Spindle Tree (Euonymus europÆus L.). According to Cornevin the spindle tree is poisonous in all its parts, especially the fruits, which are emetic and strongly purgative. Sheep and goats have been injured from eating the leaves, and children have suffered from eating the fruits.

Toxic Principle. This plant does not appear to have been closely studied from the toxicological point of view; contrary to the statements generally made in the literature Van Rijn remarks that this species does not contain the doubtfully classed Euonymin.

Symptoms. Ingestion of the plant induces symptoms and lesions such as are due to violent vegetable purgatives.

RHAMNACEÆ.

Buckthorn (Rhamnus Catharticus L.) and (R. Frangula L.). The berries of both species are toxic and purgative, but both are uncommon and rarely eaten by stock.

Toxic Principle. The berries and bark contain the glucosides Frangulin (C₂₁H₂₀O₉) and Rhamnetin (C₁₆H₁₂O₇).

Symptoms. The berries are purgative, and there is some danger from large quantities, which may induce superpurgation. The leaves are astringent and may arrest milk secretion (Cornevin). MÜller states that the inflammation of the stomach and intestines may terminate fatally.

Laburnum (Cytisus Laburnum L.). The well-known and much admired Laburnum must be regarded as one of the most poisonous species of British plants. By numerous experimental researches Cornevin proved that all parts of the plant are poisonous—root, wood, bark, leaves, flowers, and seeds, especially the seeds. In his experiments the horse, ass, sheep, goat, dog, cat, fowl, duck and pigeon, were utilized, seeds being given. He found that 80 centigrammes per kilogramme live weight would be necessary to kill a horse (say 1 lb. for an animal of 1200 lb. live weight), 60 centigrammes per kilogramme live weight to kill an ass (say 6 oz. for an ass weighing 600 lb.); and 6 grammes in the case of a fowl (say 0·4 oz. for a fowl weighing 4½ lb.). The sheep and goat he was not able to kill, as they refused the food after a certain point; the dog and cat he was not able to kill because they so readily vomited; and the duck and pigeon vomited with extreme facility.

Many cases of the poisoning of children have occurred through the ingestion of the flowers and seeds. In 1908 a case was recorded by the Board of Agriculture and Fisheries, in which two horses were alleged to have been poisoned in North Wales by laburnum seeds, a very small quantity of which was found in their stomachs after death.

MÜller states that in Dalmatia goats which had eaten Cytisus Weldeni, though themselves uninjured, produced milk which was poisonous to man.

Toxic Principle. All parts contain the toxic alkaloid Cytisine (C₁₁H₁₄N₂O), said by Moer and Partheil to be identical with Ulexine; it is found in the seeds to the extent of 1·5 per cent. Cornevin states that the root, wood and bark are nearly constant in toxicity, but that the leaves and pods present remarkable seasonal variations owing to the migration of the poison into the seeds. The toxic property is not destroyed by drying of the plant.

Symptoms. Laburnum poisoning is of the acrid, narcotic type, with, in man, nervous symptoms, abdominal pain, vomiting, purging, tetanic spasms and convulsions.

Cornevin’s observations show that the symptoms occur in three consecutive stages,—(1) excitement, (2) coma and incoordination of movement, and (3) convulsions. The order of the appearance, their duration, and the association of each with the others depend upon the susceptibility of the animal and the quantity ingested. Thus the symptoms of excitement may be present alone if only a small quantity is eaten; the duration of the symptoms in this case is never considerable, and the normal is gradually regained. In general, however, the symptoms are associated in pairs; thus when an average quantity is fed there is excitement and coma but no convulsions; when large quantities are fed the first stage is suppressed or is so short as to be almost imperceptible, the coma and convulsions being present simultaneously. As regards temperature, there is, in stage (1) a rise, in stage (2) a drop, and in stage (3) a rise again near death. In stages (2) and (3) there is a slackening of respiration, the arterial tension is raised, there is an increase in the number of pulsations and a modification of the rhythm. In stage (3) near death there is a lowering of the arterial tension, and the pulsations become gradually less perceptible, but with a uniform rhythm; there is a slackening in respiration, and by the time this finally ceases the heart beats have become imperceptible.

When horses, asses or mules have eaten a small quantity of the seeds or leaves, there is simply yawning and uncertain gait, these symptoms lasting for two hours, and the normal being regained after urination. Considerable (but not fatal) quantities cause unsuccessful attempts at vomiting, sometimes opisthotonos in asses, sweating, muscular tremors, and then a deep coma which may last 15 hours. Fatal quantities cause yawning, sexual excitement, accelerated and noisy respiration, wheezing, muscular tremors followed by contractions which commence in the posterior limbs and spread to the anterior limbs, facial contractions, staggering and copious sweating. A rapid fall in temperature follows, but there is a slight rise during the period of convulsions; the pulse is at first quicker and stronger, but the number of beats rapidly comes back to the normal, to rise again shortly before death; the rhythm of the pulse is at first regular (in groups of 2, 3 or 4) but becomes irregular again just before death. The animal at length falls, and cannot get up, the nostrils are distended, the mouth is wide open, respiration becomes gradually slower, and death takes place in great agony.

