Chapter III: Front Matter (3)

_Bacteriology. The bacillus of Swine Plague_ (_B. Pestis Suis_) has already been described in the differential table of allied bacteria given under hog cholera. It is a short rod, with rounded ends, 0.8 to 1.5μ. × 0.6 to 0.8μ, staining readily in aqueous basic aniline colors and bleaching in Gram’s iodine solution. The staining is distinctly polar, the colored portions being more or less crescentic with the concave or straight border turned inward toward the central clear space. It is destitute of flagella and distinctly nonmotile unlike the very active bacillus of hog cholera. It further differs in its growth on potato which is slight, gray and waxy. On gelatine, too, it gives a feeble growth (or none) unlike the brownish colonies of the bacillus of hog cholera. It fails to liquefy gelatin. On agar the growth is more active, being grayish, translucent or brown. Those forming under the surface are like flat horizontal discs with a small microscopic elevation or knob in the center. It grows in milk producing little or no acid and no clot. It produces gas with none of the sugars—glucose, lactose, saccharose—in contrast with the gas production in glucose by the hog cholera bacillus. It shows much less vitality and hardihood than the hog cholera bacillus, growing but feebly between 65° and 70° F., and most actively at 97° to 100° F.; dying in 7 minutes at a temperature of 58° (moist); dying in 3 days when dried, in 4 to 6 days in the soil, in 10 to 15 days in water and instantly in 0.04 per cent solution of lime water.

_Pathogenesis._ It is pathogenic to swine, hens, pigeons, pheasants, sparrow, mice, guinea pigs, rabbits, cattle, deer, etc., showing not only a wider range than the hog cholera bacillus, but a more deadly action outside the genus suis. Inoculated birds die in 2 days, rabbits in 16 to 20 hours and guineapigs in 1 to 4 days.

_Accessory Causes._ These agree in the main with those of hog cholera already described so that it is needless to repeat them here. The principal distinctions depend on the lesser vitality of the swine plague bacillus outside of the animal body, and its wider range of pathogenesis outside the genus suis. Infecting materials that have been thoroughly dry for a week may be considered harmless, also that which has been more than two weeks in water, and that which has been more than a week in the soil. If, therefore, the buildings have been thoroughly disinfected, the simple disuse of yards and pastures for a fortnight, and of ponds of water for three weeks may suffice. In the case of hog cholera it may be necessary to abandon such places for 5 months or for the season.

Abandonment by swine is, however, insufficient: all susceptible animals, wild and tame, (see pathogenesis) must be excluded as any one of these may maintain the infection. The preservation of recovered swine on the premises, or the early return of the immune may become a means of preserving the bacillus for the next susceptible pigs that may be introduced. The bacillus of swine plague may be found on the air passages of swine and other animals that are not themselves, at the time, susceptible to the disease, and these animals accordingly become the occasions of what have been thought to be spontaneous outbreaks, and of invasions of fresh herds after the introduction of healthy pigs which have been thought to be beyond suspicion. The danger of the communication of the germ by wild birds and rodents would be enormous, but for the fact that it is so much more deadly to these animals than the microbe of hog cholera, that few survive to maintain the infection. Yet the rule ought to be, to exclude from the fields or premises occupied by new or susceptible pigs, all animals, that may by any possibility become the means of introducing the infection so recently prevalent. Though so easily destroyed when outside the living body, the microbe of swine plague can be carried by the apparently healthy living animal and we must rigidly exclude the possibility of this occurring.

