CHAPTER II

RANUNCULACEÆ.

=Traveller’s Joy= (_Clematis Vitalba_ L.). The extent to which this

species is poisonous is not clear, though all parts are stated to be

poisonous, acrid and narcotic, while the juice tends to blister the

skin. It is remarked by Cornevin that it is less poisonous in spring,

when the ass and goat browse on it to a considerable extent without

serious trouble, than later, when it cannot be eaten without danger.

_Toxic Principle._ Traveller’s Joy appears to contain strongly poisonous

substances which have not been closely investigated. Greshoff found a

_Saponin_ in the leaves[2]. The poison is dissipated by heat.

Footnote 2:

Kobert states that various species of _Clematis_, _Ranunculus_,

_Anemone_, and also _Caltha palustris_ and _Trollius europæus_,

contain _Anemonal_ or _Pulsatilla-camphor_, which causes strong local

irritation, burning and swelling in the mouth, vomiting, intestinal

inflammation, etc.

_Symptoms._ When eaten in quantity the young shoots are diuretic,

violently purgative, causing dysentery, and in rare cases death. Applied

to the exterior it is irritating and even vesicatory. (Cornevin.)

REFERENCES.

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

=Anemone= (_Anemone_ sp.). Both our native species of Anemone appear to

be more or less poisonous in character: the Wood Anemone or Wind Flower

(_A. nemorosa_ L.), and also the Pasque Flower (_A. Pulsatilla_ L.).

These plants, the former of which grows in woods and damp shady spots in

fields, and the latter on chalk downs and limestone pastures, may on

occasion be taken by stock in early spring, when green herbage is not

too plentiful, but deaths appear to be rare, even if they have occurred.

All parts of the plants contain a toxic principle, which is volatile and

destroyed by drying.

_Toxic Principle._ The toxic substance is stated to be _Anemone-camphor_

(oil of Anemone) which imparts a bitter taste to the plants, and itself

gives rise in the plant to _Anemonic acid_ and _Anemonin_

(C_{10}H_{8}O_{4}), a very poisonous, narcotic substance, stated to be

neither a glucoside, nor an alkaloid, but a ring ketone with the

properties of an acid anhydride.

_Symptoms._—The symptoms recorded by Cornevin in the poisoning of

animals by the fresh plants are nausea, coughing, vomiting (if

possible), stupefaction, muscular tremors, and violent colic,

accompanied at times by hæmaturia and always by diarrhœa and dysentery.

There are pronounced respiratory and heart troubles.

Pott confirms the symptoms of hæmaturia, diarrhœa, and inflammation of

the stomach and intestines in the case of _A. Pulsatilla_ when fed in

the green condition. According to Esser, the plant poison affects the

spinal cord and the brain, the symptoms being similar to those produced

by _Aconitum Napellus_.

REFERENCES.

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

=Buttercups= (_Ranunculus_ sp.). A number of species of _Ranunculus_ are

acrid, irritant or severely poisonous, as the case may be. There are

variations in the poisonous character according to the season, and some

parts of the plant are more toxic than others. At the time the young

shoots develop in the spring but little of the poisonous principle is

present, and some (_e.g._ _R. Ficaria_) are not then poisonous, but a

larger quantity of the poisonous principle forms later, and some species

are especially dangerous at the time of flowering, after which the

toxicity decreases with the maturity and state of dryness of the plant.

The flowers are the most poisonous, and then the leaves and stem. It

does not seem to have been demonstrated that the seeds of any species

are dangerous, though Henslow states that the fruits of some species,

when green, appear to be most intensely acrid.

Some species of _Ranunculus_ are especially harmful (_R. sceleratus_,

_R. Flammula_, and _R. bulbosus_), while others are less so (_R.

lingua_, _R. Ficaria_, _R. acris_). The toxic principle is volatile, and

buttercups are easily rendered innocuous by drying or boiling—so much so

that when dried in hay they may be regarded as a nourishing food for

stock, and are readily eaten. Indeed, _R. repens_ is scarcely, if at

all, injurious even when green, though a case of fatal poisoning to

sheep said to be due to this species was reported in the _Veterinarian_

in 1844. Fresh _R. aquatilis_ is held to be quite harmless, and has been

used as a fodder. “Along the banks of the Hampshire Avon, and other

places in the same neighbourhood, it is used by the peasantry as fodder.