In cases of poisoning of horses and asses noticed by Pott animals that could not vomit died very quickly. The symptoms were excitement, nausea, coma, slower breathing, convulsions, paralysis of the motor nerves, and finally cessation of the action of lungs and heart.

Ruminants are much less susceptible than horses. Cornevin’s attempts at poisoning failed through their refusal of the plant. MÜller observed in a case of cattle poisoning, bloating, paralysis of the limbs (especially fore limbs), sleepiness, dilatation of pupils, and later salivation, nausea, coma and occasional convulsive movements of the muscles of the extremities. These symptoms persisted through several days and then disappeared.

Broom (Cytisus Scoparius Link.). This very plentiful and widely distributed plant is undoubtedly to some extent poisonous, though perhaps only feebly so in the quantities likely to be eaten by domestic animals. Blyth records 400 cases of poisoning from it, however. Very hungry animals might eat too much of it, and hence show symptoms of poisoning.

Toxic Principle. The plant contains the alkaloid Cytisine (C₁₁H₁₄N₂O); also the volatile alkaloid Sparteine (C₁₅H₂₆N₂), a single drop of which, according to Blyth, killed a rabbit, which showed symptoms similar to those of nicotine poisoning.

Symptoms. Taken in sufficient quantity broom induces narcotic poisoning, with symptoms resembling those caused by Coniine, with central nervous paralysis.

Cornevin gives the symptoms as similar to those due to C. Laburnum.

Indian Peas (Lathyrus sativus L.). A type of poisoning that deserves attention here is that known as Lathyrism, since it is due to the consumption of peas of the genus Lathyrus, the most dangerous being the “Indian Pea,” L. sativus. The peas of this plant (see Frontispiece) are small and dark-coloured, and are imported largely from India and other countries under the general name of Mutter peas, a name which they share with the ordinary pea Pisum sativum. In addition to the seeds of this species the seeds of two South European and North African species—L. Cicera and L. Clymenum—have commonly caused poisoning both in man and in animals, not infrequently leading to fatal results. Horses, cattle, sheep and pigs have been affected—horses particularly so—and many cases have been recorded in the veterinary journals since 1885. Very heavy losses have occasionally resulted from the use of the raw peas as a food for stock. For example, in 1884 Messrs. Leather of Liverpool had 35 out of 74 cart horses ill through eating Indian peas at the rate of 3 to 4 lb. per head per day. Of the 35 no less than 19 died, and 2 were slaughtered, while 14 recovered. In the famous Bristol Tramways case (1894) 123 out of 800 horses became ill owing to being fed on the peas of L. sativus, and many died. There are few records of harm to cattle, sheep and pigs, and Watt quotes Don to the effect that pigeons lose their power of flight by feeding on the peas. Very large quantities of the peas are used for feeding purposes, and the fact that the losses are not larger is probably because the peas only comprise a small proportion of the ration or are cooked before use.

After boiling or roasting the peas appear to be less harmful, as they are eaten in India when cooked, or ground into flour and converted into bread—though Cornevin states that drying and cooking does not destroy the toxicity, while boiling for some time showed that at any rate part of the toxic substance passed into the water, which became toxic and caused death, the boiled seeds losing the greater part of their poisonous property and not causing accidents when the water was rejected. MacDougall states that as far as experimental evidence was available (1894) it seemed to show that boiling the seeds before use renders them innocuous.

Lathyrism usually only supervenes when the use of the peas for food is prolonged, and the peas are taken in considerable quantity, but it is possible that there is wide variation in the toxicity of different samples, owing to differences in soil, climate, and other factors. In man, Lathyrism is stated to be common in Spain, Italy, Russia and India, owing to continued use of bread from flour of the three species of Lathyrus mentioned above. It is said especially to affect males.

Toxic Principle. Nothing certain as to the poisonous properties is known, attempts to isolate the toxic substance having failed (Kobert), though Smith gives it as prussic acid, apparently indicating a cyanogenetic glucoside. This, however, can hardly be so, as the poison is cumulative, and may not show its effects for weeks or months, or, in man, even years—according to the quantity of peas eaten.

Symptoms. Lathyrism is only produced when the ration consists largely of the pea for a considerable period (see above); in the horse fed exclusively on the pea, the tenth day; but when one or two quarts are given daily, only towards about the 80th day. Moreover, the malady may declare itself as long as fifty days after the cessation of the pea feeding (Lander).

