Pampered artificial life of dogs as predisposition. Eating carrion. Chills especially when heated and exhausted. Infection from bowels. Obstruction of gall duct by inflammation, calculi, neoplasms. Catarrhal exudate as a protector of microbes. Toxins from intestines, food or water. Youth, lack of acclimation, mental shock, blocking of bowel, blood effusion in gall bladder, incubation. Symptoms: signs of gastro-enteritis, prostration with invasion of the liver and especially of the kidney. Icteric urine without jaundiced mucosa. Gravity of icterus with suppression of urine. Hypochondriac tenderness, arched back, dullness, irregular bowels, excited circulation and breathing, preliminary fever tends to subside, tympany, colic, trembling. Death in one or two days or more. Lesions: congestion, degeneration, ecchymosis, ulceration of gastro-duodenal mucosa, extending into liver ducts and acini, bile inspissated, liver enlarged, yellowish brown, softened, fatty, shrunken, distorted hepatic cells. Kidneys congested, ecchymosed, cortical part with necrotic foci; lymph glands congested. Diagnosis: by icterus of tissues and urine tests. Prognosis: grave in acute cases, more hopeful in tardy ones. Treatment: antiseptics, cholagogues, salol, salicylates, alkalies, carbonates, tartrates, iodides, laxatives, cold enemata, aloes, electricity, water freely, pilocarpin, strychnia, aqua regia, digitalis, bitters, muriatic acid, convalescent diet.
Causes. The dog is much more subject to jaundice than the horse, and the affection is liable to be much more severe, than in solipeds. He leads a more artificial life, especially in cities, where the lack of open air exercise, and of the facility for attending to nature’s wants, together with an excessive, varied, stimulating diet predisposes him to constipation, indigestion, and disorders of the stomach, bowels and liver. In other cases the devouring of decomposing food and foul water proves a cause of direct microbian infection, and of poisoning by ptomaines and toxins generated out of the body. Exposure manifestly has something to do with the prevalence of canine icterus, which is more common in spring and especially in autumn than at other seasons. In hunting dogs, out of condition, the suddenly induced over-exertion and fatigue, and the succeeding chill in cold air or water, become accessory factors.
It appears to be most commonly the result of the transference of germs from the intestine, either by way of the bile ducts, or with the blood through the portal vein. The first form is usually the sequel of muco-enteritis affecting the duodenum, with swelling of the walls of the common bile and pancreatic duct at its orifice, or from obstruction by gall-stones, concretions, impacted bowels or neoplasms. With the arrest of the biliary flow the intestinal ferments gain an entrance into the common duct and the sac of Vater, finding protection from the antiseptic bile in the resulting catarrhal exudate, and in this way they reach the gall-bladder, the biliary radicles and the acini. With the entrance of bacteria or toxins by the portal vein on the other hand, there is first a troubled condition of the acini and hepatic cells, an over-secretion of thick bile, and blocking of the passages so that little is passed into the intestine, the greater part being absorbed into the hepatic veins. Fermentation microbes in the stomach and intestines, the germs of suppuration and septicæmia, and saprophytic germs from outside the body are held to be causative of icterus. Cadeac lays much stress on the putrefactive germs in water, and traces different attacks to marshes and foul ponds.
As in other infecting diseases, early age has a predisposing influence. The older subject has presumably been already exposed to the microbe and acquired some measure of immunity. Animals coming new to the locality and poison, are equally susceptible with the young. Trasbot found that 14 out of 17 dogs thus attacked were between three and eighteen months.
Leblanc and Trasbot claim mental shock as a cause of icterus in the dog. The disappointment and weariness caused by the master’s absence, the excitement of a fiercely contested fight, and brutal punishment are adduced as cases in point. Abuse of emetics and purgatives, in connection with a pre-existing hepatic or duodenal disorder or as a supposed prophylactic of canine distemper has induced jaundice.
Obstruction of the small intestine has proved a factor, partly by the reflex irritation through the splanchnic nerves, and partly through obstruction to the common bile and pancreatic duct.
Walley records a case of obstruction of the cystic duct by extravasation of blood in the gall bladder.
Icterus not infrequently supervenes during canine distemper in which the early gastric and duodenal irritation becomes an occasion of the extension of the catarrhal infection to the common bile duct. Even apart from this Trasbot has seen the majority of cases ushered in by a gastro-duodenitis. In this connection it is interesting to quote the remark of Pfuhl that 26 out of 27 persons using the foul baths of a given establishment contracted icterus, while the soldiers bathing in another branch of the Elbe entirely escaped.
The fact that icterus usually sets in several days after such an exposure, whether in man or dog, indicates a period of incubation, and thereby sustains the theory of infection.
Symptoms. In the majority of cases, gastro-enteritis constitutes the first step of this affection and the early symptoms are characteristic of that disease. Frequent vomiting, at first of food, and later of a glairy fluid which may be discolored by bile, redness of the tongue, especially along its margins, bloodshot, watery eyes, lying down with the nose on the right side of the abdomen, or standing with the abdomen tucked up and the back arched, halting movements of the limbs, wincing if manipulation is made of the spine or the epigastrium, elevated temperature, accelerated pulse and breathing, anorexia and perhaps purging, mark the onset. So long as the liver is unaffected prostration is not a marked feature.