_Lesions._ _Acute_ and _rapidly fatal cases_ of swine plague furnish lesions indicative of a hæmorrhagic septicæmia. The abundance of petechiæ on the skin, mucosæ, serosæ, and tissues generally, with circumscribed hæmorrhages, congestions, inflammations and exudations, agree in the main with what is observed in the acute examples of hog cholera. If the congestive or inflammatory lesions, concentrate in the lungs rather than the bowels it assists in the diagnosis of swine plague. The swelling and blood engorgement of the lymph glands are nearly alike in the more acute types of the two diseases. The spleen is less constantly enlarged than in hog cholera or swine erysipelas. In the _subacute_ and _chronic forms_ the lesions may be almost entirely confined to the enlarged and congested or hæmorrhagic lymph glands. Usually, however, the lungs are the seat of lobular or lobar pneumonia, affecting by preference the lower portions of the anterior and median lobes, and sometimes also the posterior lobe. The pleuræ are often involved, showing arborescent congestion, thickening, exudate, false membranes and hydrothorax. The exudate may at times fill up the interlobular connective tissue, even before the pulmonary tissue is materially involved suggesting a local infection starting at the pleural surface. The hepatised lobule has a general red color varying in depth at different points, and showing lighter yellowish or grayish spots representing the purulent air sacs and terminal bronchia, and necrotic foci. On section the bronchia often yield pus, while the pulmonary tissue oozes a bloody liquid rich in small lymphoid cells.

The liver and spleen may be all but normal, though in a number of cases they may be congested and softened. The stomach and bowels may be virtually sound, or they may show extensive congestion, petechiation and thickening of the mucosa at different points, with, in some cases ulcers, but these latter are mostly excavated and rarely assume the projecting, button-like, laminated form which is so characteristic of chronic hog cholera. Emaciation is a marked feature as in hog-cholera.

_Symptoms._ In the most acute type these may not differ from those of similar cases of hog-cholera. If there has been any opportunity of estimating the incubation it will be found to have been shorter, the skin and mucosæ have a darker red blush, showing first on the ears, breast, belly and inner sides of the thighs and forearms, the lymph glands are enlarged, and there is cough and dyspnœa if the patient is roused to exertion. The presence of petechiæ on the skin and of a very high temperature (107° to 109°) is to be specially noted. There are great prostration and dulness, complete anorexia, hiding under the litter, indisposition to rise, often weakness, staggering, paresis or even paraplegia, somnolence, and death in coma or convulsions.

In the _subacute_ and _protracted_ cases, there is the short incubation (1 day), followed by hyperthermia, drooping tail, hiding under the litter, flushed eyes, nose and mouth, impaired appetite, arched loins, hollow flanks, retracted abdomen, cough easily roused by driving, and signs of consolidated lungs in their lower parts (crepitation, suppressed murmur, abdominal or heart sounds etc.). After a day or two the skin becomes flushed and together with the visible mucosæ the seat of petechiæ. The superficial lymph glands are enlarged. The bowels are usually confined but as the disease advances diarrhœa may set in. There is rapid loss of condition, and the patient may die as the result of exhaustion, toxin poisoning, colliquative diarrhœa, or other condition.

_Diagnosis during life_ is based largely on the shorter incubation, the greater reddening of the visible mucosæ, the comparative absence of abdominal tenderness, and offensive diarrhœa, and the constancy of the cough and other symptoms of broncho-pneumonia.

_Post-mortem._ It is marked by the constancy and predominance of the lung lesions, and the comparative absence of ulceration of the ileum, cæcum and colon, and especially of the projecting, laminated, button-like, necrotic sloughs.

The morphology of the bacillus, its habit of polar staining, its lack of automatic movements, its comparatively poor growth in alkaline bouillon, on potato, gelatine and agar, its inability to ferment glucose with the production of gas, its rapidly fatal action on hens and pigeons as well as on rabbits and guinea pigs serve to distinguish it from the microbe of hog cholera. (See table p. 38).

_Prevention._ In this connection the reader is referred to the precautions, given under hog cholera, against conditions, hereditary, hygienic, climatic, dietetic, parasitic, etc., which lay the system more open to microbian invasion. In the matter of exclusion of the bacillus, the swine plague germ is less difficult to deal with, because it is so much more easily destroyed. Disinfect the buildings, and all contaminated objects as advised under hog cholera, clean yards, and shut up these and pastures or runs, and all infected water for one month. In case of public market yards and alleys, and railway loading banks, chutes, and cars, a thorough cleansing and disinfection may warrant that they may be put to use again immediately. No animals that occupied the yards before disinfection should be allowed to mingle with the new stock, as they at times carry the microbe, though themselves apparently healthy and immune. All regulations as to railway and boat transit, recommended under hog cholera, are equally applicable to swine plague. The possibility of protecting private herds, by keeping them in special pens, holding two or three each, is also the same for swine plague.

