Part 11

Then as regards varieties in the individual germ. Th. Smith recognizes this as a frequent condition and describes no less than seven different types of bacillus choleræ suis which he had studied and which varied in morphology, cultural qualities and virulence. Lignieres found that the virulence especially of bacillus suis pestis is very easily affected by successive passages through the bodies of small experimental animals. We ought not to be surprised then if we find in different epizoötics, in different countries and even in the same, bacilli which for the time at least show characteristics different from those to which we have been accustomed. These give us varying phases of septicæmia which however come together in one great class. Two of these types which have been placed on record may be here named. For others see septicæmia hæmorrhagica of cattle and sheep.

=McFadyean’s Swine Fever Bacillus.= The characters of this microbe found constantly by McFadyean in swine fever, approximates closely to the hog cholera germ in morphology and motility and in its deadly action when eaten, while it approaches toward the swine plague germ in its cultural habits on potato, gelatine and agar, and in alkaline culture liquids, and finally it differs from both in the absence of pathogenesis to Guinea pigs and in its very moderate action on rabbits. The symptoms and lesions of the swine fever of Great Britain are those of the hog cholera of America rather than of swine plague.

=Marseilles Swine Plague Bacillus.= This microbe was found by Rietsch and Jobert in a febrile epizoötic of swine at Marseilles, and was studied by Caneva and Bunzl-Federn separately. The latter identified it with the bacillus of ferret septicæmia, as described by Eberth and Schimmelbusch. It was longer and thicker than the hog cholera bacillus, twice as long as broad, actively motile, with flagella, and differed from bacillus choleræ suis, in its polar staining, its free growth in acid media, in acidifying and coagulating milk, and in its forming both indol and phenol in peptonized bouillon.

In this case the source of the disease was in importations from Africa (Fouquet), and it spread widely in Southern France for nine months. It proved almost constantly fatal, in from four days to two or three weeks. The symptoms were weakness especially in the hind limbs, with more or less fever, constipation often followed by diarrhœa, an infrequent cough, and red blotches on the skin. In chronic cases ulcers formed in the mouth and intestines especially the cæcum and colon. Appetite was often retained to the end. The young, under a year old, were the chief sufferers. It made 20,000 victims in several months in the province of Bouches-du-Rhone.

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.