Plants Poisonous to Live Stock — Inside the Classic
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not paralyse the vagus terminations, nor depress the motor and sensory nerves or muscles. The circulation is but slightly influenced, and vasomotor depression only occurs in the later stage of lethal poisoning. Death occurs from paralysis of the respiratory centres. Poisoning in animals is exhibited by loss of muscular power, slowing and failure of respiration, stupor, and asphyxia. The pulse may be infrequent, the pupils are dilated, and the skin is moist rather than dry.
The following symptoms in animals are given by Welsby: Nervo-muscular exaltation, eyelids and irides much dilated, eyes amaurotic and very bright, pulse full, temperature normal, respiration difficult and hurried, profuse salivation, muscles of neck and extremities in a state of tetanic rigidity, considerable abdominal distension, stercoraceous and renal emunctories entirely suspended, death.
In a _cow_ there was observed, two hours after eating, dilatation of pupils, the conjunctivæ were injected, and the carotids beat violently. There were general convulsions, loud respiration, salivation, and purgation. According to Pott the milk of affected cows is of an unpleasant taste.
4, 16, 39, 57, 68, 73, 81, 128, 141, 151, 157, 161, 190, 203, 205, 213, 257.
=Garden Nightshade= (_Solanum nigrum_ L.). This species is described as “one of the widest spread weeds over every part of the globe, except the extreme north and south; varying so much in warmer regions as to have been described under more than forty names” (Bentham and Hooker). In the same way there can be no doubt that, though it must always be regarded as poisonous, this plant varies considerably in toxicity according to soil, climate, and general condition of growth. For this reason the plant may sometimes be eaten in considerable quantities without ill effects, while in other cases it will undoubtedly prove poisonous.
Children have been poisoned by the berries, but may on occasion eat them with no other ill effect than a stomach ache, or, if eaten in excess, sickness and purging. The berries “have even been used instead of raisins for plum puddings with no effects out of the ordinary” (Ewart). The plant has also been used in Queensland and elsewhere as a substitute for spinach. In several cases the plant has proved fatal. Gohier gave 3 kilogrammes (6½ lb.) of the green plant to a horse and observed no serious symptoms. Cases of poisoning are recorded for calves, sheep, goats and pigs (Chesnut and Wilcox). According to Lehmann, Schraber and Haller, the berries are poisonous to ducks and chickens. Over thirty years ago the death of a number of cattle in Victoria was recorded as being due to poisoning by this weed.
Though cases of poisoning of stock are rare, partly perhaps because the plant is a weed of arable land and partly because animals are likely to avoid it unless starved, _Solanum nigrum_ must be regarded as a poisonous plant, any examples of which may prove toxic. The downy and more prostrate form has been considered the most poisonous.
The “Wonderberry,” said to be a hybrid between _Solanum guineense_ and _S. villosum_, which are probably varieties of _S. nigrum_, cannot in England be distinguished from the last named, the fruits of which appear to be edible in some countries and poisonous in others. Greshoff found that fruits of the “Wonderberry” contained more Solanine than the wild English _S. nigrum_ or the Canadian form known as the “Huckleberry,” and hence they should not be eaten.
_Toxic Principle._ The Garden Nightshade, in particular the berries, contains the alkaloidal glucoside _Solanine_, of which the formula is considered doubtful. Solanine is readily converted into sugar and the poisonous _Solanidine_. It was isolated from the berries in 1821, and though decidedly active in sufficient quantity is not a violent poison. A small quantity of _Solanine_ is present in the stem and berries, but these are probably less poisonous than green potatoes (p. 54).
_Symptoms._ The symptoms of poisoning are apparently much the same in man and animals: “Stupefaction; staggering; loss of speech, feeling, and consciousness; cramps and sometimes convulsions. The pupil is generally dilated.”
4, 10, 11, 16, 17, 52, 53, 57, 73, 81, 82, 128, 141, 161, 203, 235, 240.
