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CAMBRIDGE AGRICULTURAL MONOGRAPHS

PLANTS POISONOUS TO

LIVE STOCK

CAMBRIDGE UNIVERSITY PRESS

C. F. CLAY, Manager

London: FETTER LANE, E.C.

Edinburgh: 100 PRINCES STREET

London: H. K. LEWIS AND CO. Ltd., 136, GOWER STREET, W.C.

London: WILLIAM WESLEY AND SON, 28, ESSEX STREET, STRAND

New York: G. P. PUTNAM’S SONS

Bombay, Calcutta and Madras: MACMILLAN AND CO., Ltd.

Toronto: J. M. DENT AND SONS, Ltd.

Tokyo: THE MARUZEN-KABUSHIKI-KAISHA

All rights reserved

a Reddish-brown to reddish-purple “Java” Beans (Phaseolus lunatus); b “Red Rangoon” Beans (P. lunatus); c “Large White” Beans (P. lunatus); d Castor Oil Beans (Ricinus communis); e “Indian Peas” (Lathyrus sativus), from Bombay; f Ergot (Claviceps purpurea), from Spain. All natural size.

PLANTS POISONOUS TO LIVE STOCK

BY

HAROLD C. LONG, B.Sc. (Edin.)

of the Board of Agriculture and Fisheries

Author of Common Weeds of the Farm and Garden

Cambridge:

at the University Press

1917

PREFACE

As in the case of a previous volume, Common Weeds of the Farm and Garden, the preparation of this handbook was undertaken because of the great lack of readily available and reliable information on the subject in English scientific literature. Many of the facts were known to a few interested persons, but many others were so scattered here and there in technical reports and journals that they were scarcely known even to expert chemists and botanists. The bringing of this information together in some sort of order has involved considerable labour extending over several years, but if the volume be found helpful to those for whose use it has been prepared I shall feel more than gratified.

That the subject is of importance is fully realised by farmers and veterinary surgeons alike, for the annual loss of stock due to poisonous plants, though not ascertainable, is undoubtedly considerable. It was felt that notes on mechanical injury caused by plants and on the influence of plants on milk might usefully be included, as in some degree related to poisoning; this has therefore been done. On the other hand, a number of cultivated plants (e.g. Rhus, Wistaria) which are poisonous have not been included because exotic and hardly likely to be eaten by stock. Fungi generally also find no place in the volume, as they are sufficiently extensive to deserve a volume to themselves, and are far less readily identified than flowering plants.

The dividing line between plants which are actually poisonous and those which are only suspected is far from clear, but a division was considered desirable for the convenience of the reader, and an endeavour has been made to give a sound but brief statement as to the present information on plants poisonous to live stock in the United Kingdom, with symptoms, toxic principles, and a list of the more important references to the bibliography in relation to each plant included in Chapters II to VI (the numbers corresponding with the numbers in the Bibliography).

Regarding symptoms it is to be regretted that in many cases they appear to be the result of injections of the toxic extracts, and not observations made after natural poisoning by ingestion of the plants. Further, there may frequently be doubt as to the identification of the plant suspected of causing poisoning; indeed, in some cases it is possible that the identification rests on the veterinary surgeon or the stockman thinking a certain plant is the cause. The most complete and systematic account of European poisonous plants is that of Cornevin (1887), and references to poisonous plants in the ordinary literature are heavily indebted to him. In so far as the toxic principles of the plants are concerned, however, his book is in many instances no longer reliable.

The chemical formulae, quoted for the use of students and research workers, have been checked by consulting works by the following authors, the reference to the bibliography being given in brackets: Henry (128), Dunstan (76), Allen (4), Haas and Hill (114), Thorpe (240), Van Rijn (252), Kobert (161), Esser (81), and Beilstein (16).

Apart from the literature consulted I desire to acknowledge my great indebtedness to the Board of Agriculture and Fisheries for kind permission to make use of official records; to Mr F. W. Garnett, M.R.C.V.S., for kindly reading the proofs from the veterinary standpoint; to very many Experiment Stations, State Departments of Agriculture, and other authorities in Australasia, America and the Continent of Europe, for assistance given and literature sent; to Sir David Prain and members of the staff at Kew for much friendly advice, and aid in consulting the Kew library; to Sir James Dobbie for permission to spend some time at the Government Laboratories to consult certain volumes; to Mr T. H. Middleton, C.B., Dr. E. J. Russell, Professor W. Somerville, Sir Stewart Stockman, Professor T. B. Wood, and others, for information and many helpful suggestions; to my friend Mr W. A. Whatmough, B.Sc. (Lond.), for many suggestions and kindly reading the proofs; and to my colleague Mr W. R. Black for invaluable help in preparing notes, checking data and reading proofs. To all these, and many others who are not mentioned by name, I tender my sincere thanks.

For any shortcomings I crave the indulgence of my readers, only requesting that they be friendly enough to spare a moment to call my attention thereto.

H. C. LONG.

Surbiton,

October, 1916.

CONTENTS

CHAPTER I
INTRODUCTION.

What is a Poisonous Plant? As will be shown later, so-called “poisonous” plants differ widely in “degree of harmfulness,” and it is highly probable that under ordinary conditions many of the plants commonly reputed to be poisonous are really almost or quite harmless. It is possible, however, that a plant usually unsuspected may on occasion prove noxious—for example, Nepeta Glechoma (p. [96]), included as suspected of poisoning horses. For these reasons, no line of demarcation can be drawn to separate actually poisonous plants from those which are suspected or are almost certainly quite harmless; and a large number of species is included in Chapter VII as suspected, many of them, however, being almost certainly more or less poisonous in certain circumstances. In many cases it is practically impossible to come to any conclusion as to the degree of toxicity of a plant, owing to the want of exact information. Many plants are quite harmless except when affected by fungi, moulds, etc.