In general Lathyrism is marked by paralysis of the lower extremities in man and the hind limbs in animals, owing to the degeneration of the muscle fibres, and possibly to affection of the nerves. In horses there is paralysis of the hind limbs, dyspnoea and roaring—with paralysis of the recurrent laryngeal nerve, and transverse myelitis. The horse thus shows weakness of the hind quarters, staggering in the effort to stand, difficulty in breathing, abnormally fast and irregular pulse, open mouth, distended nostrils. Tracheotomy often gives almost immediate relief.

Lander mentions in cart horses grinding of teeth, and convulsive movements of the eyes, recalling epilepsy. In one outbreak there was thick wind, staggering gait, weakness of hind quarters, and general signs of intoxication; and sudden violent attacks of laryngeal paralysis and dyspnoea during which there was palpitation, frothing, tongue protruded, eyes staring, bluish tint of buccal membranes, and palpitation. Paroxysms sometimes proved fatal.

An attack among 125 lambs is mentioned by Cornevin. The lambs could not stand on their fore legs and were obliged to go down on their knees. On setting them up again, they were only able to keep up while motionless or moving slowly. There was loss of sensibility in the front members. In spite of this the eye was alert, they were attentive to everything that went on around them, and were easily frightened.

In pigs paralysis of posterior members has been observed.

In cattle there was staggering, blindness, and stiffness of the lower joints. In sheep and pigs there was also paralysis of the hind limbs.

Yellow Vetchling (Lathyrus Aphaca L.). To what extent this vetchling is poisonous to stock is not clearly known, but it is cultivated in India as a fodder for cattle. The seeds, however, are not altogether safe when ripe, and MacDougall says “The seeds and pods have been known to be used in soup in their young state and without harm resulting, but the ripe seeds are narcotic and cause sickness and headache.”

Lupines (Lupinus sp.). Different species of Lupinus have been found to cause poisoning of live stock, more particularly sheep, which, when fed largely on lupines, develop a chronic type of poisoning known as Lupinosis, or poisoning may be acute and rapid in its effects, as in the United States. Records of large numbers of sheep being affected at a time date from 1872, in various parts of the German empire. In Europe by far the most harmful species is the Yellow Lupine (L. luteus), which has been the cause of heavy losses of sheep, though horses, cattle and goats may also be affected. The Blue Lupine (L. angustifolius) and White Lupine (L. albus) may also be toxic. L. luteus has caused lupinosis in Germany since 1860, and Cornevin states that in 1880 no less than 14,138 out of 240,000 sheep fed upon it (or 5·89 per cent.) died. Of 44 horses affected 11 died.

It must not be thought that all crops of lupine are poisonous, as lupines are extensively grown on the Continent for fodder purposes and are usually harmless. Even where Lupinosis occurs, considerable quantities of the lupine must be ingested to cause poisoning. The toxicity appears to vary according to soil and certain indefinite conditions, and sometimes even a kilogramme (2·2 lb.) of the plant would suffice to kill a sheep. Poisonous symptoms may sometimes be observed after a single meal. Desiccation does not render the plant innocuous, the seeds and hay being poisonous.

In the United States species of Lupinus have caused great loss. In 1898 no fewer than 1,150 of a flock of 2,500 sheep died from eating one species; one sheep farmer lost 700 sheep from the same cause; and 1,900 out of 3,000 sheep died from Lupine poisoning in Montana in 1900. Lupine hay is found to be less harmful to horses and cattle, and Chesnut and Wilcox suggest that this is possibly because as a rule they avoid the pods, while sheep eat them. Lupines in America are very rapid in their action on sheep, which may often die in one-half to three-quarters of an hour after eating a quantity of the pods. Further, there is evidence that sheep may gradually become immune to the poison by eating Lupines regularly, since sheep fed regularly on hay nearly half lupine were unaffected, but others eating the same hay for the first time died in considerable numbers. The lupines are certainly far the most dangerous when they bear ripe seeds—cut and made into hay before the pods form they are much less dangerous.

In regard to L. luteus Lander says: “According to the German authorities a daily ration of 1 pound of the whole plant, ? pound of empty pods, or 1? pound of seeds, will produce poisoning.”

Various means have been tried to render Lupines harmless, and success is stated to follow heating with steam under a pressure of 2 to 2½ atmospheres.

Toxic Principle. A very full account of Lupine poisoning is given by Pott, and from this a brief summary may be made. Siewert and Wildt (1879) found two substances very like the alkaloids of Conium maculatum—one like Coniine and the other like Conhydrine, the former only being proved to be very poisonous. Baumert states that in L. luteus there are only two bitter alkaloids, Lupinine (C₁₀H₁₉ON) and Lupinidine = Sparteine (C₁₅H₂₆N₂). Many investigators (e.g. KÜhn at Halle) held that lupinosis was not identified with the presence of lupine alkaloids. Then, in 1883, Arnold and SchneidemÜhl caused the disease (lupinosis) in sheep with lupines freed from all alkaloids, and they isolated from the seeds a substance they named Lupinotoxin, which they found to be poisonous. The nature of the poison cannot yet be said to be fully understood. The Lupine does not always appear to be poisonous—only under certain conditions which are not too well defined. One farmer had Lupines on the same soil for twelve years without ill effects when fed to sheep, and then of 450 sheep 120 were severely ill, and 80 died; they had had unthrashed Lupine, not quite ripe, to the extent of one-fourth of the ration. It is held to be definitely established that the presence of this poison is due in turn to the presence of a saprophytic fungus; when the fungus is absent or only present in small quantity the lupine is not at all or only slightly poisonous.