_Immunization_ is somewhat more promising than in hog cholera. Metchinkoff and Th. Smith working independently found a fair measure of success in inoculating rabbits and guinea pigs with three to five small injections of sterilized bouillon cultures, agar cultures or blood, intravenously, intraabdominally or hypodermically. But as applied to swine it has not proved satisfactory, and the irregularity of the results and the tendency to induce unthriftiness have caused it to be abandoned.

_Treatment._ The therapeutics of swine plague like that of hog cholera is essentially unsatisfactory. Benefit might be derived in individual cases from a careful and judicious use of drugs to meet the special indications, but with the comparatively low value of the individual animal, the certainty of the multiplication of the deadly poison by the preservation of the diseased, and the extreme danger of its diffusion and extension, treatment is anything but commendable.

_Serum-therapy_ has been advocated for years by De Schweinitz, and under the auspices of the Bureau of Animal Industry it has been given a wide trial, but it has not met with the full success that was at first claimed for it. The serum is prepared in a similar way to that of hog cholera and is similarly employed. It is open to the same class of objections, and though when skillfully employed it will reduce the mortality, it does not yet seem to have reached the point at which it can be recommended as a profitable investment. Like all temporizing measures it draws attention from the sounder and more economical measure of extinction and is indirectly a means of the perpetuation and even the diffusion of the infection. So long as extinction cannot be secured, this is a less valuable alternative for the adoption of owners of high priced hogs.

MODIFIED AND COMPLEX FEVERS OF SWINE.

Double infections. Varieties of bacillus choleræ suis, and bacillus
suis pestis. McFadyean’s swine fever bacillus. Marseilles swine plague
bacillus.

We accept fully the duality of the Hog Cholera and Swine Plague, though this duality has been hotly contested on both sides of the Atlantic. Many of the best observers in Europe now support this position. These include Selander, Bang and Jensen who are familiar with the _svinpest_ (hog cholera) of Scandinavia; Kitt, Friedberger and Fröhner who are familiar with the _Schweineseuche_ (swine plague) of Germany; Raccugla, Canova and others in Southern Europe; and Lignieres and others in France who have studied the hog cholera and _pasturellose porcine_ (swine plague).

But the conceded duality of these two diseases as they occur in typical examples in swine, does not account for all the infectious fevers of swine, in which these microbes or others closely allied to them may figure. Salmon, Smith and their coadjutors describe double infections in the same system, in which both the bacillus choleræ suis and the bacillus pestis suis figure, and in which there result a combination of symptoms and lesions, that together represent both of these germs. It may be that one or other of these germs in a given outbreak, shows a predominance in potency so that the symptoms are more characteristic of it than of its companion; it may be that the more potent germ kills the victim, quickly by an acute septicæmia and gross lesions that would apply almost as well to one germ as to the other; or it may be that both act moderately and the attack is protracted with resulting lesions in both lungs and bowels that respectively suggest the plague and the cholera.

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.

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.

SEPTICÆMIA HÆMORRHAGICA OF THE SHEEP: LOMBRIZ.

Synonyms. Definition. Geographical distribution, Argentina, France,
etc. Causes: bacillus; intravenously, etc., youth, verminous
affections, low condition. Bacteriology: ovoid bacillus with polar
stain, bleached by Gram’s solution, ærobic, nonmotile. Symptoms:
Chronic form in summer, diarrhœa, arched back, stiffness, emaciation,
flattened wool, segregation, impaired or depraved appetite, shedding
wool, anæmic skin, dependent dropsies, sunken eyes, weak small pulse,
temperature variable—elevated, nasal and buccal discharge, weakness,
paresis, dulness, torpor, lung symptoms, arthritis. Diagnosis: from
distomatosis and strongylosis. Acute form with high fever,
constitutional disorder, colics, diarrhœa, death in 24 to 36 hours,
subacute form. Lesions: black blood, congestions, and general
petechiæ. Lungs, liver, kidneys and spleen, congested, swollen.
Subacute cases have lighter blood, and lesions. Chronic cases anæmic,
blood diffluent, lymph glands enlarged, congested; connective tissues
and serous cavities dropsical, gastric, intestinal and hepatic worms,
spleen shrunken. Mortality: great in acute, less in chronic.
Prevention: segregation, exclusion of all sheep from unknown or
suspected flocks, antiseptic dip and quarantine for new purchases,
expose a few as a test; cleanliness, disinfectants, avoid watershed
from infected lands, wide range, outdoor life, generous diet, remove
weak, emaciated, anæmic. Immunization. Treatment.

