivre. There was loss of appetite, great
thirst and passage of greenish-yellow fcetid freces. Schaper and
Liitje (r93I) also record acute cases of copper poisoning in which
15 per cent. of the sheep as well as a few cows and calves on fruit
farms became affected as a result of contamination of the herbage
with a mixture of copper sulphate and slaked lime used to spray
the fruit trees. In this case, the chief symptoms were accelerated
pulse and respirations, raised temperature and severe gastro-
enteritis.
Chronic poisoning occurs particularly amongst animals in the
neighbourhood of smelting works. Thus, W~iman (I939) records
that 25 per cent. of the cattle turned out on to p~sture contam-
inated with dust from a copper works were affected after six weeks.
In chronic cases the chief symptoms are loss of appetite, increas-
ing emaciation, weakness, staggering gait, digesfive disturbance
with constipation followed by diarrhcea, jC!,undice and hrematuria
indicating destructive changes in- the liver and kidneys, thickening
of the skin, and loss of hair and death in several weeks. In sheep
cedema of the ears and loss of wool may be noted.
Post-Mortem Appearances.-Inflammation of the stomach and
intestines with thickening of the mucous membrane, which may
be stained a green to blue colour, is the chief lesion in acute cases.
There may also be evidence of a hremorrhagic nephritis and de-
IIlIlNERAL OR INORGANIC POISONS 59
generation of the liver, which is usually enlarged and friable. In
the case of the foals quoted by Reimers (1908), the abdomen was
greatly distended and contained about a litre of reddish-yellow
serum; the stomach was full of food, mucous membrane inflamed
and thickened, that of the small intestine being also thickened
and covered with hremorrhagic patches; the liver enlarged,
brownish-yellow and friable; the spleen enlarged and kidneys
congested; the heart dark red and covered with hremorrhagic
patches.
In chronic cases, in addition to evidence of gastro-enteritis and
liver degeneration, there may be signs of a generalised icterus and
c:edema, together with myocarditis, nephritis and cystitis. The
post-mortem appearances of the chronic cases of Baum and
Seeliger (1898) varied. There was evidence of chronic catarrh of
the small intestine with thickening of the mucous membrane and
swelling of lymph follicles; swelling, inflammation, fatty degenera-
tion, atrophy and necrosis of the liver and kidneys; copious
deposits;f hremoglobin and subserous hremorrhages on the heart;
in one case there was general icterus.
Treatment.-The usual treatment for irritant poisoning should
be carried out. As chemical antidotes to copper, potassium ferro-
cyanide, fructose, lactose, iron filings, sulphur and animal charcoal
have been recommended. Egg albumin, milk and magnesia may
also be given, together with mucilages and stimulants. The source
of the poison should be removed if possible.
Chemical Diagnosis.-After destruction of the organic matter
by the method of Babo and Fresenius, the residue is dissolved
in dilute nitric acid, filtered and made alkaline with ammonia;
the production of a blue colour indicates the presence of copper.
The formation of the reddish-brown ferrocyanide on the addition
of potassium ferrocyanide is an exceedingly delicate test, showing
the presence of copper even when present in insufficient quantity
to respond to the ammonia test. For the quantitativ; estimation
of copper, the colour produced on the addition of potassium ferro-
cyanide may be compared with a standard solution prepared from
a known amount of copper.
From what has been said, it is evident that the detection of
copper in the liver or kidneys is no evidence of copper poisoning.
For example, Eden (I940) found the copper content of normal
sheep's liver varied between 02 to 29 mg. per 100 g. of tissue.
However. its presence in the stomach contents, vomit or freces,
60 VETERINARY TOXICOLOGY
if the quantity be considerable, will, together with the symptoms,
point to copper as the particular agent of the observed. corrosive
pOisoning.
REFERENCES.
Baum and Seeliger (1898), Vet. Rec., 11,249.
Eden, A. (1940)' J. Compo Path. and Therap., 53,9.
Ogilvie, D. D. (1942), Vet. Rec., 54,31.
Reimers (1908), Vet. I, 64,215.
Rose, A. L. (1933), Austral. Vet. J., 9,63.
Schaper and Liitje. (1931),.Berl. tieriirztl. Wschr., 47,36.
Theiler, A. (1912), South Afric. Agric. j., 3,321.
Weiman (1939', Dtsch. tieriirztl. Wschr., 47, 279.

ZINC .
. Forms and Occurrence.-Although metallic zinc and its com-
pounds are widely encountered, the poisoning of animals by them
is a rare event. The sulphate (white 'vitriol) fi"nds use as an emetic,
and is liable to be mistaken for Epsom salt, which has the same
crystalline appearance. The chloride is a very soluble and deli-
quescent substance, having a powerful corrosive action, and is
not given internally. The solution in water is faintly acid in reac-
tion, and constitutes Burnett's fluid, used as a strong disinfectant
for unhealthy wounds. A concentrated solution of zinc chloride
is used in plumbing, and a mixed solution of the chloride with
sulphurous acid used to be employed as a Idisinfectant.
Each of these salts is irritant, and causes poisoning. The double
salts with potassium or ammonium are less powerfully irritant.
The oxide and carbonate are extensively used as pigments-zinc
white-and in antifouling preparation for ships. They and the
salts of weak acids, such as zinc acetate and zinc benzoate, are
astringents, and are used internally in medicine.
Zinc phosphide has come into use as a chea:p rat poison. It is
usually mixed with grain or other suitable material and is ex-
tremely toxic, but its toxicityis due not so much to the zinc as to
the contained phosphorus.
Zinc cisterns and galvanised vessels yield zinc to soft water
under the same conditions as those governing the solution of lead.
Although poisoning from this source is rare, illness may be caused
from drinking water contaIning zinc; thus Blampied (I93 0 )
records illness amongst cattle from- drinking water containing
Ii grains of zinc per gallon. The metal is also dissolved by means
MINERAL OR INORGANIC POISONS 61
of org_anic acids from zinc-lined troughs and pipes, and so may find
its way into foodstuffs, particularly milk and milk products
which have been kept for any length of time in gal vanised iron
vessels owing to the formation of zinc lactate. Such cases have
been reported by Grimmet and McIntosh (1936), Grini (1938),
and others; as little as 0005 per cent. of zinc in milk being suffi-
cient to cause illness and deaths in pigs.
Apart from zinc-contaminated food, poisoning is only likely to
occur from the accidental administration of zinc chloride or
sulphate, in spite of the wide diffusion of zinc compounds. In the
latter case dogs and cats promptly reject the dose by vomiting,
and under proper treatment a fatal termination is unlikely.
Absorption and Elimination.-The insoluble compounds of zinc
are not very easily absorbed, being found only in traces in the organ
after lengthy dosage. The greater part of a dose of the oxide is
excreted as sulphide in the fieces. The soluble and irritant salts
are absorbed, and may be found in the liver, kidneys, and spleen.
Elimination takes place chiefly by the kidneys, but zinc is stored,
and only slowly eliminated from the liver. Thus, the author
found zinc in the liver of a calf which had received 100 g. of
zinc potassium chloride (equivalent to 42 grains of pure zinc
chloride) three weeks before death. One ounce of the organ
contained -;fIJ grain of zinc; there were traces in the kidney and
bile, but it was absent in the spleen.
Toxic Doses.-lJun (1910) found that l ounce of zinc sul-
phate daily for a fortnight had no marked effect on horses,
though larger doses caused loss of appetite, nausea, and diuresis;
and Graham, Sampson, and Hester (1940) failed to observe any
effects in mares which had received as much as 35 g. of zinc lactate
daily in the food for over a year.
In experiments with zinc potassium chloride the author found
that roo g. (nearly 4 ounces)_ caused illness, but was not fatal
to a young calf which had already received several smaller doses.
A full-grown sheep was not seriously affected by 20 g., but
was killed by 60 g. of the same salt.
When given intravenously zinc sulphate acts rapidly; thus
30 grains depresses the heart's action, and may kill a dog in a
few' seconds.
Symptoms.-Poisonous doses of zinc salts produce the general
symptoms of acute metal poisoning, and are not marked in
animals by remote effects.
62 VETERINARY TOXICOLOGY
In the case of the calf above referred to, the administration of
IOO g. of zinc potassium chloride caused at once blowing and
distress, the animal lying down. After twenty-four hours the
temperature was 98 F., pulse 88 (strong), fceces watery, abdomen
tucked up, back arched, and there were rigors of fore and hind
quarters. The symptoms passed off slowly, the animal remaining in
an emaciated condition.
In sheep and pigs the irritan't salts produce loss of appetite,
frothing, nausea, dulness, and general loss of condition.
Post-Mortem Appearances.-These are of acute gastro-enteritis.
A sheep poisoned by zinc potassium chloride showed slight in-
flammation of the first and third stomachs, but intense croupous
inflammation, with fibrinous exudate, of the fourth stomach. The
whole of the alimentary contents were very fluid and watery, and
there was diffuse but slight inflammation throughout the small
and large intestines and ccecum. Kidneys and liver were normal,
and the bladder empty. The lungs were highly engorged.
Treatment.-Alkali carbonates tend to render the zinc salts
insoluble, and may be given as antidotes. Gastro-enteritis is com-
bated by demulcents. Vomitories or the pump are used to remove
the cause.
Chemical Diagnosis.-Zinc is separated from organic matters
in the systematic analysis by means of nitric acid. Other metals
having been removed or proved to be absent, it is easily recognised
by giving the colourless sulphide as a precipitate when ammonium
sulphide or sulphuretted hydrogen is added to the ammoniacal
solution.
A delicate test consists in the precipitation of colouriess zinc
ferro cyanide by means of potassium ferro_cyanide from neutral
solutions, or in the presence of acetic acid. -
For the quantitative estimation of zinc, Birchner (I9IS) re-
commends a turbidity comparison. ,The zinc is precipitated from
the solution obtained after tne destruction of organic matter by
means of hydrogen sulphide in the presence of calcium citrate.
The pure zinc sulphide thus obtained is dissolved in dilute, hot
hydrochloric acid and the turbidity produced on the addition of
potassium ferrocyanide compared with the turbidity produced
by a known quantity of zinc when. . .similarly treated. .
As a point of medico-legal value, it may be observed that traces
of zinc'are very often found in alimentary contents, but must not
be taken as indicative of poisoning in the absence of concordant
MINERAL OR INORGANIC POISONS 63
symptoms and lesions. When, however, the metal is found in the
liver, there are stronger, though not absolutely conclusive grounds
for suspicion.
REFERENCES.
Birchner (1918), ]. Biol. Chem., 38, 191.
Blampied, T. Ie Q. (1930), Vet. Rec., 10,191.
Dun, F. (1910), Veterinary Medicines, 12th ed.
Graham, R, Sampson, J., and Hester, H. R (1940)' ]. A mer. Vet. Med.
Ass., 97,41.
Grimmett, R E. R, and McIntosh, I. C. (1936), New Zealand ]. Agric.,
53,34
. Grini, O. (1938), Norsk. Vet.-tidsskr., 50, 746.

SILVER.
Forms and Occurrence.-Metallic silver is not important from
the standpoint of pharmacy and toxicology. The commonest
soluble compound is the nitrate, very easily soluble in water, and
stable on heating, being fused and cast into sticks for use as lunar
C'alfstic. The halogen salts (the chloride and bromide) are very
extensively used in photography, but are not dangerous. The very
dangerous cyanide is also used in photography and largely in
silver plating. Colloidal silver is the metal reduced in the presence
of solutions of colloids, and is soluble. It is used in medicine, and,
like the organic salts the lactate or aciol, and citrate or itrol, does
not act as an irritant. An efficacious non-irritant silver preparation
is protargol, a compound of silver with albumose.
Poisoning by silver is rare, and the acute form follows .the
admirtistration of large doses of soluble salts. Accidents in the case
of the dog may result from the swallowing of a stick of lumar
caustic. Smaller and repeated doses give rise to the condition
known as argyria.
Absorption.-Soluble salts of silver form albuminates like those
of the heavy metals, and these are but slowly absorbed. The
astringent and caustic actions of the nitrate are thus confined to
the parts in contact. In the stomach the salts are decomposed by
the hydrochloric acid giving silver chloride, which is very sparingly
soluble in acids and water, but slightly dissolved by sodium
chloride solutiqn. The greater part of a dose of silver nitrate is
thus rendered unabsorbable, but in contact with organic matter
the chloride is reduced, and the silver converted into black silver
sulphide, which passes into the freces.
VETERINARY TOXICOLOGY
Nevertheless, some proportion is absorbed, and in the case of
prolonged dosage is deposited with blackening of the skin,
especially when exposed to light, in the condition known as
argyria.
Silver is stored in the liver, spleen, pancreas, and bones, and is
mainly excreted through the bile.
Toxic Doses.-Dogs are poisoned by from 30 to 60 grains of
silver nitrate. The larger animals would doubtless require doses of
considerable magnitude, but data on the point are wanting.
Symptoms.-Large doses of silver nitrate cause the symptoms
of gastro-enteritis, with vomition of blood-streaked clots in dogs.
Great prostration is caused with weakening of the heart's action,
and often paralysis, convulsions, and death from shock.
Chronic poisoning, argyria or argyrism is often attended in
animals by the same blackening of the skin as in man. There is
chronic indigestion, loss of appetite, weakness, an;emia, and
emaciation.
Post-Mortem Appearances.-Beyond the signs of gastro-
enteritis the lesions due to acute silver poisoning are not charac-
teristic. With large doses, and when vomition has not been
profuse, flakes of discoloured silver chloride might be noticed.
The bowel contents are black from the presence of silver sulphi<;le.
In chronic poisoning, there is fatty degeneration as with arsenic,
antimony, and phosphorus.
Treatment.-Sodium chloride is a chemical antidote td acute
silver poisoning, acting by formation of silver chloride. It must be
remembered that silver chloride dissolves slightly in salt solution,
so the dose given should not be disproportionately large, and
should be diluted. Demulcents and opium should follow the
ordinary measures to secure removal of the cause.
Chemical Diagnosis.-Silve~ is dissolved in the nitric acid
extraction process, and separated according to that scheme, as
sulphide along with the other 'metals (q.v.). In seeking for silver
the sulphides are to be extracted with warm nitric acid (not hydro-
chloric as in the ordinary routine), and the characteristic tests for
silver perfor,med on the solution of the nitrate. The precipitation
by hydrochloric acid of flocculent silver chloride, colourless, but
blackened on exposure to light, is characteristic. It should be
further shown that the chloride is soluble in excess of ammonia,
whereby it may be separated from the sparingly soluble lead
chloride, which does not dissolve in ammonia. From the ammonia
MINERAL OR INORGANIC POISONS 65
solution silver chloride is reprecipitated by acidifying with nitric
acid.
Other tests are also delicate, but most of them not very charac-
teristic. Thus potassium chromate from a neutral solution gives
reddish-yellow silver chromate, but confusion with the yellow
chromates of lead and barium is possible. Potassium iodide gives
yellow silver iodide, which in very small traces is not easily dis-
tinguished from other insoluble iodides, such as those of bismuth,
copper, and lead.
Phosphates and arsenites give yellow precipitates of the corre-
sponding silver salts, and arseniates give brown silver arseniate.
All these are only formed in the absence either of free acid or
ammonia, and are of little value in practical toxicology.
Silver also coats copper in Reinsch's test, and o~ warming the
copper with dilute nitric acid both metals dissolve to form the
nitrates. Hydrochloric acid precipitates silver chloride from the
solution of the mixed nitrates.

THALLIUM.
Forms and Occurrence.-Thallium is a heavy metal, found in
small amounts as an impurity in pyrites and zinc bien de, which
in many respects resembles lead in its toxicological action, but is
much more poisonous. The metal forms monovalent and trivalent
compounds, the toxicity of the monovalent salts being propor-
tional to their thallium content; also they are more toxic than the
trivalent salts. Thallous acetate and sulphate are the chief salts
encountered. .
In medicine, thallium is mainly used as a depilatory either in
the form of an ointment containing 5 to 10 per cent: of the
acetate or given by the mouth in single doses of 8 mg. per kg.
body weight, but numerous accidents have occurred, since the
depilatory and toxic doses are very close to one another, and its
use for this purpose is not to be recommended. The sulphate has
recently come into use as a vermin poison, as it is soluble, colour-
less, practIcally tasteless, and extremely efficient, but even when
all precautions have been taken the danger of accidental poisoning
of domestic anirp.als is very great, as Larson, Keller, and Manges
(1939) point out.
Absorption and Elimfnation.-The soluble salts of thallium are
rapidly absorbed even from the intact skin, but after absorption
5
66 VETERINARY TOXICOLOGY
there is the formation of the comparatively insoluble chloride, so
that the metal is only excreted slowly and becomes widely dis-
tributed throughout the body, particularly in the liver, brain, and
skeletal muscles. Approximately 60 per cent. of the thallium
absorbed is excreted in the urine, the remainder being excreted
in the bile, milk, and other secretions.
Toxic Dose.-The toxic dose of thallium both for animals and
man appears to be very constant, lying between I5 to 25 mg.
per kg. body weight, the general rule being that adults are more
susceptible to the effects of the poison than young animals.
Newsom, Loftus, and Ward (I930) found experimentally that the
minimal lethal dose of thallium sulphate for sheep when given
mixed with oats was 24 mg. per kg. body weight; with death in
nine days, and that the smallest dose which caused shedding of
the wool was 8 mg. per kg. body weight. McCrory and Ward
(I936) found experimentally that 25 mg. per kg. body weight was
the approximate minimal lethal dose- for cattle, with death in
fourteen days, and Ward (I93I) found that 25 mg. per kg. body
weight was the minimal lethal dose for the fowl.
Symptoms.-Even in acute cases symptoms set in gradually,
taking some days to develop. The chief signs of poisoning are in-
appetence, vomition, salivation, mucous discharge from the
nostrils, weakness, staggering gait, and evidence of an acute
gastro-enteritis. There is thirst, abdominal pain, the passage of
blood-stained, mucus-covered freces, and later diarrhrea, which
may alternate with constipation; finally, collapse and death,
probably from respiratory failure. Following- the ingestion of a
single sublethal dose of thallium, shedding of the hair as a result
of direct injury to the hair follicle occurs after an interval of a few
days to several weeks; depilation may also occur in acute cases
of poisoning. In chronic cases,- in addition tQ depilation and the
general symptoms associated~with a chronic intoxication, indica-
tion of damage to the central nervous system, such as muscular
tremors, paralysis, and convulsions, may be seen, death occurring
after several weeks' illness, most probably as a result of the injury
to the higher centres. .
Post-Mortem Appearances.-Th), chief lesions are an intense,
hremorrhagic gastro-enteritis with ulceration, particularly of the
stomach and abomasum; enlargement and fatty degeneration of
the liver, congestion of tbe spleen and kidneys, with evidence of
a parenchymatous nephritis and hyperremia of the brain. Larson,
MINERAL OR INORGANIC POISONS 67
Keller, and Manges (1939) describe the lesions in the central
nervous system as being characterised by fragmentation of the
axis cylinders, foci of softening in the basal ganglia, mid-brain,
hypothalamus, cerebellum, and pons, and the appearance of peri-
vascular cuffs of exudate round the arterioles in the basal ganglia
and mid-brain. In addition they record degeneration of the semin-
iferous tubules, necrosis of the myocardial fibres, h~morrhagic
pulmonary cedema, and general degeneration of parenchymal
organs.
Chemical Diagnosis.-The method ~depends on the conversion
of the thallium to the iodide and was first proposed by Lynch
(193 0 ). After destruction of the organic matter by the method
of Babo and Fresenius, the :6.ltrate is made alkaline with ammo-
nium chloride and ammonia and boiled to precipitate the phos-
phates, which are filtered off. Hydrogen sulphide is then bubbled
through the filtrate and the thallium sulphide so formed removed
by filtration. This is dissolved in hot dilute hydrochloric acid and
the solution made alkaline with ammonia and boiled, any pre-
cipitate which appears being filtered off and discarded. The
solution is then acidified with hydrochloric acid and excess of
potassium iodide added, when a precipitate of yellow thallium
iodide forms. This is collected, washed with potassium iodide
and alcohol until free from excess of iodide, dried, and weighed.
Thallium salts give a characteristic green band in the spectrum
which serves as identification.
REFERENCES.
Larson, C. P., Keller, W. N., and Manges, ]. A. (1939), ]. Amer. Ve1. Med.
Ass., 95,486.
Lynch, R. (1930), Lancet, 2, 1340.
McCrory, B. R., and Ward, J. C. (1936), J. Amer. Vet. Med. Ass., 89,301.
Newsom, 1. E., Loftus, ]. B., and Ward, ]. C. (1930), ]. Amer. Vet. Med.
Ass., 76, 826.
Ward, J. C. (1931), ]. Amer. Pharm. Ass., 20,1272.

BARIUM.
Forms and Occurrence.-Barium is the most toxic of the metals
of the alkaline earth series-calcium, strontium, and barium-,--
and cannot replace calcium in its relations to life; for instance, in
respect to blood coagulation, and bone formation. Barium is,
however, stated to be deposited in the bones in barium poisoning.
Of the salts, the sulphate, or heavy spar, is insoluble in water and
68 VETERINARY TOXICOLOGY
acids, and is consequently inactive. The carbol1ate is soluble in
hydrochloric acid and is therefore converted into the chloride in
the acid stomach. It is used as a component-of some arsenical rat
powders. The nitrate and chlorate are both soluble, and are used to
make green fires in pyrotechny. The chromate is used as a yellow
pigment, and barium also finds a limited application in glass
making. By reason of the great density of the barium compounds,
the sulphate is sometimes used to bulk fabrics, and has been
found in the coatings of cheeses. But there is no ground for regard-
ing this as likely to cause poisoning. In veterinary therapeutics
barium chloride is given intravenously in 8 to 20 grain doses to
the horse, or It to 2 or even 3 drachms by the mouth, and 75-
gramme drenches to cattle. It is e.mployed in impaction of the
colon, and causes violent contraction of the intestine.
All the preparations of barium excepting the sulphate, which is
harmless, must be regarded as dangerous. The use of barium car-
bonate as a vermin killer has been the cause of loss, especially
among sma,!l animals, within the author's more recent experience
(I9I8-1920).
Toxic Doses.-Sixty grains proves poisonous to dogs, and horses
have been killed by five daily doses of 75 grains of the chloride.
These isolated examples must be taken with reserve. By injection
far smaller amounts are dangerous. Thus Gray (1924) records.
convulsions and death in a large cart horse after intravenous
injection of 39 grains of barium chloride.
Symptoms.-When concentrated, the barium salts act as irri-
tants; but are not easily absorbed from the alimentary tract. By
whatever channel given l barium acts as a. powefu} purge, and when
possible causes vomiting. There is staggering, loss of control of
movements, and difficu~ty in standing.
Barium acts on the heart like' digitalis, the ventricular con-
tractions being slowed, and the heart eventually arrested in
systole. Given intravenously, barium causes clonic and tonic con-
vulsions, and the same general symptoms of vomition and purging.
Post-Mortem Appearances are not characteristic. Some in-
flammation of the stomach is seen after large doses of the soluble
salts. Congestion of the lungs, kidneys, and brain will be observed.
Treatment.-Soluble sulphates, sU,ch as those of sodium or
magnesium, are indicated as chemical antidotes, operating by
the formation of the insoluble barium sulphate. Removal of the
cause by purgatives, emetics, and the pump is required. When
MINERAL OR INORGANIC POISONS 69
given intravenously the prognosis is grave. The depressant action
is combated by stimulant and excitant drugs, and oxygen has
been recommended.
Chemical Diagnosis.-Since the sulphate of barium is so very
insoluble in acids, the salts of this metal are converted into the
sUlphate and lost in the residue of the nitric acid extraction process
used for lead. Special search may be made for barium in a hydro-
chloric acid or nitric acid residue, the former being preferable, as
nitric acid might oxidise barium sulphide to sulphate. By boiling
the clear extract in hydrochloric acid with calcium sulphate
solution, or dilute sulphuric acid, a white precipitate of the
sulphate is got. This is collected and .fused in a crucible with a
mixture of potassium and sodium carbonates. After washing with
water, the residue of barium carbonate is dissolved in acetic acid
and special tests applied-viz., formation of insoluble barium
sulphate with calcium sulphate, or sulphuric acid solution; for-
mation of yellow insoluble barium chromate by addition of potas-
sium chromate. To distinguish from lead, the acetic acid solution
is shown to give no black sulphide with sulphuretted hydrogen
and no insoluble iodide with potassium iodide.
REFERENCE.
Gray, H. (1924), Vet. j., 80, 50.

CHROMIUM.
Forms and Occurrence.-Chromic acid is a powerful corrosive
which destroys all tissues. The corrosive effect is shared to a less
extent by the orange potq,ssium bichromfl,te, and still less by the
yellow potassium chromate. The green basic, chromhtm oxide, is
stated to be harmless. Several cases of poisoning by potassium
bichromate, which is widely used in the arts, have been recorded
in man, and the salt appears to operate occasionally less by reason
of its irritant than by reason of its indirect nervous effects.
Chromates of lead and of barium are yellow paints very commonly
used, and large quantities of chromate are used in the chrome
tanning process for leather.
Toxic Dose.-That for the horse is given by Kaufmann (r90r)
as 450 grains, for the dog 45 to 60 grains, but according to
Desoubry (r906) 300 grains proved fatal to a horse.
Effects.-Chromates are never given internally, but are ab-
sorbed through wounds or through the skin, producing dyspnrea,
70 VETERINARY TOXICOLOGY
general lowering of the temperature, acceleration of the pulse,
convulsive movements, followed by weakness, insensibility, and
death. In the case referred to above, 300 grains of potassium
bichromate were given, to the horse in the morning in mistake for
sodium bicarbonate. In view of the fact that bichromate is orange
and bicarbonate colourless, this seems a most extraordinary
mistake, unless, indeed, the bicarbonate had been coloured by a
yellow dye.
There was no appetite in the evening, and on the next day there
were observed stiffness, frequent pulse, heart excited and irregular,
temperature rorlo F., respiration slow, mucous membranes
cyanotic, abdomen painful, intense thirst. Later the breathing
became hurried and short, the temperature rose to r02'7 F., and
the stiffness passed off; but in spite of treatment the animal died
forty hours after ingestion of the poison.
Post-Mortem Appearances.-On post-mortem the conjunctival
membranes were found to be covered with hremorrhagic .-spots,
the buccal membranes having small, shallow ulcers; the mucous
membranes of the stomach showed numerous blackish spots, the
small intestines were covered with a diphtheritic layer and con-
tained a blood-coloured fluid, as also did the large intestines; the
membranes of the lungs, heart, kidneys, blad'der, and spleen were
destroyed.
Chemical Diagnosis.-After destruction of the organic matter,
removal of insoluble sulphides by means of hydrogen sulphide
and filtration, the filtrate is evaporated to dryness and any
chromium present converted into chromate by fusion with
sodium carbonate and potassium nitrate; the perchromic acid test
may then be performed. A portion of the residue is acidified with
sulphuric acid and hydrogen peroxide added; a blue colour due
to the formation of perchromic acid which on shaking with ether
passes into the ethereal layer, indicates the presence of a chromate
in the residue. Chromates yield a reddish-violet colour in the
presence of a 0'2 per cent. solution of diphenylcarbazide dissolved
in nine parts of alcohol and one part of glacial acetic acid, and also
a green colour in the presence of sulphuric acid and a reducing
agent such as formaldehyde.
REFERENCES.
Desoubry (lg06). Vet. Rec., 19, 2g0.
Kaufmann, M. (IgOI), Th6rapeutique eb Matiere M6dicale V6t6rinaire,
3rd ed.
MINERAL OR INORGANIC POISONS 7l

IRON.
Iron filings are stated to act as a mechanical poison similar to
powdered glass, but such cases are rare, if not entirely absent,
from our literature. Nor are there recorded cases of poisoning by
sulphate of irolt (copperas, or green vitriol). This salt is not an
active irritant; it produces violent pain, vomiting, and purging
in the human subject.
Only a very small proportion of ingested iron is absorbed, and
it is extremely doubtful whether this salt would produce death,
at any rate in the larger animals. It is now agreed that a small
proportion of a dose of an iron preparation is absorbed, probably
in the form of albuminate, but the greater part of the material is
excreted as iron sulphide in the freces. When iron albuminate or
iron sodium tartrate, which do not coagUlate albumin, is injected,
poisoning results, but this is a case which does not come within
the range of practice. Absorption from the intestines is so slight
and so slow that poisoning does not arise when iron is given by
the mouth. A case is recorded by Hoare (l893) of death of cows
by iron perchloride. The symptoms noted were dulness, loss of
appetite, quick and weak pulse, hurried respiration, cessation' of
lactation, and obstinate constipation. Administration of mag-
nesium sUlphate caused inky-black evacuations. On post-mortem
examination the fourth stomach was found to be thickened and
perfectly black, with some erosion of the mucous membrane; the
intestines were slightly congested, and the contents black.
Analysis revealed an abnormal proportion of iron, stated as
equivalent to 285 drachms of iron perchloride per l'5 gallons of
liquid contents. As regards this case the effect must be ascribed
to the astringent and irritant action of the perchloride on the
alimentary system.
REFERENCE.
Hoare, E. W. (1893), Vet. Rec., 5, II8.

PHOSPHORUS.
Chemical Characters.-Of the numerous derivatives of the
element, only the "ordinary," free, or white phosphorus, and less
frequently the hydride, and hypophosphorous acid are of sig-
nificance in toxicology. Poisoning by the very highly toxic hydride
72 VETERINARY TOXICOLOGY
is not likely to occur outside the laboratory, although, when
calcium carbide contains traces of calcittm phosphide, phosphoretted
hydrogen is given by the action of water; and, moreover, calcium
phosphide itself is a moderately accessible substance,
Ordinary phosphorus forms a waxy solid, of characteristic
garlic odour, very inflamma.ble, and oxidised rapidly with emission
of a glow in the dark, Red, or amorphous, phosphorus is formed
from the ordinary on heating, is insoluble in oils and carbon
bisulphide, and is not toxic,
Preparations.-Those most likely to be met with are phosphorus
rat and mice pastes, which are made by incorporating finely divided
phosphorus with a suitable grease, and colouring with blue.
Although often marked as non-poisonous to cats and dogs, most
of the accidents with these animals and fowls are due to them.
The grease protects the phosphorus from rapid oxidation and spon-
taneous ignition, and also facilitates its absorption on ingestion,
Phosphorus matches are less likely vehicles, and are being rapidly
superseded by so-called "safety-matches," whose headls are free
of phosphorus.
Toxic Dose.-Great uncertainty exists as to the toxic dose of
phosphorus, and the figures given are to be accepted with reserve,
A great deal depends on the state of subdivisiort, a more finely
divided preparation being more easily absorbed. It has, indeed,
been stated that coarse particles are harmless, For the horse and
ox, 8 to 32 grains; pig, 2'5 to 5 grains; dog, 0'7 to r'5 grains; fowl,
0'3 grain.
Absorption and Elimination.-Dissolved or finely divided phos-
phorus is absorbed as such, absorption being facilitated by the
emulsifying action of the alkaline biie. Phosphorus is in part
oxidised in the alimentary tract, to which is ascribed its irritant
effect. In the blood stream it is carried to the tissues, and is
eventually oxidised to phosphoric acid. No positive evidence of
the formation of the lower phosphorous acid in the blood has been
obtained. It is excreted as phosphates in the urine. The free phos-
phorus in the blood is also in part given off in the lungs, and causes
the exhaled air to smell of phosphorus and to glow in the dark.
Symptoms.-Phosphorus acts as a iocal irritant on the mucous
membranes, but is only slowly absorbed, the onset of symptoms
being delayed some hours, and in exceptional cases days, after
taking. Uneasiness, nausea, vomiting, and eructation ensue; the
vomit, f<ecal and urinary excretions may be luminous in the dark,
MINERAL OR INORGANIC POISONS 73
as ,also may be the breath. There is fever, thirst~ and abdominal
pain. IIi the second phase jaundice and nervous effects, delirium,
convulsions and coma precede death, which may not occur until
after the lapse of several days. Jaundice is an almost invariable
concomitant, being attributable to the enlargement of the liver
cells preventing the flow in the bile-ducts.
Slow phosphorus poisoning in the dog might be compared with
canine typhus (Stuttgart dog disease; infective gastro-enteritis).
In birds, which are frequent victims of phosphorus poisoning,
there is great stupor, the patient being huddled up, beak open,
comb blanched; thirst, -diarrhcea, convulsions, and coma precede
death.
The chronic phosphorism, with its well-known necrosis of the
jaw, observed in workers in phosphorus is rare among animals.
Post-Mortem Appearances.-Besides inflammation and ulcera-
tion of the mucous membranes of stomach and intestines, there
is to be observed well-marked fatty degeneration, especially of
the liver, of the heart, and even of the skeletal muscles. The liver
is friable and yellow with occasionally red patches. The bile ducts
may be enlarged so as to obstruct the flow of bile and thus cause
jaundice. Perforation of the stomach has been observed in the dog
after taking phosphorised oil. The alimentary contents are usually
liquid and dark brown in colour, and the intestines often heavily
charged with bile.
Treatment.-The stomach should be emptied, if necessary, by
the tube. As an emetic copper sulphate is used. It may be repeated
as an antidote, being supposed to remove the poison in the form
of copper phosphide. A well-known antidote is -old-that is,
oxidised-French turpentine, but doubt has been recently ex-
pressed as to its value. Purgation may assist in the elimination
of the poison. Oils promote absorption, and must be avoided.
In treating the dog, give 3-grain doses of copper sulphate in
water every five minutes till vomiting is caused. Thereafter
I-grain doses every quarter of an hour, and if rejected combine
this with morphine.
Chemical Diagnosis.-The garlic odour and luminosity of vomits
clearly indicate phosphorus poisoning. In the case of the fowl the
crop acts as a storehouse of p~osphorus, which can be detected
(as free phosphorus) after death; but in the dog and cat at the
period of death the phosphorus will either have been eliminated
or more or less completely oxidised.
74 VETERINARY TOXICOLOGY
Scherer's test is a useful preliminary test which can be applied
directly to the material under examination. The test depends on
the fact that phosphorus vapour blackens filter paper soaked in
silver nitrate, but it must be remembered that other substances,
particularly hydrogen sulphide, have the same effect, so that,
whilst a negative result indicates the absence of phosphorus, a .
positive result must be confirmed by other tests. The material is
mixed with lead acetate solution, made acid with dilute sul-
phuric acid, and heated in a flask in the mouth of which a piece of
filter paper soa,ked in 5 per cent. silver nitrate solution is sus-
pended; blackening of the paper suggests the presence of phos-
phorus, but confirmation by means of a Mitscherlich test is neces-
sary. This latter test is carried out by distilling the suspected
material acidified with sulphuric acid, and allowing the vapour
to condense in a water-cooled, vertical condenser which is kept
in the dark. Phosphorus vapour as it condenses to the liquid form
is strongly luminescent. Certain volatile substances such as
alcohol, chloroform and essential oils prevent the phosphorescence
as long as they continue to distil over, so that heating should be
continued for some time. The residue in the flask may be tested
for phosphate by heating with ammonium molybdate after
boiling with nitric acid to oxidise any phosphorus which may be
present.
In a case investigated in 19II, a sow had died from phos-
phorus poisoning by having eaten the bodies of fowls similarly
poisoned. The ingesta of the sow's stomach contained frag-
ments of fowls, and free phosphorus was present in the pro-
portion of ! grain per ounce of ingesta. The gizzard of one of the
dead fowls gave t grain pbosphorus per ounce. After seven days'
exposure the material in each case no longer contained free phos-
phorus. After the phosphorus has been fully oxidised to phos-
phoric acid its detection is impossible, phosphates being -normally
present in ingesta and organs. In the lower stages of oxidation
the detection is, briefly, as follows: (a) ~ct gn the material with
zinc and dilute sulphuric acid, passing the gas through silver
nitrate solution. This yields a precipirttte of silver phosphide.
(b) Collect the silver phosphide, and introduce it into a hydrogen
generating apparatus, passing the hydrogen over solid caustic
potash. The flame is green, due to the presence of phosphoretted
hydrogen.
In this way evidence is easily obtainable. For instance, in a
MINERAL OR INORGANIC POISONS 75
recently observed case no free phosphorus or lower acid was
found in the viscera of a dog; and in the dried-up vomit several
days after emission no free phosphorus was present, but lower
acids were easily recognised.
In medico-legal work no case of phosphorus poisoning can be
established unless either free Phosphorus is found in the ingesta
or vomit, or, failing this, unless in the same materials the lower
acids are detected. The symptoms and lesions must also be con-
sistent with phosphorus poisoning. It is hopeless to attempt to
prove that the quantity of phosphate is excessive, phosphates
being found in all animal matter, and in the case of the dog in
particular in large and variable amount on account of the eating
of bones.
REFERENCES.
Beaudette, F. R., Hudson, C. B., and Weber, A. L. (1933), North. Amer.
Vet., 14, 39.
Danckwortt, P. W. (1935). Dtsch. tieriirztl. Wschr., 43,406.
Hastings, C. C. (1939), North Amer. Vet., 20,29.
Pritchett, H. D. (1939), Cornell Vet., 29,391.
Sassenhoff, I. (1939), Arch. wiss. prakt. Tierhlk., 74, 513.

AMMONIA.
Forms and Occurrences.-The only compounds of ammonia
of significance in toxicology are free ammonia and ammonium
carbonate. Free ammonia is encountered in the form of the solu-
tion in water-the so-called ammonium hydrate-or liquor am-
monice jortissimum, of the Pharmacopceia. It contains in con-
centrated condition 36 per cent. of ammonia, has the specific
gravity 088, and evolves ammonia gas on exposure to air.
Diluted ammonia is a 10 per cent. solution. Ammonia gas can be
easily condensed to a liquid by pressure, and is used to produce
cold in refrigerating plants by the rapid evaporation of the
liquefied gas. Dilute ammonia solutions along with soap form
popular cleansing agents and adjuncts to the bath. Along with
turpentine or vegetable oils and soap, ammonia, or the carbonate,
forms. valuable embrocations. Ammonia is present in coal-tar
liquors and coke-oven affluents, but the proportion is not high
enough to cause danger. The poisonous effects of such liquors are
due to other constituents, chiefly creosote. Mishaps occur some-
times through mistakes in dispensing, strong ammonia being taken
instead of ammonium acetate, dilute ammonia, or nitrous ether.
VETERINARY TOXICOLOGY
Such errors lead to serious results, involving injury to the mouth,
pharynx, and resophagus. .
Toxic Doses.-Ammonia and ammonium carbonate, especially
the former, possess a high degree of toxicity, although it is not
possible to state accurately the doses. Kaufmann (r90r) gives
480 grains as toxic for the horse, 1,000 for the ox, and 30 for the
dog; of the carbonate, for the horse 1,200 grains. Hertwig (I9II)
found that ! ounce of the shong solution, when diluted, had no
bad effect on horses, but that when concentrated I ounce killed in
sixteen hours, and 3 ounces in fifty minutes. These figures agree
with those quoted by Kaufmann.
Eflects.-Strong ammonia acts as a corrosive poison like the fixed
alkalis, destroying the tissues "by dehydration, solution of the
epidermic and epithelial cells, liquefaction of albumins, and
saponification of fats.
Ammonia is readily absorbed by the skin, lungs, and mucous
membranes, and exerts on all animals a stimulation of the reflexes,
marked by general excitation. When injected, ammonia produces
general tetanic convulsions, which are absent in a muscle after
severance of the motor nerve. In toxic doses coma, insensibility,
and paralysis follow the first transient period of violent excita-
tion. Ammonia and its salts are transformed in the liver into urea
and excreted as such in the urine.
The corrosive effects of strong ammonia are marked in the
mucous membranes of the mouth and pharynx, and in addition
the simultaneous inhalation of the gas gives rise to the bronchial
disturbances characteristic of it, the swelling of the membranes
of the larynx and trachea often causing asphyxia. The tendency
to the formation, as a secondary effect, of false membranes is
noteworthy.
The effect of ammonia on the blood is first one of deoxidation,
followed by dissolution of the corpuscles, and formation of
hrematin from the hremoglobin. The proteins combine to form
soluble ammonia albuminates, and the blood becomes incoag-
ulable, and dark brown or black in colour.
Symptoms.-Recorded instances of death from ammonia poison-
ing among animals are rare, but Verlinde (tgo6) observed a case
in Belgium. A steel cylinder of compressed ammonia fell from a
dray, and, being smashed, involved the driver and team for some
time in an atmosphere heavily charged with ammonia gas. Similar
accidents have been recorded amongst operatives of ammonia re-
MINERAL OR INORGANIC POISONS 77
frigerating plants. The symptoms observed in the horses were: cau-
terisation of the mucous membranes of eyes, nostrils, and cornea;
the buccal epithelia exfoliated in large flakes, exposing raw and
inflamed surfaces, from which blood exuded; blood-stained dis-
charge from both nostrils, which were partially obstructed by
cedematous swelling; the eyes were closed, eyelids swollen, and
tears flowed; respiration laboured and panting. On the next day
the observations were: dull, depressed, pulse 60, respirations 26,
temperature 39 C., no appetite. Intense photophobia keratitis
and muco-purulent conjunctivitis, with profuse yellow discharge
mixed with flakes of epithelium fro~ both nostrils. Frequent
short, painful cough and loud, sibilant rales, and dull patches
pointed to bronchitis, congestion, and pulmonary redema.
On the third day in the first case the pupil became visible and
appetite improved. About the twelfth day the animal became
convalescent, but bronchial complications lasted some time.
The second animal was, however, worse, broncho-pneumonia
and septicremia set in, and it was slaughtered on the tenth day.
Post-Mortem Appearances.-In the above cases there were
observed patches of purulent broncho-pneumonia; the bronchi
of greyish colour, the smaller filled with purulent casts containing
debris of mucous membrane. The lower borders of the lungs were
particularly implicated.
In a case of poisoning of a dog, observed some years ago, the
stomach showed violent inflammation, was distended with gas,
and contained brownish bloody fluid. Death had occurred in two
days after bloody vomiting at the end, but the symptoms unfor-
tunately were not under expert observation.
Treatment.-Ammonia poisoning is treated by dilute acids,
preferably diluted vinegar, as a chemical antidote; demulcents,
honey, and belladonna as a stimulant.
Chemical Diagnosis.-The recognition of free ammonia is a
matter of great case from the well-known smell and other pro-
perties of that substance. In the above-mentioned case the gas
contained in the stomach was ammonia, and 2 ounces of the fluid
yielded i- gr~in of ammonia on distillation. In seeking for ammonia
a precaution is necessary, since volatile bases of ammoniacal
odour may be found in putrefaction. The distinction, however, is
easy, since ammonium chloride does not fuse on heating, but
sublimes, and is ins.oluble in strong alcohol, properties not shared
by the chlorides of the organic bases.
VETERINARY TOXICOLOGY
In cases such as those of poisoning by vapour it need hardly
be remarked that chemical diagnosis is superfluous and im-
possible, for long before death, which results as an after-effect,
the absorbed substance will have been eliminated.
As a point of medico-legal significance, it must be remembered
that ammonia is developed in putrefaction. Judgment will there-
fore need to be exercised in expressing an opinion.
REFERENCES.
Hertwig, (I9II), See Dun, F" Veterinary Medicines, I2th ed,
Kaufmann, M. (I90I), TMrapeutique et Matiere Medicale Veterinaire,
3rd ed.
Verlinde (I906), Vet, j., 62, 526,

STRONG ACIDS AND ALKALIS.


Eflects.-The effects of concentrated alkalis (caustic soda and
caustic potash) and acids (sulphuric, nitric, and hydrochloric) are
due to the profound chemical action which they exercise upon the
living tissue, leading to its destruction, to intense corrosion, and
local lesion, followed by vomit ion , colic, purgation, exhaustion,
and death by shock.
All these agents attract water, and thus act as powerful de-
hydrants, a property which is, however, particularly characteristic
of strong sulphuric acid. The alkalis, further, decompose fats and
proteins; whilst the acids-in particular nitric acid-coagulate
the latter.
Corrosion of the mucous membranes of the mouth, tongue, and
pharynx will be observed.
When strong sulphuric acid is swallowed it casues retching, and,
if possible, vomit ion of blood-stained matter, with shreds of mucus.
The local irritation and swelling of the lips, tongue, fauc_es, and
throat are very marked, and cause suffocation.
Characteristic of nitri!;: acid is the intense yellow- coloration of
the epithelium, which has been known in man to extend through
the whole of the alimentary tract.
Dilute sulphuric or other acid is often given to horses to improve
condition. This it fails to do, and an overdose causes acute poison-
ing. If this treatment is persisted in, chronic disturbance of the
digestion, with serious loss of condition and general health,
results.
Concentrated alkali (caustic potash or caustiG soda) destroys
MINERAL OR INORGANIC POISONS 79
the membranes, and sometimes causes perforation. According to
Hertwig, 2 drachms of caustic potash in 6 ounces of water killed
a horse in thirty-six hours, and Orfila observed the death of a dog
in three days after having 32 grains.
Treatment.-The treatment of alkali poisoning is by means of
very dilute acids, preferably vinegar, followed by fatty oils, and
later sedative or stimulating agents; whilst in acid poisoning ,dilute
alkali-e.g., chalk, burnt magnesia, soap solution, weak soda
solution-is indicated, and later mucilaginous and stimulating
agents. .
Cases of poisoning by these agents are rare, and should they
occur offer little difficulty in diagnosis and treatment.
The question of alkali contamination of water may from time
to time demand attention. In a recent legal case it was held to
have been proved that a stream had been contaminated with
caustic soda, but there could be no doubt that the death of a
heifer which had access to the stream was certainly not due to
caustic alkali. I

An extremely interesting case of poisoning by hydrochloric acid


gas is reported by Stordy (1908). The fumes, which were of volcanic
origin, emanated from a small hole in a gully in the Kelong Valley,
Africa. Around the hole were the carcasses of buffaloes. Fowls tied
near the hole were rapidly affected, whilst a man who put his head
in it was seized with a severe headache and vomiting. Sheep, dogs,
and cows placed near the hole immediately began to heave
violently, collapse, and die~the sheep in a few seconds, the cows
within half a minute. Inhalation of ammonia assisted resuscitation
immediately after the first collapse. The gas proved to be that of
hydrochloric acid extending at a maximum height of 18 inches
from 20 to 30 feet of ground round the fissure.
Post-mortem revealed dark-coloured, incoagulable blood, and
the heart in all cases arrested in diastole.
Leccus (1915) observed injury to two horses as the result of
taldng oats which had been washed with hydrochloric acid to
improve their appearance. In ol}e case ulcerous stomatitis and
in the other gastro-enteritis were the most marked symptoms.
Warm bran, sodium bicarbonate, and access to pure water
assisted recovery in four days.
Chemical Diagnosis.-Valuable indications are afforded in nitric
acid poisoning by the yel10w colour imparted to the tissues, which
may, however, be marked by blood. The reaction of the contents
80 VETERINARY TOXICOLOGY
to test papers is a valuable guide, and the degree of alkalinity or
acidity should be determined and compared with that of the nor-
mally alkaline rumen or intestine contents and the normally acid
stomach contents respectively. To separate the acids or alkalis
from organic matter the process of dialysis through a parchment
membrane with water should be used. The suspected compound
may then be tested for in the purified dialysis liquid. Steyn (I939)
. considers that the vomit is the most suitable material for
analysis.
REFERENCES.
Leccus (1915). See Abstracts from Foreign Journals, Vet. Rec., 27, 516.
Steyn, G. D. (1939), Ondersterpoort J. vet. Sci., 13,347.
Stordy, R. J. (1908), J. Camp. Path. and Therap., 21, 75.

SODIUM.
Sodium Chloride.-It is generally accepted that large doses of
sodium chloride, or ,common salt, may lead to poisoning, par-
ticularly in the pig and fowl, although it must be stated that the
evidence for this is largely circumstantial. A diet containing a
high proportion of salt is not readily eaten by animals, and
attempts to produce experimental poisoning have not been very
successful. For example, a pig was given five daily doses of
I ounce, six of 2 ounces and six of 3 ounces of salt consecutively
mixed with its food. Although the 3-ounce doses were not eaten
readily, no abnormal effects were observed. Slavin and Worden
(I94I) fed pigs increasing amounts.of salt until the ration con-
tained 20 per cent. of salt without producing any ill-eHects save
slight diarrhcea in the case of one pig, and they also administered
single doses of salt, up to 8 ounces, to pigs without producing
symptoms of poisoning except vomition in one pig. Similarly,
Tochter (1935), having fed pigs with varying amounts of salt
added to the diet, concludes that salt has no toxic effects on pigs
when given in quantities up to 3 ounces daily provided that the
salt is given in gradually increasing amounts. Wautie (I935) also
failed to produce acute symptoms of poisoning, although up
to 4,000 g. of salt were consumed by pigs in the space of thirty-
three days. Daily doses of 250 g. produced intense thirst, diar-
rhcea, and polyuria, but no deaths. He suggests, however, that
the toxic effects of salt may be influenced by such factors as the
amount of water available, the type of food consumed, and the
tolerance of the animal.
MINERAL OR INORGANIC POISONS 8I
On the other hand, there are numerous cases recorded in which
animals have died following the ingestion of salt without there
being any other cause of death apparent. Clough (I928 and I929)
has collected a number of such cases in the fowl, the usual history
being that the fowl died suddenly, post-mortem examination
revealing no definite lesions, only a high concentration, up to 2
per cent. in some cases, of salt in the crop; and Worden (I94I) has
collected a number of cases in the pig. In one case, pigs died after
eating about 4 pounds of flour sweepings containing 32 per cent.
of sodium chloride, and 36 g. of the sweepings caused the death
of a rabbit within twenty-four hours. Edwards (I9I8) records the
death of pigs following the ingestion of floor sweepings from a
bakery which were found to contain 22 per cent. of sodium
chloride.
Circumstantial evidence of poisoning in cattle, sheep, and dogs
has also been recorded. In cattle and sheep, poisoning is'usually
ascribed to the fact that the animals have been gra:ling on salt
pastures, drinking water with a high salt content, or been given
large doses of salt. Scott (I924) observed salt poisoning of cattle
arising from drought conditions. In this case, a locked waterway
which served irrigation, boundary, stock water, and drainage
purposes was also the recipient of effluent from a salt works. By
reason of the silting up of the gates, due to the abnormal drought,
the water eventually attained a total salt concentration of no less
than I'7 per cent. in the vicinity of the grazing pastures. This
percentage is approximately one-half of that of average sea water
and nearly double that of physiological saline.
Damage was indicated by the beasts becoming emaciated, hide-
bound, with rough staring coats; lack of energy and profuse diar-
rhcea. Two pairs of healthy beasts were given sound fattening
rations, but one pair received "salted" water from the drain,
whilst the other pair received pure water. After a fortnight, the
pair on pure water had gained I75 pounds, the pair on salted
water had lost 358 pounds.
In addition to the symptoms noted above, there were observed
bronchial rales with peripheral crepitus and difficult breathing;
evacuations thin and watery, with considerable foul gas emission.
On the ninth day profuse diarrhcea, slightly hremorrhagic, and
tenesmus were seen.
Autopsy of two fatal cases showed great emaciation; dropsical
heart sac and thorax; cedematous lungs; inflammation of the
6
82 VETERINARY TOXICOLOGY
stomach and bowls. The flesh was watery, soapy to touch and
pale yellow. Blood was thin and showed lack of coagulatory power,
and diminution of both Ieucocytes and red blood corpuscles.
-Eighteen of the subjects of this poisoning aborted.
Since the practice of giving farge doses of salt to cattle in the
treatment of red water has, come in, dangerous effects of depres-
sion, abdominal pain, extreme thirst and often collapse have been
observed after doses of I to I t pounds, especially if not well
diluted, and Rambe (1935) 'considers that the practice of giving
freshly calved cows up to 250 g. of salt per day in the food is
responsible for producing anorexia, inanition, and pica.
Brine poisoning and poisoning by household swill is more
obscure, since the fluids usually contain other constituents besides
salt. It is not unlikely that brines may contain organic poisons
derived from the breakdown of proteins; herring brine, which has
been held responsible for some cases of poisoning, contains potas-
sium nitrate and the volatile base trimethylamine as well as salt,
and in the case of household swill containing salted potato there
is the possibility of poisoning by the alkaloid solanine contained
in the potato. Arising no doubt from the general acceptance of
salt poisoning as liable to afiect pigs, there is a widespread idea
that household waste liquors of all sorts may kill these animals,
but in a very large number of alleged salt or soda cases, analysis
of the stomach contents fails to reveal an excess of either sodium
chloride or sodium carbonate.
It may be concluded that whilst the question of salt poisoning
requires a great deal of further investigation, the actual recorded
cases are sufficient to establish its existence as a matter of practical
fact. '
Toxic Dose.-It is not possible to state the doses of salt necessary
to cause death; records indicate that from 4'5 to 7 pou~ds may
prove poisonous to cattle; from 2 to 4'5 pounds to the horse; and
from 4 to 8 ounces to -the sheep and pig. In the ,fowl, Ed'.Vards
(1918) was able to cause death following the injection into the
crop of 20 g. of salt dissolved in 70 mI.-of water, corresponding to
a dose of 10 g. per kg. body weight, and: French (1936) considers
that salt is toxic to fowls when fed in amounts greater than 2 per
cent. of the total food intake.
Symptoms.-There is no doubt that very large doses of many
salts can produce harmful effects, although the salt in question
has no specific action. All concentrated solutions of salts when
MINERAL OR INORGANIC POISONS 83
taken into the stomach and intestines cause osmotic disturbance
and. the withdrawal of water from the surrounding tissues which
may set up irritation and vomition, but in addition to the gastric
disturbances naturally to be anticipated, definite nervous symp-
toms appear to be associated with poisoning by sodium chloride,
particularly in cases of poisoning by brine.
From the recorded instances, the general symptoms of salt
poisoning in the pig involve loss of appetite, thirst, salivation and
diarrhcea; the animals may sit like dogs on their hind legs and then
roll over on to their sides; vertigo, dilation of the pupils, blindness,
and convulsions are also seen; the convulsions increase in fre-
quency and the subject loses power over the hind quarters; the
temperature is normal, but the ears and skin feel cold; death takes
place in convulsions. The onset of symptoms is rapid and death
occurs within three days.
Suffran (1909) describes a case in which thirteen out of fifteen
fowls died after eating a salted potato mash, symptoms setting
in within twelve hours. The birds fell from their perches, showed
signs of great thirst and weakness, and there was a viscous discharge
from the beak. Suffran (1909) produced experimental poisoning
in fowls by the injection of 4 g. per kg. body weight of salt into
the crop. The symptoms observed appeared to show a special
action on the muscles, illustrated by progressive' difficulty in
walking, with eventual inability to stand, but there was no true
paralysis because the muscles still exhibited reflex action. Death
was attributed to asphyxia, due to loss of power of the respiratory
muscles. The symptoms of somnolence, hyperresthesia and vertigo
seem further to indicate an action upon the nervous centres.
In cattle, the general symptoms appear to be intense thirst,
staggering gait, dilated pupils, rapid pulse, and muscular tremors.
Seven cattle given 12 kg. of salt dissolved in water showed agita-
tion, loss of appetite, suspended rumination, thirst, a slight
increase of pulse, and normal evacuations on the first day. On the
next day, the animals were recumbent; head and back legs ex-
~ended; foaming at the mouth, body cold, moaning, moderate
,:ympanites; evacuations liquid, greenish and mixed with mucus
and blood. Death occurred within twenty-one to twenty-four hours.
Post-Mortem Appearances.-General inflammation of the
mucous membranes of the stomach and intestines and injection
of the cerebral membranes appear to be the chief lesions, but, on
the other hand, no definite lesions may be discovered.
VETERINARY TOXICOLOGY
Treatment.-Symptoms should be treated as they arise.
Emetics, demulcents, and stimulants are indicated; cerebral
symptoms may be treated with bromide or chloral hydrate.
Chemical Diagnosis.-Salt may be separated from organic
matter most readily by diffusion or dialysis, and the recorded
cases show that a high concentration of salt in the ingesta can be
detected by this means, so that in most cases the chemical diagnosis
of salt poisoning is a matter presenting little difficulty, even allow-
ing for the fact that sodium chloride is a normal constituent of
the body fluids. On the other hand, this may not always be the
case, for the absqrption of salt is extremely rapid, and the salt
content of the ingesta may be found to be within physiological
limits a few hours after the ingestion of a large quantity of the
substance.
Sodium Chlorate.-In recent years, sodium chlorate in a 4 to
5 per cent. aqueous solution sprayed on to pastures has been
increasingly used as a cheap and convenient means of destroying
ragwort, buttercups, and other broad-leaved plants. Although its
toxicity is low and animals eat plants so treated apparently with-
out ill-effect, nevertheless cases of poisoning by sodium chlorate
have been reported. 1\1cCulloch and Murer (1939) record several
cases in which cattle and sheep died after grazing on pastures
treated with sodium chlorate, and Moore (1941) records the poison-
ing of fifteen cattle with six deaths following the application of
I,460 pounds of sodium chlorate to ~ acre of a lIo-acre field.
There is also no lack of experimental evidence of the toxicity
of sodium chlorate, as shown by Seddon and McGrath (1930),
Steyn (1933), and others.
Toxic Dose.-From the experimental evidence available, it
seems that the minimal lethal dose for' cattle is about 400 g.,
90 to 120 g. for sheep, and 5 g. per kg. body weight for fowls.
Steyn (1933) was able to produce fairly severe symptoms of
poisoning in a horse followi'ng the administration of I20 to 130 g.
of sodium chlorate, and two sheep, one weighing 40 kg. and the
other 45 kg., died within twenty hou'rs of the last dose following
the administration respectively of 15 g. daily for three days and
30 g. daily for two days. Seddon and McGrath (1930) found that a'
steer became ill after the consumption of 266 g. of sodium chlorate
mixed with bone mt;al over a period of fourteen days and state
that certain cattle show a liking for the substance.
Symptoms.-The chief effect of chlorates in tg,e body is to bring
MINERAL OR INORGANIC POISONS 85
about the formation of methremoglobin and hrematin from hremo-
globin or oxyhremoglobin probably owing to their oxidising
action. Very little of the chlorate ion appears to be used up in this
process, so that the reaction is severe and prolonged. In addition,
they cause hremolysis and hremoglobinuria. Excretion is mainly
by way of the kidneys, but also by the saliva, mille, sweat and other
secretions when there is a rapid reduction of the chlorate to the
chloride.
In sodium chlorate poisoning, whicH may be acute or subacute,
the symptoms are mainly referable to the rapid formation of
methremoglobin. In acute cases, there is vomition where possible,
dyspnrea, rapid pulse, collapse and death within a few hours.
In subacute cases, there is loss of appetite, cessation of rumination,
gastro-enteritis, rapid pulse,. dyspnrea, and a raised temperature.
A dark discoloration of the visible mucous membranes with
ecchymoses and, at times, evidence of a hremolytic jaundice may
also be observed. Blood samples when first drawn appear a dark
chocolate brown colour, which lightens on exposure to air.
Post-Mortem Appearances.-The most characteristic lesion of
sodium chlorate poisoning is the dark, almost black appearance
of all the tissues and organs of the body due to the presence of
large quantities of methremoglobin. The organs are hyperremic
and patches of inflammation with hremorrhages may be present
in the mucous membrane of the alimentary tract, particularly
in the abomasum and upper part of the duodenum. Enlargement
of the spleen, redema of the lungs, hepatic degeneration, nephritis,
and evidence of hremoglobinremia may also be observed.
Treatment.-McCulloch and Murer (I939) were unable to find
a successful antidote for sodium chlorate poisoning in the sheep,
but the administration of reducing agents such as sodium thio-
sulphate and alkalis such as sodium carbonate is indicated and
may be helpful provided that the interval between ingestion of
the poison and the administration of the. antidotes is short.
Inhalations of oxygen, artificial respiration, and blood transfusion
have been found to be of value in the treatment of chlorate poison-
ing in the human subject. Since the beneficial effect of the intra-
venous injection of methylene blue in cases of methremoglobin-
remia (see Nitrates) seems to be established, this drug may also
be ofyalue in the treatment in cases of chlorate poisoning.
Chemical Diagnosis.-Owing to the .fact that chlorates are
rapidly reduced to chlorides in the presence of organic matter,
86 VETERINARY TOXICOLOGY
their chemical detection in cases of poisoning is extremely diffi-
cult. An attempt should be made to separate the chlorate from
organic matter by dialysis as soon as possible, and the dialysate
concentrated and tested for the presence of chlorate. This may be
done by means of ammonium thiocyanate paper or a few drops
of potassium iodide, starch solution, and acetic acid may be added
to the concentrate, the formation of the blue starch-iodine com-
pound indicating the presence of a chlorate. However, in spite
of the difficulty of demonstrating- the presence of a chlorate,
diagnosis of sodium chlorate poisoning should present little diffi-
culty if consideration be given to the symptoms, post-mortem
findings, and the presence of large amounts of methremoglobin.
The latter substance is best detected by shaking some blood with
water and submitting the solution to spectroscopic examination.
Sodium Carbonate - and Bicarbonate.-These are weak alkalis
which have on occasion been held responsible for poisoning
animals. Frohner (1927) observed mness in a cow which had re-
ceived 800 to 900 g. of sodium carbonate, and Reid (1921) records
the death of 150 sheep as the result of drinking water contaminated
by the effluent from a dairy factory which was found to contain
a large quantity of sodium carbonate. Linton and Wilson (1933)
record that flo_or sweepings containing 33'7 per cent. of sodium
bicarbonate caused illness- amongst five sows with one death.
In the fowl, Witter (1936) was able to produce a condition resem-
bling visceral gout, together with injury to the kidneys, particu-
larly in young 'chicks, following the addition to the drinking water
of as little as 06 per cent. of sodium bicarbonate.
In such cases the chief symptoms are thirst, severe abdominal
pain, and evidence of gastro-enteritis. On post-mortem examina-
tion, patches of inflammation are present in the alimentary tract,
particularly the stomach, with redema and thickening of the
mucous membrane and hyperremia of the small intestine.
Treatment should follow the usual lines for poisoning with alkalis,
and the chemical diagnosis should present little difficulty, although
in cases where the examination is delayed it may be impossible
to recognise the particular alkali responsible for the poisoning.
REFERENCES.
SODIUM CHLORIDE.
Clough, G. W. (1928), Vet. Rec., 8,247.
Clough, G. W. (1929), Vet. Rec., 9,1099.
Edwards, J. T. (1918), ]. Compo Path. and Therap., 31,40.
MINERAL OR INORGANIC POISONS 87
French, M. H. (1936), Rep. Dept. Vet. Sci., Tanganyika, 1935,25.
Rambe, I. (1935), Svensk. Vet-Tidskr.,-40, 30r.
Scott, W. ,(1924), Vet. ]., 63,19.
Slavin, G., and Worden, A. N. (1941), Vet. Rec., 53,694.
Sufiran, F. (1909), Rev. gen. Med. vet., 13, 698.
Tochter, J. F. (1935), Vet. Rec., 15,477.
Wautie, A. (1935), Ann. Med. vet., 80,253.
Worden, A. N. (1941), Vet. Rec., 53,695.

SODIUM CHLORATE.
McCulloch, E. C., and Murer, H. K (1939),]. A mer. Vet. Med. Ass., 95,675.
Moore, G. R (1941), J. Amer. Vet. Med. Ass., 99,50.
Seddon, H. R, and McGrath (1930), Agr. Gaz., New South Wales, 41, 765.
Steyn, D. (1933), Ondersterpoort ]. vet. Sci., 1, 157.

SODIUM BICARBONATE.
Frohner, E. (1927), Lehrbuch der To xi kola gie , 5th ed.
Linton, R G., and Wilson, A. N. (1933), Vet. ]., 89,80.
Reid, H. A. (1921), Vet. j., 78, 177.
Witter, J. F. (1936), Poult. Sci., 15,256.

NITRATES.
Sources and Doses.-The nitrates of sodium and potassium have
both been known to give rise to poisoning, the general character
of which is not unlike salt poisoning, and attention was drawn to
the question at an early date. Sodium nitrate is very commonly
used in the form of Chile saltpetre as a manure. This may be con-
sumed after it has been spread on the pastures in sufficient
amount to cause toxic effects, as Crawford (I94I) records, or
animals may have acc~ss to the sacks or containers in which the
manure has been stored; it may also be admInistered in mistake
for Glauber salt (sodium sulphate). There is also ample evidence
to show that certain plants may contain sufficient nitrate to render
them toxic when consumed by animals; thus, Bradley, Eppson
and Beath (I939) proved conclusively that the toxic principle in
oat hay was potassium nitrate, and Williams and Hines (r940)
showed that nitrate is the toxic principle of Saliva rejtexa, the
mint weed of Australia.
The toxicity of nitrates is usually regarded as being low. Smith
(r898) gave potassium nitrate to two bullocks in daily doses of
8 ounces, increased to ro ounces twice, and then to I2 ounces
three times without ill-effect; and Seekles and Sjollema (r932)
found that a cow could consume 300 g. of potassium nitrate in a
day without evidence of poisoning. On the other hand, three
88 VETERINARY TOXICOLOGY
bullocks died after having I pound each of a mixture containing
80 per cent. of potassium nitrate and zo per cent. of magnesium
sulphate. Hoare (I924) records the death of four cows which had
received I pound of potassium nitrate sold in mistake for Epsom
salt, and Taylor (I9I8) records a similar case in which a cow was
killed by I pound of potassium nitrate. Seekles and Sjollema
(I93Z) were able to set up symptoms of nitrate poisoning by the
administration of 100 to ZOO g. of potassium nitrate directly into
the rumen, and Williams and Hines (I940) caused the death of a
sheep by drenching with 80 g. of potassium nitrate dissolved in
It litres of water. With regard to nitrate-containing plants,
Bradley, Eppson and Beath (I939) found that 15 pounds of oat
hay containing 7'2 per cent. of potassium nitrate was sufficient
to kill calves.
Symptoms.-Following absorption, a portion of the nitrate is
reduced to nitrite and slowly absorbed and eliminated in the urine
and other secretions. The effect of the poison is in part due to an
irritant action, partly to the action of nitrite on the vascular
system, and mainly to the formation of methremoglobin, toxic
symptoms being shown when the concentration of methremo-
globin reaches about 50 per cent. There is abdominal pain, tym-
panites, rapid pulse, dyspnrea, and abortion in pregnant animals;
there may also be a staggering gait, muscular tremors, severe
diarrhrea, convulsions, dilation of the pupils, and collapse.
Post-Mortem Appearances.-Evidence of a gastro-enteritis, par-
ticularly inflammation of the abomasum, may be observed, to-
gether with hyperrePlia of the liver and kidneys and all the signs
associated with a methremoglobinremia.
Treatment.-Bradley, Eppson and Beath (I940) report that
the intravenous injection of 2 g. of methylene blue in a 4 per cent.
solution protected cattle against doses of up to 350 g. of potassium
nitrate, and Scott (I94I) was able to bring about the recovery of
a sheep experimentally poisoned by 80 mg. of sodium nitrite per
kg. body "veight by the intravenous injection of 10 ml. of a 06
per cent. 8olution of methylene-blue in normal saline, so that it
seems that methylene blue should be a valuable agent for the
treatment of nitrate poisoning, provided that the methremo-
globinremia is not greater than 70 per cent.
Chemical Diagnosis.-After evaporation of the dialysed fluid,
sodium or potassium nitrate may be easily recognised. A delicate
test for nitrate is the addition of a .few drops of concentrated suI. .
MINERAL OR INORGANIC POISONS 89
phuric acid and a crystal of brucine, when a bright red colour is
produced; nitrites may be tested -for by'the Griess-Ilosvay test,
using a-naphthylamine and sulphanilic acid. For the quantitative
estimation of nitrates Williams and Hines (I940) recommend a
colorimetric estimation, using phenol disulphonic acid as the
reagent.
REFERENCES.
Bradley, W. B., Eppson, H. F., and Beath, O. A. (1939), J. A mer. Vet
Med. Ass., 94, 54!.
Bradley, W. F., Eppson, H. F., and Beath, O. A. (1940), J. A mer. Vet.
Med. Ass., 96, 41.
Crawford, M. (1941), Vet: Rec., 53,650.
Hoare, E. W. (J924), Veterinary Materia Medica and Therapeutics, 4th ed.
Scott, M. 1. R. (1941.), Aust. Vet. j., 17, 7I.
Seekles, L., and Sjollema, B. (1932), Vet. Rec., 12,1416.
Smith, S. M. (1898), Vet. Rec., 11,85.
Taylor, H. (1918), Vet. Rec., 31, 1.
WiIIiams, C. H., and Hines, H. 1. G. (1940):A1I5t. Vet. j., 16, {4.

