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

Toxic Principle. This is probably the glucoside Bryonin, which occurs in Bryonia dioica (p. 35).

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

LILIACEÆ.

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

Toxic Principle. Walz isolated the glucoside Paridin; and Esser states that the toxic property is due to a Saponin,—the bitter irritant glucoside Paristyphnin (C₃₈H₆₄O₁₈), which is convertible into Paridin (C₁₆H₂₈O₇ + 2H₂O) and sugar.

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

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

Toxic Principle. All parts of the plant contain the bitter poisonous glucoside Convallamarin (C₂₃H₄₄O₁₂), the glucoside Paridin (C₁₆H₂₈O₇ + 2H₂O), and the glucoside Convallarin (C₃₄H₆₂O₁₁)—the first a dangerous purgative, and the last a cardiac poison resembling Digitalis. Convallamarin is a very poisonous crystalline substance, with at first a bitter and afterwards a sweetish taste.

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

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

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

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

Toxic Principle. Meadow Saffron contains in all parts the acrid, poisonous alkaloid Colchicine (C₂₂H₂₅NO₆) stated by Esser to occur to the extent of 0·2 per cent. in the corms, 0·4 to 0·6 per cent. in the seed coats, but only traces in the leaves. Hertel obtained 0·38 to 0·41 per cent. of alkaloid from the seeds, Farr and Wright from 0·46 to 0·95 per cent., and Carr and Reynolds 0·12 to 0·57 per cent.; the U.S. Pharmacopoeia, 1905, required a Colchicine content of 0·45 per cent. in the seeds, and 0·35 per cent. in the corms (Allen).

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

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

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

GRAMINEÆ.

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

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

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

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

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

Toxic Principle. The grains only are harmful, and contain the narcotic alkaloid Temuline (C₇H₁₂N₂O), which Hofmeister showed to be a strong nerve poison, and which is said to occur to the extent of 0·08 per cent. in the seeds. Other authorities impute the toxic property to Loliine, while Smith states that the toxic principle is Picrotoxin. In relation to the grain fungal hyphÆ have usually been found, though not invariably, 20 to 30 per cent. of the plants sometimes being free from it. The fungus (Endoconidium temulentum) is propagated vegetatively by means of mycelium. It appears to live symbiotically in the maturing grain, and perhaps to a slight extent renders possible the assimilation of nitrogen from the atmosphere; but Freeman observed that though generally stimulating to the Darnel, it is occasionally injurious to it. Esser sums it up by saying that according to most authorities who have investigated Darnel the fungus alone contains the toxic substance—the Temuline—and hence the grains in which the fungus does not occur should be harmless. The fungus is found in Darnel grain in all countries—Chile, Brazil, S. Africa, Persia, Spain, France, Sweden, Germany, etc. So far as can be ascertained there have been no feeding experiments to determine the difference in toxic character between fungus-infested and fungus-free grains. The dangerous properties are said to be most pronounced in wet seasons.

Symptoms. In France Darnel is called Ivraie, because, when brewed with barley, it acts as a narcotic intoxicant.

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

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

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

EQUISETACEÆ.

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

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

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

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

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

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

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

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

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

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

FILICES.

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

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

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

Toxic Principle. Continental authorities say that Bracken contains the poisonous Pteritannic acid, which is identical with the Filicic acid of the Male Fern (Aspidium filix-mas).

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

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

FUNGI^[6].

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

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

Toxic Principle. Ergot of rye is used in medicine. It contains 0·20 to 0·25 per cent. of Ergotinine. In the British Pharmaceutical Codex, 1911, the grains (sclerotia) of Ergot (see Frontispiece) are described as longitudinally furrowed, 1 to 4 cm. long, slender, curved, tapering to both ends; they break with a short fracture, and are somewhat triangular in transverse section; they have a characteristic and disagreeable odour and taste, are dark violet to black in colour, and whitish within. Ergot contains the physiologically active alkaloid Ergotoxine or Hydroergotinine (C₃₅H₄₁O₆N₅), also known as amorphous Ergotinine, and, when formerly obtained in an impure state, as Cornutine and Ecboline. It is the hydrate of the crystalline base Ergotinine (C₃₅H₃₉O₅N₅). There are also other physiologically active constituents derived from amino-acids.

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

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

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

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

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

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

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

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

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

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