Symptoms. The disease is either acute or chronic according to the amount of poison ingested. Most writers describe the disease in sheep, but symptoms given vary somewhat.

In the acute form sheep become ill suddenly. There is loss of appetite, dyspnoea, intense fever, hÆmaturia, circulatory and digestive troubles, grinding of teeth and trembling, which may pass into spasmodic contractions. Vertigo is sometimes present. Jaundice then appears and is evidenced by the yellow colour of the mucous membranes. Tumefaction of the eyelids, lips and ears is common, but not invariably present. Micturition is frequent, but not abundant, and the urine contains albumen; the excrements are few and dry. There is collapse, and loss of condition progresses rapidly, death occurring on the fourth to the sixth day after the commencement of the illness.

In the chronic form the interstitial hepatitis predominates. Tumefaction of the head may also appear as in the acute form. Digestive troubles indicate chronic gastro-enteritis. This condition lasts for from 15 to 20 days, during which the cephalic oedemÆ are eliminated by gangrene and the animals remain listless and without appetite. The illness in sheep is grave, and affected animals are rarely completely cured. The mortality in other species does not seem to be less than in sheep. (Cornevin.)

In describing the acute form of lupinosis Pammel adds that the initial temperature may be as high as 104° to 106° F., but that it is intermittent and gradually falls just before death. The pulse may reach 130 per minute and the respirations 100. A bloody froth may issue from the nostrils. Animals apparently prefer the recumbent position, extend the head on the ground, and seem entirely oblivious to all surroundings. At first there is constipation, but later diarrhoea may set in and the excreta be tinged with blood. In the chronic form the symptoms are not so violent. Jaundice may be entirely absent, and emaciation and anÆmia may be the chief signs.

Chesnut and Wilcox record a case in which two sheep were each given 150 medium-sized pods of a native lupine, and seemed to like them. In 45 minutes, however, they became frenzied and died an hour later. They give the symptoms as practically the same as those caused by European species of Lupinus; acute cerebral congestion, with great mental excitement, the sheep rushing about and butting into things; following is a stage characterized by irregularity of movement, violent spasms, and falling fits; in most cases collapse and death occur within half-an-hour to an hour and a half; the pulse is strong and regular; the convulsions resemble to some extent those caused by strychnine; the excretion of the kidneys is much increased and sometimes bloody. In post-mortem examination the kidneys are found affected, the lungs slightly congested, the cerebral membranes in all cases congested, and in violent cases small blood vessels are ruptured in different parts of the body.

“Java” Beans (Phaseolus lunatus). Though not native to Great Britain, the so-called Java Beans have been imported in considerable quantities for stock feeding, and in the past nine years have caused the death of a large number of animals. For example, in March, 1906, the Board of Agriculture and Fisheries published an account of the poisoning of animals by these beans at eight centres; at six of the centres 133 cattle were involved and 43 died. The beans are of varying origin, and pass under the name of Java beans, Rangoon beans, Burma beans, Lima beans, and Paigya beans. They are considerably different in colour according to origin, the Java beans being pale brown to almost black; Rangoon, Burma or Paigya beans smaller, plumper, and lighter in colour (“red Rangoon beans” are pinkish with small purple splotches, and “white Rangoon beans” are pale cream); and Lima beans are much larger than the last-named and pale cream or white in colour (see Frontispiece).

It has long been known that beans of certain forms of Phaseolus lunatus are poisonous, and the fact is noted by Church (Food Grains of India, 1886), and by Watt (Dictionary of the Economic Products of India, 1889–96). The coloured forms, and particularly the wild forms, are the most dangerous, the white types being in general safe for stock feeding. Some forms have a general similarity to butter beans and haricots, and have hence been favourably regarded by farmers, but it is a sound plan to purchase under a guarantee beans with such names as those given.

Toxic Principle. It was shown in 1903 (Proc. Roy. Soc., Vol. 72) that the seeds of P. lunatus, uncultivated in Mauritius, contained a cyanogenetic glucoside, Phaseolunatin (C₁₀H₁₇O₆N). This glucoside, under favourable conditions, such as are present when the beans are moist, masticated and ingested at the temperature of the animal body, gives rise to prussic acid, which is the direct cause of poisoning. The seeds of the wild forms yield, like bitter almond seeds, considerable quantities of prussic acid, while the cultivated forms resemble sweet almonds in yielding only traces of the acid, or none at all. Determinations of the yield of prussic acid by various investigators show percentages of from 0·027 to 0·137 in Java beans, and 0·004 to 0·02 in Burma beans. The largest proportion therefore occurs in the coloured beans, while the white forms contain much less or none at all, and may be generally regarded as safe for stock.

