SEPTICÆMIA HÆMORRHAGICA OF BOVINE ANIMALS.
Synonyms. Definition. Historic notes. Resemblance to black quarter. Bacteriology; saprophytic cocco-bacillus, nonmotile, ærobic, related to microbe of swine plague, chicken cholera, and rabbit septicæmia. Pathogenic to deer, buffalo, cattle, horses, swine, rabbits, rats, mice, goats, and sheep. Variability. Vitality: great in soil, dies in 6 to 20 days when dried, and quickly in antiseptics, resistant to heat. Accessory causes: rise of soil water in winter or in spring, drying of marshes in summer, wet, rich, swampy, mucky soils; youth, gregariousness, carnivorous habit, insects, vermin, wild animals and birds, epizoa, entozoa, wire fences, wounds of all kinds, hard, woody provender; inoculations in wounds the most fatal. Symptoms: superficial with hyperthermia, functional disorder; muscular tremors; violet mucosæ; segregation; swelling in intermaxillary space, tongue, throat, neck, dewlap, or elsewhere, not pitting on pressure. Petechiæ. Death in six hours to four days; thoracic form kills in four to eight days; abdominal form with colics, and bloody often frothy fœtid fæces. Chronic forms usually pulmonary. Lesions: straw-colored exudations subcutem or intramuscular; blood extravasations; in lungs resembles lung plague; on bowels blood effusions, and exudates; softened, blood-stained lymph glands. Spleen usually normal in size. Blood black. Petechiæ extensive. Chronic lesions. Bacillus in exudate, blood and bronchial mucus. Diagnosis: from anthrax, black quarter, lung plague, rinderpest, and malignant œdema. Mortality 50 to 80 per cent. Prevention: isolate and kill affected; destroy or disinfect carcasses and infected things and places, feeding and drinking troughs and manure. Close and drain infected fields. Immunization, by three inoculations with cultures made at a high temperature (86° to 90°) in free air; or with virus that has been grown in pigeon. In case of deer, drive a few days into a noninfecting enclosure, and then on to a sound range. Treatment.
Synonyms. Wild—und Rinderseuche (Bollinger), Buffalo Disease, Barbone (Oreste and Armanni), Cornstalk Disease (Billings, Moore), Sporadic Pneumonia (Smith), Pneumo-enteritis (Galtier.)
Definition. An acute bacteridian disease of domestic and wild herbivora and swine, characterized by sudden onset, rapid and fatal course, marked hyperthermia, accelerated breathing and pulse, and extensive gelatinoid or sanguineous extravasation in the intermaxillary space, tongue, skin, subcutaneous or intermuscular connective tissue, lungs, pleura, pericardium or intestine.
Historic Notes. It is almost certain that in earlier times this affection was often mistaken for gloss-anthrax, blackquarter, or even lung plague. Metaxa, in 1816 in Italy, manifestly describes it. Oreste and Armanni, in 1882 and 1887, traced Italian cases to the microbe. In 1854 it destroyed many cattle and deer in England (Veterinarian). In 1878 Bollinger records its great fatality among the deer, wild boars, cattle and horses in and near the royal parks at Munich, and for a number of years after in Bavaria. Friedberger records its presence in Schlüchtern, Prussia, in 1885–6, Condamine in Cochin China in 1868, and Guillbeau and Hess in Switzerland in 1894. In America, what appears to be the same affection is noted as corn-fodder disease in Nebraska (Billings), as Wildseuche in Tennessee (Norgaard), and as hæmorrhagica septicæmia in Minnesota (Reynolds). I have repeatedly met with the affection in New York in cows arriving from the west, and in the indigenous cattle on wet, mucky, undrained land in spring, about the period of the melting snows.
Bacteriology. The essential cause of the disease is a saprophytic cocco-bacillus, ovoid, with rounded ends, about 1μ long by 0.3 to 0.6μ broad, but showing involution forms and a variable size. It is nonmotile (Kitt claims motility), ærobic (facultative anærobic), takes a polar stain with clear centre in aniline colors, bleaches in Gram’s (1) solution, shows neither spores nor flagella, grows readily in bouillon, on gelatine, (a bluish transparent layer without liquefying), serum at 98° F., milk (without acidifying or coagulating), and alkaline potato (not on the acid). The cultures have a peculiar odor and yield no indol.