_Synonyms._ Pasteurellosis Ovina. Infectious Pneumo-Enteritis.

_Definition._ An infectious febrile affection of the sheep, chronic or acute, characterized by dulness, stiffness, or paresis, anorexia, thirst, disorder of the breathing and digestive organs, black diffluent blood, petechiæ, reddish effusions in the serosæ or connective tissue, and congestive or inflammatory lesions of the lungs, liver, kidneys and intestines. The presence of a cocco-bacillus (diplococcus, strepto-cocco-bacillus, pasteurellosa) in the lesions is especially characteristic.

_Geographical Distribution._ Though Lignieres first demonstrated this as a bacteridian disease in the Argentine Republic, he was, after his return, able to identify the same affection in the flocks of almost every department of France, in newly imported English Lincolns and German Merinos, so that there can be little doubt that the malady exists in all or nearly all countries engaged in sheep husbandry, though it has been usually attributed to parasitisms of the lungs, liver or alimentary canal alone.

_Causes._ The essential cause is manifestly the bacillus, which Lignieres has isolated, cultivated in vitro, and successfully inoculated intravenously in the sheep, which he also infected by feeding the pure cultures. Intravenously it proved fatal to Guinea pig, rabbit, pigeon, chicken, rat, mouse, horse, ass and ox. Yet many other accessory causes must be admitted as operating in different cases.

_Youth_ shows the greatest susceptibility whether the victim be mammal or bird. So marked is this influence that the principle sufferers are lambs just weaned or yearlings. Yet mature animals, that are debilitated from any cause, also fall victims. The measure of immunity usually noticed in mature sheep may well be attributed to a previous mild and non-fatal attack of the bacillus.

_Verminous affections_ are undoubtedly predisposing causes, hence, the common practice of attributing the malady to the worms alone. This again in part explains the susceptibility of the young which so often harbor worms to a dangerous extent. It seems to matter less what worms are present than, that they are in sufficient numbers to greatly deteriorate the health. It is noticeable, however, that those worms that make breaches in the mucosæ, have been noted as infesting the victims of this malady. In the stomach worms sent from Argentina, Railliet identified Strongylus Contortus, S. circumcentus, and S. instabilis and in the duodenum S. filicollis and S. Curticei. These, like the distomata often found in the liver, are blood suckers and not only render the animal anæmic, but make numerous perforations to act as infection-atria. The various lung worms, encysting themselves in the air sacs and determining local congestions may act in the same way, opening channels for the entrance of the microbe.

_Low condition_ or a _low tone_ of health from any cause predisposes. Old, worn out animals, ewes in lamb, or those just lambed, sheep that have been shut up and denied proper exercise in winter, those on poor feeding and perhaps nursing twins, those that have suffered from any debilitating disease of any kind are especially obnoxious to a dangerous attack.

_Microbiology._ The microbe, which Lignieres found in the pulmonary lesions, is one of the colon group of pathogenic bacteria that have been classed together as _pasteurella_. It usually appears as a very minute ovoid bacillus which stains promptly and deeply at the poles in fuchsine or gentian violet, leaving a clear median part, so that it seems a _diplococcus_. It bleaches readily in Gram’s solution. Its form varies in different culture media sometimes showing long _bacilli_, and sometimes _streptococco-bacilli_, but the usual and characteristic appearance is that of a _cocco-bacillus_, and to this it constantly returns. The microbe is ærobic and nonmotile (the slow zig-zag motion sometimes seen does not seem to be automatic). In peptonised bouillon it produces opacity in 18 hours, or in simple bouillon in 24 to 48 hours, the best temperature being 100° F. Gelatine plate cultures are slow because of the compulsory low temperature, yet in 36 to 48 hours it forms pale blue, translucent, round colonies the size of a pin head. It never liquefies. In coagulated blood serum it forms only a thin transparent pellicle hardly visible, and there is no growth on potato.