=Bittersweet= (_Solanum Dulcamara_ L.). Some doubt exists in regard to the toxic character of this common denizen of the hedge-row, some persons regarding the berries as harmless and others as poisonous. Possibly the plant varies in toxicity. Floyer states that 30 berries killed a dog. Though stock rarely touch the plant there seems to be no doubt that it is poisonous, stem, leaves, and berries containing the toxic alkaloid found in _S. nigrum_ and the potato (_q.v._), and it is especially possible that poisoning may follow the ingestion of the berries. Johnson and Sowerby (1861) say that the leaves are narcotic, causing nausea and giddiness, and that the fruit is equally harmful, though no fatal cases then seemed to be recorded. Gillam records (_Vet. Record_, 1906) a case of poisoning of sheep. An anonymous writer in the _Mark Lane Express_ (July 24, 1911) states emphatically that this plant is very poisonous, and that he has known 14 per cent. of the sheep on a farm to be killed by it in a year, while his veterinary surgeon had had 40 cases that season, some proving fatal.
_Toxic Principle._ Like _S. nigrum_, the stems, leaves, and berries of Bittersweet contain _Solanine_. The berries are stated by Esser to contain 0·3 to 0·7 per cent. of Solanine. The stems also contain the glucoside _Dulcamarin_ (C_{22}H_{34}O_{10}), which imparts a bitter taste to the plant, but which has not been fully studied.
_Symptoms._ In the case recorded by Gillam (see above) the symptoms observed in sheep were small intermittent pulse, temperature 104° F., quickened respiration, staggering gait, dilated pupil, and greenish diarrhœa. The symptoms appear to be the same in the case of cattle (_Farmer and Stockbreeder_, July 10, 1911).
4, 16, 40, 50, 52, 73, 81, 141, 147, 203, 213, 257.
=The Potato= (_Solanum tuberosum_ L.). Though potato haulm is more or less commonly utilised on the Continent as a green fodder, and has been so used in England, yet there are good grounds for the general belief that it is not a suitable food for stock. The tubers may in general be eaten with impunity, but, under certain conditions, cannot be regarded as blameless, since they have caused serious injury. There are certainly records of injury to man from eating Potatoes, and accidents with animals have occurred more commonly. “Greened” tubers, and tubers with young shoots appear to be the chief cause of accidents, and, as regards live stock, usually when fed raw.
Cornevin knew of no case of poisoning in man, and considered that this was probably because man (1) eats only the part poorest in the toxic principle (see below), (2) does not eat the skin, (3) always cooks the tubers, and (4) rarely subsists only on potatoes for a considerable time. He found accidents among _animals_, however, not rare. In fact, eliminating cases possibly due to changes caused by weather, cryptogams, and ferments, he found poisonings every year unquestionably due to Solanine, chiefly among cattle. Cows will eat the haulm without trouble in times of scarcity of green fodder, but to the detriment of their health if such feeding is prolonged.
Macfadyen showed some time since that old sprouted Potatoes, even after boiling, are poisonous to horses. In 1896 eleven horses died from eating in most instances small quantities of spoiled and somewhat sprouted Potatoes, and two test-horses fed on the Potatoes died. In this case, however, it was conjectured that the poison was probably some organic substance generated by the bacteria or fungi growing on the Potatoes.
Chesnut and Wilcox (1901) recorded the death of six pigs due to eating sprouted uncooked Potatoes; after cooking the potatoes did not cause poisoning. With sufficient boiling most of the poison appears to remain behind in the water and might be thrown away.
Cases of poisoning of stock by Potatoes appear to have occurred more or less frequently in Germany. Two such cases were noted in the _Berliner Tierärztliche Wochenschrift_ in 1909, in one of which 64 cows developed symptoms of poisoning after being fed on a large quantity of raw tubers, while in the other instance two cows became ill after eating Potato parings—which, as shown below, contain more Solanine than the “flesh.”
In the case of two children who died, F. W. Stoddart, Public Analyst of Bristol, after a post-mortem in one case, gave a very guarded opinion that death was probably due to Solanine poisoning, due to eating raw Potato peel, but was not confident. A most interesting case of severe but not fatal poisoning is described in _The Lancet_ (1899). No less than 56 soldiers in Berlin were badly affected, until the supply of Potatoes was stopped, but the men recovered.
Pammel (1911) states that some persons cannot eat Potatoes because poisonous to them, but such persons must be extremely rare, and hypersensitive to minimum quantities of Solanine, which is almost if not quite absent in the “flesh” of Potatoes.