They collect it in boats and give it to their cows and horses, allowing

the former about twenty to thirty pounds a day. One man is said to have

kept five cows and a horse, with little other food but what they could

pick up on the heath, using no hay but when the river was frozen. Hogs

eat it and will live upon it alone until put up to fatten.” (Johnson and

Sowerby—_Useful Plants of Great Britain_.)

_R. sceleratus_ L., or Celery-leaved Buttercup, is probably the most

toxic species, and it is stated that in man a single flower may cause

poisonous symptoms resembling those due to _Anemone_ and _Colchicum_. It

is considered especially dangerous to cattle, and has caused many

losses: among its French names are _Mort aux Vaches_, and _Herbe

sardonique_. Poor people have been known to eat the young shoots when

boiled, heat dispelling the poison.

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

horses and cattle.

_R. bulbosus_ L., the Bulbous Buttercup, is somewhat variable in

toxicity, and is least dangerous after the flowers have dropped their

corolla, and the bulb-like rootstock is most harmful in autumn and

winter. The flowers are the most dangerous part.

_R. Ficaria_ L., Lesser Celandine, varies in toxicity with locality and

season, being most harmful at the flowering period. It is stated that

wood-pigeons eat the roots with avidity, and that the young shoots have

been eaten as a salad in Germany, as they are not toxic. An English

veterinary surgeon (Flower) recorded that three heifers were poisoned by

it (_Vide_ Cornevin).

_R. acris_ L., Acrid Buttercup or Tall Crowfoot, is a frequent cause of

poisoning in cattle, and Cornevin says it is perhaps the species which

causes the most accidents.

_Toxic Principle._ The buttercups contain an acrid and bitter juice, the

chemical properties and composition of which are not well known, but it

is believed that the substance is identical with the _Anemonin_ of the

_Anemone_ sp. (_q.v._). Beckurts isolated _Anemonin_ and _Anemonic acid_

from _R. acer_. Pott, however, states that the poisonous species contain

the two alkaloids _Aconitine_ and _Delphinine_.

_Symptoms._ The buttercups are acrid, burning and narcotic, causing

irritation of the mucous membrane, with inflammation of the intestinal

tract.

Cornevin shows that _R. sceleratus_ induces gastro-enteritis, colic,

diarrhœa with excretion of black foul-smelling fæces, vomiting when

possible, falling-off in milk yield in cows, nervous symptoms, reduction

in pulse, and stertorous respiration, dilation of the pupils, enfeebled

condition, difficult mastication, spasmodic movements of the ears, lips,

etc.,—followed in serious cases by convulsions, sinking of the eye in

its socket, possibly stoppage, and death in 6 to 12 hours after

convulsions first appeared.

In the _horse_ symptoms substantially similar to the above have been

recorded (Lander).

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

_Sheep_ after eating _R. repens_ have been noticed to fall suddenly in

the field; their eyes rolled, and some animals showed dizziness, and

died with the head inclined over the left flank (Lander).

REFERENCES.

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

=Marsh Marigold= or =King-Cup= (_Caltha palustris_ L.). Like the species

of _Ranunculus_, the Marsh Marigold is to some extent poisonous in

character, and both animals and man have suffered. Cattle have died from

eating it, and Müller records the poisoning of many horses, one of which

died. In general, animals refuse it, but may possibly eat it when

pressed with hunger in times of scarcity of green herbage. Cornevin

states that it has little or no acrid properties when very young, but

that it is toxic by the time of flowering—acridity increasing with age.

_Toxic Principle._ The toxic character of the Marsh Marigold has not

been fully investigated, though the presence of an alkaloid has been

determined, and A. B. Smith states that the toxic properties are due to

the alkaloid _Jervine_ (C_{26}H_{37}O_{3}N2H_{2}O) and the glucoside

_Helleborin_ (C_{36}H_{42}O_{6}). On drying—_e.g._ in hay—the plant

becomes harmless, as in the case of most species of _Ranunculus_.