_Symptoms: Chronic Form._ In Argentina, Lignieres observed the disease especially during the hot summer months (December to May), and after weaning in the lambs. This may be from the marked change of food, from the greater activity of microbian life at this season, from the exhausting effect of the heat, or from a combination of two or more of these conditions. It appears alike in the sheepfold, and on the open prairie. In considerable flocks the symptoms may be at first overlooked, so that the death of several sheep may be the first thing to draw attention. Then a certain number are found to scour, arch the back, walk stiffly, lose condition, and have the wool flattened and devoid of yolk (_clapped_ wool). The sheep may be dull, lagging behind its fellows, or lying apart by itself, ruminating infrequently and for shorter periods than natural, and there may be inappetence, or depraved appetite (eating earth), though some eat well to the end. Irregular and at intervals capricious appetite is a frequent condition. When caught and examined, the wool is easily torn out, the muscles are soft and wasted, (the leg muscles may have practically disappeared), the bones stand out at all points, the skin is pale, thin, bloodless and devoid of its subcutaneous fat, (paper skin), there may be œdemas along the ventral aspect of the body, pitting on pressure, and between the branches of the lower jaw (poked), the eyes are sunken, the conjunctiva may be puffy and œdematous, but like the muzzle and mouth they are pale and anæmic and the pulse is small, though the excitement may have roused cardiac palpitations. The temperature varies from time to time often reaching 105° or 106° F. There is liable to be a muco-purulent discharge from nose and mouth especially noticeable during drinking. As the disease advances the subject becomes weak, paretic, dull and stupid, it remains down without interest enough to seek food, though still eating if it is brought to it. The head is usually rested on the flank, and the animal often lies so for days in a state of semi-stupor without disposition or ability to rise, paretic or paraplegic. Auscultation may sometimes detect a mucous râle or crepitus, and percussion a flatness of sound over some part of the lung. Chronic arthritis is an occasional symptom.

_Diagnosis._ The symptoms closely resemble those of distomatosis or strongylosis, and the disease is often complicated with one or more of these, so that it may become difficult to judge how much is due to the microbian infection and how much to the helminthiasis. The presence, continuously or intermittently, of the hyperthermia is almost pathognomonic of the operation of the microbe.

_Acute Form._ This has been particularly observed in the ewe just after lambing, when the system is especially susceptible to microbian invasion, and little able to cope with it. There are hot ears, nose and feet, temperature of 104° to 106° F., accelerated pulse and breathing, anorexia, ardent thirst, deeply congested mucosæ, colicy pains, pawing the ground, frothy or bloody diarrhœa, arched back, pendent head, ears and eyelids, muscular trembling, albuminous urine, plaintive cries, dark red vaginal discharge, muco-purulent or glairy nasal discharge, and death in 24 to 36 hours. Such animals may be in fair condition or even fat, no time having been allowed for emaciation.

In other cases death may be delayed for three or four weeks, with the same general symptoms, only less marked. In such cases, pregnant ewes are likely to abort, and the lambs are born dead, or prove weak and listless, and die when a few days old. Some have too little energy to suck; others suck heartily but perish all the same on the second or third day, after diarrhœa, thirst, hyperthermia, prostration, and stupor.

_Lesions._ These vary according to the type. In the _rapidly fatal cases_ there is dark colored blood, with congestion of the serous and mucous membranes, which, together with the skin and often the solid tissues, are covered with petechiæ, and even circumscribed hæmorrhages. The lungs, liver, kidneys, spleen, and many of the lymph glands are congested and swollen, seeming at times of a black hue as if blood-saturated. The lesions, indeed, indicate an acute septicæmia.

In _cases that have survived three or four weeks_, the morbid changes are slighter, the blood is brighter in tint, and the congestions less deep in color, ecchymoses may be especially confined to the heart, abomasum and small intestines, which may also show hæmorrhages. Enlargement and congestion of the lymph glands are the rule, while pulmonary consolidation and gastro-intestinal mucous inflammations are frequently found. As in the more acute types the urine is albuminous.

