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.

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.)

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 (C₁₀H₈O₄), 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 diarrhoea and dysentery. There are pronounced respiratory and heart troubles.

Pott confirms the symptoms of hÆmaturia, diarrhoea, 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.

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, diarrhoea 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).

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 (C₂₆H₃₇O₃N2H₂O) and the glucoside Helleborin (C₃₆H₄₂O₆). 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, diarrhoea, 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 diarrhoea and general oedematous swelling over the whole body,” but they recovered (Johnson and Sowerby).

Hellebores (Helleborus sp.). Two poisonous species of hellebore may on occasion be taken by live stock, though rarely—Stinking Hellebore (H. foetidus 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. foetidus, 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 (C₃₆H₄₂O₆), a highly narcotic and powerful poison; Helleborein (C₂₆H₄₄O₁₅); and the alkaloid Jervine (C₂₆H₃₇O₃N2H₂O).

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 diarrhoea, 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, diarrhoea, 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.

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 (C₃₁H₄₉O₇N), very poisonous and having a bitter taste; Delphisine (C₃₁H₄₉O₇N), which is extremely poisonous; Delphinoidine (C₄₂H₆₈N₂O₇), 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).

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 (C₃₄H₄₅NO₁₁), and also Aconine (C₂₅H₃₉NO₉). 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 oesophagus, 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 ? oz. respectively.

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 (C₁₇H₁₉NO₃) and Rheadine (C₂₁H₂₁NO₆), 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 diarrhoea, convulsions, and epileptic symptoms, the animals falling over and rolling.

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 (C₂₀H₁₉NO₅ + H₂O), which, especially occurring in the root, does not appear to be poisonous, or is of feeble activity; the alkaloid Chelerythrine (C₂₁H₁₇NO₄), which is poisonous; and Protopine (C₂₀H₁₉NO₅). 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.

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 (C₃H₅NCS), the alkaloid Sinapine (C₁₆H₂₃NO₅), 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 diarrhoea); 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 diarrhoea, 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.

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 (C₁₈H₂₈O₁₀)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 foetid and mixed with blood.

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:—

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 (C₁₇H₂₆O₁₀)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, diarrhoea, 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 diarrhoea 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 diarrhoea, and nerve troubles, death taking place in marasmus and decline. The active principle acts as an irritant on the digestive tract, causing colic, diarrhoea 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 diarrhoeic and foetid. 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 foetid diarrhoea, 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 diarrhoea, 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.

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).

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 diarrhoea, and in the case of sheep even be fatal. Pott says that the milk of cows eating it is with difficulty converted into butter.