Professional Documents
Culture Documents
VETERINARY
TOXICOLOGY
REVISED BY
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
MGIPC-S2-rII-6-2!iIPD\-6-6-38-250.
First Edition
Second Edition-
Third Edition -
BOOK
PRODUCTION
WAR ECONOMY
STANDARD
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
<
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
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
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
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,
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.
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
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 "
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,
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.
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
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.
/
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.
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
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
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.
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
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.
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.
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
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.
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-
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'
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.
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
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.
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
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.
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
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
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
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
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
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
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
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
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
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
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-
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
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
OLEANDER.
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.
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-
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.
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.
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.
RHINANTHUS.
Cornevin, C. (1893), Des Plantes Veneneuses.
Mirande, M. (I907), Campt. Rend., 145, 439.
PHYTOLACCA~ElE.
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,
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.
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
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.
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.
J
change).
Turpentines.
Poisons distilled either from lEssential oils.
acid or alkaline solution Alcohol.
Ether.
Chloroform.
Sulphuric
Acid. FroMe. Marquis. I Ma~delin. Benzalde-
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.
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