In _chronic cases_ the anæmia is prominent. The clot is soft, relatively small, elastic and black, the serum is relatively very abundant and pale. The red globules are greatly reduced in numbers, and there are a number of giant cells which stain deeply as in chlorosis. The lymph glands are usually enlarged, softened and slightly congested but rarely the seat of blood extravasation. The tissues generally are pallid, soft and shrunken. There is a marked absence of subcutaneous and intermuscular fat, while the connective tissue is more or less infiltrated with a transparent, watery lymph. The serous cavities usually contain more than the normal amount of fluid, transparent or straw-colored, and with few globules or granules. Congestions and even shreds of false membrane are sometimes present on the serosa. In some cases the lungs and bronchia are the seat of inflammatory exudates, causing nodular consolidations of from one-half to one inch in diameter. Not unfrequently the lungs show strongylosis as the fourth stomach shows strongylus contortus, the small intestines strongylus filicollis, tæniae (expansa, fimbriata, etc.), the large intestines æsophagostoma Columbiana, and tricocephalus affinis, and the gall ducts distoma hepaticum and distoma lanceolatum. In these chronic cases the spleen is usually shrunken, and the liver firm, sometimes even cirrhotic.

_Mortality._ The acute cases are usually fatal. Those that assume a chronic form, if free from local lesions in important organs, well-fed, and, above all, kept in the open air, and changed to a different pasture, tend largely to recovery.

_Prevention._ The propagation of the infection from animal to animal is slow and somewhat uncertain, and when introduced by the purchase of a new ram or other animal, it may take a considerable time to affect the stock extensively, but for this reason, and because an apparently sound sheep may harbor the germ, it is difficult to oppose it successfully by segregation. All the same, it is desirable to take all possible precautions against its advent, and among these, the exclusion of strange sheep from noninfected pastures and flocks. When the time comes to make an outcross from the home strain, the ram must be selected not only for his pedigree and individual qualities, but no less for the soundness of the flock from which he is taken. If the lambs of that flock have been decimated by disease, the best blue blood, and most faultless form should not tempt the flockmaster. He should be rejected in favor of one taken from a flock that is above suspicion. It matters little if it can be plausibly argued that the mortality came from worms of the lungs, liver, or digestive organs; these in themselves may soon ruin any flock, but they, too, often coexist with the microbe of infectious septicæmia, and, when this is the case, they prepare the system and open a way for its invasion.

New purchases should not only be selected from apparently sound and guaranteed stock, but they should be passed through an antiseptic dip on arrival, and then if possible quarantined in a special enclosure until they shall have proved their freedom from infection. A valuable ram may be placed with some lambs or yearlings in close quarters to ascertain whether he has brought the infecting matter with him. If all escape after some months the presumption is that he is sound. Perfect cleanliness of the fold should be maintained, and disinfectants may be freely used in it.

The water supplies should be watched, rejecting streams that have drained sheep-pastures where there have been marked losses of lambs and ewes. Water from deep wells without any surface leakage is to be preferred.

When new stock (ram, ewes, lambs) are of necessity mixed with the sound herd, a wide range, an open air life, and abundant dietary must be secured. The system that is full of strength and vigor can better resist the microbe and even throw it off entirely, whereas the weak, confined subject succumbs. For the same reason, the weak, emaciated and debilitated subjects should be at once separated from the sound flock, and kept in a special enclosure, in the open air, on a rich diet. Should they harbor worms, this seclusion is even more imperative. (See parasites of lungs, liver, stomach and bowels).

