Text book of veterinary medicine, Volume 2 (of 5)

by James Law

The disease caused by altered seeds and straw of the lupin is mainly characterized by jaundice, fatty degeneration of the hepatic cells and hypertrophy of the connective tissue of the liver causing acute atrophy of the organ.

Causes. The essential cause of the disease appears to be the consumption of lupins. But all lupins are not equally poisonous. Those taken from one portion of a field are harmless, while those from another are toxic. In stacks built in the field and weathered the upper and outer portions are often harmless while the interior remains poisonous. It would seem as if the poison were washed off by the rain, or deprived of its potency by the action of the air. It successfully resists dry heat, for three hours at boiling temperature, but is rendered harmless by steam acting under the pressure of two atmospheres for the same length of time. A poisonous principle (lupino-toxine) has been obtained from the toxic lupins but it is not quite certain that this is the sole toxic ingredient. This agent is extracted from the powdered seeds by macerating them for two hours in a soda solution (in which it is very soluble) at 102° F., and purified by treating the solution successively with acetic acid, lead acetate, hyposulphuric acid and alcohol. This agent produces the symptoms of lupinosis in the acute or chronic form according to the doses of the agent administered. Eichhorn and Baumstarch have isolated from lupins an alkaloid analogous to conicine: Stener found an alkaloid which he believed to be methylconicine: Baumert attributed the activity to another alkaloid lupinine. It is not definitely known whether the poisoning is usually effected by a simple poison or by a combination of several. Nor is it certain whether the toxic matter is a normal product of lupins grown on particular soils and under given conditions and harvested at a particular stage of growth, or if it is the product of a cryptogamic or bacterial growth. Some leguminous seeds are poisonous at a given stage of ripening but there is as yet no proof of lupinosis being confined to any particular stage. The common moulds often grow on lupins without rendering them poisonous, but it does not follow that some less familiar cryptogam is equally harmless under all circumstances. The soda extract of the poisonous lupins was deadly though it contained no cryptogams, but it is not shown that it was free from soluble chemical products (toxins) of the cryptogams. The same remark applies with equal force to the bacteria which have been invoked as the cause of the poisons. Though not themselves present in a given deadly extract of the lupins this does not exclude from such extract the toxic products of bacterial growth. It is claimed that Arnold has produced lupinosis with lupins that had been first robbed of their alkaloids. But the absence of alkaloids does not prove the absence of nonbasic (neutral) poisons, of vegetable, cryptogamic or bacterial origin.

That certain lupins contain a deadly poison is certified, but the precise source of the poison remains to be demonstrated.

In estimating causes we must take into account the lessened power of resistance of animals lacking in constitutional strength and vigor. Thus sheep suffer far more severely than horses, oxen, or even goats. Ewes and lambs perish in greater numbers than rams, hoggets and wethers.

Symptoms in Sheep. In the acute form the disease appears suddenly, as manifested by anorexia, hyperthermia, rapid and oppressed breathing, accelerated pulse, stupor, vertigo, and not unfrequently swellings of lips, ears or face. Inappetence may be first manifested by the rejection of poisonous lupins, while sound ones and especially other food are still eaten, but soon all are refused alike. Temperature, which may reach 104° to 106° F. on the next day after feeding on the poison, may rise and fall day by day, and finally fall materially as a herald of death. Respiration rises to 100 per minute and becomes labored or panting, with, in some cases, a bloody froth in the nostrils. The pulse rising to 130 and upwards keeps pace with the hyperthermia and general excitement. Vertigo is shown in the staggering gait when moved, and by a tendency to steady by resting the head on the trough, rack, fence or ground. The recumbent position is often preferred, the head being extended on the ground, and the animal remaining oblivious to all efforts to raise him—even to blows. Sometimes there is stupor, and at others hyperæsthesia, or indications of fear. There is grinding of the teeth, and sometimes trismus (Schütz, Kotelman).

In two or three days jaundice is shown, more especially in the conjunctiva and the urine. The latter, however, is not unfrequently colored with blood, and contains albumen, bile acids, and renal epithelium and casts. It is passed frequently in small quantity, so that its condition is easily ascertained.

The fæces are at first scanty and hard with a coating of yellowish mucus, and it may be streaks of blood. Later they are uniformly stained of a dark brown, and diarrhœa may alternate with the constipation. Emaciation advances with rapid strides.

Death may occur as early as one day after the attack but is usually deferred to the fourth or fifth.

A steady amelioration of all the symptoms may be welcomed as a precursor of recovery.

In the chronic form jaundice may be entirely absent, and a subacute gastro-enteritis may be attended by emaciation and anæmia. Roloff has frequently found the implication of the other mucosæ especially those of the nose and eyes which become catarrhal, and Zurn notes the implication of the skin of the face with exudations, swellings and the formation of sores and scabs on the eyelids, lips, ears, etc.