_Toxic Principle._ The Potato plant, like the other species of _Solanum_ mentioned above, contains _Solanine_, which occurs not only in the haulm, but in the flowers and fruits, and in the peel of the tubers. _Solanidine_ also occurs ready-formed in the young sprouts of potatoes to the extent of 1·5 per cent. (Allen). In the case of the soldiers poisoned in Berlin analysis demonstrated the presence of Solanine to the extent of 0·038 per cent. in boiled tubers and 0·024 per cent. in raw tubers, and on an average every man who fell ill had 0·3 gramme of the alkaloid, a sufficient quantity to produce toxic results. Esser (1910) states that in midsummer the haulm contains 0·0925 per cent. of Solanine but late in summer only 0·0374 per cent. In the tubers the alkaloid occurs in the inner layers of the peel to the extent of 0·0124 per cent., red or pink varieties containing rather more than yellow sorts. The same authority says that damp soils tend to a higher percentage of Solanine than dry soils[3], and that nitrogenous manuring as compared with potash tends to an increase of Solanine. In fresh spring shoots 1·5 per cent. of the alkaloid has been found, and the percentage is especially high in tubers which have been “greened” by long exposure to light. As already stated it is the greened tubers which appear to be the chief cause of accidents. Tubers with young shoots are richer in poisonous alkaloids than those which have not yet been sprouted; such tubers when fed raw to stock may on occasion induce poisoning, unless fed only in small quantities.
On the other hand, potatoes grown in a dry sandy soil are stated to contain more Solanine than those grown in other soils.
Writing in 1887 Cornevin remarked that Solanine, though neither very active nor very abundant in Potatoes, nevertheless causes accidents, as it is cumulative, or, to be more exact, is eliminated slowly.
_Symptoms._ In poisoning by potato _haulm_, Cornevin records constipation, loss of appetite, rise in temperature, accelerated circulation, normal respiration, salivation, tumefaction of eyelids, eyes watery, conjunctivæ injected, and hair erect. The skin is covered with scabs which exude matter, the skin being cracked. These scabs are found especially on the scrotum of male cattle and the udder of female cattle, but also in the caudal region and round the anus. An examination of the mouth shows places on the upper jaw which are devoid of mucus and are purulent at the centre, the mucus round the edges being swollen. The posterior members are similarly but not so badly affected. Movement of these members seems to cause the animal much pain. Defecation is frequent, the fæces being liquid and dark in colour. The animals are recumbent for a considerable time with the posterior members stretched out. In the worst cases there is pronounced emaciation.
According to Friedberger and Fröhner (_vide_ Pammel) animals affected by potato tops show symptoms resembling those of foot-and-mouth disease.
According to Pott the _berries_ cause colic and foul smelling diarrhœa in _cattle_. A German veterinary surgeon after feeding the green plant observed symptoms of delirium, paralysis, and flatulence. In other cases trembling and uncertain gait, with paralysis of the spinal cord, have been observed in _cows_.
In poisoning by _tubers_ there is depression, loss of appetite, cessation of lactation, gritting of teeth, profound prostration, with a remarkable somnolence, but no dilatation of the pupils. The animals remain recumbent, with closed eyes, and refuse to get up. Respiration is somewhat retarded, and the pulse is small and accelerated. There are digestive disturbances, tympanitis, diarrhœa succeeds constipation, and there is vomiting (where possible). The poisoning is usually fatal.
Where a large quantity of sprouted Potatoes has been fed the prostration becomes paraplegia, with loss of sensibility, stupefaction, and death. Where there is prolonged ingestion of a large quantity of unsprouted tubers there is prostration, intestinal irritation, rapid emaciation and death in marasmus after an illness of from one to three weeks (Cornevin).
Pott states that potatoes diseased with wet rot, when fed raw, cause digestive troubles, bloating, diarrhœa, abortion, and decrease in milk yield, with fatal results in some cases. Potatoes diseased with dry rot cause constipation in sucking pigs, and a “fishy” butter from cow’s milk.
