Chapter XX: Part 20

_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.

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 of 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.

European 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.

CONGESTION OF THE LIVER.

Physiologically after a meal is hyperæmic, and may increase one-third.
Rich feed and temporary idleness may cause morbid congestion. Other
causes are: ptomaines and toxins in spoiled food, hepatic irritants,
damp, hot, tropical climates, warm, damp, buildings, overfeeding,
dilated right heart, insufficiency of tricuspid valve, pulmonary
emphysema or congestion. Absence of valve between the right heart and
hepatic veins, slow hepatic circulation, dilatability of hepatic
vascular system, compression of lung by false membranes, œdema,
hepatization, infarction, hydrothorax. In horse: special causes:
spoiled fodders, carminatives, volatile oils, work in hot sun,
vaso-dilatation in heat and atony, falls, kicks, goring, blows;
passive forms from obstacles to the circulation. Lesions: Hepatic
enlargement to 20 or 30 pounds, and dark red color, darker spots of
extravasation, hepatic vein congestion in centre, and portal vein
congestion in periphery of acinus, softening, granular, fatty, nuclei
disappear from hepatic cells, nutmeg liver, cirrhosis. Symptoms:
general febrile symptoms, great prostration, drowsiness, slight
colics, arched loins, trembling or jerking, lies on right side,
percussion on last ribs painful, slight icterus and increased
urination and urea. In passive cases, less icterus and kidney trouble;
tends to intestinal catarrh and ascites. Prevention: good hygiene,
moderate laxative ration, cool air, exercise. Treatment: green or
laxative foods, salines, derivatives, water at will, always before
morning feed. In dog: overfeeding, indolence: pulmonary and
circulatory troubles. Lesions: nutmeg liver, degeneration, cirrhosis.
Symptoms: pampered idleness, obesity, pulmonary or cardiac disease,
intestinal catarrh, piles, ascites, slight icterus, percussion
tenderness of right hypochondrium, lying on right side, increase of
percussion flatness. Treatment: saline purgatives or laxatives,
antiseptics, restricted laxative diet, open air exercise, derivatives,
etc.

Physiologically the liver undergoes hyperæmia in connection with an abundant meal and active digestion. Within the limits of health it may increase one-third in bulk and weight. When this hyperæmia attends on temporary idleness and rich feeding it may overstep the limits of health and become pathological. Other causes of pathological congestion are, tainted food rich in ptomaines and toxins, food injured by cryptogams, and food that contains principles irritating to the liver. It is especially common in swampy regions in tropical or semi-tropical latitudes, and where the warm air is surcharged with moisture. Hot, close, damp stables, with overfeeding and lack of exercise in the pampered horse or dog, or under the forcing system of feeding for exhibition, or for the butcher, acts in a similar manner. Dilatation of the right heart, or imperfection of the tricuspid valve is a direct cause of mechanical congestion and emphysema, congestion or other obstruction in the lungs has a similar effect. In short the absence of valves between the right heart and the hepatic veins determines a passive congestion of the liver whenever there is any serious hindrance to the passage of blood through the right heart and lungs. The tardy circulation through the liver (5 mm. per second) also predisposes to congestion. The great development of the circulatory system in the liver, and its dilatability predisposes it to such congestions in a pre-eminent degree. For the same reason the liver suffers in the horse that is attacked with pulmonary congestion, whether as the result of overwork or of heat congestion. It will also suffer from compression of the lungs by false membranes or hydrothorax, or obstruction, by œdema, hepatization or infarction. The toxic matters produced in infectious diseases, and especially those affecting the intestinal canal and its connections, are arrested in the liver and contribute to hyperæmia.

CONGESTION OF THE LIVER IN THE HORSE.

_Causes._ Beside the general causes above mentioned, may be specially named, musty, decomposed, and irritant fodders: those which like green legumes, are easily fermented; and those which contain stimulating volatile oils or carminative principles. They are also especially exposed to such causes as severe and prolonged work under a hot sun, the nervous atony which causes vaso-dilatation in a hot climate, and such traumatisms as come from falls, kicks, goring, and blows by shafts, poles and clubs. These especially induce _active congestion_. The _passive_ forms come mainly from obstruction in the lungs, or heart (dilatation, right valvular insufficiency, pericarditis, hydropericardium, myocarditis, fatty degeneration, endocarditis), or in the posterior vena cava.

_Lesions._ The congested liver is enlarged and deeply colored with blood. The weight of twenty to thirty pounds is often attained. While the color is of a deep red throughout, there are spots of a still darker hue indicating the seat of subcapsular or deeper seated hemorrhages. The color varies according as the congestion is passive or active. In the former the coloration is deeper in the centre of the acinus (nutmeg liver) indicating congestion of the hepatic veins, while in the latter the periphery of the acinus may be most deeply stained implying congestion of the portal vein. The consistency of the organ is diminished, and the more acute the attack the greater the friability. In such cases there is a parboiled appearance indicating granular and commencing fatty degeneration. Under the microscope the relative distension of the intralobular, and interlobular veins and the hepatic capillaries becomes more distinctly marked and the presence of pigment and fatty granules and the lack of protoplasm and nuclei in the hepatic cells indicate their progressive changes. When the peripheral cells are pale from fatty granules the contrast between the light margin and dark centre of the acinus, makes the mottled or nutmeg aspect of the liver much more pronounced.