SULPHUR.
In large doses sulphur is poisonous, cases of death in the horse
and dog being on record. .
Impure sulphur is liable to contain arsenic and free sulphuric
acid; but the poisoning is not to be attributed to these, for in one
case sulphur which had caused the death of horses was proved by
analysis to be free of these impurities.
Free sulphur is not acted upon by the acid gastric juices, but
in the intestines it is converted, to a small extent, into the soluble
and absorbable alkali sulphides, and is further reduced to sul-
phuretted hydrogen, which enters into the circulation, so that not
only is sulphuretted hydrogen given off per rectwm, but also may
be detected in the exhaled air.
It is to be remarked that sulphuretted hydrogen is intensely
poisonous, an atmosphere containing I per I,OOO of that gas being
held to be rapidly fatal to man.
The formation and absorption of these products lio doubt
accounts for the nervous effects of sulphur poisoning, which, for
the rest, is characterised by the production of super-purgation
and its attendant weakness and collapse.
Toxic Doses.-The purgative dose for the horse and ox is given
by Kaufmann (I90I) <l;s from 7 to 14 ounces. Percy (I9IO),
Ales (1907), and Mosselman and Hebrant (1898) found that in
90 ,VETERINARY TOXICOLOGY
one case horses were killed by 8 ounces each, in a second by
10 ounces each, and in a third by 10 to 14 ounces each. Harvey
(I924) records that 8 ounces killed a heifer in forty-eight
hours.
Symptoms.-The onset of symptoms is fairly rapid-from three
to eight hours after dosage. In the horse, dulness, pain, and diar-
rhrea, with black or grey liquid fceces smelling of sulphuretted
hydrogen, and highly coloured acid urine, sometimes albuminous,
have been observed. The conjunctivce and other mucous mem-
branes are injected, the respiration rapid and laboured, pulse
weak and rapid, temperature 1040 F., extremities cold; great de-
pression and tottering gait are followed by death within a few
hours, or gradual recovery under treatment.
Hebrant (I900) records that in a case of a dog, eight hours
after administration of a large unknown dose of flowers of
sulphur, there was violent colic, diarrhrea, and vomition, the
ejections being at first bloody, and afterwards consisting of pure
blood; pulse almost imperceptible and coma. In this case there
was recovery after twenty-four hours.
Post-Mortem Appearances.-Intense inflammation of the gastric
and intestinal mucous membranes, which are sometimes gan-
grenous. The blood is dark coloured and fluid; viscera and lungs
engorged; fibrinous clots in the portal venous system, spleen, and
liver; all the tissues and fluids of the body smell strongly of sul-
phuretted hydrogen. Particles of sulphur may be noticed in the
stomach, intestines, and fceces.
Treatment.-In one case castor oil, eggs and milk, chlorodyne
and whisky, were successful in curing horses so treated. In
another case milk, flour, gruel, white of eggs, subnitrate. of bis-
muth, and rice-water enemata were employed.
Chemical Diagnosis.~Earticles of sulphur may be recognised
by inspection. If no such particles are found, the material -is
thoroughly dried in the steaIl1; overt, extracted with carbon bi-
sulphide, and the sulphur recovered by evaporation of the liltered
solution. In this way sulphur in the proportion of 2t grains per
ounce and 21- grains per ounce has been recovered from the
stomach and colon contents respectively of a horse. It may also
be mentioned that the extraction of sulphur is frequently a
valuable guide as to the sources of arsenic (from sheep dip) or
antimony (from condition powders) in cases of'poisoning by those
agents.
MINERAL OR INORGANIC POISONS 91
REFERENCES.
Ales (1907), Vet. j., 63, 254.
Harvey, F. T. (1934), Vet. Rec., 4, 1023.
Hebrant (1900), Vet. Rec., 13,167.
Kaufmann, M. (1901), Therapeutique et Matiere Medicale Veterinaire,
3rd ed.
Mosselman and Hebrant (1898), Vet. Rec., 11,249.
Percy, H. W. (1910), Vet. j., 66,29.

SELENIUM.
The condition variously referred to as "Blind Staggers,"
"Alkali Disease," or "Locoism," causes considerable losses
amongst stock, particularly in certain parts of the Western Great
Plains of the United States, Western Canada, and elsewhere. The
disease has been known for many years and was first recorded
by Marco Polo in the thirteenth century, who encountered it in
Western China and correctly observed that it resulted from the
ingestion of certain plants. The first modern description of the
disease was given by Madison (1860), who recorded it as occurring
in cavalry horses, but it was generally ascribed to drinking water
contaminated with some "alkali" or simply to the effects of
extreme cold, and it was not until Robinson (1933) demonstrated
the presence of toxic amounts of selenium in plants grown on
affected areas that the true cause of the disease came to be
realised. It was then established by Franke (1934) and others
that the dis~ase only occurred in animals kept in seleniferous
areas or fed on food grown in such areas, and that the removal of
selenium from the diet caused the disease to disappear, so that
there is now no doubt that the condition is in fact selenium
poisoning.
Selenium occurs together with sulphur, and shows a close
analogy in its chemical behaviour to the latter substance. In soils
it is found in the form of the element or as inorganic or organic
compounds, but from the toxicological point of view it is the
amount of selenium available to the plant which is of importance.
This question has received much attention, and the work of
Franke and Painter (1937) and others has clearly shown that
inorganic selenium compounds are comparatively insoluble, and
that in many cases the selenium, probably in the form of selenite,
is firmly bound to the soil, so that it is not available to the plant;
on the other hand, organic selenium cor1\pounds are more soluble
VETERINARY TOXICOLOGY
and appear to be absorbed fairly readily by plants. The rainfall
in seleniferous areas is also of som.e importance in this connection,
since where the rainfall is low, the soluble selenium compounds
will not be washed away and dangerous amounts will accumulate
in the soil; on the other hand, where the rainfall is high, the
amount of available selenium in the soil is likely to be low. In
addition to these considerations, the ease with which plants
absorb selenium varies considerably, Beath, Gilbert, and Eppson
(I937) established that certain plants, particularly Astragalus,
Stanleya, and Oonopsis species, readily absorb selenium, and on
their decomposition leave behind organic selenium, which thus
becomes available to other plants, such as cereals, which normally
do not take up any great amount of selenium from the soil. For
this reason, these species have been termed "indicator" or "con-
verter" plants, since they are found growing abundantly on
seleniferous soils and convert the selenium which they themselves
have taken up into a readily available form. For example, a
common converter plant such as Astragalus bisulcat1tS may
contain as much as 2,000 to 6,000 parts of selenium per million.
In plants and in animals selenium follows the metabolism of
sulphur, the greater part being built up into the protein molecule,
as was shown by Horn and Jones (I940), who were able to isolate
a crystalline amino-acid containing selenium; a little may also
be present in the elemental form. Plants containing more than
5 parts of selenium per million must be considered dangerous and
unsuitable for fodder. As a rule, animals avoid plants with a high
selenium content, but they will consume them when other foods
are scarce.
Symptoms.-Poisoning may be acute or chronic; in the former
case it is usually called "Blind Staggers," and in the . latter
"Alkali Disease." In acute cases, symptoms set in rapidly and may
be present within eight days or so of the ingestion of a seleniferous
diet. An affected animal loses weight) has a poor, staring coat,
wanders away from the rest of the herd, and develops a staggering
gait and impairment of vision. As the .disease progresses the
animal moves .in circles, and, owing to increasing blindness,
cannot avoid obstacles; there is salivation, lachrymation and
severe abdominal pain, inability to swallow, and finally complete
paralysis, collapse, and death from respiratory failure. In chronic
cases the characteristic symptoms are loss of copdition, depraved
appetite, anq damage to the extremities as a result of failure of
MINERAL OR INORGANIC POISONS 93
the peripheral circulation. Rings appear on the hoof just below
the coronary band, the hoof becomes overgrown and deformed,
but does not fall off, which produces a characteristic high-stepping
gait~ and there is increasing lameness, mainly as a result of
erosion of the articular surfaces of the long bones. Signs of the
disease may be present at birth, and deformities, especially in
chickens hatched from eggs laid by fowl fed seleniferous grain,
are frequently observed.
Post-Mortem Appearances.-Draize and Beath (1935) found
that congestion of the bloodvessels, evidence of stasis of the
gastro-intestinal tract, congestion and necrosis of the liver, and
engorgement of the gall-bladder are the chief lesions present in
acute cases of poisoning. Evidence of inflammation and degenera-
tion of the epithelium of the abomasum and small intestine,
petechial hremorrhages on the endocardium, congestion of the
lungs, and erosion of the articular surfaces of the long bones may
also be observed. In chronic cases atrophy of the heart is pro-
nounced, and there is evidence of inflammatory changes in the
endocardium and myocardium, the liver is atrophied and cirrhotic,
the spleen and lungs congested, and there is a glomerular nephritis
and inflammation of the gastro-intestinal tract.
Treatment.-Davidson (I940) found that treatment of acute
cases may be successful if carried out before the stage of paralysis
is reached. The treatment consists of hypoder:mic injections of
strychnine repeated at two-hourly intervals until three to four
doses have been given, together with copious draughts of hot
water every two hours for two days. Moxon et al. (1940) found
experimentally that the administration of p-bromobent;ene to
dogs and cattle increased the urinary excretion of selenium ~?
such an extent that the latter disappeared from the blood stream,
so that this s~ould prove to be a valuable therapeutic agent in
cases of poisoning.
Chemical Diagnosis.-Since. selenium in biological material is
in organic form, Painter (1941) recommends the complete oxida-
tion of organic matter. Selenium gives various colour reactions,
the best reagent to use being codeine phosphate. The material
is dissolved in IO m!. of sulphuric acid, heated for thirty
minutes with I ml. of 30 per cent. hydrogen peroxide, and
2 drops of 4 per cent. codeine phosphate added. A green colour
changing to bluish-green develops on standing. This reaction has
been proposed by Schultz and Lewis (1940) as a satisfactory
94 VETERINARY TOXICOLOGY
method for the colorimetric estimation of selenium, using sodium
selenite in concentrated sulphuric acid as the standard.
REFERENCES.
Beath, O. A., Gilbert, C. S., and Eppson, H. F. (1937), A mer. J. Botany,
24,96 .
Davidson, W. P. (1940)' Canad. J. Camp. Med,. 4, 19.
Draize, J. W., and Beath, O. A. (1935), ]. Amer. Vet. Med. Ass., 86, 753.
Franke, K. W. (1934), J. Nutrit., 8, 597.
Franke, K. W., and Painter, E. P. (1937), Ind. Eng. Chem., 29, 291.
Horn, M. J., and Jones, D. B. (1940)' ]. Amer. Chem. Soc., 62,234.
Madison, T. C. (1860), U.S. Congr., 36th Session, 52,37.
Moxon, A. L., et al. (1940)' ]. Bioi. Chem., 132,783.
Painter, E. P. (1941), Chem. Rev., 28,179.
Robinson, W. D. (1933), j. Ass. Official Agr. Chem., 16,4 23.
Schultz, J., and Lewis, H. B. (1940)' ]. Bioi. Chem., 133, 199.

MOLYBDENUM.
Forms and Occurrence.-Molybdenum, the chief sources of
which are the minerals wulfenite, PbMo0 4 , and molybdenite,
MoS 2 , is only likely to cause poisoning under special circumstances,
since it is not a common substance and finds its chief use in the
chemical laboratory as a means of testing for phosphate, with
which it combines in the presence of nitric acid, forming a heavy
yellow precipitate of phospho-molybdate. However, like selenium,
it has been found that where molybdenum is present in the soil
it can be absorbed by plants in sufficient quantity to make them
toxic to stock on ingestion. In Great Britain, the herbage growing
on soils arising from the Lower Lias formation in parts of Somerset-
shire, Warwickshire, and Gloucestershire has been analysed
spectroscopically by Ferguson, Lewis, and Watson (1943), and
found to 'have a molybdenum content of 20 to 100 parts per
million, whereas herbage normally only contains traces of the
element, on the average 4 parts per million. If animals, par-
ticularly ruminants, are grazed on pastures with a __high molyb-
denum content, they suffer from a disease known locally as-!'teart."
Ferguson, Lewis, and Watson (1943) further showed that "teart"
disease could be set up in healthy cattle by the administration of
three to six daily doses of 5 g. of sodium molybdate and also by
the application to healthy pastures of 20 pounds of sodium
molybdate per acre, so that there is no longer any doubt that the
disease is, in fact, molybdenum poisoning.
Gimingham (1914) made a detailed study of the "teart"
MINERAL OR INORGANIC POISONS 95
pastures of Somersetshire and found that the disease occurred to
the greatest extent on well-managed pastures containing a high
proportion of clover and leafy, palatable grasses, but no relation-
ship has been established between the botanical composition of
the pastures and the incidence of the disease. This varies con-
siderably from year to year and even from field to field; it is
highest in the autumn, particularly in mild, wet seasons when
there is an abundant growth of grass, and lowest in dry seasons.
Hay made from such pastures or the grass obtained from them
after there has been a frost is comparatively harmless, presumably
because under these conditions the molybdenum becomes con-
verted into some insoluble form, since analyses show that the
molybdenum content still remains high.
Symptoms.-Cattle, particularly milch cows, and also sheep are
the animals chiefly affected and may show symptoms of the
disease within twenty-four hours to a few days after first being
turned on to a "teart" pasture. The symptoms closely resemble
those seen in J ohne's disease, the most characteristic being a
chronic diarrhrea with the passage of yellowish-green, watery
freces, loss of condition, and a reduced milk yield; in severe cases,
death may result from exhaustion.
Treatment.-Muir (I936) found that if affected animals were
removed from the pastures and given a diet consisting of hay
and undecorticated cotton cake, recovery was uneventful, and
Ferguson, Lewis, and Watson (1943) were able to prevent the
onset of the disease by the daily administration of 2 g. of copper
sulphate to cows and I g. to young stock, but at present there is
no satisfactory way of treating the pastures themselves so as to
render them harmless.
REFERENCES.
Ferguson, W. S., Lewis, A. H., arid Watson, S. J. (1943),]. Agr. Sci., 33,44.
Gimingham, C. T. (1914), ]. Agr. Sci., 6,328.
Muir, W. R. (1936), A gr. Progr., 13, 53.

HALOGEN ELEMENTS AND THEIR COMPOUNDS.


Chlorine, Bromine, and Iodine.
Forms and Occurrence.-The halogen elements, chlorine,
bromine and iGJdine, though not found in the free condition in
nature, are employed in the arts to a limited extent, an~ free
iodine is a valuable drug. Chlorine and bromine rank as amongst
96 VETERINARY TOXICOLOGY
the most chemically active elements, and are both, in the state
of vapour and diluted with air, most powerful disinfectant agents.
In Germany stable disinfection by evaporation of bromine is
practised. N ei ther the gaseous chlorine nor the volatile liquid
bromine is encountered outside special work, and both are most
dangerous substances to handle. Liquid bromine has a most
powerful corrosive action, destroying the skin and mucouS surfaces,
and causing wounds which heal with difficulty. The solutions in
water-viz., chlorine water and bromine water-find some applica-
tion in pharmacy as caustic disinfectants.
Bleachzng powder (chloride of lime or calcium chlorohypochlorite)
and sodium hypochlorite (or eau de] avelte), the so-called chlorinated
alkalis, owe their efficiency to the ease with which they part with
chlorine, and thus effect oxidation. Bleaching powder is given
internally to the horse and ox in doses of 450 and 750 grains re-
spectively, and in proportionately smaller amounts to sheep. It
must be remembered that contact :with acids, even when very
weak and dilute, generates free chlorine, and large doses are there-
fore liable to cause injury.
The simple salts, such as sodium chloride and potassium
bromide and iodide, are in common use, and have great thera-
peutic value. All are liable to cause dangerous symptoms in large
doses.
The oxygenated salts, potassium and sodium chlorates, bromates,
and iodates, are increasingly toxic in the order named, and it is
very probable that the presence of iodate in Chile saltpetre accounts
in part for the toxicity of that substance (see Nitrates).
Symptoms.-Poisoning by the above-named substances is rare,
and a brief summary of the general effects of the agents named
will therefore suffice.
Chlorine and bromine, in the condition of concentrated vapour,
are very dangerous, and primarily attack the respiratory system.
They cause intense pulmonary irritation by directly attacking
the mucous membranes. There is suffocation, cough, violent
retching, and discharge of bloody mucus. In fatal cases a comatose
condition precedes death. The pulmonary troubles may eventuate
in broncho-pneumonia, and even with recovery there is great loss
of condition and resistant power.
Treatment must include immediate removal, of the cause.
Small quantities of sulphuretted hydrogen or ammonia act as
direct chemical antidotes against both chlorine and bromine.
MINERAL OR INORGANIC POISONS 97
Vapour of alcohol or ether is, however, preferable, as the above
agen ts are also themselves very toxic.
Chemical Diagnosis will not be possible if any length of time
elapses before death, and, indeed, is scare ely necessary, since
there can be little doubt as to the cause. The faint odour of chlorine
or bromine may be observed. To test chemically the parts are
distilled into water, and the halogen recognised in the watery
distillate. Bromine imparts a brown or orange colour to water,
and extraction with chloroform gives a heavy orange-coloured
lower layer. Both agents liberate iodine from solutions of iodides,
such <l;s potassium iodide, and this gives a blue colour, discharged
on heating and reappearing on cooling, with dilute starch solution.
The test is not characteristic of chlorine and bromine, since many
substances-e.g., nitrous fumes and hydrogen peroxide-also
liberate iodine from iodides.
When given internally bromine is very poisonous. According to
Law, 120 grains killed a dog in five hours; 10 to 12 drops in an
ounce of water intravenously proved suddenly fatal (Orfila).
Iodine in doses of 5 to 6 drachms by the mouth killed dogs in a
few days (Orfila), a half-ounce of iodine caused colic in a horse
(Tabourin), and 2 drachms intravenously killed (Patu). Hertwig
gave horses 40 to 60 grains of iodine twice daily for fourteen days,
without causing death, and larger doses of several ounces have
failed to injure cattle. .
Very large doses of these agents cause acute abdominal pain,
diarrhrea, which has the bromine or iodine odour, general weak-
ness, vertigo, and convulsions.
Iodism, following protracted administration of full doses, is
marked by catarrh of the nostrils, throat, and alimentary organs,
suppressed urination, weakness, emaciation, scaly skin eruptions,
and the hair falls off in patches.
Boiled starch is recommended as an antidote in fixing free
iodine, but is of doubtful value, and certainly useless, apart from
its demulcent effect, for bromine.
Bromides of sodium and potassium, which closely resemble
common salt in appearance, are more dangerous than it (see
Common Salt). But the doses required to exercise toxic effects
are very large, and.not likely to be the cause of accidental poison-
ing. There is so great a difference in the cost of the iodides and
bromides as compared with chlorides that risk of substitution of
them for chloride is very greatly minimised. One ounce of bromide
7
98 VETERINARY TOXICOLOGY
to a horse causes listlessness, muscular feebleness, unsteadiness of
gait, impaired reflex movements; the pulse is feeble, respiration
slowed, rectal and cutaneous temperatures are diminished, and
secretion of urine increased. D1Sn (I9IO) observes that dogs dis-
play similar symptoms after 45 grains. The vomition, diarrhcea,
and diuresis are general effects of salt administration.
Bromism, with cerebral depression, increased secretion, anremia,
weakness, and eczematous eruptions, results from prolonged
administration of bromides.
Like the bromides, large doses of iodides. cause enfeeblement of
the heart and cerebral and spinal depression, prolonged exhibi-
tion causes iodism, and large doses are fatal to dogs, which show
depression and gastric irritation due to salt administration.
But.large doses of iodide are given to horses and cattle. Thus,
in actinomycosis of cattle 2 drachms twice" daily cause no toxic
effects even after prolonged treatment, and in obstinate cases
Hoare (I924) prescribes 2 drachms potassium iodide with 5 grains
mercury biniodide twice daily for several weeks.
Iodojorm, so valuable as an antiseptic dressing, is :r:arely given
internally. Not being easily absorbed from the skin, it does not
often give rise to poisoning; but this may happen with dogs
through licking. In dogs and cats it causes gastric irritation,
vomiting, muscular spasms, a lowered temperature, enfeebled
heart action, and narcosis. There is albuminuria, and in chronic
poisoning emaciation and fatty degeneration of muscles and
glands. According to Fr6hner (I927), dogs are killed by I5 grains
per 2 pounds body weight by the mouth, by 20 to 30 grains sub-
cutaneously, or 7 grains injected into a serous cavity. Dun (I9IO)
records that an old cow died in thirty-six hours with spasms and
narcosis after I! ounces.
In any case of poisoning by iodoform no difficulty ought to
be experienced in diagnosis, because the drug will be known to
have been accessible, the odour is characteristic, and the symp-
toms are in accordance.
REFEl{ENCES.
Dun, F. (f910), Veterinary Medicines, 12th ed.
Frohner, E. (1927), Lehrbuch der Toxikologie, 5th ed.
Hoare, E. W. (1924), Veterinary Materia Medica and Therapeutics, 4th ed.
MINERAL OR INORGANIC POISONS 99

FLUORINE.
Forms and Occurrence.-Fluorine is a widely distributed
element which occurs naturally in many rocks, being found
chiefly as fluorspar, CaF2.; cryolite, AIF3 ,3NaF', a double fluoride
of aluminium and sodium extensively used for the manufacture
of aluminium; and apatite, Ca5F(P04)a, a natural fluophosphate
present in many phosphatic rocks, which may contain as much as
2'0 to 4'0 per cent. fluorine. It thus comes about that the element
can readily find its way into soils and water supplies, in which it
may be present in considerable amounts, particularly in areas
where rock phosphate is found, as, for example, in North Africa,
parts of North <l;nd South America, India, and China. In certain
areas the fluorine content of the soil may reach 0'I5 per cent., and
water, particularly' from underground sources in contact with
marine clays, has been found to contain as much as I5 mg. per
litre. Owing to the prevalence of the element, it is not surprising
that traces are normally 'present in plant and animal tissues,
usually in the form of the comparatively insoluble calcium
fluoride, 3Caa(P04)z,CaF2, IO to 40 mg. per IOO g. being a not
unusual amount of fluorine to find in the teeth and bones of healthy
cattle. Little significance was, therefore, attached to fluorine as
a toxic agent until Velu (1932) in North Africa and Roholm
(1931) in Denmark sho~ed conclusively that the ingestion of
small amounts of fluorine over long periods produces characteristic
signs of chronic poisoning. Velu (I932) and his' co-workers in-
vestigated the disease known as <tEl Darmous," which affects
particularly the teeth of animals and human beings inhabiting
the phosphatic areas of Morocco, and they were able to reproduce
the condition by feeding rock phosphate containing fluorine.
Roholm (1934) studied the disease of sheep in Iceland known as
"Gaddur," which occurs after volcanic eruptions and is charac-
terised by osteodystrophic changes in the long bones. This also
was shown to be caused by the ingestion of 'fluorine distributed
over the pastures as a result of volcanic activity. It is now well
established that where fluorine occurs in abnormal amounts in
the soil or water a chronic endemic fluorosis is likely to exist, the
most obvious signs of which are characteristic changes in the
teeth of the local popUlation.
In addition to naturally occurring fluorine, fluorosis may
result from the contamination of pastures and feeding stuffs by
100 VETERINARY TOXICOLOGY
the smoke from factories using raw material containing fluorine
in their manufacturing processes. The most likely sources in this
case are superphosphate works, aluminium, glass and enamel
factories, chemical works, and brick works using clay containing
fluorine. On being subjected to heat, the fluorine volatilises and
is carried away in the smoke in the form of a heavy, oily mist,
which is. rapidly deposited on the surrounding pastures. The
presence of fluorine in the atmosphere itself may also be dangerous,
as was the case in the Meuse valley disaster of 1930, when fog
containing fluorine and other irritant substances enveloped the
valley for several days.
In addition to the above, poisoning may result from the
ingestion of fluorides, usually sodium fluoride or cryolite, used as
insecticides and vermin poisons, and also as bactericidal agents,
the latter particularly by breweries to inhibit excessive fermenta-
tion in the lees. There is also the possibility that phosphate licks
or mineral mixtures supplied for animal feeding may contain an
injurious amount of fluorine.
Toxic Dose.-The toxicity of fluorine shows considerable
variation, depending on such factors as the type of compound,
the species and age of the animal, and the nature of the diet.
Hydrofluoric acid itself is a powerful, corrosive poison, but is not
likely to be encountered in veterinary toxicology; sodium fluoride
and silicon fluoride are also extremely toxic, the fluorine in rock
phosphate less so, and cryolite and calcium fluoride the' least
toxic. The toxicity of fluorides dissolved in water appears to be
high, I part per million in drinking water being sufficient to cause
changes in the teeth of ~hildren. Roholm (1937) considers that, on
the average, 23 to go mg. per kg. body weight is the minimal
lethal dose for animals, though IS mg. of sodium fluoride per
kg. body weight caused-the death of sheep. Although there is a
tendency for fluorine to accumulate in the bones with age, young
growing animals are more susceptible to the effects of fluorine
than are adults, and a daily intake of m9re than 3 mg. per kg.
body weight, which appears to be about the limit of tolerance for
calves, may in time set up symptoms of poisoning. There is also
evidence to show that where there is a deficiency or imbalance
of minerals, particularly of calcium, in the diet, the susceptibility
to fluorine is enhanced. On the other hand, th~e are indications
that a plentiful supply of green food may reduce the toxicity of
fluorine compounds, and also that where its ingestion is inter-
MINERAL OR INORGANIC POISONS lor
mittent larger quantities may be consumed without producing
symptoms of poison"ing.
Symptoms.-In acute cases, the main symptoms are those
associated with a corrosive poison. There is gastro-enteritis,
abdominal pain, diarrhcea, muscular"Weakllcss, dyspncea, collapse,
and death, probably from arrest of the heart and respiration. Ill-
ness may be only of short duration, but usually lasts several days.
In chronic poisoning the symptoms show considerable varia-
tion, depending on the amount of fluorine ingested. In the mildest
form, which is usually due to drinking water containing a high
fluorine content, the only noticeable symptom is the characteristic
dystrophic changes of the teeth. These fail to-grow properly, the
enamel shows patches or spots of a chalky white deposit and is
frequently stained a chocolate brown colour. This mottling of the
teeth is more evident on the permanent teeth, but may also be
seen on temporary teeth. The enamel becomes eroded and pitted,
large cavities with evidence of excessive wear eventually appear,
and the teeth are extremely brittle. These changes are mainly
due to faulty calcification, both the enamel and dentine being
affected. Iil more severe cases, such as may arise from contamina-
tion of pastures by factory smoke, etc., as recorded by Hupka
and Goetz (1931), Bosworth (1941), and others, symptoms set in
rapidly, young growing animals and milch cattle being par-
ticularly affected, probably because of their enhanced need for
calcium. There is failure of growth, unthriftiness," anorexia,
diarrhcea, and progressive emaciation. Evidence of osteomalacia
with exostoses of the long bones, particularly the jaw bones, is
pronounced, and spontaneous fractures may be present on account
of the brittleness of the bones. Overgrowth of the hoof may also
be present, and affected animals are usually lame and remain
lying down. Osteosclerosis has been reported to occur in cryolite
workers, but this has not been observed in animals.
Post-Mortem Appearances.-In acute cases, the main lesions
are a hremorrhagic gastro-enteritis, acute nephritis, and paren-
chymatous degeneration of the visceral organs. In chronic cases,
the changes in the bones and teeth may be the only lesions
present. The bones are thicker than normal, very brittle, and show
chalky deposits on the surface. Poorly calcified new bone forma-
tion from the periosteum is present, and an excessive amount of
osteoid tissue with atrophy of the bony tissue may be seen.
Treatment.-Treatment should follow general lines for irritant
102 VETERINARY TOXICOLOGY
poisoning. In chronic cases, improvement may be expected on
the removal of fluorine from the diet and the' provision of whole-
some food. Care must be taken to ensure that any phosphatic or
other mineral supplement is free from fluorine.
Chemical Diagnosis.-The presence of fluorine may be demon-
strated by means of the etching test, in which the fluorine is
liberated as hydrofluoric acid by heating the material with con-
centrated sulphuric acid at 175 0 C. in a lead crucible and allowing
the fumes to act on a glass cover-slip. Soluble fluorides may be
recognised by their bleaching properties when added to a zir-
conium-alizarin solution in the presence of acid. Henry and
Benjamin (1936) found the most convenient and reliable method
for the estimation of fluorine was to liberate the fluorine as hydro-
fluorsilicic 'acid by distilling the material in the presence of silica
with 60 per cent. perchloric acid and titrating with a standard
thorium nitrate solution, using a zirconium-alizarin solution as
indicator.
REFERENCES.
Bosworth, T. J. (1941), Froc. Roy. Soc. Med. London, 34,391.
Henry, M., and Benjamin, M. S. (1936), Aust. Vet. ]., 12,8.
Hupka and Gotze (1931), Deuts. tieriirztl. Wschr., 39,203.
Roholm, K. (1934), Arch. wiss. Prakt. Tierhlk., 67, 420.
Roholm, K. (1937), Fluorine Intoxication, H. K. Lewis and Co., Ltd.
Velu, H. (1932), Arch. Inst. Pasteur Algerie, 10,41.

CARBON MONOXIDE.
Occurrence.-Carbon monoxide, or carbonic oxide, is to be
clearly distinguished from carbon dioxide, or carbonic acid. It
is inflammable and chemically neutral. Carbon monoxi.de is
formed in the incomplete combustion of carbon, and is contained
in "producer gas" to the extent of about 23 per cent., in "water
gas" about 44 per cent., in "Dowson gas" 24 per cent., in "coal
gas" from 6 to I I per cent., and is further also formed in the ex-
plosion without complete combustion of fire-a amp in mines-; and
is thus a constituent of choke-damp.
Toxicity.-Estimates as to the toxic proportion of carbon
monoxide in air vary, but according to some authorities (Gruber
and Hempel) it is less than I per cent. On this account, and in
consideration of the numerous technical and domestic employ-
. ments of the above-named gases, a description of carbon monoxide
poisoning is desirable. But recorded cases of death amongst
animals are very rare.
MINERAL OR INORGANIC POISONS r03

Absorption and EfIects.-Carbon monoxide is rapidly absorbed


by the pulmonary mucosa, and passes into the blood stream in
the form of carboxyhcemoglobin, a combination of the monoxide
with hcemoglobin, which is more stable than the oxygen compound
(oxyhcemoglobin). It is therefore an exceedingly toxic compound,
since the stability of the carboxyhcemoglobin prevents oxygena-
tion of the blood, and poisoning in an atmosphere containing over
3 per cent. is almost instantaneous.
In smaller proportions there is vertigo, 'and loss of power and
muscular tremors. Respiration is difficult, rapid, and stertorous.
The heart's action is intermittent, power over the sphincters is
lost, and death ensues in coma.
Post-Mortem Appearances.-The most notable post-mortem
appearance is the bright redness of the blood, which gives a pink
or violet froth, but the lesions are not characteristic.
Treatment in suspected cases such as of coal-gas or choke-damp
poisoning will take the form of inhalation of oxygen, in the hope
of dissociating the carboxyhcemoglobin, by means of excess of
oxygen. Electrical treatment, the positive pole in the rectum and
the negative in the 'mouth, has been recommended as valuable
for small animals.
Chemical Diagnosis.-The best test for carbon monoxide
depends on the character of the absorption spectrum of carbon
monoxide blood, wh,ich may be observed in a dilution of r of de-
:fibrinated blood in 1,000. This test may therefore be applied to
blood post-mortem, or used for air by agitating the suspected
sample with normal de:fibrinattid blood of the above strength.
The absorption spectrum of carboxyhcemoglobin is similar to that
of oxyhcemoglobin-viz., two bands in the yellow-but displaced a
little to the right. The difference is in the fact that reducing
agents such as ferrous salts, but better ammonium sulphide,
reduce oxyhcemoglobin, with fusion of the two bands into one,
larger and indistinctly outlined, whilst reduction does not alter
the carbon monoxide blood spectrum.
A chemical method of detection consists in passing the suspected
gas over gently warmed pure iodine pentoxide. Even with very
small proportions of carbon monoxide iodine is liberated which
is absorbed in potassium iodide solution, and recognised by the
starch or other of the well-known tests for iodine. The reaction
is not absolutely conclusive, since such hydrocarbons as acetylene
(which is also present in coal gas) behave similarly.
ORGANIC POISONS AND DRUGS

HYDROCYANIC OR PRUSSIC ACID.


Occurrence.-Hydrocyanic acid is one of the most powerful
poisons known, and poisoning by it may arise not only through
the use of the acid and its salts in the arts-e.g., in the cyanide
gold extraction process, in electroplating, and in pharmacy-but
also because hydrocyanic acid is, under certain circumstances,
generated by many plants. In the vegetable kingdom, hydro-
cyanic acid most probably represents a stage in the metabolism
of nitrates, which are absorbed from the soil and eventually built
up into plant proteins, and occurs either free or more usually
in combination in the form of cyanogenetic or cyanide-producing
glycosides.
A glycoside is an organic compound of vegetable origin which,
by hydrolysis with dilute mineral acids, or by the agency of certain
vegetable enzymes, is decomposed, yielding always sugars and
at the same time other compounds. Amygdali1~, C2oH27NOll' the
glycoside of the bitter almond, is an excellent typical example.
The almond seed also contains the enzyme or ferment emulsin. On
macerating the seed with water the emulsin is brought into
contact with the dissolved glycoside, and CaUses the decomposi-
tion represented by the equation C26H27NOn +2H zO =2C 6H 120 6 +
C6H 5CHO+HCN-i.e., the amygdalin yields glucose, benzalde-
hyde (or oil of bitter almonds), and hydrocyanic acid. In smaller
proportions amygdalin is also found in the peach, plum, 'cherry,
and apple seeds, and the formation of the poisonous prussic acid
from such sources appears to have been known to the early
Egyptian priests. The cherry laurel. (Prunus lamoceraS2ts) , one
of the commonest ornamental shrub~, contains amygdalin-in the
leaves, and gives rise sometimes to poisoning. In the South-
Eastern United States the Prunus caroliniana, laurel cherry, or
mock orange, which is cultivated as a hedge, and P. serotina, or
wild black cherry, an Eastern forest tree, both similarly have
proved dangerous; in South Africa Rimington (1932) and others
have shown that varieties of Dimorphotheca contain the cyano-
genetic glycoside linamarin, and therefore can develop hydro-
cyanic acid. In addition to the above-mentioned, many of the
I04
ORGANIC POISONS AND DRUGS 10 5

Legulninosc:e, in particular Phaseolt:s lunatzts (Java or Rangoon


bean, Haricot de Lime), and species of vetch (Vicia); certain of
the Graminec:e, Leeman (1935) lists eighty-eight members of the
family in which prussic acid has been reported to occur-e.g., the
millet or sorghum, the maize, etc.-and certain of the Linaccee-
e.g., common flax, Linw1Z usitatissimttm and its varieties (L. cathar-
ticmn, etc.)-also contain cyanogenetic glycosides, such as phaseo-
lunatin (or linamarin), which yields on fermentation glucose,
acetone, and hydrocyanic acid.
The quantity of glycoside present varies widely and it is un-
evenly distributed throughout the whole plant, but occurs chiefly
in the leaves; thus it is present in sufficient quantity in the young
sorghum to cause poisoning, but is absent or in insufficient
quantity to prove dangerous in the mature plant, and, at any rate
in the case of the Grami.nec:e, both diurnal and seasonal variations
in the hydrocyanic acid content have been shown to occur. It
has also been established that wilting of the plant is accompanied
by an increase in its hydrocyanic acid content; the composition
of the soil and the manurial treatment may also affect it. In the
Phaseolus or Java bean the percentage of glycoside in the wild.
East Indian varieties, which vary in colour from pale, reddish-
brown to purple, amounts to rather more than 01 per cent. The
white beans of the same species contain only about one-tenth part
of this proportion, and in cultivated varieties the proportion is
smaller still. From the practical point of view only the dark-
coloured, and especially the purple, beans are to be regarded with
suspicion. In 1906 considerable poisoning took .place through the
importation of the wild Phaseolus from the East under the name
of Java or Rangoon beans.
As regards the mechanism of poisoning by these materials it
is necessary to emphasise several important points:
1. In the drierl material the enzyme and glycoside are not in
contact, and therefore no fermentation with formation of hydro-
cyanic acid Occurs.
2. After mastication the pulped mass at the body temperature
is in a most favourable condition for fermentation, and the dis-
engagement of hydrocyanic acid is therefore rapid in the rumen
or stomach.
0
3 A moist heat of over 60 C. destroys the enzymes, but it
must be remembered that their destruction by dry heat re-
quires prolonged heating to at least 100 0 C., the cyanogenetic
106 VETERINARY TOXICOLOGY
glycosides in themselves neither appearing to be particularly
poisonous nor to be acted upon by the various digestive fer-
ments.
In spite of hot pressing, which would be expected to destroy
the enzyme, the great majority of linseed cakes still contain
active enzymes. Linseed cake rarely, however, yields more than
0'025 per cent. of hydrocyanic acid, although as high a percentage
as 0'055 has been observed. It will therefore be only under ex-
ceptional conditions that linseed can prove poisonous, as has been
shown by feeding experiments.
As regards the preparations likely to be encountered in
pharmacy and the arts, the B.P. hydrocyanic acid is a 2 per cent.
and Scheele's acid is a solution of from 4 to 5 per cent., whilst
the very volatile and exceedingly poisonous anhydrous acid is
never encountered outside the laboratory.
Potassium cyanide is the commonest salt, and is also very
poisonous. It is a colourless crystalline solid, having a faint
smell of prussic acid, and yielding an alkaline solution in
water.
Potassium cyanide appears to be slightly less toxic than the
equivalent quantity of the acid-at any rate, on intrathoracic
injection; but this <;lifference is probably due to the fact that
potassium cyanide solution does not disengage prussic acid
vapour, and is therefore less rapidly absorbed by the pulmonary
system. By the acid gastric juices hydrocyanic acid is, however,
readily liberated from potassium cyanide.
It must also be remembered that it is the cyanogen acid
radicle or ion CN' which is poisonous and therefore the complex
cyanides (e.g., potassium ferrocyanide) and the sulphocyanides
(e.g., KCNS) are practically harmless. '
Notable also is merc'uric cyanide, Hg(CN)2' which is not
easily dissociated-i.e., does not readily yield hydrocyanic,~cid
and is therefore no more toxic than mercuric chloride.
Toxic Doses.-Kaufmann (rgOI) quotes' for the horse 6 grains in
the form of the 2 per cent. solution, and 06 grain similarly for the
dog. Dun (rgro) st~tes similarly that 4 to 5 drachms of the 2 per
cent. acid (equivalent to 6 grains pure acid) may kill a horse in an
hour. As regards potassium cyanide, Kaufmann (Igor) gives the
dose for the horse as 60 to 120 grains (equivalen( to 25 to 50 grains
of pure acid). For the dog he gives 4'5 grains (equivalent to 1'75 of
pure acid). The very much larger doses-of cyanide as compared with
ORGANIC POISONS AND DRUGS 10 7
free acid are no doubt heeded, because liberation of the acid is
necessary when the salts are given. A heifer withstood 22'5 grains
pure acid in the form of potassium cyanide, but was killed by
30 grains taken by the mouth, and Tochter (1935) was able to
cause the death of pigs in thirty minutes following the administra-
tion of 6 grains of hydrocyanic acid in a capsule; likewise, 37
grains of potassium cyanide also caused the death of a pig when
given in a capsule, but not when mixed with the food, owing to
the fact that the animal refused the food for several hours, by
which time volatilisation with the production of formic acid was
probably complete. For the rapid destruction of dogs by intra-
thoracic injection on the average r} grain of free acid in the form
of Scheele's acid are commonly used:
As regards doses of cyanogenetic feeds, such as Java beans,
assuming 20 grains as the minimum toxic dose for cattle; and an
average hydrocyanic acid yield of 9 grains per pound for dangerous
Java beans, it will be evident that at least 2 pounds of' beans will
be required. In the case of linseed an average hydrocyanic yield
of 1'75 grains per pound may be expected, and thus at least I I
pounds of cake would be needed to produce poisoning. Even such
an unusually large feed would probably fail in this effect, since
the gradual evolution of the acid leaves time for elimination and
consequent diminution of the total effect.
The case of linseed, one of our most valued farm foods, merits
particular attention. Amongst others, Tochter (1939) and Worden
(1940) have examined this question in some detail, and it may be
concluded that poisoning is unlikely to arise from this source,
since the amount of hydrocyanic acid available for absorption at
anyone time is unlikely to reach a lethal dose. Indeed, no well-
authenticated records of damage by . linseed to mature cattle
exist, but there is some evidence that calves occasionally may be
the victims of prussic acid poisoning from linseed cake. On this
point the observations (amongst others) of Dunne (1924) and of
Wilson (1924) are decisive. The symptoms observed follow those
described below. As stated above, the available hydrocyanic acid
of commercial cakes may run to 0'05 per cent. or 3'5 grains per
pound. In the cases reported, the proportions were of this order.
The conditions under which the food is used for calves, moreover,
favour hydrocyanic acid generation by fermentation, in so far as
the ground food is commonly made into a mash with cold or luke-
warm water. In this way the available poison is offered in a single
108 VETERINARY TOXICOLOGY
dose, in sharp distinction to the conditions obtaining on dry
feeding.
Absorption and Elimination.-Hydrocyanic acid and its soluble
salts are absorbed through the skin, speedily producing the
general symptoms. Similarly, the vapour is rapidly absorbed
through the lungs, and thus acts more quickly than by the other
channels of absorption. The respiration, at first stimulated, is
speedily inhibited. In the circulation the venous blood, at first
redder, is eventually darker. In a test tube hydrocyanic acid
forms a combination with hremoglobin, thus preventing the
absorption of oxygen. This effect appears to be absent in the
living animal, but instead tissue respiration is profoundly affected
owing to interference with the cytochrome reaction, so that the
cells can no longer take up the oxygen carried to them by the
blood. A condition of asphyxia is thus produced and tissue
respiration may be so completely inhibited that the venous blood
retains the colour of arterial blood, and there is a rise in the
blood sugar level. Hydrocyanic acid also exercises a retarding
effect on the activity of such inorganic ferments as colloidal or
finely divided platinum. When, for example, hydrogen peroxide
is being decomposed with evolution of oxygen by means of finely
divided or colloidal platinum, the addition of a cyanide greatly
checks the rapidity of the change.
In addition, experiments upon the frog, which is very resistant
to ordinary asphyxiation, tend to show that the poison also
exercises a paralysing effect on the central nervous system-
rather more upon the medulla and lower brain than upon the
cerebral cortex. .
Elimination takes place. partly through the lungs, the exhaled
air having a faint almoncf-like odour, and also partly as a result
of thiocyanate formation with excretion in the urine.
Symptoms.-Very large doses are exceedingly rapidly- fatal,
owing to the arrest of the heart in diastole. Toxic doses usually
exercise a brief powerfully stimulant effect, followed by depres-
sion, paralysis, and diminution of blood tension. Given by the
alimentary tract, the diluted acid causes salivation, vomition if
possible, and diarrhc:ea with the herbivorre. There are convulsions,
spasms, vertigo, paralysis, stupor, and cessation of respiration
before that of the heart-beats.
Several cases are on record relating to Java bean poisoning.
McCall (1906) gave 'Java bean meal to a collie, a cow, and a horse,
ORGANIC POISONS AND DRUGS 10 9
that supplied to the horse having first been boiled for one hour.
Fifteen to twenty minutes elapsed before the appearance of
symptoms, which ended fatally in the case of the dog within two
hours, and in the cases of th~ cow and the horse within four hours.
Damman and Behrens (1906) describe the following symptoms:
vertigo, tympany, and falling, with a fatal issue in nearly every
case. Mosselmann (1908) describes the effect of about one pound of
the beans on four oxe;~ and two heifers. There was a preliminary
.period of great excitement and salivation. After two hours the
animals were swollen, with slight diarrhcea, quick pulse and res-
piration, muscular spasms, and in one case paralysis of the hind
quarters. There was rapid recovery.
Aggio (1907) observed poisoning of.ewes by cherry laurel. There
was loss of appetite, vomition, inability to rise, and several deaths.
Adsetts (1871) describes a similar case in a horse. There was an
indistinct and feeble pulse, mucous membranes ingested, difficult
respiration, uneasiness, prostration, coldness of the extremities,
loss of appetite, consVpation, diminished urination, and acute
pain; protracted over three days, these eventuated in death.
It will be readily perceived from these examples that one has
not to deal here with simple cyanide poisoning. It is well known
that the train of symptoms and the post-mortem lesions in cases
of the ingestion of a plant often suggest irritation which is by no
means typical of the pure active principle. Plants may contain
some other more slowly acting poisonous principle in addition to
a cyanogenetic glycoside, as has been pointed out by Green and
Andrews (1923), and irritant substances may 3Jso be present, as,
for example, in the cherry laurel, which contains an essential oil
analogous to turpentine.
Post-Mortem Appearances.-In cases where death has been due
to the effects of ingestion of plants containing cyanogenetic
glycosides, inflammation of the gastro-intestinal tract may be
observed, but such irritation is not typical of cyanide poisoning.
Animals poisoned with hydrocyanic acid show congestion of the
venous system, the blood remaining unclotted in the vessels;
reddening and congestion of the mucous membrane of the stomach
and all parts of. the body may have a faint smell of bitter almonds.
Otherwise few characteristic post-mortem signs are to be seen.
Treatment.-The poison should be removed by emetics or the
stomach pump, and measures taken to combat prostration-
e.g., stimulants, warmth, and artificial respiration. Atropine has
no VETERINARY TOXICOLOGY
been recommended, also the injection of sodium sulphide and
sodium thiosulphate, in the hope that the comparatively harm-
less sulphocyanides may be formed, but at best this process is a
slow one. The most hopeful line of treatment is the administration
of substances which cause the formation of methremoglobin.
Cyanides in the presence of methremoglobin immediately form the
non-toxic cyanhremoglobin compound, and if sufficient methremo-
globin can be formed in the body to inactivate the hydrocyanic
acid present, whilst leaving enough hremoglobin available for
respiration, the chances of recovery are good. With this object in
view, intravenous injections of methylene blue or sodium nitrite
ha.Ve been recommended, sodium nitrite being the most effective
given either alone or combined with inhalations of amyl nitrite,
but the latter must be given with caution as there is a danger of
collapse. A suggested line of treatment is to give inhalations of
amyl nitrite for fifteen to thirty seconds, repeated at two to three
minute intervals, and the intravenous injection of 2 to 5 m!.
of 4 per cent. sodium nitrite, followed by 5 ml. of 50 per cent.
sodium thiosulphate intravenously.
The classical antidote is freshly precipitated ferrous hydrate,
which is made by mixing iron sulphate and liquor potassre, and
which may be given ad lib. It must not be made with the carbon-
ates, for ferrous carbonate does not readily form ferrocyanide,
and the production of this harmless salt is the object of the treat-
ment. However, unless antidotal treatment is instituted early
there is little hope of recovery in cases of true hydrocyanic acid
poisoning.
Chemical Diagnosis.-Since hydrocyanic acid is volatile, the
separation from tissues is effected by slow distillation in a current
of steam, after aci<;lific<'!:ti~n of the material with tartaric or dilute
sulphuric acids. The exit tube of the condenser is allowed to dip
into a dilute solution of caus6c alkali and the process continued
until about 100 ml. of distillate have been collected.
The tests for hydrocyanic acid are exceedingly delicate; the best
is the absolutely characteristic formation of prussian blue by the
action of precipitated ferrous hydroxide on a caustic alkali
solution of the cyanide. This leads to the formation of ferro-
cyanide, and after acidification the ferric salts present yield with
the ferrocyanide prussian blue. The delicacy of the test is in the
neighbourhood of 1 ln 100,000; the thiocyanate test is, however,
even more delicat~. For this reaction a portion of the distillate is
ORGANIC POISONS AND DRUGS III

evaporated to dryness on a water-bath after the adpition of a few


drops of ammonium sulphide. The residue is then moistened with
dilute hydrochloric acid and a drop of ferric chloride added; the
development of a red colour, which disappears on the addition of
mercuric chloride, indicates the presence of a cyanide. For the
quantitative estimation of hydrocyanic acid, titration of the
distillate with a standard solution of silver nitrate is the best
procedure to adopt. By the aid of these tests, prussic acid may be
detected post-mortem, not only in the viscera but also in the
blood and tissues.
As a general test for the presence of hydrocyanic acid in plants,
the picrate paper test gives satisfactory results, but it is not
suitable for animal tissues owing to the presence of reducing
substances. The papers are prepared by dipping filter paper cut
into suitable strips into a solution of sodium picrate prepared
by dissolving 5'0 g. of sodium carbonate and 0'5 g. picric acid
in 100 ml. of water and allowing the papers to dry. The
paper turns a reddish-brown colour in the presence of hydrocyanic
acid, but the colour may be slow in developing and a negative
result is not established until the suspected material and paper
have been incubated for at least sixteen hours at 40 C. Steyn
(1939) found that the limit of sensitivity of the test lies at about
oooosmg. of hydrocyanic acid.
REFERENCES.
Adsetts, F. (1871), Veterinarian, 44,336.
Aggio, C. (1907), Vet. I, 63,599.
Damman and Behrens (1906), Vet. j., 62, 396.
Dun, F. (1910), Veterinary Medicines, 12th ed.
Dunne (1924), Vet. j., 80,40.
Green, H. H., and Andrews, W. H. (1923), 9th and loth Rep. Dir. Vet.
Educ. Res., S. Africa, 381.
Kaufmann, M. (1901), TMrapeutique et Matiere MMicale Veterinaire,
3rd ed.
Lander, G. D. (1'910), I. Board Agric., 904.
Leeman, A. C. (1935), Ondersterpoort J. Vet. Sci., 5, 97.
McCall, G. (1906), Vet. Rec., 18, 776.
Mosselman (1908), Vet. I., 64, 265.
Rimington, C. (1932), 18th Rep. Dir. Vet. Servo Anim. Indust., Union of
5. Africa, 955.
Steyn, G. D. (1939), I. s. Afr. Vet. Med. Ass. 10,65.
Tochter, J. F. (1935), Vet. Rec., 15,477.
Tochter, J. F. (1939), Vet. Rec., 51, 929.
Wilson (1924), Vet. I., 80, 79.
Worden, A. N. (1940)' Vet. Rec., 52,857.
II2 VETERINARY TOXICOLOGY

CARBOLIC ACID AND ALLIED PREPARATIONS.


Sources and Preparations.-Carbolic acid [phenol (C 6H oOH)] is
a constituent of the tar either of coal or wood. The proportion of
carbolic acid in crude coal tar is about 0'5 per cent., and it is
separated in the distillation in the so-called middle oil. The three
isomeric cresols (C 6 H"CH 3 0H)-ortho, meta, and para respectively
-form about 3 per cent. of the heavy or creosote oil of tar dis-
tillation. In wood tar there is also found guaiacol (C6H"OCH30H),
the methyl ether of orthodihydroxybenzene. Of these various
phenols, carbolic acid is the only one prepared in a pure condition
on anything like a large scale. The complex mixture of the various
phenolic bodies is commonly known as cresylic or tar acid, and
finds several technical applications. Creosote or tar dips are
mixtures of tar acids with the hydrocarbons that accompany
them in the tar oils with hydrocarbon oils, alkali, and resin soaps.
Pyridine bases derived from the coal tar are also present, and the
following is a good example of the composition of such a dip:

Per Cent. Per. Cent.


Water 8'20 Rosin acids 1~'73
Soda .. 2'27 Phenols 14'I I
Pyridine 2'25 Hydrocarbons 54'44

It may be pointed out at this stage that the solubility of


carbolic aCid in water is about 5 per cent., and that of the cresols
about 2! per cent. ; but that these compounds are soluble in caustic
alkalis, whilst the neutral hydrocarbons are emulsified, yielding
turbid opalescent solutions with soaps.
Based upon these principles is the preparation. of such disin-
fecting agents as ere olin and lysol, which essentially are feebly
alkaline mixtures, having as their/active principles phenols, and
capable of forming emulsions by reason of the resin or fatty soaps
which they contain. In spite of frequent claims to the contrary,
all phenolic preparations must be regarded as poisonous; thus
with a carbolic dip the dilution for use should be such that the
phenols do not exceed 0'75 per cent. ./
Tar oil, or oil of Pitch distilled from wood tar, resembles creosote,
but contains chiefly guaiacol and its allies.
Oil of tar with vaseline or mineral lubricating oil is a very
ORGANIC POISONS AND DRUGS II3
common mange dressing for horses, and sometimes finely divided
mercury is also added.
Crude creosote is very widely used for the .impregnation of
wood sleepers and fence spiles.
From all thes.e sources, and even from tar itself, poisoning may
arise; and under this general heading must also be included cases
of poisoning due to the contamination of water by coke oven and
gasworks effluents.
As regards tar, it must be remembered that crude tar contains
some 3 per cent. of cresols or tar acids, nearly all of which pass
into water when the tar and water are mixed with one another.
In a similar way water may take up sufficient cresols from creo-
soted sleepers to cause poisoning. But creosote, as it contains a
larger proportion of cresols, is naturally more 'dangerous than
crude tar. Cases of poisoning by both these means have been
investigated.
Effluent waters from coke ovens and gasworks contain sulpho-
cyanides and tar acids. An example of a coke oven effluent,
analysed in 1909, showed:
Sulphocyanide I 82 grains per gallon
Cresols (tar acids) .. 5. 81

Large quantities of such a water would be required to cause


death. Nevertheless, an effluent of such composition must be
regarded as a dangerous contamination to drinking-water.
Hoare (1924) saw a case of a cow (poisoned by effluents from a
disinfectant factory) in which the milk smelled of carbolic acid,
as alSo did the dejecta. Recovery after purgation and olive oil
took place slowly.
Toxicity.-The toxicity of phenol varies according to the
channel of absorption. The lethal dose for the horse by the ali-
mentary tract is about I ounce, for the dog from I to 2 drachms,
although 15 grains is said to have caused death.
Of the cresols, the ortho compound is more poisonous than
carbolic acid, para-cresol still more so, but meta-cresol less. All
the phenols thus appear to be powerful poisons of the same order
as hydrocyanic acid and arsenic. It is exceedingly difficult-in
fact, impossible-to give quantitative data" regarding poisoning
by absorption through the skin, but in the. case of creosotic
sheep-dips a Departmental Committee found that a It per
cent. tar acid dip caused grave symptoms, one sheep dying
8
II4 VETERINARY TOXICOLOGY
about three hours after dipping, whilst a ! per cent. dip was
safe.*
Kaufmann (19II) further cites cases of death in horses by the
external application over the whole body of 2 and 3 per cent., and
of fowls by 5 per cent., lysol.
Hoare (I924) communicates a case in which z-ounce doses of
lysol were prescribed for parasitic gastritis in sheep: According to
the owner the treatment killed more aniIYlals than the disease!
On the other hand, Shawcross (1933) records that a mare recovered
after an illness of ten days from the effects of I pint of lysol
administered in mistake for linseed oil.
Symptoms.-Concentrated carbolic acid precipitates albumins,
with which it appears to form a loose combination, and is more
penetrating to the tissues than the -majority of corrosives. The
concentrated acid is a violent corrosive, and its local effects may
prove fatal from shock and collapse after the ingestion of large
doses. In the dilute condition carbolic acid manifests after
absorption marked effects on the central nervous system, illus-
ti-ated by weakness, stupor, and tetanic convulsions, similar to
those produced by strychnine, choreic movements, followed by
paralysis of the locomotor system, and death. With very large
doses the collapse may be immediate without convulsions.
In one case recorded by Loft (I906) carbolic acid had been
poured upon the food of cows. They showed loss of appetite; tJ:le
bodies distended by food; constipation; respiration slow; temper-
ature 1050 F.; weak and very quick pulse; soreness of mouths;
salivation; and, in two cases, partial coma.
In another case recorded by McKenny (1904) horses which had
drunk water -containing carbolic acid showed a blanching of the
buccal membranes, staggering~ twitching muscles, eyes staring,
pJ.1pils dilated, and incipient coma.
In a third case Slipper (1906) <;!-ttended a horse which had been
given by mistake 8 ounce"! of creolin in water. After twelve
hours it showed dulness and general restlessness; quick pulse;
temperature above normal; mUCO)1S membranes pale; the urine
was almost black, and had a tarry odour. After three days'
prostration symptoms of acute enteritis set in, and t~e animal
died in violent abdominal pain.
Harris (1905) records that a bull terrier, after eating a mouthful
of carbolised bran, nine hours later displayed muscular twitchings,
* Report of Committee on Sheep-Dipping, 1904.
ORGANIC POISONS AND DRUGS IIS
followed by paralysis of the hind quarters; abdominal distension;
difficult respiration; the mucous membranes of the mouth white
and hardened. The symptoms lasted about four hours, with
occasional attacks of convulsions, and recovery took place within
twenty-four hours. The amount of carbolic acid taken could not
have exceeded I2S grains.
Prime (1908) observed a dog with a crushed foot. This was
dressed with ointment, and four pills containing creosote were also
given, after which there was vomiting and diarrhrea, the ejecta
smelling of creosote; a weak and quick pulse; temperature 1050 F.
Under treatment with stimulants, alternating with sodium
sulphate, there was gradual recovery.
Begg (1924) reported the causing of dangerous symptoms by
the injection per anum of a teaspoonful of I in 50 carbolic acid
to a Yorkshire terrier. '
An interesting case of Gillam (1896) refers to the poisoning of cats
by carbolic disinfectant powder. In this c,ase clonic and tonic spasms,
dilatation of thepupils,salivation,irregular and feeble heart action,
well illustrate the nervous symptoms of carbolic acid poisoning.
Bennett (1914) reported an interesting case in which a pony was
dressed all over with oil of tar (mange was feared) in mistake for
train oil. After an hour the subject manifested great pain, and
was blowing badly. , Later the pony fell and was lying on its off-
side, limbs stretched out and quite rigid; jaws tightly clenched;
pulse imperceptible at submaxillary artery. Consciousness was
quite lost, and in spite of washing, the application of emollients,
and giving of stimulants, death occurred in about three hours.
Hobday made a series of very careful observations on the
dangers of disinfectants, and investigated creolin (1896), chino sol
(1898), and izal (1900). Chino sol is a derivative of the base
quinoline, but for convenience may be included here. The results
confirmed the toxicity (in spite of exaggerated statements to the
contrary) of these agents when improperly employed. With
delicate breeds of dogs and cats Hobday (1896) advises that the
total application of creolin should not exceed 10 to IS minims. In
poisoning by it he indicates subnormal temperature, paralysis of
hind legs, followed by complete paralysis, prostration, and clonic
spasms, well marked in limbs, jaws, and eyelids. Death from
collapse follows co a.
Cats are more susceptible than dogs to chinosol, and it should
not be injected in doses exceeding In- grain and t grain per pound
1I6 VETERINARY TOXICOLOGY
body weight of the cat or dog respectively. The chief symptoms are:
Sneezing and coughing and increased salivation; temperature
subnormal; staggering gait, commencing with loss of motor power
of hind quarters; great prostration; and death from heart failure.
Izal is less dangerous than creolin, but may poison, showing
similar symptoms. Applications of it to the skin ought not to
exceed 10 to 15 minims per pound body weight of dogs or cats.
According to Dollar (1896), who investigated the clinical value
of "]eyes" and creolin, these agents are safe as ordinarily used with
the horse. With the dog his observations on the whole agree with
Hobday's, and he advises 10 to 15 minims of creolin per pound
live weight as the upper limit for fine-skinned, delicate, and
in-and-in bred dogs, such as toy varieties, although as large a
proportion as 40 minims may be safe for adults and mongrels.
He found that a cat of 7 pounds weight, three years old, after
well rubbing with 5 drachms of "Jeyes" in 5 per cent. solution was
poisoned, and died within fourteen hours. But he forcibly argues
that this preparation is no. worse than any lotion or any other
efficacious agent.
Animal oil (oZe'lt1Jt animale jcetid1t1n) is derived from the dis-
tillation of bones, and is thus a tarry product. Although it differs
chemically from coal and wood tars, reference to it may perhaps
be most conveniently made at this point. The oil is a complex
mixture consisting of hydrocarbons and bases differing in this
respect from the acid containing coal and wood tars. The chief
bases are pyridine and its analogues. Pyridine is related chemically
to coniine and nicotine, and is very toxic, about half an ounce for
man and 5 ounces for- the horse causing death in convulsion;; and
asphyxiation.
Clough (1925) has encountered two cases of damage due to
animal or bone oil. Two cqws died within--a few days after chewing
sacking impregnated with the oil, which had been placed at
rabbit-holes in order to cause the rabbits to bolt.
The second case related to two colts, which had been dressed
with this oil (8 parts) along with oZ. picis (I part) and sulphur
(I part). Next morning both were dead and post-mortem revealed
slight gastric enteritis and partial asphyxiation.
Post-Mortem Appearances.-Follo/wing internal administration
of tar acids, there is observed intense irritation of the gastro-
intestinal mucous membranes; that of the rumen may become
detached, but this is a frequent post-mortem observation of no
ORGANIC POISONS AND DRUGS II7
special significance. Frequently there is a strong smell of carbolic
acid in the viscera; the pharynx and resophagus exhibit pallor.
In creolin poisoning, one notes the smell of the agent; the heart
cavities contain dark blood clots, and the small vessels, par-
ticularly of the brain, are congested.
As characteristic of chinosol are the' smell and colour of the
agent, and the presence of frothy saliva in the pharynx, cesophagus,
and stomach.
Treatment.-Carbolic acid after absorption is eliminated in the
form of sulphuric acid derivatives or sulphocarbolates in the urine.
These compounds are comparatively harmless, and in using
sodium sulphate as an antidote it is intended to facilitate their
formation. Sucrate of lime and the intravenous injection of
ammonia are both also recommended. In the case of the cats
above referred to, 20 grains of zinc sulphate speedily acted in one
instance; this was followed by egg albumin in milk, and every
three hours by a mixture of chlorodyne and lime water. In a
second case, the emetic proving ineffectual, the animal died.
With the large animals strong purgatives and whisky have .proved
successful when the purge acted. Repeated gastric lavage and
the administration of large quantities of olive or cottonseed oil
are also indicated.
Chemical Diagnosis.-Carbolic acid and its allies, being volatile,
may be recovered from organic matter by distillation from the
acidified mass in a current of steam. They are recognised in the
distillate by their odour, by the production of a red coloration
when a few drops of the distillate are boiled with Millon's reagent,
by the ferric chloride coloration (carbolic acid gives a violet,
creosote a smoky tint), and by the formation of the sparingly
soluble bromination compounds on the addition of excess of
bromine water. These compounds are crystalline in the case of
carbolic acid and gummy in the case of the cresols.
REFERENCES.
Begg, H. (1924), Vet. j., 80,47.
Bennett, R. (1914), Vet. Rec., 26,798.
Clough, G. W. (1925), Vet. Rec., 5, 720.
Dollar, J. A. W. (1896), Veterinarian, 69, 839.
Gillam, W. G. (1896), Vet. Rec., 9,614.
Harris, P. J. (1905), Vet. j., 61,268.
Hoare, E. W. (1924), Veterinary Materia Medica and Therapeutics, 4th ed.
Hobday, F. T. G. (1896), }. Compo Path. and Therap., 9,1.
Hobday, F. T. G. (1898), j. Compo Path. and Therap., 11,33.
Hobday, F. T. G. (1900), j. Compo Path. wnd Therap . 13, 250.
lIB VETERINARY TOXICOLOGY
Kaufmann, M. (1901), TMrapeutique et Matiere Medicale Veterinaire,
3rd ed.
Loft, J. H. (1906), Vet. Rec., 9, 733.
McKenny, J. (1904), Vet. Rec., 7, 628.
Prime,.T. F. (1908), Vet. ]., 64, 134.
Shawcross, C. F. (1933), Vet. Rec., 13, 92.
Slipper, T. (1906), Vet. j., 62, 75.