_Symptoms._ Cornevin records that _cattle_ have died from inflammation

of the digestive tract, and gives the symptoms as those of _Ranunculus_

poisoning. There seem to be digestive troubles, diarrhœa, and loss of

milk production, even (according to Rusby) when fed with hay. In the

_horse_, there is colic, bloating, and inflammation of the bladder,

while the urine is dark red. According to Cornevin, the symptoms are

similar to those produced by _Ranunculus_ sp. Pammel quotes Friedberger

and Fröhner as stating that the plant causes hæmaturia. Five persons who

ate it as a herb were “seized with violent sickness and pain in the

abdomen, followed by diarrhœa and general œdematous swelling over the

whole body,” but they recovered (Johnson and Sowerby).

REFERENCES.

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

=Hellebores= (_Helleborus_ sp.). Two poisonous species of hellebore may

on occasion be taken by live stock, though rarely—Stinking Hellebore

(_H. fœtidus_ L.) and Green Hellebore (_H. viridis_ L.). The much

esteemed Christmas Rose (_H. niger_) is also toxic, but unlikely to be

eaten by stock. In no case should trimmings of these plants from

shrubberies, etc., be thrown to stock—cows have died from eating such

trimmings. The two species first mentioned are equally toxic, all parts

are poisonous, and drying does not render them innocuous. Cornevin

records that animals have been killed by _H. fœtidus_, and says that 9½

oz. of the fresh root or 2½ oz. of the dried root are poisonous doses to

the horse, while 120 to 150 grains are fatal to sheep. It was recorded

in 1847 (_Veterinarian_) by Mayer that a horse was fatally poisoned

through eating five half-pints of the chopped-up leaves of this species

in two days in a bran mash. In regard to this species also Johnson and

Sowerby write: “The Bear’s-Foot has been used as a vermifuge ever since

the days of Hippocrates, notwithstanding its dangerous qualities. Every

part of the plant is a violent cathartic, but far too uncertain in the

degree of its action to be safely administered.”

_Toxic Principle._ Both species contain the poisonous glucosides

_Helleborin_ (C_{36}H_{42}O_{6}), a highly narcotic and powerful poison;

_Helleborein_ (C_{26}H_{44}O_{15}); and the alkaloid _Jervine_

(C_{26}H_{37}O_{3}N2H_{2}O).

_Symptoms._ The Hellebores are cathartic, narcotic, and drastically

purgative. Stupor is followed by death with spasms in the case of _H.

viridis_ (Pammel). In general there is in the horse and ox bloody

purgation, salivation, attempts to vomit, and excessive urination,

according to Lander, who cites Mayer as noting violent straining and the

discharge of frothy mucus, but no effort to vomit, the heart action

resembling that observed in Digitalis poisoning, showing periodic

intervals of arrest in systole.

Müller gives the symptoms in cattle and sheep after eating the leaves as

loss of appetite, nausea, and even vomiting, salivation, grinding of

teeth, wind, colic, bloody diarrhœa, decrepitude, giddiness, loss of

sensation, convulsions, and not seldom death.

Affected cows are stated to give bitter milk which has purgative effects

(Pott).

The poisoning of two cows by _H. viridis_ came under the notice of

Cornevin. There was observed loss of appetite, diarrhœa, tenesmus,

violent attempts to evacuate, which after 5 or 6 days resulted only in

the expulsion of glareous blackish matter; to the end the pulse was slow

and intermittent. The heart beats were weak, and after 5 or 6 beats

there was a stop equal in duration to at least a beat and a half. A

remarkable fact was the very gradual loss of condition, while the milk

secretion was maintained until the last day. In one case death occurred

after 12 days and in the other after 28 days.

REFERENCES.

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

=Larkspur= (_Delphinium Ajacis_ Reich.). In the United States of America

certain species of Larkspur are exceedingly harmful to live stock, and

it has been said that “with the exception of the Loco weeds there is

probably no poisonous plant on the cattle ranges of the West that has

caused such heavy losses to stockmen as has larkspur” (_Far. Bul. 53, U.