In old standing cases of passive congestion the liver may be the seat of fibroid degeneration, extending from the capsule inward in bands or trabeculæ, and giving to the organ a firm resistant character (sclerosis, cirrhosis).

_Symptoms._ The symptoms are general and suggestive rather than pathognomonic. There are dullness, prostration, unsteady walk, pendent head, with occasional jerking, semi-closed eyes, redness of the conjunctiva, slight colicy pains, arching of the loins, muscular tremblings and decubitus on the left side rather than the right. The more definite symptoms are tenderness on percussion with the closed fist over the last ribs (the liver) especially on the right side, increase of the area of hepatic percussion dullness (which may be rendered valueless by a loaded colon), the presence of a slight icterus in the conjunctiva and urine, and an increase of the urine secreted and an excess of the contained urea.

In _passive_ cases however the obstruction to the escape of blood from the liver prevents the development of icteric symptoms, of uræmia and of polyuria. In all such cases however there follows a general congestion of the portal system and if it persists for any length of time gastro-intestinal congestion and catarrh and even ascites may develop.

In all cases alike the history of the attack will help towards a satisfactory diagnosis.

_Prevention._ A rational hygiene embracing daily work or exercise, moderate laxative diet, green food in its season, pure cool air are important precautions.

_Treatment._ A moderate supply of green or laxative food, the withholding for the time of grain, and especially of maize, wheat or buckwheat, saline laxatives daily, and a stimulating embrocation or blister to the tender hypochondrium are the most important measures. Exercise in a box stall, or still better in a yard or paddock in the intervals between more systematic work forms an important adjunct to medicine. As a laxative sulphate of soda is to be preferred at first in a full cathartic dose and later in a daily amount sufficient to relax the bowels. Given in a bucket of water every morning before the first meal a very small dose will be effective.

CONGESTION OF THE LIVER IN THE DOG.

_Active_ congestion is very rare excepting in over-fed and indolent family pets. _Passive_ congestion induced by diseases of the lungs and heart is however far from uncommon.

_Lesions._ True to their origin these usually appear as the spotted nutmeg liver with the deep congestion in the centre of the acini. For the same reason the fibroid degenerations shown in chronic cases, show the firm fibroid neoplasm chiefly around the hepatic veins. Granular, fatty and pigmentary degeneration of the cells are found as in the solipeds.

_Symptoms._ These are as obscure as in the horse. There is always a history of a sluggish, gourmandizing life, and in the early stages, a manifestation of embonpoint which suggests a torpid liver. Further suggestions may also be obtained from coexisting diseases of the lungs, or heart, from gastro-intestinal catarrh, from piles, or ascites. Then there is at times a slight icterus of the conjunctiva and urine. Finally tenderness on percussion on the right hypochondrium, decubitus on the left side, and an increased area of dullness on percussion may afford useful hints for diagnosis.

_Treatment._ In the rare cases due to infection from the intestine, an active saline purgative followed by antiseptics (salol, naphthalin, naphthol, etc.,) daily will be of value. It is also desirable to keep up the action of the bowels by morning doses of salines. In cases consequent on chest disease attention must be given to such primary trouble. In all cases a restricted laxative diet, and graduated but increasing exercise in the open air are demanded.

HEPATIC HÆMORRHAGE OR RUPTURE.

Causes: Mechanical injuries, falls, blows, kicks, degenerations,
amyloid, fatty, granular, congestion, neoplasms, glanders,
tuberculous, myomatous, microbian infection. In the horse, disease of
liver, heart, lungs, hepatic artery, portal vein, degenerations
following overfeeding, idleness, foreign bodies, arsenic, phosphorus,
parasites, violent movements in colic, running, draught, leaping. In
the dog, pampering and traumatism. In cattle forced feeding,
emaciation, microbian infection. In birds, tubercle, tæniasis,
microbian infection. Lesions: extravasation, intracapsular, or through
capsule into the peritoneal cavity. The extravasation bulges of a deep
black, covering a dark softened, pulpy, hepatic tissue, with light
colored fatty tissue around. Clots may be stratified from successive
bleedings. Liver usually enlarged. Symptoms: onset sudden, or preceded
by stiffness, soreness and other signs of hepatic trouble. Extensive
rupture, entails weakness, unsteady gait, perspiration, pallor of
mucosæ, small weak rapid pulse, palpitations, dilated pupils, rolling
eyes, amaurosis, tremors, convulsion in case of survival, coldness,
œdemas. Death in five hours to five days. Risk of relapse in
recovering cases. Treatment: rather hopeless, rest, laxative, ergot,
ferric chloride, tannic acid, witch hazel, cold water, snow or ice to
right side. In meat producing animals fatten.