Symptoms.—The symptoms given by Damman and Behrens (Veterinary Journal, 1906) were vertigo, tympany, and falling, with death in most cases. Mosselmann (Vet. Jour., 1908) observed the symptoms due to the ingestion of a small quantity of the beans by six head of cattle. They were: great excitement, salivation, swelling, slight diarrhoea, quick pulse and respiration, muscular spasms, and paralysis of the hind quarters in one instance; all recovered rapidly.

Castor Oil Plant (Ricinus communis L.). The beans (see Frontispiece) of this exotic are toxic, and poisoning is only likely to occur if they are sold in error as a feeding stuff, or from the use for feeding purposes of the press-cake after the extraction of the well-known castor oil, a purgative commonly used medicinally, of which the beans contain about 50 per cent. According to Cornevin four seeds suffice to cause accidents in man, eight lead to very grave results, and beyond that number death may ensue. Pigs and poultry have been poisoned by the seeds, and M. Audibert (near Beaucaire) reported the death of 80 sheep from eating the press-cake, which is stated to have more pronounced properties than the oil. It has been found as an impurity in linseed cake and maize meal. (Jour. Roy. Agric. Soc., 1892.)

Toxic Principle. The toxic properties of the bean are due to Ricin, a toxin which is similar to bacterial toxins, and the activity of which is destroyed by heating to 100° C. The beans also contain the alkaloid Ricinine (C₈H₈O₂N₂), the toxic properties of which are regarded as doubtful. (See Deane and Finnemore, Yearbook of Pharmacy, 1905, p. 473.)

Symptoms. These usually appear some days after the ingestion of the beans or press-cake. There is generally purging. Broad observed in an affected horse loss of appetite, shivering, cold extremities, dejection, abdominal pain, constipation, temperature 103° F., pulse 70, and death in about three days.

ROSACEÆ.

Cherry Laurel (Prunus laurocerasus L.). This exceedingly common ornamental shrub has caused the poisoning of numerous cattle and sheep on the Continent, but is apparently less harmful in Great Britain—and in any case animals are not much given to eating the foliage of this shrub, the strong smell of the leaves when bruised affording a warning of its unwholesome character. Gerlach recorded the intoxication of 25 sheep. Bibbey also records the poisoning of 15 sheep by laurel, some of them dying (Farmer and Stockbreeder, Jan. 29, 1912). On the other hand, Henslow wrote of his cows that they “completely ruined a long laurel hedge adjoining the field in which they lived; but this abnormal food did no harm either to themselves or the milk they produced.”

Toxic Principle. So long ago as 1803 Schrader showed that the cherry laurel contains a substance yielding prussic acid. The leaves contain the cyanogenetic glucoside Prulaurasin (C₁₄H₁₇O₆N), and an enzyme-emulsin which, by its action on the cyanogenetic glucoside, induces the formation of prussic acid, which is the actual cause of poisoning. The percentage of the glucoside appears to be greatest about July and August. By a microchemical examination Peche has clearly localised hydrocyanic acid compounds in the leaf parenchyma.

Symptoms. In poisoning by Cherry Laurel there is bloating, inability to rise, loss of sensation, difficult breathing, convulsions and dilatation of pupils, and the results may be fatal if unattended to, prussic acid being formed.

In the case of poisoning of ewes Aggio observed (Veterinary Journal, 1907) loss of appetite, vomiting, and inability to rise, followed by several deaths. In 1871 Adsetts described (Veterinarian, 1871) symptoms of poisoning in the horse: indistinct and feeble pulse; congested mucous membranes, difficult respiration, uneasiness, prostration, coldness of the extremities, loss of appetite, constipation, diminished urination, and acute pain, eventuating in death in three days. In sheep Bibbey observed salivation, grinding of teeth, brain symptoms, paralysis in the back, coma, and death.

CUCURBITACEÆ.

Bryony (Bryonia dioica L.). This widely distributed hedge climber, which produces large quantities of scarlet berries, is a highly irritant plant, with an unpleasant odour and a nauseous juice. The large fleshy tuberous rootstocks have caused the poisoning of whole families who have eaten them in mistake for turnips and parsnips. The berries may tempt children, and cases of poisoning have occurred. Cornevin estimated that 15 berries would cause the death of a child and 40 that of an adult. No deaths of domestic animals have been observed in searching the literature, but animals may possibly eat it along the hedgerows at times when grass is scarce. Pigs might possibly eat sufficient of the rootstock, or poultry of the berries, to cause poisoning.

Toxic Principle. The plant contains the bitter and poisonous glucoside Bryonin (C₃₄H₄₈O₉).