Even when the liver is invaded, a fair measure of life and activity may often be retained so long as the kidneys remain sound and active. The bile pigments and salts, and the toxins generated by the invading microbes are alike eliminated in large part in the urine, and the profound poisoning and prostration of the nervous system are in a measure prevented. In many cases therefore the urine is strongly jaundiced without much or any discoloration of the mucosæ and in such cases the prospects are usually good for an early and complete recovery. It must not, however, be inferred that such a happy issue will always follow, as the pigments are by no means as toxic as are other hepatic products and fatal results may ensue with very slight jaundice of the tissues.
As a rule, however, the jaundice of the tissues (eyes, nose, mouth, white portions of the skin) is to be accepted as a grave manifestation, indicating either an excessive production and absorption of bile, or a suppressed secretion through the kidneys, or both. Then the poisoning by biliary salts and bacterial toxins is shown in profound dullness, prostration, muscular weakness, indisposition to rise, moving stiffly and only when dragged by the collar, the limbs trembling and the back arched. The tender back is arched, the right hypochondrium sensitive, the expression dull, stupid and listless, and constipation or a fœtid diarrhœa is liable to set in. The heart beats may be strong and irregular, the breathing is easily disturbed and hurried. The temperature at first 104° to 107° may descend to the normal as the system becomes charged with the toxic products, and does not usually exceed 99.5° after two or three days of jaundice of the tissues.
The icterus is shown in the eye or mouth, or on any white portion of the skin, and in the urine it will be detected by the eye or by the tests above given.
In the worst cases the urine is very scanty and of a deep yellowish brown color, prostration is extreme, tympany, colic, obstinate constipation or bloody diarrhœa may set in, the breathing, hurried or not, is trembling, the pulse small, and the temperature at first high may descend to 95° or even much lower before death.
The course of the disease varies according to its gravity. If there is complete retention of bile, and abundant production of toxins, the animal dies in one or two days in a state of collapse. If there is general progressive degeneration and destruction of the hepatic tissue without at first absolute suppression of the discharge of bile into the duodenum, the patient may last till the fourth or fifth day, or later.
Lesions. There are usually congestion, tumefaction, friability, ecchymosis and even ulceration of the gastric and duodenal mucosa. The organs are empty, but show a reddish brown exudate of a glairy consistency, and containing red blood globules and pus corpuscles. The same inflammatory lesions are to be traced into the common bile duct, the cystic duct and bladder, the biliary ducts, and the acini. The mouth of the common duct is usually blocked with a plug of tenacious mucus, the gall bladder having been unable to expel this and the inspissated bile into the intestine. The liver is slightly enlarged, yellowish, with patches of brownish yellow more or less deep, and the acini contain an abundance of oily globules, and yellowish brown granules. The acini have no clear line of delimitation, and the contained hepatic cells are shrunken and distorted, standing apart from each other in a dropsical or watery medium.
The kidneys are congested and ecchymosed; the cortical substance brown, friable, and with numerous areas of necrosis of a bluish white color, and even abscesses. The medullary substance is yellow and the uriniferous tubes contain an abundance of yellowish brown granules.
The lungs have a yellowish red color, with patches of ecchymosis.
The lymph glands generally are congested and many of them gorged with blood, of a dark red color, and lacking in consistency and cohesion.
Diagnosis. The characteristic icterus is lacking in the early stages, and active treatment gives good hope of success. When indigestion, persistent vomiting and tenderness of the epigastrium, and right hypochondrium, are associated with diarrhœa, it is highly important to examine the urine for even slight traces of bile. When the jaundice is due to impaction of a biliary calculus, the symptoms may increase slowly, and yet reach a sudden climax with acute colicy pains and tenderness of the right hypochondrium.
Prognosis. In acute rapidly developing cases a fatal issue is to be expected. In those which develop more slowly, recovery may be hoped for if early treatment is instituted.
Treatment. Cases due to biliary calculus must be treated for that lesion.
In purely infective icterus attempts must be made to arrest the intestinal and hepatic fermentation. As intestinal antiseptics, naphthol, benzo-naphthol, naphthaline, 5 grains four to six times a day. As hepatic antiseptics, salol 5 grains, salicylate of soda 8 grains, or calomel 1 grain four times a day. The salol and salicylate tend to increase biliary secretion and to render it more fluid. The same end is attained by alkalies (carbonates of potassa, or soda or lithia, bitartrate of soda, iodide of potassium). These are further valuable in hastening the elimination of toxic matters by the kidneys. The expulsion of bile, and of intestinal microbes and toxins may be sought by laxative doses of Glauber salts, or by cold enemas of the same. Verheyen recommends aloes in laxative doses for six days. Siedamgrotzky had good results from induction currents of electricity, sent through the region of the liver twice a day for ten minutes on each occasion. To assist in elimination abundance of pure water or of watery fluids may be used. The most effective eliminating agent is pilocarpin in ⅙ gr. dose hypodermically, repeated daily. In weak conditions frequent small doses of strychnia, ether, aqua regia, or digitalis may prove valuable.