_Causes._ Hemorrhage and rupture of the liver are closely correlated to each other, the accumulation of extravasated blood in the parenchyma in the one case leading to over distension of the capsule, and the laceration of this capsule and of the adjacent substance of the liver occurring in the other as a mere extension of the first. They usually occur as the direct result of mechanical injury (falls, blows, kicks) acting on a liver already softened and friable through disease. These predisposing degenerations may be amyloid (Caparini, Johne, Rabe), fatty (Julien, Gowing, Adam, Siedamgrotzky), granular softening, hepatitis or congestion (Zundel), glander neoplasms (Mathis), tubercles, angiomata (Trasbot), microbian infection (Stubbe), tumors (Brückmüller).

In the horse predisposing conditions may be found in diseases of the liver, heart or lungs, in embolism of the hepatic artery (Wright), in obstruction of the portal vein (Pierre), in infarction of the liver, in degeneration with softening, in sarcomatous, melanotic, glanderous or cancerous deposits in its substance, in degenerations consequent on over feeding, idleness, congestions, on the penetration of husks of grains into the liver substance, on arsenical or phosphorus poisoning. The presence of flukes, echinococci and other parasites may also cause congestion and softening. To the _immediate_ or _traumatic_ causes above named may be added the violent movements attendant on a severe attack of colic, and violent exertions in running, draught, leaping, etc. (Friend).

In the =dog= we must recognize all the pampering conditions which predispose to congestion and degeneration, together with more direct operation of kicks, blows, falls, fights, over exertion, etc.

In =cattle= a forcing regimen is especially predisposing, and yet the loss of vigor resulting from a diametrically opposite treatment, must be accepted as an occasional cause. Stubbe found in emaciated cows miliary hemorrhagic infarcts of a dark red color which gradually extended to an inch or more in diameter. These he traced to microbian infection coming by way of the chronic intestinal lesions which are common in old cows. The final result of such infarctions was loss of hepatic substance and the formation of cicatricial tissue with a marked depression on the surface of the organ.

In =birds= fatal hepatic hemorrhages occur in connection with local tubercle (Cadiot), tæniasis of the liver, or microbian infection.

_Lesions._ The hemorrhage may take place into the substance of the liver only, or the capsule may be lacerated so that the blood escapes into the peritoneal cavity in considerable quantity.

In the _horse_ it usually occurs in the right or middle lobe, rarely in the left. There may be one or more hemorrhagic effusions varying in size from a cherry to a duck’s egg, or even an infants’ head (Lorge). This projects from the surface of the organ and its deep black contrasts strongly with the white of the adjacent capsule. When laid open the hepatic tissue is seen to be softened and pulpy, and its dark color forms a striking contrast with any surrounding fatty liver. Any form of degeneration may be revealed on microscopic or chemical examination. Not unfrequently small clots of blood form under the capsule raising it in the form of little sacs. Such clots are usually stratified indicating a succession of small hemorrhages.

When the capsule is torn, the lesion may extend from one surface of the organ to the other, and the edges, smooth, uneven or fringed, are united together by a blood clot.

In case of hemorrhagic infarcts the lesion usually has a distinctly conical outline corresponding to the vascular distribution. These are especially characteristic of cases supervening on heart disease.

The volume of the liver is usually increased and the weight may reach 30 lbs. (Schmeltz), 34 lbs. (Lorge), or even 66 lbs. (Trasbot).

In _other domestic animals_ analogous lesions are found modified largely according to the size of the subject.

_Symptoms._ These may develop instantaneously without any marked premonitory indication. In other cases tenderness on percussion over the liver, stiffness or groaning under sudden movements or turning, arching of the back, hanging of the head, slowness in rising, costiveness, slight transient colics, and even icterus may have been detected on close observation. The symptoms of actual rupture are essentially those of internal hemorrhage. The animal becomes weak, or unsteady upon its limbs, perspires, arches the back, and shows a marked pallor of the visible mucosæ. The pulse is small, thready, weak and accelerated, and the heart beats violent or palpitating. The percussion dullness over the liver is extended (Weber), the loins become insensible to pinching, and there may be some distension of the abdomen. Dilatation of the pupils, retraction or rolling of the eyes, amaurosis, tremors of the muscles of the neck, lying down, or falling, and general convulsions may precede death. This may occur in a few hours or it may be delayed if the lesions are restricted. In case of survival, coldness and œdema of the extremities and sheath have been observed. The lesser hemorrhages may terminate in recovery if there is no attendant incurable disease. In anthrax, glanders, cancer, tuberculosis, septicæmia, etc., a favorable issue is not to be looked for.