Symptoms. The symptoms are those resulting from inflammation of the stomach and intestines, together with convulsions. According to Cornevin consumption of the plant promotes sweating, and causes a livid hue, nausea, diuresis and abundant painless, watery defÆcation, to which are added in cases of poisoning nervous symptoms of stupor and tetanic convulsions. There may be superpurgation or a suppression of defÆcation.

Lander states that 2 lb. of fresh or 6 to 8 oz. of dried root given to horses did not cause purging, but there was abdominal pain, loss of appetite, accelerated breathing, fever, dullness and copious urination.

Cases may end fatally.

Cowbane or Water Hemlock (Cicuta virosa L.). This plant is undoubtedly exceedingly poisonous, and fatal cases have occurred in both man and farm live stock. It has been mistaken by man for parsley, celery or parsnip, with fatal results, many persons having succumbed to it. The rootstock is attractive to children on account of its sweetish taste. Pott says that either fresh or dry it is poisonous to all animals when only a small quantity is eaten, and often causes rapid death. Sheep and goats appear to be less readily affected than other domestic animals, and cattle to be most sensitive. The loss of eleven animals in Brittany was noted in the Veterinarian in 1877, and a number of cattle died in Ireland (Veterinary News, 1911), death in both cases being due to Cowbane. It is clearly dangerous to grazing animals which have easy access to it, especially if ordinary herbage is scarce. Hedrick (Canada) is quoted as stating that a piece of the root about the size of a walnut is sufficient to kill a cow in about fifteen minutes; and MÜller says that the quantity of dried plant sufficient to kill a horse appears to be about 1 lb. According to Kanngiesser the mortality in human poisoning due to this plant amounts to 45 per cent. of the cases.

Toxic Principle. The poisonous character of Cowbane has not been fully investigated, and the toxic principles are given as the alkaloid Cicutine, with Oil of Cicuta, and Cicutoxine. The last is a bitter resinous substance classed by Cushny in the picrotoxin group; it occurs in the dry root to the extent of 3·5 per cent. The toxicity is stated to vary with season and climate; the rootstock is most poisonous in spring.

Symptoms. In man the yellow poisonous juice in the rhizome induces epileptic convulsions, followed by death. The cicutoxine gives acrid narcotic symptoms quickly followed by fatal results. The symptoms usually appear within two hours, and death ensues in half-an-hour to several hours. The symptoms which appear in an hour or so are given as loss of appetite, salivation, vomiting (in swine), nausea, colic (in horse), bloating (in cattle), diarrhoea, irregular pulse and heart, dilatation of pupils, rolling of eyeballs, vertigo, reeling in circles, twisting of neck, falling down, automatic movement of limbs, opening and shutting of mouth, and death, usually with convulsions, in from half an hour to an hour after first manifestation of symptoms.

For cattle, Lander gives hurried respiration, collection of froth at the mouth and nostrils, and tympanites. The limbs are extended and alternately stiffened and relaxed.

In his description of the symptoms Esser states that swallowing is difficult, the tongue is stiffened, there is salivation, and death takes place after loss of consciousness and convulsions.

Water Parsnip (Sium latifolium L.). The leaves and especially the root of this species are regarded as poisonous, and the plant is described as “poisonous” by Strasburger.

According to MÜller the symptoms resemble those produced by Chaerophyllum (p. 40). After eating the roots cows showed symptoms of excitement, leading, in some instances, very quickly to death. The milk, according to Cornevin, is of a disagreeable flavour.

The related S. angustifolium has also been mentioned as objectionable. As regards the toxic principle these plants have not been closely studied, and it is not possible to give detailed symptoms.

Water Dropwort (Oenanthe crocata L.). This weed of marshes, ditches, and similar wet spots, has been a frequent cause of loss of stock. Cases of fatal human poisoning have also occurred, owing to the leaves having been mistaken for celery and the rootstock for parsnips. Several cases of the poisoning of cattle have been recorded in the veterinary journals, and sheep and cattle died on a farm near Bristol (Jour. Roy. Agric. Soc., 1898). Horses have also been poisoned. Johnson and Sowerby (1861) record the poisoning of 17 convicts near Woolwich, the leaves and roots being eaten in mistake for celery and parsnips respectively. Nine suffered from convulsions and became insensible; one died in five minutes, a second in a quarter of an hour, a third in an hour, and a fourth a few minutes later, while two more died during the next few days.

Cornevin says that this plant causes the poisoning of animals every year—they eat it willingly, showing an enfeebled instinct owing to domestication. The plant is poisonous in all its parts, the root being the most toxic, and drying does not destroy the toxic property. Cornevin gives the following quantities of the fresh root as necessary to poison various animals:—

Holmes described Oenanthe crocata as the most dangerous and virulently poisonous of all our native plants (Pharm. Jour., 1902).

Other species of Oenanthe are also poisonous in a less degree—e.g. O. fistulosa L., and O. Phellandrium Lamk.