The microbe shows a very close relationship with those of swine plague, chicken cholera and rabbit septicæmia, but it sometimes differs in showing little or no pathogenesis for the Guinea-pig.
Animals susceptible. It is pathogenic to deer, buffalo, cattle, horses, swine, rabbits, rats, mice, and to a lesser extent to goats and sheep.
The pathogenesis varies with the immediate source of the microbe. When obtained from cattle a drop of blood kills rabbits in twelve to twenty hours, with intense hæmorrhagic laryngitis and tracheitis. Guinea pigs die in forty to eighty hours. When obtained from the buffalo it killed horse, ox, or pig in twenty to forty-eight hours. That obtained from barbone (buffalo) appears to be more potent than that from septicæmia hæmorrhagica (cattle).
Vitality of the microbe. Simple drying destroys virulence in six to twenty-two days. Virulence is retained for nine days in putrid flesh. It is preserved, and the microbe multiplies in soil or water containing organic matter and nitrates. It is easily destroyed by ordinary antiseptics 1:5000 of mercuric chloride destroying its vitality in one minute (Hueppe). On the contrary it shows a great resistance to changes of temperature. It grows in the soil at 55° to 60° F. (Hueppe), and in old cultures may resist for an hour a temperature of 175° to 195° (Oreste and Armanni).
Accessory Causes. These are such conditions as favor transmission of, or receptivity to the microbe. In Southern France the disease is most common in the winter months, probably because the soil water rises then; on the Roman marshes on the other hand, it prevails especially from May to October, when the water is lowest and most impure. In New York I have seen it especially at the breaking up of the winter frosts, when the water, pent up in the rich organic soils, is suddenly released. It is pre-eminently the disease of wet soils, rich in the debris of decomposing organic matter, of the rich prairies and bottom lands of the Mississippi Valley, of springy, swampy or mucky soils elsewhere, of the Pontine marshes at Rome, of the Delta of the Nile, of the rich virgin soils in Asia. Youth has the greatest receptivity, the older animals having probably acquired immunity through an earlier attack. The animals that live in herds infect each other by contact, fighting, licking, etc., others are affected by eating the vegetation or drinking the water soiled by the diseased, wild boars by eating the carcasses, and all animals by the attacks of biting or blood-sucking insects which have just come from the diseased. It is claimed that the infection is carried by men and animals, and by the sale in villages of the flesh of infected animals. Dogs, wolves, foxes, and other carnivorous animals and birds will also carry the infection for long distances. Finally, it will travel to a greater or lesser distance with running water.
The entrance of the microbe by wounds must always be counted on, and explains the casual inoculations, by bites of dogs, insects, worms, by barbed wire fences, by wounds with horns, tusks, or feet, by nails, etc., and in winter by hard, woody aliment scratching the lips, mouth, fauces or pharynx. Shedding of teeth, diseased teeth or gums, and everything that causes abrasion of the alimentary mucosa must be admitted into the list of causes. Infected traumatisms of any kind, like intratracheal and intravenous inoculations usually prove fatal, while infection by ingestion is not necessarily so. The pathogenic potency appears to be impaired in the stomach or intestines.
Symptoms. These vary widely according to the subject, the seat of infection and the violence of the attack. They may be classed under three principal heads: superficial, thoracic and intestinal, and in addition into acute and chronic cases.
In the superficial, external or cutaneous form there is usually a sudden onset with high fever (104° to 107° F.), accelerated pulse, (70 to 90), and breathing (24 to 50), anorexia, suspended rumination, muscular tremors or shivering, staring coat, dry, hot muzzle, burning of ears, horns and hoofs, suppression of milk, and more or less stringy salivation. The visible mucosæ are of a deep red or violet tinge, and the patient will often remain apart by himself when the herd has moved elsewhere. Soon there develops a tense, hard, hot, painful swelling of the intermaxillary space, tongue, throat, neck, dewlap or elsewhere, amounting to perhaps six inches in thickness, extremely resistant and not usually indented on pressure with the finger. The breathing becomes stertorous and deglutition difficult or impossible. The mouth is hot and filled with tenacious saliva, and the tongue may hang pendant while on its borders and lower surface are projections of the mucosa swollen by infiltration, yellowish and semi-transparent, or blood-stained. At other points petechiæ are more or less abundant.