_Duration. Termination._ In severe cases a fatal issue may be expected in from five hours to five days. In the milder cases which make a temporary recovery there is great danger of a second hemorrhage from the new vessels in the tissue undergoing organization or from the adjacent degenerate liver tissue. The course of the affection may be altered by such complications as arthritis (Dieckerhoff), pneumonia, pulmonary thrombosis (Leblanc), enteritis or peritonitis (Cadeac).

_Treatment_ is usually of no avail. Rest, and the administration of laxatives and hæmostatics, have been especially recommended. Of the latter, ergot by the mouth or ergotin subcutem, tends to contraction of the blood-vessels and to check the flow. Ferric chloride is also used, though apt to interfere with hepatic function. Tannic acid, hamamelis, and other astringents may be used instead. Cold water, snow or ice applied to the right hypochondrium may act as a check to the hemorrhage. Unless in purely traumatic cases in an otherwise healthy liver, a recovery is at best temporary, and the already degenerate liver is liable to relapse at any moment. In horses and dogs, therefore, recovery is by no means an unmixed good. Meat producing animals that recover should be prepared for the butcher.

HEPATITIS.

Forms of hepatitis: Parenchymatous hepatitis. Definition: Degeneration
of hepatic cells. Relation to enteritis and nephritis. In
horse—causes:—as in congestion, pampering, spoiled fodder, malt,
inundated meadows, chill, overfeeding, hot moist climate,
hæmoglobinæmia, infection. In cattle—causes:—forcing ration, hot
weather, overwork, infection. In dog—causes:—infection from alimentary
canal. Lesions: Enlarged, softened liver, round edges, a week later
yellow atrophy, granular on section, bloodless. Acini with indefinite
margins, cells granular, nuclei lost. In dog centres of softening.
Symptoms:—in horse: Attack sudden, rigor, fever, dullness,
prostration, yellowish red mucosæ, unsteady gait, slight colic,
anorexia, urine decreased, glairy, brownish red, groaning in
defecation, excited circulation and breathing, increased icterus by
third day, fœtid, colorless diarrhœa. Diagnosis: Coincidence of fever,
prostration, icterus, painful defecation, fœtid diarrhœa, light color
of stools, tenderness and flatness on percussing hepatic area. From
influenza by absence of watering eyes and contagion. Prognosis in
horse: Very grave unless urine is free. Treatment in horse: Portal
depletion, calomel, ipecacuan, salines, diuretics, fomentation of
loins, antiseptics, derivatives, mineral acids, bitters. Careful
laxative diet in convalescence. Symptoms in cattle: Slower onset,
anorexia, dullness, depression, drivelling saliva, grinding teeth,
icterus, constipation, later fœtid diarrhœa, pale colored stools,
recumbency, groans on rising, arching back, tender right
hypochondrium, fever. Prognosis grave. Death in five to six days.
Treatment as in horse: Only saline laxatives. Symptoms in dog:
Muscular tremors, staring coat, hyperthermia, icterus, fœtid breath,
ventral decubitus, extreme prostration, anorexia, tender right
hypochondrium, diminished urine, death in two or three days. Treatment
in dog: Calomel and jalap, diuretics, laxatives, derivatives,
germicides, in convalescence, mineral acids, bitters, careful diet.

The different forms of inflammation of the liver are distinguished according as they affect, especially the hepatic cells and tissue of the acini (parenchymatous), as they result in suppuration (suppurative, catarrhal, abscess), as they cause necrobiosis in nodular masses (infectious or necrotic), as they lead to fibroid thickening under the peritoneum and proper capsule (perihepatitis); or as they cause general fibroid induration of the organ by increase of its connective tissue (cirrhosis).

PARENCHYMATOUS HEPATITIS, ACUTE YELLOW ATROPHY OE THE LIVER.

The characteristic morbid lesion in this disease is the degeneration of the liver cells, loss of their protoplasm and nuclei and of their normal functions. It may be circumscribed to limited areas, or may affect the liver, generally. As the hepatic functions, are so intimately related to those of the bowels and kidney, the affection is usually accompanied by inflammations of these organs as well.

_Causes in horses._ The same general causes which produce congestion, may also determine the further morbid stage of inflammation. Cadeac mentions a case which developed in a horse kept alone and idle in the stable. He makes no mention of condition, food, cleanliness nor ventilation. Haubner and Franzen have traced it to a diet of malt or of hay harvested from inundated meadows. Zundel records a case following exposure to extreme cold. More commonly the disease is secondary to the overtaxing of the liver, by heavy feeding in warm moist climates, or in hæmoglobinæmia, or to the arrest of the micro-organisms of the food, or of infectious diseases.

_Causes in Cattle._ These suffer rarely, but from essentially the same conditions. It has followed aphthous fever (Eletti), and arisen under a forcing ration, in hot weather (Callot, Cruzel), or under overwork (Cruzel).