Lander notices two cases of poisoning of _horses_ by tubers. In the first case the symptoms were a small and weak pulse, normal temperature and loss of coordination in movements; complete loss of appetite, excessive thirst, but inability to drink; mydriasis, stertorous breathing, suspension of peristalsis, and slight tremors over the crural muscles. In the second case there was a rapid and feeble pulse, temperature 103° F., intense congestion of the mucous membranes, and very fœtid diarrhœa, terminating fatally.
In poisoning of _horses_ after receiving large quantities of raw Potatoes, Pott records boil-like swellings on the skin, loss of hair, diarrhœa, inflammation of the stomach and intestines, skin irritation, and swollen fetlocks and hocks.
In reference to the horses mentioned above (p. 55) it is stated that an affected animal seems dull, and dies within twelve hours after being first observed, without evincing any sign of pain. The first symptoms in ten cases were weakness and loss of power over the limbs.
In _cows_ the symptoms (Müller) are loss of appetite, bloating, diarrhœa, staggering, dilatation of pupils, convulsions, loss of sensation and paralysis. In many cases, however, these symptoms do not appear, but instead there are outbreaks on the skin of the hind legs similar to those in foot-and-mouth disease. Pott mentions abortion as a symptom. After the ingestion of green Potato parings by dairy cows he remarks catarrh of the stomach and intestines, and bad milk and cheese; consumption of diseased Potato parings resulted in the flow of hard mucus from the mouth, the legs being badly swollen, and covered with scabs, and the mouth and body covered with boils. Symptoms of paralysis were noticed after feeding dirty Potato parings to four cows and four bulls, and one cow died.
In the case of the cows already referred to (p. 55) as poisoned in Germany, it was remarked as a noticeable feature in both instances that there was the appearance of eczema on the hind limbs, causing lameness.
A case in which _pigs_ were fed on uncooked, sprouted Potatoes is noticed by Chesnut and Wilcox; there was slowly progressing paralysis, which became complete after about 24 hours, increased salivation, and a regurgitation of the stomach contents. According to Pott death may result in pigs. The symptoms given by Lander for poisoning in pigs are loss of appetite, dullness, exhaustion, imperceptible pulse, watery diarrhœa, low temperature and comatose condition.
In the case of the poisoned soldiers the symptoms were those of acute gastro-enteritis; rise in temperature to 103° F.; headache, colic, diarrhœa, general debility; in some cases vomiting, in others nausea only; several men fainted, and one had convulsions; the majority were drowsy and apathetic; but all recovered.
4, 16, 19, 57, 73, 81, 128, 130, 141, 170, 190, 196, 203, 204, 205, 213.
=Deadly Nightshade= (_Atropa Belladonna_ L.). This plant has long been known to be exceedingly poisonous, all parts containing a toxic principle. Both man and domestic animals may be poisoned, though the latter are very unlikely to touch the plant. As regards man, children are most likely to be affected, owing to the attractive character of the large bright black berries. Domestic animals appear to be rarely poisoned and are less affected than man, and in any case the susceptibility of various species—and even individuals of the same species—is very variable. Human beings are most susceptible, followed by the cat and dog; the horse is much less so; and the pig, goat, sheep, and rabbit are little susceptible to poisoning, even on eating the root—the most poisonous part (Cornevin). Gohier and others have given over 2 lb. of the green plant to horses without ill effects, and this repeated on three days did not cause marked pathological troubles. Hertwig considered large ruminants to be more sensible than horses to the action of Belladonna. It appears to be agreed that small ruminants are very slightly susceptible to this plant. Birds are considered almost insensitive, while rabbits may be fed for weeks on the leaves without poisoning, as also sheep, goats, and pigs. Horses and cattle are more sensitive but nevertheless resistant. The poison is no doubt quickly removed by the kidneys, since ordinary injection of Belladonna causes the usual symptoms. It is stated that the flesh of rabbits and birds which have eaten the plant and have been slaughtered apparently healthy is poisonous to man.
One berry can induce symptoms of human poisoning, and a child died after eating only three berries. Mortality in human cases of poisoning by Belladonna is given by Kanngiesser as 10 per cent.
