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).