_Causes in Dogs._ Most cases result from infection by way of the stomach and intestines, or by the transfer to the liver of the ptomaines and toxins of such infections. It is thus related in its origin to catarrhal jaundice and hyperæmia.

_Lesions._ In the earliest stage with albuminoid exudation into its substance the liver may be greatly enlarged, its sharp edges rounded, and its consistency softened. After a week’s illness atrophy may have set in and the organ appears shrunken and of ocherous yellow. In the early stages there may be sanguineous engorgement, the cut surface may bleed freely, and small extravasations may show throughout the liver substance, later the clay yellow hue, the granular aspect and the absence of blood on the cut surface are characteristic. The margins of the adjacent acini are indefinite or lost, and under the microscope the hepatic cells are charged with granules (albuminoid, fatty and pigmentary), while the nuclei are no longer demonstrable.

In _cattle_ the liver may be double the normal size and at first of a deep purple red, which may change later to the earthy yellow.

In _dogs_ the liver is tumid and yellow, and marked by small pea-like centres of softening. There is marked softening and the microscope reveals the characteristic degeneration of the hepatic cells.

_Symptoms in the Horse._ These resemble those of congestion rendered more intense and therefore somewhat less obscure. The attack is usually sudden, there may be rigor followed by hyperthermia, dullness, pendent head, drooping eyelids, injected conjunctiva with a yellowish tinge, unsteady gait and slight indications of colic. There is anorexia, partial suppression of urine, and what is passed is thick, glairy and brownish red, fæces are passed with pain, and groaning, probably from compression of the liver, the heart beats violently, while the pulse is small, breathing accelerated and perspiration abundant. The temperature rises (101° to 106°) and remains high throughout unless lowered through biliary intoxication. Percussion over the liver and especially on the right side shows increased area of dullness and marked tenderness. On the second or third day the icterus usually increases, and a slight fœtid diarrhœa may set in with marked fœtor of the pale or colorless discharges. The jaundice is not, however, a criterion of the danger, as it may become less marked or entirely disappear because of the extensive degeneration of the hepatic cells and the arrest of the formation of bile.

_Diagnosis in the horse._ The disease is recognized by the coincidence of fever, with great depression, icterus, painful defecation, constipation followed by a fœtid diarrhœa with lack of color in the stools and by increased area of dullness and tenderness in the region of the liver and especially on the right side. From influenza which it resembles in many respects, it is distinguished by the absence of watery discharge from the eyes, and by the entire absence of all indication of contagion. The cases occur one at a time.

_Prognosis in the horse._ The disease is exceedingly fatal. When the kidneys remain active, the poisons are eliminated and there may be hope of recovery, but when urine is suppressed an early death by poisoning is to be expected.

_Treatment in the horse._ A most important indication is to secure depletion from the portal system. Calomel 1 dr., aloes 4 drs., ipecacuan 1 dr. may be given in bolus, and followed by small daily doses of sulphate and nitrate of soda with bitters, with or without the ipecacuan. Action on the kidneys is essential to secure elimination of the poisons which threaten a fatal poisoning if retained. To favor the same action fomentations may be applied to the loins. The frequent presence of pathogenic microörganisms either in the bowels or liver suggests the use of germicides (salol, salicylic acid, salicylate of soda, naphthalin, naphthol, beta-naphthol, etc.) as in catarrhal jaundice. Sinapisms or blisters applied to the right side of the chest and over the short ribs may be useful, and after the subsidence of the more violent symptoms, dilute mineral acids and especially nitro-muriatic acid may be resorted to in combination with diuretics and bitters.

When appetite returns succulent, laxative, non-stimulating food in small quantity should be given. Wheat bran mashes, carrots, turnips, potatoes, apples, fresh grass, ensilage may be adduced as examples. Throughout the disease the ingestion of an abundance of pure water should be encouraged.

_Symptoms in the ox._ These may appear more tardily than in the horse, loss of appetite, staring coat, dullness, pendent head and ears, unsteady movements, rigors, drivelling of saliva from the mouth and grinding the teeth are usually noted. To these are added the more diagnostic symptoms of slight (or severe) jaundice, constipation followed by a fœtid light colored diarrhœa, a strong disposition to remain recumbent, marked suffering attendant on rising, arching of the back when up, and tenderness on percussion over the right hypochondrium. The temperature gradually rises, though more slowly than in the horse, and may again descend under a profound poisoning.

_Course._ The disease reaches its acme in four to six days, and generally has a fatal issue.

_Treatment_, is on the same lines as for the horse only as a purgative, sulphate of soda may advantageously replace the aloes.

_Symptoms in the dog._ The symptoms are those of congestion in an exaggerated form. There are muscular tremors, erection of the hair, followed by rising temperature up to 105° or 106°, an icteric hue of the mucosæ, the pulse is accelerated, strong, irregular, respiration rapid, panting, fœtid breath, ventral decubitus, and prostration extreme. Appetite is completely lost, the bowels become relaxed, the stools fœtid, the right hypochondrium painful on pressure or percussion, and the urine greatly reduced and icteric or suppressed. This feature of urinary suppression, determines a rapid poisoning and death in two or three days.

