Ivy (Hedera Helix L.). The berries of the Ivy are said to be largely eaten by certain birds (e.g. blackbirds, thrushes, wood-pigeons), but have poisoned children. The plant has long been said to be poisonous, but no definite case of poisoning of live stock has been discovered; possibly farm live stock would need to eat a considerable quantity for serious effects to be induced. Indeed, when keep is short, it is quite common in some districts to see Ivy strewed on the fields for cattle and sheep to eat, and it is very frequently given to sick animals by country people (Garnett).

Toxic Principle. This has not been closely studied, but ivy contains a bitter principle which is strongly cathartic, emetic and purgative. Ivy contains a poisonous glucoside Hederin (C₆₄H₁₀₄O₁₉) and a resin (Gummi hederÆ).

Symptoms. As suggested above, it is doubtful whether animals have been poisoned by Ivy. Symptoms given appear to refer to children, and consist in sickness, diarrhoea, nervous symptoms, excitement at first, then convulsions and paralysis (MÜller). Sickness and purgation (Esser).

Cornevin states that the symptoms are complex, emeto-purgative effects being present, with nervous symptoms resembling those of intoxication, viz. excitement, then coma, convulsions, uncertain gait, and stertorous respiration.

CAPRIFOLIACEÆ.

Common Elder (Sambucus nigra L.) and Dwarf Elder (S. Ebulus L.). These two plants are usually avoided by stock, no doubt in view of their odour, more particularly in the case of the latter species. The bark, leaves and berries of both species were noticed by Cornevin as having pronounced purgative properties, and the berries of S. Ebulus as having poisoned turkeys. Esser remarks that the use of S. Ebulus by country folk as a purgative has caused fatal poisoning. The leaves of S. nigra have caused severe irritant poisoning in a child.

Toxic Principle. Some doubt exists as to the poisonous principle of the Elders, the leaves of which contain Sambunigrin (C₁₄H₁₇O₆N), a cyanogenetic glucoside; the alkaloid Sambucine; and a purgative principle. According to Cornevin drying reduces the toxicity but does not destroy it.

Symptoms. The symptoms are not very definite, but small quantities cause purgation, while large quantities induce depression and violent emetic and cathartic effects, with diarrhoea, abundant diuresis and acceleration of pulse. The leaves of S. Ebulus have caused vomiting, obstinate constipation and enteritis in a boy, and in the case of another boy the flowers caused vertigo and headache.

COMPOSITÆ.

Tansy (Tanacetum vulgare L.). Live stock are most unlikely to eat this plant, as it is bitter and acrid. Cattle appear to have been poisoned by it in Germany, Kobert’s opinion being that death had resulted from tansy. There have also been many serious cases of human poisoning.

Toxic Principle. Tansy contains the bitter, volatile and poisonous Oil of Tansy.

Symptoms. Tansy Oil has been employed as an abortifacient, and produces convulsions, violent spasms, frequent and feeble pulse, and paralysis of the heart and lungs, inducing a condition similar to that observed in rabies.

Pammel cites cases of the action of the oil from the plant on dogs. According to Pott the tansy imparts a bitter taste to the milk of cows which eat it.

Ragwort (Senecio Jacoboea L.). No suspicion appears to have been focussed on Ragwort in Britain, but it must be recorded here as the cause in Canada of the Pictou cattle disease, or hepatic cirrhosis, a somewhat fatal disease which has caused much loss during the last few years. In New Zealand also the same disease has been experienced, and has caused considerable mortality among sheep. In one case sheep were closely pastured on about 4000 acres with the object of eradicating the too prevalent weed, but after a year losses ensued. Gilruth concluded that if the weed does not monopolise the ground, sheep may, with few exceptions, eat it daily without suffering ill effects. Cattle and horses avoided it when possible.

It may be remarked that in Britain feeding the young shoots off with sheep, which seem to like the plant, is regarded as the best plan of reducing Ragwort in grass land. So far there seems to be no record of injury from this cause.

In South Africa cirrhosis of the liver in cattle (locally termed Molteno cattle sickness) has been traced to S. latifolius, 8 to 10 lb. of which in daily feeds of 2 to 6 oz. caused death in about six weeks. Another species, S. Burchellii, is similarly poisonous, ½ lb. daily for four days having killed an ox on the fifth day; at Molteno half the quantity proved fatal. Both species are fatal to cattle and horses.

Toxic Principle. As regards S. Jacoboea nothing appears to be known as to any toxic principles, though an alkaloid has been isolated by Watt (1911), but not fully described. The South African S. latifolius, however, was examined at the Imperial Institute, and two new crystalline alkaloids were isolated—Senecifoline (C₁₈H₂₇O₈N) and Senecifolidine (C₁₈H₂₅O₇N)—1·20 per cent. being present in the plant before flowering and 0·49 per cent. after flowering.