S. Dept. Agric._). _D. Ajacis_ is the only British species, occurring in

cornfields in Cambridgeshire, Sussex and elsewhere, and, like the

Continental species _D. Consolida_, must be regarded as poisonous and

fatal to cattle, while horses and sheep may also suffer. Sheep and

goats, however, appear to resist the poison unless taken in considerable

quantity. Wilcox fatally poisoned a yearling lamb within an hour of

administering per os the extract from less than 1 oz. of the dried

leaves of an American species. The seeds are the most dangerous part of

the Larkspur, and should never be ground up with wheat should the two

plants grow together. The seeds of _D. Staphisagria_ are used in

medicine.

_Toxic Principle._ The species _D. Ajacis_ has been little studied, but

_D. Consolida_ and _D. Staphisagria_ contain the alkaloids _Delphinine_

(C_{31}H_{49}O_{7}N), very poisonous and having a bitter taste;

_Delphisine_ (C_{31}H_{49}O_{7}N), which is extremely poisonous;

_Delphinoidine_ (C_{42}H_{68}N_{2}O_{7}), which is poisonous; and

_Staphisagrine_.

_Symptoms._ The seeds are stated to be emetic and purgative, and _D.

Consolida_ is stated by Pott to be an acute narcotic poison to horses

and cattle. In general the symptoms appear to resemble those produced by

_Aconitum_ (p. 15). There is salivation, vomiting, colic, convulsions,

and general paralysis (Müller).

REFERENCES.

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

=Monkshood= (_Aconitum Napellus_ L.). The extremely poisonous character

of this plant has been recognised since ancient times, and it is

mentioned by Pliny, Dioscorides, etc. It is not common in the wild state

in Britain—chiefly occurring in some Welsh and one or two West of

England counties—and is not very liable to cause poisoning of live stock

in Britain. Cases of poisoning of horses, cattle, sheep and pigs have

been recorded on the Continent, however (Cornevin), and cows died in

Victoria. Linnæus says that it is fatal to cows and goats when they eat

it fresh, but that when dried it does no harm to horses. Medical works

record many cases of human poisoning, particularly in cases where the

root has been mistaken for horse radish—from which, however, it markedly

differs. The leaves at first taste insipid and then sharply burning; the

root when fresh smells like the radish and has a slightly sweetish

taste, which is succeeded by characteristic tingling of the tongue and a

sensation of numbness in the mouth.

_Toxic Principle._ Monkshood is very poisonous, and though all parts are

toxic the root is the most dangerous, and next the seeds and leaves. The

plant seems to vary in toxicity with age and climate, being but slightly

active when very young, most active just before flowering, and at the

minimum of activity when the seeds ripen. The cultivated form is stated

to be much less poisonous than the wild one. Drying removes a part of

the toxic substance, and boiling removes most of it. The plant contains

the toxic alkaloid _Aconitine_ (C_{34}H_{45}NO_{11}), and also Aconine

(C_{25}H_{39}NO_{9}). The root contains 0·17 to 0·28 per cent. of

_Aconitine_, but the leaves and flowers less.

_Symptoms._ The chief symptoms are those of depression, and are

manifested through the nervous system and the circulatory and

respiratory organs. Tetanic symptoms are also present. There is loss of

appetite, salivation, inflammation of the mucous membrane of the mouth

and jaws, grinding of teeth, nausea and vomiting, great restlessness and

colic; the animal groans and walks with an uncertain gait owing to

bodily weakness, giddiness and paralysis of hind feet or of all limbs;

there is also a notable slackening in the pulse, breathing becomes

difficult, consciousness is lost and the pupils are dilated. Death

ensues in most cases within a few hours, and after convulsions.