_Treatment_ must follow the same lines as in other animals, a purgative of calomel and jalap, followed by diuretics, laxatives, derivatives, and above all germicides. In case of survival mineral acids, aqua regia, bitters, and a carefully regulated diet will be in order.

SUPPURATIVE HEPATITIS. HEPATIC ABSCESS.

Causes in horse: pyæmia, omphalitis, thrombosis, infection, biliary
calculi, concretions or parasites, foreign bodies, hot, damp climates,
strangles, brustseuche, glanders, endocarditis. Lesions in horse: from
parasites and mechanical irritants, pea-like or hazelnut; embolic
abscess, pin head to hen’s egg; infection from strangles, foreign
bodies, etc., may be of large size, and burst into adjacent organs,
the peritoneum or externally. Symptoms in horse: of pre-existent
malady, remitting fever, successive chills, intermittent icterus,
hypochondriac tenderness. Spontaneous recovery, aspiration, opening,
antiseptics locally and generally. Lesions in ruminants; secondary
multiple abscesses, bean-like or (with foreign body) very large, may
extend into adjacent parts. Symptoms in cattle: fever, chills,
jaundice, tympany, diarrhœa, dysentery, wasting, tender right
hypochondrium. Treatment: as in horse. Causes in dog: foreign bodies,
tumors, infections, blows, traumas. Lesions: traumatic abscesses,
single, large, infectious abscesses multiple, small. Former fœtid.
Symptoms in dog: hepatic congestion or colic, then chills,
prostration, irritability, tenderness of right hypochondrium, nausea,
vomiting. Treatment in dog: antiseptic aspiration, laparotomy.

_Causes in the Horse._ Hepatic abscess arises from a great many primary morbid conditions. As a secondary abscess it is seen in the different forms of pyæmia and especially in suppurative omphalitis in young animals. It may start in thrombosis determined by clots or septic matters carried from a distance through the portal vein or hepatic artery, in biliary calculi or concretions, in parasites introduced from the duodenum, in barbs or husks of the cereals that have penetrated through the biliary ducts, or in bacteria or their toxins which have been carried from the bowels, spleen or pancreas. The government veterinarians have found it a comparatively common lesion in the hot damp climate of Hindoostan, and a similar frequency has been noticed in west Africa. Among general affections it is liable to occur in strangles, contagious pneumonia, glanders, endocarditis of the left heart and phlebitis with the formation of thrombi in the lungs. In the two last named disorders, the affection takes place by the simple transference of detached clots to the liver to block its arteries or capillaries. Or it may be that micro-organisms are transferred in the same way. With modern views of suppuration the presence of the pyogenic organisms must be conceded.

_Lesions in the horse._ Cadeac distinguishes the different types of hepatic abscess as: _1st biliary abscess_ in which suppuration commences in the interior of the biliary ducts and usually from parasites or mechanical irritants introduced or from calculi or concretions formed within them: these rare abscesses contain biliary salts, pigments, and epithelium and acquire the size of a pea or hazelnut: _2d Metastatic abscesses_ which start in the arterial, portal, or capillary vessels, by the arrest of infecting clots, which determine a further clotting, the obstruction of the vessel, the accumulation of leucocytes and the formation of abscess of the size of a pin head or larger up to a hen’s egg, surrounded by a hæmorrhagic infarct softening in the centre: these are numerously disseminated through the liver: _3d Mechanical Abscess_ due to the penetration of foreign bodies or parasites: 4th Infection as in strangles. These may attain a large size, cause adhesion to adjacent organs, and rupture into the chest, the colon, stomach or peritoneum. The pus may even escape externally through the right hypochondrium.

_Symptoms in the horse._ These are always obscure and vary much with the source of the malady. If there has been a pre-existing hepatic malady the symptoms of that will be in evidence; if an omphalitis its existence may still be recognizable; if pulmonary or cardiac disease, that may be detected; if parasites, evidence of their existence may perchance be found; if gall stone, a previous violent hepatic colic with icterus may have occurred; and if intestinal septic disorder, there may be the testimony of intestinal troubles. The more diagnostic symptoms are a fever of a remittent type, one or several violent shivering fits, a marked jaundice which like the fever shows exacerbations, and a similar irregularity of the condition of the urine which may be successively of a dark brown, a deep yellow, and a transparent amber color. Tenderness and grunting on percussion of the right hypochondrium would be an additional aid in diagnosis.

_Treatment._ Death has been hitherto considered as the inevitable result, yet recoveries may ensue after rupture into the colon or through the abdominal walls. If the seat of the abscess can be ascertained its evacuation through an aspirator and the subsequent injection of an antiseptic would be appropriate. The concurrent use of antisuppurants like hyposulphite of soda, or sulphide of calcium would also be in order.