Symptoms. As they may to some extent serve as a guide in relation to possible Ragwort poisoning in Britain the symptoms observed from poisoning by the South African species may be given: Severe and strained purging: fÆces yellowish to dark brown; cows cease to give milk; abdominal pain, groaning; animal may go mad and charge anyone approaching, or lie with outstretched head, drooping ears, staring coat, and dull glaring eyes; death usual within three days from commencement of purging. The post-mortem shows an inflamed fourth stomach; hardened condition of the liver, often dull grey with spots in the interior; expanded gall bladder, with dull yellow viscid bile.

Wild Lettuce (Lactuca sp.). Just how far the two species L. scariola L. and L. virosa L. are really poisonous is not clearly known, and it is probable that to be seriously harmful to farm live stock they would need to be ingested in considerable quantity, and this they never seem to be. They are certainly not actively poisonous, though Bailey and Gordon say that “we have been informed that this European plant—now a national pest—is sometimes eaten by cattle, on whom it has been observed to have had an injurious effect.”

Toxic Principle. Authorities differ as to the substances to which the toxic property, if any, is to be attributed. According to Ludwig the milky juice, known as Lactucarium, includes Lactucone, Lactucin, and Lactucic Acid, the second of these being the narcotic substance. Nearly half the weight of Lactucarium (a form of dried juice) consists of the tasteless inodorous Lactucone or Lactucerin (C₁₄H₂₂O), and the bitter taste is due to Lactupicrine, Lactucin and Lactucic Acid. In the leaves of L. virosa, Dymond found traces of Hyoscyamine or a similar substance (Jour. Chem. Soc., 1892, Vol. 61, p. 90).

Symptoms. Intoxication is produced similar to that caused by poppy heads; the narcotic effects are dominant (Cornevin).

ERICACEÆ.

Rhododendron (Rhododendron sp.). The literature points to there being no doubt as to the poisonous character of a number of species of Rhododendron, and indeed most species are suspected. Animals do not appear to eat Rhododendrons very extensively, but both English and Belgian veterinary surgeons have published records of poisoning of sheep and goats by R. ponticum. Suspected cases were recorded in the Journal of the Board of Agriculture (1907 and 1914); three cases of cattle poisoning in the Veterinary Record (1900, 1906, and 1907); one of calves in the Veterinarian (1859); and three of sheep-poisoning—one in the Veterinary Journal (1906), and two in the Veterinarian (1865); but these cases were not all fatal. The death of 19 out of 21 cross-bred Scotch lambs due to eating R. ponticum was reported by C. T. Baines in the Journal of the Land Agents Society (Aug. 1914, p. 373). The plant was eaten after a heavy fall of snow. Chesnut includes R. maximum as one of the thirty most poisonous plants of the United States. According to Cornevin, R. ferrugineum causes frequent poisoning of animals which graze on the plateaux where it grows—especially sheep and goats, the latter providing the most victims, as they willingly browse the young shoots and leaves. R. californicum is said to be poisonous to sheep in Oregon. R. Chrysanthum, the leaves of which have been used in Russia and Germany for rheumatism, has caused poisoning in man. R. punctatum and R. hirsutum appear to be not less poisonous.

Both leaves and flowers are narcotic, and even the honey in the flowers is regarded with suspicion. The following quotations are not without interest:—

“In these regions (Tungu) many of my goats and kids had died foaming at the mouth and grinding their teeth, and I have discovered the cause to arise from their eating the leaves of Rhododendron cinnabarinum (“Kema Kechoong,” Lepcha; Kema signifying Rhododendron); this species alone is said to be poisonous, and when used as a fuel it causes the face to swell and the eyes to inflame, of which I observed several instances.” (Hooker, Himalayan Journals, ii. p. 150).

“Rhododendron arboreum becomes plentiful at 5000 to 6000 feet (East Nepal), forming a large tree on dry clayey slopes.... In the contracted parts of the valley the mountains often dip to the riverbed in precipices of gneiss under the ledges of which wild bees build pendulous nests looking like huge bats suspended by their wings; they are two or three feet long and as broad at the top whence they taper downwards; the honey is much sought for except in spring, when it is said to be poisoned by Rhododendron flowers just as that eaten by the soldiers in the retreat of the Ten Thousand was by the flowers of R. ponticum.” (l.c. i. p. 200).

Toxic Principle. The leaves and flowers contain a bitter poisonous glucoside, Andromedotoxin (C₃₁H₅₀O₁₀), which has been regarded as more poisonous than Aconitine. Other glucosides found in Rhododendrons are Ericolin (C₃₄H₅₆O₂₁), Arbutin (C₁₂H₁₆O₇), and Rhododendrin (C₁₆H₂₂O₇), but it is not clearly shown whether these are poisonous when ingested; Kobert, however, includes the two former among cerebro-spinal poisons.