A really poisonous plant may be defined as one a small quantity of which when eaten induces some form of indisposition with irritant, narcotic, or nervous symptoms, with serious or even fatal consequences either immediately or by reason of cumulative action of the toxic property.

Harm done by Poisonous Plants. A perusal of the following pages will afford convincing proof that the question of the general “wholesomeness” of wild plants is worthy of serious consideration by all who are interested in the practice of agriculture. Still more important is a satisfactory knowledge of the extent to which plants are actually poisonous—that is, sufficiently injurious when eaten in small or large quantities to induce more or less severe indisposition, illness or death, with the consequent losses which such bring in their train—loss of milk and meat production in the case of cattle, of meat and wool production in sheep, of power in the horse, of expenditure in attendance and veterinary treatment generally, and possibly total loss by death of the animals concerned.

The losses due to Poisonous Plants in Great Britain happily afford no comparison whatever with the immense losses sustained in some other countries, such as the cases of lupine poisoning mentioned at p. [29], but deaths are sufficiently numerous to make it certain that financial losses are in the aggregate very heavy. In this connection it may suffice to refer to the many cases of yew poisoning, the losses due to Umbellifers (pp. [36]–42), and the instance reported in the Staffordshire Weekly Sentinel in relation to meadow saffron and water hemlock (p. [80]). Further, it appears to be extremely likely that many losses due to unascertained causes are really due to plant poisoning. For this reason veterinary surgeons will be well advised always to consider this possibility and, if need be, to obtain the services of a trained botanist to survey the farm or field involved, with the object of deciding whether poisonous plants are present.

Circumstances in which Poisoning occurs. It may be assumed that many plants are to a considerable extent protected from animals by the fact that they have an unpleasant odour, are acrid or bitter to the taste, or are actually toxic in character, just as others assume such protective devices as spines. In a state of nature animals appear to avoid instinctively such plants as are toxic or “unwholesome,” and to be less readily poisoned than are domesticated animals living under artificial conditions. Indeed, it has been remarked that farm stock reared in a locality where certain poisonous plants abound are much less likely to be injured by these plants than animals imported from a district where they do not occur.

The individuality of stock is also a factor which may be responsible for poisoning, some animals having what may be described as a depraved appetite for unusual and unappetising food plants. It would appear that animals are often tempted to eat dark-green plants of luxuriant growth which are soft and succulent. This is especially true when the plants are young and tender, particularly as regards sheep, which, however, usually avoid tall, old rank-growing and coarse herbage—unless absolutely pressed by hunger. Cattle, however, are not so particular, and will commonly eat large coarse-growing plants.

Sheep have been observed to be particularly variable in their choice of food plants, not only individually in the flock, but from day to day. Chesnut and Wilcox remark[^[1]] that “there seems to be no way of accounting for the appetite or taste of stock. This statement is perhaps especially true of sheep. We have often observed sheep eating greedily on one day plants which they could scarcely be persuaded to eat on the following day on the same range.” In the case of one flock of sheep on a foothill range at an altitude of 4,600 ft. “a few of the sheep were observed eating large quantities of wild sunflower (Balsamorhiza sagittata), a few ate freely of false lupine (Thermopsis rhombifolia), some confined their attention largely to the wild geranium, while others ate false esparcet (Astragalus bisulcatus) almost exclusively. Two sheep were seen eating the leaves of lupine, and about fifty ate a greater or less quantity of Zygadenus venenosus, while the majority of sheep in the band fed exclusively upon the native grasses on the range.”

[1]. “The Stock-Poisoning Plants of Montana,” V. K. Chesnut and E. V. Wilcox. Bul. No. 26. U.S. Dept. Agric., Div. Bot., 1901.

Horses also have been known to acquire in America a depraved appetite for horsetail and loco-weed.

The different species of live stock are often quite differently affected by poisonous plants, some being very susceptible to a given plant while others may be little or not at all susceptible. One species (e.g. the pig) may readily vomit the poison of a plant which is emetic, while another (e.g. the horse) may be unable to do so and hence be the more seriously injured. The variability of the different classes of live stock in this respect is frequently brought out in Chapters II to VI. Poisonous effects may also vary with the individuality and age of animals of the same species.

At certain periods of the year—e.g. in early spring, and during dry summers,—there may be a scarcity of green herbage, and this may induce animals to eat any green plants which are especially early, including poisonous ones, which they would otherwise refuse.

In some cases poisonous plants which do not lose their toxic properties on drying (e.g. meadow saffron) may be included in hay, and hence find their way to stock in such a form that they may not be distinguished. It has been found, however, that some poisonous plants or parts of them are refused by stock when mixed with good herbage in hay. Care should be exercised that poisonous plants are not included with hay or green fodder, and in cases of poisoning all forage should be examined.

Animals may also be poisoned by certain toxic seeds (e.g. corn cockle) fed to them with cereal grains, in feeding stuffs generally, or in the refuse seeds from the sources mentioned. Here again judgment is necessary, and it is probably advisable on all counts to burn the weed seeds and similar refuse from the sources mentioned. Poisonous seeds may occur in low quality feeding stuffs, and poisonous seeds of foreign origin are occasionally sold for food purposes owing to the mistaken idea that they are a valuable addition to the ration (e.g. the poisonous “Java” beans). In any case in which an animal is believed to have been poisoned purchased feeding stuffs should always be considered as a possible source of injury and be submitted to examination.