Kaufmann (quoted by Cornevin) observed in the _horse_ champing of the

jaws, salivation, fibrillous contraction of the muscles of the

olecranon, then of the buttocks, then of the whole body. The intestinal

pains were shown by the blows of the animal’s hind feet under and at the

back of the belly. There was also observed an intense and painful

contraction of the muscles in the inferior cervical region, the hyoid

and the abdomen; an increased sensibility; repeated evacuations; at

first congestion, then great paleness of the mucous membranes;

diminution in the volume of the arteries; faint whinnyings at the moment

of the contraction of the muscles of the neck, shoulders and stomach;

muscular rigidity of the posterior limbs; uncertain gait; laboured

breathing; and finally paralysis of motion, respiration and senses.

Lander in giving similar symptoms for the horse notices also choking

movements of the œsophagus, eructation of frothy matter, dilatation of

pupils and low temperature.

Kaufmann gives the poisonous doses of powdered root for the horse and

dog as 13 to 14 oz. and ⅙ oz. respectively.

REFERENCES.

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

PAPAVERACEÆ.

=Poppies= (_Papaver_ sp.). Poisoning by the two common poppies (_P.

Rhoeas_ L. and _P. dubium_ L.) is not common, but Cornevin says that the

former is poisonous in all its parts, and sufficiently so to cause

accidents every year. Animals may be affected by eating the plant when

mixed with green fodder, or by ingesting the seeds and capsules with

waste material after the winnowing and grading of cereals. Stock,

however, will most likely reject the plants, owing to their unpleasant

odour and taste, but cattle have been poisoned by eating unripe heads of

_P. Rhoeas_ when the plant was mixed with clover and sainfoin. _P.

dubium_ has caused poisoning of horses, cattle and pigs.

_Toxic Principle._ Both species contain the alkaloids _Morphine_

(C_{17}H_{19}NO_{3}) and _Rheadine_ (C_{21}H_{21}NO_{6}), which are

present in the milky juice of the plant. The latter, which was isolated

by Hesse, is believed to have no narcotic effects. The toxic principle

is not destroyed by heating, and the plant is therefore poisonous both

in the green state and when dried in hay.

_Symptoms._ It is remarked by Cornevin that cattle poisoned by _P.

Rhoeas_ at first exhibit symptoms of excitement, shown by continual

movement, by pawing of the soil or litter, increased respiration and

more rapid pulse; this is followed by stoppage of the digestive

functions, sometimes a little swelling of the eyelids, and coma, one

affected animal appearing to sleep while standing, remaining motionless,

and if forced to move walking in an unsteady manner. Finally, the animal

falls, and if a fatal result is likely (which is unusual) it remains

stretched on the ground; respiration becomes slower, the temperature

falls, and after a few convulsive movements death occurs owing to

asphyxia.

Müller notes excitement, wildness of look, dilatation of pupil,

convulsions; then coma, loss of sensation and symptoms of depression

replace those of excitement. There is salivation, bloating,

constipation, and in many cases also bloody diarrhoea. Death, however,

is rare.

Pott gives stupidity, retention of urine, colic, with sickness and

diarrhœa, convulsions, and epileptic symptoms, the animals falling over

and rolling.

REFERENCES.

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

=Greater Celandine= (_Chelidonium majus_ L.). This common plant exhales

an unpleasant odour, and when bruised or broken shows the presence of a

yellowish acrid juice, which becomes red immediately on exposure to the

air. It is an old medicinal drug plant, but is dangerous, being emetic

and purgative, with a strongly irritating effect on the digestive tract.

Animals are but rarely likely to take it, and no record of the death of

domesticated animals has been found.

_Toxic Principle._ Among the substances contained in the Greater

Celandine may be mentioned the bitter alkaloid _Chelidonine_

(C_{20}H_{19}NO_{5} + H_{2}O), which, especially occurring in the root,

does not appear to be poisonous, or is of feeble activity; the alkaloid

_Chelerythrine_ (C_{21}H_{17}NO_{4}), which is poisonous; and

_Protopine_ (C_{20}H_{19}NO_{5}). It is stated by Cornevin that the

toxic substance is not removed on drying, but Pott (1907) remarks that

the dried plant is harmless to animals, the poisonous alkaloid being

volatile and disappearing on drying.