STRYCHNINE.
Forms and Occurrence.-The alkaloid strychnine C21H2202N2
occurs, along with brucine C23H2604H2 and vomicine C22H2404H2,
in the seeds of certain species of the Loganiacere: the Strychnos
-nux vomica in the East Indies; the Strychnos ignatii in the Philip-
pines; the upas-tree (or Strychnos tieute) in Java; snake-wood tree
(or S,trychnos cohtbrina) in the East Indies; and Strychnos gauther-
iana.in Tonquin. In the Strychnos toxifera of Guiana strychnine is
associated with brucine and curarine.
The nux vomica seed, incorrectly often called the "nux vomica"
or "strychnine bean," forms to the number of fourteen or fifteen
the seeds of the fruit, resembling an orange in size, and having a
harmless pulp. The seeds have an average weight of 23 grains,
and are about the size of a shilling. They have a concavo-convex
shape, with a well-defined umbilical centre, are covered with soft
velvety hairs, and are brownish-grey in colour. The taste is acrid
and intensely bitter. The beans are rarely the cause of poisoning,
but it is stated that they have been known to be accidentally
incorporated into oil cakes. The powdered bean forms the nux
vomica, whence is also derived the extract and tincture of the
pharmacy.
The content of strychnine in the bean varies between 0'5 and
2 per cent. Brucine is present in larger proportion, and both it
and vomicine show the same action as sti!llulants to the motor
nerve centres, but are considerably less active. Strychnine, or
nux vomica, is frequently encountered outside th~ pharmacy.
Vermin powders very commonly consist of mixtures of strychnine
with starch or flour and blue, or soot, and such powders are the
commonest
, causes of poisoning amongst dogs, cats, and foxes.
/

Strychnine preparations have also been used to protect stacks


from'vermin. The free and general sale and use of strychnine rat
powders leads to many cases of poisoning of the smaller animals,
and strychnine occupies the first place, numerically, among the
ORGANIC POISONS AND DRUGS II9
poisons. Cases of poisoning of the large animals by strychnine
are, however, rare. Since its discovery in 1818 strychnine has also
acquired an evil repute as an agent of malicious poisoning in the
human subject.
Absorption and Elimination.-Strychnine is absorbed, without
local effect, slowly from the intact skin, giving rise to general
symptoms. Absorption is rapid by way of the mucous surfaces,
or on injection. From the stomach strychnine is easily absorbed
at a rate depending on the condition of the organ, the absorption
being more rapid from an empty than from a fu~l stomach. 'Free
strychnine is but slightly soluble in water, the salts, especially
those of the organic acids, such as the tartrate and acetate, being
more freely dissolved. The absorption from the rumen is, as might
be expected, not considerable, and no doubt the alkalinity of the
contents of that organ is partly responsible for this. The pre-
cipitation of strychnine by alkalis makes it very inadvisable to
prescribe it with them-e.g., with liq. arsenicalis, etc. The last
dose may contain an excess of subsided strychnine, and prove
poisonous. The period between dosage and the onset of symptoms
is often a question of great medico-legal significance. Manifestly,
it cannot be precisely answered, and it rarely happens that one
has the opportunity of observing the point. It will depend on the
nature of the dose-e.g., as to whether given as solid, as a salt, or
in solution; on the quantity administered; on the state of the
digestive organs; and on the individuality and species of the
subject. Doses given hypodermically may be expected to act
within ten minutes, and from one-half to two hours might reason-
ably be stated as the interval in the case of the administration of
solid strychnine in lethal doses by the mouth to the dog.
By whatever channel absorbed, strychnine is quickly trans-
ported by the blood to the central nervous system and organs.
Strychnine is not eliminated very rapidly. It passes into the
saliva and urine, but the elimination is not complete even in
three days. It thus results that the drug in therapeutic quantities
exercises an apparently cumulative effect, so that the administra-
tion of the tenth dose may kill, whereas the first had scarcely any
. appreciable effect. For this reason-viz., that at least three days
are required for elimination-it follows that the idea of an
increased susceptibility to strychnine is fallacious. The effect is
that of a fresh dose plus the fractional residues of previous
doses.
120 VETERINARY TOXICOLOGY
Toxic Doses.-The toxic doses of strychnine and of powdered
nux vomica are given by Kaufmann (IgOI) as follows:
Strychnine. Nux Vomica.
Horse 3.0 to 45 grains 300 to 450 grains
Ox .. 3.0 to 60 " 300 to 525 "
Pig 015 to 075 grain 60 to go'"
Dog 0075 to 0.30 75 to 15

The dose for a dog is thus roughly in ordinary fractions between


113and 1- of a gr;)_in.
The relative sensibility is shown by Kaufmann's figures dis-
playing the number of milligrammes of strychnine per kilogram me
of body weight:
Man 0.40 mg. I Dog .. 075 mg.
Rabbit .. 060 " Fowl .. 200 mgs.
Cat 075" '

The limits above set forth will probably with justice be regarded
as low, especially in the dog, where l~o-grain doses are given with
caution to toy varieties; indeed, in modern practice strychnine
is given only in very small and carefully regUlated doses to these
animals ..
Hodgkins (1907) records typical strychnine convulsions and
death in a toy spaniel which ate an Easton syrup tabloid after a
meal, the dose of strychnine being probably :h grain.
Similarly, strychnine spasms followed by recovery have been
noticed in a fox terrier after two laxative pills for human use
found to contain lo grain each of strychnine.
According to Bock (1907), th~ injection into the jugular vein of
IO c.c. of a glycerin solution containing 6 grains of strychnine
destroys a horse in three to four seconds without the convulsions
witnessed when a water solution is. employed.
The dosage for birds is very erratic. Thus, Youatt (1840) records
the administration of a total of 95 grains of strychnine in twelve
weeks to an owl, the dose increasing from 1 to -i grain, when death
resulted.
Guinea-pigs and some monkeys appear to be remarkably in-
susceptible to strychnine when given by the mouth.
Action and Symptoms.-Strychnine acts as a powerful stimulant
to the central motor cells, and thus affects chiefly the spinal cord.
The reflex irritability is greatly increased, probably by reason of a
reduced resistance to the passage of peripheral stimuli along the
ORGANIC POISONS AND DRUGS 121
sensory nerves. When the peripheral nerve-endings are paralysed
by cocaine, injection of strychnine fails to produce the tetanic
convulsions, and severance of the posterior roots of the spinal
nerves in frogs has been shown to inhibit the convulsions,
save when the nerve ending is stimulated. In a frog in which
the anterior portion only is. effused with strychnine solution,
stimulation of the hind extremities is followed by ordinary
reflexes, but stimulation of the anterior extremities leads to
general tetanic convulsion. After the intense stimulation, depres-
sion and paralysis follow.
Under the influence of strychnine an exceedingly sligpt external
stimulus, such as a current of air, induces a normal reflex, imme-
diately followed by the characteristic general tetanic spasms,
during which the back is curved (opisthotonos), respiration
arrested, and the muscles are tense. Death results from asphyxia-
tion; usually the respiration ceases after tWo or three spasms.
Animals tend to avoid light, and display marked hyperresthesia.
During the spasms the rigidity of the extended limbs is so great
that a small animal may be lifted in a perfectly straight position
by one extremity:
In horses symptoms set in some hours after such doses as 5 to
6 grains, and involve an accelerated pulse, laboured breathing,
abdominal pain, sensitiveness to touch, and tetanic spasms.
From I to 2 ounces of nux vomica are required to poison the horse.
Macqueen observed strychnine symptoms in the treatment of
paralysis in the horse by doses of strychnine, increasing from
r grain to 5 grains twice daily. Twitching of the superficial muscles
is a preliminary warning. Within about twenty minutes after a
further dose the horse rears, falls, and makes galloping move-
ments, so that it moves backwards on its side in a circle. The
spasm is followed by a period of quiescence. If relieved by tobacco
there is recovery.
Cattle withstand relatively large doses. Thus Macgillivray
(1910) gave an old cow in all 90 grains in solution, and
this induced a few spasmodic tremors, which lasted about
twenty minutes. Dun (I910) gave a small red cow, affected
with pleura-pneumonia, in all 47 grains within two hours and
a quarter. The pulse rose to r60; the symptoms were quickly
induced and included nausea, attempts to vomit, laboured
breathing, and the typical tetanic rigidity.
Dogs become very uneasy, whine, are nauseated, and often
r22 VETERINARY TOXICOLOGY
vomit. This is an important point, and emphasis must be. laid
on the fact that vomiting does not always save the patient. The
rectal temperature rises 2 to 4 F., and general tetanic spasms
occur with increasing violence at intervals of one, two, or more
minutes, until death, which is rapid after the first onset of
symptoms.
As to differential diagnosis, it may be recalled that strychnine
spasms are clonic, whereas those of tetanus are tonic. But tetanus
in the dog is very rare, whilst strychnine poisoning is very common.
Post-Mortem Appearances.-These are the appearances of
asphyxi~, the venous blood being dark and fluid, lungs and
cerebral meninges engorged. The left heart is often firmly con-
tracted and nearly empty. Very rarely, and in protracted cases,
the intestines may show a little patchy congestion. The rigor
mortis is a post-mortem appearance often held to be very charac-
teristic, but its absence is not to be taken as a decisively negative
sign. The feet, or the claws of birds, are generally incurved, and
the muscles of the jaws are rigid. In one of the best observed cases,
quoted by Taylor (r934) from the observations of Caspar of Berlin,
the corpse was described as like a thousand others. The duration
of rigor mortis among dogs is certainly not invariably more pro-
longed in consequence of strychnine poisoning. It may pass off
within twelve hours.
Treatment consists in removal of the poison, when possible by
emetics, fo grain apomorphine hypodermically having induced
vomition in three minutes in a dog. The patient should be kept
quiet and protected from external stimuli as much as possible.
McCall (1907) records a successful cure of a dog by chloroform
inhalation, To grain .apomorphine, and after vomit Ion if grain
morphine repeated two or three times.
The best physiological antidote is chl6ral. Howe (r898) gaye
6 grains chloral hydrate in solution to a dog, repeated in one hour
and then in three hours. There were no fits after the first dose,
and next day the dog was better. As an emergency treat-
ment an infusion of tobacco has been successfully employed by
Macer (r870) ..
Prudames, in treating strychnine poisoniug of stag hounds,
found it necessary in some cases to inject! grain apomorphine
to secure vomiting. Followed by 20~ grains chloral by the mouth,
this proved effective. .
There is danger in giving antidotes by the mouth, for if a spasm
ORGANIC POISONS AND DRUGS I23
occurs the liquid may pass into the trachea, and cause suffocation
or pneumonia. It ought also to be borne in mind that after
absorption emetics may do more harm than good. According to
Hoare (r924) a large dose of chlorodyne and a full dose of castor
oil have proved successful, probably by both hastening expulsion
and retarding absorption.
Chemical Diagnosis.-Strychnine is obtained as a residue from
organic solvents in the course of the systematic separation of
vegetable principles, according to the scheme outFned later.
When a large dose has been given, there may be obtained a crys-
talline deposit weighing several grains, but very often only a
gummy smear rendered impure by the organic matter, always
separated during the extraction, may result. Steyn (r935) recom-
mends that the extract be purified by dissolving the residue in
water acidulated with sulphuric acid and shaking the solution
with ether. The aqueous solution is then made alkaline with
potassium hydroxide and re-extracted with chloroform. By this
means certain ptomaines which give colour and biological reac-
tions closely resembling those of strychnine may be removed,
since the ptomaines or their salts are soluble in ether.
The recognition of strychnine depends on three tests: (r) The
substance must hav~ an intensely bitter taste, a solution of r grain
of strychnine in a gallon still exhibiting distinct bitterness.
(2) Strychnine dissolves without colour in concentrated sulphuric
acid, and the introduction into the solution of a fragment of
potassium bichromate yields a characteristic violet colour, passing
quickly into rose-pink, which is persistent for some time. The
colour is produced in streaks on moving-the bichromate crystal
through the liquid. (3) When bichromate solution is added to a
solution of strychnine in dilute acetic acid, the sparingly soluble
strychnine chromate separates in crystals. The precipitate gives
with concentrated sulphuric acid the same colour reaction as
described under (2).
Although strychnine is amongst the mast stable and easily
recognised alkaloids, error is possible. When organic impurities
are considerable, reduction of chromate and sulphuric acid may
occur with simulation of the strychnine colours, and, moreover,
those colours proper to strychnine may be effectually masked.
Furthe~, many residues, especially those derived from herbivorous
stomach contents, give a precipitate with chromate in dilute
acetic acid, which is, however, amorphous, although with con-
124 VETERINARY TOXICOLOGy
centrated sulphuric acid it gives a red colour. In such doubtful
cases the physiological action of the extract ought to be tested
on a mouse, for which rloo grain of strychnin~ is lethal within
ten minutes.
REFERENCES.
Bock (lg07), Vet.]., 63, 447.
Dun, F. (1910), Veterinary Medicines, 12th ed.
Hoare, E. W. (1924), Veterinary Materia Medi~a and Therapeutics, 4th ed.
Hodgkins, T. (1907), Vet. I, 63, 4 I I .
Howe, N. (1898), Vet. Rec., 11,325.
Kaufmann, M. (1901), TMrapeutique et Matiere Medicale Veterinaire,
3rd ed.
McCall, G. (1907) , Vet. I, 63,277
Macer, J. (1870), Veterinarian, 43, 20 9.
Macgillivary (1910). See Dun, F., Veterinary Medicine~, 12th ed.
Macqueen, ]., Private Communication.
Prudames, W. C., Private Communication.
Steyn, G. D. (1935), Ondersterpoort,]. Vet. Sci., 5, 139.
Taylor, A. S. (1934), Principles and Practice of Medical Jurisprudence,
9th ed.
Youatt> W. (1840 Veterinarian, 13,28.

MORPHINE AND OPIUM.


Forms and Occurrence.-Opium is the inspissated juice of the
opium poppy, Papaver somniferum, which is native to Southern
Europe and the Levant, though cultivated and occasionally found
wild in England. Poisoning of animals by eating the opium poppy
is, however, unknown.
The juice contains some fifteen alkaloids, most of which are
present in very small proportions. The table displays .the chief
of these with the average percentages in which. they are found in
opium.
Per Cent. ' Per Cent.
Morphine C17H rg 0 3 N 10'0 Thebaine C 19 H 21 0 3N 0'15
Codeine C1sH 21 0 3 N 0'3 Papaverine C2oH~lO.N 1'0
Narceine C23H270sN.3H20 0'02 Narcotine C22H230,N 6'0

The other alkaloids are not important.


Poisoning by morphine is rare amongst animals, this alkaloid
affording a good illustration of the variation in the action of a
cerebral,Poison according to the degree of nervous development.
Doses ordinarily given to dogs for ana:stheti(: purposes would
prove fatal to a man. Horses and r],lminants are less susceptible,
and since in the horse the brain is relatively less highly developed
than the cord, the spinal are more marked than the cerebral effects.
ORGANIC POISONS AND DRUGS I25
Toxic Doses.-Kaufmann (I90I) gives the toxic doses on sub-
cutaneous injection as:
Horse 45 to 75 grains
Ox: 75 to 120 "
Small dog 1'5
Large dog 15

These doses are probably too low; for the horse 75 to IOO grains
and for the dog about 4 grains per pound body weight are, how-
ever, fatal. Wooldridge (I934) uses! 'to t grain for an::esthesia in
small, and 2 grains in large, dogs. It is very doubtful if poisoning
by the mouth ever occurs, and it has been proved to be impossible
to kill a pigeon in this way. Doses have been given experimentally
to the pony reaching 60 grains by the mouth, without evoking
marked symptoms, and after slaughter there was no sign of
action beyond impaction of the domach contents dut! to gastric
paralysis.
Absorption and Elimination.-Morphine is somewhat slowly
absorbed from the alimentary mucosa. When given hypo-
dermically, it is excreted into the stomach. In a recent experi-
mental case the writer found morphine by means of Pellagri's
test in the urine, and in the abomasum of a calf which had received
30 grains of morphine under the skin thirty hours before death.
In the system morphine is rapidly eliminated, being oxidised in
the blood stream to oxydimorphine, or at any rate modified
chemically to a substahce closely allied to morphine.
Symptoms.-In the horse and ox toxic doses of morphine give
rise to a period of excitement IT).arked by restlessness, bellowing,
laboured breathing, full pulse, sweating, and dilatation of the
pupil. Later, coma sets in with general loss of sensibility, slow
pulsation and breathing, and a subnormal temperature. There is
arrest of the digestive functions leading to nausea, indigestion,
and tympany.
The excitant effects of morphine on the horse are sometimes
seen when it or opium' is given in colic. The animal moves in a
circular direction ("circus mode of progression"), an effect which
used to be ascribed to the disease, but is in reality due to the drug.
The action on the ox is similar, and the excitement often gives
the impression of madness or marked delirium. .
\Vhen poppy-heads are eaten the gastric symptoms become
more pronounced.
126 'VETERINARY TOXICOLOGY
Sheep display similar symptoms to cattle.
In the cat an hypnotic effect is rarely seen, the action being that
of motor excitement.
In dogs, as in man, a toxic dose induces excitement and reflex
irritability, vomiting, contracted pupil, sometimes convulsions.
Thereafter follow coma, respiratory failure, and death.
Oeller (1914) reports the following case. The subject was a
dachshund, fourteen years old, living a very pampered life,
although apparently healthy. B~fore removing a small papilloma
from the skin of the right humeral region 00I5 gramme of morpho
hydrochlor. was given subcutaneously. Usually the dog was fed
regularly at midday; but on the day of operation, in order to
avoid vomiting after the injection, it was not fed at all, and
operated upon about 5.30 p.m. .
The dog had been treated for dental trouble previously, and on
that account, when the morphia was injected, the animal was
distrustful and nervous. Directly after the injection salivation and
movement of the jaws set in. The dog became more and more
excited, and finally broke into loud plaintive howling. A contrac-
tion of the pupils had already appeared; and the heart was beating
powerfully at the rate of 120 per minute. Finally the operation had
to be performed without any lessening of the sensibility having
taken place. The condition of excitement continued unabated
without the least interruption until nine o'clock the following
morning, when another examination was made. The dog had been
howling persistently throughout the night.
The morning examination resulted as ~ollows: The pupils were
still more contracted. and_ the conjunctivce more reddened than on
the day before. The sounds of the heart had become distinctly
weaker, and the pulse-rate was 140 pet minute. The breathiQg was
hurried and, in consequence of the howling, was very irregular.
The whole of the abdomen was very distended. Percussion in the
region of the stomach yielded a tympanitic sound, but in the right
hypochondrium the splenic area of dulness was sharply defined.
The stomach was considerably dilated. The examination of the
bladder by palpation and percussion showed it was markedly
enlarged and apparently somewhat displaced towards the right.
Its area of dulness extended almost to the umbilicus. There was
no especial sensitiveness to pressure. .-
A temporary paralysis of the bladder due to the action of
morphine was suspected; it was uncertain, however, whether the
ORGANIC POISONS AND DRUGS I27
gastric distension suspected was due to the same cause, as the
restless dog's constant changes in position during the night might
have resulted in a torsion of the stomach. The dog was still so
excited that the passage of a probang was out of the question; the
stomach was therefore punctured. This collapsed after the escape
of its accumulation of gas. Immediately afterwards, for the first
time since the operation of the day before, the dog ceased to howl.
After only five minutes' rest from. howling a visible improvement
could be seen, which was maintained thenceforward.
A few hours later, it was found that urine had been passed
voluntarily, and some food taken. The excitement, although
markedly lessened, still persisted till the late afternoon, and
towards evening a general exhaustion succeeded it. After taking
somemore food the dog had a good night,and no further symptoms
appeared. The pupils, which in the evening were still contracted,
were normal again the next morning, and reacted well to light.
No more gastric tympany appeared after the puncture, and the
bladder did not refill to the former degree. The paralysis of both
these organs was therefore relieved. '
It is surprising that so sma~l a dose of morphia caused such
severe toxic symptoms, which aroused suspicion as to the purity
and accuracy of dosage of the drug. But the injection had been
given from a sterile solution supplied in an ampoule; and on
analysis it was found that the solution was pure and the dosage
accurate.
The case was therefore undoubtedly one of idiosyncrasy
towards morphia. Perhaps the idiosyncrasy was individual, and
perhaps the advanced age of the dog may have had something to
do wi th it; but the extremely -pampered life the animal had led for
years previously was a more probable cause of the condition.
Finally attention may be drawn to the great similarity of the
symptoms in this case to those commonly seen in cats after the
subcutaneous injection of morphia.
Post-Mortem Appearances are not characteristic, being those
of asphyxia.
Treatment consists in removal of the cause by em~sis, the
pump, and purgation. The depressant effects are combated by
caffeine hypodermically, or in cerebral excitement cold applica-
tions to the head. The stimulant action of small doses of atropine
seems useful. Potassium permanganate, slightly acidified, is
valuable to destroy unabsorbed morphine.
1:28 VETERINARY TOXICOLOGY
Chemical Diagnosis.-Morphine is separated in the course of
the alkaloid research by means of amyl alcohol extraction from
an ammoniacal solution. Morphine possesses many reactions, few
of which have any value in practical toxicology. Ferric chloride
gives a purple colour with solutions of morphine, but the test is
not delicate, a fair amount of morphine being needed. -Many of the
reactions are reduction processes, and therefore most unreliable,
if not absolutely misleading. A good test is that of Pellagri, which
depends on the formation of apomorphine, and is thoroughly
diagnostic. The suspected residue is warmed with concentrated
hydrochloric acid and a few drops of sulphuric acid until heavy
fumes begin to be evolved, cooled, diluted, and neutralised with
sodium bicarbonate. The solution is usually pale pink at this stage.
Solution of iodine is added very slowly in small quantities, when
an emerald green colour develops. On shaking with ether, two
layers form; the lower aqueous layer is green, and the upper
ethereal layer red.
Several experiments have been made at the Royal Veterinary
College to test the reliability of the methods of extraction and
recognition of morphine. A pony had 55 grains morphine in ball,
and was killed after four and a half hours. The urine was tested
and gave a good reaction for morphine by Pellagri's test. Another
animal was killed three days after receiving 60 grains, and on
analysis gave no reaction from ingesta, and doubtful tests from
freces and urine. No Pellagri test was got in extracts from the
lungs, liver, and stomach of a dog which had had IS grains of
morphine acetate subcutaneously.
In opium the alkaloids are combined with meconic acid, which
is separated in the routine process, and gives a dark red colour
with ferric chloride, stab_l~ to acids. The recognition of meconic
acid is usually taken as satisfactory evidence of the presence of
opium.
REFERENCES.
Kaufmann, M. (I90r), Therapeutique et Matiere Medicale V6terinaire,
3rd ed.
Oeller, A. (I9I4), Vet. Rec., 27,286.
Wooldridge, G. H. (1934), Encyclopredia of Veterinary Medicine, Surgery
and Obstetrics, 2nd ed.
ORGANIC POISONS AND DRUGS I29

COCAINE.
Occurrence.-Cocaine C17H2104N is the active alkaloid of the
coca plant, Erythroxylon coca, indigenous to South America. In
small doses it is a powerful stimulant, causing exhilaration and
enhanced muscular activity, for which reasons it is used by the
natives when performing long journeys without food. On the same
grounds horses are sometimes "doped" with cocaine, or cocaine
preparations, such as powders containing go per cent. strychnine.
Cocaine is valuable as a powerful local anresthetic, especi::}lly
in eye diseases. For local amesthesia in dogs Wooldridge (I934)
uses to grain per pound body weight, with a maximum dose of
2 grains.
POisoning may result from accident or from excessive "doping"
and depends (In the general action of cocaine as a convulsant,
. producing spasms, which may be confounded with those due to
strychnine.
In the horse toxic doses (60 to IOO grains) produce restlessness
and excitement, salivation, dilatation of the pupil, acute mania,
and intense excitement. In the dog there is first observed anxiety
and fear, then exhilaration, followed by weakness, muscular
twitching, rl).ythmical movements, convulsions and stupor,
dyspnrea, feeble pulse, and weakened respiration. The respirations
diminish in amplitude, but increase in frequency, and cease from
20 to 25 seconds before the heart.
Examples of cocaine poisoning are rare, not at all likely to
occur with the horse or ox, and not often with the dog.
At the present time cocaine is often replaced by the substitutes
such as novocaine and eucaine, or conjoined with adrenaline. This
acts by causing anremia of the part injected, and thus preventing
the carriage of the cocaine to the vital organs.
The toxic doses in grains per pound body weight are ap-
proximately:
Horse it grain
Ox; .. ~o
Dog .. 'Tlrs

but these are probably too low.


In the system cocaine is largely oxidised, and only in part
excreted by the kidneys, which renders its detection as a dope a
matter of some difficulty.
9
130 VETERINARY TOXICOLOGY
Treatment of cocaine poisoning requires rapidly acting
stimulants, such as nitroglycerin, strychnine or atropine,
together with the usual steps towards securing elimination.
Chemical Diagnosis.-Cocaine is separated in the general
search for alkaloids and may be recognised by producing local
anresthesia on the tongue and by Hankin's reaction. A few drops
of potassium permanganate solution are evaporated to dryness
on a glass slide by the aid of gentle heat and a drop of half-
saturated alum solution, together with a little of the purified
alkaloid, added. A cover-glass is then put on and the slide
examined under a microscope. Oily drops form at first, but later
rectangular, purplish-red crystals appear if cocaine be present.
The test fails, however, unless the alkaloid is fairly pure. A drop
of cocaine solution placed in the eye of a cat produces dilatation
of the pupil.
REFERENCE.
Wooldridge, G. H. (1934), Encyclop~dia of Veterinary Medicine, Surgery
and Obstetrics, 2nd ed.

ESERINE OR PHYSOSTIGMINE.
Occurrence.-The alkaloid eserine C15H2102Na occurs III the
:seed of Physostigma venenosum (Calabar bean, chop nut, or
ordeal bean), native to West Africa, and used by the natives as a
primitive method of trial by ordeal. Eserine is not likely to give
rise to poisoning among animals, but is used somewhat extensively
as a powerful defrecant in obstruction of the bowels. In this
capacity caution is needed, as some subjects are very sensitive to
the toxic effects. Crude eserine is further liable to be contaminated
with calabarine, an alkaloid which causes severe muscular tremors.
The dose of eserine as sulphate or salicylate is from I to It grains
for the horse hypodermically.
The toxic doses by' subcutaneous injection are, according to
Kaufmann (Ig01):
Dog .. 110 to 1'. grain
Horse 2t grains
Ox .. 5
The doses are probably underestimated, for a horse received
two doses of 3 grains each within twenty-five minutes, which
evoked symptoms, but there was recovery in two hours. In another
case, an aged horse which had suffered for a Week from impaction
ORGANIC POISONS AND DRUGS I3I

of the colon was given 12 grains of a commercial extract of Calabar


bean. The animal fell almost immediately, perspired, exhibited
muscular tremors, and died within a few minutes.
Dunning (1914) reported dangerous symptoms in a horse after
! grain eserine intravenously, and further noted death of a cow
after subcutaneous injection of I grain each of eserine, strychnine,
and pilocarpine.
Symptoms.-After a toxic dose of eserine there are powerful
muscular tremors resembling convulsions of central origin,
eserine acting like strychnine in augmenting the reflex activity
of the cord. The excitement is followed by paralysis, eventually
affecting the respiratory muscles, and death results from asphyxia.
The animal falls and the breathing is rapid, laboured, and ster-
torous, and in the later stages feeble and irregular. There is
increasing salivation, sweating, vomition when possible, and
increase4 peristalsis with expUlsion of dung and gas. The myotic
action of small doses is often replaced by mydriasis after large
toxic administrations.
Post-Mortem Appearances.-The large intestine is empty,
ana;mic, wrinkled, and hard. Bladder empty and contracted, as
also is the uterus. The muscles and motor nerves retain sensibility
for some time after death.
Treatment consists in emetics or the pump. After respiratory
failure life may be prolonged, or even saved, by artificial
respiration. Atropine is antagonistic to eserine, and should
be given subcutaneously. In distinction to eserine, atropine
inhibits secretion, diminishes reflex excitability, paralyses the
alimentary organs and bladder, accelerates the heart by paralysis
of intracardiac vagi, and is mydriatic, but large doses of atropine
are to be avoided, as aggravating the eserine effects.
Alcohol, digitalis, and ammonia may be given by the mouth,
whilst strychnine is stimulant to the respiratory centres.
Chemical Diagnosis.-Eserine is separated in the ordinary
procedure for alkaloids. Its solutions on keeping assume a reddish
colour, without loss of activity. The myotic effect may be
observed, but other myotics such as pilocarpine and muscarine
must be excluded.
Eserine gives the following colour tests: Sulphuric acid, yellow;
bleaching powder solution, red; bromine, red; but none of these
is characteristic. When an ammoniacal solution of eserine is
shaken in air, a pink colour develops which is soluble in chloro-
VETERINARY TOXICOLOGY
form. On evaporation of eserine or its salts to dryness in the
'presence of excess of ammonia, a blue-green residue remains.
This changes to red on the addition of dilute acetic acid, and it
becomes decolorised in the presence of reducing agents such as
hydrogen sulphide.
REFERENCES.
Dunning, F. ]. (1914), Vet. Rec., 27,2.
Kaufmann, M. (1901), TMrapeutique et Matiere l'vIMicale Veterinaire,
3rd eel.

PILOCARPINE.
Occurrence.-The leaves of Pilocarpus jaborandi, indigenous to
Brazil, contain the alkaloid pilocarpine C1iH1602N 2' which is
usually prescribed in the form of the nitrate.
Pilocarpine is allied in its physiological actions to eserine, and
more closely to muscarine. Muscarine is the active alkaloid con-
tained in the fungus Agaricus muscarius, or the fly-blown agaric.
This plant is used by the Siberian natives to produce a kind of
intoxication, and by long use they appear to gain a degree of
tolerance to its toxic effects.
Effects and Symptoms.-Pilocarpine stimulates glandular excre-
tion and involuntary muscle. Horses salivate copiously; after
3 grains subcutaneously the horse champs its jaws and salivates
freely, but does not sweat; the bowels move freely by stimula-
tion of the involuntary intestinal muscles. With large doses the
mucous secretion of the bronchi is so great that taken along with
the contraction of the tubes, great dyspnrea, which may be fatal,
is produced. According to Kaufmann (rgor), horses are poisoned
by 5 grains subcutaneously, but cattle are less sensitive; T.he dog
and cat are more sensitive, Frohner (I927) stating that! grain
killed a dog weighing I32 pounds by pulmonary redema.
Poisoning by pilocarpine could scarcely occur as the result of
accident or malice. It is only likely to happen under treatment,
and it is not therefore necessary for present purposes to do more
than signalise its possibility and main features. Atropine, which
stop~ secretion and paralyses involuntary muscle, is clearly the
proper physiological antagonist, and is the remedy to be used
in the contingency of an overdose of pilocarpine or eserine.
Chemical Diagnosis.-An alkaloid suspected to be pilocarpine
may be tested for as follows: A small quantityof the cl;lloride is
shaken in a test-tube with a crystal of potassium bichromate,
ORGANIC POISONS AND DRUGS I33
I to 2 c.c. of chloroform, and I c.c. of 3 per cent. hydrogen peroxide.
After a few minutes the chloroform layer becomes blue-violet to
indigo, according to the quantity of pilocarpine. Like nicotine,
pilocarpine gives a colour reaction with runman's p-dimethyl-
amino-benzaldehyde reagent. This becomes yellow when warmed
with the alkaloid or its salts.
REFERENCES.
Frohncr, E. (1927). Lehrbuch der Toxikologic, 5th ed.
Kaufmann, M. (I90r), Therapeutique et Matiere Medicale V6terinaire,
3rd ed.

IPECACUANHA AND EMETINE.


Occurrence.-Ipecacuanha is the dried root of the Cephaelis
ipecacuanha, indigenous to South America, and owing its activity
to the alkaloids emetine C29H4004N2' which is present in the dry
root in the proportion of I to 2 per cent., and in smaller proportions
cephaeline C28 H as 0 4N 2 arid psychotrine C2a:;Ef3604N2.4H20. In
pharmacy emetine is rarely used, the extract, syrup, and Wine of
ipecacuanha being the usual forms.
Effects.-There is very little chance of poisoning being caused
in the ordinary applications of this drug, large doses of which are
needed to give toxic symptoms. Thus, 3 ounces are quoted by
Winslow as having killed a horse, whilst Dun (I9IO) gives 3!
ounces. As regards pure emetine, Winslow gives 2 grains as fatal
to a dog, and Dun (19IO) gives for the dog !- to 8 grains, and for
the cat i grain. The latter authority describes 2 grains swallowed
by a dog as having caused violent vomiting, increased mucous
secretion from the respiratory and alimentary membranes, in-
flammation of the stomach and intestines, stupor and death in
twenty-four hours. The emetic effects of these drugs are prob-
ably due to local gastric action, for when given under the skin
emetine is excreted into the stomach and may be found in the
first vomitus.
Chemical Diagnosis.-Emetine may be separated in the general
search for alkaloids. With Frohde's reagent emetine gives a
. yellow colour, changing to green, and with Mandelin's reagent a
green colour. The alkaloid also gives a colour reaction in the
presence of nascent chlorine. This reaction may be carried out by
dissolving the ~lkaloid in concentrated hydrochloric acid, adding
134 VETERINARY TOXICOLOGY
a trace of potassium chlorate, and evaporating to dryness on a
water-bath. A pink colour is produced which changes to brown
when exposed to ammonia, fumes if emetine is present.
REFERENCE.
Dun, F. (1910), Veterinary Medicines, 12th ed.

GELSEMIUM. '
Occurrence.-GelseIl1ium is the root of Gelsemiu11t sempervirens,
or yellow jasmine, native to the Southern United States. The
rhizome and roots contain three alkaloids-gelsemine C2oH2202N2'
gelsemicine C2oH2504Nz, and sempervirine C19H161'f2.H20. Ac-
cording to Cushny (1941), gelsemine exercises an effect on frogs
like strychnine, but not on mammals, and it is probable that in
this case the effects of gelsemium are due to gelsemicine. Gelse-
mium is, however, very little used in practice, and cases of
poisoning are unlikely to be encountered.
Effects.-The genera.l effect is a prQgressive depression of the
respiratory centres, which are at first stimulated and then
paralysed. In poisoning there is muscular weakness, staggering,
and falling, with convulsive movements of the head and limbs.
Respiration is slow, pulse feeble, and temperature reduced. Con-
sciousness is preserved, and death occurs from asphyxia with
almost simultaneous arrest of the heart.
The lesions are those of asphyxia, as with coniine. Stimulants
such as strychnine, atropine, digitalis, and alcohol, along with
general measures of elimination, are indicated as remedies.
Chemical Diagnosis.-Preparations of gelsemium root are
identified by testing for gelseminic acid (!3-methyl-resculetine), a
substance present in many of the Solanacece. It is left as a residue
after evaporation of a chloroform extract from acid ~olution, and
is characterised by giving- a beautiful blue fluorescence- in water
or watery alcoholic solution. Gelsemine gives a bright red colour,
changing to brown when dissolved in sulphuric acid, and a- crystal
of potassium bichromate is drawn throlJgh the solution; with
potassium permanganate a red colour changing to violet is pro-
duced, and with Mandelin's reagent a red colour, which later
becomes reddish-violet.
REFERENCE.
Cushny, A. R. (1941), Pharmacology and Therap~utics, 12th ed.
ORGANIC POISONS AND DRUGS 135

VERATRINE.
occurrence.-Commercial veratrine is usually obtained from
the seeds, known as Sabadilla seeds, of the Mexican Schoenocaulon
officinale and contains a mixture of alkaloids, the more important
being cevadine C32H490sN and veratridine C36HsI011N. Many of
the false hellebores contain the same or closely related alkaloids
particularly in the rhizome; thus, the white and green hellebores,
Veratmm album and V. viride, contain jervine C26H3703N, rubi-
jervine C26H4302N, pseudo-jervine C29 H 43 0"N and protovera-
tridine C32H51011N, as well as cevadine and veratridine. The action
of these alkaloids resembles that of aconitine, the chief effects
being irritation of sensory nerve endings, particularly of the
mucous membranes, a characteristlc action on muscular contrac-
tion in which the muscle fails to relax after stimulation, and
paralysis of the higher centres, death being due to failure of
respiration.
Toxic Doses.-Commercial veratrine is exceedingly poisonous,
the toxic doses given by Kaufmann (rgor) being:
By the Mouth.
Horse 15 to 45 grains
Ox .. 15 to 45
Dog .. I to 5

According to Cornevin (r893), I gramme per kilogramme body


weight of the fresh root of Veratrum album kills the horse, and
2 grammes per kilogramme the cow.
Symptoms.-Dogs to which veratrine is given hypodermic-
ally salivate profusely, perform movements of mastication and
deglutition, and vomit profusely. Similar symptoms affect horses
and cattle, and actual vomition occurs with the latter. In all
cases there is profuse purgation, and frequently excessive urina-
tion. After a period of ~xcitability there is calmness, prostra-
tion, inability to rise, and inco-ordinated movements of the
members. There is an increase in muscular contractibility accom-
panied by a marked prolongation of the period of relaxation.
Poisonous doses lead to a weak, irregular pulse, owing to the
effects on the heart muscle, inhibitory apparatus, and vasomotor
centres. The respiration is deep and slow, and death occurs in
convulsions or paralysis.
Cresswell (r886) saw a horse seriously poisoned three hours
VETERINARY TOXICOLOGY
after having been given a ball containing Veratntm 'album as a
remedy for grease. There was continual retching, but no actual
vomiting; pulse 86, irregular and feeble; 'respiration 68.
Post-Mortem 'Appearances.-These are more or less extensive
inflammation and hcemorrhagic patches in the pyloric end of the
stomach and in the intestines. The bladder is empty, kidneys
inflamed, and liver often but not always congested. The blood is
black and fluid.
Treatment consists in, elimination of the cause, respiratory
stimulants, and warmth. Artificial respiration, if possible, is
effective. Carbonates and demulcents are indicated, tannin as an
alkaloid prec::ipitant, and ~orphine against the nausea and gastric
irritation.
Cresswell (1886) gave' 3 ounces of whisky and 3 ounces of
ammonia carbonate hourly for six doses, and then two-hourly.
In twelve hours there was improvement, and, under tonics and
stimulants, recovery.
Chemical Diagnosis.-Veratrine is remarkable in causing violent
sneezing when a little of the powder is sniffed: The quantities
isolated in a toxicological research are rarely sufficient for this
excellent test.
A characteristic reaction is that given by warming with hydro-
chloric acid, which yields a green passing to red colour. The rea
coloration with sulphuric acid is also given by the constituents of
hellebore. Sulphuric acid and sugar yield with veratrine succes-
sivelya yellow, green, and violet colour. _
The general effects of veratrine ought to be observed by injec-
tion in a mouse.
- REFEREN"CES.
Cornevin, C. (1893), Des Plantes Venemeuses.
Cresswell, ]. B. (1886), Veterinarian, 59, '227.
Kaufmann, M. (1901), Therapeutique et Matiere Medicale Veterinaire,
3rd ed. -

CURARINE.
Occurrence.-The alkaloid curarine C19H 260 2N is contained in
the' curara, wourara, wourali, or arrow poison, Strychnos taxi/era
of Guiana, and is associated therein with strychnine and brucine.
Effects.-Curarine paralyses the peripheral endings of motor
nerves. The first parts to be affected ~re the limbs, then the trunk
and head, and finally the respiration, which, with poisonous doses,
is gradually enfeebled, and ultimately ceases. Consciousness and'
ORGANIC POISONS AND DRUGS 137
intelligence are unimpaired. For the horse 32 to 48 grains sub-
cutane~usly are fatal, and for the dog f to 3t grains.
When taken by the mouth curarine is absorbed slowly. It is
eliminated rapidly, and unaltered in the urine, by whatever
channel it is given.
Artificial respiration is successful in combating curare poisoning
mainly by reason of the rapid elimination of the alkaloid.
As with the other medicinal alkaloids, there is little likelihood
of curare poisoning occurring outside of possible overdosage.
Chemical DiagnOSis-Curarine like strychnine gives a reddish-
violet colour when dissolved in concentrated sulphuric acid and a
crystal of potassium bichromate is drawn through the solution.

YOHIMBINE.
Occurrence.-Yohimbine C21H2603N2 is an alkaloid derived
from the bark of the Coryanthe yohimhi (Schumann), found in
the Cameroons.
I t is given in the form of the chloride in doses of grains ! for
the stallion, It for the bull, I! for the cow, l for the sheep, m to
rlo for small dogs, to for dogs from 20 to 50 pounds, and t for dogs
over 50 pounds. These doses may be repeated three times a day.
Efl'ects.-Yohimbine has some importance as a non-irritant
aphrodisiac drug, which excites the spinal erection centre and
congests the genital organs.
Poisoning has not often been observed, but Dun (1910) states
that dogs have been killed by ! grain, displaying dyspnrea,
depression of the heart, salivation, diarrhcea, a low temperature,
partial paralysis, and convulsions.
Although poisoning could not occur save as the result of care~
less dosage, it is well to point out its possibility, especially in view
of the rather wide use of the drug, and the likelihood of inexpert
employment.
Chemical Diagnosis.-Yohimbine gives with strong sulphuric
acid and potassium bichromate a dirty greenish-blue colour,
rapidly passing to dirty green (not characteristic). When yohim-
bine is mixed with a drop of a solution of benzaldehyde in alcohol
(I to 4), and a drop or two of sulphuric acid is added, the mixture
i.s at "first dark brown, then gradually (first at the edges) becomes
cherry-red, and finally violet.
REFERENCE.
Dun, F. (1910), Veterinary Medicines, 12th ed.
VETERINARY TOXICOLOGY

COCCULUS INDICUS.
Occurrence.-The seed kernels of A namirta paniculata, or
Levant nut, well known as Coccul1tS indicus, contain a chemically
neutral active principle, picroto'J(in C30H34013' The Levant nut
has an interesting toxicological history, but cases of poisoning by
it of the large animals are not described, although it is stated that
a small percentage of malicious poisonings of cattle in India are
due to it. Taylor (1934) relates cases of picrotoxin poisoning which
will show the possible vehicles. The principle is very bitter and
-intoxicating, though in large doses it causes intense pain and
frequent vomiting. It used to be employed as an adulterant to
beer, and Taylor (1934) cites cases of poisoning by this means.
It was also used as a fish poison, to poison wheat for the destruc-
tion of birds, and by robbers to render their victims powerless or
"hocussed. "
Cushny (1914) classes picrotoxin, as regards its effects, along
with cicutoxin and renanthotoxin, the active principles of Cicttta
virosa and CEnanthe crocata respectively (see these).
Chemical Diagnosis.-Picrotoxin is yielded to organic solvents
from the acid liquid in the systematic search for poisons. Sulphuric
acid and ammonium molybdate (Frohde's reagent) gives a gold
to saffron-yellow colour. If picrotoxin is evaporated to dryness
with a little strong nitric acid, the residue just moistened with
concentrated sulphuric acid and caustic soda added, a red colour
is produced.
REFERENCES.
Cushny, A. R. (1914), Pharmacology and Therapeutics, 12th ed.
Taylor, A. S. (1934), Principles and Practice of Medical Jurisprudence,
9th ed.

CANNABIS INDICA, OR INDIAN HEMP.


Cannabis indica is the dried flowering Q.r fruiting tops of tht:
female plant of Cannabis sativa, native to India, and is officina:
in the British Pharmacopreia. In India the drug is rarely used for
homicidal purposes, but is sometimes employed to produce
narcosis and facilitate the commission of crime. In that country
three forms are used to secure pleasant dreams/viz., bhang, tne
powdered ears and stalks; ganja, the dried flowering tops; and
charas, the resin extracted from the green plant. The first t:"o are
ORGANIC POISONS AND DRUGS 139
used to prepare drinks and sweetmeats, and the third (charas), or
a similar preparation, sometimes containing datura and called
"majun," is used for smoking.
Ganja is used in India as an anodyne-e.g., in the shoeing of,
or surgical operation on, the horse, and is neariy, if not equally,
as good as morphine. Rutherford (I9IO), who used the drug in
India against equine colic, states that it is as rapid as opium,
and has the advantage of not arresting the action of the bowels
or causing delirium. It is also stated that the duration of the
narcosis is longer.
The toxic doses for animals must be large. In the literature
there are few, if any, references to poisoning of aninals either by
the plant or extract. Hobday (I9IO) states that doses of 10 grains
to 2 drachms of extract given to dogs cause stupor, with paralysis
of the hind quarters, which might last two days, but are not fatal.
Smith (I9IO) and Rutherford (I9IO) both used Indian extract
in veterinary work, and the latter observed the effects of doses
of I to 8 drachms in bolus to horses. Only the I-drachm doses
caused preliminary excitement. The general symptoms were
dulness and sleepiness, pulse and respiration slowed, food
, neglected. When trotted, the animals moved as if drunken, side-
ways and unsteadily. Defrecation was suppressed, and the dulness
lasted up to thirty-five hours, after which recovery ensued.
From these valuable observations it is clear that fatal poisoning
by Indian hemp need not be seriously apprehended in its applica-
tions to animals.
REFERENCES.
Hobday, F. T. G. (1910). See Dun, F., Veterinary Medicines, 12th ed.
Eutherford, C. (1910), See Dun, F., Veterinary Medicines, 12th ed.
Smith, F. (1910). See Dun, F., Veterinary Medicines, 12th ed.

SANTONIN AND WORMWOOD.


Occurrence.-The shrubs santonica (Artemisia maritima) and
wormwood (Artemisia absinthium) of the order Compositre, both
grow in Great Britain, but are not likely to be eaten by small
animals. The effects of the active principles on larger animals are
not serious. Wormwood yields oil of absinthe, a narcotic poison
causing trembling, stupor, and convulsions in dogs. It is used as a
remedy for worms. Its consumption in the form of absinthe gives
rise to the very grave chronic absinthism in man.
Santonin, derived from the flower heads of A. maritima, is very
VETERINARY TOXICOLOGY
commonly used as a vermicide for round and thread worms, the
doses for dogs being from i to 3 grains, and for cats and small
dogs from 1 to i grain.
Symptoms and Treatment.-Overdoses are dangerous and some-
times fatal. They cause in dogs twitching of the head muscles,
rolling of the eyes, grinding of the teeth, rotation of the head,
and epileptiform convulsions, followed by clonic spasms. During
the spasms the respiration is disturbed, and asphyxia may occur.
Santo~in imparts a blood-red colour to the urine. It has been
'known to cause temporary blindness in the dog.
Poisoning is to be treated by emetics and purgatives. The con-
vulsions are prevented by chloroform, chloral, or bromides, and
artificial respiration is used if necessary.
Chemical Diagnosis.-(r) Santonin in solution in a little alcohol
is heated in a dish at'roo o C. with r or 2 drops of 2 per cent.
alcoholic furfural solution, and 2 to 3 C.c. of strong sulphuric
acid. The liquid becomes purple-red, blue-violet, dark blue,
and after sever~l hours deposits a black precipitate (delicacy
o~o grain). (2) Santonin is heated with a mixture of 2 parts of
strong sulphuric acid to I part of water until the liquid is yellow,
and after cooling a trace of ferric chloride is added. This gives,
as a rule, a turbidity, whilst on again heating there is a violet
coloration (delicacy 6~O)'
When a suspicion arises that harm has .been caused by over-
dosage of santonin tablets, the recognition and, if possible,
weighing of santonin removed from organs becomes a very
important matter from the medico-legal point of view.

TURPENTINE, CAMPHOR, AND ESSENTIAL OILS.


Occurrence.-Under tp.is heading may be conveniently collected
those cases of poisoning arising either from oils, essences, or the
plants which contain them. The general effect of this class is
irritant, and after absorption narcotic or paralysant.
Turpentine is the hydrocarbon, or mixture of hydrocarbons,
distilled from the oleoresin of the pine, Pinus sylvestris, etc., of
the order Conifera. Turpentines are optically active, rotating the
plane of polarised light, and this affords an excellent qualitative
guidt1. Thus, in examining a tar-oil preparation the obtaining of
an active distillate indicates turpentine or wood tar, as dis-
tinguished from coal tar. Oil of savin is chemically a turpentine,
.
and is contained to the extent of about 3 per cent. in the tops of
ORGANIC POISONS AND DRUGS 141

the common savin (Juniperus sabi1ta-Coniferce) , a cultivated


evergreen shrub, commonly credited with abortive properties.
Savin possesses a very characteristic acrid taste and smell, and
probably contains other principles than turpentine, for its activity
is certainly greater. Savin, American red, or pencil, cedar (Juni-
perus virginian a) , and Wellingtonia sequoia, are conifers not
indigenous to Britain, but cultivated in our gardens, and must be
held liable to be possible causes of poisoning. Like savin, the two
last-named species contain essential turpentine oils.
The rue (Ruta grav(oZe1ts} is an exotic member of the Gerania-
cece, cultivated in this country, and which contains, according to
Cornevin (r893), an essential oil, and an acid mtinic acid.
Camphor is a neutral, crystalline, volatile solid of the class of
ketones allied to turpentine, and is obtained from the evergreen
camphor laurel, native to"East Asia. Artificial camphor is prepared
by the action of dry hydrochloric acid gas on turpentine.
The common tansy (Tanacetum vulgare of the Compositce), allied
to the Artemisia, is a herb often used in this country to make
tansy tea. It contains a volatile ketone tanacetone, and has been
credited with causing poisoning.
In detailing the nature of the poisoning caused by the above-
named active principles, or the corresponding plants, it may be
again remarked that they present the same general features of
local irritant and remote paralysant action. And, further, that the
ill-judged exhibition by inexpert persons of all varieties of turpen-
tine, such as eucalyptus, is liable to cause serious results.
Poisonous Effects.-The symptoms, lesions, treatment, and
chemistry of these agents are here shortly summarised.
Turpentine.-Gamgee (r868) grouped turpentine with oil of
tar and naphtha as an active irritant, and pointed out that as an
antispasmodic it is a dangerous drug, often aggravating the
disease it is intended to cure. Large. doses cause irritation and
sometimes ulceration of the bowels. Turpentine is quickly
absorbed, and exercises paralysant effects in the same order as
those of alcohol.
Elimination occurs by the lungs and kidneys, and the urine
acquires the characteristic odour. Repeated small doses are more
likely to cause renal inflammation than one large dose, which
mostly passes off in the freces.
On examining the alimentary organs after overdosages of
turpentine, one observes marked congestion and fluidity of the
contents. In the horse the stomach is devoid of solid, and contains
VETERINARY TOXICOLOGY
brownish-yellow liquid, on which turpentine may be floating in
'large quantities. Such a result leaves little room for doubt that
poisoning has occurred.
Turpentine is easily recovered from organic matter by dis-
tillation in a current of steam. It reacts vigorously with iodine,
and on mixing equal parts of turpentine, amyl nitrite, and acetic
acid a crystalline precipitate is produced. Similarly, on the
addition, drop by drop, of hydrochloric acid, a blue colour is
produced and then a crystalline precipitate. A drop of the oil
mixed with concentrated hydrochloric acid and ferric chloride pro-
duces on warming a rose colour, changing to violet and then blue.
Savin.-Gamgee (r868) records a case in which the abortion
of foals had been secured by repeated dosage of savin. The
foals were dropped dead, and from the state of the membranes
it was thought that they had died some ten to twelve days pre-
viously to abortion. The condition of the mares was poor, and
there was a mucous discharge of an irritant nature from the anus.
The urine and freces smelt strongly of savin. The mares recovered
under treatment. The poisonous dose is uncertain. Hertwig gave
half a pound daily for si;x: or eight days to l;lOrses, without effect.
With large doses there is in general: diarrhcea, thirst, accelerated
pulse and respiration, and great prostration.
Fuller (r860) observed in horses pois'oned by savin: heavy
appearance, tucked-up flank, difficulty in swallowing, salivation,
and thirst; respiration quick and laboured, pulse quick and weak;
fceces hard and covered with mucus, urine dark and scanty; tem-
perature variable, and patches of cold perspiration. The symptoms
lasted four to five days, when there was great prostration and
deafh.
Moir (r862) recorded savin poisoning of an eight or nine year
old bay horse. He observed staring coat, sunken eyes, mouth
clammy, and viscid saliva; fceces slimy, great urination, corded
pulse, watery discharge from eyes and nostrils. The respiration
was not much increased.
On post-mortem both these observers found inflammation and
mucous discharge of the mouth, gUllet, stomach, and intestines.
In Fuller's cases the ccecum was full of yellow liquid, but in some
instances empty and contracted to about one-fourth. The colon
was full of undigested food, rectum thickened and inflamed, and
bladder full of offensive urine. In Moir's case, he found the
stomach full of oily liquid, in which savin was detected.
The treatmenF of savin poisoning is by means of opium to
ORGANIC POISONS AND DRUGS r43
allay pain, followed by mild aperients, demulcents, and stimu-
lants.
The oil gives an intense red colour with concentrated sulphuric
acid, and reacts vigorously with fuming nitric acid, yielding an
orange-brown solution.
Rue.-Corhevin (1893) states that the leaves of rue are some-
times used, occasionally with fatal results, to procure abortion.
He characterises its effect as those of a gastro-irritant causing
a period of excitement, followed by depression, weakened heart
action, lowering of surface temperature, abundant salivation,
and swelling of the tongue.
The lesions are those of gastro-enteritis, the posterior parts of
the alimentary canal being often normal. In females phere is con-
gestion of the uterus, with a violent colour if abortion has occurred.
Gamgee (r868) similarly remarks that in large doses the plant
acts as a narcoto-irritant. Well-authenticated cases of poisoning
by this plant are hard to find, and not very likely to occur
in Great Britain.
The oil, unlike savin, does not react with fuming nitric acid,
but effervesces on the addition of a drop of nitric acid, sp. gr.
1'42. It gives a colour reaction when added to an alcoholic solu-
tion of p-dimethylamino-benzaldehyde acidified with sulphuric
acid, a violet colour slowly appears which becomes brownish-red
on warming, and leaves a reddi!'\h-purple residue when evaporated
to dryness.
Tmtsy.-Poisoning by tansy has been placed on record by
Kobert (I908). The subjects were cattle, and the symptoms in-
cluded refusal of food, rumination slow, dung hard, dark, dry,
and covered with slime; shaking movements of head and neck,
pulse strong (64), temperature 38.6 C.; eyelids half-closed, pupils
contracted, and globe of eye flickering; dulness, staggering gait,
and weakness.
The oil produces a violet colour with fuming nitric acid and
reacts violently with iodine, leaving a greenish solution and a
black precipitate.
Camphor.-Hertwig (I91O) states that from! to ! ounce of
camphor proves fatal to the dog, whilst 2 to 4 ounce doses to
horses a:pd cattle, and 2 to 4 drachms to sheep, accelerate respira-
tion, heighten sensibility, and occasionally cause convulsions.
The general effects of camphor recall those of turpentine,
causing preliminary stimulation, with subsequent paralysis of
the central nervous system.
144 VETERINARY TOXICOLOGY
Camphor poisoning is rare, and not very likely to be en-
countered. Diagnosis is made easy by the elimination of the
poison in the exhaled air, to which the familiar odour of the
substance is imparted.
REFERENCES.
'TURPENTINE.
Gamgee (1868), Veterinarian's Vade-Mecum.
SAVIN.
Fuller, A. (1860), Veterinarian, 33, 135.
Gamgee (1868), Veterinarian's Vade-Mecum.
Moir, C. (I862), Veter'inarian, 35,643.
RUE.
Cornevin, C. (1893), Des Plantes Veneneuses.
Gamgee (1868), Veterinarian's Vade-Mecum.
TANSY.
Kobert (1908), Vet. ].,,64,375.
CAMPHOR.
Hertwig (1910). See Dun, F., Veterinary Medicines, 12th ed.

OIL OF CHENOPODIUM.
OcCurrence.-Chenopodium is a volatile oil distilled from the
seeds of Chenopodittm ambros'oides anthelminticum or American
wormseed, which is widely used as an anthelmintic against
roundworms and hookworms. The toxic and anthelmintic con-
stituent is ascaridol, CloH1602, which is found in the less volatile
fraction of the oil to an extent varying between 45 and 70 per cent.,
the remaining portion being made up of various terpenes. The
variation in the amount of ascaridol'present in different samples
of the oil makes exact dosage difficult, and it is probably on
account of this that fatalities occasionally arise, particularly in
pigs and dogs, following the administration of the accepted
anthelmintic dose of 3'5 ml. for the former and 1'0 mL for the
latter.
Symptoms.-The oil is readily absorbed from the alimentary
tract, where it acts as an irritant and is excreted at least in part
by the lungs; it does not appear in the urine. The. chief symptoms
of poisoning are gastro-entcritis ;:tnd evidence of involv:ement of
the central nervous system. Vajda (1935) reports that in pigs
the chief symptoms are muscular spasms, convulsions, and death;
and Clough (1936) records that in sbeep, convulsions are the most
ORGANIC POISONS AND DRUGS I45
prominent symptoms, 4 ml. by the mouth being fatal to lambs.
Cats as well as dogs are extremely susceptible to the effects of
the oil, and in these animals depression of the central nervous
system and vital centres controlling the heart and respiration is
usually well marked, the main symptoms being paralysis, coma,
and death, although in some cases convulsions may also be seen.
Treatment can only be carried out on general lines as the
symptoms arise. The administration of purgatives and stimulants
is indicated.
Chemical Diagnosis.-The oil may be recovered from the
viscera by steam distillation and the distillate extracted with ether.
When pure, the oil is yellowish in colour, with a characteristic
smell and, like turpentine, it reacts vigorously with iodine; it also
gives a brown colour when warmed with alcoholic potash, a
reddish-brown colour with concentrated sulphuric acid, and a
reddish colour with concentrated hydrochloric acid.
REFERENCES.
Clough, G. W. (1936), Vet. Rec., 48,53.
Vajda, T. (1935), Wien. t~erdztl. Wschr., 22, 142.

OXALIC ACID.
Occurrence.-Salts of oxalic acid are found in many plants,
notably in rhubarb and sorrel, which contains-the acid potassium
oxalate. Many plants also contain calcium oxalate deposited in the
microscopic quadratic, or envelope-shaped crystals, in which the
same salt is so generally observed Lin urinary deposits of the her-
bivorous animals.
Oxalic acid is used on a fairly large scale commercially as a
straw-cleaning agent, and under the name of salts of sorrel or
salts of lemon, oxalic acid is used for domestic purposes, such as
the cleaning of straw hats and brasswork, and the removal of
ink stains. It resembles Epsom salts in appearance, and confusion
with it has caused accidents. Oxalic acid is a common poison in the
human subject, but cases of the poisoning of large animals by it are
very unusual. Dogs may, however, be poisoned accidentally by this
agent in doses of about 15 grains, and cats by about 3 grains. In the
horse, Stewart and McCallum (1944) found that very large doses
of oxalic acid and oxalates were necessary before symptoms of
poisoning set in. In one case, a horse was given 200 g. of oxalic
10
VETERINARY TOXICOLOGY
acid daily for ten days without showing symptoms of poisoning
until the eighth day, and another animal received 200 g. of calcium
oxalate daily for six days, but no clinical symptoms of poisoning
were observed in this case. However, two doses of 454 g. sodium
oxalate, given with an interval of twenty-five hours between
them, produced symptoms of poisoning within a few hours after
the administration of the second dose and death in twenty-seven
hours, and similar doses of ammonium oxalate caused death in
three hours.
Symptoms.-Concentrated oxalic acid causes, in dogs, nausea
and vomiting of black or brown acid material. Difficulty in
swallowing, thirst, diarrhrea, and colic are alimentary symptoms
common to irritant poisoning. Gamgee (1868) indicates labouring
and spasmodic respiration; injection of conjunctivre, and dilatation
of pupil; small and irregular pulse; and with advancing stupor
and prostration tetanic twitchings of the muscles.
Oxalic acid and oxalates are absorbed slowly and excreted by
the kidneys as calcium oxalate, which, being insoluble, may cause
calculi.
Post-Mortem Appearances.-These are: a blanched appearance
of the membranes of the mouth, fauces, and gullet. The stomach
contains much gelatinous mucus, and is rarely perforated. More or
less intestinal inflammation is observed, and the blood is dark and
fluid. It will be remembered that oxalates prevent the coagula-
tion of blood by removing the soluble lime in the form of calcium
oxalate. In the experimental cases of poisoning of horses with
large doses of oxalic acid and oxalates, no characteristic lesions
were observed in the internaPorgans, but blood analyses showed
that there was anhydrremia with a high hremoglobin and low blood
calcium content.
Treatment.-Burnt magnesia or chalk is better than car-
bonate of potash or soda, since the fortller renders oxalic acid
insoluble. Lime water and oil and- demulcents are valuable, with
stimulants as indicated.
Chemical Diagnosis.-Oxalic acid may be extracted from organic
matters by feebly acidified water, but the 'best method is that of
dialysis through parchment as practised for salt, nitre, and
mineral acids. The diffusate may be Pllrified by neutralising and
adding lead a<:etate, which precipitates insoluble lead oxalate.
This is collected, washed, suspended in water, and sulphuretted
hydrogen passed into the turbid fluid. Lead sulphide is thus pre-
ORGANIC POISONS AND DRUGS I47
cipitated, and after filtering the solution on evaporation deposits
oxalic acid. A quantitative estimation may then be carried out
by dissolving the acid in hot hydrochloric acid and titrating with
N /ro potassium permanganate.
Two tests sufficiently cha,racterise oxalic acid, if sufficient
material is available: (r) Warmed with a strong sulphuric acid,
oxalic acid (and its salts) gives carbon monoxide and carbon
dioxide, and does not char. (2) Calcium chloride precipitates
calcium oxalate from a neutral solution. The calcium oxalate
is insoluble in ammonia and in acetic acid (distinction from
tartaric, citric, malic, and succinic acilis).
In medico-legal work oxalic acid or a salt must be recovered
from alimentary contents or vomit. The detection of calcium
oxalate in the urine is not evidence, especially with the her-
bivorre, in which a, diet of sorrel will cause increased excretion
of this salt.
REFERENCES.
Gamgee (1868), Veterinarian's Vade-Mecum.
Stewart, J., and McCallum, J. W. (1944), Vet. Rec., 56,77.

ALCOHOL.
Occurrence.-Alcohol results from the fermentation of sugar
by yeast, and thus ,enters into the composition of ale, wine, and
distilled liquors. The latter rarely exceed a strength of 50 per cent.
by weight of alcohol.
Acute alcohol poisoning is very occasionally observed in
animals, and, as in man, follows the consumption of a large do'se
of pure spirit or spirituous beverage. The chronic alcoholism of
man is not observed in animals, possibly from the inaccessibility
of alcoholics, for goats and sheep are stated quickly to acquire a
liking and tolerance for spirits, taking 6 or 8 ounces of brandy
without serious effect. Ducks, fowls, and parrots also take alcohol
readily after having had it given a few times.
Alcoholic intoxication is stated to occur amongst stock fed on
brewery and distillery residues, but the statement must be taken
with reserve, for in such residues the dilution is very great, and
this appears to be a most important factor. A dose of alcohol
which, when highly diluted and slowly consumed, causes no
harm, would, if concentrated and given in one dose, cause grave
intoxication, or even death. Cases of death in man after taking
VETERINARY TOXICOLOGY
a few ounces of undiluted spirit in one draught are common, and
the poisoning is often fatal in a very' short time.
Toxic Doses.-According to Hertwig (1910),8 ounces of concen-
trated alcohol caused the death of an old but sound horse in about
ten minutes. According to Dun (1910), four to five ounces of
whisky (of about 45 per cent. alcoholic strength), if retained,
kill a zo-pound dog in a few minutes. Eight grammes (about
120 grains) per kilogramme (about 2 pounds) body weight has
been stated as the toxic dose of alcohol. The higher alcohols-
propyl, butyl, and amyl-are more toxic and more irritant than
ethyl alcohol, or common alcohol. Crude spirit, however, ~n
doubtedly owes a part of its noxious qualities to the presence of
aldehydes, which are the first oxidation products of the alcohols,
and which are only slowly eliminated from raw spirit in the
process of maturation. . '
Symptoms.-A1cohol in large doses paralyses the nerve-centres
in the order of their development, the higher cerebral fun.ctions
being "first affected, the cardiac and respiratory last. In animals
the motor paralysis thus declares itself as a prominent feature, as
compared with the mental derangement of man.
In acute poisoning of animals there is a period of great excite-
ment, during which the patient exhibits brightness of the eye,
contraction of the pupils, and irregular movements. The horse
prances and strikes out with its feet. Very soon there is collapse,
with a small, weak pulse, coldness, coma, and death.
Post-Mortem Appearances.-The digestive organs show irrita-
tion after concentrated doses. The blood is dark, and clots are
found in the heart and large vessels. There is congestion of the
meninges of the brain, of the lungs, and other organs.
Treatment.-Antidotes are tea, coffee, or caff~ine. Strychnine
is a physiological antagonist, and may be injected. Ammonia as
a stimulant by the mouth, and purgatives, are indicated.
Chemical Diagnosis.-The separation of alcohol from tissues
is easy, but its exact identification is surrounded by pitfalls.
Distillation of the parts from' a neutral solutiOil will yield the
alcohol in the first part of the distillate. If the quantity permits,
the concentration may be increased by redistillation and dehydra-
tion with quicklime. If the alcohol can thus be got free of water,
the boiling point (780 C.) may be observed even with very small
quantities, and, taken along with the iodoform test, is sufficient
absolutely to identify. The iodoform test depends on the forma-
ORGANIC POISONS AND DRUGS 149
tion of the very characteristic iodoform on gently warming a
dilute solution of alcohol with sodium car1;>onate and a scrap of
iodine. It is, however, given by other compounds-e.g., aldehyde
and acetone-and therefore taken alone is not characteristic. In
medico-legal work it is valuable evidence to show that alcohol
is present in the blood and in the brain.
REFERENCES.
Dun, F. (1910), Veterinary Medicines, 12th ed.
Hertwig (1910). See Dun. F . Veterinary Medicines. 12th cd.

CANTHARIDES.
Occurrence and Uses.-The Spanish blister-fly, Cantharis vesica-
toria, is found in Southern Europe, Germany, and Russia, and con-
tains a powerful vesicant active principle, cantharidin, CloH1204'
The powdered insects form the ordinary cantharides of pharmacy,
and are sometimes adulterated with euphorbium and the China
blister-fly (Mylabris). Characteristic of Spanish fly is the brilliant
coppery-green of the wing sheaths. The Chinese fly is larger, has
two orange-coloured bands and spots on the wing sheaths. Can-
tharides, besides its use as a vesicant, is employed against exces-
sive urination, and in large (dangerous) doses as an aphrodisiac.
Poisonous doses of cantharides, according to Gamgee (1868), are,
for the horse or ox, ! ounce and upwards; for the sheep, I drachm;
and for the dog, t drachm. It is dangerous to employ too large or
too extensive applications of cantharides blisters, for poisoning
may result from absorption. Dogs lick the blistered parts, and
this leads to swelling and engorgement of the tongue.
Symptoms.-Large doses of cantharides cause strangury,
frequent passage of small quantities of urine, or its total sup-
pression, a small and rapid pulse, quickened breathing, and excite-
ment, followed by coma and collapse.
An interesting case of poisoning 0' a horse is recorded by
King (1907), The animal had 8 ounces of a mixture composed of
5 ounces each of linseed and turpentine oils, and 14 drachms of
powdered cantharides in mistake for linseed oil.
Next day the mouth and lips were seen to be blistered, the
horse was blowing slightly, and passing large quantities of urine.
The pulse was go, very quick and feeble, and temperature 100 0 F.,
soon becoming subnormal. The whole of the mucosa of lips and
150 VETERINARY TOXICOLOGY
mouth became blistered, and subsequently destroyed, the .mouth,
throat, and neck being very painful, causing much dribbling.
There was constipation and refusal of all food for five days, when
the patient took some oatmeal gruel and soft food. Belladonna
and nutrient enemata were given by the rectum.
On the sixth day the urine contained blood, and there was
slight abdominal pain. Injections of ether were given thrice daily,
but death occurred on the tenth day.
Smith (1924) recorded the deaths of seven horses resulting from
dosage with Chinese blister-fly in mistake for ipecacuanha. All
cases exhibited continuous though not very acute abdominal
pain, but no symptoms specially directed to the kidneys or
bladder. Treatment was unavailing.
On Post-Mortem'in King's case the kidneys were found to be
much inflamed, and each contained large abscesses. There were
large hremorrhagic spots on the bladder, and an ulcerated patch
the size of a crown piece in the stomach. The intestines and lungs
were much congested, and the endocardium of an intensely deep
purple hue.
In the Treatment of cantharides poisoning mucilages and
albuminous draughts, such as linseed tea, white of egg and the
like, are indicated. Oils are to be avoided, as they favour the
solution and absorption of the poison.
Cantharidin is present in all organs after death, but is especially
to be sought in the urine. It is insoluble in water, but is dissolved
by caustic alkalis. From urine, or an alkaline extract of organs,
cantharidin is extracted by chloroform after acidification. From
viscera cantharidin may be obtained by distillation in a current
of steam after the previous addition of phosphoric acid. The dis-
tillate is concentrated by repeated redistillation, made alkaline
",:ith caustic soda, and evaporated to dryness. The residue is
again heated with excess of ph.osphoric acid under a reflux con-
denser, and the solution extract~d with chloroform. The chloro-
form is then evaporated to dryness. The only test of any value
is the observation of the blistering effect, which is produced by as
little as 0'05 mg.
REFERENCES.
Gamgee (1868), Veterinarian's Vade-Mecum.
King. H. (1907), Vet. j., 63,270.
Smith, F. (1924), Vet. j., 80,38.
ORGANIC POISONS AND DRUGS 151

CARBON TETRACHLORIDE.
Forms and Occurrence.-Carbon tetrachloride, or tetrachloro-
methane, CC14 , is a colourless, non-inflammable liquid with a
boiling point of 76 C. and specific gravity 1600; it has a charac-
teristic smell resembling that- of chloroform. It was originally
introduced as a substitute for chloroform, but its use as an
anresthetic was soon abandoned, and it was not used in medicine
until Hall (I92I) demonstrated its value as an anthelmintic
against hookworm; subsequently, ~Montgomery (I926) showed-
that it was extremely efficacious in the treatment of fascioliasis,
and it is now widely employed for this purpose. It is also
extensively used in industry as a solvent for substances of a
fatty nature, tar, etc., and in fire-extinguishers, but, both in
animals and man, fatal cases of intoxication have arisen from
its use.
Absorption and Elimination.-Carbon tetrachloride vapour is
readily taken up by the lungs on inhalation; when given by the
mouth the liquid is slowly absorbed from the alimentary tract,
where it exercises an irritant effect. Following absorption, its
action in many respects resembles that of chloroform, narcosis
and, on occasion, serious liver disturbance being produced.
Elimination of therapeutic doses is mainly by way of the lungs,
only traces appearing in the urine. After the administration of
large doses it is also excreted with the freces.
Toxic Dose.-Montgomery (1926) administered up to 50 ml.
in capsule to individual sheep without causing ill-effect, and Ross
and McKay (1928) gave up to 100 ml., only causing the death of
one animal from asphyxia. As it had been established that as
little as 5 ml. was sufficient to destroy liver fluke, there appeared
to be a sufficient safety margin to warrant its use on a large scale,
but unfortunately this has not always proved to be the case.
Although very large numbers of sheep are treated annually without
ill-effect, there are many cases on record in which small doses
have caused fatal intoxication. Thus Norris (1927) records tha.t
sheep died after the administration of 2 ml. in capsule; Clough
(I936) records several cases in which sheep died after receiving
the usual anthelmintic dose of I ml. in capsule; and Rose (1932)
found that a dose of I ml. may in some flocks cause a mortality
rate of up to 30 per cent. of the treated animals. There is thus a
152 VETERINARY TOXICOLOGY
wide range in the susceptibility of sheep to the effects of the drug,
which is also the case in other species. Cattle, particularly milch
cows, show this variation, 10 ml. being sufficient in some cases
to cause severe symptoms and death, whilst in other cases doses
of 20 ml. are well tolerated; in dogs, 3 ml. per kg. body weight
may be harmless, but it has been possible to cause liver damage
in these animals with as little as 0'25 ml. per kg. body weight;
in pigs, White (1939) found that, whilst' a dose of 06 ml. per kg.
body weight was usually insufficient to produce symptoms of
poisoning, yet in some cases 0'2 ml. per kg. body weight caused
creath within twelve hours.
Numerous attempts have been made to determine the factors
responsible for producing individual susceptibility to carbon
tetrachloride, but up to the present experimental work has failed
to reveal the cause. In cases where the drug is given in a capsule
there is no doubt that occasionally a fatal pneumonia results
from breakage of the capsule in the mouth, and for this reason
Australian workers recommend that the drug be mixed with
liquid paraffin and given by means of a syringe, but such cases
do not occur often. The purity of the drug has also been ques-
tioned, but, although carbon tetrachloride will yield phosgene
when heated to a high temperature and may contain carbon
bisulphide as an impurity, the purity of commercial samples is
usually beyond question. Minot (1927) and others have connected
a hypocakremia with a susceptibility to the action of carbon
tetrachloride, but experimental evidence has not shown this to
be the case. A high protein diet has also been associated with a
susceptibility to carbon tetrachloride, since there' is a certain
amount of evidence that fatalities are more often encountered
in hand-fed animals in good condition than in animals in low con-
dition on the range. However, although carbon tetrachloride
poisoning is associated with a high guanidine content of the blood
and an increase in the total nitrogen excretion, indi'cating some
disturbance of protein metabolism, as well as with a hypoglycremia,
these effects are probably the result of liver injury and not the
cause of the susceptibility. Until further knowledge is obtained,
the safest procedure to adopt is to test the susceptibility of the
animals by dosing one or two before dosin_g them all, avoid giving
the drug to animals that are fat or are receiving a high protein
diet, and provide the treated animals with a mineral supplement
to their diet.
ORGANIC POISONS AND DRUGS 153
Symptoms.-In veterinary medicine,' poisoning by carbon
tetrachloride is usually acute following the administration of the
drug as an anthelmintic. The chief symptoms, which, as a rule, set
in rapidly, but may be delayed for two or three days, are loss of
appetite, dulness, staggering gait, somnolence, evidence of gastro-
intestinal disturbance with the passage of blood-stained freces,
constipation followed by diarrhrea, collapse, and death within
twelve to twenty-four hours. Signs of jaundice may be observed,
but are not always present.
Post-Mortem Appearances.-A gastro-enteritis of varying
intensity, particularly congestion of the abomasum and upper
part of the small intestine, with petechial hremorrhages on the
mucous surfaces, is the most constant lesion. The liver may show
congestion and fatty degeneration, with evidence of a central
necrosis, and the kidneys may also show congestion, cloudy
swelling, and necrosis of the tubular epithelium, but in some
acute cases of poisoning liver and kidney lesions may not be
observed. In cases where the drug has entered the lungs, septic
pneumonia, with acute inflammation of the bronchi and trachea,
are to be noted. In chronic cases, cirrhosis of the liver is the most
prominent lesion.
Treatment.-N 0 specific antidote' has yet been discovered for
carbon tetrachloride poisoning, and treatment should follow
general lines. Rose (1932) found that the oral administration of
4 g. of ammonium chloride in 60 ml. of water was of some benefit
to poisoned sheep; the administration of calcium chloride to
overcome the hypocalcremia has also been recommended, buHittle
evidence has been forthcoming to show that 'the symptoms are
relieved when the blood calcium level has been brought back to
normal. In this connection, there is some evidence that exercise
increases the hypocalcremia, so that this should be avoided in
cases of poisoning. Leach and Forbes (1941) have found that the
subcutaneous injection of xanthine prevents the onset of liver
cirrhosis in rats poisoned with carbon tetrachloride, and also that
the oral administration of sulphanilamide prevents liver necrosis
in acute cases, but the mechanism of this action is still un-
known.
Chemical Diagnosis.-It is usually possible to obtain a sample
of the drug which has been responsible for poisoning; this should
be examined for impurities, particularly carbon bisulphide. The
identification of carbon tetrachloride in viscera is difficult unless
154 VETERINARY TOXICOLOGY
sufficient can be obtained to carry out a boiling-point deter-
mination; it gives the general reactions of the organic chlorine
derivatives and possesses a characteristic smell. It may be
distilled in a current of steam, and chlorine detected by
means of starch-iodide paper on decomposition of the vapour
by heat; carbon tetrachloride also gives the isonitrile reaction
when heated with aqueous caustic potash solution and a drop
of aniline.
REFERENCES.

