Part 82

In case of recovery, there is an improvement of the general symptoms, the heart and respirations become moderate, appetite is restored, the little animal sucking the teat, there are abundant, yellow, semi-solid defecations, the strength increases day by day, and convalescence may be fully established by the twelfth to the fifteenth day.

Diagnosis. This is mainly based on the extreme weakness and prostration, the violent heart action, the jaundiced hue of the mucous membranes, and the bloody urine. Confirmation may be sought in the presence of streptococci in the fresh urine, kidneys, liver and blood, and in the artificial cultures made from them. The presence of omphalitis is further significant.

Prognosis. Bernardin says that if hæmaturia is present nine out of ten cases are fatal, while in the absence of this feature nine-tenths recover.

Lesions. The jaundiced appearance of the conjunctiva and other tissues is constant. The heart is pale, soft and flaccid, with petechial patches of a deep red extending into the muscular substance; the lungs are congested with similar patches of blood-staining; the blood in the heart and larger vessels is dark, and fluid or only loosely clotted. The liver is congested to twice or thrice its normal size (10 lbs. in place of 3 or 4 lbs.); the spleen is enlarged, softened, and shows spots of brownish yellow. The small intestine contains a yellowish or dark red meconium, and it may contain effusions of dark blood, while its mucosa is inflamed, thickened, easily lacerated, and pigmented, or marked by petechiæ. The large intestines and especially the rectum are packed with hard dry balls.

The kidneys are enlarged, often to double their volume, and deeply congested, with infarcts, and patches of necrosis, of a pale brownish yellow hue. The urine in the bladder is deeply stained with blood coloring matter.

Treatment. For congenital cases it is manifest that treatment must be preventive and applied to the dam, before parturition. An open air life, moderate exercise, sound, easily digestible and nourishing food; grooming; in the stable, cleanliness, dryness and good ventilation; good water, are essential.

For the offspring, antiseptics (tannin, mercuric chloride lotion, copperas, calomel, iodoform), applied to the navel, and protection against cold winds and rains, and damp lairs. For mules and other young animals born in severe, winter weather a dry, warm, foaling box is desirable, and the little animal should be rubbed dry and covered with a warm woolen blanket. When the temperature approaches zero or the barn is cold, the smaller animals, as soon as they are dropped, should be placed under a box with a jar of hot water wrapped in woolen coverings, or with hot bricks similarly wrapped, and should only be let out for food when they are completely dried, or when the weather has moderated.

Therapeutic treatment may be commenced by a dose of aloes given to the dam, or of olive or castor oil or manna given to the offspring. As a substitute sulphate of soda may be used. Antiseptics like salicylate of soda, salol, or the sulphites may be added. To act as a demulcent on the alimentary and urinary tracts, well boiled flaxseed tea is usually recommended. Weakness may be met by warm strong coffee, salicin, quinia, or other bitters, and more stimulating agents like camphor, angelica, assafœtida, or even oil of turpentine may be added. Diarrhœa may be checked by linseed tea, mustard plasters, or in obstinate cases, by opium. Elimination should be sought by administering abundance of pure water or watery demulcents, and even by the use of alkalies like bicarbonates of soda or potash. A moderately free action of the bowels must be constantly maintained.

Antiseptic treatment of the navel and umbilical veins must not be overlooked.

LUPINOSIS, ACUTE TOXÆMIC ICTERUS, ACUTE YELLOW ATROPHY OF THE LIVER.

Attacks sheep, goat, ox, horse, stag; and, experimentally, dog. Causes: consumption of lupins, at a given stage of ripeness, from a given part of a field, or from centre of a stack. Lupinotoxine, conicine, methyl conicine, lupinine. Cryptogamic or bacterial poison. Weak subjects, sheep and even ewes and lambs, suffer most. Symptoms: Acute form: anorexia, fever, excited pulse and breathing, stupor, or hyperæsthesia, vertigo, swellings on head. Poisonous lupins are first rejected. Bloody nasal froth. In two or three days icterus. Urine may be bloody. Fæces at first hard, coated, bloody, later dark brown and often liquid. Emaciation. Death in 1 to 5 days. Chronic form, gastro-enteritis, emaciation, anæmia. Nasal catarrh. Facial swellings and sores. Lesions: hepatitis, nephritis, muco-enteritis, enlarged spleen, icterus, blood extravasations; hepatic tissue, infiltrated, cloudy, granular, fatty, later cirrhosis. Kidneys contain casts: Spleen tumid, blood gorged. Prognosis: grave: acute cases die, chronic may recover. Prevention: feed no lupins, avoid dangerous fields, wash off poison from lupins with a soda solution. Ensilage with acid producing fodder in alternate layers. Treatment: avoid alkalies, give acids, purgative, castor oil, water. In horse, causes anorexia, anæsthesia, dullness, stupor, colic, constipation, urinary irritation, fever, slight jaundice, vertigo, orange nasal discharge, sores on tongue and face, and lower part of limbs. Diagnosis. Prognosis hopeful. Treatment as in sheep. Icterus from other fodders.

This affection has been noticed especially in sheep, but also in the goat, horse, ox and stag as the result of eating lupins. The dog has contracted the disease under experiment. It has been studied especially in Northern Germany where the lupin is largely cultivated as a fodder crop. The yellow lupin (Lupinus Luteus) is mainly to blame for the disease, but the Lupinus Albus and Augustifolius are also spoken of as factors.

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.

Lesions in Sheep. The prominent lesions are parenchymatous inflammation of the liver and kidneys, muco-enteritis, enlargement of the spleen, and icterus, with more or less blood extravasation.

The liver is the seat of acute hepatitis. It is usually swollen and abnormally friable, with a yellowish color often as deep as citron. The parts recently attacked exhibit albuminoid infiltration and cloudy swelling, the older lesions show fatty or granular degeneration. These changes exist especially in the hepatic cells, and fatty metamorphosis bears a direct relation to the obesity of the sheep. If the patient has survived the first few days, the liquefied products are absorbed, there is a relative increase of the interstitial connective tissue and the volume of the organ is materially decreased (acute yellow atrophy of the liver, Schütz). In chronic cases, the hypertrophy of the interstitial connective tissue is the most prominent feature, constituting a distinct cirrhoses (fibroid induration) and the atrophy becomes very pronounced while the surface is very irregular and uneven. The gall bladder is distended, and its mucosa congested.

Jaundice, which may be little marked apart from the conjunctiva, is usually shown in the subcutaneous connective tissue, the skin of the abdomen, the omentum and mesentery, but according to Cadeac is never shown in cartilage, bone nor tendon.

The kidneys show parenchymatous inflammation, congestion, swelling which gives a hardness of touch through the resisting fibrous envelope, and often a pervading shade of yellow. The epithelium of the uriniferous tubes is cloudy, turbid and granular and the tubes themselves contain cylindroid casts. The bladder is catarrhal and has been too irritable to contain urine.

The spleen is tumid, soft, reddish gray, and on section shows excess of blood, pulp, and here and there marbling by fibrinous exudate.

The heart is pale, granular, friable, with a tinge of yellow and with a slight citron colored effusion in the pericardium. The cardiac blood is dark and thick but coagulates and brightens in color on exposure to the air.