_Symptoms._ The action of this plant is acrid, irritant and narcotic,

emetic and purgative. Esser remarks that when Chelerythrine is

introduced on the nasal mucous membrane it causes violent sneezing, and

taken internally causes vomiting. Müller says that poisoning of

domesticated animals is not recorded, but that according to old accounts

500 grammes (about 1 lb.) of the fresh plant eaten by the horse will at

most cause slight diabetes.

REFERENCES.

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

CRUCIFERÆ.

=Charlock= (_Brassica Sinapistrum_ Boiss.), also known as _B. Sinapis_

Visiani and _Sinapis arvensis_ L., may be regarded as harmless in the

young state, but liable to cause injury after flowering, when the seeds

have formed, when it may occasion serious accidents if eaten by live

stock. A case in which rape cake containing the seeds of charlock caused

poisoning was recorded in 1875 (_Jour. Roy. Agric. Soc._). The seeds

only are dangerous.

_Toxic Principle._ The seeds contain minute quantities of volatile _Oil

of Mustard_ or _Allyl-isothiocyanate_ (C_{3}H_{5}NCS), the alkaloid

_Sinapine_ (C_{16}H_{23}NO_{5}), and the alkaloidal glucoside

_Sinalbin_.

_Symptoms._ Ingestion of the seeds may cause inflammation of the stomach

and intestines (with loss of appetite, wind, colic, and diarrhœa);

inflammation of kidneys (difficult, excessive or bloody urination); and

nervous symptoms, with great exhaustion, uncertain gait, paralysis of

limbs and in isolated cases convulsions (Müller).

Pott also records increased salivation.

In the _horse_ Cornevin records great depression, difficult and

accelerated respiration, yellowish mucus and convulsive cough. A

characteristic symptom is the emission of frothy liquid through the

nostrils (as much as 10 litres in one hour). Death often occurs from

asphyxia in a fit of coughing.

In _cattle_, cake containing the seeds caused inflammation of the

intestines, exhausting diarrhœa, and unquenchable thirst.

The cultivated Mustards may induce similar effects, and Lander records

the following symptoms as caused by _Brassica nigra_:—In the _horse_,

bronchial symptoms, marked by difficulty in breathing and the discharge

of great quantities of yellowish frothy matter from the nose; in

_cattle_, uneasiness, restlessness and intense colic, with frantic

rushing about and mania, ending in exhaustion, falling, struggles and

collapse; in a recent case there were dullness, coldness, some tympany,

laboured respiration, staggering and falling, and in fatal cases,

immobility and a semi-comatose condition.

REFERENCES.

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

=Wild Radish= (_Raphanus Raphanistrum_ L.). As in the case of charlock,

the seeds of wild radish are very acrid, and susceptible of introducing

intestinal troubles if eaten by animals when mixed with cereals.

=Garlic Mustard= (_Alliaria officinalis_ Andrz.) and =Treacle Mustard=

(_Erysimum cheiranthoides_ L.). The seeds are stated to have properties

similar to _Brassica Sinapistrum_ (p. 18) owing to a pungent oil; and

when eaten in quantity to induce poisoning, inflammation of the

digestive tract and of the kidneys, as well as nervous symptoms

(Müller).

CARYOPHYLLACEÆ.

=Soapwort= (_Saponaria officinalis_ L.). This plant is more or less

poisonous, but is rarely, if ever, eaten by stock, and no recorded case

of the poisoning of stock has been met with.

_Toxic Principle._ The whole plant, especially the root, contains the

poisonous glucosidal _Saponin_ (C_{18}H_{28}O_{10})_{4}, a peculiar

substance which causes intense frothing when stirred in water.

_Symptoms._ No symptoms of animal poisoning by the plant are recorded,

but the action of Saponin in the blood stream is to induce dissolution

of the red cells, with stupefaction and paralysis, as in the killing of

fish by poisoning. It also causes vomiting and purging. Taken by the

mouth it causes inflammation of the alimentary tract, the contents of

which are fœtid and mixed with blood.

REFERENCES.