Toxic Principle. Poehl (1895) obtained from the root of this species an amorphous neutral product which he designated Oenanthotoxin. The latest investigation is that by Tutin, who examined entire dried plants collected in early spring, and the experiments confirmed the conclusion arrived at by Poehl, that the toxic principle is a neutral resin. A dark-coloured, viscid resin, insoluble in water, and equal to 3 per cent. of the weight of the plant, was extracted, and it is stated that the neutral portions of the petroleum and ether extracts of this resin represent the toxic principle of the plant. As there is no evidence of the homogeneity of this product, and it is probably complex in character, it was given no name or formula. The fact that it has poisonous properties was ascertained by administering the various products to guinea pigs per os.

Symptoms. In poisoning by O. crocata the symptoms generally appear very quickly, and in serious cases death may follow in from one hour to a few hours. In Tutin’s experiments on guinea pigs the extracts referred to above rendered the animal hypersensitive in two to four hours, while marked convulsions, with trismus soon appeared; the heart-beat became very noticeably slow and the convulsions persisted until death ensued. There is great restlessness, difficult breathing, convulsions, loss of sensation, blindness and stupefaction (MÜller); Lander says the symptoms recall hemlock poisoning, with the addition of green foetid diarrhoea.

In cattle, one hour after eating, there is depression and accelerated respiration; the conjunctivÆ are injected, the eye turns in its orbit, the pulse is weak but rapid, and there is foaming. Later, there is colic, and spasmodic contractions of limbs and jaws. If the quantity ingested is sufficient to cause death, the animal falls, but still moves its limbs. There is bellowing, contraction of pupils, insensibility, and death in convulsions—or, if not fatal, cattle may remain paralysed.

In the horse, the appearance of the symptoms and the course of the illness are much more rapid and the nervous symptoms are accentuated.

If the pig has consumed only a small quantity it soon gets rid of the poison by vomiting; but if the quantity is considerable there is no vomiting and death is as rapid as with cyanide poisoning (Cornevin).

Fool’s Parsley (Aethusa Cynapium, L.). Much has been written about the toxic properties of this weed of cultivated fields, principally because, owing to the fact that the foliage has often been mistaken or misused for parsley and the roots for radishes (!), it has been the cause of human poisoning, though it seems to be one of the least active of the poisonous Umbellifers. Its poisonous character is undoubted, but it is unlikely to cause the poisoning of stock, which seem to refuse it. Some authors regard it as strongly poisonous, but others as more or less harmless. Johnson and Sowerby cite a case in which a child of five years old died within an hour after eating the root, and a second death (in Germany) within twenty-four hours from the use of the leaves in soup.

The most complete account of this plant is that by Power and Tutin, issued from the Wellcome Chemical Research Laboratories in 1905. Many authors since 1807 are cited as writing of its poisonous properties, and of cases of poisoning, two of which terminated fatally. Miller (1807) says that “most cattle eat it, but it is said to be noxious to geese.” Bentley and Trimen write that “in all recorded experiments with it on animals, it has had poisonous effects.” Dr. John Harley (1876 and 1880), after experiments on a child and adults, concluded that the plant was absolutely free from the noxious properties attributed to it. In 1904, however, a case of severe poisoning by it was recorded (Brit. Med. Jour., July 16, 1904, p. 124).

Toxic Principle. This has for many years been stated to be the alkaloid Cynapine. For their investigation Messrs. Power and Tutin collected the plant round London in July and August, with the fruits still green, and after thorough chemical examination found 0·015 per cent. of an essential oil of rather unpleasant odour; 0·8 per cent. of resinous substances; and an exceedingly small amount of a volatile alkaloid having the peculiar characteristic odour of Coniine. The amount of hydrochloride of the alkaloid obtained showed that if the base were Coniine it would correspond to only 0·00023 per cent. of Coniine in the plant. In a degree this confirms the statement by Walz (1859) that the fruit “contains a volatile base, very similar in odour and chemical behaviour to Coniine, and probably identical with it.” The investigators suggest that the alkaloid is Coniine, and the small amount would justify the opinion, but there may be variation in toxic property according to stage of development and climate. The authors conclude that “it cannot be considered improbable that under favourable conditions of growth, the proportion of alkaloid may be increased to such an extent as to impart to the plant the poisonous properties ascribed to it.”

Symptoms. In a child which died, there were abdominal pain, a feeling of sickness, and a tendency to lockjaw, and death supervened within an hour; and in a German case, vomiting, diarrhoea, lockjaw, and death in 24 hours. (Johnson and Sowerby.) The plant causes convulsions and stupor, with nausea and vomiting (Henslow).

The symptoms observed in cows are loss of appetite, salivation, fever, uncertain gait, and paralysis of hind limbs (MÜller).

Pott refers to a case which occurred in Guernsey among horses. Animals with white muzzles and feet had diarrhoea, while other horses remained healthy. All white places on the body were badly inflamed. Pammel states that the plant causes stupor, paralysis and convulsions in domestic animals.