Symptoms. In the case of goats Cornevin records intense pain, diarrhoea, discomfort, gritting of teeth, salivation, and frequently vomiting; while there is reduced lactation, trembling, spasms, vertigo, loss of power, and death. Lander notes similar symptoms in cattle and sheep.

According to Eve (Veterinary Record, 1907), a reddish colour was observed in the milk of a cow poisoned by Rhododendron.

Azalea (Azalea sp.). A suspected case of poisoning was recorded in the Journal of the Board of Agriculture in 1907. No British record of poisoning has been found. Various species of Azalea (A. pontica, A. indica, A. arborescens, A. nudiflora, etc.) are stated to be very poisonous to all animals which browse on them in the East. Cuttings should never be thrown down where they can be eaten by stock.

Toxic Principle. Little work has been done on these plants, but they are believed to contain Ericolin, Arbutin, and Andromedotoxin as in the case of rhododendrons (p. 47).

Symptoms. Azaleas appear to be narcotic, and to produce symptoms resembling those caused by Lolium temulentum (Cornevin).

PRIMULACEÆ.

Scarlet Pimpernel (Anagallis arvensis L.). Unless it occurs in very considerable quantity this little plant is unlikely to be eaten to an extent sufficient to cause definite poisonous symptoms, as it is a cornfield weed. It may be taken, however, if animals are allowed to run over stubble. Sheep are said to refuse it in general, but have died from eating it (see below).

There seems to be no doubt that if eaten in sufficient quantity it has a poisonous action, having an irritant action on the digestive tract—the intestines—as well as producing narcotic effects. Strasburger notes it as “slightly poisonous”; Bailey says “a dog is stated to have been destroyed by making it swallow three drachms of the extract,” while according to Hyams the fluid extract in 4 drachm doses is fatal to dogs (the size of the dog is not mentioned!); at the Veterinary School at Lyons horses were intentionally killed by administering a decoction of the plant; in America Chesnut notes it as suspected of killing a horse; Ewart says it “has been reported to render the chaff from oat crops infested by the weed unpalatable to stock”; and Gilruth states that a year or two ago it was responsible for the death of a large number of sheep in Victoria, apparently acting as a narcotic poison (Amer. Vet. Rev., July, 1913, p. 383.). On the Pacific coast the plant is known as “Poison Weed.” Grognier and Orfila are stated to have put its poisonous properties beyond doubt.

Toxic Principle. The plant contains the glucoside Cyclamin (C₂₀H₃₄O₁₀), and a saponin-like substance (Pammel). Van Rijn says it contains two glucosides.

Symptoms. The plant has an irritating effect on the intestines and a stupefying effect on the nervous system. Cornevin states that it is never taken by the larger domestic animals in quantity sufficient to cause poisoning.

OLEACEÆ.

Privet (Ligustrum vulgare L.). The facts as to the poisonous character of Privet are by no means clear, but Taylor records a case in which three children who ate the berries were attacked by violent purging, and a boy and girl died. Turner observed a case in which horses died after eating Privet.

Toxic Principle. The Privet is stated to contain the poisonous glucosides Ligustrin and Ligustron, not mentioned by Van Rijn, who says it contains Syringin (C₁₇H₂₄O₉), while Pammel (1911) adds the bitter glucosidal principle Syringopicrin (C₂₆H₂₄O₁₇).

Symptoms. In horses Turner observed loss of power in the hind limbs, with a pulse of 50, temperature 102° F., slightly injected mucous membranes, and dilated pupils, with death in 36 to 48 hours. The berries are stated by MÜller to cause sickness and diarrhoea.

CONVOLVULACEÆ.

Bindweeds (Convolvulus sepium L. and C. arvensis L.). The creeping rootstocks and foliage, as well as the seeds, are held to be more or less poisonous if eaten in quantity, and as long ago as 1872 Olver recorded (Veterinarian, 1872) that pigs which ate freely of Convolvulus died. These species, when eaten in considerable quantity, appear to be cathartic and purgative, causing symptoms resembling those due to jalap.

Thorn Apple (Datura Stramonium L.). This species is an escape from cultivation, but on occasion occurs plentifully in gardens, and if allowed to seed may escape to arable fields and find its way to stock, though it does not appear to have done so in Britain. Several species of Datura are recognized as virulent poisons in North America, where they are known as Jimson Weeds. All parts are poisonous, especially the seeds, which have a somewhat sweetish taste, and have frequently caused accidents to children who have eaten them. Cases are recorded in the United States in which cattle have been poisoned by eating the leaves of young plants in hay. Live stock, however, usually avoid the plant, which has an unpleasant odour and taste, while the seeds are enclosed in thorny capsules. Walsh states that the seeds are very fatal to young ostriches. Drying does not destroy the toxicity.

