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.