In case of improvement a course of bitters is usually demanded, and these may be combined with hydrochloric acid or small doses of sodium bicarbonate.
Throughout the disease, gruels, beef tea, buttermilk, whey or any simple nutritive aliment which the animal relishes may be given, but both then and during convalescence fatty matters and indigestible materials should be carefully withheld.
Usually with gall-stones or concretions, or distomata. In sheep from decomposing vegetation. Symptoms: anæmia, emaciation, pallor, icteric mucosæ. Digestive disorder and bilious stools suggest worms. Treatment: as in horse, or vermifuge.
Though less common than in the dog icterus in ruminants occurs, but most commonly in connection with gall stones and concretions, or with trematodes in the gall ducts. These forms will be noticed under these respective headings. Verheyen describes an icterus of sheep which occurs enzootically in damp low undrained localities, and is attributed by shepherds to the consumption of dead and fermenting leaves. The symptoms are those of anæmia, emaciation, and increasing weakness, with a pallor and more or less dull yellow of the conjunctiva, and, later, of the other mucosæ. The loss of appetite, indigestion, yellow liquid fæces, suggest the possible presence of parasites as a cause, and the prescribed treatment by common salt, juniper berries and tonics strengthens the suspicion. Other forms must be treated according to cause on the lines laid down above.
In mules; less frequently in horses and cattle. Bacteridian. Predisposition from alleged miscegeneration. Offspring of lymphatic mares. Spoiled fodders, foul buildings, exposure, infection by umbilicus. From gastro-enteritis, diarrhœa, dysentery. Congenital. Symptoms: refuses the teat, scours, red urine, palpitation, colics, perspirations, inflammations, or abscesses of navel, arthritis, other internal disorders. Death from exhaustion or in convulsions. Or symptoms subside and pass in 15 days. Diagnosis: prostration, palpitation, icterus, and bloody urine with omphalitis. Streptococci. Prognosis: with hæmaturia nine-tenths fatal. Lesions: icterus, heart soft, flabby, lungs congested, general ecchymosis, blood black, clot diffluent, liver congested, enlarged, spleen, swollen, softened with spots of brownish yellow, meconium bloodstained, kidneys swollen, congested, points of infarction or necrosis, urine bloody, navel lesions. Treatment: for congenital cases improve hygiene for dams; for offspring, antiseptics to navel, shelter, warm box; aloes to dam, or oil to colt, antiseptics internally, demulcents, stimulants, derivatives, opium, water, alkalies.
This has been observed in cattle (Kitt), and in horses (Levrier, Bernadin, Lhomme) but above all in mules (Villa-Roya, Carrere, Levriere, Bernadin, Lhomme, Hartmann, Dieckerhoff).
The affection is a bacteridian disease, in which there is a great destruction of red globules, and liberation of hæmatin, with hæmaturia and yellow coloration of the tissues.
Causes. Carrere attributes much to a supposed congenital weakness induced by the unnatural generation of ass with mare. Cadeac noticed that the offspring of certain mares and horses remained sound, while the progeny of the same animals, and asses suffered largely from icterus. Levrier found it especially in the mules born of mares having a lymphatic temperament or suffering from canker, grease or chronic lymphangiectasis. Bernadin and Lhomme attribute much to bad hygiene, and especially to poor or spoiled fodders. Lhomme, Lafosse and Trasbot find accessory causes in cold and wet weather. Retention of the meconium is another cause. Dieckerhoff, Hartmann, Cadeac and Bournay trace the disease to bacterial infection as the essential cause. Many cases originate in septic infection and inflammation of the navel and umbilical veins. Others commence with mucous gastro-enteritis, attended by diarrhœa or dysentery. In other cases the germs appear to have reached the liver through the circulation as the animal is already affected at birth.
Symptoms. When not congenital, symptoms are usually seen in the first few days of life, usually before the fifth day.
In congenital cases the new born animal is unable to stand at all or for longer than a very short time, it lies listlessly and makes no attempt to suck even when held up to the teat. There is acceleration of pulse and respiration, the heart beats are tumultuous, the mouth is dry, the mucosæ of a straw yellow, the bowels are costive, and the urine, whether discharged in life, or found in the bladder after death, is bloody.
When attacked later, the animal becomes dull, weak, and stupid, refuses the teat, and has the bowels relaxed. The mucosæ become pale yellow, the breathing accelerated, the heart beats violent, and the pulse rapid, small and weak. The urine is passed slowly and with effort and has a red hue more or less deep according to the severity of the attack. Colics are not uncommon, causing uneasy shifting of the limbs and tail, cries, frequent lying down and rising, and partial or general perspiration. Complications on the part of the navel and umbilical veins are to be looked for, in open sores, swellings, abscess, phlebitis, and in arthritis and secondary abscesses in different organs. Death may occur quietly, as from exhaustion, while in other cases it is preceded by convulsions.
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.
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.
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.