Clough. G. W. (1936). Vet. Rec., 48,551.


Hall, M. C. (1921), ]. Agr. Res., 21,157.
Leach, B. E., and Forbes, J. C. (1941), Proc. Soc. Exp. Biol., N. Y., 48,
3 6 1.
Minot, A. S. (1927), ProG. Soc. Exp. BioI., N. Y., 48,361.
Montgomery, R. F. (1926), J. Camp. Path. and Therap., 39, II3.
Norris. ]. H. (1927). Vet. Rec., 7, 598. .
Rose, A. L. (1932), Aust. Vet. J.. 8,122.
Ross, I. C., and McKay, A. C. (1928), Aust. Vet. J., 5,17.
White, E. G. (1939), J. Path. and Bact., 49, 95.

PHENOTHIAZINE.
Occurrence.-Phenothiazine, or thiodiphenylamine, is a second-
ary amine prepared by heating diphenylamine and sulphur in the
.presence of an oxidising agent. It occurs as a fine, smooth,
yellowish-green powder, which is insoluble in water but readily
soluble in the fat solvents, and which crystallises from alcoholic
solutions in fiat, leafy crystals with a soapy feel and sharp melting
point of 180 0 C. It is the parent substance of such dyes as methy-
lene blue, thionin, etc., and has been used in industry since its
synthesis by Bernthsen in 1885. It was not, however, until
1934 that it was introduced into medicine as an anthelmintic
and urinary antiseptic, and it is now extensively employed
as an anthelmintic, particularly in the treatment of helmin-
thiasis.
When dry, phenothiazine is perfectly stable, but under moist
conditions spontaneous oxidation occurs with the formation of
two red dyes, thionol and phenothiazone. These substances are
easily reduced to the corresponding colQurless leuco-forms, the
reaction being rev~rsible:
ORGANIC POISONS AND DRUGS 155
H

r
N N
("'/~/~'
H
HO
?' '\/
IlJl)OH
s -?" --- HO~)U~)=O
----,>

s
.l'V~"/,\- /// Leucothionol Thionol

l/~J,,)(
s
Phenothiazine
"'-
\.a. I
~AA.I'
H
N
("'-A/'\-
I I IOH
Leucophenothiazone
-<-- r'A N

I I I
'\/V~/=O
s
Phenothiazone

As pointed out by Davey and Innes (1942) and others, these


derivatives arise in the body following the administration of
phenothiazine, the particular compound produ~ed depending
on the oxidation-reduction potential present at the time;
Collier (1940) obtained some evidence that these derivatives inter-
fere with tissue oxidation, whilst phenothiazine itself does not,
so that they may be the toxic principle and not phenothiazine
itself. .
Toxic Dose.-The earlier work of Lapage (r940) and Taylor and
Sanderson (1940) showed that in most cases domestic animals are
very resistant to the effects of phenothiazine, but since the
administration of the drug has been practised on a large scale,
cases of poisoning, particularly in horses and pigs, have been
recorded, although the incidence is very small in proportion to
the large number of animals treated. The general conclusions may
be reached that an individual susceptibility to the drug does exist,
that repeated small doses are more likely to produce toxic effects
than a larger single dose, and that young animals are more
susceptible to the drug than adults; however, the cause of this
apparent susceptibility has yet to be explained, and it is difficult,
therefore, to state precisely the toxic dose of phenothiazine.
Taylor (1942) has collected a number of cases in which horses
died following the administration of 30 g., the usually accepted
anthelmintic dose for these animals, although Lapage (1940)
found that a single dose of 500 g. had no ill-effect on a 9S2-pound
thoroughbred mare, and 125 g. produced no toxic effect in calves;
Roberts (1941), however, found that for pigs 0'5 to 08 g. per
pound body weight may be dangerous.
156 VETERINARY TOXICOLOGY
Symptoms.-Evidence of poisoning as a rule sets in a few hours
after administration, but occasionally may be delayed for several
days. The chief symptoms are restlessness, staggering gait"
muscular weakness; there is destruction of red blood corpuscles
with anc:emia, jaundice and hc:emoglobinuria, weak rapid pulse,
respiratory distress, colic, diarrhcea, prostration, and death after
a short illness; in pigs, inco-ordination of movement, weakness of
the hind limbs, and inability to stand are the most prominent
symptoms.
Approximately 50 per cent. of the phenothiazine administered
is excreted unchanged in the fc:eces, the remainder in the form of
its derivatives, or perhaps a conjugated form of phenothiazine is
excreted in the bile, urine, milk, and other secretions. The colour-
less leu co-derivatives are present in the urine, which is usually
colourless when voided, but turns red on exposure to air.
Post-Mortem Appearances.-The most constant findings are
enlargement of the liver and kidneys, the bladder full of dark red
urine, and evidence of jaundice, but in some cases no diagnostic
lesions may be present.
Treatment.-Symptomatic treatment is all that can be at-
tempted, since no specific" antidote as yet has been discovered.
Owing to the destruction of red blood corpuscles, blood trans-
fusion is in<;licated, but Taylor (I942) does not consider that this
or any treatment holds out much hope of success.
Chemical Diagnosis.-This should present little difficulty,
since poisoning is only likely to follow the administration of the
drug as an anthelmintic. Phenothiazine, being soluble in fat
solvents, may be extracted from the ingesta by ether, the ether
evaporated, and the residue _dissolved in alcohQI, from which the
phenothiazine will crystallise o_n the addition of water; a melting
point determination will then establish its identity.
REFERENCES.
Bernthscn, A. (1885), Liebig's Ann. Chem., 230, 187.
Collier, H. B. (1940), Canad. ]. Res. Sec. D., 18,272.
Davey, D. G., and Innt!s, J. R. M. (~942), Vet. Bull., 12, R7.
Lapage, G. (1940), Vet. Rec., 52, 648.
Roberts, F. H. S. (1941), Aust. Vet. ].,17,130.
Taylor, E. L. (1942), Vet. Rec., 54, 95.
Taylor, E. L., and Sanderson, K. M. (1940)' Vet. Rec., 52,635.
POISONOUS PLANTS
IT will be very readily admitted that anything approaching a
full enumeration of the plants which are, or are suspected of being
poisonous to animals, still more a reliable account of their effects,
would be a task of extreme difficulty and outside the scope of a
book of this nature. A mere catalogue has little value, so that the
attempt has been made to collect primarily well-substantiated
information relating to common poisonous plants. This naturally
involves a preferential treatment of British and European
genera, since there have been for a longer time opportunities of
exact study, but attention will also be given to the valuable work
which has been done and is still going on in America, South Africa,
Australia, and elsewhere. This has made great advances in recent
years and has considerably increased the knowledge of the in-
digenous poisonous plants of these countries.
Much of the literature of the subject is scattered throughout
veterinary, botanical, and agricultural journals, reports of
institutes and colleges, and Government publications, the more
important of which will be mentioned in the text. Of the older
literature, the report of the United States Bureau of Animal
Industry, I898, contains a summary of numerous American
species by V. K. Chesnut; several important papers have appeared
in the Transvaal, Cape, and Union of South Africa agricultural
journals; and F. N. Windsor in "Indian Toxicology" makes
reference to some Indian plants commonly used as poisons. All
these sources of information have been freely drawn upon. Many
tropical plants have been well known for a long time as the
sources of valuable drugs, some of which have been mentioned
in the preceding section, so that they are not referred to in the
present connection, although it is possible that the plant may act
as a vehicle of poisoning to animals.
With regard to the textbooks available, "Des Plantes Vene-
neuses," Cornevin (1893), and "Die Giftpflanzen Deutschlands,"
Esser (I9IO), are still invaluable standard manuals; to these may
be added "Poisonous Plants of the United States," Muenscher
(I940), and "The Toxicology of Plants in South Africa," Steyn
(I934). In addition, the mpnumental work, "Biochemie der
Pflanzen," Czapek (I92I), and "The Plant Alkaloids," Henry
(1939), are of great value. To all of these the author is greatly
157
VETERINARY TOXICOLOGY
indebted. The botanical descriptions given in the text are for the
most part taken from "British Flora," Bentham and Hooker
(I9 08).
The loss to agriculturalists in anyone year from poisonous
plants must be enormous, but there is no way of assessing what
this may be, for in most cases no record is available. Moreover,
it may not always be possible to come to a definite conclusion,
since so many factors must be taken into account. The toxicity of
a plant may show considerable variation under different con-
ditions of soil, climate, and stage of growth; the susceptibility of
the animal and the parts of the plant eaten must also be con-
sidered. Cultivation may also have an effect'on toxicity, rendering
some plants comparatively harmless, and in some cases altering
the alkaloidal content. There is also a certain amount of evidence
to suggest that strains of the same plant grown under similar
conditions may show a variation in toxicity, owing to hereditary
factors, but these are at present not well understood. It will be
evident, therefore, that great care must be exercised before
coming to the conclusion that a particular plant has been the
cause of poisoning.
As a general rule, cases of plant poisoning are more numerous
in winter and early spring or under conditions of drought when
green food is scarce and the animals are tempted to eat .plants
which they would not otherwise touch. Young animals are more
susceptible to poisons than adults, and in districts where poisonous
plants are prevalent newly introduced animals are more likely to
be affected, since they have not learnt to discriminate between
the wholesome and.unwholesome plants of the district.
Although many plants contain traces of toxic substances, it
does not necessarily follow that th~y will give .rise to cases of
poisoning. For example, many most valuable forage plants
contain traces of hydrocyanic acid, out are only dangerous under
certain limited circumstances; thus, the hydrocyanic acid content
of sorghum is only likely to be dangerous when the plants are very
young or after wilting. Perhaps the point of greatest importance
to consider is whether the amount of the plant eaten at anyone
time contains poisonous material, whicn can be absorbed from
the alimentary tract in sufficient amount to bring about harmful
effects. ,
Craig and Kehoe (I925), in a valuable paper on plant poisoning,
base their classificatjon according to the nature of the active
POISONOUS PLANTS 159
principle: (I) alkaloids, (2) glycosides, and (3) phytotoxins, to
which must be added (4) unclassified. But after consideration, it
appeared more satisfactory to deal with the poisonous plants in
the sequence of their natural orders, although it is arguable that
a more rational procedure is to classify them according to the
pharmacological subdivisions of the active principles. But such a
classification is not satisfactory, since it cannot be precise, and it
seemed better to follow the line of least resistance, or, it is hoped,
of least controversy.
REFERENCE.
Craig, ]. F., and Kehoe, D. (I925), Vet. Rec., 5, 795.

CONIFERlE.
The chief poisonous species of the Coniferro, or pine family,
found in Gn~at Britain and Europe are T axus baccata, or yew,
and the shrubs of the juniperus species, such as savin. Poisoning
by turpentine and savin have been described under a previous
heading, and therefore a description of yew poisoning only will
be given at this point.
Yew.-The leaves of the common yew, or Taxus baccata, and
its varieties, such as the Irish yew (T axtts fastigiata) , and yellow
yew, have long been known to be poisonous, and contain as active
principle the alkaloid taxine. The same active principle is probably
contained in the American species, Taxus minor, found in the
North-Eastern United States, and l,nown there as common yew,
ground hemlock, or poison hemlock.
This alkaloid occurs in the leaves of all species, but only in
small proportion in the berries. According to Thorpe and Stubbs
(1902), the undried leaves yield on extraction 01 to 0r8 per cent.
of taxine. It seems likely, further, that the leaves of the male
contain slightly more alkaloid than those of the female tree, but
the difference is trifling.
Much controversy formerly existed as to the poisonous effects
of yew, it having been held that the poisonous qualities vary with
the season, with the freshness of the leaves, and with the species
of the animal. But there can no longer be any doubt that the
leaves at all times may be poisonous. The alkaloid may be easily
separated and detected from dried or undried leaves. Well-
authenticated examples of poisoning among the domesticated
animals are very numerous, and the definite toxicity of the
r60 VETERINARY TOXICOLOGY
alkaloid extracted chemically from the leaves may be readily
observed upon experimental animals. Such variations as have
been observed are readily comprehensible in consideration of the
known variability in the action of any poison according to the
condition of the alimentary system and individuality of the
subject. When a few sprigs of
yew are eaten by an animal on
a full stomach, it is quite to be
expected that dangerous results
may not ensue.
Action and Toxic Doses.-The
action of yew, as of so many
plants, is complicated by the
fact that, in addition to the
chief alkaloid, other toxic sub-
stances are present as well.
The sap is acrid owing to the
presence of a volatile oil, oil of
yew, and the leaves contain
traces of the alkaloid ephedrine
and traces of hydrocyanic acid.
However, there is little doubt
that the chief action of yew
is due to the alkaloid taxine,

i~
C37H51010N, which is non-irri-
tant.
Accord~ng to Cornevin (I893),
the poisonous doses are:
Horse .. 2 g. per kg. body weight.
FIG. I.-TAXUS BACCATA (COMMON Ox 10 g.
YEW). Sheep .. 10 g.
(From Smith's "Veterin-ary Goat 12 g.
Hygiene.") Pig 3 g.

The doses refer to ingestion of autumn and winter leaves and


show, as is usual, a relatively great degree of resistance on the
part of the ruminant.
There are several recorded in~tances of yew poisoning in man,
generally of lunatics, from which it appears that the poisonous
dose of leaves for the human subject is small. In these cases,
quoted by Taylor (1934), it is noteworthy that, as with animals,
POISONOUS PLANTS 161
a comparatively short period of time elapses between taking the
poison and the onset of symptoms and death.
The alkaloid is rapidly absorbed from the alimentary tract, and,
as sp.own by Nicholson (1933), it exercises its chief effect on the
heart. This is at first slowed owing to depression of the conducting
tissue, and finally standstill of the heart in diastole results. No
evidence has been obtained to indicate that taxine directly affects
the respiratory centres or central nervous system, the pronounced
respiratory distress being due to asphyxia as a result of the heart
failure. The alkaloid, however, even in small doses, depresses the
smooth muscle of the body.
Taxine is rapidly broken down in the body, probably by the liver,
and is excreted in the form of benzoic acid, so that the alkaloid
cannot be demonstrated in the urine, milk, or other excretions.
Symptoms.-A remarkable feature of yew poisoning is its
rapidity. Often the effects only appear in cattle when chewing
the cud. Whilst quietly chewing, they drop as if shot. In some
examples recorded in the literature the animal died whilst in
the act of eating the plant, or was found to have fallen and died
suddenly without evidence of a struggle. The animal will stop
suddenly whilst working, start blowing and trembling, stagger,
fall on haunches, then on side, and die quietly. Death occurs
in about five minutes, with symptoms like apoplexy. A case of
death after sixteen to seventeen hours of a colt is recorde<l by
Jarvis (1893), who points out that the plan't was taken on a full
stomach, but that paralysis of the alimentary system, with
stoppage of digestion, immediately ensued.
Post-Mortem Appearances.-The stomach is generally distended
with gas, owing to fermentation following the arrest of digestion.
Intense inflamm.ation is almost invariably observed, but does not
appear to be a salient feature in the cases amongst the human
subject quoted by Taylor (1934). The stomach is found to contain
dark green ingesta, and sprigs, berries, or leaves of yew may be
easily recognised, but if dry sprigs were eaten they may not be
recognised. The inflammation rarely extends to the intestines,
which also rarely contain fragments of yew. The liver, spleen, and
lungs are engorged with dark blood. The right heart is empty,
and the left heart contains more or less of dark, tarry-looking
blood. Similar observations are recorded by Gillam (1906) in the
case of the pig.
Treatment.-The prognosis of yew poisoning is grave. Cases
II
r62 VETERINARY TOXICOLOGY
of recovery are few, but one is recorded by M'Phail (r900). An
emulsion in sodium bicarbonate solution of r pint linseed oil,
with 2 ounces each of chIaro dyne and nitrous ether, was given,
followed after some hours by whisky and linseed oil. Stimulants
and chlorodyne were repeatec1next day. After a purge and further
dose of opiate, recovery ensued after the fourth day.
Another. similar case is that recorded by Stanley (r859), in
which the remedial measures were bleeding, sodium carbonate,
and turpentine, followed by drenches and stimulants.
When possible, purgatives and demulcents are indicated, and
stimulants, caffeine, alcohol, etc., to combat the depressant action
of taxine. The heart should be supported by injections of adrenalin
and barium chloride, and a respiratory stimulant such as lobeline
is also indicated, but so long as much yew remains in the stomach
medicinal treatment is of little use. If the diagnosis is certain
rumenotomy offers the best chance of success. .
Chemical Diagnosis.-The alkaloid taxine is extracted, though
not without' loss, in the general scheme of search for vegetable
poisons. Risk of decomposition is minimised by operating at a
low temperature, as is done by evaporating extracts in a partial
vacuum. Taxine is not well defined chemically, it being not
absolutely established that it is a single substance. But the sub-
stance extracted in the usual way is characterised by giving a
pure rose-pink colour with strong sulphuric acid, which is fairly
permanent, but disappears on dilution; with Frohde's reagent, a
violet colour is produced.
In practice, however, the finding of yew fragments offers an
amply sufficient proof of poisoning, taken along with the clinical
and post-mortem observations, and it is also to be noted, as a
caution, that many other substances give a red colour with
sulphuric acid. But of these many are not basic, and can therefore
be distinguished from taxine, which is; whilst the veratrine and
hellebore principles do not give the red colour in the cold, and,
further, also, give other characteristic tests. Fina:lly, a physio-
logical test on a mouse or rabbit -should be used in additional
confirma tion.
REFERENCES.
YEW.
Cornevin, C. (1893), Des Plantes Venlmeuses.
Gillam, W. G. (1906), Vet. Rec., 1;8, 88.
Hoare, E. W. (1893), Vet. Rec., 6,588.
Jarvis, H. (1893), Vet. Rec., 6,398.
POISONOUS PLANTS
McPhail, J. (1900), Vet. j., 56,27
Nicholson, J. A. (1933), 3rd Rept. Dir. lnst. Anim. Path. Cambs., 169.
Stanley, F. T. (1859), Veterinarian, 23,450 .
.Taylor, A. S. (1934), Principles and Practice of Medical Jurisprudence,
9th ed.
Thorpe, T. E., and Stubbs, G. (1902), J. Chem. Soc., 81, 874.

ARACElE.
The only member of the Aracere, or arum family, found wild in
Britain is the Arum nzaculatum, known under the common names
CUckoo-pint, lords-and-ladies, wild arum, water robin, Portland
sago, etc. Cornevjn (I893) further name_s A. italieum, A. draeun-
elflus, and the marsh plant Calla palustris as being similar to
A. maeulatum in effects. In America, A tisa}'}Jza triplzyllum and
Symploearpus fcetidus also belong to the arum family and have
been reported to give rise to cases of poisoning ..
The Cuckoo-Pint (Fig. 2) is a familiar hedgerow' plant having
a tuberous root-stock, flowering in May, and having clustered
scarlet berri'es in August. The leaves are glossy, halberd-shaped,
and spotted. Cases of the poisoning of animals by it are rare,
although several cases, chiefly of children, are on record in human
toxicology. Numerous other species of the arums have similar
toxic properties, but they do. not appear to have caused poisoning
of animals to a notable extent.
Active Principle and Effects.-Like the allied species, this plant
contains an acrid juice of unknown chemical nature, a:t:d has the
effect of a powerful irritant. The juice is found in all parts, and
drying or boiling to a great extent deprives the plant of its
activity. Formerly starch for laundry purposes and a kind of sago
used to be made from the plant, and preparations of the root also
enjoyed some repute as cosmetics. The old herbalists used to
recommend the juice as a purgative, a practice which must have
been attended with grave risk.
Animals do not eat the plant readily, even if kept from other
foods. If a dangerous quantity is taken, there is intense irritation,
purgation, and vomiting (when possible), with the after-effects of
convulsions, exhaustion, and possibly death from shock.
In the Treatment of a case of poisoning demulcents and
stimulants are indicated.
REFERENCE.
Cornevin, C. (1893), Des Plantes Ven{meuses.
VETERINARY TOXICOLOGY

IRIDACElE.
The Iridaceffi, or iris family, includes the numerous cultivated
species of our gardens, and there are found in the wild state Iris
pseu,dacor/ls-yellow iris, yellow flag, or water flag; and I. fceti-

FIG. 2.-ARUM MACULATUlIl (CUCKOO-PINT).

dissima-stinking iris, stinking gladwyn, or glader. They contain


as active principle iridin, C24H26013, a glycoside belonging to the
group of vegetable purgatives. Poisoning of animals is rare, and
the effects are those of a drastic purgative. It will thus be
POISONOUS PLANTS
sufficient to signalise the possibility of danger through the giving
of parts of such plants to animals, especially to pigs.
The American Gyrotheca capitata, red-root, or paint-root, of the
Atlantic coast and Cuba, belongs to the r..1ated order of Hcemo-
doracece, and has a red sap. It is supposed to be dangerous to pigs.
This order also includes the South African "tulps" or "tulips,"
which give rise to the so-called tulp poisoning. Thl'Y are dis-
tributed throughout the country, and some have been introduced
from Australia, where their dangerous character has also been
noted. They thrive_in various localities-in sandy soil, in vlei lands,
a
and on hillsides. Tulp is frequently prominent plant after the
first rain~ on burnt veldt. Steyn (I934) lists seven Homeria species
and five M orcea species as being poisonous, the more prevalent
being H. collina (Groot tulp) and Morcea polyanthus (Elou tulp).
Poisoning.-The dangerous character of the tulps seems estab-
lished beyond all doubt, although little is known as to the active
principle. Mackenzie (I9IO) found that the corm of H. collina
contains a glycoside with a digitalis-like action, and tinctures
have been prepared from other tulps with a similar action, but in
the case of H. pallida Rindl (I924) obtained an alkaloid which
he named homeridine. The active principle present in M orcea
species has not yet been determined. Diagnosis of tulp poisoning
must therefore depend on circumstantial evidence.
Steyn (1928) found that the fresh bulbs and leaves of H. callina
and M. polystachya caused the death of sheep in twenty to thirty
hours when administered by stomach tube, the most constant
symptoms being dulness, colic, diarrhrea, and tympany. Bowhill
(I900) has described tulp poisoning of horses, the chief symptoms
being a rise of temperature, thready but strong pulse, loss of
appetite, dulness, with drooping of the head and ears; the mouth
is burnt, there is some frothing and grinding of the teeth, and in
some cases arching of the neck, regurgitation of gas and attempted
vomition; the colic, slight at first, increases rapidly in severity, and
in about two hours there is well-marked tympanites; finally, there
is coma, in some cases convulsions, and death in five to ten hours.
Williams (I902) distinguishes subacute cases with tympanites
and the usual symptoms of flatulent colic and acute cases, in
which there is extreme tympanites, the animal dashes about
with staggering gait, pupils dilated, convulsive twitchings, lips
retracted, and symptoms of asphyxia. The patient falls and dies
immediately.
r66 VETERINARY TOXICOLOGY
Treatment follows general lines. Turpentine, linseed oil, and
tapping the distended bowl are indicated. Stimulants, such as
caffeine, alcohol, and camphor, should also be given, but digitalis
is contra-indicated.
The lesions are those of acute gastro-enteritis, with large
ecchymosed patches at the entrance to the pylorus. Hyperremia
and congestion of the liver, kidneys, lungs, and hremorrhages in
the spleen may also be observed.
REFERENCES.
HOMERIA.
Bowhill (1900), Vet. Rec., 13,229.
MackenziE!!, A. T. (1910), S. Afric. Med. Rec., 8,94.
Rindl, 1\1. (1934), Trans. Roy. Soc. S. Afric., 11,251.
Steyn, G. D. (1928), 13th and 14th Repts. Dir. Vet. Educ. and Res.,
S. Africa, 187.
Steyn, G. D. (1934), The Toxicology of Plants in South Africa.
Williams, A. T. (1902), Vet. Rec., 15,421.

AMARYLLIDACElE.
The Amaryllidacere, or amaryllis family, includes numerous
species of narcissus or daffodil, so well known as garden plants,
some of which may be found wild, probably having established
themselves from garden culture. The same order also includes the
Galanthus or snowdrop. None of these is likely to be the cause of
poisoning, as animals refuse the leaves. They all contain an
essential oil and have powerful emetic and 'purgative properties.
The atamasco lily, Zephyranthes atamasco, of the South-Eastern
United States, is believed to cause staggers in horses. Several
poisonous members of this family occur in South Africa, the
best known being A maryllis belladonna and Buphane disticha.
The active principle of the amaryllis family is probably the
alkaloid lycorine, C16H1P4N, which has been isolated from
A. belladonna and other members of the family, and which in
large doses produces a hydrastine-like action with vomition and
diarrhcea. Other alkaloids and amorph-ous basic substances have
also been isolated, which may have a: toxic action; thus, in addi-
tion to lycorine, B. disticlza contains another alkaloid, buphanine,
C23H2406N2, and two amorphous bases, one of whicI:t is a con-
vulsant poison, and the other posseses -a colchicine-like action.
The plants have powerful emetic and purgative properties and
set up all the symptoms of irritant poisoning. Treatment of the
symptoms as they arise is all that can be attempted.
POISONOUS Pf--ANTS

DIOSCORIDACElE.
The Dioscoridacere, or yam family, includes one poisonous
British species-namely, Tamu(communis-black bryony, ladies'

FIG. 3.-TAMUS COMMUNIS (BLACK BRYONY).

seal, or Isle of Wight vine (Fig. 3). This plant is a climber, twining
over hedges, known by its heart-shaped, shining'leaves, with a
r68 VETERINARY TOXICOLOGY
tapering J?oint turning blackish in autumn. The berries are scarlet.
It is found extensively in England, not in Scotland, and in Ireland
only on the shores of Lough Gill in Sligo.
The active principle probably resembles bryonin, the purgative
glycoside of the white bryony. Cornevin (r893) states that the
black bryony acts as a narcoto-irritant when the fruit is eaten,
but that the leaves are eaten by goats and sheep without ill-effect.
The chief symptoms are vomition, colic, paralysis of the hind
quarters and rapid death. Blackwell (r93r) records three cases of
suspected bryony poisoning in horses, the chief symptom being
subacute' gastro-enteritis.
REFERENCES.
T AMUS COMMUNIS.
Blakewell, W. E. (1931), Vet. Rec., 11, 9IL
Cornevin, C. (1893), Des Plantes Veneneuses.

LILIACElE.
This order contains a large number of species, widely dis-
tributed throughout the world, many of which are certainly known
to be poisonous; some provide valuable drugs.
Veratrum.-The veratrums, or false hellebores, V. album and
V. officinale, found in Europe, and V. viride and V. calijornicztm,
of North America, contain poisonous alkaloids similar to those
present in Schcenocattlon officinale of Mexico, the seeds of which,
known as sabadilla seeds, provide the veratrine of commerce.
The veratrums are not eaten readily by.animals owing to their
burning taste, although sheep are said to eat the young leaves
and shoots with apparent relish. The seeds are undoubtedly
poisonous and have been recorded as causing the death of chickens.
For an account of veratrum poisoning, refereuce may be made to
veratrine. ' .
Zygadenus.-The zyga,denus species, or death camas, of
America owe their poisonous properties to the- presence of
veratrine-like alkaloids, one of whjch, zygadenine, C39H6301ON,
possesses an action similar to that of cevadine. Z. venenostts is
found in meadows and retains its poisonous properties after
drying, so that hay cut from such meadows may possess poisonous
properties. The alkaloids are chiefly found in the seeds, but all
parts of the plants are poisonous. Tl1.e chief symptoms are
POISONOUS PLANTS 16 9
vomition, staggering gait, collapse, coma, and death. Treatment
is unsatisfactory, but recovery may occur if the affected animals
are kept quiet.
Other dangerous American species of this order are Chrosperma
1n'lfsccetoxicum, fly poison, or stagger grass, which contains an
alkaloid, particularly in the bulbs; these are mixed with molasses
and used to stupefy flies. The foliage is also poisonous to cattle
and sheep, producing staggering gait, and gastro-intestinal dis-
turbance. J1.1elanthi1t11t species, or bunch flower, are also reported
to be poisonous to horses when present in hay, as is Lettcocrin1t11t
montanum.
Of the European species, the most important and best known
from the point of view of toxicology is C.olchicum autttmnale, and
the literature contains several records of its toxic properties.
Colchicum autumnale.-The common colchicum, meadow
saffron, or autumn crocus (Fig. 4). "At the time of flowering, in
August, there are no leaves, the brown bulb ending in a sheath of
brown scales, enclosing the base of the flower, whose long tube
rises to 3 or 4 inches above ground, with six oblong segments of a
reddish-purple or rarely white, and nearly It inches long. Soon
afterwards the leaves appear, and attain in spring a length of
8 or 10 inches, by about I or I! inches in breadth. The capsule is
then raised to the surface of the ground by the lengthening of the
peduncle, soon after which the leaves wither away."* The habitat
is in moist meadows and pastures. It is rare in Ireland, and
naturalised in Scotland.
Toxic Principle and Doses.-Colchicum contains in all parts the
active alkaloids colchicine, C22H2506N, and colchiceine, C21H2306N
(about 0'05 per cent.), which is net destroyed on drying or on
boiling, passing into the water. Poisoning of animals may result
in the spring from the eating of the young leaves, or in autumn
through the flowers in pastures.
Cornevin (1893) estimates the' toxic dose of green leaves per
pound body weight of the ox at 60 to 75 grains, and of the bulb
for pigs at 3 grains per pound.
Colchicine, being absorbed slowly, only exercises its effects after
a comparatively long period, and is gradually eliminated, mainly
by the urine and milk, so that there is danger of a cumulative
effect. Its most marked effect is as a violent purgative, animals
suffering from it passing fcetid, green or black evacuations. The
* Bentham and Hooker.
170 VETERINARY TOXICOLOGY
nervous symptoms of stupor, coma, and paralysis are probably
referable to the general collapse, rather than to a specific action.
Death occurs from respiratory failure.

FIG. 4.-COLCHICUM AUTUMNALE (MEADOW SAFFRON).

Symptoms.-The general toxic symptoms occur after several


ours, and death up to several days, aCGording to the amount
1gested. Nausea, abdominal" p?-in, violent purgation, sometimes
rolapse of the rectum, ce,ssation of urinagon and lactation,
vmpanites, gritting of teet~, weak pulse, coldness, progressive loss
uf power from posterior outwards, are features of this poisoning.
POISONOUS PLANTS I7 I
Barret and Remli:qger (I9I2) observed sudden illness of thirty-
one out of fifty-one cattle, and five deaths. Calves showed slight
affection through the secretion of the poison into the milk.
Post-Mortem Appearances are those of acute gastro-enteritis,
the rumen distended, and probably containing leaves or seeds of
the plant. The other organs do not .show notable or characteristic
appearances.
Treatment should consist of oily and mucilaginous drinl<:s; there
is no satisfactory chemical or physiological antidote. Barret and
Remlinger (I912) used milk drenches, with egg-white and black
coffee, injections of caffein, and external applications of mustard.
Chemical Diagnosis.----:-The alkaloids of colchicum are feebly
acid, and are separated in the course of the general search for
vegetable poisons. The residues have an acrid bitter taste, are
coloured yellowish-brown by concentrated sulphuric acid, and
blue passing to olive-green and yellow by nitric acid.
Paris quadrifolia.-Herb Paris, or four-leaved grass, is a rare
plant, but widely diffused over the temperate zones; it occurs
locally in England, but not in Ireland. It grows in woods and
shady places, has' a whorl of four ovate leaves from 2 to 4 inches
long, and bears bluish-black berries. All parts of the plant are
stated to be toxic and contain a saponin, paristyphnin, which on
hydrolysis yields a sugar and an active glycoside, paridin, C16H 2S0 7 .
Convallaria majalis.-The "\Yell-known lily of the valley con-
tains two crystalline glycosides, convallamarin and convallarin,
which are found in all parts of the plant. Convallamarin possesses
a purgative action, and convallarin has a digitalis-like action.
The plant and its extracts are thus very dangerous, though few
cases of poisoning are to be found. According to Cornevin (I893),
4 drops of the extract injected intravenously killed a dog in ten
minutes.
Fritillaria meleagrJs.-Snake's head, fritillary, drooping tulip,
or chequered daffodIl, a bulbous herb having lanceolate leaves
and bearing single red or pink flowers. It grows in meadows and
moist places in a few localities in the south and east of England,
but not in Scotland. Poisoning by it is not common, but little
being known of its effects, and there are no cases of accidental
poisoning on record. F. imperialis resembles F. meleagris in its
action and is a more common plant on the continent of Europe.
In both plants the active principle is probably an alkaloid,
imperialine, C35H6004N, which possesses an action on the heart.
172 VETERINARY TOXICOLOGY'
Urginea.-The official Urginea maritima, medicinal squill, or
sea onion, is a maritime plant common on the Mediterranean
littoral, in South Africa, and very abundant in Algeria, where the
poisoning of pigs and of young animals has been observed. The
lanceolate leaves grow from the base of the flowering stem and
die before flowering. The greenish flowers are numerous on long
pedicles in an erect raceme. The root is a bulb covered with scales,
and about 6 inches in size. The plant reaches 1-~- to 2 feet in height,
and two varieties, the red and the white, are found.
All parts are poisonous, but chiefly the bulb. The active prin-
ciple is a crystalline glycoside named by Stoll (1937) scillaren A,
which has a cardiac action and yields the aglucone scillaridin; in
addition, an amorphous substance, scillaren B, has been isolated,
but this is probably a mixture of substances of unknown con-
stitution. According to Cornevin (r893), the probable toxic doses
of the pulp by the mouth are: for the horse 0'2 g., for ruminants
. 0'5 g., and for the pig 0'25 g. per kg. body weight.
Symptoms.-When taken in a large dose or in repeated moderate
doses, the diuresis observed with small doses gives place to
anuria and hrematuria; there is nausea and diarrhcea with colic
in ruminants. When possible, vomition occurs. The respiration is
laboured and pulse quickened, and there is agitation and con-
vulsions, followed by a phase of prostration and death. Cornevin
(r893) states that, in spite of the smell of the plants, pigs in Algeria
have died through eating the plant eraaicated from pastures and
thrown on to the roadside, whilst young animals have succumbed
to the leaves in pastures infested with the plant. The lesions are
those of alimentary and renal irritation.
Recently the red variety of U. maritima has come into favour
as a rat poison, since it is said to be non-toxic to domestic animals.
In this case, Winton (r927) considers that the toxic action is not
due to the glycosides, but to an unstable substance which acts on
the central nervous system, causing an ascending paralysis, con-
vulsions, and death in two days. ~
No record of poisoning by the British squills-Scilla verna,
the spring, and S. autumnalis, the autumn squill-is to be found,
although related plants are officinal and poisonous.
The South African Urginea species, or slangkops, are also very
poisonous and cause heavy losses, particularly /
amongst sheep.
They resemble U. maritima in action, and probably contain the
same or closely related cardiac glycosidcs.
POISONOUS PLANTS 173
Botanical Characters.-U. Burkei, or Transvaal slangkop, has
a reddish-brown bulb from 3 to 4 inches in diameter. The outer
scales are easily removed, and have a blood-like colour when held
up to the light. With the first rains it puts up a succulent stalk
bearing the green flower-buds, resembling a snake's head, whence
the vernacular name, slangkop. The bluish-green leaves "form a
spike of from five to seven leaves, about 6 to 9 inches long, t inch
wide, with curved edges, and tapering to a point. The flower-spike
and leaves may thus each cause poisoning at different seasons.
Steyn (1934) found that 500 g. of the fresh bulb of U. Burkei
caused the death of a sheep in fifteen hours, symptoms setting in
in about one and a half hours, although in some cases of poisoning,
the onset of symptoms may be delayed for several days.
U. macro centra, or Natal slangkop, and U. capitata, or Berg
slangkop, are also extremely poisonous.
Symptoms.-Poisoning by slangkops is characterised by
diuresis, tympanites, diarrhcea, acute abdominal pain, irregular
pulse, lachrymation, muscular tremors, laboured respiration,
collapse, coma, and death after several days' illness. In aggra-
vated cases the patient lies on its side, and death may occur
suddenly.
Post-Mortem Appearances.-These are not characteristic. There
is patchy inflammation of the intestine and fourth stomach, acute
congestion of the kidneys, and enlargement of the liver.
Treatment.-The treatment is, directed against the inflammation
by means of emollients, demulcents, and purgatives, such as
arecoline hypodermically. Stimulants are also indicated.
Ornithogalum species are also known to be very poisonous.
The common name for these plants in South Africa is chin~erin
chee, but O. glaucum is referred to as Cape slangkop. O. 1tmbel-
tatum of Europe and North America is usually called Star-of-
Bethlehem.
O. glaucum has a flowering stem 6 to 9 inches long, with scent-
less green flowers edged with purplish-brown. The bulb is small,
egg-shaped, and has a thin underground neck 2 to 3 inches long.
The leaves are shiny green, long and lanceolate. O. thyrsoides has
a white bulb of It inches diameter and a round, green, succulent
stem It to '2 feet high. The flowers are white, with a brown centre
and yellow stamens, and form a cluster on short stalks at the top
of the stems. The fruit is a capsule bearing many seeds.
Active Principle.-The active principle of these plants has not
174 VETERINARY TOXICOLOGY
yet been isolated in a pure form, but is probabjy associated with
a dark green resin. All parts of the plants are poisonous; Steyn
(1929) found that goo g. of fresh O. lacteum caused the deatH of
a sheep, and Quinn (1927) found that 10 g. of the bulbs of
O. Saundersic:e caused symptoms of poisoning in cattle, and 5 g .
. the death of a horse in three days.
Symptoms.-The chief symptoms are dulnes[S, depression, and
loss of appetite, followed by severe purgation. abdominal pain,
and drowsiness. The purging continues, the eyes are staring and
glassy, .and the heart beat becomes irregular, with an abnormally
loud beat. Violent struggling, kicking, and foaming from the
nostrils may precede death.
Post-Mortem Appearances.-The chief lesion i:'> a marked gastro-
enteritis and thick, cyanotic blood; the alimentary contents are
ft.uid and stinking. .
Treatment.-Sedatives and purgatives, together with stimulants,
are indicated; alkali, such as bicarbonate, is said to be of some
value.
REFERENCES.
COLCHICUM AUTUMNALE.
Barret and Remlinger (1912), Vet. ]., 68,306.
Cornevin, C. (1893), Des Plantes Veneneuses.
CONVALLARIA MAJALIS.
Cornevin, C. (1893), Des Plantes Veneneuses.
URGINEA.
Cornevin, C. (r893), Des Plantes Veneneuses.
Steyn, G. D. (1934), The Toxicology of Plants in South Africa.
Stoll, A. (1937), The Cardiac Glycosides.
Winton, F. R. (1927), ]. Pharnz. and Exp. Therap., 31, 12 3.
ORNITHOGALUM.
Quin, J. 1. (1927), S. Afric. J. Sci., 24,431.
Steyn, G. D. (1929), 15th Rept. Dir. Vet. Servo S Africa, 777.

GRAMINlE. ,
Of the very large family of grasses, only a-few species are known
to produce specific poisoning, but many contain hydrocyanic acid,
which, und~r certain circumstances, may be ptesent in sufficient
amount to cause toxic effects; nevertheless, IJ].any of these are
also valuable fodder grasses. In this connection,ti:le more important
are the sorghums, particularly S. halepense, Johnson grass;
S. vulgare, Indian millet or guinea-corn; and S-: v~tlgare var.
POISONOUS PLANTS I75
Szedanense, Sudan grass: These contain a glycoside, dhurrin,
which, on hydrolysis with the enzyme emulsin, yields hydrocyanic
acid, glucose, and parahydroxybenzaldehyde. The hydrocyanic
content of the young grasses may be sufficient to produce poison-
ing, but from the work of Henrici (I926) it appears that the
greatest amount of hydrocyanic acid is present during wilting of
the mature grass, so that they are most dangerous under drought
conditions or when they are frosted or otherwise damaged. How-
ever, when dried slowly, their hydrocyanic acid content is greatly
reduced, so that they may be fed safely in hay. Other graminre
which may at times contain hydrocyanic acid in sufficient amount
to be poisonous ar~ Holctts lanatus, velvet grass, and Zea mays,
maize, mealie, or Indian corn. The latter is associated with a
disease of cattle, "corn-stalk disease," which occurs particularly
during a drought, when the animals are grazed on wilting maize.
The retiology of this condition is obscure. Walsh (I909) found that
the male flowers contain hydrocyanic acid, as do the stems, but
Schwarte, Eveketh, and Biester (I939) consider that the disease
is due to the presence of unidentified substances in the stems of
the wilting plant. To these may be added the arrow grasses,
Triglochin maritima and T. pahestris, which do not belong to
this order, but to the Juncaginacere. However, they contain
hydrocyanic acid, particularly in the leaves, which may be present
in sufficient amount to be poisonous. For a consideration of hydro-
cyanic acid poisoning, see previous section.
Lolium temulentum.-Darnel is the only species found wild and
native to Great Britain; it is widely distributed, particularly in
South Africa and parts of America, and is probably the "tares"
mentioned in the Bible.
L. temulent'/,tnt (Fig. 5) is closely allied to L. perenne (Fig. 6), the
rye grass, known in two varieties, the English and Italian. The
distinguishing points between the species temulentum and perenne
are:
Temulentum.-Outer glume as long or longer than the spikelet.
Some of the glumes with awns as long as themselves.
Perenne.-Outer glume shorter than the spikelet. Awns short
or absent.
The poisonous properties of L. temulentum are confined to the
grains, which have a yellowish-green colour, in distinction to the
violet seeds of Bromtts. The flour is colourless and tasteless, and
the starch grains have a dimension of 4 to 8 jk.
176 VETERINARY TOXICOLOGY
Accidents 'due to L. te11tulentuln commonly arise from the
admixture of the grains with barley or other cereals, or from the
addition of the flour to ordinary flour.
The detection of L. tem1tlentum flour in the ordinary material
may be effected by means of a microscopic examination of the

FIG. 5.-LoLIUM TEMULENTUM (DARNEL).


(From Smith's "Veterinary I:ygiene.")

starch granules; ether extracts an olive-coloured fat, which may


be shown to be poisonous on a small animal; or a flour, shaken
with alcohol, will give a yellowish-green c'olour if L. temulentttm
be present in significant amounts.
Toxicity.-According to Cornevin (1893), thelethal doses of the
seeds are:
POISONOUS PLANTS 177
Horse 7 g. per kg. body weight.
Dog 18 g.

Ruminants and birds are less sus-


ceptible.
The toxic principle is probably an alka-
loid, temuline, C7H 120N2 , first 'isolated
by Hofmeister (1892) from the seeds of
darnel. Freeman (1902) found evidence
to support the idea that this alkaloid
was only present in darnel seeds affected
with a fungus, probably Endocladium
temulentum, which is frequently found
between the hyaline layer and the
aleuro'ne layer, but Steyn (1934) fed
large quantities of fungus-infected darnel
seeds to rabbits, pigs, horses, and dogs
without producing any symptoms what-
soever, so that further research is neces-
sary be~ore a definite conclusion can be
reached.
Symptoms.-The alkaloid possesses nar-
cotic and mydriatic properties. In horses,
there is dilatation of the pupils, vertigo,
uncertain gait, and trembling. The sub-
ject falls, the body is cold and extremities
stiff, respiration laboured, pulse slow and
small, and there are convulsive move-
ments of the head and limbs. There is
rapid enfeeblement and death within
thirty hours. No special lesions beyond
a little intestinal irritation are to be seen.
This account is abridged from experiments
quoted from Cornevin (1893), in which
2 kg. of the grains were given to a horse.
According to the same authority, the
yellow ether extract of the grain appears
to act as a hyperresthetic, causing sali-
vation and vomition, trembling, con-
vulsions,. and tetanic rigidity. The water FIG. 6.-LoLIUM PERENNE
(PERENNIAL RYE-GRASS).
extract displays anresthetic and narcotic (From Smith's "Veter-
properties, causing drowsiness, coma, inary Hygiene.")
12
VETERINARY TOXICOLOGY
prostra'tion, and lack of co-ordination of movements, as well as
salivation and vomition.
A case of poisoning of pigs through the admixture of L. temu-
lentwn grains with barleys was noted by Tait (r842). There was
foaming, convulsions, and paralysis; the stomach and intestines
w.ere inflamed and the lungs congested.
Of the other grasses thought to contain specific poisonous pro-
perties, the best known are Stipa robusta, sleepy grass, which is
reported to cause losses amongst sheep in Arizona and New
Mexico (the grass possesses narcotic properties, but affected
animals usually recover); Eragrostis cilianensis, stink grass, which
is reported to be poisonous to horses; and Melia decumbens, dronk
grass, which is found in South Africa, and is reported to have
poisonous properties similar to L. temulentum.

RF;FERENCES.
Henrici, M. (1926), Ilth and 12th Repts. Dir. Vet. Educ. and Res. S. Afric.,
495
Schwarte, L. H., Eveketh, D. F., and Biester, H. E. (1939), Vet. Med.,
34,648.
Walsh, L. M. (1909), South African Poisonous Plants.
LOLIUM TEMULENTUM.

Cornevin, C. (1893), Des Plantes Veneneuses.


Freeman, E. M. (1902), Proc. Roy. Soc., 71, 27.
Hofmeister, F. (1892), Arch. Exp. Path., 30,202.
Steyn, G. D. (1934), The Toxicology of Pla~ts in South Africa.
Tait, ]. (1842), Veterinarian, 15,212.

EQUISETACElE.
Equisetum species, or horse-tails, are widely distributed, and
many reports are on record of their poisonous properties. The
common European horse-tail is E. palt/stre (Fig. 7); in North
America E. arvense, the scouring rushes, E. hyemale and
E. lavigatum, and E. sylvaticum are also abundant; in South
Africa E. ramosissimmn is found.
Toxicity.-Young animals, particularly young horses, appear
to be more susceptible than adults to the toxic action of horse-
tails. Poisoning of sheep and cattle, as well as horses, has been
reported, although Canadian authorities consider that cattle are
but little affected by the plants. Equisetum species do not lose
their toxicity on drying, 'so that they remain dangerous when
present in hay, which is probably the most common vehicle of
, The .toxic principle is as yet unknown. Earlier sugges-
poisoning.
POISONOUS PLANTS 179
tions were that the symptoms might be due t<:> mechanical injury
from the silica present 1.0 the extent of about 8 per cent. in mature
plants, but young cquisetum shoots, which ~ontain little silica,
are extremely poisonous, so that the active
principle is probably some organic substance.
Aconitic acid has been isolated from E.
palustre, as well as an alkaloid named palus-
trine, C12H2402N2' by Glet, Gutschmidt, and
Glet (I936), and this latter substance is prob-
ably the active principle of that particular
cquisetum.
Symptoms.-Rich and. Jones (I902) ob-
served in horses poisoned with horse-tail
unthriftiness, muscular wasting, and in two
to five weeks staggering gait and loss of
power to stand. The pulse was slow at first,
but later became fast and weak; there was a
rise in temperature, and the visible mucous
membranes were pallid. Although the appetite
remained good, the animals finally died from
exhaustion. Hudson (1924) noted in cattle
grazing clover on a pasture where E. arvense
was somewhat abundant, diarrhrea, weakness
of the hind limbs, and a slightly tucked-up
appearance. There were no fatalities, and
speedy recovery followed removal to another
pasture. Steyn (1932) found that 800 g. of
fresh E. ramosissimum given to a sheep pro-
duced symptoms in twenty-four hours which FIG7-EgUISETUM
PALUSTRE (HORSE-
were characterised by dyspnrea, accelerated, TAIL).
strong ,pulse, frequent lying down, and stagger- (From Sm,ith's "Yet-
ing gait; a furth~r dose of 800 g. aggravated erinary Hygiene.")
theprevioussymptoms,but recovery was compl~te on the third day
Treatment.-Recovery is generally to be eXpected on changing
the diet. Purgatives are indicated, and affected animals should
be kept as undisturbed as possible.
REFERENCES.
Glet, Gutschmidt, and Glet (1936), Zeit. Physiol. Clwn ., 244, 229.
Hudson, R. (1924), Vet. I., 80, 40.
Rich, F. A., and Jones, L. R. (I902)~ Vermont Agrio. Exp. Sta. Bull., 95.
Steyn, G. D. (1932), 18th Rept. Dlr. Yet. Servo a,nd Anim. Indust. S.
Africa, 87!.
180 VETERINARY TOXICOLOGY

POISONING DUE TO DISEASED FORAGE.


The fungi apt to affect forage are very numerous, the more
common being Ustilago carbo, or smut, attacking grasses and
grains; U. maydis, affecting maize;
Pttccinia graminis, causing rust and
mildew in grains; Claviceps purpurea,
or ergot, attacking cereals, particu-
,I larly rye; C. paspali, attacking pas-
palum grasses; and Tilletia caries,
attacking wheat-all of which cause
disease of .the growing grain. Moulds
affect damp, badly harvested or
stored forage, and cause fermenta-
tion, loss of colour and aroma. The
commonest are Botrytis, Penicil-
limn, Aspergill1ls, Oidium and Mucor,
which have been examined by Burgi
(1931) and others. The evidence
that moulds themselves are poison-
ous is, however, conflicting. Steyn
(1934) carried out experiments with
a number of moulds given directly
to rabbits and pigs with entirely
negative results, but he concludes
that fungus-infected food must be
considered poisonous until the con-
trary has been proved. Danckwortt
FIG. S.-SMUT OF OATS. (1926) suggests that it is not the
A, panicle of oats attacked from moulds themselves but products
below upwards; B, spikelet
with the fungus in an. early derived from them which may be
stage of growth; C, free spores harmful; of these, the most likely
of Ustilago carbo; D, spores are amine derivatives such as cholin,
germinating and producing
yeast-like buds. trimethylamIne, neurin, etc., but
(From Smith's "Veterinary
these substances do not appear to
Hygiene.") be of a high order of toxicity when
taken by the mouth.
As regards active principles, the only member of this group
concerning which there is at present definite knowledge is ergot,
the sclerotium of the fungus Claviceps purpurea. It is probable
that C. paspali possesses the same action and is responsible for
POISONOUS PLANTS iSr
producing "paspalum staggers," a disease sometimes seen in
animals grazing on paspal urn grasses.
Ergotism is a well-known disease of animals and man, which in
the past has assumed epidemic proportions, particularly in Central
Europe, where it was known under the name of tiS t . Anthony's
Fire," since the Saint was supposed to have suffered from it.
In the acute form of the disease the chief symptoms are hyper-
sensibility, severe nervous disturbance, blindness, and death in
convulsions. This form, however, is seldom seen in animals, which

FIG. 9.-RpST AND MILDEW.


A, part of s.tem of oat-plant attacked by Puccinia graminis; B, two of the
blotches from A enlarged 20 diameters; C, P. graminis within the stem,
but near the surface, bursting the cuticle at D, beneath which are seen
the teleutospores; E, E, spores of Cfredo linearis, which sometimes sur-
round the teleutospores of P. graminis; G, teleutospores germinating
and producing sporidia at H. These sporidia, on germinating, give rise
to .7Ecidium berberidis.
(From Smith's "Veterinary Hygiene.")

more usually suffer from chronic ergotism. In this form there is


gastro-intestinal disturbance with vomition, diarrhcea or con-
stipation, colic, coldness, and anresthesia of the extremities;
nervous symptoms may appear in some cases, and in others there
may be dry gangrene of the feet, ears, or tail, or of the comb,
tongue, and beak in birds. The parts usually drop off without pain,
and death results from asthenia. Abortion or mummification of
the fcetus has been reported to occur in pregnant animals, but
this is by no means a constant feature of the disease.
r82 VETERINARY TOXICOLOGY
Much research has been carried out to determine the active
principles of ergot, and it has now been established, mainly as a
result of the work of Barger (193I) and his co-workers, that five

FIG. II .-ERGOTS GERMINATING.


(From Smith's "Veterinary Hygiene ..")

FIG. I2.-BOTRYTIS GRISEA.


(From Smith's" Veterinary Hygiene.")

Fw. 10. - SPIKE OF


ERGOTISED RYE.
(From Smith's "Vet- FIG. I3.-PENICILLIUM GLAUCUM.
erinary Hygiene.") (From Smith's "Veterinary Hygiene.")

pairs of alkaloids' are usually present in ergot, tp.e total alkaloidal


content of which varies between o'or to 0'4 per cent. In each pair
of alkaloids, one possesses physiological activity and the other is
an isomer with little or no action. The main active alkaloid is
POISONOUS PLANTS r83
ergotoxine, C35H3SQsNs' its isomer being ergotinine; the others
so far isola ted are ergotamine and ergotaminine, C33H3505N5 ;
ergosine and ergosinine, C30H3705N5; ergometrine and ergometri-
nine, C19H2302N3; and erg<?cristine and ergocristinine, C35H3905N5'
In addition, numerous simple bases, such as acetyl choline, tri-
methylamine, putresceine, etc.; amino-acids such as histidine,
tryptophane, etc.; and a pigment, sciererythrin, which gives the
fungus its characteristic purplish-red colour, are also present.
The symptoms of ergot poisoning are undoubtedly due to the
alkaloids it contains; ergotoxine paralyses sympathetic nerve-
endings, which have an augmenting effect, but leaves inhibitor
endings unaffected. It also causes primary stimulation of smooth
muscle .and sub-
sequent paralysis
oft h e s y m p a-
thetic nervous sys-
tem. The other
active alkaloids
have a similar but
less pronounced
action. Ergomet-
rine, however,
seems to be the
principal agent
which causes con- FIG. 14.-0IDIUM AUREUM.

traction of uterine B, spores further magnified.


muscle, . but it is (From Smith's" Veterinary Hygiene.")
not present in aU
samples of ergot. The gangrene seen in chronic ergotism is due
to an endarteritis obliterans and thrombosis. This is readily
. produced in the comb when ergot is injected into a cock, and
the reaction is used for the detection and assay of ergot samples.
Chemical Diagnosis.-The preliminary extraction may be carried
out by the Stass-Otto process, using 80 per cent. alcohol as the
extractive and removing fat by means of light petroleum. On
extracting the acidifi~d residue with ether, the pigment sclerery-
thrin is obtained, which colours the solution red, changing to
purple on the addition of an alkali. It shows two absorption
bands, one in the green and one in the blue, on spectroscopic
examination. The alkaloids, which will also be extracted, give
certain colour reactions with sulphuric acid; in the pres~nce of
VETERINARY TOXICOLOGY
sulphuric acid, ergotoxine gives a yellow colour, changing to
green, or on adding a trace of ferric chloride to the sulphuric acid
an or~nge-red colour changing to red and then bluish-green.
These colour reactions, however, are not specific, since they are
given by many indol derivatives, so that confirmation of the
presence of ergot alkaloids should be made by means of the cock's
comb test. This is carried out by injecting a small portion of the
extract intramuscularly into a young cock, when the comb and
wattles will become cyanotic if the alkaloids be present. A micro-
scopic examination of the food material suspected to contain
ergot should be made, in an attempt to detect the fungus, and, if
flour is suspected, 2 g. of this should be shaken with 10 m!. of
70 per cent. alcohol and 0'5 ml. sulphuric acid, and the mixture
warmed to 50 C.; the supernatant fluid will become red on
standing, owing to the extraction of the pigment, sclererythrin.
The symptoms of poisoning by moulds appear capable of dis-
tinction into two phases-the production of alimentary and
urinary disturbances, and action on the central nervous system.
Thus, there are shown colic and tympany, and frequently exces-
sive, constant urination, and also dejection, staggering gait,
dilatation of the pupil, blindness, and .paralysis, especially of the
hind extremities.
Varnell (1862) gave an old but healthy mare twelve feeds of
oats infected with Aspergillus during four days, and observed
the above indicated nervous disorders. Death was painless on the
sixth day. He found, on autopsy, the stomach and intestines pale
and flaccid, liver paler than normal, and spleen very small.
The effects of the mould Oidium (on bread) on the horse have
been recorded by Perrin (1907). There were internal rumblings,
frequent defrecation and passage of small quantities of urine,
difficulty in moving, membranes injected, pulse 60, full and hard.
Later the animal fell, the pulse was weak, there was coma followed
by vertigo, and death after repeated seizures. -
On post-mortem examination, he found congestion of the mucous
membranes; the liver yellow and friable, and the brain congested.
Muller (1909) has described extensive disease amongst horses,
cattle, and sheep in Alsace-Lorraine, due to grain infected by
Puccinia. It was characterised by myopathic paresis or paralysis,
and excessive salivation. Acute cases termin-ated fatally in one
or two hours; subacute cases in from ten to forty-eight hours; and
in chronic cases there was death from inanition. The post-mortem
w:as negative.
POISONOUS PLANTS 185
Bansse (1903) studied the effects of mouldy clover on the horse,
observing delirium, with staring eyes, perspiration, and foaming,
followed by weakness, loss of power of the hind legs, and muscular
tremors of elbow and thigh.
Aspergill1ts jumigat1ts or glaucus gives rise to aspergillosis in all
mammals and birds, causing a pneumonia with many of the
symptoms of tuberculosis. It is frequently transmitted by food,
or may be inhaled, and is communicable from animals to man.

REFERENCES.
CLAVICEPS.
Barger, G. (I93!), Ergot and Ergotism.
MOULDS.
Bansse, (lg03) Vet. ]., 45, 80.
Biirgi, o. (1931), Tieriirztl. Rdsch., 37,484.
Dankwortt, P. W. (1926), Deutsch. tierdrztt. TVschr., 34, 639.
Miiller (lg0g), ]. Compo Path. and Therap., 22,66.
Perrin, M. (lg07), Vet. J., 63,248.
Steyn, G. D. (1934), The Toxicology of Plants in South Africa.
Varnell, G. (1862), Veterinarian, 35,65.

RANUNCULACElE.
This order contains the following poisonous genera: Clematis,
Tlzalictmm, Anemone, Adonis, Ranuncultts, Caltha, Helleborus,
Aqltilegia, Delphinium, Aconit1lm, and Actcea, members of which
are found wild, or are cultivated in Britain, and are widely dis-
tributed, especially over northern temperate regions. Only
clematis is tropical. Of these the most important, from the stand-
point of toxicology, are aconitum, helleborus, delphiniwlZ, and
ranwncultls, and these will therefore be first described.

Aconitum and Aconitine.


Botanical Characters.-Aconitum napellus (Fig. IS), monk's-
hood or wolf's-bane, is the chief species of the genus aconittftn
found in Great Britain. "Stem firm and erect, It feet to 2 feet high.
Leaves stalked, or the upper ones nearly sessile, of a dark green,
glabrous or slightly downy, divided to the base into five or seven
deeply cut, linear, pointed segments. Flowers large, dark blue, on.
erect pedicles, forming a handsome, dense, terminal raceme. The
upper helmet-shaped sepal at first conceals the lateral ones, but
is ultimately thrown back. Spur of the small upper petals short,
I86 VETERINARY TOXICOLOGY
conical, and more or less bent downwards. Carpels three, often
slightly united at the base. Habitat moist pastures, thickets, and
waste places in mountainous districts. In Britain wild in the West
of England and South Wales."*

FIG. IS.-AcONITUM NAPEl:LUS (MONK'S-HoOD).


(From Smith's "Veterinary Hygien~")

The plant is exceedingly dangerous, owing its poisonous pro-


~rtiesto the alkaloid aconitine, C34H;i7011N, which js present in the
ot to the extent of about 2 to 4 per cent., and in less proportions
* Bentham and Hooker.
POISONOUS PLANTS
in the leaves, flowers, and seeds. The maximum content of alkaloid
is attained just before flowering, and the proportion is less in the
plant growing in higher than in lower latitudes, and also after
several generations of culture as an ornamental plant. In the
Himalq_yas the species Aconi~um laciniatum and A. spicatum-
Bish, Indian or Nepaul aconite-contain more poisonous alkaloids
than the European plant.
In America A. napellus is a garden plant, and A. colttmbianum
is native to the North-West, where it sometimes poisons sheep.
Toxic Doses.-Kaufmann (IgOI) gives the POis9nouS doses of
powdered root by the mouth as 13 to I4 ounces for the horse and
-! ounce for the dog. Of the preparations of aconite the B.P.
tincture is I in 20, and Fleming's tincture I in It. Of the latter
120 to ISO minims are stated as poisonous to the horse, and 50
to 60 minims to a dog of 40 pounds. The alkaloid aconitine is
exceedingly poisonous, t grain killing a dog of 30 pounds in sixty-
five minutes. The toxic dose on injection is estimated at i grain
for the horse and -io grain for the dog.
EtIects.-Aconitine is speedily absorbed, and is eliminated
slowly, chiefly by the kidneys. Its local effect is irritant, producing
tingling and twitching, followed by numbness. It acts as a gastro-
intestinal irritant, causing diarrhcea. The general effect is exercised
upon the medullary vagus centre, producing cardiac depression
and fall of blood pressure, and on the respiration, the breathing
becoming slow.
Symptoms.-In the horse there are noticed champing and
copious salivation, with choking movemel1ts of the cesophagus,
eructation of frothy matter, and continued attemps to vomit.
The gait is staggering and pulse weak. Intense colic, purgation,
and spasmodic contractions of the diaphragm are observed.
Paralysis follows, the respiration being difficult and heart and
pulse weak; the pupils are dilated, membr:anes blanched, and
temperature low; there is loss of power and sensation, convulsions,
and'death by asphyxia.
In the dog aconite poisoning is marked by salivation, nausea,
violent vomiting, and purgation. The jaws are champed, and the
dog rubs its nose with its paws. The heart action and respiration
become progressively more feeble.
Post-Mortem Appearances.-Notable gastro-enteritis is not
found in cases or rapid poisoning. The lungs contain little blood
and are collapsed, the passages containing frothy mucus. The
188 VETERINARY TOXICOLOGY
lungs are extensively studded with patches of extravasated blood,
the right heart is engorged, and the left nearly empty.
Treatment.-If possible, the stomach is, to be emptied by
emetics or the pump. Tannin or iodine in potassium iodide may
be exhibited as alkaloid precipitants, but with doubtful value.
As physiological antidotes to the depressant action on the heart,
digitalis, ether, or atropine may be given. \iVarmth and friction
will assist in stimulating the heart and lungs.
Chemical Diagnosis.-Aconitine and pseudo-aconitine (con-
tained in Indian aconite root) are isolated in an impure condition
in the routine alkaloid separation. Chemical tests are very un-
reliable, though when pseudo-aconitine is present Vitali's test
(see Atropine) is given. Concentrated sulphuric acid or phosphoric
acid, warmed with aconitine, both eventually give a reddish-
violet colour. But the test ,is absolutely unreliable, for almost
always there are traces of organic bases, or ptomaines, which
behave similarly.
Aconitine induces a burning, tingling effect, followed by numb-
ness, on the tongue or lips, and this observation has value (use
with caution!). The only satisfactory proof is by an observation
of the physiological effects on a small animal.