Death may take place from pharyngeal obstruction or closure, or as the disease advances, there may be indications of implication of the viscera, of the chest or abdomen: encreasingly difficult breathing, a mucous or suffocative cough, colicy pains, tenesmus, and the passage of moulded glazed fæces, of pseudo-membranous casts, or of profuse liquid stools. The animal may move the hind feet uneasily, lie down and rise alternately, may remain persistently recumbent until death, or he may stand up until he falls to perish of asphyxia. Death may occur in six hours, or may be delayed four days.
In the thoracic form the extreme hyperthermia is complicated by early lesions in the lungs, while the muscular or cutaneous ones are omitted or deferred. So long as the lesions are confined to the chest, they are betrayed by hurried and even oppressed breathing or dyspnœa, a frequent, moist, suffocative cough, persistent standing to favor respiration, and there are the percussion and auscultation indications of consolidated lungs or hydrothorax. The mucosæ are usually of a darker red, than in the external form, cyanotic indeed, and the peculiar asphyxial position, with legs apart, head extended, dilated nostrils and open mouth may be very significant. These symptoms are likely to be modified or supplemented before death, by those caused by intestinal or renal disorder. In the thoracic form in young animals death by suffocation may occur in a few hours, but more commonly the disease progresses slowly and a fatal result is not reached until the fourth day or even the eighth. This form is common in the deer, and less so in cattle.
In the intestinal or abdominal form the usual sudden onset and high fever, are complicated by inappetence, tympany, rumbling of the bowels, uneasy movements of the hind feet, perhaps twisting of the tail, looking at the flanks, and even lying down and rising. There is frequent, violent straining with the passage of fæces at first glazed, later streaked with blood, or mixed with pseudo-membranous casts, and very soon soft, watery, frothy and fœtid. These are usually black or reddish black from contained blood.
The urine may also be blood-stained.
Before death, complications on the lungs or skin will often come in to assist in diagnosis.
In the chronic and subacute types the lesions are often concentrated on the lungs, and there are a moderate fever cough, hurried breathing under exertion, dulness on percussion over limited pulmonary areas, blowing sounds, mucous râles, crepitations and more or less muco-purulent expectoration. These phenomena are all the more significant if complicated by digestive disorders, costiveness, fœtid mucous diarrhœa, tympany, or by the eruption of the superficial swellings.
Lesions. The swellings on or under the skin or among the muscles show extensive straw-colored exudations, colored at points with blood, with enlargement, infiltration and staining of the adjacent lymph glands. On the chest walls the sero-sanguineous exudate may extend from the root of the lungs, through the intercostal spaces to the skin in the breast, the axilla and behind. The tongue is often enormously swollen and black, charged with extensive blood extravasations in addition to the yellowish exudate. Along its sides and on its lower surface, the mucosa stands out in projecting masses of yellowish infiltration, which may show equally on the fauces, pharynx, larynx, trachea and bronchi.
In the lungs the pleuræ and subpleural and interlobular tissue are extensively infiltrated and thickened by a profuse yellowish serous or sero-sanguineous exudate, so that the appearance may closely resemble that of lung plague. The lung tissue is consolidated, hepatized and dark red, with at some points emphysema. The pleural sac is usually filled by a serous or bloody effusion (2 to 25 quarts) and there is often extensive implication of the pericardium. The tracheo-bronchial mucosa and bronchial glands show extensive infiltration and thickening.
In the abdomen are found extensive infiltrations and blood extravasations in the mucosa and submucosa of the stomachs and intestines, softening and shedding of the epithelium, infiltrations of the peritoneum, diaphragm, and sublumbar adipose tissue, and softening and degeneration of the liver and kidneys. The intestinal gastric and mesenteric glands are usually infiltrated, softened and blood-stained. Engorgement of the spleen is exceptional.
The blood is very black but not usually materially changed in consistency nor coagulability. Petechiation of the different serosæ and other tissues is a prominent feature.
In chronic cases the lesions are mostly shown in the lungs and lymph glands. The lungs show circumscribed lobular islets of congestion, induration or caseation, offering a suggestion of tubercle, which is all the more deceptive when cretifaction has set in. The caseous centres may vary in size from a pea to a walnut, and some may have ruptured to form a vomica discharging into a bronchium. Bronchia leading to affected lobules are blocked with muco-purulent matter, yellowish, thick and tenacious, and their mucosa is thickened and puckered. The enlarged lymph glands are especially those of the bronchia, trachea, mediastinum, bowels, mesentery and sublumbar region.