Clippings and trimmings from gardens and shrubberies have proved a more or less common cause of live stock poisoning, such material being too often carelessly thrown out for animals to pick over. In such circumstances it may quite easily happen that the animals get yew, daphne, privet, rhododendron, azalea, solanums, and other plants of a poisonous character. For this reason it is better to destroy such trimmings, etc., by burning them, or by adding them to the compost heap as the case may be.

A further source of poisoning must be noted here—fleshy and parasitic fungi (toadstools, rust fungi), moulds and similar organisms. Many toadstools are directly poisonous when eaten, but the microscopic organisms are probably in themselves harmless, though taken with food which they are responsible for injuring (bad hay, cakes, etc.), the poisoning being due to the changed and damaged feeding stuffs, or possibly to poisonous principles directly elaborated by the microscopic fungi. Fungi and related organisms cannot be dealt with in this volume, but it may at least be said that the use of mouldy hay and similarly affected feeding stuffs is attended with some danger, which is not yet very clearly defined.

Effect of Soil, Climate and Cultivation on the Toxic Properties of Plants. In general, wild poisonous plants are richer in either alkaloids or glucosides than the same species when cultivated, though there are exceptions. In many cases it is found that plants vary considerably in toxicity, or the percentage content of the poisonous principle, according to soil, light, moisture, etc. Solanaceous plants in particular vary in this way, and one or two instances may be given as examples. Solanum nigrum varies so much that it has been regarded as harmless in one country and quite poisonous in another (p. [52]).

Experiments conducted at the Arlington Experimental Farm, Virginia, showed that in 24 first-year plants of Atropa Belladonna grown in 1910 the alkaloid contents of the leaves varied from 0·334 to 0·700 per cent., and averaged 0·547 per cent. In 1911 the alkaloid contents (usually the average of five pickings) of the leaves of 59 plants varied from 0·306 to 0·766 per cent., and averaged 0·532 per cent. In 1912 the alkaloid contents (commonly the average of 5 pickings) of the leaves of 57 plants varied from 0·352 to 0·768 per cent., and averaged 0·545 per cent. In individual plants at a single picking the highest alkaloid content in 1911 was 0·925 and the lowest 0·200, and in 1912 the highest was 0·882 and the lowest 0·292. (Jour. Agric. Res., I. 2, Nov., 1913.)

The variation in the percentage of poisonous principle was well shown in several papers read at the International Congress of Applied Chemistry held at Washington and New York in 1912 (see Chemist and Druggist reports). For example, Carr stated that at the Wellcome Materia Medica Farm, Dartford, Kent, the effect of manuring on medicinal plants has been tested for some years, and the effect of the more common fertilisers on Atropa Belladonna was shown by the following table:—

In considering these results it must be remembered that the soil is naturally suited to the plant, and the percentage of alkaloid obtained without added fertilisers is already high. The low figures obtained in 1907 were probably due to the seasonal conditions. Atmospheric conditions have a modifying influence.

It was also shown that the Belladonna root of commerce varies greatly in alkaloid strength. “In a number of analyses made of commercial roots, variations from 0·27 to 0·69 per cent. have occurred. The average of twenty-one analyses of German and Austrian commercial roots was 0·40 per cent. Other observers have recorded similar results. Chevalier (Compt. Rend., 1910, 150, 344) gives the following figures for Continental roots: French, 0·300 to 0·450 per cent.; Austrian, 0·251 to 0·372 per cent.; Italian, 0·107 to 0·187 per cent. Henderson has shown the average of thirty samples of foreign root to be 0·3 per cent. It is interesting to observe that the average of nine samples of root grown at Darenth is 0·54 per cent. In order to determine whether this variation was due to collecting at different times of the year, roots from the same plot, derived from second year’s plants, which were sown at the same time, were dug up at intervals and dried. The following is a record of the analysis of these samples:—

“The amount of variation throughout the year is thus seen to be very small.”

Dunstan (Bul. Imp. Inst., 1905) has shown that Hyoscyamus muticus grown in India yielded 0·3 to 0·4 per cent. of hyoscyamine, but that the same species grown in Egypt produced 0·6 to 1·2 per cent.

According to Esser no coniine is found in Conium maculatum growing in the far north. The same authority says that the root of Hyoscyamus niger is quite free from toxic properties in winter.

Variation in the Poisonous Parts of Plants. As will be shown in succeeding chapters, many plants (e.g. meadow saffron) are poisonous in all their parts, though the amount of the toxic substance may differ according as to whether the seeds, leaves, stem or roots are severally considered. In other cases one part of the plant alone is toxic (e.g. the seeds, as in corn cockle). Further, some species vary in the percentage of the toxic substance in the leaves before and after flowering. Frequently the root is the most toxic portion of the plant. This point may be usefully recollected in relation to poisoning of live stock, which are in general affected by the foliage or ripe seeds.

Eradication of Poisonous Plants. Wherever poisonous plants are found, particularly in quantity, where they are liable to be eaten by live stock, an attempt should be made to eradicate them. They may be simply dealt with as weeds as may be necessary according to the species concerned. When any difficulty is experienced in regard either to determination of the species or to methods of eradication the advice of the Board of Agriculture and Fisheries (Whitehall Place, London, S.W.) should be requested. Stock should at once be removed from a suspected pasture, which should be immediately and thoroughly examined by a competent botanist. Harmful plants should be eradicated and their place filled by better herbage.