Helleborus.
The three species of helleborus found in Great Britain are
Hellebones niger (Fig. 16), Christmas rose or black hellebore, native
to South-Eastern Europe, and a garden plant in this country;
H. viridis, green hellebore or bear's foot, a European plant some-
times found in American gardens; and H. jatidus, or setter-wort.
Care must be exercised in distinguishing these from the so-called
white hellebore, or Veratrum album, an Alpine plant belonging to
the Liliacere. .
Botanical Characters.-Only H. viridis and H. jat,id1;S, which
grow wild, need be described here.
H. viridts (Fig. 17), green helieb!)re _or bear's-foot: "Radical
leaves large, on large stalks, divided il}to seven to elev"en oblong,
acute, toothed segments, 3 to 4 inches long, the central ones free,
the lateral ones on each side connected together at the base, so
as to form a pedate leaf. Stem scarcely exceeding the leaves,
bearing usually two, three, or four large drooping flowers of a
pale yellowish-green, and at each ramification a sessile leaf, much
./
POISONOUS PLANTS r89
less divided than the radical ones, and the segment usually
digitate."*
H. jmtidus (Fig. IS), or setter-wort: "Lower leaves not all
radical, but mostly raised on the short perennial base of the stems,
forming a larger and thicker tuft than in H. viridis, their segments

FIG. 16.-HELLEBORUS NIGER (BLACK HELLEBORE).

narrower, less toothed, stiffer, darker green, and more shining,


their outer lobes at a less distance from the central ones. Flower-
stem about a foot high, with a large close panicle of drooping
flowers, of a pale green, tinged at the apex with purple, the
concave sepals giving them a globular form. Bracts at the rami-
* Bentham and Hooker.
I9 VETERINARY TOXICOLOGY
fication of the panicle ovate and entire, or shortly lobed at the
summit."*
Habitat of both species chiefly South-E'astern England.
All parts of the hellebores are poisonous, particularly the root,
whence the extract is made. The tincture at one time had repute

FIG. I7.-HEl.LEBORUS VIRIDIS (GREEN HELLEBORE).

as an abortifacient, but is not now used, and H. jmtidus used to be


given for quarter-evil. The active principle is the glycoside helle-
borein,' along with a little of the lesS' powerful helleborin. The
former is a drastic purgative with a digitalis-like action and the
latter is a narcotic.
Toxic Doses.-Cornevin (r893) gives 9 ounces of the fresh root
'" Bentham and Hooker.
POISONOUS PLANTS r9 I
as poisonous to the horse. The dried root he states as toxic in
2l ounce doses to the horse, and r20 to i50 grains to the sheep.
Mayer (r847) records that a horse had in all 5 half-pints of
the chopped leaves of H. fcetidus in a bran mash during two days,
and was fatally poisoned.

FIG. IS.-HELLEBORUS F<ETIDUS (SETTER-WORT).

Symptoms.-A full dose of hellebore causes in the horse and ox


bloody purgation, ~alivation, attempts to vomit, and excessive
urination. Mayer (r847) similarly found violent straining and the
discharge of frothy mucus, but no effort to vomit. The heart
action resembles that observed in digitalis poisoning, showing
periodic intervals of arrest in systole.
Post-Mortem Appearances.-Helle,bore acts as an irritant, and
r9 2 VETERINARY TOXICOLOGY
congestion of the fourth stomach and small intesLHv ~lave been
recorded. The rumen is full, but the fourth stomach and intestines
may be empty, the inflammation of the pylorus preventing the
passage of food. .
Treatment.-This consists of purgatives, mucilaginous draughts,
stimulants, and in general measures similar to those employed
against digitalis.
Chemical Diagnosis.-The glycosides of hellebore are yielded
to solvents in the systematic extraction of the acid liquid in the
search for organic poisons. There are no satisfactory tests. Sul-
phuric acid on warming causes a coloration passing from pink to
red-violet, but a similar reaction is given by many other sub-
stances.
Delphinium.
Delphinium staphysagria (Fig. r9), or stavesacre, a native of
the South of Europe, is not found wild in Great Britain. The seeds
of the plant contain four alkaloids-delphinine, C34 H 47 0 9N, its
isomer delphisine, the amorphous delphinoidine, C25H4204N, and
staphisagroine, C4oH4607N2' of which delphinine is the most
poisonous. resembling veratrine and aconitine.
The powdered seeds are used as a valuable agent against lice.
In addition to D. staphysagria, the species requienii, pict'ltm,
and consolida occur in Central and Southern Europe, whilst in the
United. States D. tricorne, consoli dum, menziesii, geyeri, recltr-
vatum, scopulorum, and trollifoliu11t have been suspected of being
poisonous. Nelson (r8g8) fed as much as 240 pounds of the fresh
leaves of D. 11tenziesii to sheep within five days without ill-effect;
but, on the other hand, Wilcox (r898) killed a yearling lamb in two
hours by the extract from less than an ounce of the dried leaves.
Symptoms.-Poisoning by stavesacre very. closeiy resembles
that by aconite,fand, moreover, being rare, need not receive de-
tailed treatment here. Macgregor (1908) observed a case of poison-
ing of a horse, which showed dulness, excessive salivation, de-
glutition, and attempts to vomit. These symptoms, along with the
weak pulse, display the likeness to aconite. In this case recovery
followed the exhibition of a pint of whisky in it pint of linseed oil.
The lesions are similar to those of aconite.
Chemical Diagnosis.-The delphinium alkaloids are obtained
by the extraction from alkaline solution in systematic work.
Delphinoidine gives definite tests which, therefore, serve to
POISONOUS PLANTS I93
characterise the nat"ure of the poisoning. The other alkaloids do
not interfere. (I) Concentrated sulphuric or phosphoric acid gives
a brown colour, slowly passing to red-brown. (2) When a drop of
sugar solution is added, and then concentrated sulphuric acid, a

FIG. Ig.-DELPHINIUM STAPHYSAGRIA (STAVESACRE).

brown and eventually deep green colour is given. (3) A trace of


bromine water added to the sulphuric acid solution gives a violet,
slowly changing to a cherry-red and blood-red colour. None of
these tests is satisfactory. The first may be confused with aconite,
13
I94 VETERTN ARY TOXICOLOGY
the second with veratrine, and the third with digitalis, and pto-
maine bases and biliary pigments often confuse and mask these
tests. A physiological test is therefore to be preferred.

Ranunculus.
Description.-The species of this genus which are poisonous
include: Ranunculus sceleratus, or celery-leaved crowfoot; R.
acris, or upright meadow crowfoot; R. bulbosus, or common
buttercup; R. arvensis, or corn crowfoot; R. repens, or creeping
ranunculus; R. lingua, or great spearwort; R. jlammula, or
lesser spearwort; and R. jicaria, or lesser celandine. These plants
are well known, and detailed descriptions are superfluous, but
attention may profitably be drawn to some of the particular
characteristics of the several examples. The general characters are:
annual or perennial leaves divided or entire, flowers generally
yellow, with double perianth, five sepals and five petals, numerous
uniovular carpels.
T~ose having divided leaves:
R. acris (Fig. 20): Leaves hairy; calyx spreading, but not
reflexed; stems erect, without runners; lower leaves palmately
divided; carpels in a globular head. Flowers early summer till
late autumn.
R. repens: Runners creeping and rooting.
R. arvensis: Leaves _glabrous; segments narrow: carpels very
prickly; plant erect. Abundant in slovenly farms in South of
England. Flowers and ripens seed with the corn.
R. bulb os us : Calyx closely reflected on the peduncle; rootstock
or thickened base of stem, forming a kind of bulb; carpels per-
fectly smooth. Flowers early summer.
R. sceleratus (Fig. 2I): Petals very small; carpels small,
numerous, in an ovate or oblong head.
Those having undivided leaves: .
R. lingua (Fig. 22): Flowers, large, plants 3 feet high; and
R. jlammula, about I foot high, flowers small, having leaves long
and lanceolate, growing in marshes and wet places.
R. jicaria (Fig. 23): Leaves cordate, smooth and shining.
Flowers early spring.
'All the above have yellow flowers . ./
Active Principle.-The Rammculi all contain an acrid juice, the
active principle in which was shown by Shearer (1935) to be
POISONOUS PLANTS
identical with the protoanemonin isolated by Asahina and Figita
(1922) from Anemone Japonica. Protoanemonin, C5H 4 0 2 , is a
volatile, yellow oil which causes intense irritation to the mucous
membranes and blistering when applied to the skin. It is, how-
ever, an extremely unstable substance, two molecules readily

FIG. 2o.-RANUNCULUS ACRIS (UPRIGHT MEADOW CROWFOOT).

combining to form anemonin, C1oH s0 4 , which rapidly precipitates


in long needle-shaped crystals or amorphous flakes when the oil
is allowed to stand. Nicholson (1933) showed that anemonin is
entirely non-irritant and possesses little or no physiological
action, so that there is no doubt that it is the protoanemonin in
buttercups which gives them their irritant properties; it is present
196 VETERINARY TOXICOLOGY
to the greatest extent at the time of flowering. It has been sug-
gested that the alkaloid, aconitine, is also present in ranunculus
species, but Shearer (1935) could find no evidence that such is the
case, nor could he show that hydrocyanic acid was present in
significant amounts, although he was able to demonstrate the
presence of a cyanogenitic glycoside in R. arvensis and R. jicaria.

FIG. 2I.-RANUNCULUS SC!>LERATUS (CELERY-_L_EAVED CROWFOOT).

Toxicity.-Ranunculus speCies are not readily eaten by animals,


and their toxicity is low; thus a three-year-old ram ate 47 pounds
of R. jicaria in eight days without showing any signs of ill-health,
but when buttercups are present in pastures in considerable
amounts there is little doubt that they are a potential source of
danger. Protoanemonin will itself cliuse illness and death, but even
if the plants are not eaten in excessive amounts they may cause
POISONOUS PLANTS 197
a mild gastro-enteritis, which may lead to more serious con-
sequences. Buttercups should, therefore, be eradicated from
pastures, which, as Stewart and Wright (1933) found, can be
satisfactorily accomplished by spraying with a 3 per cent. solution
of sodium chlorate at the rat~ of 50 pounds per acre.

FIG. 22.-RANUNCULUS LINGUA (GREAT SPEARWORT).

Symptoms.-The first symptoms induced by ranunculus are


those of gastro-enteritis, colic, nausea, vomiting (if possible),
salivation, emission of black fceces, and sometimes hcematuria. To
these are added nervous symptoms, retardation of pulse, slow and
stertorous respiration, weakness of the posterior parts, difficulty
in mastication and drinking, and blindness. With large quantities
r9B VETERINARY TOXICOLOGY
,there may be convulsions, with the eyes retracted in the orbits,
an exaggeration or absolute arrest of defrecation" and death
usually within twelve hours after the appearance of convulsions.
Gerrard (r874) observed the
effects of common buttercups
on the horse. The symptoms
accorded with those above
named. A change of diet and
mild aperient effected a cure.
A case of the poisoning of
sheep is described in the Veteri-
narian of r844, p. 488. The
cause was R. repens. A few
hours after the sheep had been
in the field several suddenly
. fell, the eyes rolled, and some
showed dizziness, and died with
the head inclined over the left
flank. The shepherd bled them,
which probably hastened the
deaths of eleven. Mulvey (1919)
records the deaths of four
heifers which, on circumstantial
evidence, were probably due to
the ingestion of R. acris. The
chief symptoms were gastro-
enteritis, depression, abdominal
pain, blindness, collapse, and
death. The only post-mortem
finding was acute inflammation
of the stomach and intestine.
Post-Mortem Appearances.-
These consist of inflammatory
FIG. 23.-RANUNCULUS FIC,ARIA
(LESSER CELANDINE). lesions of the alimentary tract,
particularly of the' intestines.
As a rule, no other lesions are present, but there may be some
evidence of renal damag.e. Valuable evidence may be forthcoming
from finding fragments of the plant in the ingesta.
Treatment.-Mild purgatives, demulcents, and stimulants are
indicated. Gerrard (1874) gave nitrous ether, aromatic ammonia,
extract of hyoscyamus, peppermint water, tincture of opium, and
POISONOUS PLANTS 199
a 4-drachm ball in the case of a: horse ~ there was purgation and
gradual recovery. The blistering action of protoanemonin may be
overcome by the application of a dilute solution of potassium
permanganate.
Chemical Diagnosis.-Diagnosis of ranunculus poisoning must
depend on the post-mortem findings and the' demonstration of
portions of the plant in the ingesta, since the isolation and
chemical recognition of protoanemonin in ingesta is impossible.
This is owing to the fact that the oil reacts with many compounds,
thereby losing its chemical characteristics. It may, however, be
readily obtained from the fresh plant by steam distillation, satur-
ation of the distillate with sodium chloride, a.nd extraction with
chloroform, benzene, or ether. It is destroyed by heat or drying.

Other Genera of the Ranunculacere.


Clematis.-The Clematis vitalba, traveller's joy or old man's
beard, is a well-known climbing plant, the white flowers of which
are common on hedgerows in June and July. All parts of the
mature plant are dangerous, but cases of poisoning are rare: It
contains an active principle probably resembling protoanemonin,
which acts as an irritant purgative and diuretic, causing enteritis,
and, in quantity, fatal dysentery. Externally it is a powerful
irritant and vesicant.
Thalictrum.-The exotic Thalictrze1n macrocarpum has been
shown to contain in the root an alkaloid, thalictrine, whose effects
are like those of aconitine. The alkaloid was originally isolated by
Drassans and Mourrut (1880), but its characteristics and even its
existence require confirmation. In Great Britain the species
T. flavum, yellow thalictrum or meadow rue, is sometimes found
in moist places and along ditches. It is not common, nor does it
appear to be so dangerous as the cultivated T. macrocarpum. In
poisoning the general character of the symptoms would probably
recall those of aconite, but no cases are recorded.
Anemone.-The anemones have a perennial rootstock, leaves
radical, flower-stem naked, excepting an involucre of three
leaves, usually at a considerable distance from the flowers. Sepals
five or more, frequently six, coloured and petal-like, longer than
the stamens. No petals; stamens numerous; carpels numerous,
one-seeded, pointed, or ending in a long feathery awn.
A. pulsatilla has purple flowers, silky outside, and carpels
ending in feathery awns.
200 VETERINARY TOXICOLOGY
A. nemorosa has white or pink glabrous flowers, and carpels
~nding in a point.
The anemones contain protoanemonin, which is identical with
the protoanemonin occurring in ranunculus species and produces
similar effects. Accidents sometimes occur to animal~, owing to
the prevalence of the plant in woods in springtime when fresh
green food is'most greedily eaten.
Adonis.-The Adonis autumnalis, or pheasant's eye, having
five to eight bright scarlet petals, with a dark spot at the base,
is rarely found in the warmer counties of England and Ireland.
A. vernalis, or ox-eye, has a yellow flower, and is cultivated in
Britain.
These plants contain a glycoside, adonidin, which is credited
with abortive properties. In large doses death is caused by super-
purgation and cardiac disturbance, but cases are not common.
Caltha.-Caltha palustris, marsh marigold or king-cup, with
bright yellow flowers, is abundant in marshy places and on brook-
sides. It flowers early in the spring. The nature and symptoms of
poisoning by it are like, those of Ranunculus.
Aquilegia is represented by the species Aquilegia vulgaris, or
columbine, which grows wild in chalky woods and pastures.
According to Cornevin (1893), poisoning by it resembles that
by aconite as regards symptoms and lesions.
Actrea.-This genus is represented by the rare Actcea spicata,
baneberry or herb Christopher, very local in Britain, and only
found in the northern counties. It is found in mountain woods,
and has white flowers and black berries. The active principle is
apparently an essential oil. When eaten in sufficient quantities,
the plant causes violent gastro-enteritis, purgation, and vomition,
followed by drunkenness and delirium. The nature of the toxic
substance and the effects merit further study'.
In America there occur A. alba, white baneberry, and A. rubra,
red baneberry, but animals refuse the plants, so poisoning is
unlikely.
REFERENCES.
ACONITUM.
Gillam, W. G. (1906), Vet. Rec., 18, 8.
Kaufmann, M. (1901), TMrapeutique et Matiere Medicale Veterinaire,
3rd ed.
Moore, R. C. (1909), Vet. ]., 65, 136.
Morgan, C. (1882), Veterinarian, 55,457.
POISONOUS PLANTS 20I

HELLEBORUS.
Mayer (1847), Veterinarian, 20,5.
DELPHINIUM.
Macgregor, A. (1908), Vet. j., 64,502.
Nelson, S. B. (1898), Rept. Bureau. Anim. lndust. U.S.A., 421.
Wilcox, E. V. (1898), Rept. Bureau. Anim. lndust. U.S.A., 479.
RANUNCULUS.
Asahina, Y., and Figita, A. (1922), Acta Phytochim., 1, I.
Gerrard, J. (1874), Veterinarian, 47,654.
Mulvey, W. S. (1919), Vet. ].,26,55.
Nicholson, J. A. (1933), Proc. Roy. Soc. Med., 26,1273.
Shearer, G. D. (1938), Vet. ]., 94,22.
Stewart, J., and Wright, C. W. B. (1933), 3rd. Rept. Dir. lnst. Anim.
Path. Cambridge, 298.
THALICTRUM.
Drassans and Lourrut (1880), Bull. Soc. Chim., 34, 85.

PAPAVERACElE.
Poisonous members of this order belong to the genera Papaver,
Rcemeria, Chelidonium, and Glaucium.

Papaver.
The opium poppy, Papaver somniferum, occasionally assumes
the wild state in England in cornfields and in the fens. Poisoning
by it is most unlikely, and, should it occur, will recall that of
opium or morphine (q.v.).
The common cornfield red poppy, P. Rhceas, is so well known
as not to require description in this place.
Active Principle.-The red leaves are so'inetimes used to make
coloured syrup for medicines (syrupus rhceados), and are harm-
less. The plant does not contain 'the opium alkaloids, but yields
a sparingly soluble alkaloid, rhceadine, C21H2106N, decomposed
by warm, diluted acids w~th formation of a blood-red colour.
Symptoms.-Fatal poisoning by the common poppy is rare,
but its possibility ought to be kept in mind in those conditions
where animals might get it along with fodder on account of its
relative abundance.
The plant causes in the ox arrest of digestion, following a period
of excitement. Immobility, coma, low temperature, slowed res-
piration, convulsive movements, and death in asphyxia are to
be anticipated. The lesions are as in opium poisoning, with more
pronounced alimentary disorder.
202 VETERINARY TOXICOLOGY
P. dubium, the long-headed poppy, is distinguished from
P. Rhceas chiefly by the capsule, which is oblong, about twice as
long as broad, and narrow at the base, whilst that of common
poppy is globular or slightly top-shaped.
It is less common than P. Rhaas in England and Ireland, but
more frequent in Scotland. Poisoning by it is even less likely than
with P. Rhceas.
The exotic species, Rmmeria hybrida, violet-horned poppy, of
the genus rameria, having purple flowers, red at the base, has
established itself very locally in cornfields in the eastern counties.
It also contains rhceadine.

Chelidonium.
Botanical Description.-Chelidonium majus (Fig. 24), the
greater celandine. Rootstock perennial. Stems erect, slender,
branching, I or 2 feet high, full of a yellow fcetid juice, and
generally bearing a few spreading leaves. Leaves thin, glaucous
underneath, once or twice pinnate, the segments ovate, coarsely
toothed or lobed, the stalks often dilated into a kind of false
stipules. Flowers small and yellow, three or six together, in a
loose umbel, of! a long peduncle. Pod nearly cylindrica], glabrous,
It inches long.
Common or roadsides, near houses, more in England and
Ireland than in Scotland.
Active. Principles.-Celandine contains four closely related
alkaloids, which are present more particularly in the root. They
are chelidonine, C20~1905N; a-homochelidonine, C21H2305N;
chelerythrine, C2oH1,o4N; and sanguinarine, C2oH1304N.H20.
Chelidonine and a-homochelidonine are related chemically to
papaverine and have a similar action, depressing smooth muscle
and the central nervous system, and, on local application to the
skin, producing paralysis of sensory nerve endings. Chelerythrine
and sanguinarine, which also _occ_urs in Sanguinaria canadensis,
probably have a similar action. -
Symptoms.-The juice of the plant acts as an irritant, and
internally causes nausea, vomiting, and violent purgation.
Reeks (I903) describes a most interesting c'ase of the
poi.soning of cows by celandine, in which the effects due to
chelidonine predominate. He observed drowsiness, salivation,
thirst, uncertain gait, torpid bowels, kidneys active. On
POISONOUS PLANTS 20 3

attempting to touch the cow she fell in convulsions, limbs


stretched out and quivering, moaning, and beating about with
head, eyes retracted in orbits. Death occurred within two
hours.
Some of the animals recovered under oleaginous purgatives,
but one which had not responded showed drowsiness, was given

FIG. 24.-CHELWONruM MAJUS (GREATER CELANDINE).

castor oil, and displayed symptoms of gastro-enteritis and kidney


irritation. Offensive purgation set in, with death from exhaustion
after a few days.
Chemical Diagnosis.-The reactions of the alkaloids of celandine
are not very characteristic. Chelidonine is coloured greenish-
yellow, brown, cherry-red, and finally violet by concentrated
204 VETERINARY TOXICOLOGY
sulphuric acid. Sanguinarine, which is only present in traces, is
characterised by giving blood-red-coloured salts.

Glauciurn.
Glaucittm luteum, the well-known horned or sea poppy, with
large yellow flowers, and pods from 10 to 12 inches long, is
alleged to cause poisoning similar to that of celandine; but cases
are not to hand and the point needs revision. It is a very abundant
maritime plant in the South, but is rarer in Scotland. Animals do
not eat it; but there is a chance of its accidental inclusion in forage.
REFERENCE.
Reeks, H. C. (1903), J. Compo Path. and Therap., 16,367.

CRUCIFERlE.
The genera of this order found wild or cultivated in the tem-
perate parts of the Old World, and credited with poisonous or
objectionable properties, are Brassica, Cochlearia, Raphanus, and
Sisymbrium.
Active Principles.-All the plants implicated owe their activity
to volatile or essential oils of the type of mustard oil. In black
mustard seed is a glycoside, sinigrin, which, in the presence of an
enzyme, myrosin, is decomposed into allyl isothiocyanate (volatile
oil of mustard, C3H 5CNS), potassium hydrogen sulphate, and
glucose. White mustard contains the glycoside, sinalbin, which,
in the presence of myrosin, yields parahydroxylbenzyl isothio-
cyanate, sinapine sulphate, and glucose; and the wild radish,
Raphanus raphanistrum, contains a glycoside similar to sinalbin.
Botanical Characters.-The plants likely to cause harm are all
well known, and it will therefore suffice to name those which are
stated to have caused poisoning. They are:
Brassica alba (Sinapis alba Linn.), cultivated or white mustard;
B. sinapis (5. arvensis Linn.), charlock or wild mustard; B. nigra
(5. nigra Linn.), or black mustard; and Cochlearia armoracia, or
horse-radish. To these may be added the wild onion, Allium
sativum, which, although pelonging to the Liliacere, is stated to
contain a volatile oil similar to oil of mustard .
. Symptoms.-In the horse black mustard/produces bronchial
symptoms, marked by difficulty in breathing and the discharge
of great quantities of yellowish frothy matter from the nose, the
POISONOUS PLANTS 205
post-mortem showing pulmonary congestion and bronchi injected,
dark red, and full of frothy yellow liquid.
Black mustard seeds* are sometimes found in cake, such as
that of rape seed, and Gerrard (I875) records the effects of such
a cake on cattle. Uneasiness, restlessness, and intense colic, with
frantic rushing about and mania, ending in exhaustion, falling,
struggles and collapse, were prominent features, and Gerrard
gave the case as a good example of the action of a purely irritant
poison.
Anderton (I86I) similarly records a case in which cows were
made fatally ill after about I pound each of an' oil-cake, shown by
Tuson to be composed chiefly of mustard seed., Salivation, colic,
respiratory distress, and accelerated pulse were noticed.
The case recorded by Roub (r906), in which cattle ate
mustard on pasture, appears very different, for he noted dul-
ness, coldness, some tympany, laboured respiration, staggering,
and falling. In fatal cases there was immobility and a semi-
comatose condition.
Cozetta records cattle poisoning by a colza cake of Indian
origin containing various 'species of mustard seed, and remarks
that steeping in boiling water withdraws the essential oil, and
renders the cake harmless.
Mustard cake, or cakes largely containing mustard seed hulls,
reappeared during the war period I9I4-I918, when foods of all
sorts were scarce, and Hughes (I924) has also noted mustard
in a cake. The symptoms observed coincided remarkably with
those quoted by Gerrard (r875).
Cochlearia armoracia, or horse-radish, has been held responsible
for poisoning in England, but is not reckoned amongst the
poisonous plants by the Continental authorities. Since it also
yields allyl sulphocyanide, there seems little doubt that it might
equally with mustard prove dangerous.
Litt (1894) observed in cattle: wildness, lowing, excitement,
and rushing about, recalling the symptoms noted by the earlier
observers on mustard. Thereafter, in conformity with Roub's
observations, he noted collapse and coldness, with low pulse and
staring eyes.
It appears most likely that the nervous symptoms here, as in
* Whole seeds pass through unaltered in the f~ces. They may be eaten
by the pound without any effect. In cake, however, they may be in the
crushed condition.
206 VETERINARY TOXICOLOGY
so many cases, are due to exhaustion, and not to any specific
action of the active principles.
Hackett (I9I7) examined three dead cows and found about
three-quarters of a peck of horse-radish in each rumen. He noted
swelling of the anterior third of the tongue, and inflammatory
congestion of the mucous membrane of the rumen, but for the rest
no gross lesion.
Comparable with the poisoning by mustard is that observed by
Goldsmith (I909), in which onion was the cause. He remarked
that cows, after eating freely of onions in a .cart, some of which
were sprouting, ana others decayed, displayed severe colic. Some
were constipated, others slightly purged, and in one case there
was vomition. In the worst case there was severe constipation,
staggering, tenderness in the loins, temperature I03 F., and the
dark-coloured urine smelt of onions.
Post-Mortem Appearances.-The prominent lesions in these
cases were inflainmation of the resophagus and trachea, and less
characteristic inflammation of the rumen, and patchy inflamma-
tion of the intestines. Roub (1906) found the abdominal cavity
and bladder to contain abundant yellow fluid, smelling of mustard.
In the onion case the viscera all smelt strongly of onions.
Treatment.-Roub (1906) gave I! pounds Glauber's salt, fol-
lowed by I pound every twelve hours till purgation resulted, and
as stimulants nux vomica and spirits of nitre. Change of diet,
oleaginous purgatives, and stimulants are indicated.
Chemical Diagnosis.-Mustard oil is volatile from neutral or
acid media in a current of steam. It is thus sep3;rated in the search
for volatile poisons, and its characteristic odour suffices for its
recognition. When in sufficient quantity it may.be got pure and
definitely identified by its physical properties.

REFERENCES.
Anderton, J. W. (1861'), Veterinarian; 34, 265.
Cozetta (1905), Vet. j., 61, 95. ~
Gerrard, J. (1875), Veterinarian, 48, 396.
Goldsmith, W. W. (1909), j. Compo Path. and Therap., 22, i51.
Hughes, H. T. (1924), Vet. I., 80,43. .
Litt, W. E. (1894), Vet. Rec., 7,546.
Roub, F. ]. (1906), Vet. J., 62,166.
POISONOUS PLANTS 20 7

VIOLACElE.
The members of this family, well known in Viola odorata, the
common violet, contain the active principle iridin of the iridacece
. (q.v.). The poison is contained in the roots, and when these are
eaten symptoms of nausea, vomiting, nervous, respiratory, and
cardiac disturbances are set up. Poisoning is, however, very rare,
and the possibility of its occurren.ce alone warrants its inclusion
here.
CARYOPHYLLACElE.
This family includes the genera Saponaria, Lychnis, .Arenaria,
and Stellaria, members of which are poisonous.
Botanical Characters.-Saponal'ia is represented by S. officinalis,
soap-wort, hedge-pink, or crow-soap. It frequents hedge-banks
and waste places, attains a height of about 2 feet, and is a peren-
nial. The leaves are ovate lanceolate, and opposite; calyx cylin-
drical, petals pink, and flowers in August.
Lychnis is represented by L. githago Scop. (Fig. 25) (Agrostemma
githago Linn.), the corn-cockle, in cornfields. It attains 2 to 3 feet,
is covered with silky hairs, and bears purple flowers in July. The
seeds are small, dark coloured, and wrinkled, and number thirty
to forty in a capsule. Occasionally the grain gets mixed with
cereals, and thus enters flour or forage. The starch is small, having
the dimension I to 2 JL, as compared with wheat, which has
I5 to 35JL.
Arenaria includes A. serpyllijolia, or the thyme-leaved sand-
wort, and is common on walls, dry sands, and waste places. "A
very much branched, slender, and slightly downy annual, seldom
attaining 6 inches. Leaves very small, ovate, and pointed. Pedic1es
from the upper axils or forks of the stem, 2 or 3 lines long, and
slender. Sepals pointed, about Ii lines long. Petals usually much
shorter, but variable in size, obovate. Capsule opening in six
narrow valves."*
Stellaria.-This genus (the star-worts), represented by several
British species, was noted by Cobbold (I880) as being responsible
for the poisoning of horses in Russia, and as having occasioned
losses in the Crimean campaign.
Active Principle.-All these plants owe their pois.onous pro-
perties to glycosides of the saponin type, which are widely
'" Bentham and Hooker.
:208 VETERINARY TOXICOLOGY
diffused in the plant kingdom, and which present minor differences
to one another. The officinal Quillaja saponaria (Rosacere) is a
chief source of saponin. It is native to South America, and is
known as Chile soap bark, or Panama root. The saponins possess
certain interesting properties
which throw light on their
physiological effects. They do
not form true solutions in
water, but give colloid sus-
pensions, and impart remark-
able and permanent frothing
qualities to the liquid. For
this reason saponin is used as
an adulterant to such bever-
ages as lemonade. The sapo-
nins are not diffusible, being
colloidal and are therefore not
easily absorbed. When taken
by the mouth it is probable
that absorption only occurs
when inflammatory lesions are
also caused, as happens with
some of the plants. When
introduced into the blood
stream the saponins cause
hremolysis, or dissolution of
the red cells, and also simi-
larly act on other cells-e.g.,
of ganglia. To these effects
are due the nervous symp-
toms of stupefaction and
paralysis. Saponin is taken
up from water by the gills of
FIG. 2s.-LYCHNIS GITHAGO
(CORN-COCKLE).
fishes into the blood stream,
and thus produces poisoning,
even in a dilution of I to 200,000. The hremolytic action is
stopped by cholesterol, which thus directly neutralises or antag-
onises saponin poisoning.
It has been stated that animals develop tolerance after continual
feeding on small doses of corn-cockle meal.
Symptoms.-=-Animals refuse to eat the corn-cockle plant, and
POISONOUS PLANTS 2 09

generally poisoning is the result of the ignorant feeding of the


grains, or fraudulent admixture of the flour with meal. Cornevin
(1893) gives the approximate lethal dose of the flour as 18 grains
and 7 grains per pound body weight for the ox and pig respec-
tively, about twice that proportion of the whole grain being
needed. Pigs reject large doses by vomiting, but small doses
repeated over a long interval give rise to chronic poisoning.
In the acute poisoning of horses there is copious salivation, colic,
pallor of the mucous membranes, pulse small and rapid, elevated
temperature, and accelerated respiration. The freces are diarrhceic
and fcetid. Muscular tremors and rigidity set in, followed by
collapse, coma, and death, without convulsions.
Cattle display similar gastric disturbances. A period of coma is
also reached, during which there is continual passage of diarrhcea,
gradual loss of motor and sensory powers, and death.
According to Cornevin (1893), Arenaria does not poison, but
causes great salivation.
Post-Mortem Appearances.-After .subcutaneous injection of
saponin there is no gastro-enteritis, although the alimentary
canal is emptied by reason of the purgation and vomiting. But
after the poison has been taken by the mouth there is inflamma-
tion, sometimes extending throughout the alimentary tract. The
contents are always fcetid, and mixed with bloody mucus. There
is congestion of the cerebral meninges and lungs, the kidneys may
be a little inflamed, and the liver normal.
Treatment.-The treatment of poisoning should consist of
removal of the cause, opiates against pain, and stimulants as
indicated.
Chemical Diagnosis.-There is little prospect of a satisfactory
recovery of saponin from ingesta or organs after poisoning.
Search should be directed to the discovery of the starch grains
of corn-cockle in the food. The starch of corn-cockle requires
more iodine to induce the blue starch iodine coloration than
wheat, or other cereal, or potato starches. Roughly, about
seven to ten times as much iodine is required. Com-cockle flour
(like that of lolium) gives a full orange-yellow solution when 10
grammes are warmed with 30 to 40 C.c. of 70 per cent. alcohol,
with 5 per cent. of dilute hydrochloric acid (Vogl's test). Under
the same conditions various other flours give to the acid alcohol
the following tints: fine wheat and rye, colourless; coarse wheat
and rye, pale yellow; barley and oats, straw yellow; pea meal,
14
210 VETERINARY TOXICOLOGY
full yellow; vetch and bean meal, purple-red; ergot, blood-red;
meals containing rhinanthin, green. Rhinanthin is a glycoside
contained in certain of the ScrophHlariacece-e.g., Mela1J1,pyrum,
Rhinanthus, etc. (q.v.).
REFERENCES.
LYCHN1S.
Cobbold (1880), Veterinarian, 52,453.
Cornevin, C. (1893), Des Plantes Veneneuses.

HYPERICACEJE.
The only member of this family reputed to be dangerous is
Hypericum perforatttm, or St. John's wort, which is abundant in
woods, thickets, and hedges in both Europe and America; it
reaches about I to It feet, and bears a yellow flower. On ingestion
of the plant, symptoms of photosensitisation may set in, especially
in animals with an unpigmented skin exposed to strong sunlight.
Many other plants are known which produce a similar effect,
particularly in countries like South Africa. and Australia, where
prolonged exposure to sunlight is likely to occur. These plants
belong to different natural orders, but for the sake of convenience
may be mentioned here. The best known are Fagopyrum eSC2t-
lmtum, or buckwheat, N.O. Polygonacere; Medicago denticulata,
or trefoil, Trifolium hybrid'ttm, or alsike clover, T. pratense, or
red clover, N.O. Leguminosre; Tribulus terrestis, or devil's thorn,
N.O. Zygophyllacere; and Lippia rehmanni, N.O. Verbenacere.
Active Principles.-The substance present in H. perforatmn
possessing a photodynamic action is probably the pigment,
hyerpicum red, C16HI005' isolated. by Cerny (19II) from the
petals. The active principles of the other plants are still unknown,
with the exception of Lippia rehmanni, from which Rimington,
QUin, and Roets (1937) were able to isolate a crystalline substance,
icterogenin, C34H 520 6 . On the adlI!inistration per os of I to 4 g. of
this substance to a normal sheep, symptoms of disease set in
within twenty-four hours.
Symptoms.-In South Africa the disease known as geeldipkop,
or swelled head, has been shown to be the result of photosensitisa-
tion. In this condition, the first symptoJl1s noticed are an intense
irritation of the skin, the animal scratching and rubbing against
objects whenever possible; there may also be a slight rise of tem-
perature. A dermatitis, particularly affecting the area ?f the head,
POISONOUS PLANTS 211
then develops, and cedematous swellings appear on the face, ears,
lips, round the eyes, and under the jaw; other parts of the body,
particularly the limbs, may also be affected. The swellings
rupture, and a purulent discharge oozes from them; the skin
becomes hard, dry, and covered with dark brown crusts, and may
become so tense that it is impossible for the animal to open its
mouth. These symptoms are, in most cases, accompanied by
evidence of bile stasis and jaundice.
Quin (1936) found that similar symptoms could be produced
experimentally by ligation of the bile duct, which permits of the
accumulation of bile pigment in the blood stream, and Rimington
and Quin (1934) found evidence that it was failure to excrete a
porphyrin, phylloerythrin, derived from chlorophyll, which was
responsible for causing photosensitisation following. the ingestion
of T. terrestris. It thus seems probable that when porphyrins or
their derivatives are present in the blood stream in abnormal
amounts, photosensitisation is likely to result on exposure to
strong sunlight. 'Since porphyrins are normally excreted in the
bile, it suggests that there must first be some injury to the liver,
but it is still uncertain what the nature or extent of this damage
must be before disease is produced; certainly ordinary liver
poisons, such as chloroform, phosphorus, or carbon tetrachloride,
do not produce it.
In northern latitudes, plants .like H. perforatum are not so
likely to produce severe photosensitisation, as is seen, for example,
in South Africa, because of the reduced sunlight, but they are
generally held to be poisonous. Thus, Cornevin (1893) records
that, following the ingestion of H. perforatum, a mare became
semi-comatose, the head dropping between the outstretched fore-
legs. The pulse was full and slow, respiration deep and slow, and
the appetite lost. The pupils were dilated, conjunctivre injected,
and the unpigmented skin of the nose coloured wine red as in
purpura. In about twelve hours the condition passed off. In
Australia, however, severe photosensitisation in cattle, sheep,
and guinea-pigs following the ingestion of H. perforatum has been
observed.
Post-Mortem Appearances.-In acute cases of photosensitisa-
tion, in addition to the skin lesions, there may be evidence of
gastro-enteritis and cholecystitis, with enlargement of the spleen
and kidneys and hepatic degeneration.
Treatment.-It is essential to provide affected animals with
2I2 VETERINARY TOXICOLOGY
shade and to change the diet. No specific treatment is known, so
that all that can be attempted is to treat the symptoms as they
arise. A purgative and cholagogue, such as calomel, is indicated,
and the sw~l1ings should be incised and an antiseptic dressing
applied.
REFERENCES.
HYPERICUM PERFORATUM.
Cerny, C. (lgIl), Zschr. Physiol. Chem., 73, 371.
Cornevin, C. (1893), Des Plantes Veneneuses.
Quin, ]. I. (1936), Ondersterpoort]. Vet. Sci., 7,351.
Rimington, C., and Quin, ]. I. (1934), Ondersterpoort J. Vet. Sci., 1,137
Rimington, C., Quin, J. I., and Roets, G. C. S. (1937), Ondersterpoort J.
Vet. Sci., 9, 225.

MELIACElE.
This order is tropical, and comprises Melia azedarach, or the
Chinese umbrella-tree, grown in Central Europe and the United
States, and escaped from cultivation in the South. Hogs are stated
to have been poisoned in Arizona by ignorant feeding of the seeds.
Symonds (1886) refers to Azadirachta indica as a drastic purgative,
the juice of the leaves being used as an anthelmintic, emmena-
gogue, and diuretic.
Poisoning, which specially affects Pigs, is marked by nausea,
vomition, violent colic, and. tympanites, followed by diarrhcea,
sweating, convulsions, uncertain gait, and intense thirst. The
lesions are those of intestinal inflammation. Steyn (I934) found
that sheep, goats, and'rabbits, as well as pigs, are susceptible, and
that the active principle is chiefly present in the drupes. Its
chemical composition is unknown, but is probably a bitter
principle which acts as a narcotic on the central nervous
system.
REFERENCE.
Steyn, G. D. (1934), The Toxicology of Plants in South Africa.
Symonds, T. J. (1886), Quart. J. Vet. Sci. India, 77

CELASTRACElE.
Botanical Characters.-This order is represented in Britain by
Euonymus europteus, spindle-tree or skewer-wood (Fig. 26), and
in America by E. atropurpureus, burning bush or wahoo, and
Celast1'1ts scandens, climbing bittersweet. E. ettropteus is a glabrous
shrub, about 3 to 5 feet high. Leaves shortly stalked, ovate-
POISONOUS PLANTS 213

oblong, or lanceolate, pointed, and min.utely toothed. Peduncles


shorter than the leaves, with seldom more than three or five
flowers, of a yellowish-green colour. Petals four, obovate, about
2 lines long, the stamens half that length. Fruit quadrangular,

FIG. 26.-EuONYMUS EUROPlEUS (SPINDLE-TREE).

red when ripe, opening at the angles so as to show the seeds


enclosed in a brilliant orange-coloured aril. The shrub is frequent
in parts of England in hedges. Animals eat the young leaves in
early summer, when the poisonous effects are greater than in the
autumn.
2I4 VETERINARY TOXICOLOGY
Active Principle.-Euonymus contains a glycoside called
euonymin, which belongs to the group of purgatives and pos-
sesses a digitalis-like action on the heart.
Effects.-The effects, lesions, and treatment of poisoning by
euonymus are like those o.f other vegetable purgatives, and need
not therefore be again detailed, especially as recorded cases are
very few. .
The leaves of the American Celastrus scan dens, climbing bitter-
sweet or staff-vine, are reported to have seriously, though not
fatally, poisoned a horse.

RHAMNACElE.
Botanical Characters.-Two species of the Rhamnus, or buck-
thorn, genus are poisonous-viz:, Rhamnus catharticus, the
common buckthorn, and R. fr~ngula, the alder buckthorn.
Neither species is very common in Britain, the former less so than
the latter, and both grow in hedges or bushy places. The flowers
are small and green, and the fruit about the size of a pea, that
of R. catharticus being black, and that of R. frangula dark
purple. R. cath~rticus usually grows on calcareous and R. fran-
gula on peaty or leafy soil.
Active Principle._:_The fruit contains a glycoside or glycosides,
which are themselves without action, but on hydrolysis they
yield emodin, trioxymethylanthraquinone, C15HIOOS' and thus
belong to the group of vegetable purgatives. This group also
include aloes, the dried juice obtained from the leaves of Aloe
chinensis; the dried bark of the North American R. purshiana,
which forms the cascara sagrada of medicine; and the official
rhubarb, Rheztm officinale, as well as the common rhubarb,
R. palmatum.
Effects.-The berries of rhamnus species are purgatives, and
dangerous effects, which are rarely likely, take the form of super-
purgation.
LEGUMINOSElE.
This natural order contains many important poisonous species,
few of which are native to Britain, though several are cultivated.
Amongst British wild plants are found Cytisus scoparius, the
common and very abundant broom, which resembles the culti-
vated SPartium junceum, or Spanish broom, in containing the
POISONOUS PLANTS 2r5
alkaloid sparteine, and Lathyy'lts aphaca, the yellow vetchling,
which contains a cyanogenetic glycoside, as does the exotic
Phaseolus lunatus, or Java bean (see under Cyanides). Of culti-
vated species, mention must be made of C.labttrnum, the laburnum
tree; varieties of lupins grown' as ornamental plants and also as
forage crops; and the seeds of such exotic species as L. sativus,
the Indian pea, which are definitely and seriously poisonous. The
cultivated Coyonilla and Wistaria are reputed to be dangerous,
but are not important. This order also includes those species of
Trifolium and Medicago which under certain conditions produce
photosensitisation (see under Hypericacere), as well as the
Astragalus species or locoweed, which are concerned in selenium
poisoning (see Selenium).

Laburnum.
Cases of poisoning by laburnum are not numerous, but Cornevin
(r893) submitted the question to experimental test and estab-
lished the toxicity of the plant beyond doubt. Poisoning of horses
has resulted from the injudicious administration of the seeds,
which are said to impart a gloss to the coat. Moreover, poisoning
in the human subject, usually from eating the flowers, is well
recognised.
Active Principle.-The active principle is the strongly basic
alkaloid cytisine, Cn H 140N 2. All parts of the plant are poisonous,
the greater part of the poison being, however, found in the seeds.
Desiccation does not destroy the activity, and the poison is not
entirely removed from the seeds by boiling.
Effects.-Cornevin (r893) found it impossible to kill the dog or
cat by feeding (on account of vomition); or the sheep, goat, or ox by
reason of refusal, after a certain point, of the food. The horse and
ass could be killed by feeding, and all animals by injection of the
poison. Taylor (1934) records similar failure to poison the dog
and cat. . .
Vomition, excitement, followed by clonic contractions and
coma, appear to be produced in carnivores.
In the horse Cornevi:iJ. (r893) observed general and sexual excite-
ment, muscular tremors, followed by contractions, beginning in
the posterior parts. In general the poisoning is in three stages-
(r) excitement; (2) coma and inca-ordination of movements;
(3) convulsions.
The lesions are not characteristic.
2I6 VETERINARY TOXICOLOGY
Chemical Diagnosis.-The alkaloid cytisine is separated in the
routine method of search for alkaloids. It is not very easily
recognised, since confusion with other alkaloids may arise. It
gives a yellow, brown, and finally green colour on solution in
strong sulphuric acid, with nitric or chromic. acids. Van der
Moer's reaction is characteristic, but difficult to apply, since the
substances ought to be in fairly definite proportions (one mole-
cule of each), and free acid absent. It consists in the production
by ferric chloride of a blood-red colour, destroyed by adding
. hydrogen peroxide and then passing on warming to blue. On the
addition of thymol to a solution of the alkaloid in concentrated
sulphuric acid, a yellow colour appears, changing to red on
warming.
Brooms.
Spartium junceum, Spanish broom, and Cytisus scoparitts,
common broom, merit mention as a precaution, for they contain
the volatile alkaloid sparteine, C15H 26N 2 , which is identical to
lupinidine, one oJ the alkaloids present in the seeds of Lupinus
luteus. Sparteine closely resembles coniine in its chemical and
physiological properties, but is less toxic. It causes paralysis of
sympathetic ganglia and motor nerve endings, and depresses the
heart. A neutral resin, scoparin, is also present in brooms, which
has been used in medicine on account of its diuretic effect.
The therapeutic dose of sparteine sulphate for the horse is
IO to 40 grains, and the plant yields about 0'3 per cent. of active
principle, whence it appears that from about 25 pounds of the
plant about I ounce would result. This would be, therefore, an
average poisonous dose-i.e., ten times the average therapeutic
dose. Poisoning by brooms is therefor~ only likely in exceptional
cases.
Spartine may be extracted by means of the Stas-Ofto method,
and occurs as a volatile liquid, which becomes brown on exposure
to air. Its most chara.cteristic reaction is the production of black
crystals, when an ethereal solution of iodine is added to an
ethereal solution of the alkaloid.

Lupines.
Although lupines are extensively used as fodder plants, they
appear at times to be the source of poisoning, particularly in
America and Europe, where they are grown for hay. The
POISONOUS PLANTS 2 17

sporadic nature of outbreaks of lupinosis has led to the suggestion


that it is only when the plants are contaminated with some
fungus or bacterial agent that 'they are poisonous, but there is
little evidence to support this idea, and it is most probable that
the alkaloids which they contain are responsible for causing the
disease. Poisoning is only likely when the plants are eaten in
excessive quantities, since the alkaloids are rapidly excreted in
the urine and do not accumulate in the body. They are distributed
throughout the plant, but are present to the greatest extent in
the seeds and pods. According to the German authorities, a daily
ration of 500 g. of the whole plant, 300 g. of empty pods, or 100 g.
of seeds will produce poisoning in sheep. Poisoning is more
common in autumn, and sheep are the animals most usually
affected, but other animals are also susceptible.
In Europe, the species of lupines most commonly found are
Lupinus [/iteus, yellow lupine; L. angustijolia, blue lupine; and
L. alba, white lupine; in America, Couch (1926) and others have
found L. leucophyllus, L. spathulattts, L. palmeri and'L. argentus
to contain alkaloids, so that it is very probable that they are
present in all lupine species.
Active Principles.-In addition to sparteine (lupinidine),
the more important alkaloids isolated from lupines are lupi-
nine, ClOH 190N; lupanine, C15H 240N 2; and hydroxylupanine,
C15H2402N2; of these, d-lupanine is considered to be the most toxic.
Symptoms.-Acute lupinosis is marked by inappetence, dysp-
nrea, and a slight rise of temperature. Hrematuria, circulatory
and digestive disturbance, trembling, spasms, and vertigo may
also be seen. Jaundice is characteristic. In the chronic form,
symptoms associated with a chronic interstitial hepatitis pre-
dominat~.
Post-Mortem Appearances.-The liver shows hepatitis with
fatty degeneration; nephritis, evidence of jaundice, and enlarge-
ment of the spleen are also present. The first stomachs are inflamed,
and then~ is effusion of blood in the intestines, peritoneum, and
other organs. (Edema of the lungs and larynx is frequently seen.
Treatment.-The treatment of lupinosis consists in the ad-
ministration of oily purgatives and acidified water to hinder
absorption; acetic, tartaric or tannic acids are the most suitable
for this purpose, since they cause precipitation of the alkaloids.
A change of diet is essential.
218 VETERINARY TOXICOLOGY

Lathyrism.
Several varieties of Lathyrus have long been known to be
poisonous, particularly in India and Mediterranean countries, and
in this connection were mentioned by Hippocrates and Pliny.
The commonest variety, L. sativus, often though wrongly called
Indian or mutter pea, is frequently present in samples of Pis1t1n
arvense or field pea-the true mutter pea-imported from India,
as well as in samples of P. sativus. Another strain, commonly
known as the Riga or dog-tooth pea, is a large white variety of
L. sativus, which is also poisonous; in addition, L. cicera and
L. clymenum are recorded as having poisonous properties.
Poisoning is usually due to the ingestion of the seeds, either
alone or mixed with other peas, but much confusion has arisen
since samples of L. sativus are usually contaminated with such
pulses as P. arvense, P. sativum, and Vicia sativa, which may
account for the discrepancies in the observations made in different
parts of the world. In addition to the seeds, Steyn (1933) showed
that fresh L. sativus in the pre flowering and flowering stages was
toxic at least to horses, one animal dying with typical symptoms
after it had eaten II4 kg. of the plant in thirty-five days. There
is little doubt, however, that the seeds are the most dangerous
part of the plant, particularly when they are ground into
meal.
Active Principle.--Much research has been carried out to
rletermine the active principle present in Lathyrus species, but so
far with little success. Anderson, Howard, and Simonsen (1925)
suggested that the trouble arose from contamination with V.
sativa, the seeds of which contain cyanogenetic glycosides, but
the symptoms produced following the ingestion of Lathyrus do
not suggest poisoning by hydrocyanic acid. Stockman (r934),
after prolonged research, isolated phytic acid from Indian
L. sativus and showed that the acid and its salts were. toxic to
monkeys, rabbits, and frogs on intravenous injection, causing
degeneration of the nerve cells and fibres of the central and
sympathetic nervous systems. But phytic acid is found in many
plants, particularly cereals, which do not produce symptoms
typical of Lathyrus poisoning, so that the acid cannot be the
specific poison concerned in this case. Whatever it may be, the
active principle does not appear to be destroyed by drying nor
boiling, though possibly prolonged boiling- may destroy it, and
POISONOUS PLANTS 21 9

there is a certain amount of evidence to .suggest that it is soluble


in water.
Symptoms.- The effects of Latltyrus are very characteristic,
and the condition known as "lathyrism" has been observed in
man and all the domestic animals. Lathyrism is only produced
when considerable proportions of the pea enter into the rations
over a prolonged period of time: in man, generally in the fourth
month; in the horse, fed exclusively on the pea, the tenth day;
but when I or 2 quarts are given daily, only towards about the
eightieth day. Moreover, the malady may declare itself so long
as pfty days after the cessation of the pea feeding ..
In' man a constant sign is paralysis of the lower extremities;
speech, intelligence, and power over the upper extremities are
preserved. The symptoms resemble those of. dorsal tabes, and
lathyrism has further been compared with beri-beri.
The first complete observations on the horse were made in
this country by McCall (1886). An animal was feeding well, but
thick in his wind. After going about 200 yards with an empty
lorry it stood with the forelegs forward, neck stretched, elbows
out, and laboured breathing. It was kept on its feet, until u'n-
yoked, with difficulty; each breath gave a loud sound from the
larynx. There was profuse sweating; quick, irregular, and inter-
mittent pulse; increased impulse of the heart; venous pulsations;
normal temperature; and a vibration over the region of the larynx.
After about five minutes the symptoms disappeared, the animal
seemed well, and began to eat hay.
The horses had been having a mixture containing 20 per cent.
of Indian pea meal. Some had it boiled, others wetted, and it
was noticed that only those which had had unboiled meal were
affected .
. McCall (1886) experimentally fed an old but sound cart mare,
whose pulse rose in eleven days from 52 to 84, temperature normal;
but after exercise the pulse was 130, and the~e was vibration over
the larynx. Later vesicles and inflamed spots formed in the
mouth, and there was extensive loss of hair, not caused by
parasites.
King (r892) observed similar symptoms with gritting of teeth,
frothing, and convulsive movements of the eyes, recalling epilepsy,
in cart horses.
Slidders (r894) and Abson (r894) record the effects... of the dog-
tooth pea on horses and ponies. The dog-tooth pea is much larger
220 VETERINARY TOXICOLOGY
and whiter than the mutter pea. The symptoms observed were
thick wind, a staggering gait, weakness of hind quarters, and
general signs of intoxication were noticed, and sudden violent
attacks of laryngeal paralysis and dyspncea, during which there
was palpitation, frothing, tongue protruded, eyes staring, bluish
tint of buccal membranes, and palpitations. The paroxysms some-
times proved fatal, otherwise there would be a speedy temporary
recovery. Change of diet is ineffectual in arresting the malady, at
any rate at first.
Meachem (I8g6) noticed no ill-effect in horses until after twelve
months' feeding.
Cases of disease in cattle have been observed with L. c~'YmeJtum
and with the Indian vetch, in both cases in France. Cows had
green vetches containing L. clymenum for ten days. Three weeks
later they were ill; they lay on sternum with neck muscles on non-
affected side contracted, the mouth closed, thick viscid saliva,
suspended rumination, constipation,. paralysis of the limbs, loss
of sensibility in the skin, pulse small and weak.
In the Indian vetch case the cause was a cake containing
Lathyrus, and there was stiffness of the lower joints, staggering,
blindness, and other symptoms, as in the preceding case.
With sheep and pigs paralysis of the hind extremities is notable.
Cornevin (r893) found that water extracts of L. sativus on
hypodermic injection into dogs produced trembling and spas-
modic movements, beginning in the hind extremities and pro-
pagated eventually to the muscles of the neck and front legs;
later, nausea and vomition, profound depression, and loss of
power of the hind limbs; eventually complete motor paralysis
and death without convulsions from the twenty-fourth to the
fortieth hour.
Post-Mortem Appearances.--In chronic lathyrism of the hors~
there are thickened, congested patches in the stomach and
intestines; lungs hyperremic and bronchi showing--signs of catarrh
and congestion. The larynx shows irregular congested patches,
especially round the glottis, the intrinsic muscles of which are'
paler and smaller on the left than on the right and show fatty
degeneration. Degenerative changes are to be observed in the
ganglion cells of the spinal cord and medulla.
In the case of cattle, the blood is tbick and dark; the cranium
and anterior portions of the spinal cord containing a large amount
of hremorrhagic serum; the 'meninges, deeply congested, forming
POISONOUS PLANTS 221

a well-marked network over both hemispheres, with black


hremorrhagic patches extending a considerable depth into the
tissue.
The only effective treatment beyond removal of the cause and
rest would appear to be tracheotomy and the administration of
stimulants such as strychnine.

Other Leguminosere.
The European Ervum ervilia, bitter vetch of bastard lentil.
produces in pigs symptoms of somnolence, passing into coma,
interrupted by muscular tremors, and occasionally with nausea
and vomition. Sheep and cattle appear to be tolerant, and the
pig also to acquire tolerance. It seems possible that mishaps
are du'e rather to malnutrition than to a definite toxic sub-
stance.
Numerous other species of this order are held responsible for
poisonings, of which mention may be made of the following:
Erythrophleum guineense and E. cOltminga have caused poison-
ing in Guinea and the Seychelles. E. guineense, and probably also
other species, contains a glycoside, eryth1'ophlein, of the digitalis
class.
The North American Gymnocladtts dioica, or coffee-tree, is
stated to contain a saponin, but cases of animal poisoning are not
recorded.
In South Africa, America, and Australia numerous Crotalaria
species have proved poisonous, including C. spectabilis, which is
sometimes grown as a fodder plant on light sandy soils. Theiler
(19II) showed that the South African disease known as stiff-
sickness is due to the ingestion of C. burkeana, the most charac-
teristic symptoms of acute poisoning being laminitis, and of
chronic poisoning a stiff, staggering gait and abnormal growth
of the hoof. Theiler (1918) also found that C. globifera and C. dura,
wild lucerne, are responsible for causing "jaagsiekte" in horses,
in which there is a rise of temperature, dyspnrea, rapid weak
pulse, collapse, and death; these plants also cause similar
symptoms in sheep. In Australia, White (1934) found C. acicularis
and C. incana to be poisonous, and in America, Emmel (1937)
and others have studied the poisonous properties of C. retusa,
C. sagittalis, and C. spectabilis. All parts of these plants, com-
monly known as rattle-pods or wild peas, are poisonous either
222 VETERINARY TOXICOLOGY
fresh or dried, and the seeds have been responsible for poison-
ing pigs and poultry. Poisoning may be acute or chronic, and
symptoms may not develop for several months after feeding has
stopped. In pigs, the most characteristic lesion in acute C. spec.ta-
biUs poisoning is hremorrhages on the serous membranes, and in
chronic cases anremia, necrotic enteritis, and induration of the
liver. .
The active principle of Crotalaria species has not yet been
identified. Since the symptoms and lesions set up by the various
species differ in certain respects, it is probable that they do not
all contain the same active principle. Treatment appears to be of
little avail.
Melitotus species, particularly M. alba, white sweet clover, and
M. ojjicinalis, yellow sweet clover, are frequently grown as fodder
plants, but under certain circumstances they are also poisonous.
Outbreaks of a condition known as "sweet clover disease" have
been reported from numerous parts of the world,. particularly
from North America and Russia. From the work of Scofiel~
(1924), Roderick and Shalk (1929), and others, it is now estab-
lished that the disease is due to feeding sweet clover which has
been damaged by unfavourable weather conditions when made
into hay or ensiled; in this case, the plants develop poisonous
properties, not due to the moulds or fungi which may also be
present.
Active Principle.-Sweet clover, like many other plants, con-
tains a bitter principle, coumarin, a lactone of coumarinic acid,
itself an oxy-derivative of cinnamic acid. Coumarin is com-
paratively harmless, but from damaged sweet clover plants
Campbell and Link (1941) and others were able to isolate a white,
crystalline derivative, dicoumarin, C19H1206, which produces all
the symptoms of sweet clover disease in experimental animals
and is undoubtedly the active principle concerned in clinical
cases of poisoning. Dicoumarin has assumed some im:R_ortance in
human medicine, since it is of great value for the prevention of
thrombus formation. -.
Symptoms.-Sweet clover disease occurs chiefly in young
cattle, but all animals appear to be susceptible. After feeding
on damaged sweet clover for a few weeks or perhaps months,
characteristic symptoms of poisoning set in. Profuse hremorrhages
occur after minor injuries, since the coagulation time of the
blood becomes progressively prolonged owing to a fall in the
POISONOUS PLANTS 223

prothrom.bin level; hremorrhages also occur in the internal


organs and subcutaneously, so that pronounced swellings, due to
extravasated blood, are seen all over the body, particularly in
the limbs. The mucous membranes are pale, there is progressive
weakness, the animal becomes stiff, unable to rise, and death
from loss of blood occurs in a few days after the onset of
symptoms.
Treatment.-Blood transfusions are the only treatment likely
to be of any avail. A change of diet is essential, and care must be
taken not to perform any operation even of a minor character
until the coagulation time of the blood has become normal.
Abrus precatorius, jequirity pea, which yields the toxalbumen
abrin, and Robinia pseudoacacia, which yields the toxalbumen
robin, also belong to the leguminosere, but are considered together
with Ricinus cU11l1ltunis.

REFERENCES.
LABURNUM.
Cornevin, C. (1893). Des Plantes Veneneuses.
Taylor, A. S. (1934), Principles and Practice of Medical Jurisprudence,
9th ed.
LUPINE.
Couch, J. F. (1926), I. Agric. Res., 32, 51.
LATHYRUS.
Abson, J. (1894), Vet. Rec., 7,159.
Anderson, L. A. P., Howard, A., and Simonsen, J. L. (1925), Indian I.
Med. Res., 12, 613. .
Cornevin, C. (1893), Des Plantes Veneneuses.
King, G. E. (1892), I. Compo Path. and Therap., 5,371.
McCall (1886), Veterinarian, 59, 789.
Meachem, F. (18g6), Vet. I., 43,77.
Slidders, ]. P. (I894), Vet. Rec., 7,90.
Steyn, G. D. (1933), Ondersterpoort I. Vet. Sci., 1, 163.
Stockman, R. (1934), ]. Pharm. and Exp. Therap., 37,43.

CROT ALARIA.
Emmel, M. W. (1937), I. Amer. Vet. Med. Ass., 90,627.
Theiler, A. (19II), Agric. I. S. A/ric., 1,10.
Theiler, ,A. (1918), 7th and 8th Repts. Dir. Vet. Res. S. Africa, 82I.
White, C. T. (1934), Queensland Agric. I., 41,692.
MELILOTUS.
Campbell, H. A., and Link, K. P. (194'1), J. Bioi. Chem., 138,1.
Roderick, L. M., and Shalk, A. F. (1931), N. Dakota Agric. Exp. Sta. Bull.,
25 0
Scofield, F. W. (1924), I. Amer. Vet. Med. Ass., 69,553.
VETERINARY TOXICOLOGY

ROSACElE.
A'I11ygdalus andPntmts species contain cyanogenetic glycosides,
and an account of poisoning by them is to'be found under hydro-
cyanic acid. The e~otic species, Quillaja saponaria, native to
South America, is a source of... saponin, and for an account of
poisoning by this agent reference may therefore be made to the
description of the Cacyophyllace.:e.

CUCURBITACElE.
The Cucurbitace~, or- gourd family, is represented in Britain by
Bryonia dioica, white bryony; Ecbalium elaterium, the squirting
cucumber; and Ciirullus colocynthis, the bitter apple, are found
in Southern and Central Europe; and Cucumis a/ricanlts, the wild
cucumber, is fairly general in South Africa.
Botanical Characters.-Bryonia dioica (Fig. 27), the wild white
bryony, which must not be confused with Tamtts communis,
black bryony, which belongs to the Dioscoridacere, although it
probably contains the same or a closely related active principle,
is a perennial climber common in hedgerows in England, though
not found in Scotland and Ireland. It differs from T. communis
in having leaves divided into five or seven broad, deep lobes, as
compared with the entire leaves of black bryony. The flower is
green and the berry red.
Active Principles.-B. dioica contains an amorphous, neutral
glycoside, bryonin, C2o H 300 5, isolated by Power and Moore (I9u)
from the root; E. elaleritmz contains elaterin, C2oH2S05, a crys-
talline substance examined by Power and Moore (I906); C. colo-
cynthis yields colocynthin, probably a complex substance con-
sisting of alkaloid/al and glycosidal components and a resin; and
from C. africanus Quin (I9I6) was able to obtain a toxic resin.
These substances belong to the jalap or colocynth group of
drastic purgatives, which also includes jalap, gamboge, podo-
phyllin, leptandrin, and euonymin. Some, such as jalap and
colocynth, are irritants to the mucous membrane of the eyes,
nose, and throat.
Symptoms.-The literature is not rich in examples,of poisoning
by bryony or by the allied purgatives. Gamgee (1868) quotes Orfila
on the effects of the root of white bryony on animals, stating that
dogs show great dulness after t ounce, and die within twenty-
POISONOUS PLANTS :225

four hours, not showing other symptoms. Ac;cotding to Hertwig,


:2pounds of the fresh or 6 to 8 ounces of the dried root given to
horses did not cause purgin~, but abdominal pain, loss of appetite,

FIG. 27.-BRYONIA DiorCA (WHITE BRYONY).

accelerated breathing, fever, dulness, and copious urination.


Cornevin (I893) states that bryony promotes sweating, and
causes a livid hue, nausea, diuresis, and abundant painless
15
226 VETERINARY TOXICOLOGY
watery defrecation, to which are added in case of poisoning
nervous symptoms of stupor and tetanic convulsions. There may
be superpurgation or a suppression of defrecation.
The lesions are not significant, and Cornevin (r893) concludes
that the purgative effect is not primary but secondary, and of
reflex origin. The active principle is found in the alimentary
tract, urine, blood, and bile.
As regards other observations on bryony, King (r85S) noted
hrematuria in horses to which white bryony had been given
to improve the condition. Auger (r899) encountered a case
in which a horse ate garden clippings containing white bryony,
and observed no abnormal symptoms save stiffness of the muscles
of the loins, which passed off on application of mustard and
embrocation. Blackwell (r93r) records three cases of suspected
bryony poisoning in the horse.
Chemical Diagnosis.--Bryonin and the glycosides of allied
nature are separated by organic solvents (e.g., chloroform) from
the acid liquid in seeking for vegetable poisons. Sulphuric acid
colours bryonin orange-yellow, then red, and, on warming,
violet. Colocynth similarly gives a yellowish-red and then brown
colour, and elaterin a yellowish-brown and then dark red
coloration.
The chemical tests are not satisfactory or clearly diagnostic.
Taken in conjunction with the finding of parts of the suspec'ted
plants, such results of analysis are, however, valuable confirmatory
evidence.
REFERENCES.
Auger, J. S, (1899),-Vet. Rec., 12,254.
Blackwell, W. E. (1931), Vet. Rec., 11, 9Il.
Cornevin, C. (1893), Des Plantes Venencuses.
Gamgee (1868), Veterinarian's Vade"Mecum.
Power, F. B., and Moore, C. VY. (1909), Pharm. ]., 83, SOL
Power, F. B., and Moore, C. W. (1910), j. Chem. Soc., 99,937.
Quin, ]. I. (1929), 15th Rept. Dir. Vet. Servo S. Africa, 769.

CRASSULACElE.
The only species of this family native to Britain, and to which
poisonous properties are commonly assigned; belong to the stone-
crops-viz., Sedum acre, common stone-crop, wall-pepper, creep-
ing jack, or gold-dust; and Sed'ltffl album, the white stone-crop.
Both are found on walls and rocks, the former having yellow and
the latter white flowers ..
POISONOUS PLANTS 227

They are stated to contain an acrid juice, and in S. acre an


alkaloid sedine, C17H190aN, allied to piperine of pepper, but
nothing of a precise nature is known as to its composition.
Poisoning is not likely to occur, save, perhaps, among birds.
Cornevin (1893) injected juice corresponding to 105 grains per 2
pounds body weight intp a dog, and noted salivation and muscular
tremors, developing into choreic movements, more marked in the
posterior than the anterior members. The respiration was deep
and accelerated, and sense impaired. To this succeeded som-
nolence and coma, lasting about t.welve hours, when the normal
condition was regained. There was abundant urination and
diarrhcea.
Amongst the South African plants belonging to this order.
varieties of Cotyledon-e.g., C. ventricosa, C. eckloniana, C. ~val
iichii, etc.-are known to be poisonous. Kamerman (1932) i,>olated
a neutral principle, cotyledontoxin, Ca2H2s07' from these plants,
which is probably the active principle. The chief symptoms of
poisoning are abdominal pain, torticollis, convulsions, collapse,
and death.
REFERENCE.
Kamerman, P. (1932). See Steyn, G. D. (1934), The Toxicology of Plants
in South Africa.

UMBELLIFERElE.
The umbel family contain important poisonous plants, of
which those belonging to the genera Conium, Cicuta, CEnanthe,
'/Ethu~a, and Cluerophyllum (Anthriscus) are the commonest.

Conium.
The only member of this genus is the very common and well-
known Conium macuZat'l-tm, or spotted hemlock, the poisonous
nature of which has been known for centuries. Infusion of the
hemlock was a favourite poison among the Greeks, and was the
agent of the official suicide of Socrates.
Botanical Characters.-Conium mawiatttm (Fig. 28), or spotted
hemlock. An erect, .branching annual or biennial, 3 to 5 feet high,
or sometimes more, glabrous, and emitting a nauseous smell
when bruised. Leaves large and much divided into numerous
small ovate or lanceolate deeply cut segments; the upper leaves
gradually smaller and less divided. Umbels terminal, not large
228 VETERINARY TOXICOLOGY
for the size of the plant, of 10 to 15 rays. Bracts short and lanceo-
lated; those of the general involucre variable in number; those of
the partial ones turned to the outside of the umbel. Fruit about
2 lines long. The s~em is often conspicuously marked with purplish-

FIG. 2B.-CONIUM MACULATUM (SPOTTED HEMLOCK).