The bacillus is present in the exudate but is especially abundant in the blood, and in the chronic cases in the bronchial mucous.
Diagnosis. From anthrax (gloss-anthrax) this affection is easily distinguished by the absence from the blood and exudates of the large, square ended anthrax bacillus, by the absence of enlargement and blood engorgement of the spleen, and of the softness and diffluence of the blood clot which characterize anthrax. Swine which are with difficulty inoculated with anthrax are very susceptible to hæmorrhagic septicæmia. Sheep which are very receptive to anthrax are somewhat refractory to the disease now in hand. Pigeons resist anthrax but readily contract septicæmia hæmorrhagica.
From black quarter it is readily distinguished by the absence of emphysema and crepitation and of a secondary cooling in the external swellings, by the presence of the germ in abundance in the blood, by its smaller size, its bipolar staining, and its lack of motility and of spores. Inoculation with black quarter bacillus kills the guinea pig, but spares the pigeon.
From lung plague it is distinguished by the suddenness of its attack and rapidity of its progress to a fatal issue; by the usual coincidence of skin and bowel lesions, while the lung plague affects the chest only; by its communicability to pigs, sheep, pigeons, and even horses, which are all immune from lung plague; and by the usual absence of lung lesions of different ages, which are so characteristic of lung plague. The abundance in the blood of the cocco-bacillus with bipolar staining in hæmorrhagic septicæmia is characteristic. Lung plague spreads slowly to exposed cattle, but spares all other domestic animals.
From Rinderpest it is differentiated by the history of its advent, by the presence of the surface œdematous swellings, by the absence of the whitish epithelial concretions on the mouth or vulva, and of the deep dark portwine discolorations of the mucosæ of the mouth, rectum and vulva, and by the fact of its inoculability on domestic animals generally. Rinderpest spreads rapidly to all exposed ruminants, but spares pigs, rabbits, Guinea pigs, horses and birds.
From malignant œdema it differs in its inoculability on the surface in place of subcutaneously only, in the presence of the cocco-bacillus in the blood during life, whereas in malignant œdema the germ is confined to the local lesion, in the absence of crepitation, which may be present in the swelling of œdema, in the greater facility with which cultures can be made of the septicæmic cocco-bacillus and in the absence of gas production in such cultures. The malignant œdema comes from a single accidental deep inoculation from almost any rich soil, and is not a malady spreading widely and generally on given limited damp, rich lands which have become infected. Finally the cocco-bacillus of septicæmia hæmorrhagica is found singly in the blood or exudate, whereas the microbes of malignant œdema may be found in form of sporeless filaments intermingled with the bacilli.
Mortality. The hæmorrhagic septicæmia of cattle cuts off from 50 to 80 per cent. of the animals attacked.
Prevention. The first consideration is to isolate and kill all the affected animals, to destroy the carcasses by burning or boiling and to burn or disinfect all objects that may have become contaminated. The buildings, yards, and fences, must be disinfected, and as the bacillus is very resistant a solution of corrosive sublimate and sodium chloride, a drachm of each to the gallon of water may be freely used after thorough cleansing. Or a whitewash containing ¼ lb. chloride of lime to each gallon may be substituted. Feeding and drinking troughs may be burned. Manure may be freely treated with sulphuric acid. Infected fields should be closed for years and if possible drained.
Immunization of buffalo and sheep has been secured by making cultures of the microbe in free air at 86° to 90° F. and inoculating the animals with the weakened virus, on three successive occasions with intervals of several days. It induces a transient fever, with no serious phenomena (Oreste and Armanni). A second available method is to pass the virus through the system of the pigeon and inoculate with the pigeon’s blood, on three successive occasions, the animals to be protected. It is manifestly impossible to put such immunizing methods in force on wild deer, and for these probably the best course is to drive them from the infected range, to an uninfected one, having retained them for a few days interval in a confined area, to allow of any already infected animals developing the disease. A similar avoidance of waters running from the infected tract is imperative.
Treatment, has been unsuccessful. Friedberger failed with hypodermic injection of carbolic acid, and internal administration of salicylic acid. Gal gave subcutem 5 per cent. solution of creolin, and doses of 1½ oz. of the same agent by the mouth. Five buffaloes out of seventeen recovered. Friedberger suggests deep incisions of the swellings so as to admit the air, and treatment of the wounds with strong antiseptics.