Treatment of Poisoned Animals. This volume makes no pretensions to deal with the veterinary treatment of cases of plant poisoning. Whenever poisoning is suspected the services of a veterinary surgeon should be sought without delay; the text books at his disposal will aid him in the treatment of any case which presents unusual difficulties. The symptoms indicated in the following pages, together with the possible discovery of a suspected plant, may be utilised in diagnosis.

Tests with Suspected Plants. The action of plants on animals may be ascertained (1) by observing the effects in cases in which it has been established that the plants have been eaten, or (2) by direct experimental feeding of animals with the plant. In the first case the results may be accurate and satisfactory if observations have been made from the outset.

As regards (2) the results may or may not be satisfactory according as the plan pursued is sound or otherwise. For example, it cannot be considered altogether reasonable and satisfactory to extract the principles present in the plant, inject them into the blood stream, and conclude from any ill effects that the animal may exhibit that the plant is poisonous, since the substance extracted may be poisonous under such conditions but little or not at all harmful when the plant is eaten in the small quantities commonly taken by animals. Again, it cannot be held satisfactory to feed an animal on a heavy and exclusive diet of the suspected plant for a considerable period. The real test would, in general, consist in a feeding trial in which the suspected plant occupied a place in the ration in reasonable quantity—such a quantity as might well be taken in natural circumstances, in view of its relative abundance in regard to other food available; and if considered likely that the plant would be eaten daily it may be fed regularly for some days. Should such a test prove negative it may generally be held that the plant is not poisonous, or only so in exceptional circumstances.

Legal Aspect of Plant Poisoning. There is clearly some legal liability in regard to poisonous plants which may, by hanging over a boundary, cause injury to a neighbour’s stock. The only cases known to the author are in relation to the yew. In the case of Crowhurst v. Amersham Burial Board (48 L. J., Ex. 109; 4 Ex. D., 5) a Burial Board was held liable for the loss of a horse poisoned by eating leaves of a yew tree planted in the cemetery owned by the Board, the tree having grown through and over their fence and projected on to the meadow occupied by the plaintiff. In Ponting v. Noakes (63 L. J. B. 549; (1894) 2 Q.B., 281) the defendant was not held liable for the death of a horse which ate off the branches of a yew tree, because the tree did not extend up to or over the plaintiff’s boundary, though it overhung a ditch, the edge of which was the boundary, and was hence accessible to the plaintiff’s stock.

The Toxic Principles of Plants. The poisonous substances in plants may be grouped either (1) according to their physiological effects on certain organs; (2) according to the principal outward and perceptible symptoms caused; or (3) in accordance with their chemical relationships.

In regard to (1) the poisons may be nerve, heart, blood-poisons, etc. (2) The poisons may be acrid, narcotic, or both. Acrid poisons are those which cause irritation or inflammation of the digestive tract (Euphorbia, Ranunculus, Daphne, etc.); narcotic poisons affect only or chiefly the brain (Agrostemma, Papaver, Atropa) or chiefly the spinal cord (Claviceps purpurea, Lolium temulentum); acrid-narcotic poisons induce to a greater or less extent the symptoms of both the foregoing groups (Taxus, Colchicum, Cicuta, Solanum, etc.).

(3) As the accounts of the individual plants will show, the toxic principles of many plants are not yet well understood, either as regards chemical constitution or symptoms caused. Many poisons may be driven off by heat (boiling, drying), and some plants may thus be rendered harmless.

Most of the toxic principles of our native poisonous plants are Alkaloids or Glucosides. The former all contain nitrogen, differ considerably in molecular constitution, and are usually combined with widely distributed organic acids. In the pure state they are colourless and usually stable, crystalline or amorphous solids, or readily volatile liquids; they usually have a burning taste. In general the same base is confined to species of the same order—e.g. Solanine to the Solanaceæ. The alkaloids include the most powerful poisons.

The term “Glucoside” indicates a group of substances which by the action of an acid or enzyme are split up into a sugar (grape sugar, galactose or rhamnose) and other substances (alcohol, aldehydes, acids). They have a bitter taste and are generally readily soluble in water. Related to the glucosides are also the Saponins, remarkable for the fact that they induce an exceedingly frothy condition in water; the prussic acid yielding compounds or cyanogenetic glucosides (e.g. Amygdalin and Phaseolunatin) also belong to this group. Other substances will be mentioned in the succeeding chapters.

CHAPTER II
RANUNCULACEÆ.

Traveller’s Joy (Clematis Vitalba L.). The extent to which this species is poisonous is not clear, though all parts are stated to be poisonous, acrid and narcotic, while the juice tends to blister the skin. It is remarked by Cornevin that it is less poisonous in spring, when the ass and goat browse on it to a considerable extent without serious trouble, than later, when it cannot be eaten without danger.

Toxic Principle. Traveller’s Joy appears to contain strongly poisonous substances which have not been closely investigated. Greshoff found a Saponin in the leaves[^[2]]. The poison is dissipated by heat.

[2]. Kobert states that various species of Clematis, Ranunculus, Anemone, and also Caltha palustris and Trollius europæus, contain Anemonal or Pulsatilla-camphor, which causes strong local irritation, burning and swelling in the mouth, vomiting, intestinal inflammation, etc.