(From Smith's "Veterinary Hygiene.")

red spots. The plant is common on the banks of streams, in hedge-


rows, and the borders qf fields.
Active Principles and Doses.-C. macttlatum is most poisonous
in the green state, the leaves and unripe fruits containing up to
POISONOUS PLANTS 229

2 per cent. of alkaloids; only small amounts are present in the


roots. The alkaloids are. v9latile, so that they are lost on slow
drying or boiling. The plant is more readily eaten by animals in
the early spring, when its alkaloidal content may be low; sheep
have been stated to have eaten the plant without ill-effect, but
there is no doubt that all domestic animals are susceptible.
According to Cornevin (r893), 4 to 5 pounds of the fresh plant
will kill a horse and 8 to ro pounds an ox.
The more important alkaloids so far isolated from the plant
are coniine, CSH17N; methylconiine, CSH16N.CHa; coniceine,
CSH15N; and. conhydrine, CSH170N. All these alkaloids are
poisonous and have a similar action, coniceine being probably
the most toxic.
Poisonous Effects and Symptoms.-The general effect'of coniine
in some respects resembles nicotine and in others curare. There
is nausea, vomition, moderate dilation of the pupils, and weakness
and staggering gait from partial paralysis of the peripheral
nerves. The sympathetic ganglia are at first stimulated and then
paralysed; the heart is at first slowed and then accelerated
through paralysis of the vagus nerve; respiration becomes slow,
laboured, irregular, and is arrested before the heart ceases to
beat. Death is due to respiratory failure, probably as a result of
paralysis of the higher centres, but consciousness is not lost.
In the horse there is nausea, gritting of the teeth, accelerated
respiration and dyspncea, muscular trembling, beginning first in
the posterior members, difficulty in walking, and paralysis; loss
of sensibility, low temperature, rapid pulse, and death by arrest
of respiration.
With the 0-1'; there is salivation, arrest of digestion, constipation,
and profound stupor; the respiration is rapid. In some instances
bloody evacuations have been noticed.
In sheep the ahdomen is tucked up, there is a dazed appearance,
dilatation of pupils, unsteady gait, the hind limbs being dragged,
coldness, and death after a few convulsive movements.
In the Pig there have been noticed prostration and inability
to move, coldness, slow breathing, livid mucous membranes,
eyes amaurotic, imperceptible pulse, paralysis, particulafly of
the posterior members, and no convulsions.
Coniine is eliminated by the urine and by the lungs, imparting
its peculiar odour to the exhaled air.
Post-Mortem Appearances.-As regards the alimentary tract,
23 0 VETERINARY. TOXICOLOGY
these are not characteristic, the poison not being an irritant,
but some congestion may be noticed: The organs are engorged,
blood black and tarry; the right heart filled, the left almost empty.
Treatment should consist in the evacuation of the stomach and
purgation; tannic acid, to remove the alkaloid; warmth and
stimulants-e.g., strychnine, atropine, and alcohol.
Chemical Diagnosis.-Coniine, being volatile, is separated by
steam distillation from the material made alkaline with sodium
carbonate. The distillate is neutralised with hydrochloric acid,
evaporated to dryness, and the residue extracted with alcohol;
the alcoholic extract is then filtered, evaporated t.o dryness, and
the residue shaken up with water; the water solution is then made
alkaline and extracted with ether. The ethereal solution is then
evaporated, leaving a mixture of the alkaloids; these may be
separated by fractional distillation. If much coniine is present,
oily drops may be seen in the distillate and a characteristic mouse-
like smell may be noticed, but this is generally masked by the
smell natural to the organic matter present.
Coniine gives no colour wjth sulphuric or nitric acids, but in
the presence of hydrochloric acid, dense white fumes are produced
with the formation of the hydrochloride, which may be obtained
in a crystalline form on evaporation. Bamford (1940) considers
the most reliable test for the alkaloid is to dissolve it in a little
benzene, and on the addition of I per cent. chloranil solution in
benzene, the solution becomes green, green crystals appearing
on evaporation. Confirmation bv means of biological tests should
be obtained. - .
Cicuta.
Botanical Characters.-Ciwta virosa (Fig. 29), cowban~ or
water hemlock. Stem hollow, somewhat branched, attaining 3 or
4 feet. Leaves twice or thrice pinnate or ternate, with narrow
lanceolate acute segments, I to I!- inches long, bordered with a
few unequal acute teeth. General umbels of from ten to fifteen
or even more rays. Bracts of the partial involucres subulate, not
quite so long as the pedicels. The habitat is in wet ditches and on
the edges of lakes, and it is very local in England, Ireland, and
southern Scotland.
The roots are hollow and septate in structure, from 2 to 4
inches long, and about It inches in diameter, and marked by
transverse scars of leaf bases. .
POISONOUS PLANTS 23 1
The Cicuta species are confined to the northern hemisphere. In
North America, C. mawlata, water hemlock or beaver poison, is
widely distributed; C. vagans has killed cattle in Oregon and

FIG. 2g.-CICUTA VIROSA (COWBANE).


(From Smith's "Veterinary Hygiene.")

Washington; C. bolaltderi is found in marshy land in California;


C. douglassii in British Columbia. All of these plants, together
with the other Ciwta species, are highly poisonous, particularly
the root.
VETERINARY TOXICOLOGY
Toxic Principle.-The root, and to a lesser extent the stems,
contain a yellowish acrid juice with a characteristic smell, from
which a resinous material may be extracted with ether. This has
been named cicutoxin, and is undoubtedly the active principle,
the fresh roots yielding 0'3 to 0'4 per cent. of this substance.
Jacobson (1915) suggested that cicutoxin has the empirical
formula C19H260a, and is a complex pyrone derivative. It resembles
picrotoxin in being a convulsant poison. .
Symptoms.-Cicuta species rank as being the most dangerous
of the Umbelliferre. Boehm (1896) found the minimal lethal dose
of cicutoxin per as for mammals was 50 to IIO mg. per kg. body
weight, and a piece of the fresh root the size of a walnut is con-
sidered to be fatal to horses and cattle.
The general symptoms of poisoning are uneasiness, salivation,
and abdominal pain; later champing of the jaws, frothing at the
mouth, and violent tonic and clonic convulsions occur. The pupils
are dilated, pulse slow, rapid shallow respirations, collapse, and
death from asphyxia. The poison acts on the higher nerve centres,
first stimulating and then paralysing them. .'
Cobbold (1877) noted a case in Brittany when eleven beasts
died with violent symptoms of vertigo, which set in within
two hours of eating, the first death occurring within six hours.
Addison (I9II) observed a case of poisoning of cattle by eating
the roots which had drifted to the side of a lake at Clones, in
Ireland. The animals were lying on their right sides, head extended,
and respiration very hurried. Froth had collected at the mouth
and nostrils, and there was tympanites, which greatly increased
shortly after death. The limbs were extended, and alternately
stiffened and relaxed. Some animals appeared to have died without
a struggle. The post-mortem revealed nothing; there was no
gastric irritation, and there were no extravasations of blood.
Chemical Diagnosis.-Cicutoxin gives ~ precipitate with _dilute
barium hydroxide, which becomes green on standing, changing
to reddish-brown on addition of excess of the reagent. If possible,
diagnosis should be confirmed by the discovery of parts of the
plant, especially the root, in the ingesta. Like many Umbelli-
ferre, the plant contains the substance umbelliferone. A water
extract of the plant shows a blue fluorescence due to this sub-
stance, but this does not definitely establish cicuta, merely
pointing to the presence of an umbelliferous plant.
POISONOUS PLANTS 233

mnanthe.
Botanical Characters.-(Enanthe crocata, or water dropwort
(Fig. 30).-A stout, branched species, attaining 3 to 5 feet; the
root-fibres forming thick, spindle-shaped tubers close to the stock;
the juice both of the stem and roots becoming yellow when
exposed to the air. Leaves twice or thrice pinnate; the segments
much larger than in the other species, always above t inch long,
broadly cuneate or rounded, and deeply cut into three or five
lobes. Umbels on long terminal peduncles, with fifteen to twenty
rays, 2 inches long or more; the bracts of the involucres small
and linear, several in the partial ones, few or none under the
general umbel. The pedicellate flowers at the circumference of
the partial umbels are mostly, but not always, barren, the central
fertile ones almost sessile. Fruit cylindrical, with long erect styles,
the ribs broad and scarcely prominent. The habitat is similar to
that of Cicuta virosa, and the plant is common in Great Britain.
The root of CEnanthe crocata has been the cause of several poison-
ings, as, f'or instance, of a gang of convicts at Woolwich in r835;
and, like the Cicuta, has an extremely rapid paralysant effect.
The active principle is probably a resinous substance, cenatho-
toxin, which resembles cicutoxin, It is also present in O. aqua-
tica and O. fistulosa. However, Tutin (r9IJ) does not consider
cenathotoxin to be a single chemical entity.
Symptoms.-According to Gillam (r906), symptoms of cenanthe
poisoning resemble those of hemlock poisoning, with the addition
of convulsions and green fcetid diarrhcea.
Cornevin (r893) gives the toxic quant~ties of the root for the
horse 0'1, the ox 0'125, the sheep O'Z, the pig 0'r5, the rabbit 2'0,
per cent. of the body weight.
The juice of CEnanthe has a powerfully irritant effect on the skin.
~n the ox there is foaming, distended nostrils, shivering, rapid
and laboured respiration, spasmodic contractions of the limbs;
the subject reels in a circle for several minutes, falls and dies.
Should death not occur, the paralysis persists. Hoare (r887) saw
cows poisoned by the roots left in a field after a flood, and observed
well-marked delirium, succeeded by rapid death.
\\lith the horse the onset of symptoms is rapid, the nervous
predominating; and with the Pig large doses fail to cause vomition,
and death occurs with the rapidity of cyanide poisoning.
Post-Mortem Appearances.--- In acute poisoning the thoracic
234 VETERINARY TOXICOLOGY
and abdominal viscera are normal, there is some congestion of
the nervous centres, the veins of the pia 1ttater distended, and

there are apoplectic foci. In more protracted/cases ecchylllosed


patches are found in the abdominal viscera.
POISONOUS PLANTS 235

Other Genera.
lEtlmsa cynapium, or fool's parsley, is not a dangerous plant
to animals. From confusion with edible parsley it has led to
poisoning of the human subject. It is said to contain coniine-like
alkaloids, which are also present in lEthusa jattta.
Chcerophyllum sylvestre, wild chervil or asses' parsley, is one of
the commonest British Umbelliferre. In spite of its odour and
acrid taste the ass eats it, and other animals also take the plant,
apparently without serious results, for it is a common food for
tame rabbits. According to a German observer quoted by Cornevin
(1893), pigs, having eaten the green plant, displayed paralysis,
dilatation of the pupils, refusal of food, and enteritis. The post-
mortem revealed acute gastro-intestinal inflammation.
Other species have been named by various authorities as
dangerous or objectionable; but further evidence being wanted,
it will suffice to name them here as suspected. They include:
Daucus carota, the wild carrot, which forms a bitter acrid root in
distinction to the cultivated carrot; H eracleum sphondylium, cow
parsnip or hog weed, which appears under certain conditions to
develop an irritant juice; Siu11t angustijolium, cow-cress or fool's
watercress;. and S. cicutcejolium, the hemlock water parsnip of
the United States.
REFERENCES.
CONIUM MACULA TUM.
Bamford, F. (1940), Poisons, their Isolation and Identification.
Buckingham, J. L. (1936), Vet. j., 92,3 01 .
Cornevin, C. (r893), Des Plantes Ventmeuses.
GIllam, W. G. (1906), Vet. Rec., 19, 88.
Macdonald, H. (1937), Vet. Rec., 49, IZII.

CrCUTA.
Addison, C. W. (19II), Vet. News, 83.
Boehm, R. (1876), Arch. Exp. Path. Pharm., 5, 279.
Cobbold (r877), Veterinarian, 24,572.
Jacobson, C. A. (1915), j. Amer. Chern. Soc., 37, 916.

CENANTHE.
Cornevin, C. (1893), Des Plantes Veneneuses.
Gillam, W. G. (r906), Vet. Rec., 19,88.
Hoare, E. W. (1887), Vet. ]., 23,301.
Tutin, F. (19II), Pharm. ]., 33,296.
CHlEROPHYLLUM.
Cornevin, C. (1893), Des Plantes Veneneuses.
VETERINARY TOXICOLOGY

ARALIACElE.
The only representative of this family found in Britain is
Hedera helix, the very common and well-known ivy. The berries
have been long known to be poisonous, having been mentioned
by Pliny, and cases of the poisoning of children by them have been
recorded. Over and above an emetic and purgative action, the
berries produce nervous effects like drunkenness, involving ex-
citement, then coma, laboured respiration, and thelike symptoms.
-Cases of the poisoning of animals are not on record. The leaves are
eaten by cattle without effect; indeed, are sometimes given to
,sick cows by country people as a dainty. Birds and small animals
might possibly be poisoned by the berries.

CAPRIFOLIACElE.
Belonging to this family are the elders, Sambucus nigra, the
common elder, and S. ebulus, the dwarf elder. The former is
common in hedges, attains R to 15 feet, has ovate leaves, white
flower, and black berries; whilst the latter is found on waste
ground, reaches 2 to 3 feet, has lanceolate leaves, pink flowers,
and black berries. All parts of these plants exhale a strong and
repulsive odour, and have been found to contain an emetic and
purgative oil, a resin, and traces of valerie acid. Animals do not
eat the plant spontaneously, and in the very rare cases of poison-
ing the symptoms and lesions ~re those of superpurgation.

VALERIANACElE.
Similar remarks to tp.<?se above made apply to Valeriana
officinalis, common valerian, cat's valerian, or all-heal, and
V. dioica, or marsh valerian, which contain an essential oil, or
mixture of oils, and valerie acid. It is most unlikely that sufficient
of these plants would be eaten by animals-to cause serious func-
tional disorder.
DIPSACElE.
A case of injury by Scabiosa succisa, or devil's-bit, has been
placed on record by Moir (r899). Bullocks and heifers which had
broken into a plantation 'and eaten the herb showed salivation,
champing, gritting of the teeth, and twitching of the facial
muscles. The tongue, whieh was slightly protruded, had an
POISOf'{OUS PLANTS 237
abraded patch about as large as a crown piece, about 3 inches
from the tip, and was very swollen and sensitive.
In a test experiment on cattle 'the plant was found to pro-
duce violent inflammation of the tongue and mouth.
REFERENCE.
Moir, J. (r899), Vet. Rec" 12,523.

COMPOSITlEo
The very large and widely-distributed order of ,Compositre
fortunately embraces comparatively few poisonous plants, but
in all parts of the world poisoning has been more or less definitely
attributed to some species.
In Europe the possibility of poisoning by Artemisia on account
of the volatile oil of absinthe has been noted (q.v.), whilst Lactuca
virosa, closely allied to L. scariola, the wild or prickly lettuce,
has a whitish latex of disagreeable odour. It is not eaten willingly
by animals, and no doubt large quantities would be required to
cause harm. Its effects recall those of opium, the general action
being one of narcosis.
In AIge'fia the roots of A tractylis gummifera are noted by
Cornevin (1893) as being sometimes eaten by stock in times of
scarcity, and to exert narcoto-irritant, conjoined to cardiac effects,
resembling those of colchicum.
In the United States H~lenium autumnale, sneeze-wort, stagger-
weed, or false sunflower, and H. hoopesii, western sneeze-weed or
yellow weed, are alleged to be poisonous to sheep, cattle, and
horses unfamiliar with the plants, but they are generally avoided
by stock. They cause salivation, vomition, diarrhrea, and a
copious nasal discharge. Actinea odorata, bitter rubber-weed, and
A. richardsoni are also poisonous, particularly to sheep, causing
abdominal pain and gastro-intestinal disturbance. Iri addition,
Solidago species, or golden rod, are thought to be poisonous, but
in this case the damage may be due to a parasitic growth on
.the plants. E1tpatorium urticcefolium, white snake-root, causes
trembles or milk sic;kness in animals and man. The characteristic
symptoms are muscular tremors, nausea, vomition, weakness, and
finally collapse. Marsh and Clawson (1917) showed that the active
principle was tremetol, a higher alcohol. This is readily excreted
VETERINARY TOXICOLOGY
in the milk, so that milk from affected animals is unwholesome to
drink.
In South Africa numerous members of the Compositre are re-
sponsible for causing poisoning;the more important of them being
as follows: Dim,orphotheca species, particularly D. spectabilis and
D. cuneata, which contain the cyanogenetic glycoside linamarin,
so giving rise to symptoms of hydrocyanic acid poisoning;
Geigeria species, the most toxic of which is G. aspera. These plants
produce the condition known as vermeersiekte, outbreaks
of which occur chiefly in sheep and goats; the characteristic
symptoms are continual vomition and diarrhcea, followed by
paralysis and death from exhaustion. Rimington and Roets
(1936) found that G. aspera contained vermeeric acid, ClsH240S,
and consider it to be the active principle, since 10 to 15 g. of the
substance caused typical symptoms of the disease and death
owhen given to a sheep by the mouth. Chrysocoma tenuijolia has
been shown 'by Steyn (1931) to be the cause of severe gastro-
intestinal disturbance, dermatitis, and alopecia, particularly in
lambs and kids. Matricaria species, particularly M. 1tigellifolia,
cause staggers or pushing disease in cattle. This condition was
studied by Andrews (1923), who found that the active principle
is probably a volatile oil; the characteristic symptom of poison-
ing is for the animal to press the head against some solid object;
illness lasts several weeks and trea tmen t is of Ii ttle a vail.

Senecio.
Senecio species are widely distributed throughout the world
and form by far the largest genus of the Compositre, over 1,000
species having been 'identIfied. All the members of this group,
usually called ragworts or groundsels, are suspected of possessing
poisonous properties, and a large number are definitely known
to be toxic. Some of the more common senecios are S. jacobClJa
and S. vulgaris in Europe; S. jacobClJa, S. ridellit, and S. longilobtts
in North America; and S. burchellii, S. retl'orsus, S. ilicijolius,
and S. isatideus in South Africa.
In Great Britain and Ireland S. jacobClJa is responsible for
causing losses amongst cattle and horses;sheep are said to ingest
the plant without suffering harm, but this would appear to be
very doubtful, and in any case animals avoid the plant if at all
possible. S. jacobClJa is also responsible for causing Pictou disease
POISONOUS PLANTS 239
in Eastern Canada and Winton disease in New Zealand; in South
Africa, Molteno straining disease is caused by the ingestion of
S. bttrcllellii or S. retrorus, and S. ilicifolius is the cause of bread
poisoning. S. sceleratus is considered to be the most toxic of the
South African senecio species.
Active Principles.-Senecio species have received considerable
attention from the chemical point of view, and it has been estab-
lished that they contain a number of toxic alkaloids. The plants
were first examined bv Grandval and Lajoux (r895). who isolated
senecionine, ClsH2505N, from S. vulgare; Watt (r909) isolated
senecifoline, ClsH270sN, from S. retl'ors1ts, called by him S. lati-
folius, and Manske (r93r) isolated retrorsine, ~lsH250sN, from
S. rety01's'Us and jacobine', ClsH250sN, from S. jacobcea. More
recently de \\Taal (r94r), in a series of studies, has found ros-
marine, C1sH 2P sN, to be present in S. iticifolius, and lists eighteen
alkaloids which have beep isolated from Senecio species up to
the present time. The toxicology of these alkaloids has received
little attention, but from the observations of Cushny (I9II) it
is probable that their chief effect is to cause petechial hremor-
rhages in the internal organs, particularly in the liver, which
would account for the characteristic liver cirrhosis seen in chronic
cases of poisoning.
ToxIc Doses.-Senecio species are poisonous when fresh as well
as when dried and made into hay; they are probably least toxic
when young. There is also every indication that the flowering
and seeding heads are also poisonous, since the seeds of S. ilici-
folius, which infests South African wheat fields, may pass into
the flour and so give rise to typical chronic senecio poisoning,
known as bread poisoning, in human beings.
The onset of poisoning is usually slow, and animals may con-
sume the plant for weeks or even months before they become
affected; indeed, symptoms of poisoning may not appear until
some weeks after the plant has been withdrawn from the diet.
It is difficult, therefore, to determine the toxic dose under natural
conditions, but experimentally Chase (r904) found that in cattle
8 ounces of S. burchellii daily for four days caused death on the
fifth day; 8 to 10 pounds of S. retroS1ts given daily in 2 to 6 ounce
doses caused death in about six weeks; and in horses, 2 ounces
daily of S. burchellii for thirteen days caused death in sixty-six
days.
Symptoms.-In acute poisoning there is dulness, accelerated
VETERINARY TOXICOLOGY
pulse, rapid respirations, weakness, colic, jaundice, and death
in a few days to several weeks. Cases of poisoning are, however,
usually chronic. In this case the general symptoms are loss of
cond,ition, inappetence, dulness, staggering gait, constipation or
sometimes diarrhrea, pallid mucous membranes; later more
violent symptoms suggesting involvement of the central nervous
system may appear, followed by death after a long illness, most
probably from complete cessat~on of liver function.
Chase (1904) observed in cattle persistent diarrhrea, reduced
lactation, dry, staring coat, no desire for food, and straining
movements, which increased in frequency and force so that in
some cases there was eversion of the rectum. From the onset of
straining the animals showed great pain, sometimes lying down
with head outstretched and groaning, or sometimes standing and
becoming frenzied; finally, there was loss of consciousness and
death. Thompson (1918) records that a peifer turned on to pasture
infested with S. jacobCBa which had been mown but left on the
ground became affected after about a month; the animal became
dull, lost condition, and was markedly jaundiced. Craig, Kearney,
and Timoney (1910), who made a comprehensive study of S.
jacobCBa poisoning in cattle and horses, found the chief symptoms
of poisoning to be loss of condition, inappetence, constipation,
but in some cases diarrhrea, blindness, nervous excitement,
dilated pupils, staggering gait, rapid pulse, intermittent straining,
insensibility to pain, but normal respirations and temperature;
salivation, champing of the jaws, and gritting of the teeth were
also noted in some cases; finally, collapse and death in from two
to ten days after the appearance of definite symptoms.
Post-Mortem Appearances.-In acute cases the liver is enlarged
and congested and may have a nutmeg appearance, hyperremia
with petechial hremorrhages may be observed in the internal
organs and serous membranes, and there may be evidence of
gastro-enteritis with petechial hremorrhages and, in ruminants,
redema of the abomasum, but the lesions may not be very
characteristic.
In chronic cases the most prominent lesion is a well-marked
cirrhosis of the liver, which is tough, leathery, and has an adherent
capsule; the central vein is engorged with blood, and the hepatic
cells show degeneration; a marked increase of fibrous tissue
extending into the lobules and proliferation of the bile ducts is
also ,present. Theiler (1918) o,bserved in some cases a round-cell
POISONOUS PLANTS 24 I
infiltration of varying intensity, and concludes that the liver
lesions in senecio poisoning may be regarded as those of a paren-
chymatous hepatitis. The abdominal cavity is dropsical, and the
lungs may show redema; petechial hremorrhages are present in
the small intestine, heart, and serous membranes, and the kidney
has a mottled appearance due to venous congestion and may show
signs of fatty degeneration. The alimentary tract shows evidence
of a patchy gastro-enteritis, and in horses the stomach may be
greatly distended.
Treatment.-Once symptoms of poisoning have fully devel-
oped, treatment is of little avail. A purgative followed by strych-
nine and arsenic tonics and the administration of glucose may be
of some benefit.
Diagnosis of poisoning must depend on circumstantial evidence.
REFERENCES.

ATRACTYLIS GUMMIFERA.
Cornevin, C. (1893), Des Plantes Veneneuses.
EUPATORIUM.
Marsh, C. D., and Clawson, A. B. (1917), J. Agric. Res., 9,699.
GEIGERIA.
Rimington, C., and Roets, G. C. (1936), Ondersterpoort J. Vet. Sci., 7,4 85.
CHRYSOCOMA.
Steyn, G. D. (1931), 17th Rept. Dir. Vet. Servo and Anim .. Indust. S.
Africa, 729.
MATRICARIA.
Andrews, W. H. (1923), 9th and loth Repts. Dir. Vet. Servo and Anim.
Indust. S. 4frica, 123.
SENECIO.
Chase, W. H. (1904), Vet. Rec., 17,425. .
Craig J. F., Kearney, W., and Timoney, J. F. (1930), Vet. Rec., 10,159.
Cushny, A. R. (19II), Proc. Roy. Soc., Ser. B, 84, 188.
Grandval, A., and Lajoux, H. (1895), Camp. Rend., 120, II20.
Manske, R. H. F. (1931), Canad. J. Res., 5,651.
Theiler, A. (1918), 5th and 6th Repts. Dir. Vet. Res. S. Africa, 9.
Thompson, H. (1918), Vet ..Rec., 31, 105.
de Waal, H. L. (1941), Ondersterpoort J. Vet. Sci., 16, 149.
Watt, H. E. (1909), J. Chem. Soc., 95,466.

CAMPANULACElE.
Lobelia urens, or acrid lobelia, is the only poisonous species of
this family found wild in Britain, and is very rare, being found
on moist heaths in Dorset and Cornwall.
16
VETERINARY TOXICOLOGY
The genus Bobelia is widely diffused, though scarce, in the greater
part of Europe, and is found in America and Australasia. Of
American lobelias, L. injlata (Indian tQbacco), kalmii, spicata, and
syphilitica are regarded as suspicious. and are sometimes found
in meadow hay.
Active Principle.-The lobe lias contain several closely related
alkaloids, the most important being lobeline, C22H2702N, which
resembles nicotine and coniine in its action, causing paralysis,
preceded by stimulation of autonomic ganglia. Lobeline also
acts as a direct respiratory stimulant and is used for this purpose
in cases of poisoning by narcotics.
Symptoms.-Fleming (r873) observed that in Australia cattle
which had eaten plentifully of the plant showed lassitude, and on
being driven hard or suddenly startled dropped in convulsions,
death following in a few minutes. J;ornevin (r893) considers the
plant acts as an irritant.
Chemical Diagnosis.-The mixed alkaloids form a liquid which
gives a red colour in the presence of concentrated sulphuric acid,
but pure lobeline is said not to do so. Lobeline gives a reddish-
violet colour with Marquis' reagent and a brown colour changing
to green with sulphomolybdic acid.
REFERENCES.
Cornevin, C. (1893), Des Plantes Veneneuses.
Fleming, G. (1873), Veterinarian, 4.6,451.

ERICACElE.
The members of this or(leJ' are widely distributed throughout
the world, particularly in India, China, Japan,.and North America;
in Europe they are found mainly as exotic shrubs, such as
Rhododendron, Azalea, Kalmia,_, etc., which a!e extensively cul-
tivated for ornamental purposes.
The toxicity of the many rhododendron species, such as R. pon-
ticum, R. ferrugineum, R. calt/ornicum, R. maximum, etc., has
been recognised for many years, and numerous cases of poisoning
in domestic animals are on record; similarly the toxicity of Kalmia
species is well established. K.lati/olia, or poison laurel, is regarded
as being the most poisonous of the Ericacere. and K. ang"ltsti/olia,
or lambkiJI, and K. polt/olia, or Alpine laurel, are also responsible
for killing large numbers of cattle and sheep annually, as well as
POISONOUS PLANTS 243
goats and horses, as recorded by Clawson (r933) and others.
Cases of poisoning by Azalea species are not numerous, but the
Californian azalea, A. occidentalia,' is responsible for poisoning
many sheep in the Southern Sierras. Since azaleas are commonly
grown as ornamental shrubs, caution must be exercised in regard
to the disposal of clippings from the plants. Amongst the other
members of this order, Andromeda floribunda, Ledum species
(e.g., L. palustre and L. glandttlosum) and Leucothce species (e.g.,
L. catesbcei, the branch ivy or calfkill of the Alleghany mountains)
are all known to be poisonous.
Active Principles.-Plugge (r884) -isolated a neutral principle,
andromedotoxin, C19H320S' from A. floribunda, which produces
typical symptoms of poisoning and appears to be the active
principle present in all the Ericacere so far examined. In addition
to andromedotoxin, Archangelski (I90r) found rhododendrin,
ClsH2207, and ericolin., C34H56021, in the leaves of Rhododendron
chrysantlzum, but the constitution of these and other substances
said to be present is uncertain, and there is little doubt that
andromedotoxin is the chief toxic agent.
Symptoms.-Symptoms of poisoning following the ingestion of
any member of the Ericacere are essentially the same and are
characterised by salivation, vomiting, abdominal pain, depression
of respiration, weakness,' staggering gait, collapse, and death
after several days' il,lness. Hardikar (I922) examined the physio-
logical action of andromeo{)toxin and found its chief effect is to
paralyse motor nerve endings, particularly the phrenics; it also
has a direct action on striated muscle, causes stimulation followed
by paralysis of vagal nerve endings, and injury to the conducting
tissue of the heart. Although andromedotoxin is non-irritant, the
vomition constantly seen in cases of poisoning is probably due
to a direct action of the poison on the vagal nerve endings in the
stomach and is not due to a central effect; death is due to respira-
tory failure.
Typical cases of rhododendron poisoning in cattle' have been
recorded by Golledge (r900), Hoare (r906), Eve (r907), and
others, which serves to emphasise the generality of actual
vomition in cases of poisoning. In sheep, Slipper (I906) and
others record typical symptoms, hut vomition does not seem to
. be so general as with cattle; in the horse Phipps (I9I4) records
copious salivation, incessant attempts at vomition, slate-coloured
mucous membranes, rapid respiration, coldness of the extremities,
244 VHTERINARY TOXICOLOG}'
and cold patchy sweating, weak pulse, but recovery. Waud (1940)
found K. ang1/stijolia causes salivation, nausea, vomition, drowsi-
ness, dyspnrea, tremors, convulsions', and death.
Post-Mortem Appearances.-These are not well marked. The
mucous membrane of the rumen may be easily detachable, but
there is no marked evidence of inflammation. Leaves of the plant
eaten may be recognised in the stomach contents.
Treatment.-Most of the recorded cases of rhododendron
poisoning recovered nnder treatment by means' of oleaginous
purgatives, followed by chlorodyne, general stimulants, and
tonics such as ammonium carbonate and spirits of nitrous ether.
Hoare (1906) treated a young cow with brandy, chIoI-odyne,
spirits of nitrous ether, linseed oil, and opiates, with recovery on
the fifth day. '
Chemical Diagnosis.-The history of the case and the detection
of l~aves of the plant in the vomitus or stomach contents is
sufficient to make a certain diagnosis. Hardikar (1922) was unable
to detect andromedotoxin in the freces of experimentally poisoned
animals, but it may be recovered from the urine on extraction
with chloroform. The pure substance has a melting point of 228 0
to 229 0 C. and gives a'red colonr on warming with dilute sulphuric,
hycirochloric, or orthophosphoric acids.
REFERENCES.
Archangelski (1901), Arch. Exp. Path., 46, 313.
Clawson, A. B. (1930), U.S. Dept. Agric. Tech. Bull., 391.
Eve, H. B. (1907), Vet. Rec., 20,4.
Golledge, C. H. (1900), Vet. Rer:., 13,326.
Hardikar, S. W. (1922), ]. Pharm. and Exp. Therap., 20, 17.
Hoare, E. W. (1906), Vet. Rec., 19, 630.
Phipps, E. (1914) ... Vet. News, 66.
Plugge, P. C. (1883), Arch. Pharm., 221, 813.
Slipper, T. (1906), Vet. j., 62,439.
Waud, R. A. (1940), ]. Pharmacal., 69,103.

OLEACElE.
This family is represented in Britain only by Fraxinus, the ash,
d Ligustrum vulgare, the privet, which' has been introduced
from America. The common privet has been observed to cause
poisoning by Turner (1904) and is said to cOritain a glycoside,
ligustrin, C17H2209' which has not r~ceived very close study.
Turner's observations were made . . on horses put into a field
with an un clipped privet hedge.
POISONOUS PLANTS 245
The symptoms observed were loss of power in hind quarters,
pulse 50, temp~rature IOZo F., mucous membranes slightly
injected, and pupils dilated. Death occurred within from' thirty-
six to forty-eigh~ hburs. .
REFERENCE.
Turner, A. (1904), Vet. Rec., 17, 319.

PRIMULACElE.
This family includes Cyclamen europceu11l, the common cyclamen
or sow-bread, and AnagalUs arvensis, the common pimpernel or
shepherd's weather-glass.
Cyclamen is not an indigenous plant, but has established itself
locally in Kent and Sussex from garden culture. The pimpernel
is a common weed of cultivation, and of cornfields, gardens, and
waste places.
Cyclamen contains in the roots the glycoside cyclamin, and
pimpernel contains the glycoside smilacin, both of which are
varieties of saponin.
The effects are thus similar to those of other saponin-containing
plants, and reference may therefore be made to these (see Caryo-
phyllacece) .
. As regards pimpernel, the plant is too small to make it likely
that a large animal could eat enough to cause harm, but extracts
have been proved to be poisonous to the horse.

APOCYNACElE.
This family is mainly tropical, and the common and harJ?1less
Vznca, or periwinkle, is the only representative in Britain. But
many plants of this order are notable causes of poisoning through-
out the tropics. As regards the active principles, the species
involved all contain glycosides, which are classed by Cushny
(1941) in the digitalis series.
The genus Apocynum is represented by A. androscemifolium,
found in Central Europe, Asia, and America, and A. cannabinlt11t,
or Canadian hemp, used in America as a fish poison. The acrid
juices, which contain the glycoside apocynin, C9H lO0 5 , examined
by Dunstan and Henry (1898), provoke vomiting and diarrhcea,
and, if in quantity, fatal superpurgation.
VETERINARY TOXICOLOGY
Strophanthus hisPidus, or Kombe, is the 'West African arrow
poison. This plant yields several closely related cardiac glycosides
which are derived from the aglucone strophanthidin, C23H 320 6 ;
this substance in the presence of a sugar, cymarose, forms the
glycoside cymarin, CaoH4409' which is probably the chief glycoside
present in the amorphous strophanthin-k used in medicine. In the
same way S. graitts yields the crystalline glycoside ouabin or
strophanthin-g, C29H44012' which is used for the assay vf digitalis
preparations. The South African Acoca1~thera species also contain
cardiac glycosides closely related, if not identical, to strophan-
thin-g, which is also found in Acocanthera ouabis. The Madagascar
Tanghinia venenijera also belongs to this family.
Poisoning of animals by these plants is not frequently encoun-
tered, but Curs on (r928) studied the effects of South African
Acocanthera species and showed A. veneJtata to be poisonous to
cattle, goats, and donkeys.
Oleander species are well known to be poisonous and are very
important in tropical toxicology. Nerium oleander is a commonly
cultivated evergreen plant in Europe, in the Southern and
Western United States, and in South Africa; it is grown as a
garden and hedge plant. It grows wild in Mexico and is a native
of Asia. In India, the most toxic oleanders are Nerizt11t odorum,
the sweet-scented oleander with white or pink flowers called
Kaner in the vernacular; Cerbera thevetia, the yellow oleander
called Karabi; and C. odallum, which is closely related to them.
Active Principles.-These are glycosides allied to digitoxin.
From N. odoYUnt there have been separated the water-soluble
glycosides neriodorein and neriodorin and the alcohol-soluble
karabin, C21H490S. The chief action of these glycosides is to cause
stimulation of the vagus, followed by paralysis; karabin is also
said to exercise a strychnine-like effect on the spinal cQrd.
Thevetin, C72H1240 as' obtained from C. thevetia, has a digitalis-
like action and also causes convulsions. The active principles are
distributed throughout the plants, particularly in the seeds.
The toxic dose is not large, a single growing top of oleander
having been said to be fatal to cattle and horses, whilst men have
been fatally poisoned by eating meat cooked on skewers of the
wood. Three seeds of C. thevetia would probably kill a man, since
two have ca'used dangerous symptoms. /"
Symptoms.-In the experimental poisoning of animals Cornevin
(r893) distinguished, a phase of stupOl:, succeeded by convulsions,
POISONOUS PLANTS 247
insensibility, and then paralysis. Vomiting occurs when possible,
and the retching continues after the stomach is empty.
Two cases of oleander poisoning in horses were reported by
Leicht (I9i4). In one case the symptoms first noted were loss of

FIG. 31.-NERIUM OLEANDER.

appetite, cerebral depression, and violent diarrhcea, respirations


frequent and deep, pulse uneven and irregular, later becoming
almost imperceptible. There was violent trembling, and frequent
straining to defrecate and urinate. Temperature was I04So F.,
VETERiNARY TOXICOLOGY
respirations very frequent, lively peristalsis, moderate tympany,
and the mucous membranes of the head were bright red. Death
resulted in forty-eight hours.
In the other case the horse was down, lying on his right side,
groaning, and with strong and audible heart-beat. The nostrils
were elevated, eyes watering, and there Was foam on the lips.
From time to time the animal drew his legs spasmodically up to
his belly and groaned louder with pain. After rape oil and digestive
powders there was recovery within two days.
The effects of N. odorum were studied in India, and noted by
"Snipe" (I887). He gave a horse 2 ounces of the leaves night and
morning for three days, and they were readily taken with food.
He observed full abdominal pain, anorexia, yellowness and
injection of the conjunctivre, no' narcosis, and temperature
normal.
The lesions were chiefly intense congestion of the small intes-
tines, particularly of the duodenum and jejunum. The ca'cum and
colon were similarly affected; contents liquid and sanguinaceous.
There was patchy congestion of the stomach, especially at the
cardiac end. The brain and spinal cord were normal.
There is no specific antidote for oleander poisoning, so that
treatment must be symptomatic. A purgative, followed by
stimulants, such as alcohol, caffeine, etc., or sedatives if con-
vulsions occur, are indicated; salicylic acid has also been re-
commended.
N. odorum glycosides give a brownish colour with sulphuric
acid, and thevetin a blue colour on boiling with dilute hydro-
chloric acid, but the chemical detection of the glycosides is
uncertain.
REFERENCES.
Curson, H. H. (1928), 13th and 14th Repts. Dir. Vet. Educ. and Res. S.
Africa, 203.
Cushny, A . .R. (1941), Pharmacology and Therapel.!tics, 12th ed.
Dunstan, W. R, and Henry, T. A. (1898), J. Chern. Soc., 75,66.

OLEANDER.

Cornevin, C. (1893), Des Plantes Veneneuses.


Leicht (1914), Vet. Rec., 26, 800.
Snipe (1887), Quart. J. Vet. Sci. India, 50.
POISONOUS PLANTS 249

ASCLEPIADACEJE.
The order Asclepiadacere, pr milkweed family, includes plants
which have an abundance of a milky, acrid, poisonous sap, and
comprise Asclepias syrica, cultivated in Europe, but native to
America, where it is known in the North-Eastern States as milk-
w~ed; A. tuberosa is the Eastern United States "pleurisy rl)ot";
A. mexicana and A. eriocarpa are milkweeds of California, Oregon,
and Nevada; ann A. galioides is the whorled milkweed of Mexico,
Texas, and Arizona, from which Marsh, Clawson, Couch, and
Eggleston (1920) were able to isolate an alcohol-soluble resin,
which is probably the activE' principle.
In Europe Vincetoxicum officinale and Cynanchum acutum
belong to the same order and are toxic; and in South' Africa
C..vnanchum capense and C. africanum cause the disease known as
krempziekte or cramp sickn~ss.
All these plants act as drastic purgatives; poisoning is more
common in sheep, though horses and cattle may also be affected.
In cases of poisoning, the affected animals tend to lag behind
and stagger in their gait. They may fall and lie quiet, then rise
and continue to feed. Convulsions are characteristic. The head
is pushed down between the forefeet and then jerked upwards
and backwards, or from side to side. The convulsions may occur
at regular intervals or very frequently, leading to great exhaustion
and a partially paralysed condition, from which there may be
recovery.
The poisoning is treated by means of aperient (Epsom salts), and
sedatives, such as chloral hydrate or potassium bromide, which is
given to the ox in doses of I ounce thrice daily, and to sheep or
goats in doses of I to 2 drachms. Distension in the case of cattle
may be relieved by the trocar.
REFERENCE.
Marsh, C. D., Clawson, A. B., Couch, J. F., and Eggleston, W. W. (1920),
U.S. Dept. Agric. Bull., 800.

CONVOLVULACEJE.
Convolvulus.
The genus C on1'olvulus includes C. scam'l1lonia and C . .ialapa.
which contain the glycosides convolvulin and jalapin respectively.
These substance$ belong to the group of drastic purgatives. The
VETERINARY TOXICOLOGY
British species of Convolvuli, or bind-weeds, do not appear to
have been definitely proved to contain these glycosides, though
it is possible that they do so.
Symptoms.--Convolvulin acts as a local purgative, but in large
doses, when it encounters insufflGient bile.it causes an astringent
effect. The convolvulus, bind-weed or laplove, is dangerous to
pigs. A good example of its effects was recorded by Olver (1872).
The animals had eaten profusely of convolvulus, and displayed
lqss of appetite and attempts to vomit. Before death the head
hung down, and the animals had a sleepy appearance.
On post-mortem there was found serous effusion in the abdo-
minal cavity, and the intestines were empty, save for a little
fluid and gas. The stomach was full of green food containing con-
volvulus. There were a few petechial patches on the villous
membrane of the stomach; the other viscera were healthy, but
the brain was highly congested.
Cuscuta.
The genus Cuscuta includes C. europcea, the greater dodder,
whi~h has been held responsible for poisoning.
Botanical Characters.-The dodder is a greenish-yellow, tending
to red, leafless, parasitic herb. The flowers form clusters, are small,
sessile, and have broad and rounded sepals. It is not very common
in England, and is confined to the South. A variety, C. trifolii,
is found in clover-fields.
Symptoms.--Dodder is stated to cause enteritis, and to evolve
also nervous symptoms in Pigs.
Holterbach (I908) observed illness of COUIS caused by a clover
containing 50 per cent. of the C. trifolii. He noted trembling move-
ments of the hind quarters and swelling over the hock-joints.
The back was arched, head outstretched, anxious appearance,
and quick breathing. -There was violent shaking, in which the
hind feet alternately took part, increasing until the animal was
in a frenzy. The attack declined, leaving. the patient exhausted
and covered with sweat. Other attacks followed" but all the animals
recovered quickly, and remained healthy.
REFERENCES.
CONVOLVULUS.
Olver, H. (1872), Veterinarian, 45, 727.
CUSCUTA.
Holterbach (1908), Vet. j., 17,632.
POISONOUS PLANTS 25 I

SOLANACElE.
This order is widely distributed throughout the world and
includes some common and most dangerous poisonous plants.
The genera to which these belong include Atropa, Hyoscyamtts,
Datura, Solanum, and Nicotiana species, and to these may be
added Cestmm species native to South America and South
Africa.
Active Principles.-Before proceeding to details regarding e;J.ch
species, it will be convenient to describe the active principles
of the plants involved, since, from this point of view, they may be
divided into three groups: (I) the atropine group; (2) the solanine
group; and (3) the nicotine group.
(r) The atropine group comprises the genera Atropa, Hyo-
scyamus, Datura, and Cestrmn, the species most commonly
encountered being Atropa belladonna, HyoscyamtJs niger, Datura
stramonium, D. metel, D. tatula, and D. meteloides. The chief
alkaloids present in these plants are atropine, C17H230aN; apo-
atropine and its isomer belladonnine. C17H2102N; hyoscyamine,
C17H210sN; hyoscine, also known as scopolamine, C17H2104N;'
and to these may be added meteloidine, ClsH2104N, from D. mete-
loides, and parguine, C21 H 3P sN, from the South American
Cestrum parqtd. The active principle present in C. lcevigatu11t, the
inkberry bush of South Africa, has not yet been determined.
(2) The solanine group comprises the genus Solanmn and the
species S. dulcamara, S. nigrul1i, and the South African S. incanum,
found wild, in addition to the numerous cultivated species, such
as S. tuberosum (potato), S. lycopersicum (tomato), and S. melon-
gena (egg-plant). These contain the glycosidal alkaloid solanine,
C52H9301SN, which is allied to the sapouins and which, on hydro-
lysis, yields sugars and the alkaloid solanidine, C27 H 430N. Like
the saponins, solanine is colloidal and is not easily absorbed
through the intact alimentary mucosa, but the alkaloid solanidine
is readily absorbed.
(3) The nicotine group comprise the genus Nicotiana, most
commonly represented by the species N. tabacum, the tobacco
plant cultivated for smoking, for the extraction of nicotine, and
for ornamental purposes, and N. glauc(l, the wild tobacco plant.
These contain the volatile alkaloid nicotine, C10H 14N 2 , allied
chemically and physiologically to coniine.
VETERINARY TOXICOLOGY

Atropa.
Botanical Characters.-Atropa belladonna (Fig. 32), deadly
nightshade or black cherry, reaches about 3 feet, has an herbaceous
stem, ovate leaves, soli~ary dark purple flowers, and black berries.
It frequents waste, stony places in chalky districts, the vicinity
of old castles and ruins, and is rather local in the South of England,
rare in the North, but common in the South of Europe.
All parts, especially the roots, contain mainly atropine (about
06 per cent.), with variable proportions of the allied alkaloids.
Atropine usually forms a larger proportion in the old than in the
young plants.
Toxic Doses.-Poisoning by the plant is rare, in part by reason
Qf its scarcity. Cats, dogs, and birds are sensitive, the horse and
ox less so, whilst the pig, goat, sheep, and rabbit are comparatively
resistant. This is probably due to the rapid elimination of atropine
by the kidneys, for when given intravenously the alkaloid causes
typical symptoms.
According to Cornevin (I893), 2 pounds of the green herb daily
for three days produced no pathological disturbances in horses.
Hertwig states 6 ounces of the dried 'root to be a fatal dose for
the horse, and that cattle are equally susceptible.
Dangerous symptoms result in dogs from the administration
of 30 to 50 grains of the dry 'plant, and ~ grain J;lypodermically
kills dogs of from IS to I6 pounds weight.
Symptoms.--Atropine exercises both a central and peripheral
action, causing stimulation of the central nervous system, fol-
lowed by depression as well as paralysis of the cholinergi,c nerve
endings of the autonomic nervous system. When taken_ in toxic
amounts the chief symptoms are qryness of the mouth, owing to
the general inhibition of secretions, increased pulse and respira-
tion frequencies, and elevation of temperature. There is dilata-
tion of the pupil, with blindne~s, restlessness, nervousness,
delirium, and muscular trembling. After-this period of excite-
ment there ensues fall of temperature, convulsions, motor and
sensory paralysis, with staggering movements, feeble and slow
respiration, relaxation of the sphincters, and death in con-
vulsions.
In dogs the pulse-rate may be as high as 400; in horses it may be
about doubled.
Livesey (I904) recorded typical symptoms, excepting that there
POISONOUS PLANTS 253
was no mydriasis, in a fox-terrier bitch, which had licked herself
after rubbing with belladonna liniment.
The post-mortem appearances are not characteristic, being
those of asphyxia.

FIG. 32.-ATROPA BELLADONNA (DEADLY NIGHTSHADE).


(From Smith's "Veterinary Hygiene.")

Treatment.-The treatment of poisoning consists in elimination


by emetics or purgatives, and treatment of the symptoms. Seda-
tives may be desirable in the early stages of excitement, but it
must be remembered that toxic doses of atropine cause depressant
254 VETERINARY TOXICOLOGY
effects. Stupor is combated by movement, and stimulants, such
as alcohol, ammonia, or caffeine. The cautious usc of the physio-
logical antidotes, eserine against mydriasis and pilocarpine
against the drying up of secretions, is advisable.
Chemical Diagnosis.-Atropine and the allied alkaloids are
separated in the search for vegetable poisons in cases of poisoning
by any of the plants of this group. A very valuable test is an
observation of the mydriatic effect on the eye of a cat. A good
chemical test is Vitali's. The residue of alkaloid is heated on the
steam bath to dryness, with a few drops of concentrated nitric
acid. On moistening the yellow residue with alcoholic potash,
atropine and its allies give a red-violet colour. The test is ex-
ceedingly delicate.
Hyoscyamus.
Botanical Characters.-Hyoscyamtts niger (Fig. 33), or black
henbane, is a coarse, erect, branching annual, 1 to 2 feet high,
more or less hairy and viscid, with a nauseous smell. Leaves
rather large, sessile, the upper ones clasping the stem, ovate,
and irregularly pinnatifid. Flowers very shortly stalked, the lower
ones in the forks of the branches, the upper ones sessile, in one-
sided leafy cymes, rolled back at the top before flowering. Calyx
short when in flower, but persists round the fruit, and then an
inch long, strongly veined, with five stiff, broad, almost prickly
lobes. Corolla above an inch long, pale, dingy yellow, with purplish
veins. Capsu}e opening transversely, with numerous small seeds.
The henbane is somewhat rare, and of similar habitat to that
of the deadly nightshade. In the United States it occurs as a weed
of European origin. The West African H. Jalezlez, according to
Cornevin (1893), is eminently poisonous.
Symptoms.-Henbane_ poisoning is infrequent, but the plant
is sometimes cultivated for medicinal use, and Welsby (1903) has
placed upon record a case in which anjmals were poisoned in a
field thus cultivated several years previo,}sly.
There were observed 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 the neck and extremities in a state of
tetanic rigidity, considerable abdominal distension, stercoraceous
and renal emunctories entirely suspended, death.
Creuzel (1840) observed henbane symptoms in a cow two hours
POISONOUS PLANTS 255
after eating the plant. The pupils were dilated, conjunctivre
injected, carotids beat violently. The animal attempted to rise,
but fell again. There were general convulsions, loud respiration,
salivation, and purgation.

FIG. 33.-HYQSCYAMUS NIGER (BLACK HENBANE).

(From Smith's "Veterinary Hygiene.")

Black henbane contains chiefly the two alkaloids, hyoscyamine


and hyoscine (scopolamine). Hyoscyamine closely resembles
atropine in its physiological effects, the mydriasis being less
permanent and the depressant effects greater, whilst hyoscine is
VETERINARY TOXICOLOGY
an extremely powerful depressant and hypnotic drug. As regards
poisoning by henbane, it is ~nteresting to remark that profuse
salivation takes the place of the great dryness due to atropine.
Chemical Diagnosis.-Hyoscyamine and hyoscine give the same
reactions as atropine, but these' alkaloids may be distinguished
by means <;>f Gerrard's test. This is carried out by adding a few
drops of Z. per cent. solution of mercuric chloride in 50 per' cent.
alcohol to the suspected alkaloid. Atropine gives a red colour
immediately; hyoscyamine gives a yellow colour which turns red
on warming; and hyoscine gives no distinctive coloration.

Datura.
Botanical Characters.--Datura stramoniltnt (Fig. 34), or thorn-
apple, is sometimes encountered in Southern England, being a
plant originally of South American origin, now fairly widely
diffused over Southern Europe.
It is a coarse, glabrous, or slightly downy annual, 1 to 2 feet
high, with spreading, forked branches; leaves rather large, ovate,
with irregular, angular, or pointed teeth or lobes. Flowers solitary,
on short peduncles, in the forks, or at the ends of the branches.
Calyx loosely tubular, about Ii inches long, and falls off after
flowering, leaving a small rim under the capsule. Corolla about
3 inches long, bordered with five narrow, distant teeth, usually
white, but occasionally (especially in hot countries) purple.
Capsule nearly globular, very prickly, with numerous wrinkled
seeds .. In the United States it is a common weed known as
"JimsQn" weed, and in South Africa it is called the "stinkblaar."
Symptoms.-A case of thorn-apple poisoning is on record by
Sullivan (1905). A horse which had eaten datura bush was down
and unable to rise, pupil dilated, mouth partly open, tongue
peculiarly dry, pulse quick and full, and visible mucous mem-
branes slightly congested. _
Sinclair (1898) mentions the death of ostrich chicks, whose
stomachs were found to contain the th~rn-apple seeds. Ostrich
poisoning by datura seeds is marked by staggering gait and
spasmodic jerking of the neck, with unnatural contortions.
Stupor and coma precede death.
In Sullivan's case -! pint of I per cent. potas~um permanganate
was given every three hours, followed by suitable doses of mag-
nesium sulphate, and ordinary turpentine liniment was applied
to the lumbar regions and extremities. There was recovery.
POISONOUS PLANTS 257
The thorn-apple contains a mixture of atropine, hyoscyamine,
and a little hyoscine, which used to be considered a single sub-

FIG. 34.-DATURA STRAMONIUM (THORN-ApPLE).

stance, and called dait/rine. From the observations detailed it


will be seen that datura operates similarly to atropine, producing
paralysis, causing dilatation of the pupil, suspension of secretion,
17
VETERINARY TOXICOLOGY
and of the inhibitory fibres of the vagus, leading to the rapid
action of the heart.
Of the numerous exotic Solanacea: which contain atropine or
related alkaloids, Mandragora officinalis, or' mandrake, contains
in addition mandragorine, C15H1902N, and African varieties of
Scopolia contain hyoscyamine, together wHh traces of hyoscine.

Solanum.
Potato.--The unripe and green potato contain dangerous
quantities of solanin, and old, rotten or sprouting tubers, which
have been kept for a long time, are also dangerous; moreover,
the alkaloid is most abundant in the "eyes" and in the skin.
'Since, however, the potato is usually boiled, in which case the
alkaloid Pilsses into the water, poisoning in the human species
is rare.
Symptoms.-Potato poisoning amongst animals occurs when
green, old, or damaged tubers are fed in long-continued and large
quantities. After about a week of such feeding the horse, as in a
case noted by Saunders (I907), shows a small and weak 'pulse,
normal temperature, and loss of co-ordination in movements;
complete loss of appetite, excessive thirst, but inability to drink;.
mydriasis, stertorous breathing, suspension of peristalsis, and
slight muscular tremors over the crural muscles.
In cases of horse poisoning encountered by Willows, a very
rapid and feeble pulse, temperature I03 F., intense congestion of
the mucous membranes\ and very fcetid diarrhcea, were observed,
the cases terminating fatally.
McFadyean (1897) observed poisoning of horses by old, mouldy,
and decayed, but not sprouted, potatoes which were steamed and
fed with barley, bran, and chaff. Weakness, loss of power over the
limbs, but not struggling or other evidence of pain, marked the
disorder. Animals fed experimentally on - the same potatoes
evinced similar symptoms and died quietly. On the other hand,
in horses Gardner (1924) observed reeling and staggering with a
stiffened gait, profuse perspiration, breathing stertorous, pro-
trusi9n of nictitating membrane, and complete trismus The
potatoes in this case were described as frosted and diseased.
McSwiney (1914) saw two calves of ten dangerously ill and one
unwell after a heavy feed of cooked small potatoes with a little
Indian meal, hay. grass, and water. ,The dominant symptoms
POISONOUS PLANTS 259
were those of narcotic poisoning, indicated by prostration, drowsi-
ness, and the absence of c'orneal reflexes.
Other cases affecting cattle. have been described by Cummin,gs
where half a barrowful of un saleable potatoes caused inability to
rise, and vomiting in the recumbent position, in consequence
whereof asphyxiation resulted. Lactation was stopped.
Hewetson (1919) records cases of poisoning from eating green
potato tops. He noted dulness and somewhat comatose appear-
ance, dryness of muzzle, salivation, cold extremities, dilated
pupil, temperature 10Z o F., no tympanites, moan, or grunt.
With Pigs fed on steamed potatoes which were budding, and
which had the buds on, Schneider (1902) observed after a few days
loss of appetite, dulness, exhaustion, imperceptible pulse, .watery
diarrhrea, low temperature, and comatose condition. Ogilvie
(1943) considers that when about 50 per cent. of.the diet consists'
of sprouted potatoes, poisoning is likely to result in the pig. The
chief symptoms he observed in a herd of eighty pigs were ano-
rexia, subnormal temperature, marked dulness, and copious
diarrhrea, followed by exhaustion and the death of twenty of
the affected animals. The symptoms of poisoning appeared a few
days after sprouted potatoes had been added to the diet, and at
post-mortem the only lesion observed was a non-specific enteritis.
On the other hand, Ironside (1943) gave up to 16 pounds of
sprouted potatoes to two pigs daily for fifteen days without
producing any ill-effect, and concludes that sprouted potatoes
may be safely fed to pigs, provided 'that they are previously
steamed or otherwise cooked.
According to Cornevin (1893), when animals are fed with raw
and entire potatoes there is depression, loss of appetite, cessation
of lactation; gritting of the teeth, and profound prostration, with
a remarkable somnolence, but no dilatation of the pupils. After a
period of constipation there succeeds diarrhrea and, when possible,
vomiting. In the less acute forms the prostration is the dominant
characteristic, to which is added the intestinal irritation, with
rapid loss of flesh.
Post-Mortem Appearances.-The post-mortem lesions are those
of acute or chronic enteritis according to the course of the poison-
ing. The other viscera are not abnormal, but there is congestion
of the cerebral membranes.
Treatment.-In the potato poisoning of horses Saunders (1907)
gave 1 gFain of strychnine subcutaneously, and rectal injec-
VETERINARY TOXICOLOGY
tions of warm water. Next day there was purgation, and i grain
of arecoline bromide speedily caused profuse salivation and
s';Veating. Offensive black freces were expelled. Eventually the
horses recovered.

FIG. 35.-S0LANUM DULCAMARA (BITTER-SWEET).

(From Smith's "Veterinary Hygiene.")

Some of the pigs treated by Schneider (IgOZ) recovered after


tannin and linseed tea. .
Bitter-Sweet.-Sola1tu11t dulcamara (Fig. 3.5), or bittersweet:
Stem shrubby at the base, with climbing or straggling branches,
often many feet in length, but dying far back in winter. Leaves
POISONOUS PL4NTS 261
stalked, ovate or ovate-Ianceolate, 2 or 3 inches long, usually
broadly cordate at the base and entire, but sometimes with an
additional smaller lobe or segment on each side, either quite
glabrous or downy on both sides, as well as the stem. Flowers
rather small, blue, with yellow anthers, in loose cymes, on lateral
peduncles shorter than the leaves. Berries small, globular or
ovoid, and red.
Symptoms.-Gillam (1906) observed in sheep small inter-
mittent pulse, temperature 1040 F., quickened respiration,
dilated pupil, staggering gait, and greenish diarrhcea. Smythe
(1931) records two suspected cases of S. dulcamara poisoning in
pregnant cows, the chief symptoms being tympany, constipation,
dilated pupils, staggering gait, collapse, and death.
Bonner (1938) observed poisoning of cattle as the result of
grazing on S. nigrum, the black nightshade, the chief symptoms
being narcosis and paralysis.
The post-mortem lesions are not characteristic; in some cases
evidence of gastro-enteritis may be present.
Chemical Diagnosis.-Solanine may be extracted by means of
the Stas-Otto process, using amyl alcohol as the extractive. It is
insoluble in water, ether, and chloroform, and gives, with con-
centrated sulphuric acid, an orange colour changing to violet on
warming; with Mandelin's reagent it gives a yellow colour
changing to orange, then brown, red-violet, and green 'before
fading. On warming solanine with a few drops of a solution of
selenic acid in sulphuric acid (6 of acid to 8 of water by volume),
a pale red colour develops which deepens on cooling. Solanine
may be obtained from plant material by expressing the juice and
washing the residue with distilled water. The liquid so obtained
is allowed to stand, the supernatant fluid decanted, made alkaline
with ammonia, and evaporated to dryness. The residue is then
thoroughly extracted with hot alcohol, the extracts filtered and
again evaporated to dryness; the residue is shaken up with water,
acidified with sulphuric acid, filtered, and made alkaline with
ammonia, when solanine is precipitated.

Nicotine.
Occurrence.-The tobacco plant, Nicotiana tabac1t11t, and the
South African wild tobacco, N. glauca, represent the third group
of the poisonous Solanace:e. The volatile alkaloid nicotine,
VETERINARY
, TOXICOLOGY
CloH14N2' is the chief active principle, the average content of the
leaves of N. tabawm being 4 to 6 per cent. The alkaloid when pure
is a strongly basic, colourless, volatile oil which rapidly turns
brown on exposure to air, taking on the characteristic smell of
tobacco. In commerce it is usually employed as the sulphate in
40 per cent. solution, which is widely used in horticulture as a
spray for the destruction of insect pests. The solution or an
infusion of tobacco leaves are also used as a parasiticide for ecto-
parasites in domestic animals, and also as an anthelmintic in
conjunction with copper sulphate for the treatment of parasitic
gastritis in sheep. Numerous fatalities have followed its use for
these purposes, most of the accidents being due to the external
application of tobacco preparations, since nicotine is readily
absorbed through wounds and even through the unbroken skin;
there is also the danger that the dressing may be licked off.
Toxic Dose.-Two drops of the pure alkaloid are sufficient to
cause fatal convulsions in the dog when given by the mouth, and
the minimal lethal dose for the horse lies between 0'2 ml. an5i
0'3 mI., so that nicotine must be regarded as a highly toxic
substance. Giordano (I935) considers that 400 to 600 ml. of tobacco
extract is the minimal lethal dose for horses and cattle when
applied to the skin, and Hornsby and French (I942) found that
a I'2 per cent. solution of nicotine sulphate was fatal when
sprayed over cattle at the rate of :2 litres per beast. A solution of
z ounces of 40 per cent. nicotine sulphate and I pound of lime
dissolved in I gallon of water has been recommended as a dressing
for cattle infested with the larvre of Hypoderma bovis, but,' as
Jones and John (I943) found, such a dressing is likely to set up
fatal nicotine poisoning. When used as an anthelmintic, Rose
(1936) found that a mortality rate of 8'4 per cent. was caused in
five to six months old lambs following the administration of
approximately I ounce of a mixture composed 5>f I pound copper
sulphate and I6 ounces of 40 per cent. nicotine sulphate dissolved
in zt gallons of water.
Symptoms.-Owing to the rapid absorption of nicotine from
the alimentary canal or surface of the body, symptoms of poison-
ing set in rapidly, appearing in about thirty minute~or so, with
death in two to three hours if a fatal dose has been absorbed.
The symptoms are referable to the action of nicotine on the
ganglion cells of the autonomic nervous system, which are at first
stimulated and then paralysed, and also to its action on the central
POISONOUS PLANTS
nervous system; here there is stimulation of the medullary
centres and spinal reflexes, which may be sufficient to cause
convulsions, followed by depression. In cases of poisoning, the
chief symptoms observed are inco-ordination of movement,
vomition, respiration at first stimulated, but later there is
dyspncea and respiratory arrest; the heart is at first slowed, but
later the pulse becomes rapid and weak, muscular tremors and
convulsions may occur, and constipation followed by diarrhrea
may also be noted; finally, there is collapse, coma, and death. In
horses which had been treated for mange with a warm solution of
about 5 per cent. strong tobacco juice, symptoms of poisoning
set in within a few minutes, there was profuse sweating, tremors,
nausea, and disturbed respiration; after five hours one animal
collapsed and showed coldness of the extremities, imperceptible
pulse, very slow respirations, and deep coma. Recovery followed
after the administration of very" strong coffee.
Livesey (1904) describes poisoning of a fox terrier with tobacco
given as an anthelmintic. About i- ounce of tobacco was present
in the vomitus; the animal showed clonic muscular spasms,
retraction of the eyes within the orbits, mouth moist, mucous
membranes rather pale and cyanotic, quick, full pulse, cold
extremities and inability to swallow. Potassium bromide was
given; the animal showed signs of collapse, the body was cold,
respiration shallow, heart slow and feeble, muscular tremors,
particularly in the muscles of the'right shoulder, and occasional
convulsions, which ceased aft~r five hours, were noted. Following
the administration of strychnine and dilute alcohol, the animal
recovered on the following day.
Post-Mortem Appearances.-Nicotine produces no characteristic
lesions. The odour of tobacco may be detected from the ingesta
and the tissues, and there may be some evidence of congestion of
the mucous membrane of the stomach, abomasum, or upper part
of the small intestine; the heart is usually collapsed and flabby.
Treatment.-The symptoms must be treated as they arise,
since no specific antidote is available. Stomach lavage should be
applied where possible, artificial respiration given as soon as
there is sign of respiratory failur~, and injections of adrenalin
given to support the heart; the administration of charcoal,
potassium permanganate, and demulsants may also be beneficial.
Chemical Diagnosis.-Nicotine may be extracted by means
of the Stas-Otto process or, since it is volatile, by distillation in
VETERINARY TOXICOLOGY
a current of steam from the material made alkaline with caustic
alkali. Nicotine gives a white precipitate, soluble in dilute hydro-
chloric acid, with mercuric chloride, which also gives a white
precipitate with strychnine, but in this case the precipitate is
insoluble in dilute hydrochloric acid. Nicotine also gives certain
colour reactions, the most characteristic being a bright pink
colour with Tunman's p-dimethylaminobenzaldehyde reagent; on
adding a drop of nicotine to the reagent in sulphuric acid, the
colour appears in the cold but disappears on the addition of water
or concentrated sulphuric acid; with sulphuric acid and potassium
bichromate, nicotine gives a green colour. When there is sufficient
material, it is desirable to distinguish between nicotine and
coniine. An ether solution of nicotine mixed with an ether solution
of iodine gives a precipitate or turbidity, and gradually long
red crystals form which reflect blue (Roussin's test). Coniine
does not give this reaction. Another distinction depends on the
fact that a cold saturated (r to go of water) solution of nicotine
remains clear on warming, whereas a similar solution of coniine
becomes turbid, since coniine is less soluble in warm than in cold
water. Nicotine hydrochloride first separates as a resin, slowly
becoming crystalline, whilst coniine gives at once a crystalline
hydrochloride.
REFERENCES.
ATROPA.
Cornevin, C. (1893), Des Plantes Veneneuses.
Livesey, G. H. (1904), j. Compo Path. and Therap., 17,359.
HYOSCYAMUS.
Cornevin, C. (1893), Des Plantes Veneneuses.
Creuzel (1840), Veterinarian, 13, 661
Welsby, J. R. (1903), Vet. Rec., 16,181.
DATURA.
Sinclair, J. M. (1898), Vet. Rec., 11, 367.
Sullivan, H. A. (1905), Vet. ]., 61,182.
SOLANUM TUBEROSUM.
Cornevin, C. (1893), Des Plantes Veneneus~es.
Gardner (1924), Vet. ]., 80, 169. -
Hewetson, W. T. (1919), Vet. Rec., 32, 104.
Ironside, W. J. (1943), Vet. Rec., 55,268.
McFadyean, J. (1897), ]. Compo Path. and Therap,. 10,69.
McSwiney, E. (1914), Vet. Rec., 26, 433.
Ogilvie, D. D. (1943), Vet. Rec., 55, 249.
Saunders, C. G. (lg07), Vet. j., 63,699.'""
Schneider (1902), Vet. Rec., 15, 3.
Willows, G. T., Private Communication.
POISONOUS PLANTS
SOLANUM DULCAMARA.
Gillam, W. G. (1906), Vet. Rec., 19, 88.
Smythe, R. H. (1931), Vet. Rec., 11,161.
SOLANUM NIGRUM.
Bonner, W. G. (1938), New Zealand J. Agric., 57, 99.
NICOTINE.
Giordano (1935), Boll. Vet. Ital., 31, 1845.
Hornby, H. E., and French, M. H. (1942), J. S. Afric. Vet. Med. Ass., 13,21.
Jones, T. H., and John, F. M. V. (1943), Vet. Rec., 55,243.
Livesey, G. H. (1904), ]. Compo Path. and Therap., 17,359.
Rose, A. L. (1936), 4ust. Vet. ]., 12,64.

SCRO~HULARIACEJ.E.

This family cont?-ins many poisonous genera, of which those


found in Britain and on the Continent are Digitalis, Scrophztlaria,
PediC1tlaris, Rhinanthus, Melampyrlun, Verbascum, and Linaria,
whilst Gratiola is native to South-Eastern Europe. Those members
which have been definitely studied have been found to contain
glycosides of the digitalis and saponin classes.

