HÆMOGLOBINÆMIA. AZOTÆMIA. AZOTURIA. HÆMOGLOBINURIA. TOXÆMIA FROM IMPERFECT HEPATIC FUNCTION. (continued 2)

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 480days, 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.

There is usually some œdema of the lung, larnyx and pia mater.

There are catarrhal lesions of the abomasum and entire intestinal canal with granular degeneration of the epithelium and spots and patches of arborescent congestion and hæmorrhage. The icteric tint is usually distinct.

Prognosis is always grave. Acute cases are almost always fatal. Chronic cases due to eating lupins in which the poison is relatively weak, or a very restricted amount of the more poisonous lupins, may recover. This mortality is very serious in the affected districts 5.8 per cent. of all the sheep of some districts in Pommerania perishing yearly from this affection and entailing the loss of almost the same number of lambs (Von Below-Seleske).

Prevention. Radical prevention can be secured by the exclusion 481of lupins from the ration. Where this is undesirable the fields that produce poisonous lupins can be ascertained and devoted to the production of other crops. When a crop of lupins has already been produced on a dangerous field the poison may be extracted from the fodder or subjected to the action of an antidote. Fortunately the poison is concentrated on the surface of the lupin and is easily washed off.

Dammann advises to leave the cut forage exposed to the rain so that the poison may be washed off. A more prompt and effective plan would be to put the fodder under a stream of water from a hose, and it could be fed while still fresh and unaltered. Friedberger and Fröhner directs that the forage be steeped for forty-eight hours in a soda solution (1:100) to dissolve off the offensive matter, after which it may be washed and safely fed.

Glaser would put the lupins in a silo, in alternate layers with some material which rapidly undergoes acid fermentation (brewers grains, maize, pulped roots). The acid renders the poison insoluble and is directly antidotal. To develop this acid it is important to put the materials into the silo before they have become too far matured.

The destruction of the poison by steaming the fodder under a pressure of two atmospheres, as recommended by Kuhn and Roloff requires a too elaborate apparatus for ordinary use.

Therapeutic treatment. The first desideratum is to render insoluble any poison which has already entered the alimentary canal. Alkalies, as solvents and distributers of the poison must be carefully avoided and acids (acetic, nitric, hydrochloric, sulphuric) freely used. These may be mixed with the drinking water or given from a bottle. If appetite is still retained, they may be mixed with the food, or acid aliment (sour ensilage, old grains, or fermented swill) may be supplied.

The next resort is a purgative to eliminate the poison from the alimentary canal. But the cathartics usually given to the ruminants are dangerous. Sulphate of soda undergoing decomposition, furnishes an alkaline solvent for the poison. Castor oil is therefore to be preferred.

An abundance of water will favor the action of both bowels and kidneys and hasten the elimination of the poison which may have been already absorbed into the system.

482European writers recommend the use of the flesh as human food, unless the animal had reached the last stage of the disease.

Symptoms of Lupinosis in the Horse. There is always the history of the presence of lupins in the oats, or of lupin straw as a food or litter. Though less fatal than in sheep the disease sets in with great severity, the symptoms referring especially to gastro-enteritis, and disorders of innervation. There is complete anorexia, impaired sensibility, dullness and stupor, the head resting on the manger or drooping with the nose near the ground. There is grinding of the teeth, colicy symptoms, and constipation, the fæces being passed as a few small, hard balls covered with mucus and fœtid. Urine is passed frequently in small amount and albuminous. There is more or less hyperthermia (rising at times to 102° to 103°), the respiration is hurried (36 to 40 per minute) and pulse is rapid (60 per minute). Jaundice is usually present but less prominent than in sheep. When moved the animal sways unsteadily or staggers. Butzert notices, in addition to the above, a thick orange colored discharge from the nose, and the formation of sores and scabs (mummification) of the lingual mucous membrane, of the lips, of the skin, of the face, and of the pastern, and swelling of the lower parts of the limbs.

Diagnosis. The development of disease with the above symptoms, in the inmates of a single stable, or in horses having a common ration, in which the lupines are found, will make diagnosis easy and reasonably certain.

Prognosis is hopeful or confident. The disease is not fatal in the horse.

Treatment should follow the same lines as in sheep.

Allied or identical diseases. Friedberger and Fröhner quote a number of outbreaks of hepatic inflammation or disorder with icterus in the absence of lupins, but on rations that were otherwise faulty. Haubner describes a “malignant icterus” in sheep fed on malted potatoes; Sander records a “hepatic typhus” in the horse when fed on inundated pastures; Reinemann and Jansen speak of a similar affection in animals fed on the straw of peas, beans and vetches.

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