Symptoms. When eaten in quantity the young shoots are diuretic, violently purgative, causing dysentery, and in rare cases death. Applied to the exterior it is irritating and even vesicatory. (Cornevin.)

REFERENCES.

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

Anemone (Anemone sp.). Both our native species of Anemone appear to be more or less poisonous in character: the Wood Anemone or Wind Flower (A. nemorosa L.), and also the Pasque Flower (A. Pulsatilla L.). These plants, the former of which grows in woods and damp shady spots in fields, and the latter on chalk downs and limestone pastures, may on occasion be taken by stock in early spring, when green herbage is not too plentiful, but deaths appear to be rare, even if they have occurred. All parts of the plants contain a toxic principle, which is volatile and destroyed by drying.

Toxic Principle. The toxic substance is stated to be Anemone-camphor (oil of Anemone) which imparts a bitter taste to the plants, and itself gives rise in the plant to Anemonic acid and Anemonin (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 diarrhœa and dysentery. There are pronounced respiratory and heart troubles.

Pott confirms the symptoms of hæmaturia, diarrhœa, and inflammation of the stomach and intestines in the case of A. Pulsatilla when fed in the green condition. According to Esser, the plant poison affects the spinal cord and the brain, the symptoms being similar to those produced by Aconitum Napellus.

REFERENCES.

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

Buttercups (Ranunculus sp.). A number of species of Ranunculus are acrid, irritant or severely poisonous, as the case may be. There are variations in the poisonous character according to the season, and some parts of the plant are more toxic than others. At the time the young shoots develop in the spring but little of the poisonous principle is present, and some (e.g. R. Ficaria) are not then poisonous, but a larger quantity of the poisonous principle forms later, and some species are especially dangerous at the time of flowering, after which the toxicity decreases with the maturity and state of dryness of the plant. The flowers are the most poisonous, and then the leaves and stem. It does not seem to have been demonstrated that the seeds of any species are dangerous, though Henslow states that the fruits of some species, when green, appear to be most intensely acrid.

Some species of Ranunculus are especially harmful (R. sceleratus, R. Flammula, and R. bulbosus), while others are less so (R. lingua, R. Ficaria, R. acris). The toxic principle is volatile, and buttercups are easily rendered innocuous by drying or boiling—so much so that when dried in hay they may be regarded as a nourishing food for stock, and are readily eaten. Indeed, R. repens is scarcely, if at all, injurious even when green, though a case of fatal poisoning to sheep said to be due to this species was reported in the Veterinarian in 1844. Fresh R. aquatilis is held to be quite harmless, and has been used as a fodder. “Along the banks of the Hampshire Avon, and other places in the same neighbourhood, it is used by the peasantry as fodder. They collect it in boats and give it to their cows and horses, allowing the former about twenty to thirty pounds a day. One man is said to have kept five cows and a horse, with little other food but what they could pick up on the heath, using no hay but when the river was frozen. Hogs eat it and will live upon it alone until put up to fatten.” (Johnson and Sowerby—Useful Plants of Great Britain.)

R. sceleratus L., or Celery-leaved Buttercup, is probably the most toxic species, and it is stated that in man a single flower may cause poisonous symptoms resembling those due to Anemone and Colchicum. It is considered especially dangerous to cattle, and has caused many losses: among its French names are Mort aux Vaches, and Herbe sardonique. Poor people have been known to eat the young shoots when boiled, heat dispelling the poison.

R. Flammula L., the Lesser Spearwort, has repeatedly proved fatal to horses and cattle.

R. bulbosus L., the Bulbous Buttercup, is somewhat variable in toxicity, and is least dangerous after the flowers have dropped their corolla, and the bulb-like rootstock is most harmful in autumn and winter. The flowers are the most dangerous part.

R. Ficaria L., Lesser Celandine, varies in toxicity with locality and season, being most harmful at the flowering period. It is stated that wood-pigeons eat the roots with avidity, and that the young shoots have been eaten as a salad in Germany, as they are not toxic. An English veterinary surgeon (Flower) recorded that three heifers were poisoned by it (Vide Cornevin).

R. acris L., Acrid Buttercup or Tall Crowfoot, is a frequent cause of poisoning in cattle, and Cornevin says it is perhaps the species which causes the most accidents.

Toxic Principle. The buttercups contain an acrid and bitter juice, the chemical properties and composition of which are not well known, but it is believed that the substance is identical with the Anemonin of the Anemone sp. (q.v.). Beckurts isolated Anemonin and Anemonic acid from R. acer. Pott, however, states that the poisonous species contain the two alkaloids Aconitine and Delphinine.

Symptoms. The buttercups are acrid, burning and narcotic, causing irritation of the mucous membrane, with inflammation of the intestinal tract.

Cornevin shows that R. sceleratus induces gastro-enteritis, colic, diarrhœa with excretion of black foul-smelling fæces, vomiting when possible, falling-off in milk yield in cows, nervous symptoms, reduction in pulse, and stertorous respiration, dilation of the pupils, enfeebled condition, difficult mastication, spasmodic movements of the ears, lips, etc.,—followed in serious cases by convulsions, sinking of the eye in its socket, possibly stoppage, and death in 6 to 12 hours after convulsions first appeared.

In the horse symptoms substantially similar to the above have been recorded (Lander).

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

Sheep after eating R. repens have been noticed to fall suddenly in the field; their eyes rolled, and some animals showed dizziness, and died with the head inclined over the left flank (Lander).

REFERENCES.