Digitalis.
Botanical Characters.-The Digitalis purpurea (Fig. 36),
common foxglove, finger flower, or dead men's bells, is a very
common weed, often cultivated as a garden plant. It frequents
dry, hilly wastes, roadsides, and banks. Being widely distributed
and well known, a particular description is unnecessary in this
place. In the United States the plant is cultivated, and is
natudlised to some extent on Cape Breton Island.
'Active Principles.-All parts of the foxglove contain the
digitalis glycosides. These possess some of the properties of
saponins and are not destroyed by boiling or drying. The sub-
stances isolated by various workers are commonly referred to as
digitalin, digitonin, gitonin, and gitalin, but much confusion has
arisen since many of the substances isolated may not exist as
such in the plant, and many have proved to be impure mixtures.
Kiliani (1901) first showed that the substance digitalinum verum
may be regarded as the pure glycoside digitalin, Ca6H5604; this,
on hydrolysis, yields sugar and an active aglycone or genin,
digitaligenin, C2aHaoOa. In aqdition, two other crystalline glyco-
sides have been isolated by Stoll and Kreis (1933); these are
digitoxin, C41H64013' and, gitoxin, C41 H 640 14 , which on hydrolysis
266 VETERINARY TOXICOLOGY

./
FIG. 36.-DIGITALIS PURPUREA (FOXGLOVE).
POISONOUS PLANTS
yield sugars and the active genins digitoxigenin, C23H 340 4 , and
gitoxigenin, C23H 340 5 , respectively. It will be noted that all the
active genins so far obtained contain twenty-tpree carbon atoms
in their molecules, and it is probable that th~ other substances
said to be present are either impure mixtufes or breakdown
products arising from the chemical processe used during ex-
traction.
Commercial tinctures and extracts of digitalis vary in com-
position and activity, owing to their containing different pro-
portions of the glycosides. Digitoxin appear!3 to be the chief
glycoside present in D. purpurea, the leaves of' which contain up
to 0'4 per cent.
Toxic Doses.-Cornevin (I893) gives the tox.ic amounts of the
green leaves as 4 to 5 ounces for the horse, 6 to 1 ounces for the ox,
I ounce for the sheep, and t to ! 'ounce for the pig. Kaufmann
\1.'9~~) g\'V'C<;:, ~ ~\\\\~'C ~{ tb.'C !>w'N\:l'C;:'C~ \'C'd\ 'd~ ~;"'iRRl01~'S b tl."1ft
horse, 60 to 130 grains to the dog, and 3 0 grains to the cat. Of
digitalin, zt grains for the horse, ! grain for the dog, and /; grain
for the cat may be considered as being fatal.
Effects.-Apart from the irritant effects, the chief action of
digitalis is upo!J. the heart. With small doses there is increased
and prolonged systole, with a shortened diastole owing to a direct
action on the cardiac muscle, particularly on the conducting
tis~ues; with toxic doses, heart block develops and the excitability
of the cardiac muscle is increased, so that the beat becomes rapid
and irregular, with final arrest of the heart, when the auricles will
be found dilated and full of blood, but the ventricles contracted
and empty. Digitalis also causes diuresis, for w}1ich purpose it was
first introduced into medicine, but this is :tJlainly due to the
beneficial action of small doses on the circulation and not to a
direct action on the kidneys. Digitalis also has a direct action
on the central nervous system, causing stimulation of the medul-
lary centres, which may be sufficient to produce vomition, stimula-
tion of the vagal and respiratory centres, so {hat there may be
rapid, deep respiratory movements and even convulsions.
Digitalis is slowly absorbed and is excreted jn the urine, but it
is a cumulative poison, so that chronic poisoni:t1g may result from
the repeated administration of small therapeutic doses.
Symptoms.-Dun (I9IO) gives a careful account of the experi-
mental poisoning of a three-year-old brown mare, which had
received in all 9 drachms of powdered digitalis over a period
268 VETERINARY TOXICOLOGY
of three days. Towards evening of the third day the mare showed
dulness and loss of appetite. On the fourth day she was nauseated;
nose, mouth, and ears cold; abdomen tympanitic, with colicky
pain, and occasional pawing; pupil somewhat contracted; pulse
firm at axilla and heart, but not very perceptible at jaw. At
4.30 p.m. she was down, much pained, and attempting to roll;
pulse 82, but unequal. On the following day at 12 noon, 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 next day at I I a.m.
Two other animals, which had received similar doses, recovered,
not having displayed marked cardiac symptoms.
In a case mentioned by Gillam (1906) two cows and a horse,
after eating hay containing dry foxglove, were observed to feed
erratically, breathe hard, and lie down after feeding. Pulse almost
imperceptible, contracted pupil, and excessive urination.
Horses which had foxglove by mistake showed sleepiness,
swollen eyelids, dilated pupils, injected conjunctivre, considerable
swelling in submaxillary space, respiration normal, temperature
I03'5 F., pulse full, between 65 and 75, most intermittent, being
occasionally normal; the second heart sound was 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. The
respiration became more difficult and stertorous, tongue and
buccal membranes livid, jugular standing out. Tracheotomy failed
to save.
Other horses showed less aggravated symptoms, and nearly' all
recovered under treatment.
In a case of the poisoning_of Pigs the cause was the pouring by
a servant of decoction of digitalis leaves into the pigs' bucket,
whereby five animals were affected, and two, died. They w~re
languid and sleepy, refusing to eat or drink, attempting to vomit,
and repeatedly passing small quantities of freces'. Urination was
scanty and strained. In the case of those which recovered, the
effects did not pass off for more than a week.
Post-Mortem Appearances.-The pigs above referred to showed
acute inflammation of the mucosa of the stomach and intestines,
with thin yellow contents. The kidneys were sligh fly congested,
bladder empty, and other viscera healthy. These appearances
POISONOUS PLANTS 26 9
seem to point to a predominating saponin-like effect, due to
digitonin.
In Dun's case the stomach was ruptured, but there was no
inflammation of the alimentary membranes.
In digitalis poisoning, as a rule, the abdominal viscera are
healthy. The lungs are engorged with dark venous blood, and the
heart shows great distension of the auricles, so that the transverse
may be greater than the longitudinal section.
Treatment.-The treatment consists of purgatives, mucilag-
inous draughts, and stimulants. There is no specific antidote,
but atropine may be given to counteract the irregular heart
action.
Chemical Diagnosis.-Digitalis glycosides are not very soluble
in water, but are readily soluble in hot alcohol, so that they can
be extracted by means of the Stas-Otto process. The best means
of recognition is by Keller's test, which is carried out by dissolving
a trace of the substance in I ml. of glacial acetic acid containing
a little ferric chloride, and then allowing concentrated sulphuric
acid to run down the side of the tube, so that the two liquids do
not mix. A dark coloured zone forms at the junction of the two
liquids, and in about two minutes a blue ring appears, whilst after
about thirty minutes the whole of the upper acetic acid layer has
a deep indigo blue colour, gradually changing to blue-green.
Various tannins, especially from quinine barks, give a similar
reaction, as also does formaldehyde. A physiological test on a frog
is therefore necessary in cases of doubt or for strict medico-legal
purposes.

Verbascum, Scrophularia, Gratiola, and Linaria.


These genera do not contain plants which give rise to serious
poisoning, and, moreover, have not received precise stUdy. A
brief mention will therefore suffice.
Verbascum.- Verbascttm thapsus, or great mullein, is a common
roadside weed, extending as far north as Aberdeen. The leaves and
flowers afford an emollient and expectorant extract, which is
used as a medicine. The seeds are stated to be narcotic, but
animals refuse to eat the plant.
Scrophularia.-Scrophularia nodQsa, or figwort, and S. aquatica,
or water scrophularia. The former occurs in woods, the latter in
marsh or moist situations, and has a disagreeable odour. Accord-
ing to Walz, they contain bitter principles, scrophulariti and
27 0 VETERINARY TOXICOLOGY
scrophulerin respectively, which may cause fatal superpurgation.
But the plants are not eaten by animals. .
Gratiola.-Gratiola o.ffi,cinalis, or hedge hyssop, is found in
Europe and in the Southern United States. It owes its activity
to gratiolin, C43H70015' a glycoside isolated by Retzlaff (1902),
belonging to the group of drastic purgatives. Poisoning, which
might possibly arise from ingestion of the plant, would tCj.ke the
form of superpurgation.
Linaria.-Linaria vulgaris, toad-flax, L. spuria, round-leaved
linaria, L. cymbalaria, ivy linaria, and L. elatina, pointed linaria,
have a repulsive smell and nauseous taste and contain an acrid
juice, said by Klobb (1907) to contain a poisonous glycoside
linarin, CSO H SO0 25 . Animals do not readily eat the plants, and
poisoning, therefore, is ve.ry rare. To>ad-flax is common in hedges
and field borders, the others less frequent, but they ought to be
included as noxious weeds.

Pedicularis, Rhinanthus, and Melampyrum.


Pedicularis.-This genus includes Pedicularis palustris, or red
rattle, distributed over marshes, wet meadows and ditches, and
P. sylvatica, or louse-wort, more widely distributed over moist
pastures, meadows, and heaths. Many species are found in the
United States, chiefly the Western.
Rhinanthus.-Rhinantlms crista-galli, the rattle, or common
rhinanthus, is a meadow and pasture weed, which often causes
injury to the herbage, and whose grains are liable to become
mixed with cereals.
Melampyrum.-Melampyrum arvense, or purple cow-wheat,
occurs in cornfields of South-Eastern England and Norfolk, and
is injurious to crops. The grains, like those of rhinanthus, may
become mixed with cereals.
These plants contain in their seeds a glycoside rhinanthin,
C5sH52040' examined by Mirande (1907), and thus may be dele-
terious components of forage or flour. The doses for animals
would be very large, for C~rnevin (1893fquotes experiments in
which 35 grammes of the grain and over 2 pounds of the fresh
plant did not affect rabbits.
The general effect of rhinanthin is that of a saponin, and
reference may be made to that substance for an account of its
action and chemical recognition in flour or meal.
POISONOUS PLANTS 27 1
REFERENCES.
DIGITALIS.
Cornevin, C. (r893), Des Plantes Veneneuses.
Damman and Behrens (r903), Vet. j., 55, 78.
Dun, F. (r910), Veterinary Medicines, r2th ed.
Gillam, W. G. (1906), Vet. Rec., 19, 88.
Kaufmann, M. (1901), Therapeutique et Matiere Medicale Veterinaire,
3rd ed.
Kiliani, H. (190r), Ber. Chem. Ges., 34, 3562.
Olver, H. (1872), Veterinarian, 45, 173.
Stoll and Kreis (1933), Munch. Med. Wschr., 80, 723.
GRATIOLA.
Retzlaff, F. (1902), Arch. Pharm., 240, 561.
LINARIA.
Klobb, T. (r907), Campt. Rend., 145, 33I.
~

RHINANTHUS.
Cornevin, C. (1893), Des Plantes Veneneuses.
Mirande, M. (I907), Campt. Rend., 145, 439.

PHYTOLACCA~ElE.

This order is not found in England. Phytolacca decandra is


acclimatised in Southern Europe and Africa, but is native to
America, where it is known as the poke-weed, garget, or American
nightshade. I
It contains a purgative active principle in all parts. Formerly
the berries were used to colour wine, a practice which is, however,
now generally prohibited on account of possible danger. The
effects are those of superpurgation, the extract being stated to
be quickly, fatal to the dog, whilst in the States cattle have occa-
sionally been fatally poisoned by the leaves.

POLYGONACElE.
Some species of this order are held to be responsible for poison-
ing, although the records and our knowledge of the active
principles are scarcely such as to give the basis of a well-founded
narrative~ They include species of Rumex, or dock, of which
R. acetosa, sorrel dock, and R. acetosella, sheep-sorrel, may be
mentioned. These plants are well known to contain oxalates,
which may possibly account for the alleged poisonings. They are
widely distributed in the north temperate hemisphere. Whilst
27 2 VETERINARY TOXICOLOGY
it is held by some that sheep-sorrel improves the condition of
sheep that eat it, others assert that the mature and seeded plant
causes poisoning in sheep and horses.
According to Cornevin (1893), in the horse the chief symptoms
include at first a condition recalling drunkenness, marked by
vacillating gait, salivation, and cyanosis. Then there are muscular
tremors, dilatation of the pupil, relaxation of sphincters, urination,
and a feeble, slow, and intermittent pulse. There succeed to these
convulsive contraction of the lips, retraction of the eyeball,
accelerated and stertorous breathing, extreme dilatation of the
nostrils, tetanic contractions of the muscles of the neck, back,
and limbs, abundant sweating, and falling. After a period of
extreme exhaustion these symptoms are repeated, and death
occurs in convulsions. The lesions are' not characteristic, but there
may be some evidence of gastro-enteritis.
Fagopyrum esculentum, buckwheat, under suitable conditions,
is capable of causing photosensitisation in domestic animals. The
flowers appear to be the most dangerous part of the plant, but the
sensitising agent has not yet been determined.

REFERENCE.
Cornevin, C. (1893), Des Plantes Veneneuses.

ARISTOLOCHIACElE.
The genus Aristolochis is mainly tropical, although some species
are cultivated in gardens-e.g., A. clematis, which is the chief
poisonous example, although all the species should be regarded
with suspicion; and Cornevin (1893) specially names of them
A. rotunda, A. longa, A. pistolochia, and tne American A. sipho.
The poisonous effects are due to the alkaloid aristolochine,
C17H190aN, which has similar but more powerful effects than
aloin (of aloes). In rabbits it causes acute neurotic nephritis,
with albuminuria and urremic symptoms, apd in dogs marked
fall of blood pressure, intestinal hremorrhages, but no nephritis.
Cornevin (1893) relates a case of the poisoning of lwrses by.a
ration containing rather more than I parf of A. clematis to 7 of
lucerne. There were noted immobility, torpor, and a drunken con-
dition, with ~nsteady gait; pulse ample, quick and hard; periods
of comatose somnolence, marked by slight spasms and convulsions;
POISONOUS PLANTS 273
dilated and vision obscured; loss of appetite, constipation, frequent
urination, and genital spasm. Recovery was slow.
REFERENCE.
Cornevin, C. (1893), Des Plantes Veneneuses.

THYMELACElE.
This family is represented in Britain only by the genus Daphne,
also found in the Cape and Australia, of which Daphne mezeremn,
common mezereon or spurge-flax, and D. laztreola, spurge-laurel
or dwarf bay, grow wild. Of the dangerous exotic species D. cneo-
mm and D. pontica (from Asia Minor) are cultivated.
Botanical Characters.-:-Mezereon (Fig. 37) is a shrub attaining
about 3 feet, cultivated in gardens, but found wild in woods,
particularly in the Soutp. The narrow lanceolate leaves form
tufts at the ends of the branches, and the small purple, scented
flowers appear in February before the leaves are fully out. The
berry is red.
The spurge-laurel (Fig. 38) attains about 4 feet, and has clusters
of evergreen lanceolate leaves crowded at the ends of the branches.
The flowers are greenish-white and scentless, and the berries
bluish-black.
Active Principle.-The daphnes contain an acrid substance,
mezerinic acid, in all parts, particularly the bark and berries. It
is not destroyed by drying. Very little is known as to the chemistry
and properties of mezerinic acid. The physiological effect is that
of a powerful drastic, also exhibiting marked nervous effects.
The plants are very poisonous. Twelve berries of mezereon have
been stated to kill the human subject, and about I ounce of the
spurge-laurel is stated to prove fatal to the horse.
A case of poisoning of a horse by spurge-laurel (locally known
as wood-laurel) was investigated by the author (rgII) for H. D.
Sparrow, of Rochford, Essex. From Sparrow's information it
appears that the leaves are frequently dried, rubbed up in the
hands, and given to horses for worms. In a case observed by him
such administration preceded attacks of gripes. Several mysterious
cases of colic encountered in the district would appear to have
been caused by this practice.
Symptoms.-Daphne poisoning is marked by intense colic. As
an immediate effect Sparrow noted consti1?ation, lasting in one
18
274 VETERINARY TOXICOLOGY
instance forty~eight hours, in spite of aloes,' oil, and I grain
eserine and 2 grains pilocarpine intravenously. There follow
dysentery and copious evacuations of f<eces with mucus, blood,

FIG. 37.-DAPHNE MEZEREUM (COMMON MEZEREON).

and intestinal epithelium. Between the spasms the animal is


drowsy.
A similar case came under observation (1912) ,through C. F.
Parsons, of Cheltenham, in the case of a seven~year-old cart-
POISONOUS PLANTS 275
horse. The horse ate the shrub whilst waiting to be unloaded, and
refused the evening meal of the same day. On the next day there
was abdominal pain, staggering gait, anxious countenance,
laboured breathing, pulse 80, temperature 1032 F., bowels

FIG. 38.-DAPHNE LAUREOLA.

normal. On tlie following day there was excessive .purgation,


pulse I20, temperature I042 F., and death Occurred at midday.
On post-mortem the stomach and intestines were inflamed and
all the ingesta fluid, and Sparrow also found the colon very much
inflamed, the walls It inches thick, and contents loose, blood-
VETERINARY TOXICOLOGY
stained, and of a peculiar odour. There was no tympanites until
after death.
The treatment consists in elimination of the cause, 'as with
irritants in general; and treatment of the particular symptoms as
indicated. .
The detection of poisoning by analysis is very uncertain in the
present state of our knowledge. The finding and identification of
plant fragments offers the most certain means. When the bark
of the plant is chewed there is produced after some minutes a
very intense burning sensation, which lasts several hours. Extrac-
tion in the ordinary systematic routine yields an acid, which has
no burning taste. It gives a smoky colour with ferric chloride,
and a pink colour on prolonged warming ~th strong sulphuric
acid. These observations are got both with the plant and with
ingesta, but are scarcely characterisfic. It is curious to note that
after extraction of the acid, even in the cold, the toxicity, as
tested on mice, so far as present observations go, disappears.

EUPHORBIACElE.
There are three genera of this family found in Britain, and
from which poisoning may occur-namely, EHphorbia, or spurge;
Mercttrialis, and Buxus, or box.
Of exotic Euphorbiacece, Ricinus communis, or castor oil;
Croton tiglim1t, or croton; and Jatropha curcas, or purging nut, are
~mportant species.
Euphorbia.
Botanical Characters.-The chief species whiGh may give rise
to poisoning is the Euphorbia lathyris, but no doubt most, if not
all, of the euphorbice have similar effects. The E. hibernica, or
Irish spurge, is', for instance, used as a fish poison.
E. lathyris.-A tall, stout,annual or biennial, often 3 feet high,
or even more; very smooth and glaucous. Stem-leaves narrow-
oblong, the upper ones broader, especially at the base, often 3 or
4 inches long, and all opposite, not alternate, as in other euphorbice.
Umbels of three or four long rays, once or twice forked, with large
ovate-Ianceolate floral leaves. Glands of the involucre crescent-
shaped, the points short and blunt; capsules large and smooth;
seeds wrinkled. The plant grows wild in Sussex and Somerset, and
is cultivated in cottage gardens.
POISONOUS PLANTS 277
Toxic Principle.-The euphorbice, of which E. lathyris is selected
as typical, ar~ distinguished by containing an acrid juice, and in
the seeds a purgative oil. The resin euphorbin from the North
African E. resinifera is a non-officinal purgative. Very little is
known of the chemistry of the juices, which on the whole rather
recall ranunculus in their action. Desiccation does not deprive
the plant of its activity.
Symptoms.-Euphorbia is distinguished by its irritant action,
with production of vomition when possible, purgation, and in
fatal doses superpurgation, together with nervous symptoms of
vertigo, delirium, and muscular tremors.
The post-mortem appearances are those of acute gastro-
enteritis.
Piss-grass.
The South African Euphorbia genistoides, known as pis~goed,
or piss-grass, is a low shrub of about 8 inches, having close, many-
branched stems, resembling a besom, and green apetalous flowers.
Like many others of this order, the stem contains an acrid juice,
having powerful irritant properties.
Poisoning.-Poisoning by piss-grass mainly affects camels,
oxen, and geldings, probably by reason of the narrower urinary
passage. It is marked by severe urethritis. The animal appears
very uneasy, and attempts to urinate are frequent and painful.
The animal lies down, the bladder becoming more distended, and
dies in coma, or in a violent effort at relief.
The treatment is difficult save in the early stages. Epsom salts
and three-hourly doses of 10 grains of extract of belladonna have
been recommended. In the horse the catheter may be used, and
for the ox amputation of the penis is a possible measure. Turpen-
tine or any diuretic agent is to be avoided.

Mercurialis.
Both M. perennis and M. annua are poisonous, and the former
is here described as typical.
Botanical Characters.-M. perennis (Fig. 39), or dog's mercury.
Rootstock slender and creeping. Stems erect, simple, 6 or 8
inches, or rarely nearly I foot high. Leaves rather crowded in the
upper half, oblong or ovate-lanceolate, 2 to 4 or 5 inches long,
usually pointed, crenate or serrated, and rough or with short
hairs. Flowers dicecious, on slender axillary peduncles, often
27 8 VETERINARY TOXICOLOGY
nearly as long as the leaves; the males in little clusters, the females
singly or two together. Ovaries larger than the perianth, with
rather long, spreading styles. Capsules more or less' covered with
warts or soft prickles.

FIG. 39.-MERCURIALIS PERENNIS (DOG'S MERCURY).

The plant is common in England and Scotland; less so in Ireland.


Toxic Principle.-Mercurialis has been found to contain a
volatile basic oil having narcotic properties, which has been
called mermrialine, and to which, in part at any rate, the toxicity
of the plant is due. "'
POISONOUS PLANTS 279
Symptoms.-Mercurialis acts on the alimentary and urinary
systems. In a case observed by Blackhurst (1896) of the poison-
ing of cows, there was excessive bloody purgation, cessation of
lactation, temperature ros o F., pulse go, and increased respira-
tion. The disease was protracted over several weeks, the animals
being comatose after the first symptoms, and eventually the neck
assumed a curved position, like the half of the figure eight, and
the animal was unable to raise its head from the ground .
. Post-Mortem Appearances.-The thoracic viscera were normal;
on dissecting the neck the muscles of the right-hand side were
rich in fibrous tissue, and the last three joints partially anchy-
losed; the abdominal viscera showed inflammation with sloughing
of the mucous membranes; the liver and kidneys showed fatty
degeneration.
Cornevin (r893) notes, further, as a symptom of the poisoning,
hrematuria, with frequent, painful micturition, and passage of
dark-coloured bloody urine.
Buxus.
Buxus sempervirens, the common and well-known evergreen
shrub, the box, is found wild in parts of central and southern
England, but is much used as an ornamental border in gardens.
From this circumstance box may give rise to poisoning, but
cases are rare.
The plant is said to contain an alkaloid, buxine, C24H 430N3 ,
isolated by Faure (1830), but of very doubtful constitution, a~
well as a resin and essential oil. The action of the plant, probably
due to the latter constituents, is emeto-purgative. In fatal doses
there are intense abdominal pain, dysentery, convulsions, and
death by asphyxia. The lesions shown are extended gastro-
intestinal irritation and pulmonary congestion.

Other Euphorbiacere.
Ricinus communis.-The castor-oil plant is an important
exotic, yielding the well-known seeds from which castor oil is
obtained by pressure or extraction. The seeds or beans of castor
oil are oval, and about i by ! inch in size. They have a brownish
or buff colour, and are mottled or marbled with brownish specks
and streaks.
The seed is rich in oil, of which it contains 50 per cent.
The residue left after pressure cQIlta.ins the active poison, which
280 VETERINARY TOXICOLOGY
does not pass into the oil. Accidents may arise either from the
giving of the beans in other food, or from the feeding of the
residual press-cake, which is otherwise valuable as a manure.
Toxic Principle.-The effects of castor-oil bean are du.e to
ricin, a typical example of j he class formerly known as toxal-
bumins, now better designated as toxins, in the present instance
'Phytotoxins, being of vegetable origin. In distinction to the
majority of toxins-cj. snake venom and bacterial toxins-
ricin, like crotin, from Croton tiglium, is absorbed from the
alimentary tract, probably by reason of its resistance to decom-
position by digestive enzymes. But the poisonous dose by the
mouth is at least one hundred times as great as that by injection.
The toxicity of ricin is unknown and enormous. Impure pre-
parations may be purified 'by the action of trypsin, which destroys
accompanying albumens, the weight of ricin decreasing without
sensible diminution of toxicity. Like other toxins and ferments,
ricin and its allies, crotin and abrin (from Abrus precatorius),
is destroyed by prolonged heating over 60 C. in the moist con-
dition, but is more resistant to dry heat.
The formation of ricin immunity is characteristic. By increas-
ing doses an animal may be made tolerant of enormous overdoses
of such magnitude as from 400 to 800 times the normal, the
tolerance not being due to habituation of the tissues, but to the
formation of a true anti-ricin in the serum, The antibody is
capable of conferring immunity on a second subject, and is
specific against ricin, but not against other toxins.
The seeds of Croton tiglium resemble those of ricinus in size
and shape, but are dull brown in colour, and not mottled.
Those of Jatropha curcas, curcas purgans, or American, Bar-
badoes, or purging nut, are not likely to cause poisoning in Great
Britain.
Both croton and jatropha yield oils and press residues, and both
are very dangerous. The mecl~ani$m of croton p_oisoning is now
known to be due to the toxin crotin, whilst jatropha, according
to Stillmark, contains ricin. With croton it seems probable that
in part the toxin 'passes into the expressed oil.
Symptoms.-Poisoning by ingestion of castor-oil beans, or
residues, does not declare itself, as a rule, till after several days,
and does not appear to be always.marked by purgation, although
thi~ is more usual, the beans being considerably more active than
the oil. In a case observed in the horse, there was complete loss
POISONOUS PLANTS 281
of appetite, shivering, coldness of extremities, dejection, abdominal
pain, and constipation. Temperature 1030 F., pulse 70, and death
in about three days.
Shenton (1914) in the horse observed dulness, prostration, pulse
60 to 80, and temperature 102 0 to 1040 F. There was constipatioll.
in all cases except one, in which there was diarrhrea, and rapid
recovery. There was total loss of appetite, and spasm of the
diaphragm was a well-marked symptom. In only one case was
there marked abdominal pain. Recovery was obtained in two to
five days after administration of laxatives.
Wooldridge (1918) and White (1918) have also observed castor
seed poisoning of horses. Both observers -remark on the passage
of hard mucus-covered freces. Elevated temperature and weak,
rapid pulse, colicky pains and shivering, were again observed in
each set of cases. At later stages of the illness Wooldridge (1918)
signalised muscular symptoms in the form of tetanic spasms;
excitement on being approached; stiff and stilty gait, the tail
being elevated. In one case there was trismus, and in all sexual
excitement, and difficulty in swallowing.
Wooldridge (1918) found gastro-enteritis affecting the pylorus
and a variable portion of the intestine beginning at the duodenum,
whilst White (1918) noticed acute inflammation of the stomach,
and a thin yellow deposit on the intestinal mucous membrane.
A case is noted by Chambers (1910), in which death occurred
in cattle after external application of castor oil and lubricating
oil against ticks. It probably does not illustrate ricin poisoning,
but displays the possible ill-effect of lar&e quantities of the oil.
Lander and Edwards (1914) investigated ricin poisoning of cattle
experimentally. The ox is known to be more resistant than the
horse, and it was found that 12~- ounces of whole seed mixed with
bran, followed after four days by 18 ounces of pressed seeds in
ball, did not seriously affect a 4 cwt. 70 lb. calf. The highest tem-
perature noted was 102.8 0 F. The whole seeds caused diarrhrea,
and the de-fatted seeds tended to make the freces hard and dark.
The seeds were the small seeds of R. co~nmunis of commerce,
averaging about 135 per ounce. Seeds of R. sanguineus and
R. zanzibariensis are larger (66 and 39 per ounce respectively)
and appear to be more toxic, for 14 ounces of the former killed a
calf in eight days, and 16 ounces of the latter in 3i days.
Noteworthy symptoms were great weakness, loss of appetite,
diarrhcea, weak frequent pulse, and later tucked-up abdomen and
282 VETERINARY TOXICOLOGY
emaciation. No gross lesions were found: some bright red con-
gestion of the pyloric end of the fourth stomach and for about
2 feet in the small intestine in the first case, and in the second
case rose-pink to red congestion of the latter half of the mucous
membrane of the small intestine.
A case of croton poisoning of horses was seen by Godbold (1914)
and Wallis (1914). Croton seeds had been passed through a mill
subsequently used for grinding rations for pigs and horses., About
300 pigs had the food; all vomited, and were severely purged,
but none died.
Nine horses (of which one died) showed hard, wiry and quick
pulse, and accelerated breathing; sweating, pawing and crouch-
,ing; temperature r03 to r05 F., and constant and very violent
purgation.
Amongst the Leguminosce the seed of Abrus precatorius, the
crab's eye, or jequirity pea, contains the toxin abrin, and the
leaves and bark of the American Robinia pse1tdacacia, or locust-
tree, contain the toxin robin. The seed of abr2ts is about the size
of a small pea, bright red in colour, and has a black spot. Abrin
is less toxic than ricin, but has similar effects-indeed, Ehrlich
only clearly differentiated the two toxins from the fact that
anti-ricin is powerless against abrin, and similarly anti-abrin is
of no avail against ricin.
It exercises a very powerful irritant action on the conjunctivre,
and has on this account found application in ophthalmic therapy.
The natives of India practise malicious poisoning by inserting
splinters impregnated with abrus under the skins of beasts. This
malpractice was detcctcd by Calmettc by means of the specific
anti-abrin. The Quarterly Journal of Veterinary Science in India,
1883, p. 375, gives an account of such a poisoning, in which a spike
It inches long and! inch at the thick end was inserted under the
skin. It had a dark green colour, weighed I2 grains, and contained
datura opium, abrus (or gunchi) seeds, onion, and spirit daru.
Chemical Diagnosis.-The vegetable toxins ricin, crotin, and
abrin all possess the power of agglutinating red blood corpuscles.
In examining a cake or meal suspected to contain castor seeds
the powdered material (about 2 grammes) is extracted by means
of physiological saline (0'9 per cent. solution of common salt)
0
in the incubator at 37 C. for a few hours, and the solution
filtered. The clear solution is then ad<Jed to a suspension of red
corpuscles from fresh defibrinated, or citrated, blood suitably
POISONOUS PLANTS
diluted (about ten times) with salt solution. More or less rapidly,
according to the quantity of ricin present, the corpuscles clump
together, or agglutinate, and fall to the bottom of the tube in the
form of red 'flakes. With very small quantities of material the
phenomenon may be observed in a hanging drop under the micro-
scope. Much protein seriously interferes with this test.
, An alternative test consists in making a layer of a small quantity
of the suspected extract on the top of some serum from an animal
immunised to ricin. With ricin such a serum forms a zone of amor-
phous precipitate (precipitin reaction). This reaction is specific.
The researches of Green and Andrews (1923) show that the root
of the South African Adenia digitata (Burtt-Davy) or M adeeca
digitata (Harv.) contains a cyanogenetic glycQside whose hydro-
cyanic acid production may amount to 0'04 per cent. of the
fresh root, and in addition a true toxin, which the authors
propose to call "tnadeecin." Half a pound of the minced root fed
to an adult ewe caused transient symptoms of cyanide poisoning
at once, followed after three days by dulness and depression, and
insensibility to ordinary handling, although reacting to painful
stimuli. The lesions pointed to an irritant poison.
The authors extracted a protein fraction of the root fatal to
rabbits in the minute dose of one-thousandth of a milligram per
kilo body weight by subcutaneous injection.
This lends powerful support to the view that in this case a
phytotoxin is the active principle. Modeccin does not possess
the agglutinative property so characteristic of ricin.
REFERENCES.
MERCURIALIS.
Blackhurst, C. (1896), Vet. j., 43,431.
Cornevin, C. (1893), Des Plantes Veneneuses.
Buxus.
Faure (1830), j. Pharm., 16,428.
RICIN.
Broad, (1896) Vet. Rec., 9,226.
Chambers (1910), Vet. j., 66,717.
Godbold, R. E. (1914). See Lander, G. D., and Edwards, J. T. (1914).
Green, H. H., and Andrews, W. H. (1923), 9th and IOth Repts. Dir. Vet.
Educ. and Res. S. Africa, 381.
Lander, G. D., and Edwards, J. T. (1914), Vet. Rec., 36,614.
Shenton, R. (1914). See Lander, G. D., and Edwards, J. T. (1914),
Wallis, M. (1914). See Lander, G ..D., and Edwards, J. T. (1914).
White (1918), j. Compo Path. and Therap., 31, 98.
Wooldridge, G. H. (1918), j. Compo Path. and Tllerap., 31,94.
VETERINARY TOXICOLOGY

PLANTS AND FOOD REPUTED TO BE POISONOUS.


Some plant products commonly used as food mayan occasion
give rise to poisoning. In some cases this may be due to the fact
that the food material has become mouldy, but, on the other
hand, some foods undoubtedly contain specific toxic substances
which, when taken in excessive quantities or fed to susceptible
animals, give rise to poisoning. '
Of the foodstuffs known or suspected to contain specific toxic
agents, the more important are as follows:
Cotton-Seed Cake or Meal.-Undecorticated cotton cake has
been responsible for causing illness and death, particularly in
young pigs, when fed in excessive quantities. The cake, or meal,
contains up to 25 per cent. of indigestible fibre, which may cause
impaction of the alimentary canal or it may be contaminated with
some harmful seeds such as castor beans, but, as Withers and
Carruth (1916) showed, cotton seed contains a highly toxic
dihydroxyphenol, gossypol, C30H 300 5 , which may be regarded as
being the specific toxic substance concerned in these cases. The
gossypol content of llndecorticated cotton cake varies con-
siderably, depending on the solvent or method used tor extracting
the oil, and also on the variety of the seed.
Toxic Dose.-Rommel and Vedder (1916) consider that cattle
fed more than 6 pounds of undecorticated cotton cake daily may
develop symptoms of poisoning after several weeks. Binns (1938)
found a ration' containing 25 per cent. of cotton seed caused
illness and death of four- to six-months-old pigs in approximately
two weeks, and Vald (1928) considers that a ration containing
10 per cent. of cotton seed is injurious to pigs. In the dog, West
(1940) found that raw cotton-seed meal, which- formed 27 per
cent. of the ration, caused poisoning after several months.
Symptoms.-Symptoms of poisoning set in suddenly, but may
not occur for some time after first feeding the cotton seed. In
pigs, Binns (I938) observed stertorous breathi~g, cyanosis of
mucous membranes, convulsions, and death within thirty minutes
of the first appearance of symptoms; and in the dog, West (1940)
observed inca-ordination of movement, somnolence, and sudden
death after a few days' illness.
Post-Mortem Appearances.-The most characteristic lesions are
petechial hremorrhages in the various organs, together with
serous exudate in the pleural and abdominal cavities aucl J?eri.-
POISONOUS PLANTS 285
cardium. There is enlargement of the 'liver, with congestion and
hremorrhages, hremorrhagic gastro-enteritis, congestion and
hremorrhages in the kidneys, and enlargement and perhaps fatty
degeneration of the heart.
Treatment.-No specific treatment is known. Further fatalities
need not be expected on a change of diet.
Soya-Bean Meal.-The observations of Stockman (I9I6) have
established that under certain circumstances soya-bean cake or
meal may cause poisoning. No specific toxic agent has been
demonstrated in the beans, and Stockman (I9I6) found that it
was only beans extracted with trichlorethylene which were
poisonous. This has been confirmed by Samin (I93I), who showed
that beans extracted with carbon tetrachloride, benzene, alcohol,
or naphtha were harmless, so that there can be little doubt that
it is the solvent, in this case trichlorethylene, which is the toxic
agent, although Stockman (I916) failed to observe ill-effects from
thirty-nine daily doses of 3 ounces of trichlorethylene mixed with
linseed oil given to a heifer. He was, however .. able to reproduce
the condition in cattle by feeding 172 pounds of soya-bean meal
extracted with trichlorethylene over the course of thirty-six days.
Symptoms.-The chief symptoms are inappetence, cessation
of rumination, staring coat, rise of temperature, bleeding from
the nostrils, colic, and the presence of blood clots in the freces.
The characteristic lesions are petechial hremorrhages in the
alimentary canal and internal organs, particularly the sub-
cutaneous tissues and muscles. No specific treatment is available.
Cacao Meal and Cacao Husks.-The residue of the seeds of
Tlzeobl'ol1la cacao, after the removal of the fat and also the husks
left after the manufacture of cocoa, have been recommended as
suitable foods for animals, especially as a source of vitamin D,
since Kon and Henry (I935) found 300 LV. vitamin D per gramme
of husks. In addition, however, th~y contain appreciable amounts
of the alkaloid theobromine, C~H802N, as well as traces of caffeine.
Asplin and Ellenberger (1927) found the theobromine content of
cacao meal to lie between I to 3 per cent., with an average of
2 per cent., and Golding and Burr (1934) found an average of
I per cent. of theobromine in cacao husks. Whilst these alkaloids
are comparatively harmless, an excess of theobromine in the diet
may undoubtedly give rise to poisoning. The toxic does is high,
since Dowden (I938) gave 3 ounces of theobromine daily to cattle
for three weeks without producing ill-effects, but it is completely
28(1 VETERINARY TOXICOLOGY
absorbed from the alimentary tract and only excreted slowly, so
that, if feeding is long continued or if food containing theobromine
is fed in excess, a toxic amount of the alkaloid may accumulate
in the body.
Symptoms.-Theobromine is sometimes used in medicine as a
diuretic, since in therapeutic doses it increases the activity of
muscle, particularly cardiac muscle, and thus improves the
circulation, but in large doses it causes exhaustion of muscle and
gastro-intestinal disturbance; unlike caffeine, however, it appears
to have little direct action on the central nervous system. In cases
of poisoning, sudden death is to be expected from heart failure.
As a rule, few symptoms are observed. Clougn (1942) records
vomition, diarrhcea, and sudden death in an elkhound the morning
after it had been given food containing IS grains of theobromine
per pound, and also the sudden deaths of two sheep dogs after
being fed three times with similar food; Blakemore and Shearer
(1943) also report sudden death. In their case, fowl died suddenly
within forty-eight hours of ingesting 3 ounces of food containing
0'5 per cent. theobromine. Treatment is of little avail, and no
characteristic lesions are present at post-mortem.
Chemical Diagnosis.-Theobromine is a dimethyl xanthine,
soluble in alcohol, so that it will be extracted by means of the
Sats-Otto process. With meal or husks a preliminary extraction
should be made with petroleum ether, the solvent evaporated
off and the residue extracted with alcohol. The alcohol is removed,
th,e residue clarified with lead acetate, the lead removed with
hydrogen sulphide, and the theobromine, now in a reasonably
pure form, recovered by extracting with chloroform. For the
detection of theobromine, 0'5 mg. of the substance is placed on a
watch-glass, mixed with 2 drops of concentrated hydrochloric
acid, the mixture brought to the boil,S drops of bromine water
added, and the solution evaporated to dryness. The residue is
dissolved in 5 drops of water, I drop of I per cent. ferrous sulphate
added, and I drop of N ammonium hydroxide placed by the
side of the solution. These are allowed to mix slowly, when an
intense dark blue coloration develops, which qu~ckly fades on
standing or with excess of ammonia. This reaction is also given
by the homologues of theobromine, caffeine, and theophylline.
Brewer's Grains and Distiller's Grains.-The residue left after
the manufacture of beer and spirits is excellent food for stock,
but is sometimes held responsible for causing ill-effects. This is
POISONOUS PLANTS
not due to any specific substance in the grains themselves, but to
the fact that they have undergone excessive fermentation or
that some preservative has been added to prevent this.
The addition of much common salt or of fluorine preparations
is sometimes resorted to and must be regarded as making the
grains improper or possibly harmful food for animals.
Sugar Beet.-Sugar beet, Beta vulgaris, and sugar-beet pulp are
also excellent food~, but accidents have been reparted following
their ingestion. In horses, the feeding of dry sugar-beet pulp may
give rise to impaction of the stomach and choking, as pointed
out by Alley (r943), and in ruminants there may be excessive
fermentation and tympanites, as observed by Conisbee (r935),
owing to the fact that large quantities of sugar m.ay be present,
particularly in the fresh roots. The ingestion of sugar-beet leaves
may also give rise to harmful effects, since, like the leaves of
rhubarb, Rheum officinale, they contain oxalic acid. Winters-
berger (I930) found I per cent. of the acid to be present and,
although the toxic dose is large, sufficient may be taken to cause
poisoning, as was found by Bendinger and Jurkow (I935).
Undecorticated Beech-Nut Cake.-Cornevin (r893) records that
cake made from the nuts of the beech, F agtts sylvatica, may on
occasion give rise to symptoms resembling poisoning by Lalium
temulentmn, but the toxic agent responsible for these cases has
not been determined.

Poisoning by Oak Leaves and Acorns.


Reports of poisoning of cattle, sheep, pigs, and horses by
Quercus species, usually Q. robur, the common oak, are on record,
although young oak leaves and acorns are commonly eaten by
stock. They contain, however, up to 7 per cent. of tannic acid,
and if eaten in excess may undoubtedly give rise to harmful
effects. The active principle is probably the acid, although it has
been suggested that some other agent is responsible, since the
toxic dose of the former is extremely large. Marsh, Clawson and
Marsh (r9I9) failed to produce any symptoms in a cow following
the administration of 25 g. of tannic acid daily for twenty-eight
days, but 50 g. daily produced death in sixteen days.
Symptoms.-Symptoms of poisoning may not appear until
after all the ingested oak leaves or acorns have been digested and
expelled. The chief symptoms are constipation in the earlier
288 VETERINARY TOXICOLOGY
stages, followed by persistent diarrhrea with frequent small,
dark, bloody evacuations. There is loss of appetite, suspension
of rumination, wasting, colic, and excessive urination; the urine
is usually pale, but may be dark coffee coloured, and the tem-
perature subnormal. There may be soreness of the mouth, pallor
of mucous membranes, and a discharge from the nose and eyes.
In the horse, Lloyd (1920) observed obstinate cons.tipation, and
particularly d.ark-coloured urine which contained flaky material.
Post-Mortem Appearances.-The lesions are generally those of
an irritant poison, but the rumen and reticulum are usually
normal. There may also be hremorrhages in the kidneys, and
nephritis and fluid may be present in the serous cavities. Tutt
(1924) found large quantities of acorns in the stomachs of four
pigs, which also showed gastro-enteritis.
Treatment.-Gould and Morgan (1934) recommend copious
draughts of liquid paraffin or oleaginous purgatives, together with
diffusible stimulants. Saline purgatives are contra-indicated. A
change of diet is essential, but at pasture this may be difficult,
since cattle develop a craving for acorns and will seek them out
wherever possible.
Chemical Diagnosis.-The tannin may be separated by acid
aqueous extracts and recognised by the dark bluish coloration
given with ferric chloride; it also precipitates gelatin or alkaloids
from solution.
Fern Poisoning.
Male Fern.-The root of Aspidium flUx-mas contains about
8 per cent. of filicic acid, C35Hss012' which, on.hydrolysis, yields
phloroglucinol, together with an oleo-resin. It is used as an
anthelmintic, but under certain circumstances may act as a
poison.
The powdered root is irritant and laxative, and in large doses
may cause hremorrhagic gastro-enteritis and nervous symptoms
of drowsiness, occasionally convulsions, coma, and collapse;
blindness may also occur. The toxic dose is very variable. Frohner
(1919) states that 5 drachms of an ethereal extract killed a dog
of 40 pounds, 6 drachms a sheep of 88 pounds, and 3 ounces a cow
of 660 pounds, but accidents have also followed the administra-
tion of therapeutic doses. In these .cases castor oil has usually
been administered together with or shortly after the anthelmintic,
and it is suggested that the oil may increase its toxicity by
POISONOUS PLANTS
facilitating the absorption of the active principle. In the treat-
ment of poisoning, evacuation of the stomach, mucilaginous
medicines, and stimulants are indicated; oleaginous purgatives
are contra-indicated.
Bracken.-Poisoning by Pteris aquilina, the common bracken,
has been observed in horses and cattle, particularly in calves,
during the early autumn from August to November. The toxicity
of bracken has been the subject of much discussion, since Storrar
(1893) first drew attention to the disorder, but sufficient experi-
mental evidence has since been obtained to confirm that bracken,
either green or when dried, may be poisonous. Considerable
amounts require to be eaten before symptoms of poisoning set in.
Stockman (1917) gave 260 pounds of green bracken at the rate
of 10 pounds daily to an eight-months-old bull .calf before pro-
ducing symptoms of poisoning, and in another case II2 pounds
of green bracken given to a four-months-old calf at the rate of
4 pounds per day were ingested before poisoning resulted.
Similarly, Hadwen and Bruce (1917) found that 161 pounds' of
bracken eaten over the course of twenty-four days, and forming
about 28 per cent. of the total ration, were required to produce
poisoning in a horse. On the other hand, animals have been given
much larger amounts without ill-effect. Bruce (1927) gave a
three-and-a-half-year-old heifer 578 pounds of bracken in eight
and a half months without producing symptoms of poisoning, and
cattle are often fed with hay containing bracken or bedded with
bracken, which they readily consume without coming to any
harm. Nevertheless, bracken must be considered as a potential
source of danger.
Active Principle.-The root has been used as an anthelmintic
and is said to contain an acid similar to filicic acid, but this does
not appear to be present in the stems or fronds, which are the parts
of the plants usually eaten. The young shoots contain hydrocyanic
acid, but in insufficient amounts to be harmful, but when mature
the plant contains a high proportion of tannic acid. This is
probably the toxic agent, although it has been suggested that a
phytotoxin is responsible, but such a substance has yet to be
isolated from bracken.
SYmptoms.-Symptol1ls of poisoning as a rule set in suddenly
and are characterised by general dulness, loss of appetite, a
watery discharge from the mouth and nose which may be tinged
with blood, the passage of dark fleces which also contain blood,
I9
29 VETERINARY TOXICOLOGY
a raised temperature, and finally collapse and death after a few
days' illness. There may also be some evidence of jaundice,
particularly in horses, difficulty in swallowing, and struggling
shortly before death.
Post-Mortem Appearances.-The lesions resemble those found
in scurvy, but Stockman (I922) showed that in experimental
cases of bracken poisoning there was no evidence of avitaminosis,
nor can the condition be associated with any bacterial infection.
The most characteristic lesions, which have been described by
Craig and Davies (I940), are petechial hremorrhages in the
alimentary canal and internal organs, particularly in the heart,
lungs, muscles, and under the skin; congestion of the liver and
kidneys; and, in some cases, a gelatinous exudate in the serous
cavities and also in the region of the thmat. The latter was the
only lesion noted by Lynch (I935) at the post-mortem of a calf
which was thought to have died from bracken poisoning.
Treatinent.-Oleaginous purgatives and the repeated adminis-
tration of potassium iodide have been recommended. A change
of diet is essential and also a change of bedding if bracken has
been used for this purpose.
Diagnosis.-The presence of tannic acid should be demon-
strated, and if possible the alimentary canal should be searched
for identifiable portions of the plant.

REFERENCES.
COTTON-SEED.
Binns, H. R. (1938), ]. Compo Path. and Therap., 51,296.
Rommel, G. M., and Vedder, E. B. (1916), J. Agric. Re~., 5,489.
Vald, A. (1928), Derds. tierarztl. Wschr., 36, 563.
West, ]. L. (1940), J. Amer. Vet. Med. Ass., 96, 74.
Withers, W. A., and Carruth, F. E. (1916), J. Agric. Res., 5,261.

SOYA BEAN.
Samin, N. (1931), Inaug. Diss. Tieriirztl. Hochschule, Berlin.
Stockman, S. (1916), J. Compo Path. q,nd Therap., 29,95.

CACAO MEAL.
Asplin and" Ellenberger (1927), Vermont Agric. Expt. Sta. Bull., 272.
Blakemore, F., and Shearer, G. D. (1943), Vet. Rec., 55, 165.
Clough, G. W. (1942), Vet. j., 98, 196.
Dowden, H. C. (1938), Biochem. j., 32, 71./
Golding and Burr (1934), Agr. Progress, 14, (Pt. I), 44.
Kon, S. K, and Henry, K. M. (1935), Biochem. j., 29,2051.
POISONOUS PLANTS 29 1
SUGAR BEET.
Alley, J. C. (1943), Vet. Rec., 55,44.
Bendinger, G. G., and ]urkow, M. I. (1935), Tieriirztl. Rdsch., 41, 695.
Conisbee, E. G. (1935), Vet. Rec., 15,262.
Winters berger, J. (193 0 ), Wien. tieriirztl. Wschr., 17,541.

BEECH-NuT.
Cornevin, C. (1893), Des Plantes Ven{meuses.

OAK.

Gould, G. N., and Morgan, K. G. (1934), Vet. Rec., 14,33.


Lloyd, W. (1920), Vet. j., 76,113.
Marsh, C. D., Clawson, A. B., and Marsh, H. (1919), U.S. Dept. Agric.
Bull., 767.
Tutt, J. F. D. (1924), Vet. j., 80,54.

ASPIDIUM.
Frohner, E. (1919), Lehrbuch der Toxikologie.

PrERIS AQUILINA.
Bruce, E. A. (1927), Dept. Agric. Canad. Bull., 88.
Craig, J. F., and Davies, G. O. (1940)' Vet. Rec., 52,499.
Hadwen, S., and Bruce, E. A. (1920), Vet. j., 76,98.
Lynch, J. (1935), Vet. Rec., 15, 106 7.
Stockman, S. (1917), J. Compo Path. and Therap., 30,311.
Stockman, S. (1922), j. Compo Path. and Therap., 35,273.
Storrar, D. (1893), J. Compo Path. and Therap., 6,276.
CHEMICAL TOXICOLOGY
Introductory.-Under this heading the general principles of
the laboratory exa~ination of material to detect the presence
of poisons will be discussed and some details given as to the
general methods of separation of poisons from organic matter.
The more important specific tests for the individual poisons have
already been described under their respective headings, so that
they will not be referred to again, but in this connection it seemed
advisable only to name those tests which are as characteristic
as possible, can be applied to the substance in the form in which
it is obtained from the material under research, and which are
suitable for the recognition of traces of the particular poison.
For analytical purposes. the poisons fall into four groups, viz.:
A. Volatiie poisons.
B. Non-volatile organic poisons.
C. Heavy metals and metalloids.
D. Acids, alkalis, and alkaline salts.
Preliminary Observations.-It is usually unnecessary to carry
out a complete analysis of the material under examination, since,
in most cases, there will be some history or post-mortem signs
which will indicate the probable nature of the poison. If, how-
ever, little or no information is available, the procedure to adopt
is first to separate volatile poisons by distillation, then treat the
residue with alcohol to remove organic poisons, and finally search
for metallic poisons. If there has been any signs of irritation
of the gastro-intestinal tract, a Reinsch test should be carried
out directly on a portion of the visceral contents to eliminate
arsenic, antimony, mercury, etc. Indeed, in any case where the
history is unsatisfactory, this test should be performed in the
first place. If poisoning by acids or caustic alkalis is suspected,
an examination of a watery extract of the material should be
undertaken as soon as possible, since nitric and sulphuric acids
are completely decomposed 'Yhen left in contact with the
tissues. Before starting a systematic search for poisons, cert~in
general observations ought to be made, the most important being
as follows:
Colour.-The existence of coloration, either local or diffused,
is a valuable guide. A yellow colou~ suggests nitric and picric
292
CHE]}[JCAL TOXICOLOGY 293
acids; greenish-blue points. to copper; green to chromium com-
pounds; black to iron compounds of tannin; blue may be due to
indigo or Prussian blue, used as colouring agents for vermin
powders, but the quantity is usually too small to be perceived;
specks of red may be vermilion or red lead; heavy black particles
may be antimony sulphide. It is only rarely that colour is detected,
for in most cases the dilution of a coloured poison in such a mass
of green ingesta as is found in the stomach of the ox is too great
for its recognition. With smaller animals the indication is more
valuable.
Smell.-Compounds easily recognisable by their smell are
phosphorus, hydrocyanic acid, alcohol, ether, chloroform, carbolic
acid, savin, turpentine, essential oils, ammonia, and sulphuretted
hydrogen. The two last are often products of decomposition, and
caution is needed on this account in forming an opinion. In
general the smell is difficult to observe on account both of the
natural and putrefactive smell of the viscera.
The odorous substances fall into Group A' of the volatile
poisons, and their smells are best observed in the course of
analysis for that group.
SusPicious particles and vegetable fragments ought to be care-
fully looked for and picked out. Valuable guidance is thus given,
and in the case of many, or most, poisonous plants the finding
and identification of vegetable detritus gives the best chance of
correct diagnosis.
It is a good plan to stir up the semi-solid contents to a thin
paste with water, and, after ?tanding, carefully decant from
heavy particles, Which (if found) may be washed with a gentle
stream of water. Particles of such substances as white arsenic,
black antimony, vermilion, red lead, and white lead may thus
be separated.
In the case of dogs and foxes the nature of the stomach con-
tents ought to be ascertained as far as possible. This gives very
valuable information in tracing tne source of poisoning. With
these animals the presence in the stomach of scraps of fur, small
bones, or feathers usually points to a bait of rabbit or bird, which
has been the vehicle of the poison.
Disposition of the material for the special analyses. is a most
important point, which is best left to discretion. The analyst
must be guided entirely by considerations arising from the
quantity of available material, the nature of the poison 'suspected
294 VETERINARY TOXICOLOGY
and the degree of delicacy of its detection. It is always wise to
reserve a portion, preferably about one-quarter, for confirmatory
analysis, or to replace accidental loss. When the analyst has at
his disposal the whole stomachs of a horse, sheep, ox, or pig, he
may consider that he has carte blanche, for the material suffices
for more than one complete analysis. Quite otherwise when he
has a small animal such as a bird, cat, or small dog to deal with.
In such case he must use discretion in the taking of parts for the
various operations.
Apparatus.-It is the common practice in medico-legal work
on the human subject to advise perfectly new apparatus for each
analysis. The apparatus used ought to be in good condition; thus
porcelain dishes must have an unimpaired glaze; but the dogma
of new vessels is somewhat extreme. To have used a ,set of
apparatus in an analysis which has yielded negative results is
the best proof of its cleanliness. It is an elementary maxim of
the trained chemist thoroughly to clean all apparatus in such wise
as to meet the object of the intended analysis. Thus a flask and
condenser intended to be used in Reinsch's test will, as a matter
of routine, be cleansed by boiling hydrochloric acid; a dish
designed for the nitric acid solution of parts will be boiled but
with that acid; flasks intended for the alcohol extraction of
organic poisons will be cleaned with a mixture of strong sulphuric
acid and potassium chromate after the laboratory attendant has
"cleaned" them. No chemist ever uses a piece of apparatus which
he has not personally cleaned. Possibly if the Courts thoroughly
appreciated the fact that it is a chemist's business to keep his
apparatus clean, and not to get muddled, and mix the specimens
or reagents, less weight would be attached to the general pre-
liminary precautions. But, on the other hand, it is essential that
the person who issued the report should' himself either have
performed, or personally supervised, all the operations.
Reagents.-All reagents designed for toxicological analysis
must be of proved purity. The condition of reagents and apparatus
in this respect is best guaranteed by the per-formance of a blank
test. If this gives a negative result-e.g., for arsenic-the reagents
and apparatus are good. A blank ought to be carried through
from time to time as a matter of routine precaution. Fortunately,
to-day the manufacture of high-grade chemicals has reached such
a pitch of excellence that it is rarely necessary specially to purify
one's reagents.
CHEMICAL TOXICOLOGY 295
Qualitative Analysis.-This aims at the detection of the presence
of a poison. It is the fundamental apd really difficult task of
toxicology. Quantitative analysis follows the qualitative, and its
chief value is to guide the expert in the formation of an opinion
as to the significance of the qualitative revelations. It has also a
subsidiary value-that of providing a figure to be produced in
evidence. The position of a witness who states that from 8 ounces
of a maferial he separated 41s grain of strychnine is stronger than
that of the witness who states that he found a "distinct trace" of
that agent. No wise man would commit himself to the statement
that the material contains a given weight of the poison; he will
name the quantity he actually separated, and he will also be well
advised to state that the weight given is his estimate, and be
prepared to state how he determined- it, and what is the probable
error of his determination.
All quantitative data in toxicology are to be regarded as ap-
proximations. But even so they are indispensable and valuable
approximations, for the reasons set forth above. The quanti-
tative methods available for the estimation of traces of material
are:
I. Direct weighing. This is the most satisfactory and sometimes
the only possible method. It may be used for the measurement of
quantities of lead and many other common metals. A residue of
an alkaloid may also be weighed, bJIt the weight ought not to be
regarded as very exact, partly by reason of the normal error in
weighing, but chiefly because the residue is rarely pure. Alkaloid
extracts always contain traces of basic substance of animal or
vegetable origin (ptomaine bases) which, when a small quantity
of alkaloid is present-e.g., I milligramme-may equal or exceed
it in weight. Further purification leads to loss of material, which
may be so great as to extend even to the vanishing point.
2. Volumetric methods depend on the performance of a
reaction with a solution of a reagent of known stref':gth, the
end of the reaction being marked or indicated in various ways,
As an illustration, hydrocyanic acid may be determined in the
presence of sodium bicarbonate by titrating with a standard
solution of iodine of such strength that I millilitre is equivalent
to 0.025 milligramme. When all the cyanide has been converted
into cyanogen iodide a permanent yellow colour appears, or if a
little starch solution is also present the end of the reaction is
marked by the production of the blue starch-iodine coloration.
VETERINARY TOXICOLOGY
From the amount of iodine used the quantity of hydrocyanic
acid present may at once be calculated.
Free alkalis such as potassium or ammonia and free acids such
as sulphuric, hydrochloric or nitric may also be determined by
neutralisation with standard acid o'r alkali respectively in the
presence of a suitable indicator.
3. Colorimetric methods depend on the production of a coloured
derivative of the substance to be estimated and comparing it
with the same coloured derivative prepared from a known amount
of the substance. Since, according to Beer's law, the colour
intensity of a solution is directly -proportional to the number of
coloured molecules it contains, matching the intensity of the
colollrs of solutions of known and unknown strengths enables
the amount of substance present in the unknown solution to be
estimated fairly exactly, provided the colours of the two solutions
are approximately of the same intensity.
4, Precipitation methods depend on the production of a pre-
cipitate from the substance to be estimated and comparing its
size and intensity with a precipitate prepared in exactly the same
way from a known quantity of the substance. Thus, in the
determination of traces of arsenic, the size and intensity of the
mirror obtained in Marsh's test is compared with mirrors prepared
from known quantities of arsenic. In Birckner's method for the
estimation of zinc, the turbidity produced on the formation of
potassium zinc ferro cyanide is compared with the turbidity
produced by the same compound formed from a known quantity
of zinc. Such methods are extremely accurate when small amounts
of substances have to be estimated and are capable of numerous,
applications-e.g., to lead precipitated as iodide, to barium as
sulphate or chromate, to silver as chloride or iodide, to tin as
dioxide, etc.
GROUP A.-VOLATILE POISONS.
The ::oe_l)aration of volatile poisons depends Oil the fact that
they can be distilled more or less readily along with a current of
steam from a boiling paste of /the materials with water. In
practice, distillation in steam is preferable to ordinary distilla-
tion because the poiling is more regular and the operation does
not require so much attention. It is advisable to place the distilling
,flask in a boiling water bath and to regulate the steam current
so that the quantity of boiling fluid remains about constant: In
CHEMICAL "TOXICOLOGY 297
this way distillation may be allowed to proceed to any extent
desired.
The best method of procedure is to make a thin paste of the
material and ascertain its reaction (acid, alkaline or neutral), if
necessary acidify with 3 to 5 volumes of a non-volatile acid such
as tartaric or sulphuric, and distil in a current of steam. Volatile
substances separated from an acid solution include phosphorus,
hydrocyanic acid, phenols, turpentine, savin, essential oils, alcohol,
ether, chloroform, 'Chloral, sulphuretted hydrogen and sulphur
dioxide. To isolate volatile alkaloids-e.g., coniine or nicotine-
the distillation must be made from caustic alkaline solution.
Substances with a characteristic smell may often be detected
during distillation, but unless the substance is pre,sent in rela-
tively large amount, the smell may be masked more or less com-
pletely by the natural smell of the ingesta or organs. Distinct
flakes (possibly of fatty acids) always pass over, and it is therefore
a good plan to allow the distillate to drop on to a small filter and
collect the clear liquid in a flask or test-tube. Phenols (carbolic
acid and creosote), turpentines (savin), essential oils (camphor,
etc.), and chloroform in fairly large .proportions form a distinct
fluid turbidity or emulsion, and may actually separate into distinct
oily drops, whilst camphor is solid. Phosphorus forms semi-solid
globules, and the other substances named are soluble.
Phosphorus, creosotes, turpentine, and some essential oils
distil slowly, and a large bulk of liquid must be distilled in order
to effect a complete separation. The other compounds-viz.,
hydrocyanic acid, alcohol, ether, chloroform, and the gases sul-
phuretted hydrogen and sulphur dioxide-being very volatile,
concentrate in the first portions of distillate. If a large volume is
collected, the dilution may be so great as seriously to interfere
with the qualitative tests (especially with hydrocyanic acid),
and it is therefore wise to stop the distillation after about 5 m!.
of clear distillate has been obtained. Small portions are then
separately tested for the substances in question-e.g., by the
Prussian blue test !for hydrocyanic acid, by the iodoform test for
alcohol, by the neutral ferric chloride test for phenols (carbolic
acid purple, creosote smoky colour), or bromine water for phenols
(solid tribromphenol from carbolic acid, resinous bro'mcresols
from creosote).
In order to effect a partial separation and purification of the
volatile substances obtained at this stage, the distillate is made
298 VETERINARY TOXICOLOGY
alkaline with sodium hydroxide (not carbonate) and redistilled.
Turpentines, essential oils, alcohol, ether, and chloroform (also
given from chloral by alkali) distil over. If the alkaline liquid is
now maae acid with dilute sulphuric acid and again distilled,
hydrocyanic acid, phenols, sulphuretted hydrogen, and sulphur
dioxide pass over. In the course of these manipulations traces Of
phosphorus suffer oxidation, whilst with alkali on heating phos-
phoretted hydrogen and hypophosphorous acid are formed.
Having distilled from acid solution, the or1ginal residue in the
distillation flask is made alkaline with sodium hydroxide; or if
none of the foregoing is present, a fresh portion of original sub-
stance is made into a paste with water, made alkaline, and again
steam distilled. In this case there distil over-volatile bases,
ammonia, coniine, nicotine, arecoline, and some bases of putrefac-
tion-e.g., trimethylamine (from brine), putrescine, and cada-
verine (ptomaine). Chloral gives, with alkali, chloroform. The~
substances must be then detected and estimated by appropriate
special methods.
The results above described may be summarised as follows:
Hydrocyanic acid. I"
Poisons distilled from dilute Phenols.
acid solution only { Sulphuretted hydrogen.

Poisons distilled from dilut~ {~~:.~OXide


caustic alkali solution only
Arecoline.
Certain bases of putrefaction.
Chloroform (from chloral).
PhosPhorus (not entirely without

J
change).
Turpentines.
Poisons distilled either from lEssential oils.
acid or alkaline solution Alcohol.
Ether.
Chloroform.

GROUP B.-NON-VOLATIJ.E ORGANIC POISONS.