_Toxic Principle._ Deadly Nightshade is the source of drugs widely used in medicine, and its properties as regards man have been extensively studied. The principal substance present is the alkaloid _Hyoscyamine_ (C_{17}H_{23}O_{3}N), readily converted into _Atropine_ (C_{17}H_{23}O_{3}N); _Scopolamine_ or _Hyoscine_ (C_{17}H_{21}O_{4}N), and in smaller quantity _Apoatropine_, and _Belladonine_ are also present.
All parts of the plant contain the toxic alkaloids, but in unequal degree. The total quantity of the alkaloids is largest in the roots (0·4 to 1 per cent.), which in the fresh state contain no Atropine, but only Hyoscyamine; the leaves and fruits contain less of the alkaloids, and cultivated plants have been found to be poorer (0·26 per cent.) than wild (0·4 per cent). The root has been found to be five times as toxic as the berries. Drying does not destroy the poisonous properties.
_Symptoms._ In quantities which are not fatal the symptoms are nausea, dilatation of pupils, muscular weakness, stumbling, falling, and rising only to fall again. These are followed by vertigo, frenzy, and coma (more rarely). There is a slight slackening in respiration, and an increase in the rapidity of the heart’s action. Dysury and constipation are observed.
In fatal quantities the symptoms are more intense and make their appearance more rapidly. The nausea is accompanied by vomiting, and there is almost complete loss of sight. Sensitiveness is at first increased but later diminishes and gradually disappears; complete incoordination of movements; increase in the heart’s action but a gradually weakening pulse; stertorous, painful respiration; decrease in temperature. There is repeated urination at the commencement of the poisoning, and then dysury. At the approach of death there are muscular trembling and clonic contractions. This phase of convulsions is short but very clear in some cases: other cases do not leave the deep coma in which they are plunged (Cornevin).
In regard to _cattle_, the following symptoms are given by Müller: Injury to sight, dilatation of pupils, constipation, later bloody evacuations, pain in hind limbs, rapid pulse, difficult breathing, restlessness, frenzy and finally paralysis.
4, 16, 61, 73, 81, 128, 138, 143, 151, 157, 161, 190, 205.
CHAPTER V SCROPHULARINEÆ
=Foxglove= (_Digitalis purpurea_ L.). The Foxglove has been recognized as poisonous for centuries, and one of its trivial names is Dead Men’s Bells—a name suggestive of the consequences of taking it. It is the source of the well-known drug; and cases of human poisoning have been very common, though by no means always fatal—indeed, Esser says “seldom resulting in death.” Animals are not known to touch this plant, but it may possibly be included in rough meadow hay, though only one case, in which two cows and a horse became ill after eating hay containing dry foxgloves, has come to notice (_Veterinary Record_, 1906). Cornevin, however, experimented on animals, and found the following amounts of fresh leaves capable of causing death in the animals specified:—
Horse 120–140 grammes (4 to 5 oz.) Ox 160–180 „ (5·5 to 6·5 oz.) Sheep 25– 30 „ (0·88 to 1 oz.) Pig 15– 20 „ (0·5 to 0·7 oz.)
The weight of dried leaves would be only one-fourth of these figures.
All parts of the foxglove are poisonous, but especially the seeds, and the leaves are more active before than after the flowering period. Cultivated varieties are stated to be less toxic than the wild species. The effects of poisoning may terminate fatally in a few hours, or if small quantities are taken regularly the poison may be cumulative and induce chronic poisoning.
Harold C. Long opens his 1917 handbook by lamenting the "great lack of readily available and reliable information" on livestock poisoning in English scientific literature. He positions the work as a companion to his earlier Common Weeds of the Farm and Garden, aiming to consolidate facts scattered across technical reports and journals. The preface immediately establishes a practical, evidence-based tone: Long acknowledges that the annual loss of stock is "undoubtedly considerable" but not precisely ascertainable, and he deliberately excludes exotic cultivated plants and fungi, focusing instead on flowering plants likely to be eaten by stock.
Structure and Scope
The book is organized by plant families, a botanical framework that allows Long to group related species and compare their effects. Each entry typically includes the plant's common and scientific names, a description of its toxic principle, and a detailed account of symptoms observed in different livestock. For example, under Polygonaceæ, Long notes that docks (Rumex species) contain acid oxalates and can cause symptoms ranging from "drunkenness" in horses to constipation and diarrhœa in sheep. The entries also cite multiple references—often a string of numbers—directing readers to the original sources. This systematic approach reflects Long's background as a Board of Agriculture official and his commitment to making specialized knowledge accessible to farmers and veterinary surgeons.