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

Marsh Marigold or King-Cup (Caltha palustris L.). Like the species of Ranunculus, the Marsh Marigold is to some extent poisonous in character, and both animals and man have suffered. Cattle have died from eating it, and Müller records the poisoning of many horses, one of which died. In general, animals refuse it, but may possibly eat it when pressed with hunger in times of scarcity of green herbage. Cornevin states that it has little or no acrid properties when very young, but that it is toxic by the time of flowering—acridity increasing with age.

Toxic Principle. The toxic character of the Marsh Marigold has not been fully investigated, though the presence of an alkaloid has been determined, and A. B. Smith states that the toxic properties are due to the alkaloid Jervine (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, diarrhœa, and loss of milk production, even (according to Rusby) when fed with hay. In the horse, there is colic, bloating, and inflammation of the bladder, while the urine is dark red. According to Cornevin, the symptoms are similar to those produced by Ranunculus sp. Pammel quotes Friedberger and Fröhner as stating that the plant causes hæmaturia. Five persons who ate it as a herb were “seized with violent sickness and pain in the abdomen, followed by diarrhœa and general œdematous swelling over the whole body,” but they recovered (Johnson and Sowerby).

REFERENCES.

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

Hellebores (Helleborus sp.). Two poisonous species of hellebore may on occasion be taken by live stock, though rarely—Stinking Hellebore (H. fœtidus L.) and Green Hellebore (H. viridis L.). The much esteemed Christmas Rose (H. niger) is also toxic, but unlikely to be eaten by stock. In no case should trimmings of these plants from shrubberies, etc., be thrown to stock—cows have died from eating such trimmings. The two species first mentioned are equally toxic, all parts are poisonous, and drying does not render them innocuous. Cornevin records that animals have been killed by H. fœtidus, and says that 9½ oz. of the fresh root or 2½ oz. of the dried root are poisonous doses to the horse, while 120 to 150 grains are fatal to sheep. It was recorded in 1847 (Veterinarian) by Mayer that a horse was fatally poisoned through eating five half-pints of the chopped-up leaves of this species in two days in a bran mash. In regard to this species also Johnson and Sowerby write: “The Bear’s-Foot has been used as a vermifuge ever since the days of Hippocrates, notwithstanding its dangerous qualities. Every part of the plant is a violent cathartic, but far too uncertain in the degree of its action to be safely administered.”

Toxic Principle. Both species contain the poisonous glucosides Helleborin (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 diarrhœa, decrepitude, giddiness, loss of sensation, convulsions, and not seldom death.

Affected cows are stated to give bitter milk which has purgative effects (Pott).

The poisoning of two cows by H. viridis came under the notice of Cornevin. There was observed loss of appetite, diarrhœa, tenesmus, violent attempts to evacuate, which after 5 or 6 days resulted only in the expulsion of glareous blackish matter; to the end the pulse was slow and intermittent. The heart beats were weak, and after 5 or 6 beats there was a stop equal in duration to at least a beat and a half. A remarkable fact was the very gradual loss of condition, while the milk secretion was maintained until the last day. In one case death occurred after 12 days and in the other after 28 days.

REFERENCES.

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

Larkspur (Delphinium Ajacis Reich.). In the United States of America certain species of Larkspur are exceedingly harmful to live stock, and it has been said that “with the exception of the Loco weeds there is probably no poisonous plant on the cattle ranges of the West that has caused such heavy losses to stockmen as has larkspur” (Far. Bul. 53, U. S. Dept. Agric.). D. Ajacis is the only British species, occurring in cornfields in Cambridgeshire, Sussex and elsewhere, and, like the Continental species D. Consolida, must be regarded as poisonous and fatal to cattle, while horses and sheep may also suffer. Sheep and goats, however, appear to resist the poison unless taken in considerable quantity. Wilcox fatally poisoned a yearling lamb within an hour of administering per os the extract from less than 1 oz. of the dried leaves of an American species. The seeds are the most dangerous part of the Larkspur, and should never be ground up with wheat should the two plants grow together. The seeds of D. Staphisagria are used in medicine.

Toxic Principle. The species D. Ajacis has been little studied, but D. Consolida and D. Staphisagria contain the alkaloids Delphinine (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).

REFERENCES.

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

Monkshood (Aconitum Napellus L.). The extremely poisonous character of this plant has been recognised since ancient times, and it is mentioned by Pliny, Dioscorides, etc. It is not common in the wild state in Britain—chiefly occurring in some Welsh and one or two West of England counties—and is not very liable to cause poisoning of live stock in Britain. Cases of poisoning of horses, cattle, sheep and pigs have been recorded on the Continent, however (Cornevin), and cows died in Victoria. Linnæus says that it is fatal to cows and goats when they eat it fresh, but that when dried it does no harm to horses. Medical works record many cases of human poisoning, particularly in cases where the root has been mistaken for horse radish—from which, however, it markedly differs. The leaves at first taste insipid and then sharply burning; the root when fresh smells like the radish and has a slightly sweetish taste, which is succeeded by characteristic tingling of the tongue and a sensation of numbness in the mouth.

Toxic Principle. Monkshood is very poisonous, and though all parts are toxic the root is the most dangerous, and next the seeds and leaves. The plant seems to vary in toxicity with age and climate, being but slightly active when very young, most active just before flowering, and at the minimum of activity when the seeds ripen. The cultivated form is stated to be much less poisonous than the wild one. Drying removes a part of the toxic substance, and boiling removes most of it. The plant contains the toxic alkaloid Aconitine (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 œsophagus, eructation of frothy matter, dilatation of pupils and low temperature.