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

=Corn Cockle= (_Agrostemma Githago_ L.). This well-known plant of

cornfields must be regarded as poisonous, though experiments and reports

as to its effects on the different classes of live stock vary widely.

Though a poisonous principle is found in nearly all parts of the plant,

the plant in the green state appears to be innocuous, and is in any case

rarely likely to be eaten fresh by stock, which probably refuse it on

account of its hairy character. The seeds, however, are by no means

harmless. They are rather large, and somewhat troublesome to separate

from cereal grains. When ground up with wheat they both discolour the

flour and impart a grey tint and disagreeable odour to bread made from

it. Further, flour containing a considerable quantity of cockle must,

owing to the poisonous character of the latter, be held to be unfit for

consumption. Fatal results have followed the use of bread containing

Corn Cockle. The toxic principle therefore is not destroyed by heating,

even in an oven in baking.

As regards domestic animals, Corn Cockle seeds have frequently been

mixed with feeding stuffs and have caused many deaths. Cornevin’s

experiments in feeding calves, pigs and fowls led to fatal results. He

was able to say that the amounts of cockle flour necessary to cause

death were:—

Calf 0·25 lb.│per 100 lb. live weight.

Pig 0·10 „ │ „

Dog 0·90 „ │ „

Fowl 0·25 „ │ „

Among other cases, Kornauth and Arche found that in their feeding trials

pigs were not killed, but albuminoid metabolism was diminished and fat

production increased. In 1893 pigs died in Germany with symptoms of

acute poisoning, when fed on tailings containing six per cent. of

cockle. In 1903–4 experiments showed that with the cow, sheep, pig and

goat, cockle is not poisonous when fed in amounts usually found in

feeding stuffs. Millspaugh gives a case in which two calves died on

being fed with two lots of 14½ oz. each of wheat flour containing 30 per

cent. and 45 per cent. of cockle seeds. About 1892 Nevinny concluded

that six grammes of cockle seed consumed in 1200 grammes of bread were

beyond doubt poisonous in effect, and that the sale of grain or flour

containing it should be forbidden. Kobert held that the sale of feeding

stuffs containing cockle should be forbidden by law. An extensive study

of this question was made by Pesch, who concluded that “Under certain

conditions Corn Cockle is injurious to domestic animals. The amount of

the poisonous substance in the seed is variable, depending probably upon

the season and the soil. Animals become accustomed to it, so that

amounts of seed which at first cause sickness, later have no injurious

effect. The susceptibility of animals to the poison varies both with the

species and the individual. Young animals are more readily affected than

older ones. It is believed that rodents and sheep are not susceptible,

and, as far as is known, grown cattle are only slightly or not at all

affected by the poison. Calves, swine, horses, and especially dogs, are

more or less susceptible. Concerning birds and fowls there is some

doubt.”

Though animals are reputed to become tolerant of the poison if the

cockle is only taken in small regular doses, yet there appears to be a

chronic form of poisoning due to this cause and termed _Githagism_,

while there is an acute poisoning due to the ingestion of large

quantities of the seeds which may cause death in 24 hours or less.

It is clear that the evidence is quite sufficient to warrant the

statement that the ingestion of more than a very small quantity of

cockle seed is dangerous, and the consumption of even small quantities

should be avoided. Thus care should be taken to remove the seeds from

cereal grains.

_Toxic Principle._ The dangerous substance contained in cockle seeds

is the glucoside variously known as _Githagin_, _Saponin_,

_Agrostemmin_, _Sapotoxin_, _Agrostemma-Sapotoxin_, or _Smilacin_

(C_{17}H_{26}O_{10})_{2}. This principle appears to occur chiefly in

the seeds, which contain up to 6·56 per cent., but it has been found

in small quantities in other parts of the plant. It is very freely

soluble in water, in which it froths like soap when shaken up, and it

has a sharp taste and no odour.

_Symptoms._ A sufficient quantity of the toxic substance may cause

nervous debility and dysentery—according to Chesnut “intense irritation

of the digestive tract, vomiting, headache, nausea, vertigo, diarrhœa,

hot skin, sharp pains in the spine, difficult locomotion, and depressed

breathing. Coma is sometimes present and may be followed by death. In

animals chronic diarrhœa and gradual depression.”