Chervils (Chaerophyllum sp.). No investigation of these plants appears to have been undertaken, but C. sylvestre L., though eaten by some animals, including the ass and the rabbit, is stated by a German observer (vide Cornevin) to have caused the death of pigs. MÜller states that according to the literature both cows and pigs have been poisoned, even fatally, by C. temulum L. The plants have a strong odour and acrid taste.

Toxic Principle. This, if any, appears to be unknown, though MÜller (1897) says that C. temulum contains in all its parts the little known Chaerophyllin (? alk.).

Symptoms. The pigs referred to above as having died were said to show paralysis, dilated pupils, and enteritis, and to refuse food. Postmortem examination showed acute gastro-intestinal inflammation. In the case of cows there are similar symptoms.

Hemlock (Conium maculatum L.). This plant, famous from ancient times as extremely poisonous, has a foetid, disagreeable odour—a mousy smell—especially noticeable when the plant is bruised. It has caused human poisoning in three ways: the seeds have been eaten in error for anise, the leaves for parsley, and the roots for parsnips.

Animals rarely appear to eat this plant, but cases have been recorded. It is stated that in the United States many domestic animals have been killed by it; and Ewart says that it is responsible for poisoning a number of cows in Victoria. Goats are believed to be largely immune to the poison, or are less harmed than other animals, and sheep are stated to eat the plant with impunity, though cases of poisoning are recorded. Johnson and Sowerby state that horses have occasionally swallowed considerable quantities without apparent effect, while Cornevin remarks that to cause death a horse would need to eat 4 to 5½ lb. of the fresh plant, or a cow 8¾ to 11 lb.

Hemlock is probably most dangerous to live stock in the spring, when green herbage is least plentiful and the young shoots of hemlock are fresh and short. Chesnut says that the root is nearly harmless in March, April and May, but dangerous later, especially in the first year of growth; but Esser states that it is only poisonous in the spring. The foliage is more poisonous before flowering than after, when the poisonous principle passes to the fruits, which are more poisonous before ripening (three quarters ripe) than afterwards. Pott remarks that after eating hemlock cows give milk with a bad taste.

Toxic Principle. Early in summer the toxic principle appears to be chiefly contained in the foliage, but later in the fruit, particularly when still green. Among the substances contained in hemlock are the toxic alkaloid Coniine (C₈H₁₇N), the poisonous Coniceine (C₈H₁₅N), Conhydrine (C₈H₁₇NO), the alkaloid Methylconiine (C₉H₁₉N), Pseudoconhydrine (C₈H₁₇ON). Coniine may be described as an oily, colourless, quite volatile liquid, quickly turning brown on exposure to the air, and giving a mousy odour to the whole plant. The amount of Coniine in the fresh leaves is given (Pammel) as 0·095 per cent., but in the ripe seeds 0·7 per cent. English fruits contain much more of the total alkaloids than imported fruits. Owing to the volatile character of the poisons hemlock largely loses its toxicity when dried in hay, and is therefore the less likely to prove injurious to domestic animals.

Symptoms. Hemlock is a dangerous narcotic plant. Even the smallest quantities may cause inflammation of the digestive organs, paralysis and death. The general symptoms are salivation, bloating, dilatation of pupils, rolling of eyes; laboured respiration, diminished frequency of breathing, irregular heart action; loss of sensation, convulsions, uncertain gait, falling, and at the end complete paralysis. Death occurs after a few hours. The poison acts on the motor nerve endings, causing paralysis, dyspnoea resulting from paralysis of the pectoral nerves, and acceleration of the heart from that of the inhibitory fibres of the pneumogastric.

Small quantities cause in the horse a little prostration, yawning, acceleration of pulse, dilatation of pupils and sometimes muscular spasms of the neck and shoulders. Large quantities cause nausea, unsuccessful attempts to vomit, gritting of teeth, accelerated respiration and dyspnoea, and muscular tremors commencing in posterior members and spreading to anterior members and spine. There is next difficulty of locomotion, sweating (but not continual), falling, paraplegia, then paralysis, loss of feeling, lowering of temperature, rapid pulse, increasingly difficult respiration, and death from stoppage of respiration.

With cattle there is ptyalism, cessation of digestion, bloating, constipation, weakness and stupor. Pregnant cows have been observed to abort; the milk of cows has an unpleasant flavour. There are bloody evacuations in some instances in the case of the ox. In cows Chesnut says that there was “loss of appetite, salivation, bloating, much bodily pain, loss of muscular power, and rapid, feeble pulse.”

In sheep the abdomen is tucked up, the animal has a dazed appearance, there is dilatation of pupils, unsteady gait, the hind limbs being dragged, coldness, and death after a few convulsive movements.

In the pig there is prostration and inability to move, coldness, slow breathing, livid mucous membranes, imperceptible pulse, paralysis, particularly of the posterior members, and no convulsions.