_Causes in Cattle._ Hepatic abscess is much more frequent in cattle, and is commonly a result of perforation by sharp pointed bodies (needles, pins, nails, wires, etc.) from the reticulum and rumen, or of parasites, or biliary calculi. Other cases are occasioned by the presence of tubercles, actinomycosis, or omphalitis.

_Lesions in Cattle and Sheep._ Secondary abscesses are usually multiple and disseminated through the organ, though Cadeac says they are more common in the left half. They vary in size from a bean to a pigeon’s egg, project often from the surface, and contain a viscid, creamy, yellowish or greenish pus. Abscesses dependent on foreign bodies often attain a great size, so as to contain a pint or quart of pus (Landel). They may make their way through the diaphragm, rumen, or abdominal wall leaving a thick cicatrix in the liver, or they may become slowly absorbed and dry up into a putty-like or cretaceous mass. Brusaferro found hepatic abscesses in lambs twenty to thirty days old—probably of omphalic origin.

_Symptoms in Cattle_ are usually very obscure. Fever, shivering fits, jaundice, indigestion, diarrhœa or dysentery, emaciation, colics, tender right hypochondrium, and peritonitis may all be in evidence but the diagnosis is little better than a guess.

_Treatment_ when possible at all would be on the same lines as for the horse.

_Causes in the dog._ According to Cadeac these are mostly foreign bodies (needles, pins, etc.) which have been swallowed, tumors of the liver or adjacent organs, phlebitis and thrombosis of the portal vein, pyæmia, septicæmia, and external injuries (kicks, blows, contusions, falls, etc.)

_Lesions in the dog._ As in the other animals _traumatic_ abscess is usually solitary and large, _secondary_ abscess multiple and small. The pus developed around a foreign body is reddish, greenish and fœtid, that of the metastatic abscess is usually whitish or yellowish and with a sweet odor.

_Symptoms in the dog_ are those of hepatic congestion, or violent gall stone colic, followed by severe rigor, great depression, or irritability, and tenderness over the right hypochondrium. Nausea and vomiting is a marked symptom though not a diagnostic one.

_Treatment._ If the flaccid abdominal walls will allow of the locating of the abscess it should be treated by aspiration and antiseptic injections. It would even be admissible to perform laparotomy, stitch the wall of the abscess to the external wound, and empty it under due antiseptic precautions.

INFECTED HEPATITIS. NODULAR NECROBIOSIS OF THE LIVER.

In ox, sheep, pig, dog, horse. Necrotic areas projecting on surface of
liver. Causes: bacteria, toxins, from bowels, womb, navel. Lesions: In
cattle dirty gray nodules in brownish red liver, nodules firm,
granular, necrotic, elements do not stain, later leucocytes and
fibro-plastic growth in periphery. In lambs the nodules are white,
common to the lungs and pleura, pathogenic to rabbit. In pigs nutmeg
liver, cells without nuclei, fatty, granular, pathogenic to rabbits,
guinea pigs, rats and young pigs. In dog, nutmeg liver, with violet
areas, and white spots, 1–2 lines, having granular, fatty cells
without nuclei. Symptoms: fever, constant lying, tarry fæces, icterus,
tender right hypochondrium, and those of the primary disease.
Treatment: antisepsis of primary seat, and bowels, elimination by
kidneys, general antisepsis, stimulants, etc. Case usually hopeless.
Prevention.

This has been observed particularly in cattle, but also in sheep, pig, dog and horse. It is characterized by the formation of circumscribed areas of gangrene, becoming hard, dry, yellowish and usually slightly projecting beyond the adjacent surface. Its infected character is shown by the presence in the lesion and adjacent parts of the hepatic tissue of an abundance of bacteria, which, from the varied description, appear to differ in different cases. The cause may however be safely stated as one of the bacteria of gangrene. It is alleged with some show of reason, that the lesion may be determined by the action of toxins and ptomaines produced by bacteria in the alimentary canal and carried to the liver with the portal blood (Cadeac). The bacteria themselves commonly come from the same source, (Stubbe), but also from the uterus (Berndt), the mammæ (LeBlanc), and above all from the suppurating or septic umbilicus. McFadyean in five cases found a long slender bacillus, Hamilton in a single case in the horse found cocci, Rivolta in an infectious hepatitis in sheep found _bacterium subtilis agnorum_, and Semmer found the same condition in young pigs from micrococci introduced through the diseased umbilicus.

_Lesions._ In _cattle_ the liver has a general brownish red, or greenish white color, and shows projecting, hard nodules of a dirty gray color more or less tinged with yellowish brown. The margins of these hard nodules are very sharply defined, and on section show a homogeneous granular surface, devoid of areas of softening or of connective tissue, and formed of the hepatic parenchyma in a state of necrobiosis. The granules and nuclear elements do not stain like those of healthy liver. As the disease advances the periphery of the nodule may be invaded by leucocytes and become the seat of a fibro-plastic hypertrophy (McFadyean) with the ultimate formation of cicatricial tissue (Stubbe).