The chronic form, which occurs when small doses are repeated over a long

period (practically the only form found in human beings, but never in

animals, except perhaps in the pig) is characterized by gradual wasting

away, loss of breath, loss of strength, chronic diarrhœa, and nerve

troubles, death taking place in marasmus and decline. The active

principle acts as an irritant on the digestive tract, causing colic,

diarrhœa and enterorrhagia.

Cornevin describes the symptoms in the acute form of the poisoning in

the case of horses, cattle, pigs and dogs.

In the _horse_, if a small quantity only is taken, there is yawning,

heavy colic, stamping and evacuation of rather soft fæces. If larger

quantities are taken, the symptoms, which commence in about an hour, are

salivation, frequent yawning and turning of the head, colic, pale mucus,

hurried and weak pulse, rise in temperature and accelerated respiration.

Some time later there are muscular tremors succeeded by pronounced

rigidity, and the fæces are diarrhœic and fœtid. The animal lies down,

and getting up is painful; it falls into a kind of coma, stretches

itself to the utmost, and death takes place without convulsions.

In _cattle_, the symptoms observed one hour after eating are

restlessness, salivation, and grinding of the teeth. Excitement and

colic are followed sometimes by coughing, this state lasting from five

to eight hours. There is then a period of coma, characterized by

permanent decubitus, repeated fœtid diarrhœa, hurried and plaintive

respiration, accelerated and gradually weakening pulse, a gradual loss

of motor and sensory powers, and a progressive decline in temperature.

Death occurs in twenty-four hours.

In the case of _pigs_, the animal grunts, lies down and remains thus

with its snout embedded in the straw. There is vomiting, more or less

violent colic and diarrhœa, the evacuation consisting of bad-smelling,

spumous fæcal matter. At times there are clonic contractions. Young pigs

are most susceptible.

Pott cites cases in which abortion was a feature of the poisoning, both

in cows and pigs. The results of numerous experiments which he quotes

(among others some carried out for the Prussian Ministry of Agriculture)

are very contradictory, a small quantity causing death in some animals,

while others of the same species were left unharmed by large quantities.

He ascribes this to the very variable proportions of the poison present

in the seeds.

REFERENCES.

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

205, 213, 249.

HYPERICINEÆ.

=St. John’s Wort= (_Hypericum perforatum_ L.). There appears to be no

record of poisoning of live stock by this plant in Britain, but Cornevin

records that it injured breeding mares fed on lucerne containing it in

large proportion. Drying in converting into hay did not render it

innocuous. It is only poisonous if eaten in considerable quantity, and

in general animals are not likely to eat much of it voluntarily, owing

to its resinous odour when crushed, and a bitter and slightly saline

taste.

_Toxic Principle._ The poisonous properties of St. John’s Wort have not

been fully investigated, but it is stated to contain an oil and an acrid

bitter resin. Ewart says that it “contains an oil whose medicinal value

was formerly highly esteemed; but this oil, and the woody nature of the

plant, render it somewhat injurious in fodder.” Summers says (_Journ.

Agric. S. Australia_, Sept. 1911, p. 144) that “it is reported to be

decidedly injurious, causing horses who eat it to break out in sores,

while milk cows have a tendency to dry off owing to its effect on the

system.”

_Symptoms._ In mares, dullness, sinking of head, loss of appetite,

slackening of pulse and respiration, dilatation of pupils, defective

sight, and lips purple (Müller).

REFERENCES.

63, 82, 117, 190, 203.

GERANIACEÆ.

=Wood Sorrel= (_Oxalis Acetosella_ L.). Though rarely likely to be eaten

by stock this plant must be mentioned here, as it is considered

dangerous on account of its high content of oxalates, which may cause

serious illness and diarrhœa, and in the case of sheep even be fatal.

Pott says that the milk of cows eating it is with difficulty converted

into butter.

REFERENCE.

213.

Plants Poisonous to Live Stock · 第 2 / 9 章