Symptom Descriptions Across Species
Long's symptom descriptions are notably precise and species-specific. For lousewort (Pedicularis), he reports that the plants are "emetic and purgative" and may cause hæmaturia in cattle. For the cow poisoned by an unspecified plant, he provides a day-by-day account: dullness on the third day, nauseated with cold extremities on the fourth, and death on the sixth. In pigs, symptoms include lethargy, refusal to eat, and strained urination. Horses may show exhaustion, colic, and staggering. These granular observations, drawn from veterinary reports and experiments, give the reader a vivid sense of how poisoning manifests differently across species. Long often notes that some plants are "refused by all classes of stock" unless pressed by hunger, adding a practical dimension to the toxicological data.
Use of References and Sources
Each plant entry concludes with a list of numbered references, such as "REFERENCES. 4, 16, 73, 76, 79, 81, 161, 170, 187, 190, 203, 204, 205, 213, 229, 252, 257." These numbers correspond to a bibliography that Long compiled from technical reports, journals, and earlier works by authors like Cornevin, Müller, and Pott. The references serve as a trail for readers who wish to verify or explore the original studies. Long also occasionally cites specific authorities by name within the text, as when he notes that "Lindley says that both plants are acrid, but are eaten by goats." This scholarly apparatus underscores the book's role as a synthesis of existing knowledge rather than a collection of original experiments.
Practical Orientation and Limitations
Long explicitly states that the dividing line between plants that are "actually poisonous and those which are only suspected is far from clear," and he has made a deliberate division for the reader's convenience. He also includes notes on mechanical injury caused by plants and on the influence of plants on milk, topics he considers "in some degree related to poisoning." The book does not claim to be exhaustive: Long excludes fungi and exotic ornamentals, focusing on plants that British livestock are likely to encounter. This practical orientation is reinforced by the inclusion of a plate showing beans and ergot at natural size, aiding identification. Readers should treat the symptom descriptions as indicative rather than definitive, and consult a veterinary surgeon for diagnosis.
Long's handbook is best read as a reference work to be consulted when poisoning is suspected, rather than a continuous narrative. The systematic arrangement by plant family makes it easy to look up a suspect plant, but the symptom descriptions are most useful when cross-referenced with the plant's identity. Readers should note that the references at the end of each entry point to a bibliography that is not included in this digital edition, so some context may be missing. For a first reading, focus on the preface and a few representative entries to grasp Long's method and the range of symptoms he documents.
That grey afternoon, rain blurred the windows while I traced Long’s dry entries on hemlock and ragwort, imagining farmers’ quiet dread. The book’s orderly families of poison felt almost like a genealogy. Later, idly, I picked up The Principles of Breeding or, Glimpses at the Physiological Laws involved in the Reproduction and Improvement of Domestic Animals — Reading Companion—and recognised the same patient attention, turned toward life’s other side.
Alexander Walker
1 week agoIsaac Walker
3 weeks ago-
Catherine Kelley - 4 weeks ago
{'review_type': 'critical', 'content': "While the subject matter is critical, this book falls short in presentation. The text is dense and dry, making it hard to read through. More importantly, the lack of high-quality images severely limits its usefulness, as identifying plants by verbal description alone is challenging. I'd recommend looking for a more visually oriented field guide."} -
Michael Garcia - 2 weeks ago
{'review_type': 'neutral', 'content': 'This is a valuable reference for anyone dealing with livestock, as it catalogues numerous poisonous plants. The descriptions are accurate, and the importance of the topic cannot be overstated. However, the book lacks visual aids like color photos, which would have made plant identification much easier. Still, the textual information is solid.'} -
Christine Payne - 1 week ago
{'review_type': 'positive', 'content': "An indispensable guide for any livestock owner or farmer. 'Plants Poisonous To Live Stock' is meticulously researched and clearly written, offering crucial information that could save animals' lives. The identification tips and symptoms are incredibly detailed, and the safety recommendations are practical. I feel much more confident in managing my pastures after reading this book."}
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Anthony Clark
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