Kaufmann gives the poisonous doses of powdered root for the horse and dog as 13 to 14 oz. and ⅙ oz. respectively.

REFERENCES.

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

PAPAVERACEÆ.

Poppies (Papaver sp.). Poisoning by the two common poppies (P. Rhoeas L. and P. dubium L.) is not common, but Cornevin says that the former is poisonous in all its parts, and sufficiently so to cause accidents every year. Animals may be affected by eating the plant when mixed with green fodder, or by ingesting the seeds and capsules with waste material after the winnowing and grading of cereals. Stock, however, will most likely reject the plants, owing to their unpleasant odour and taste, but cattle have been poisoned by eating unripe heads of P. Rhoeas when the plant was mixed with clover and sainfoin. P. dubium has caused poisoning of horses, cattle and pigs.

Toxic Principle. Both species contain the alkaloids Morphine (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 diarrhœa, convulsions, and epileptic symptoms, the animals falling over and rolling.

REFERENCES.

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

Greater Celandine (Chelidonium majus L.). This common plant exhales an unpleasant odour, and when bruised or broken shows the presence of a yellowish acrid juice, which becomes red immediately on exposure to the air. It is an old medicinal drug plant, but is dangerous, being emetic and purgative, with a strongly irritating effect on the digestive tract. Animals are but rarely likely to take it, and no record of the death of domesticated animals has been found.

Toxic Principle. Among the substances contained in the Greater Celandine may be mentioned the bitter alkaloid Chelidonine (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.

REFERENCES.

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

CRUCIFERÆ.

Charlock (Brassica Sinapistrum Boiss.), also known as B. Sinapis Visiani and Sinapis arvensis L., may be regarded as harmless in the young state, but liable to cause injury after flowering, when the seeds have formed, when it may occasion serious accidents if eaten by live stock. A case in which rape cake containing the seeds of charlock caused poisoning was recorded in 1875 (Jour. Roy. Agric. Soc.). The seeds only are dangerous.

Toxic Principle. The seeds contain minute quantities of volatile Oil of Mustard or Allyl-isothiocyanate (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 diarrhœa); inflammation of kidneys (difficult, excessive or bloody urination); and nervous symptoms, with great exhaustion, uncertain gait, paralysis of limbs and in isolated cases convulsions (Müller).

Pott also records increased salivation.

In the horse Cornevin records great depression, difficult and accelerated respiration, yellowish mucus and convulsive cough. A characteristic symptom is the emission of frothy liquid through the nostrils (as much as 10 litres in one hour). Death often occurs from asphyxia in a fit of coughing.

In cattle, cake containing the seeds caused inflammation of the intestines, exhausting diarrhœa, and unquenchable thirst.

The cultivated Mustards may induce similar effects, and Lander records the following symptoms as caused by Brassica nigra:—In the horse, bronchial symptoms, marked by difficulty in breathing and the discharge of great quantities of yellowish frothy matter from the nose; in cattle, uneasiness, restlessness and intense colic, with frantic rushing about and mania, ending in exhaustion, falling, struggles and collapse; in a recent case there were dullness, coldness, some tympany, laboured respiration, staggering and falling, and in fatal cases, immobility and a semi-comatose condition.

REFERENCES.

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

Wild Radish (Raphanus Raphanistrum L.). As in the case of charlock, the seeds of wild radish are very acrid, and susceptible of introducing intestinal troubles if eaten by animals when mixed with cereals.

Garlic Mustard (Alliaria officinalis Andrz.) and Treacle Mustard (Erysimum cheiranthoides L.). The seeds are stated to have properties similar to Brassica Sinapistrum (p. [18]) owing to a pungent oil; and when eaten in quantity to induce poisoning, inflammation of the digestive tract and of the kidneys, as well as nervous symptoms (Müller).

CARYOPHYLLACEÆ.

Soapwort (Saponaria officinalis L.). This plant is more or less poisonous, but is rarely, if ever, eaten by stock, and no recorded case of the poisoning of stock has been met with.

Toxic Principle. The whole plant, especially the root, contains the poisonous glucosidal Saponin (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 fœtid and mixed with blood.

REFERENCES.

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

Corn Cockle (Agrostemma Githago L.). This well-known plant of cornfields must be regarded as poisonous, though experiments and reports as to its effects on the different classes of live stock vary widely. Though a poisonous principle is found in nearly all parts of the plant, the plant in the green state appears to be innocuous, and is in any case rarely likely to be eaten fresh by stock, which probably refuse it on account of its hairy character. The seeds, however, are by no means harmless. They are rather large, and somewhat troublesome to separate from cereal grains. When ground up with wheat they both discolour the flour and impart a grey tint and disagreeable odour to bread made from it. Further, flour containing a considerable quantity of cockle must, owing to the poisonous character of the latter, be held to be unfit for consumption. Fatal results have followed the use of bread containing Corn Cockle. The toxic principle therefore is not destroyed by heating, even in an oven in baking.

As regards domestic animals, Corn Cockle seeds have frequently been mixed with feeding stuffs and have caused many deaths. Cornevin’s experiments in feeding calves, pigs and fowls led to fatal results. He was able to say that the amounts of cockle flour necessary to cause death were:—

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, diarrhœa, hot skin, sharp pains in the spine, difficult locomotion, and depressed breathing. Coma is sometimes present and may be followed by death. In animals chronic diarrhœa and gradual depression.”