This group comprises non-volatile organic poisons whic~ may
be classified as basic or non-basic. The most important of the
basic poisons are the vegetable alkaloids. The non-basic poisons
include a variety of substances which cannot be classified satis-
factorily, but as they can be extracted from acidified watery
CHEMICAL TOXICOLOGY 299
solutfons by means of the same solvents as are used for the
extraction of alkaloids, it is convenient to class them together.
The most important of them are the following: glycosides and
saponins; essential oils; drastic purgatives such as aloes; resins
such as jalap; neutral principles such as picrotoxin; and deriva-
tives of barbituric acids and urea. Thesp. latter, however, do not
play an important -part in veterinary toxicology.
Alkaloids are widely distributed throughout the vegetable
kingdom, particularly in the seeds and roots of dicotyledonous
plants, although they also occur in the leaves, in certain mono-
cotyledons, in fungi and elsewhere. They exhibit all degrees of
toxicity from the extremely poisonous aconitine to the com-
paratively non-toxic caffeine. Many are, derived from pyridine or
quinoline by the substitution of one or more hydrogen atoms by
additional side chains, so that their constitution is, as a rul.e,
complex,and indeed is not known in all cases. They are usually
feebly alkaline in reaction and, like ammonia,. readily combine
with acids without the elimination of hydrogen. They are only
slightly soluble in water, but as a rule form more soluble salts.
The free alkaloidal bases are soluble in ether, chloroform, amyl
alcohol and ethyl acetate, which solvents are used for their
extraction from alkaline solutions, whereas their salts are in-
soluble in these reagents. As a general rule, both the bases and
salts are soluble in alcohol.
Glycosides occur in plants, especially in the bark, roots, fruits
and cell sap, and, like the alkaloids, exhibit all degrees of toxicity.
When pure they are white, crystalline substances with a bitter
ta;;te, only slightly soluble in water, but soluble in alcohol and the
other alkaloidal solvents. They are esters which on hydrolysis
with acids yield sugars and other components. In nature the
hydrolysis is brought about by enzymes which accompany the
glycoside in the plant, so that if a glycoside is to be looked for,
the enzyme must be destroyed by heat as soon as possible. The
sugar most commonly produced as a result of hydrolysis is
glucose, though other hexose and in some cases pentose sugars
also occur. The other component of the glycoside molecule may
be an acid, alkaloid, aldehyde or alcohol, and is the toxic prin-
ciple. For example, many glycosides on hydrolysis yield hydro-
cyanic acid, some acetic acid; others, like the digitalis glycosides,
yield components called genins, which contain the phenanthrene
ring system; others, like solanine, yield an alkaloid-in this
300 VETERINARY TOXICOLOGY
case solanidine-and so on. Since the molecular structure of the
300 or so known glycosides is for the most part still undeter-
mined, it is more convenient to classify them by their physio-
logical actions into three main groups, viz.: (r) Cyanogenetic
glycosides which on hydrolysis yield hydrocyanic acid; (2) cardiac
glycosides which affect the heart; (3) glycosides which are asso-
ciated with anthraquinone derivatives and thus are purgatives.
Saponins are glycosides which possess the special property of
forming foaming, colloidal solutions when shaken with water.
They also are widely distributed throughout the vegetable
kingdom and also exhibit varying degrees of toxicity, the more
poisonous of them usually being referred to as sapotoxins. When
pure they. are white amorphous or crystalline substances with a
bitter taste, only slightly soluble in water but soluble in alcohol
and the other alkaloidal solvents. They may be subdivided into
neutral and acid saponins. The neutral saponins, like the cardiac
glyc:::osides, yield genins containing the four-membered ring
system of the sterols. The characteristic property of saponins,
which is made use of for their detection, is their power to hremo-
lyse red blood corpuscles.
The other substances included in this group will be considered
separately, since they do. not fall into a single chemical entity. It
must also be borne in mind that certa,in basic nitrogenous sub-
stances, usually called ptomaines, arising from the decomposition
of animal matter, are soluble in alcohol and may be extracted
by the method to be described, so that care must be taken not to
mistake these for alkaloids.
The extraction of both the basic and non-basic substance~ of
this group from the original material is carried. out by the Stas-
Otto method, which depends on the fact that all the members
of this group are soluble in excess of alcohol to which a dilute
acid (tartaric, citric or sulphuric) is added in quantity sufficient
to impart a distinct acidity to the solution. 4cidification is
necessary because some alkaloids are very sparingly soluble in
.alcohol,_ but give salts which are' more easily dissolved-e.g.,
morphine. Since the organic salts of the alkaloids are more
soluble in alcohol than the mineral salts, the use of tartaric acid
is, on the whole, preferable to' that of sulphuric. When the material
is acid, no further addition is necessary ..
stas-Otto Process.-A convenient amount of the material in as
fine a state of division as possible is mixed with a large amount
CHEMICAL TOXICOLOGY 30 1

of alcohol, using approximately 200 millilitres of alcohol for


every IOO grammes of material taken. The reaction of the solution
to litmus is noted, and if not acid sufficient tartaric acid is added
to secure a distinctly acid reaction. The solution is then allowed
to stand for twenty-four hours or warmed nearly to boiling point
on a water bath. When cold, the material is filtered through muslin
and the residue thoroughly squeezed out, .preferably by means
of a press. The extraction is repeated three times, using fresh
alcohol for each extraction, the alcoholic extracts combined,
allowed to stand for some hours and then filtered. The alcoholic
filtrate contains any of the above-mentioned poisons and also
large quantities of such organic substances as fats, oils, carbo-
hydrates, the s~mpler proteins, and bases derived from their
decomposition. The residue may contain such toxins as ricin, but
is rejected, since separate special search must be made for sub-
stances of this nature.
The clear yellow to dark brown filtrate is next concentrated by
boiling in a vacuum, whereby the alcohol is rapidly removed at
. a temperature of 30 to 40 C. A very thick, dark-coloured watery
residue, amounting to about 10 to 20 millilitres and generally con-
taining fat, is left. Bamford (I940) recommends that the alcohol be
evaporated off in open dishes under a current of air rather than
in a vacuum, since this procedure eliminates frothing, which may
be very troublesome, and assists the separation of fat and protein
in a form which admits of rapid filtration.
The gradual addition of hot alcohol to the residue usually brings
about a precipitation of impurities such as carbohydrate. These
are removed by filtration and the clear alcoholic solution again
evaporated in a vacuum to a small bulk. About 20 to 50 millilitres
'of water is then added to the residue and the mixture thoroughly
shaken and filtered, the clear aqueous solution being collected
in a sepa'rating funnel. The insoluble part is mainly composed of
fat and, as a rule, need not be further examined, although it may
contain such drastic oils as croton. Any organic poison present
in the original material will now be concentrated in the acid
watery extract, which is moderately free from organic impurities,
but is always coloured, varying from pale yellow to dark brown.
Preliminary Observations of the Water Extract.-A tendency
to foam and generally to simulate soap solution points to saponins.
Ferric chloride gives a red colour with meconic acid (from opium)
in the acid solution. In a neutral solution ferric chloride gives
302 VETERINARY TOXICOLOGY
violet colours with phenol, morphine and salicylic acid, and a
blue-black or black colour with tannins and gallic acid.
Extraction of the Constituents of the Water Extract.-The
separation of the substances likely to be present in the water
extract is effected through extraction of the watery solution by
means of organic solvents which do not mix or are only partially
soluble in water, such as petroleum ether, ether, benzene, chloro-
form, ethyl acetate and amyl alcohol. The solvent to be used
depends on the nature of the dissolved substance which it is
desired to extract. Of those named, petroleum ether has the most
limited range and amyl alcohol the widest. The nature of the
substance extracted depends on the reaction of the solution.
If the solution is acid, solvents extract free acids, glycosides and
bitter principles; if it is alkaline, solvents extract alkaloids; if
neutral, glycosides. Morphine is not extracted in the presence of
strong alkali (sodium hydroxide), since, being a phenol, it forms
salts of the alkali metals. It is, however, extracted from ammonia
or sodium bicarbonate solution, since these are not strong enough
alkalis to form salts with morphine. In practice it is sufficient to
a
make alkaline with ammonia or bicarbonate as usual procedure.
On the basis of these facts, an extraction of the acid liquid
will yield glycosides, bitter principles, acid and neutral compounds,
and a subsequent extraction of the liquid made alkaline by
ammonia will yield alkaloids. The two groups are thus partially
separated, but many alkaloids are extracted from acid solution
since they are feeble bases-e.g., chelidonine, veratrine, colchicine
and solanidine.
In actual experience successive extractions with ether and
chloroform .(a) from acid and (b) from ammoniacal solution are
sufficient. Instead of chloroform it is very convenient to use
ethyl acetate, which poss~ss~s nearly as wide a range of solvent
power, separates more easily from emulsion than chloroform, and
forms a layer lighter, not heavier, th.an. wat~r. Howev:er, for
alkaloids chloroform is the best solvent to u'se.
The various extracts are evaporated clther spontaneously or
at a gentle heat in porcelain dishes or on a porcelain tile having
a number of cup-shaped depressions. Before evaporation it is
advisable to run the extract through a small dry filter-paper in
order to remove traces of water. ./
The problem of detecting the organic poison which now con-
fronts the analyst is beset with difficulties, the chief being that,
CHEMICAL TOXICOLOGY 30 3
whether a poison is present or not, a yellowish to brown-coloured
smear of impurities is always left after evaporation, which may
react with such general alkaloidal reagents as phosphomolybdic
acid and have reducing properties. The impurities are derived
from the original organic material such as fats, carbohydrates
and proteins. If, however, an organic poison is present in fair
quantity, as, for instance, about 2 milligrammes or upwards, the
difficulty on account of such normal impurity is diminished.
Another difficulty is that in many cases characteristic or dis-
tinctive reactions are lacking, particularly in the case of bitter
principles and glycosides.
Purification.-It is theoretically easy to devise methods for
the purification of any special type of organic poison, but, in fact,
it is hard to carry out because the process is wasteful and, there-
fore, when dealing with a trace there is the risk of entirely losing
it. Thi$ happens very often. Thus, a residue may show a certain
reaction in an incomplete or masked fashion which cannot be
demonstrated again after further purification. This does not
necessarily mean that the substance is absent from the original
material, but it may point..,to the fact that it is present in such
small quantity that it is not the cause of poisoning. In this sense
such an observation is valuable.
Alkaloids which are strong bases may be purified by dissolving
the residue in a dilute acid (acetic or sulphuric) and shaking the
solution with solvents, which more or less fully remove adven-
titious impurities of a neutral, acid or feebly alkaline nature.
Thereafter the acid liquid is made alkaline and the organic base
again extracted, now in purer form. If, however, impurities are
still present, an attempt may be made to get rid of them by
precipitating the alkaloid from acid solution by adding Mayer's
reagent drop by drop until .precipitation is complete. The pre-
cipitate is collected, shaken up with hydrogen sulphide solution,
and the sulphides so formed removed by filtration. The filtrate
is then made alkaline and re-extracted with the solvent. Another
method is to treat the solution with lead acetate, which pre-
cipitates proteins and many other impurities. In the case of
alkaloids, the lead acetate solution is acidified with acetic acid,
but for glycosides basic lead acetate may be used. In either case,
the addition of the lead solution produces a precipitate which is
filtered off and the lead removed from the filtrate by bubbling
a current of hydrogen sulphide through it. On removal of the
VETERINARY TOXICOLOGY
precipitate by filtration, the filtrate is made alkaline and re-
extracted with the solvent.
The residue should be as' free from impurities as possible before
proceeding with the process of identification, so that purification
must be repeated until the residue is practically pure white in
colour. As this may entail' considerable loss, a portion of the
original material should always be kept in reserve.

General Reactions of the Organic Poisons.


There are certain reactions by means of which it may be decided
whether a substance is or is not an alkaloid or a glycoside.
Alkaloids.-A characteristic of alkaloids is that they are readily
precipitated by numerous reagents. The first procedure, there-
fore, is to make sure that an alkaloid is actually present by testing
a faintly acid solution of the material with a precipitating reagent,
and then, if positive results are obtained, to attempt to identify
the alkaloid by colour reactions or, if necessary, crystallisation
and melting-point determinations.
There are numerous substances which give precipitates with
alkaloids, those most generally u~ful being Sonnenschein's
phosphomolybdic reagent, Mayer's potassium mercuric iodide
reagent, Wagner's iodine in potassium iodide reagent,s per cent.
tannic acid, cold saturated aqueous solution of picric acid, and
z per cent. gold chloride solution. A trace of the material under
investigation is dissolved in a drop of dilute sulphuric acid and
placed in a watch-glass on a black under-surface. A drop of the
precipitant is then added and the formation of a precipitate
looked for. The precipitates given by phosphomolybdic acid are
pale to distinct yellow; by potassium mercuric iodide, b~own to
red; and by tannic acid, dirty white.
Colour tests are carried out by evaporating an alcoholic solution
of the material to dryness in a porcelain dish, and when cool
adding a few drops of the reagent. The reagents most generally
useful are concentrated sulphuric acid, fuming nitric acid, Frohde's
molybdic acid reagent, Mandelin's vanadic acid reagent, and
Marquis' formalin in sulphuric acid reagent. The formation of
coloured compounds with I per cent. ,8-naphthol or p-dimethyl-
amino-benzaldehyde in sulphuric acid may also be of assistance.
In this case, Bamford (I94o) recomwends that the tests be carried
out in capillary tubes, which are also used for crystallisation tests
and melting-point determinations.
CHEMICAL TOXICOLOGY
Glycosides.-These compounds are all characterised by yielding
sugars, usually glucose, on contact with mineral acids, and thereon
is based the Brunner-Pettenkofer test, which is a modification of
Pettenkofer's well-known bile' test. A solution of the suspected
substance is made in water along with a little ox-bile and placed
in a test-tube. Strong sulphuric acid is poured down the side of
the tube,; forming a heavy layer below the water-bile solution.
At the point of juncture there is developed a cherry-red colour
which gradually extends throughout the aqueous layer. Its
formation depends on the splitting off of sugar from the glyco-
sides, thus giving with sulphuric acid the bile reagent of Petten-
kofer's test.
The chief glycosides likely to be encountered are those from
digitalis, artemesia, strophanthus, squill, and hellebore, for the
identification of which reference should be made to the special
tests already described.
Saponins.-If the presence of a saponin is suspected, a few drops
of the .extract should be added to a suspension of washed red
blood corpuscles in normal saline and the development of hremo-
lysis looked for. Since other hremolytic substances may be present
in the extract, if hremolysis occurs the test should be repeated
after the addition of a trace of cholesterol, which inhibits the
hremolytic action of sapotoxins. If hremolysis still occurs, then it
is probable that sapotoxins are not responsible for the reaction.
Gadamer (1924) describes certain colour reactions given by
saponins, the most characteristic being a :r;-ed colour darkening
to reddish-violet on the addition of concentrated sulphuric acid,
and a bluish-violet colour changing to green on the addition of
Frohde's reagent.
There are no general reactions given by the other substances
belonging to this group, so that reference should be made to the
specific tests for these substances.
COLOUR REACTIONS OF CERTAIN ALKALOIDS.

Sulphuric
Acid. FroMe. Marquis. I Ma~delin. Benzalde-
hyde.
Vitali.

Aconitine - Colourless Colourless Colourless Colourless Colourless Colourless


Apomor- Colourless Green- Violet - Purple -
phine blue
Arecolin - Colourless Colourless Colourless Colourless Colourless Colourless
Atropine - - - - - - Violet
Brucine - Colourless Red- - - - Colourless
yellow
20
VETERINARY TOXICOLOGY
Sulphuric Benzalde-
Acid. Frohde. .Marquis Mandelin. hyde. Vitali.

ChlOlidonine Yellov.-
red-
Yellow-
green
- - - -
violet
Cocaine - Colourless Colo;"rless Colourless Colourless Colourless Colourless
Colchicine Yellow Yellow Orange Green- Yellow Brown-
brown violet
Coniine - Colourless Colourless Colourless Colourless Colourless Colourless
Curarine
Cytisine -
- - Brown - Violet -
Colourless, Orange
-
Orange Red- Orange Orange
orange yellow on
warming
Delphine Brown Brown Brown Brown- COlourless, Brown
violet green-
brown on
warming
Emetine - - Yellow-
. green
- Green - -
Ergotoxine Yellow- Violet- Black- Violet- Violet Brown
green green violet green
Eserine - - - - - - Orange-
green
Gelsemine - Colourless - Red-
violet
- -
Hydrastine - Yellow-
green
- Orange-
green
Colourless,
yellow on
-
warming
- -
-- - -
Hyoscine - Violet
Hyoscy-
amine
- - - - Violet
Lobeline - Colourless Colourless Red- - Colourless -
viOlet
Lupinine Colourless CQlourless CololIriess Colourless Colourless Colourless
Morphine - Colourless Red-
violet-
Violet - Purple -
green
Nicotine - - - - - Colourless,
blue-red-
-
violet on
warmi'lg
Papaverine - Colourless Yellow- Green Colourless -
red-
violet
Pilocarpine COlourless Colourlt'Ss Colourless Colourless Colourless, -
yellow-
pink on
warming
Solanine - Yellow- Green- Violet- Pink- Colourless, -
brown lilac brown_ violet red-brawn
green on warm- -
ing
Strychnine Colourless Colourless - Blue
violet
- -
red
Taxine - Red- Violet - - - -
violet
Veratrine - Yellow- Rcd- Yellow- Red- Colourless, Brown-
violet violet orange- violet green- red-
brown .violet on violet
warming
Yohimbine - Blue - Blue - -
CHEMICAL TOXICOLOGY 30 7
ALKALOIDAL PRECIPITANTS.
SONNENSCHEIN'S PHOSPHOMOLYBDIC ACID REAGENT.-Prepared by dissolving
sodium phosphomolybdate in ten times its weight of a mixture of I volume of
concentrated nitric acid sp. gr. I '42 with 9 volumes of water.
MAYER'S POTASSIUlII MERCURIC IODIDE REAGENT.-Prepared by dissolving
1'35 grammes mercuric chloride and 5 grammes potassium iodide separately in
water. Mix and add water to make 100 milliJitres.
WAGNER'S IODINE IN POTASSIUlII IODIDE REf.GENT.-Prepared by dissolving
10 grammes potassium iodide in 30 millilitres water. When dissolved add 5
grammes iodine and distilled water to make 100 millilitres.
PICRIC ACID.-Cold, saturated aqueous solution.
TANNIC ACID.-5 per cent. aqueous solution.
GOLD CHLORIDE.-2 per cent. solution.

ALKALOIDAL COLOUR REAGENTS.


FROHDE'S REAGENT.-Prepared by dissolving 0'05 gramme molybdic acid or
sodium molybdate in 10 millilitres cold, pure sulphuric acid. The solution should
be colourless, and should be freshly prepared.
MANDELIN'S REAGENT.-Prepared by dissolving I part of ammonium meta-
vanadate in 200 parts of pure, concentrated sulphuric acid.
MARQUIS' REAGENT.-Prepared by mixing 2 drops of formalin with 3 milli
litres pure concentrated sulphuric acid. The solution should be prepared as
required.
BENZALDEHYDE REAGENT.-Prepared by dissolving I gramme p-dimethyl-
aminobenzaldehyde in 100 miIIilitres absolute alcohol and adding 20 drops of
pure, concentrated sulphuric acid.
VITALI'S REAGENT.-Fuming nitric' acid evaporated to dryness, together with
the alkaloid. When cold, add a drop of alcoholic potash.
TUNMAN'S REAGENT.-Prepared by dissolving I gramme p-dimethylamino-
benzaldehyde in 100 millilitres of absolute alcohol and acidifying with o I millilitre
of concentrated sulphuric acid.

GROUP C.-HEAVY METALS AND METALLOIDS.


The common metallic poisons are arsenic, antimony, mercury,
bismuth and silver, lead, copper, zinc, chromium, iron, manganese,
magnesium, barium, tin, cadmium, thallium, fluorine and sele-
nium. Iron is always present, mainly from hcemoglobin.
It is unnecessary to make separate tests for each of these
metals, although, having detected one or more of them, it may be
necessary to make special extractions of the original material
for the purposes of estimation and to obtain a specimen. In any
case of suspected metallic poisoning, before proceeding with the
analysis the first step is to examine the stomach contents, pick
out any solid particles which may be present and submit them to
sublimation, for in this way the presence of arsenic may be
deteCted without great difficulty. A portion of the material should
then be submitted to a Reinsch test, for it can be expected to
reveal the presence of arsenic, antimony, bismuth, silver and
mercury, even in the presence of organic matter, and finally the
complete destruction of organic matter should be undertaken.
VETERINARY TOXICOLOGY
This may be done either by the method of Babo and Fresenius
or by means of nitric acid.
I. Reinsch Test.-The material under investigation is finely
divided and from IS to 200 grammes, according to circumstances,
boiled with dilute hydrochloric acid and pieces of pure copper
foil, approximately I square centimetre in size, in a clean flask
provided with.a reflux condenser. The concentration of the acid
in the mixture should not exceed 8 per cent., as otherwise there
is risk of a loss of arsenic as arsenious chloride by yolatilisation. It
is also important to remember that hydrochloric is the only suitable
acid, and that in the event of free chlorine, potassium chlorate,
nitric acid or nitrates being present, solution of the copper will
occur. In such cases the acid mixture must be gently warmed
until free of chlorine before putting in the copper. A blank test
should be carried out first of all by boiling the acid and copper
together for about thirty minutes in the apparatus to be used for
the test, when the copper should remain clean and bright.
If the material contains arsenic, antimony, bismuth, mercury
or silver, a dark greyish deposit appears on the pieces of copper.
These should be inspected from time to time, and if the deposit
is anyway heavy they should be removed from the flask, as
other'Rise there is a risk of solution of the copper with loss of the
deposit. Fresh pieces of foil are then added and the process con-
tinued until the formation of a deposit can no longer be detected.
On removal from the flask the pieces of foil are thoroughly
washed with water and absolute alcohol and carefully dried
between pieces of filter-paper without undue friction. If the
deposit is at all considerable, that of arsenic has. a steel-grey
appearance, of antimony purplish black, of bismuth black, and
of mercury and silver the silvery lustre of these metals. When
very small quantities are present a definite deposit of indistinct
greyish-black tint may alone be seen. Occasionally sulphur may
become deposited on the copper, so that the colour of the foil is
not sufficient evidence of the presence of the metals and sub-
limation tests must be carried out.
The pieces of copper foil are cut with a clean pair of scissors
into strips 2 millimetres in width and placed in .small sublimation
tubes about 8 centimetres long with flat sides. A portion of the
tube near the closed end is then gently heated in a small flame,
and when cool the tube is examined under the low power of
the microscope. If arsenic is present it volatilises, unites with
CHEMICAL TOXICOLOGY
oxygen, and is deposited on the sides of the tube as arsenious
oxide in the form of characteristic, glistening, octahedral crystals,
the test being sufficiently delicate to detect as little as a milli-
gramme or less of arsenic; antimony sublimes, leaving an
amorphous greyish~white deposit on the sides of the tube;
bismuth does not sublime, but becomes oxidised, leaving an
amorphous black deposit; mercury sublimes with the formation
of globules of the metal; and silver remains unchanged.
The Reinsch test may not be successful if the metals are
present in the original material as insoluble sulphides, which is
likely to be the case if there has been prolonged putrefaction,
and it may also fail to detect the presence of organic compounds
of arsenic.
2. l\'1ethod of Babo and Fresenius.-A weighed sample of the
material is cut into small pieces if necessary, mixed with 2 parts
of dilute hydrochloric acid, and I gramme of powdered potassium
chlorate added for everv roo millilitres taken. The mixture is
J

then heated on a vigorously boiling water-bath, the nascent


chlorine th~s liberated bringing about the destructive oxidation
of the organic matter. If the liberation of free chlorine cannot be
'detected before liquefaction is complete, more potassium chlorate
in the form of pellets must be added and the process continued
until the organic matter with the possible exception of a certain
amount of fat has been completely oxidised. This usually requires
several hours, when the mixture is allowed to cool and is filtered.
The residue after washing several times with hot water may be
discarded, as silver chloride is the only insoluble metallic salt
it is likely to contain.
The excess of chlorine in the clear yellowish filtrate is removed
by the addition of sodium sulphate, which reduces the chlorine
to hydrochloric acid, and the excess of sulphur dioxide is removed
by bubbling a current of air through the warmed filtrate.
The next step is to precipitate any metals which may be
present as sulphides by bubbling a stream of hydrogen sulphide
through the filtrate. Here the great difficulty is to obtain hydrogen
sulphide free from arsenic, as nearly all the metallic sulphides
used for its generation contain traces of this substance. Numerous
methods have been suggested to overcome this difficulty.
Bamford (I940) recommqnds the preparation of a solution of mag-
nesium hydrogen sulphide, which will yield pure hydrogen sulphide
on heating. This is effected by treating commercial iron sulphide
3 10 VETERINARY TOXICOLOGY
with hydrochloric acid in a Kipp apparatus and allowing the gas
to bubble into a suspension of magnesium oxide until the liquid
is completely saturated. The solution is allowed to stand and is
then decanted off from any unchanged magnesium oxide. On
heating, pure hydrogen sulphide is given off with regeneration
of magnesium oxide when the boiling point is reached.
Pure: hydrogen sulphide is allowed to bubble through the
filtrate obtained as described above until it is completely saturated
with the gas and the precipitate which forms is filtered off. In
order that precipitation may be complete, the filtrate is placed
in stoppered bottles and allowed to stand overnight, again
saturated with hydrogen sulphide, filtered, and the process
repeated until no further precipitate forms on the addition of
hydrogen sulphide.
The precipitate is collected, but as it may still be contaminated
with organic matter further purification is necessary. This is
effected by dissolving the pre.cipitate in dilute hydrochloric acid,
adding a few drops of bromine, and heating on a water-bath until
the remaining organic matter is destroyed, any exces.s of bromine
being removed by reduction with a few drops of stannous chloride.
The solution is then filtered and made up to a definite volume,
aliquot portions of it being taken for the special tests.
3. Nitric Acid Digestion.-A suitable quantity of the material,
from I to 4 ounces, is mixed in a porcelain dish, with 50 per cent.
nitric acid, to a thin paste, and about I to 2 c.c. of strong sul-
phuric acid added. The mixture is then warmed over a small
flame with constant stirring. A violent reaction, accompanied
by the evolution of brown oxides of nitrogen, sets in, and the
operation must be conducted in a proper fume chamber. After
from twenty minutes to half an hour's heating the liquid will be
nearly all evaporated, and will have a.brown colour and pasty
consistency. No organic tissue remains, but fats are not com-
pletely destroyed. If heating is continued, the mass suddenly
carbonises with some violence. There' is ~ slight risk of loss if this
occurs, but it is not a fatal objection. After carbonisation, which
is unnecessary, the solutions are more d~eply coloured, but the
analysis is not hindered,
The heated mass is diluted with water, about 100 to 150 mI.,
stirred well to disintegrate solid fatty matter, allowed to cool
thoroughly, filtered, and the fatty residue waJhed with water.
T4~ _pale yellow liquid now contains all the poisonous metals,
CHEMICAL TOXICOLOGY 3I I
except barium, whose sulphate is insoluble in dilute nitric acid.
1 barium is to be looked for, the sulphuric acid must be
omitted, in which case the metal is in solution along with the
others.
The acid solution is now made strongly alkaline with ammonia,
whereby the colour changes to dark brown, and pure sulphuretted
hydrogen bubbled into the warm liquid. A little yellow ammonium
sulphide is added, and the liquid is filtered. The precipitate may
contain sulphur, sulphides of lead, mercury, silver (bismuth),
copper, zinc, manganese, and iron; phosphates of calcium and
magnesium, and phosphate or hydroxide of chromium. Arsenic
and antimony sulphides are soluble in ammonium sulphide, as
also is organic matter. After washing the precipitate, it is there-
fore free from organic impurities, and may be dealt with according
to the ordinary methods of qualitative analysis.
Iron in the form of black ferrous sulphide, sulphur, and phos-
phates (chiefly of calcium), are always present, and the other
compounds named above may also be in the precipitate.
By passing hot dilu.te hydrochloric acid repeatedly thr.ough
the filter, there are dissolved iron, phosphates, chromium, zinc,
manganese, and lead. When, however, lead sulphide is present
in considerable quantity, the sparingly soluble lead chloride forms
needle-shaped colourless crystals on the paper and in the filtrate.
Dilute hydrochloric acid also dissolves traces of copper and
bismuth.
The dilute hydrochloric acid solution is concentrated until
nearly all the free acid has been volatilised, the liquid diluted, and
sulphuretted hydrogen solution added. Leac;l is precipitated as
black sulphide, but with small quantities of the order of rrh grain
a yellow to brown coloration only is produced. In order further
to characterise it, and to distinguish from copper and bismuth,
the precipitate is collected on a small filter, washed, dissolved in
the minimum amount of dilute nitric acid, most of the acid
evaporated off, and a small crystal of potassium iodide added.
This gives with lead yellow lead iodide,.as an amorphous powder,
dissolving on boiling to a colourless solution, which, on cooling,
deposits yellow spangles of lead iodide, which ~re so characteristic
that their formation is the best test for lead.
Having removed lead as the sulphide, the liquid is evaporated
till free of sulphuretted hydrogen, oxidised by heating with a few
drops of strong nitric acid, and ammonium hydrate added in
312 VETERINARY TOXICOLOGY
excess. The precipitate always formed contains brown ferric
hydroxide and phosphates. If the phosphate is in excess, the pre-
cipitate is pale yellow, and a few drops of ferric chloride must be
added before the ammonia.' In addition to these the precipi~ate
may contain chromium hydroxide, known by its green colour.
The filtrate is tested for zinc and manganese by adding ammonium
sulphide, which gives colourless zinc sulphide and buff-coloured
manganese sulphide as precipitates.
The residue left after treatment with hydrochloric acid may
contain free sulphur, and the black sulphides of mercury, bismuth,
copper, and silver. It is to be noted that silver, mercury, and
bismuth will have been found in the Reinsch test.
Hot dilute nitric acid dissolves the silver, bismuth, and copper.
If copper is present in significant amount, the solution will be of
a pale, greenish-blue colour. Silver is recognised by adding dilute
hydrochloric acid, which precipitates colourless silver chloride.
Ammonium hydrate is now added, and precipitates bismuth
hydroxide as a colourless flocculent precipitate. The solution is
filtered, and the bismuth precipitate washed and dissolved in the
minimum quantity of hydrochloric acid. On adding the chloride
solution to water, an opalescent turbidity of bismuth oxychloride
is produced. The ammoniacal filtrate containing the copper will
have a more or less deep, pure blue colour, according to the
quantity of copper. It is made acid with acetic acid and potassium
ferrocyanide added. This gives a reddish-brown coloration with
traces of copper, and a reddish-brown precipitate with larger
amounts, and is a more delicate test than the blue aJ;l1monia
coloration.
The nitric acid leaves undissolved mercury. This is then dis-
solved in hydrochloric-acid with the addition of a little potassium
chlorate, and after boiling off the chlorine is tested by Reinsch's
test with copper, or by adding stannous chloride solution-; which
precipitates insoluble mercurous chloride (calomel), and on warm-
ing converts this into mercury as a black deposit of finely divided
metal.
The table opposite summarises the operations set forth
above. .
The delicacy of the method is amply sufficient for toxicological
purposes, and even for the recognition of traces which can hardly
have medico-legal interest. Thus t10u grain of lead can be separated
and recognised by ~ulphuretted hydrogen when originally con-
CHEl\JICAL TOXICOLOGY 3I3
31 4 VETERINARY TOXICOLOGY
tained in 2 ounces of organic matter. With this amount of
organic matter a positive reaction for lead may be anticipated
with certainty. For mercury a proportion of -S-fm- grain in 2 ounces
can sometimes be recognised, at others not-that is, the figure
quoted is an extreme lower limit. The limit for copper is r-60 grain,
and that for zinc if]O grain, each in 2 ounces. The same figures
apply to the detection of these metals when all the organic matter
is burnt off by heating with strong sulphuric acid.

GROUP D.-ACIDS, ALKALIS AND ALKALINE SALTS.


It is not possible to give a single comprehensive scheme for the
detection of the various acids, alkalis and soluble salts comprised
under this heading. An excellent method of separation for soluble
compounds of this class is afforded by dialysis throug~ a parch-
ment membrane or, failing this, a sausage-skin. The material
under examination is made into a thin paste with water and
placed in the membrane, which is then immersed in a narrow
cylinder of distilled water. The crystalloids pass through the
membrane into the surrounding water, whilst the colloids do not
so diffuse or only extremely slowly. The dialysate is removed from
time to time, fresh water being added as required.
Acids, bases and soluble salts are thus obtained in a fairly pure
watery solution. Sometimes, however, it is sufficient to dilute the
material and filter, but the filtration is often very slow and dis-
solved proteins are not removed. The subsequent handling of the
filtrate depends on the nature of the substances to be looked for,
but as a rule there is no difficulty in separating and identifying
them by means pi crystallisation, neutralisation, precipitation, etc.
Acids.-It must be 'remembered that the stomach contents
are normally acid from the presence of free hydrochloric acid, and
also that organic acids may be present in considerable quantity,
so that the amount of fre-e hydrochloric acid present may have to
be determined, and also it is necessary to distinguish mineral
from organic acids. - -
The watery extract of the material prepared as described above
is first tested with Congo red paper, which turns blue in the
presence of mineral acids, but purplish in the presence of organic
acids. Methyl violet, which turns green in the presence of mineral
acids, may also be used. Another useful reagent is neutral ferric
acetate. This, w.h~n added to a solution of potassium or ammonium
CHEMICAL TOXICOLOGY
thiocyanate, scarcely shows the red colour of the acetate, but
when a mineral acid is added the non-ionised ferric acetate yields
the ionised ferric salt of the acid, which gives a blood-red colora-
tion with the thiocyanate. Similarly, neutral ferric acetate, starch
solution, and potassium iodide show no blue coloration, but the
addition of a mineral acid produces the ferric ion which liberates
iodine from the potassium iodide with the formation of the blue
iodide of starch. Giinzberg's reagent, prepared by dissolving
2 grammes of phloroglucinol and r gramme of vanillin in roo
millilitres of 95 per cent. ethyl alcohol, is also useful to differentiate
between mineral and organic acids, for no coloration is produced
with the latter, but a purplish-red colour indicates the presence
of sulphuric or hydrochloric acid and a reddish-yellow colour
the presence of nitric acid. The test is carried out by evaporating
a few drops of the reagent to dryness in a porcelain dish and
drawing a clean glass rod moistened with the extract through the
residue. The mixture is then gently warmed, when, if a mineral
acid is present, the appropriate colour will be seen.
Having demonstrated the presence of a mineral acid, it is then
necessary to employ the special tests to determine the nature and
amount of acid .present. .
Alkalis and Alkaline Salts.-It must be remem:bered in this case
also that the ruminal and intestinal contents are normally
alkaline and contain alkaline salts, so that the presence of an
hydroxide or carbonate must be demonstrated. Moreover, if
. putrefaction has occurred, the watery extract will be alkaline
from the presence of ammonia.
A watery extract of the material is prepared as before, and its
reaction to litmus and phenolphthalein determined. Excess of
barium chloride" and a few drops of phenolphthalein are then
added to a portion of the extract, and if a carbonate is present
a precipitate of barium carbonate is formed, and the solution
becomes colourless; but if the alkalinity is due to the presence
of hydroxide, the red colour of the indicator remains unchanged.
As potassium and sodium hydroxides are soluble -in alcohol, a
portion of the extract should be extracted with alcohol, thus
making- it possible to separate hydroxid~s from carbonates.
The presence of ammonia may be recognised by smell or by
warming some of the extract and a little sodium hydroxide in a
flask and noting if white fumes appear when a glass rod moistened
with hydrochloric acid is held in the mouth of the flask. If
316 VETERINARY TOXICOLOGY
ammonia appears to be in excess, the amount should be deter-
mined by titration with standard hydrochloric acid and tests
made for ammonium salts.
REFERENCES.
Autenreith, W. (1928), Laboratory Manual for the Detection of P<?isons,
6th ed.
Bamford, H. F. (1940), Poisons, their Isolation and Identification.
Gadamer, J. (1924), Lehrbuch der Chemischen Toxikologie.
Glaister, J. (1942), Medical Jurisprudence and Toxicology, 7th ed.
Smith, S. (1943), Forensic Medicine, 8th ed.
Smith, S., and Cook, W. G. H. (1934), Taylor's Principles and Practice of
Medical Jurisprudence, 9th ed.

PTOMAINES.
Ptomaines (cadaveric or corpse alkaloids)' may be defined as
nitrogenous organic bases produced during the decomposition of
animal matter largely as a result of bacterial action, the nature
of the bases depending on the duration and type of putrefaction
-i.e., whether aerobic or anaerobic. Most are formed during the
earlier stages of decay, but later they pass into simpler or more
stable and harmless compounds. Since they appear in alcoholic
extracts made from putrefying material, give precipitates with
the common alkaloidal reagents and may produce toxic symptoms
of convulsions, paralysis and death when injected into the
animal body, the possible presence of ptomaines very naturally
complicates the task of alkaloid detection, particularly as some
of them simulate the reactions given by such alkaloids as coniine,
strychnine, morphine, colchicine, etc. Indeed, some observers
have called them corpse coniine, corpse strychnine, etc. In no
case, however, do the properties of these bases entirely coincide
with the alkaloids, and it is the rule that some one or more of the
specific tests for a vegetable alkaloid are not given by the ptomaine.
Physiological tests also help to distinguish ptQmaines from
alkaloids, as it has been conclusively proved that extracts con-
taining ptomaines have no effect on the cat's eye unless a mydriatic
alkaloid is also present. In addition, most .of the ptomaines are
soluble in water, sothat if the Stas-Ottq. process is strictly fol-
lowed, all precautions taken during the process of purification and
the special tests for alkaloids rigidJy carried out, no mistake need
be made.
In many cases the ptomaihes are relatively simple compounds
CHEMICAL TOXICOLOGY 3I 7
such as methylamine; some are liquids of low boiling point such
as di- and trimethylamine, ethylamine, diethylamine and normal
and iso-propylamine; and some are crystalline bodies such as
putrescine (tetramethylene diamine), cadaverine (pentamethy-
lene-diamine), choline (hydroxyethyl trimethyl-ammonium hy-
droxide), and substances related to choline such as choline-
muscarine and neurine. Neuridine (C 5H 14N 2) is the commonest
base present, but is non-toxic. It has been shown that basic
'substances resembling ptomaines may also be obtained from the
living animal; these have been called leucomaines to distinguish
them from the ptomaines.
Ptomaine Poisoning.-Although certain ptomaines may give
rise to serious effects when injected into the animal body, they
are comparatively harmless when taken by the mouth, so that they
are not responsible for the so-called "ptomaine poisoning." This
is usually the result of eating food contaminated with pathogenic
organisms, and it is the toxins produced by the bacteria which are
responsible for producing the symptoms. The Salmonella group
are the organisms usually involved, the best known of these being
Gartner's bacillus, B. suipestifer, B. aertrycke, and B. paratyphosis,
which all produce thermostabile toxins. B. bot1tlinus, a toxin-
producing, spore-bearing anaerobe, has also been responsible for
a large number of deaths. It follows, therefore, that in any case
of suspected ptomaine poisoning the presence of these bacteria
or their toxins must first be excluded. In the case of brine poison-
ing, the base trimethylamine may be present in considerable
quantity, and it has been held responsible for producing the
toxic symptoms.
REFERENCE.
Steyn, G. D. (1935), OndersterpoortJ. Vet. Sci., 5, 139.
INDEX
ABRIN,282 Ammonia, chemical diagnosis of, 77
Abrus precatorius, 282 effects of, 76
Absinthe, oil of, 139, 237 forms of, 75
Absorption, 6 poisoning, post-mortem, 77
by alimentary tract, 8 symptoms of, 76
by lungs, 7 treatment of, 77
by skin, 7 toxic doses of, 76
mechanism of, 9 Amygdalin, 104
of gases, 6 A mygdalus species, 224
of insoluble solids, 6 Anagallis arvensis, 245
of poisons, 6 Analysis, apparatus for, 294
of soluble solids, 6 preliminary observations in, 292
Accumulation, 13 qualitative, 295
Acetylcholine, 183 quantitative, 295
Acids, detection of, 79 toxicological, 292
poisoning by, 78 A namirta paniculata, 138
Acocanthera species, 246 Andromeda floribunda, 243
Aconite poisoning, post-mortem, 187 Andromedotoxin, 243
symptoms of, 187 A nem01le species, 199
treatment of, 188 Anemonin, 195
Aconitic acid, 179 Animal oil, II6
Aconitine, 185 Antimony, actions oI, 42
detection of, 188 chemical diagnosis of, 43
Aconitum species, 185 forms of, 41
Acorn disease, 288 poisoning, treatment of, 43
Acttea spicata, 200 Apatite, 99
Actinea odorata. 237 Apoatropine, 251
Acute poisoning, 20 Apocynacete, 245
Adenia digitata, 283 Apocynin, 245
Adonis species, 200 Apocynum species, 245
lEthusa cynapium, 235 Apomorphine, 128
Agaric, fly, 132 Apple, bitter, 224
Agaricus muscarius, 132 thorn, 256
Agrostemma githago, 207 Aquilegia species, 200
Alcohol, chemical diagnosis of, 148 Aracete, 163
occurrence of, 147 A raliacete, 236
poisoning, 147 Arenaria species, 207
toxic doses of, 148 Argyria, 63 .
Alkali disease, 91 Aristolchia species, 272
Alkalis, caustic, 78 Aristolchine, 272
detection of, 79 Arrow grass, 175
effects of, 78 Arsenic, absorption of, "33
Alkaloids, cadaveric, 316 chemical diagnosis of, 37
corpse, 316 elimination of, 34
reactions of, 304 forms of, 28
separation of, 300 toleration of, 33
All-heal, 236 toxic doses of, 33
Allium sativum, 204 toxicity of, 31
Almonds, bitter, 104 Arsenical poisoning, acute, 35
Aloe chinensis, 214 chronic, 35
Alpine laurel, 242 diagnosis of, 34
Alsike clover, 210 post-mortem, 36
Amaryllidacete, 166 symptoms of, 34
Amaryllis belladonna, 166 treatment of, 37
American nightshade, 271 Artemesia species_,.. 139, 237
American worm-seed, 144 Arum species, 163
3 1B
INDEX 31 9
Ascaridol, 144 Bread poisoning, 239
Asclepiadacece, 249 Brewer's grains, 287
Asclepias species, 249 Brine poisoning, 82
Ash, 244 Bromates, 96
Aspergillosis, 185 Bromides, effects of, 97
Aspergillus, 180 Bromine, 95
Aspidium filix-mas, 289 Bromism, 98
Asses' parsley, 235 Bromus, 175
Astragalus species, 92 Brooms, 216
Atamasco lily, 166 Brucine, 118
Atiscema eriphyllum, 163 Brunner-Pettenkofer test, 305
Atractylis gummifera, 237 Brunswick green, 29
Atropa belladonna, 252 Bryonia dioica, 224
Atropine, 251 Bryonin, 224
detection of, 254 Bryony, black, 167
effects of, 252 white, 224
Autumn crocus, 169 Buckthorn, 214
Azadirachta indica, 212 Buckwheat, 210
Azalea, 242 Bunch flower, 169
Burnett's fluid, 60
Babo and Fresenius, method of, 309 Burning, bush, 212
Baneberry, 200 Buphane disticha, 166
Barium, chemical diagnosis of, 69 Buphanine, 166
forms of, 67 Buttercup, 194
poisoning, post-mortem, 68 Buxine, 279
symptoms of, 68 Buxus sempervirens, 279
treatment of, 68
toxic doses of, 68 Cacao, husks, 286
Bastard lentil, 221 meal,286
Bay, dwarf, 273 Calabar bean, 130
Bear's foot, 188 Calfkill, 243
Beaver poison, 231 Calla palustris, 163
Beech-nut cake, 287 Calomel,52
Beet-pulp, 287 Caltha species, 200
Belladonnine, 251 Cama, death, 168
Benzaldehyde reagent, 307 Campanulacece, 241
Berg slangkop, 173 Camphor, 140
Beta vulgaris, 287 Canadian hemp, 245
Bindweed, 250 Cannabis indica, 138
Bish, 187 Cantharides, 149
Bitter almonds, oil of, 104 detection of, 150
Bitter apple, 224 Cantharidine, 149
Bitter rubber-weed, 237 Cantharis vesicatoria, 149
Bitter-sweet, climbing, 212 Cape slangkop, 173
Bitter vetch, 221 Caprifoliacece, 236
Black bryony, 167 Carbolic acid, II2
Black cherry, 252 chemical diagnosis of, II 7
Black hellebore, 188 poisoning. post-mortem, 116
Bleaching powder, 96 symptoms of, 1 14
Blind staggers, 91 treatment of. Il7
Blister-fly, 149 toxicity of, Il3
Blou tulp, 165 Carbon monoxide, 102
Bluestone, 56 absorption of, 103
BlJle vitriol, 56 poisoning, post-mortem, 103
Bone oil, u6 treatment of, 103
Bordeaux mixture, 56 toxicity of, 102
Botrytis, 180 Carbon tetrachloride, absorption of, 151
Box, 279 chemical diagnosis of, 153
Bracken poisoning, 289 poisoning, post-mortem, 153
Branch ivy, 243 symptoms of, 153
Brassica species, 204 treatment of, 153
3:20 VETERINARY TOXICOLOGY
Carbon tetrachloride, toxic dose of. Cocculus indicus, 138
15 1 Cochlearia armoracia, 204
Carrot, wild, 235 Codeine, 124
Caryophyllacem, 207 Coffee tree, 221
Cascara sagrada, 214 Coke effluents, lI3
Castor-oil bean, 279 Colchiceine, 1(/9
Causes of poisoning, 18 Colchicine, 169
Caustic, lunar, 63 Colchicttm autttmnale, 169
potash, 78 Colocynth,224
soda, 78 Colocynthin, 224
Celandine, greater, 202 Columbine, 200
lesser, 194 Common salt, chemical diagnosis of, 84
Celastracem, 212 poisoning, post-mortem, 83
Celastrus scandens, 212 symptoms of, 82
Celery-leaved crowfoot, 194 treatment of, 84
Cephaeline, 133 toxic dose of, 82
Cephaelis ipecacuanha, 133 Compositm, 237
Cerbera species, 24 6 Conhydrine; 229
Cestrum species, 251 Coniceine, 229
Cevadine, 135 Conijerm, 159
Chmrophyllum sylvestre, 235 Coniine, 229
Charlock, 204 Conium maculatum, 227
Chelerythrine, 202 Convallamarin, 171
Chelidonine, 202 Convallaria majalis, 171
Chelidonium majus, 202 Convallarin, 171
Chemical toxicology, 292 ConvolvulacetE, 249
Chenopodium, oil of, 144 Convolvulin, 249
Cherry laurel, 104 Convolvulus species, 249
Cherry, wild black, 104 Cooper's dip, 31
Chervil, wild, 235 Copper, absorption and elimination of,
Chile saltpetre, 87 57
Chile soap bark, 208 chemical diagnosis of, 59
Chinese blister-fly, 149 effects of, 57
Chinese umbrella-tree, 2J2 poisoning, acute, 58
Chinkerinchee, 173 chronic, 58
Chinosol, lI5 post-mortem, 58
Chlorates, 84, 96 treatment of, 59
Chlorine, 95 preparations of, 56
Christmas rose, 188 Copperas, 71
Chromates, 69 Corn-cockle, 207
Chromic acid, 69 Corn crowfoot, 194'
Chromium, chemical diagnosis of, 70 Corn-stalk disease, 175
preparations of, 69 Coronilla, 215
Chronic poisoning, 20 Corrosive sublimate, 52
Chrosperma muscmtoxicum, 169 Corrosives, 78
Chrysocoma tenuifolia, 238 Coryanthe yohimbi, 137
Cicuta species, 230 Cotton cake, 284
poisoning by, 232 seed meal, 284 .
Cicutoxin, 232 Cotyledon species, 227
Citrullus colocynthis, 224 Cotyledontoxin, 227 .
Claviceps purpurea, 180 , Coumarin, 222
Clematis vitalba, 199 Coumarinic acid, 222
Climbing bitter-sweet, 212 Cowbane, ~30
Clover, alsike, 210 Cow-cress, 235
red, 210 Cow par9Jlip, 235
sweet, 222 Cow wheat, purple, 270
Coca plant, 129 Crab's eye, 282
Cocaine, 129 Cramp sickness, 249
chemical diagnosis of, 130, Crassulacem, 226
poisoning, 129 Creeping buttercup, 194
toxic doses of, 129 CTeolin, 112
INDEX 3 21
Creosote dips, 112 Digitoxigenin, 267
Cresol, II2 Digitoxin, 265
Cresylic acid, 1I2 Dimorphotheca species, 104, 238
Crotalaria species, 221 Dioscoridacet:B, 167
Crotin, 280 Dipsacet:B, 236
Croton tiglium, 280 Diseased forage, poisoning by, 180
Crowfoot, celery-leaved, 194 Distiller's grains, 287
corn, 194 Distribution of poisons, 13
meadow, 194 Dodder, poisoning by, 250
Crow soap, 207 Dog's mercury, 277
Crudfert:B, 204 Donovan's solution, 29
Cryolite, 99 Dronk grass, 178
Cuckoo-pint, 163 Drooping tulip, 171
Cucumber, squirting, 224 Dropwort, water, 233
wild,224 Dwarf bay, 273
Cucttmis africanus, 224
Cucurbitacet:B, 224 Easton syrup, 120
Curarine, 136 Ecballium elaterium, 224
Cuscuta species, 250 Egg plant, 251
Cyanide poisomng, See Hydrocyanic Ela.terin, 224
acid EI darmous, 99
potassium, 106 Elder, common, 236
Cyanogenetic glycosides, 104 dwarf,236
Cyclamen europt:Bum, 245 Elimination of poisons, 14
Cyclamin, 245 Emerald green, 29
Cymarin, 246 Emetine, 133
Cynanchum species, 249 Emodin, 214
Cytisine, 215 Emulsin, 104
Cytisus laburnum, 215 Endocladium temulentum, 177
scoparius, 214 Equisetacet:B, 178
Equisetum 'species, 178
Daffodil, chequered, 171 Eragrostis cilianensis, 178
common, 166 Ergocristine, 183
Daphne species, 273 Ergocristinine, 183
Darmous, EI, 99 Ergometrine, 183
Darnel, 175 Ergosine, 183
Datura species, 256 Ergosinine, 183
Daturine, 257 Ergot of rye', chemical diagnosis of,
Daucus carota, 235 18 3 --
Deadly nightshade, 252 poisoning, 180
poisoning by, 252 symptoms, 183
Death camas, 168 Ergotamine, 183
Definition of a poison, 2 Ergotaminine, 183
Delphinine, 192 Ergotinine, 183
Delphinium, alkaloids of, 192 Ergotism, 181
detection of, 192 Ergotoxine, 183
poisoning by, 192 ErzcaceCE, 242
species, 192 Ericolin, 243
Delphinoidine, 192 Ervum ervilia, 221
Delphisine, 192 Erythrophlein, 221
Devil's bit, 236 Erythrophleum species, 221
Devil's thorn, 210 Erythroxylon coca, 129
Dhurrin, 175 Eserine, chemical diagnosis of, 131
Diagnosis of poisoning, 20 poisoning, post-mortem, 131
Dicoumarin, 222 symptoms of, 131
Digitaligenin, 265 treatment of, 131
Digitalin, 265 Essential oils, 140
Digitalinum verum, 265 Euonymin, 214
Digitalis, detection of, ;Z69 Euonymus europt:Btts, 212
effects of, 267 Eupato'Yium urtict:Bfolit!m, 237
Digitalts pU'Ypu'Yea, 265 Euphorbia spec1es, 276
.21
322 VETERINARY TOXICOLOGY
EuphorbiaceC8, 276 Gutzeit test, 40
Euphorbin, 277 Gymnocladus dioica, 221
Gyrotheca capitata, 165
Fagopyrum esculentum, 210
Fagus sylvatica, 287 HcemodoraceC8, 165
False hellebore, 135, 168 Halogen compounds, detection of, 97
Fern, poisoning by, 289 elements, 95
Figwort, 269 Hankin's test, 130
Filic acid, 289 Haricot de lime, 105
Flax, 105 Hedera helix, 236
Fluorine, chemical diagnosis of, 102 Hedge hyssop, 270
forms of, 99 Hedge pink, 207
poisop.ing, post-mortem, 101 Helenium species, 237
symptoms of, 101 Hellebore, black, 188
treatment of, 101 false, 168
toxic dose of, 100 green, 168
Fluorosis, 99 poisoning, 191
Fluorspar, 99 toxic doses of, 190
Fly agaric~ 132 white, 168
Fly poison, 169 HeUeborein, 190
Fool's parsley, 235 Helleborin, 190
Forage, diseased, 180 Helleborus species, 188
Fowler'S solution, 29 Hemlock, 227
Foxglove, 265 gIound,159
Fraxinus, 244 poison, 159
Fritillaria species, 171 poisoning, 229
Fritillary, 171 spotted, 227
Frohde's reagent, 307 water, 230
Henbane, black, 254
Gaddur,99 poisoning, 254
Galanthus, 166 Heracleum sphond,ylium, 235
Gamboge, 224 Herb Christopher, 200
Garget, 271 Herb Paris, 171
Geeldipkop, 210 Hogweed, 235
Geigeria species, 238 Holcus lanatus, 175
Gelsemicine, 134 Homeria species, 165
Gelsemine, 134 HOlllochelidonine, 202
Gelsemium sempervirens, 134 Horned poppy, 204
GeraniaceC8, 141 Horse-radish poisoning, 204
Gerrard's test, 256 Horsetail, 178
Gitoxigenin, 267 Hydrochloric acid, 78
Gitoxin, 265 Hydrocyanic acid, 104 .
Glaucium luteum, 204 absorption of, 108
Glycosides, reactions of, 305 chemical diagnosis of, 110
Golden rod, 237 elimination of, 108
Gossypol, 284 poisoning, post-mortem, I09
Goulard's solution, 44 sYlllptoms of, 108
Gourds, 224 treatlllenj; of, 109
GraminC8, 174 Hydroxy-Iupanine, -217
Gratiola officinalis, 270 Hyoscine, 251
Gratiolin, 270 Hyoscyamine, 251
Great mullein, 269 Hyoscyamus species, 254
Green hellebore, 188 poisoning by, 254
Green vitriol, 71 Hypericacece, 210
Griess-Ilosvay test, 89 Hypericum perjoratum, 210
Groot tulp, 165 Hypericum -red,- 210
Ground hemlock, 159 Hyssop, hedge, 270
Groundsel,238
Guaiacol, 1I2 Icterogenin, 21if
Guinea corn, 174 Idiosyncrasy, 15
Giinzberg's reagent, 315 Imperialine, 171
INDEX
Indian corn, 175 Lead, absorption and elimination of, 44
hemp, 138 chemical diagnosis of, 5 I
millet, 174 forms of, 44
pea, 218 metallic, 44
tobacco, 242 poisoning, acute, 47
Inkberry bush, 251 chronic, 49
Inorganic poisons, 4, 28 post-mortem, 50
Iodates, 96 sub-acute, 48
Iodine, 95 symptoms of, 47
Iodism, 97 treatment of, 50
Iotioform, 98 solubility in water, 44
Ipecacuanha, effects of, 133 toxic dose of, 47
IridacctlJ, 164 Ledum species, 243
Iridin, 164 LeguminostlJ, 214
Iris species, 164 Lentil, bastard, 221
Iron, perchloride, 71 Leptandrin, 224
Irritants, 16 Lesser celandine, 194
Isle of Wight vine, 167 Lettuce, wild, 237
Ivy, effects of, 236 Leucocrinum montanum, 169
Ivy linaria, 270 Leucomaines, 317
Izal, lIS Leucophenathiazone, 155
LeucothtlJ species, 243
Leucothionol, ISS
Jaagskiekte, 221 Levant nut, 138
Jacobine, 239 Ligustrin, 244
Jalap, 224' Ligustrt,m vulgare, 244
Jalapin, 249 LiliacetlJ, 168
Jasmine, yellow, 134 Lily, atamasco, 166
Jatropha curcas, 280 Lily of the valley, 171
Java bean, 104 LinacetlJ, 105
J equirity pea, 282 Linamarin, 104, 238
Jervine, 135 Linaria species, 270
Jeye's fluid, II6 Linarin, 270
Jimson weed, 256 Linseed cake, 106
Johnson grass, 174 Linum species, 105
JuncaginacetlJ, 175 Lippia rehmanni, 210
Juniperus species, 141 Lithopone, 44
Liver, protective action of, 13
Lobelia, acrid, 241
Kalmia species, 242 poisoning by, 242
Kaner, 246
Karabi,246 species, 241
Karabin, 246 Lobeline, 242
Keller's test, 269 Locoism, 91
Kermes mineral, 41 Locust tree, 282
King-cup, 200 LoganiacetlJ, II8
Lolium pere1lne, 175
Kombe,246 Lolium temulentum, 175
Krempziekte, 249 poisoning, symptoms, 177
toxic doses of, 176
Laburnum, alkaloids of, 215 Lords and ladies, 163
detection of, 216 Lousewort, 270
poisoning by, 215 Lucerne, wild, 221
Lactuca species, 237 Lunar caustic, 63
Ladies' seal, 167 Lupanine, 217
Lambkill, 242 l.upines, poisoning by, 217
Laplove, 250 Lupinidine, 217
Lathyrism, post-mortem, 220 Lupinine, 217
symptoms of, 219 Lupinosis, 217
Lathyrus species, 218 Lychnis githargo, 207
Laurel, alpine, 242 Lycorine, 166
cherry, 109 Lysol,112
324 VETERINARY TOXICOLOGY
Maize, 105, 175 Morphine, absorption of, 125
Male fern, poisoning by, 289 chemical diagnosis of, 128
Mandalin's reagent, 307 elimination of, 125
Mandragora officinalis, 258 poisoning, post-mortem, 127
Mandragorine, 258 symptoms of, 125
Mandrake. 258 treatment of, 127
Marquis' reagent, 307 toxic dose of, 125
Marsh marigold, 200 Moulds, poisoning by, 180
Marsh test, 38 Mucor, 180
Matricaria species, 238 Mullein, great, 269
Mayer'~ reagent, 307 Muscarine,S, 132
Meadow rue, 199 Mustard, black, 204
Meadow saffron, 169 oil of, 204
Mealie, 175 poisoning, 204
Meconic acid, 128 white, 204
Medicago denticulata, 210 Mutter pea, 218
Melampyrum arvense, 270 Myrosin, 204
Melanthium species, 169 Mylabris, 149
Melia azedarach, 212
Melia decumbens, 178 Narceine, 124
Meliace~, 212 Narcissus species, 166
M elilotus species, 222 Narcotine, 1"24
Mercurial poisoning, post-mortem, 55 Natal slangkop, 173
symptoms of, 53 N eriodorein, 246
treatment of, 55 N eriodorin, 246
Mercurialine, 278 Nerium species, 246
Mercurialis species, 277 N'eurin, 180
Mercurialism, 53 Nicotiana species, 251
Mercury, absorption and elimination Nicotine, poisoning by, 262
of,5 2 tests for, 263
chemical diagnosis of, 55 Nightshade, American, 271
forms of, 52 black,261
poisoning, acute, 53 deadly, 252
toxic dose of, 53 woody, 260
Metalloids, 4 Nitrate poisoning, post-mortem, 88
Metals, separation of, 307 symptoms of, 88
systematic analysis for, 313 treatment of, 88
Meteloidine,25 I Nitrates, chemical diagnosis of, 88
Methods, Babo and Fresenius, 309 toxic doses of, 87
colorimetric, 296 Nitric acid, 78
Stass-Otto, 300 Non-irritant poisons, 17
volumetric, 295 Non-volatile organic poisons, 17
Methylconiine, 229 Nut, purging, 280
Mezereon, common, 273 Nux vomica, Il8
Mezerinic acid, 273
Mildew, 180 Oak leaf, poisoning by, 288
Milk sickness, 237 Oat hay, 87
Milkweed, whorled, 249 CEnanthe species, 233
Millet, 105 ,Poisoning by, 233
Mineral green, 29 ffinanthotoxin, 233
Mint weed, 87 Oidium, 186
Mitscherlich test, 74 Oil of absinthe, 139, 237
Mock orange, 104 of chenopodium, 144
Modecca digitata, 283 of mustard, 204
Modeccin, 283 of pitch, Il2
Molteno disease, 239 of rue, 143
Molybdenum, forms of, 94 of savin; 142
poisoning, symptoms of, 95 of tansy, 143
treatment of, 95 of turpentine, 140
Monk's-hood, 185 of wormwood, 139
Mor~a species, 165 Old man's beard, 199
INDEX 325
Oleacet:8, 244 Phosphorus poisoning, symptoms of, 72
Oleander, poisoning by, 246 treatment of, 73
Onidn, wild, 204 toxic dose of, 72
Oonopsis species, 92 vermin pastes, 72
Opium poppy, alkaloids of, 124 Photosensitisation, 210
detection of, 128 Physostigma venenosllm, 130
poisoning by, 125 Physostigmine, 130
Organic poisons, 104 Phytic acid, 218
Ornithogalum species, 173 Phytolacca decandra, 271
Orpiment, 28 Phytolaccacece, 271
Ouabin, 246 Phytotoxin, 3, 280
Oxalic acid, chemical diagnosis of, 145 Picrate paper test, I I I
poisoning, post-mortem, 146 Pictou disease, 238
symptoms of, 146 Pilocarpine, chemical diagnosis of, 132
treatment of, 146 effects of, 132
toxic doses of, 145 Pilocarpus jaborandi, 132
Ox-eye, 200 Pimpernel, common, 245
Pinus sylvestris, 140
Paint root, 165 Piss grass, 277
Palustrine, 179 Pleurisy root, 249
Papaver somniferum, 124 Podophyllin, 224
Papaver species, 201 Pointed linaria, 270
PapaveraceaJ, 201 Poison, absorption of, 6
Papaverine, 124 accumulation of, 13
Paridin, I7I classification of, 16
Paris green, 29 definition of, 2
Paris quadrifolia, 171 distribution of, 13
Paristyphnin, 171 elimination of, 14
Parquine, 251 variations in action of, 15
Parsley, asses', 235 Poisoning, acute, 20
fool's, 235 bracken, 289
Parsnip, cow, 235 bread,239
water, 235 brine, 82
Paspalum grass, 181 causes of, 18
staggers, 181 chronic, 20
Pea, Indian, 218 diagnosis of, 20
jequirity, 282 kinds of, 20
mutter, 218 ptomaine, 316
wild, 221 subacute, 20
Pedicularis species, 270 treatment of, 21
Pellagri's test, 128 Poisons, chemical analysis for, 25
Penicillium, 180 inorganic, 4, 28
Periwinkle, 245 - mineral, 4, 28
Phaseolunatin, 105 non-volatile, 17
Phaseolus lunatus, 104 organic, 4, 104
Pheasant's eye, 200 volatile, 17
Phenol. See Carbolic acid Pokeweed, 271
Phenothiazine, chemical diagnosis of, PolygonaceaJ, 271
15 6 Poppy, horned. 204
occurrence of, 154 opium, 124, 201
poisoning, post-mortem, 156 red, 201
symptoms of, 156 sea, 204
treatment of, 156 Post-mortem examinations, 25
toxic dose of, 155 Potassium cyanide, I06
Phenothiazone, 155 nitrate, 87
Phloroglucinol, 289 Potato poisoning, 258
Phosphorus, absorption and elimina- Primulacece, 245
tion of, 72 Privet, 244
chemical characters of, 71 Protoanemonin, 195
chemical diagnosis of, 72 Protoveratridine, 135
poisoning, post-mortem, 73 Prunus species, 104
VETERINARY TOXICOLOGY
Prussic acid. See Hydrocyanic acid Rue, meadow, poisoning by, 199
Pseudo-jervine, 135 oil of, 141
Psychotrine, 133 Rumex species, 271
Pteris aquilina, 289 Rust, 180
Ptomaines, 316 Ruta graveolens, 141
Puccinia graminis, 180 Rutinic acid, 14 1
Purging nut, 280
Pushing disease, 238 Sabadilla seeds, 135, 168
Putresceine, 183 St. Anthony'S fire, 181
St. John'S wort, 210
Quantitative analysis, 295 Saliva reflex"" 87
Quercus robur, 288 Saltpetre, 87
Quillaja saponaria, 208 Salt poisoning, 80
Sambucus species, 236
Radish, wild, 204 Sand wort, 20 7
Ragwort, 238 Sanguinaria canadensis, 202
Rangoon bean, 104 Sanguinarine, 202
Ranunculacefli, 185 Santonin, chemical diagnosis of, 140
Ranunculus, poisoning by, 197 effects of, 139
species, 194 Saponaria .species, 207
Raphanus rhapanistrum, 204 Saponins, 207
Rattle pods, 221 poisoning by, 207
red,27 Savin, oil of, 140
Reagents, benzaldehyde, 307 Scabiosa suc(;isa, 236
Frohde, 307 Scheel's green, 29
Giinzberg, 315 Scheele's acid, 106
Mandelin, 307 Scherer's test, 74
Marquis, 307 Schrenocauloll- officinale, 135, 168
Mayer, 307 Schweinfurt's green, 29
Sonnenschein, 307 Scilla specieS, 17 2
Tunman, 307 Scillaren A, l72
Vitali, 307 Scillaren B, l72
Wagner, 307 Scillaridin, 172
Realgar, 28 Sclererythrin, 18 3
Red clover, 210 Scopolamine, 25 1
Red poppy, 201 Scopolia species, '25 8
Red rattle, 270 Scouring rush, 17 8
Red root, 165 Scrophularia species, 269
Red squill, 172 Scrophulal'iacefli, 265
Reinsch test, 308 Sea onion, 112
Retrorsine, 239 Sea poppy, 2 0 4
Rhamnacem, 214 Sedine, 227
Rhamnus species, 214 Sedum specieS, 226
Rheum species, 214 Selenium, chemical diagnosis, 93
Rhinanthin, 270 occurre~ce of, 91
Rhinanthtts cristagalli, 270 poisoning, post-mortem, 93
Rhododendron, 243 synIptoms of, 92
Rhododendron, poisoning by, 2-43. tre<).tment of, 93
Rhreadine, 201 Sempervirine, 134
. Rhubarb, 145, 214 Senecifoline, 239
Ricin, 280 Senecio poisoning, 2]9
Ricintts communis, 279 species; 23 8
Robin, 282 Senecionig.e, 239
Robinia pseudacacia, 282 Setterwort, 188
Rremeria species, 202 Sheep dips. See Arsenic and
Rosacem, 224 bolic acid
Rosmarine, 239 Sheep sorrel, 27 1
Round-leaved linaria, 270 Shepherd's weatherglass, 245
Roussin's test, 264 Silver, absorption of, 63
Rubberweed, bitter, 237 chemical diagnosis of, 64
Rubijervine, 135 Silver poisoningrpost-mortem, 64
INDEX 32 7
Silver poisoning, symptoms of, 64 Stinkblaar. 256
treatment of, 64 Stink grass, 178
m-eparations of, 63 Stipa robusta, 178
salts of, 63 Stone-crop, 226
toxic doses of, 64 Straining disease, 239
Sinalbin, 204 Strophanthidin, 246
Sinapis species, 204 Strophanthin-g, 246
Sinigrin, 204 Strophanthin-h, 246
Sisymbrium species, 204 Strophanthus species, 246
Sium species, 235 Strychnine, absorption of, 119
Skewer-wood, 212 chemical diagnosis of, 123
Slangkop poisoning, 172 poisoning, post-mortem, 122
Sleepy grass, 178 symptoms of, 120
Smilacin, 245 treatment of, 122
Smut, 180 toxic doses of, 120
Snake-root, white, 237 Strychnos species, 1I8
Snake-wood tree, II8 Strychnos toxijera, 136
Snake's head, 171 Subacute poisoning, 20
Sneeze-weed, 237 Sudan grass, 175
Sneeze-wort, 237 Sugar-beet pulp, 287
Snowdrop, 166 Sulphur, chemical diagnosis of, 90
Sodium bicarbonate, 86 poisoning, post-mortem, 90
carbonate, 86 symptoms of, 90
chlorate, 84 treatment of, 90
chloride, 80 toxic doses of, 89
nitrate, 87 Sulphuric acid, 78
Solanacem, 251 Sunflower, false, 237
Solanidine, 251 Sweet clover disease, 222
Solanin, 251 Swelled-head disease, 210
Solanum species, 251 Symplocarpus jmtidus, 163
Solidago species, 237 Symptoms of poisoning, 21
Sonnenschein's reagent, 307
Sorghum species, 105, 174 Tamus communis, 167
Sorrel, 145 Tanacetone, 141,
Sow bread, 245 Tanacetum vulgare, 141
Soya-bean cake, 285 Tanghinia venenijera, 246
Spanish blister fly, 149 Tansy, 143
Sparteine, 216 Tar oil, II2
Spartium Junceum, 216 Tares, 175
Spearwprt, great, 194 Tartar emetic, 41
little, 194 Taxine, 160
Species, influence on action, 15 Taxus species, 159
Spindle-tree, 212 Teart disease, 94
Spurge, 276 Temuline, 177
Spurge-flax, 273 Tests, Brunner-Pettenkofer, 305
Spurge-Iamel, 273 Gerrard, 256
Squill, 172 Greiss-Ilosvay, 89
Squirting cucumber, 224 Gutzeit,40
Staff-vine, 214 Hankin, 130
Stagger grass, 169 Keller, 269
Stagger weed, 237 Marsh,38
Staggers, blind, 91 Mitscherlich, 74
paspalum, 181 Pellagri, 128
Stanleya species, 92 Reinsch, 308
Staphysagroine, 192 Roussin, 264
Star of Bethlehem, 173 Scherer, 74
Star-wort, 207 Vitali, 254
Stas-Otto process, 300 VogI,209
Staves acre, 192 Tetrachlormethane, 151
Steltaria species, 207 Thalictrine, 199
Stiff-sickness, 221 Thalictrum species, 199
VETERINARY TOXICOLOGY
Thallium, absorption of; 65 Vetch, 105
chemical diagnosis of, 67 Vicia species, 105
forms of, 65 Vienna green, 29
poisoning, post-mortem, 66 Vincetoxicttm officinale, 249
symptoms of, 66 ViolaceaJ, 207
toxic dose of, 66 Violet, common, 207
Thebaine, 124 Vitali's reagent, 254
,Theobroma cacao, 286 Vitriol, blue, 56
Theobromine, 2S6 green, 71
Thevetin, 246 white, 60
Thiodiphenylamine, 154 Vogl's test, 209
Thionol, 154 Volatile poisons, search for, 296
Thorn-apple, 256 Vomicine, lIS
ThynielaceaJ, 273
Tilletia caries, ISO Wagner's reagent, 307
Toad-flax, 270 Wahoo, 212
Tobacco, poisoning by, 261 Watercress, fool's, 235
Tomato, 251 Water dropwort, 233
Toxicology, scope of, I Water hemlock, 230
Toxins, bacterial, 3 Water parsnip, 235
differences from poisons, 3 Water robin, 163
phyto-,3 Water scrophularia, 269
zOO-, 3 Weed-killer. See Arsenic
Transvaal slangkop, 173 Wellingtonia sequoia, 141
Traveller's joy, 199 White bryony, 224
Treatment of poisoning, 21 White hellebore, 168
Trefoil, 210 White lead, 44
Tremetol, 237 White precipitate, 52
Tribulus terrestis, 210 White snake-root, 237
Trifolium species, 210 White sweet clover, 222
Trzglochin species, 175 White vitriol, 60
Trimethylamine, 82, 180, 183 Whorled milkweed, 249
Tryptophane, IS3 Wild black cherry, 104
Tulip, drooping, 171 Wild carrot, 235
Tulp, 165 Wild chervil, 235
Tunman's reagent, 307 Wild cucumber, 224
Turpentine, 140 Wild lucerne, 221
\Vild onion, 204
UmbelliferaJ,227 Wild pea, 221
Umbelliferone, 232 Winton disease, 239
Umbrella-tree, Chinese, .212 Wistaria, 215
Upas-tree, lIS Wolfs-bane, 185
Urginea species, 172 Wood-laurel, 273
Ustilago species, ISO Woody nightshade, 20-0
Wormseed, American, 144
Wormwood, oil of, 139
Valerian, 236
Valeriana species, 236
ValerianaceaJ, 236 Yam, 167
Valerie acid, 236 Yellow jasmine, 134
Velvet grass, 175 Yellow sweet clover, 222
Veratridine, 135 Yellow vetchling, 215
Veratrine, chemical diagnosis of, 136 Yellow weed, 237
poisoning by, 135 Yew, poisoning, post-mortem, 161
toxic dose of, 135 symptoms of, 161
Veratrum species, 135, 16S treatment of, 161
Verbascum thapsus, 269 toxic dose of, 160
VerbenaceaJ, 210 ' Yohimbine, 137
Verdigris, 56
Vermeersiekte,23S Zea mays, 175
Vermeetic acid, 238 Zephyranthus atamasco, 166
INDEX
Zinc, absorption of, 61 Zinc, solubility in water, 60
chemical diagnosis of, 62 toxic dose of, 61
forms of, 60 I Zootoxins, 3
poisoning, post-mortem, 62 Zygadenine, 168
symptoms of, 61 Zygademls species, 168
treatment of, 61 I ZygophyUacem, 210

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