In _lambs_ Rivolta found the necrosed nodules standing out as white patches under the capsule of the liver, but similar lesions were met with in the lungs and pleuræ, an observation which has been confirmed by Hanbold. The affection was conveyed by inoculation to the rabbit.

In _pigs_ Semmer found nutmeg liver, deep red or grayish yellow, hypertrophied, the hepatic cells swollen and divested of nuclei but containing fatty and pigmentary granules. It was inoculable on rabbits, guinea pigs, white rats and on young pigs.

In the _dog_, Courmont and Doyon found congested liver (portal congestion) with projecting patches of a deep violet color and sharply defined borders, and one to two lines in diameter, also salient white spots with distinct outlines. In the white spots the hepatic cells had lost their nuclei and were charged with fatty granules.

_Symptoms._ These are indications of hepatic disease. In _parturient cows_, Berndt noted fever (102° to 104°), anorexia, stiffness, cough, labored breathing, intense thirst, constant decubitus, and constipation followed by lowering temperature, tarry fæces and icterus. The region of the liver was very sensitive to pressure or percussion. In the other animals the symptoms appear to be largely over-shadowed by those of the primary disease, but the same general indications of jaundice, hepatic tenderness and digestive disorder are superadded.

_Treatment_ when it can be intelligently adopted, consists largely in evacuation and antisepsis of the seat of primary infection, and of the _prima viœ_, and in maintaining elimination by the kidneys. In this way, as in congestion and hepatitis, the concentration of the poison is as far as possible counteracted, and an opportunity may sometimes be furnished for the recuperation of the liver cells. As a rule, however, the case is hopeless, and thus preventive measures, by cleanliness, disinfection and antisepsis of the ascertained sources of the infection are indicated.

PERIHEPATITIS.

Inflammation of capsule of liver (external and Glisson’s). Causes:
Traumas, infective diseases, phlebitis of the portal vein, chill,
distomatosis. Lesions: Peritonitis and inflammation of the capsule in
patches, yellowish gray exudate, fibroid thickening or pus. Adhesions
to adjacent objects. Thickening of trabeculæ. Symptoms, tardy
respiration and circulation, tender hypochondrium, colics, diarrhœa,
painful defecation, moan with expiration. Slight cases recover.
Sequelæ: compression of portal vein or bile duct, gastric catarrh,
piles, etc. Treatment: Salines, alkaline diuretics, mineral tonics,
bitters.

This is inflammation of the external capsule of the liver and Glisson’s capsule. It may arise from direct mechanical injury, or by extension of inflammation from adjacent structures, such as the peritoneum. It may also complicate contagious pneumonia in the horse, tuberculosis in the ox, pneumoenteritis in pigs, and also phlebitis of the vena portæ (Cadeac, Morot). It may follow a chill, or distomatosis.

_Lesions._ These are essentially peritonitis circumscribed by the liver, and extending to the proper capsule, and its vaginal investments of the hepatic vessels. It is usually limited to certain spots which become the seats of a yellowish gray exudation, with a tendency to fibroid development and thickening, but sometimes degenerating into pus. The deposits on the outer side of the hepatic peritoneum may develop false membranes and fibrous adhesions to surrounding objects, the diaphragm, omentum, stomach or intestine. The deposits under the peritoneum lead to similar fibrous development with hypertrophy or thickening of the capsule, the trabeculæ extending thence into the liver and the vaginal sheaths of the vessels. Such areas of thickening are revealed as depressed spots or patches of a white color, and showing a firm fibrous, pearly appearance when incised. Such lesions are not uncommon in the livers of horses, cattle and swine. In the pig they may have a violet, or brownish red color, but with spots of other colors—grayish or brownish (Kitt).

_Symptoms._ Dopheïde, who has studied the disease in cows and to a less extent in horses, found a reduction in pulsations (26 per minute) and respirations (6 per minute) in connection with a mild peritonitis, intestinal catarrh, colicy pains and diarrhœa. The conjunctiva is pale, the pulse compressible, the respirations unequal and accompanied by a moan, and the appetite impaired or lost.

If confined to mere spots on the liver, a restoration to apparently vigorous health may take place, but if extensive it may lead to compression and obstruction of the portal vein or bile duct, or to compression and atrophy of the liver, with corresponding symptoms.

_Treatment._ As in other congestions of the liver, the use of salines to deplete the portal system, and of alkaline diuretics are especially indicated, to be followed by bitters and mineral acids. Sinapisms and other counter-irritants to the region of the liver are of great service. If not complicated with abscess, or microbian infection, cases of this kind will often do well.

CIRRHOSIS OF THE LIVER. FIBROID DEGENERATION.