The chronic form, which occurs when small doses are repeated over a long period (practically the only form found in human beings, but never in animals, except perhaps in the pig) is characterized by gradual wasting away, loss of breath, loss of strength, chronic diarrhœa, and nerve troubles, death taking place in marasmus and decline. The active principle acts as an irritant on the digestive tract, causing colic, diarrhœa and enterorrhagia.

Cornevin describes the symptoms in the acute form of the poisoning in the case of horses, cattle, pigs and dogs.

In the horse, if a small quantity only is taken, there is yawning, heavy colic, stamping and evacuation of rather soft fæces. If larger quantities are taken, the symptoms, which commence in about an hour, are salivation, frequent yawning and turning of the head, colic, pale mucus, hurried and weak pulse, rise in temperature and accelerated respiration. Some time later there are muscular tremors succeeded by pronounced rigidity, and the fæces are diarrhœic and fœtid. The animal lies down, and getting up is painful; it falls into a kind of coma, stretches itself to the utmost, and death takes place without convulsions.

In cattle, the symptoms observed one hour after eating are restlessness, salivation, and grinding of the teeth. Excitement and colic are followed sometimes by coughing, this state lasting from five to eight hours. There is then a period of coma, characterized by permanent decubitus, repeated fœtid diarrhœa, hurried and plaintive respiration, accelerated and gradually weakening pulse, a gradual loss of motor and sensory powers, and a progressive decline in temperature. Death occurs in twenty-four hours.

In the case of pigs, the animal grunts, lies down and remains thus with its snout embedded in the straw. There is vomiting, more or less violent colic and diarrhœa, the evacuation consisting of bad-smelling, spumous fæcal matter. At times there are clonic contractions. Young pigs are most susceptible.

Pott cites cases in which abortion was a feature of the poisoning, both in cows and pigs. The results of numerous experiments which he quotes (among others some carried out for the Prussian Ministry of Agriculture) are very contradictory, a small quantity causing death in some animals, while others of the same species were left unharmed by large quantities. He ascribes this to the very variable proportions of the poison present in the seeds.

REFERENCES.

[4], [16], [28], [46], [52], [53], [63], [76], [81], [82], [144], [161], [172], [184], [190], [203], [205], [213], [249].

HYPERICINEÆ.

St. John’s Wort (Hypericum perforatum L.). There appears to be no record of poisoning of live stock by this plant in Britain, but Cornevin records that it injured breeding mares fed on lucerne containing it in large proportion. Drying in converting into hay did not render it innocuous. It is only poisonous if eaten in considerable quantity, and in general animals are not likely to eat much of it voluntarily, owing to its resinous odour when crushed, and a bitter and slightly saline taste.

Toxic Principle. The poisonous properties of St. John’s Wort have not been fully investigated, but it is stated to contain an oil and an acrid bitter resin. Ewart says that it “contains an oil whose medicinal value was formerly highly esteemed; but this oil, and the woody nature of the plant, render it somewhat injurious in fodder.” Summers says (Journ. Agric. S. Australia, Sept. 1911, p. 144) that “it is reported to be decidedly injurious, causing horses who eat it to break out in sores, while milk cows have a tendency to dry off owing to its effect on the system.”

Symptoms. In mares, dullness, sinking of head, loss of appetite, slackening of pulse and respiration, dilatation of pupils, defective sight, and lips purple (Müller).

REFERENCES.

[63], [82], [117], [190], [203].

GERANIACEÆ.

Wood Sorrel (Oxalis Acetosella L.). Though rarely likely to be eaten by stock this plant must be mentioned here, as it is considered dangerous on account of its high content of oxalates, which may cause serious illness and diarrhœa, and in the case of sheep even be fatal. Pott says that the milk of cows eating it is with difficulty converted into butter.

REFERENCE.

[213].

CHAPTER III
CELASTRACEÆ.

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.

REFERENCES.

[63], [81], [205], [252].

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.

REFERENCES.

[4], [63], [76], [190], [203].

PAPILIONACEÆ.

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.

REFERENCES.

[4], [16], [63], [64], [81], [128], [144], [161], [190], [205], [213].

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.

REFERENCES.

[4], [16], [82], [128], [203].

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, dyspnœa 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 dyspnœa 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.

REFERENCES.

[63], [82], [137], [170], [179], [190], [203], [205].

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, ⅗ pound of empty pods, or 1⅕ 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, dyspnœa, 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 œdemæ 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 diarrhœa 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.

REFERENCES.

[4], [16], [20], [21], [42], [57], [63], [69], [82], [93], [128], [161], [166], [170], [190], [203], [213].

“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 diarrhœa, quick pulse and respiration, muscular spasms, and paralysis of the hind quarters in one instance; all recovered rapidly.

REFERENCES.

[5], [38], [76], [77], [107], [109], [125], [129], [144], [255].

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.

REFERENCES.

[4], [16], [66], [73], [128], [205].

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.

REFERENCES.

[4], [16], [73], [76], [81], [128], [129], [130], [132], [170], [205], [232], [254], [255].

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.

REFERENCES.

[73], [76], [81], [141], [170], [233].

UMBELLIFERÆ.

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), diarrhœa, 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.

REFERENCES.

[31], [73], [81], [123], [141], [151], [170], [190], [203], [205], [213], [233], [238].

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.

REFERENCES.

[73], [81], [190], [235].

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 fœtid diarrhœa.

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).

REFERENCES.

[10], [14], [73], [81], [141], [146], [170], [190], [205], [209], [213], [235], [246].

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, diarrhœa, 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).