Toxic Principle. The Thorn Apple is usually stated to contain the highly poisonous narcotic alkaloid Daturine, but this appears to be a mixture of the two alkaloids Hyoscyamine (C₁₇H₂₃O₃N) and Atropine (C₁₇H₂₃O₃N), which, together with the alkaloid Scopolamine, or Hyoscine (C₁₇H₂₁O₄N), have been found in the plant, the principal constituent being Hyoscyamine. In some analyses as much as 0·33 per cent. of Atropine has been found in the seeds, and 0·2 per cent. in the leaves (Pammel). The three alkaloids occur together to the extent of 0·48 to 3·33 per cent. in the leaves, 0·43 per cent. in the flowers, and 0·1 per cent. in the root, Hyoscyamine predominating (Esser). An investigation conducted at the Imperial Institute (Bul. Imp. Inst., 1911) showed the amount of alkaloids in European specimens to be:—

Symptoms. The general effect of Datura poisoning appears to resemble that of Atropa Belladonna, but is by some considered more rapidly effective. There is paralysis, dilatation of the pupils, suspension of secretion and of the inhibitory fibres of the vagus, leading to rapid action of the heart (Lander). Poisoning may terminate fatally. Pammel quotes Winslow as stating that two grains of Atropine produce mild toxic symptoms in the horse; cattle are as susceptible as horses, though herbivora are not so easily influenced as carnivora. Chesnut gives the following symptoms: “Headache, vertigo, nausea, extreme thirst, dry, burning skin, and general nervous confusion, with dilated pupils, loss of sight and of voluntary motion, and sometimes mania, convulsions, and death.” Walsh gives the toxic symptoms in ostriches as staggering gait, spasmodic jerking of the neck, stupor, and death in a comatose state.

Henbane (Hyoscyamus niger L.). The poisonous character of Henbane is well known, but the plant is by no means common (except in Ireland), though found in parts of England, Scotland, and Wales. Poisoning of live stock may occasionally occur, but the disagreeable odour is likely to prevent all but abnormal or very hungry animals from touching it. The seeds are eaten by birds, apparently without injury, but poisoned chickens which ate the ripe seeds in Montana. Cornevin records that cows have been poisoned by eating the plant when given mixed with other herbage. There are numbers of cases of children having been poisoned by eating the seeds. The root has also caused accidents by being taken for other herbs, and the young shoots and leaves have been used in error as a vegetable. A case was reported in the press in 1910 in which 25 men and women visitors at a Davos pension suffered from the effects of eating the root of Henbane given in error for horse-radish, or mixed with it. All suffered from strange hallucinations, but with prompt and careful treatment all had recovered in twelve hours. Kanngiesser says that poisoning by this plant very seldom terminates fatally.

Welsby records a case in which animals were poisoned in a field in which Henbane was grown for medicinal use some years before (Veterinary Record, 1903). According to Rodet and Baillet (vide Cornevin) small quantities of the seeds are in some countries mixed with the food of fattening stock; if true that fattening is promoted, it is probably due to the inducement to quiet and repose caused by the narcotic properties of the seeds.

Toxic Principle. Poisoning by Henbane is due to the alkaloids Hyoscyamine (C₁₇H₂₃NO₃) and the closely related Hyoscine, or Scopolamine (C₁₇H₂₁O₄N). The glucoside Hyoscypicrin is also found in Henbane. The poisonous property is not eradicated by drying or boiling. The leaves of Henbane grown in Europe contain from 0·04 to 0·08 per cent. of total alkaloid, and the seeds 0·06 to 0·10 per cent. (Bul. Imp. Inst., 1911).

Symptoms. Henbane is an anodyne, and hypnotic. The symptoms resemble those caused by Atropa Belladonna (p. 58). The important differences (Cornevin) are that there is here abundant salivation and no dryness of the mouth as in Atropa. There is dilatation of the pupils; and mydriasis, which is dissipated more slowly than in Belladonna poisoning.

Further differences in the action of the two poisons are given by Winslow (via Pammel): The tetanic stage succeeding spinal paralysis observed in Atropine poisoning does not ensue with Hyoscine. The latter alkaloid slightly depresses and slows the heart and does 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.

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.”

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 (C₂₂H₃₄O₁₀), 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 diarrhoea. The symptoms appear to be the same in the case of cattle (Farmer and Stockbreeder, July 10, 1911).

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.

3. On the other hand, potatoes grown in a dry sandy soil are stated to contain more Solanine than those grown in other soils.