Lignieres advocates immunization by serum prepared on the Pasteur method, but, as he has not divulged the exact technique of its preparation, it is impossible as yet, to give this an unqualified endorsement. It has this in its favor that the mature sheep, in full vigor of middle life, though in an infected area, usually resist the infection, while the young, old, debilitated and verminous suffer. Opposed to it are these considerations that are recognized by Lignieres himself;—1st, The acquired immunity is not perfect, as shown by occasional relapses in sheep that have survived a first attack; 2d, The serum inoculation is not only useless, but dangerous in animals that already harbor the germ; I may, add 3d, Any acquired parasitism or debilitating disease may tend to break down the immunity and prostrate the system under the infection. Lignieres advises that the serum treatment should be restricted to the new born lambs in infected herds, or herds in infected areas. The first three or four weeks after birth are to be preferred for the operation, though failing this it may still be ventured on, up to a few days before weaning. The longer it is delayed the greater the danger of a preëxisting infection, and of untoward results from the new access of infecting material, on the back of an infection which varies so extremely in its pathogenic potency. Even among the new born lambs, Lignieres would restrict the serum therapy to the strong, robust and healthy, and, if they survive the resulting fever, would repeat the _treatment_ after the hyperthermia has ceased. No satisfactory treatment of the disease has been made. An open air life, a generous diet, and a course of iron, and bitters will, however, be of use in serving to improve health, digestion and vigor, to solicit a better production of red globules, and to enable the patient to survive the period of anæmia, prostration and debility. Antiseptics like quinia, the sulphites and the iodides might be used as adjuncts.

PNEUMO-ENTERITIS IN SHEEP: HÆMORRHAGIC SEPTICÆMIA: SWINE PLAGUE.

Historic note. Microbiology: ovoid bacterium, motile, with polar
stain, non-liquefying, chains, grows freely on culture media.
Pathogenic to sheep, goats, dogs, hens, rodents, calf, ass. Views of
Lignieres, Lienaux, and Conte. Symptoms: Acute form in young;
hyperthermia, rapid pulse, troubled breathing, dulness, prostration,
sopor, anorexia, congested petechiated mucosæ, offensive diarrhœa,
emaciation, wheezing, cough, râles, crepitus, percussion flatness,
abortion. Death in 6 hours to 3 days. Subacute form in mature:
symptoms moderate, recoveries the rule. Lesions: fœtid carcass, blood
staining of skin and organs, exudates, petechiæ, swollen congested
lymph glands, peritoneal exudate, congested liver and spleen,
gastro-enteritis, pleural effusion, lobular and peribronchial
exudates, caseation, congested womb, placenta and brain, bacterium in
lesions. Prevention: isolation, disinfection, secretions, manure,
drainage, exclude tame and wild animals. Disinfectants.

Among the different forms of hæmorrhagic septicæmia in sheep, that observed by Galtier in 1889 in Basses Alpes, and later elsewhere in southern and western France and in Algiers, must be specially noted. It seems to be the same affection studied later by Lienaux, Conte, Besnoit and Cuillé and which prevailed from Tarn in the south of France, to Vendée in the west, and Somme in the north.

_Microbiology._ The pathogenic factor found in the lesions was an ovoid bacterium, a little larger than that of fowl cholera, motile, non-liquefying, with polar staining, and often showing in short chains of two or three joined end to end. It grows easily and abundantly in all common culture media, even on potato which fails to propagate the cocco-bacillus of Lignieres. This, with its ready transmission from swine to sheep and _vice versa_, apparently serves to differentiate it from the cocco-bacillus, and the disease from the hæmorrhagic septicæmia of Lignieres.

_Pathogenesis._ In Galtier’s first observations in Basses Alpes four separate flocks were infected by pigs brought all from one market, and placed in or by the pens of the sheep where they sickened and one in seven died in a few days. Then the mortality began among the sheep and ranged as follows: 1st flock lost 10 in 37: 2d flock 16 in 25: 3d flock 8 in 20: 4th flock 12 in 22. On one farm 10 sheep were sent to a neighbor’s just before the arrival of the sick pigs and escaped, and on another a second flock kept in outlying pens well apart from the home flock kept perfectly sound.

With cultures of the microbe in vitro, he successfully inoculated sheep, goats, dogs, chickens, Guinea pigs, rabbits, and, finally, a calf and an ass. The cultures were inoculated in different cases; intravenously, into the trachea, pleura, lung, and subcutaneous connective tissue, and one goat was infected by ingestion.

Lignieres claims that Galtier must have worked with a complex infection in which his (Lignieres’) cocco-bacillus was an essential constituent. The evidence of this is, however, lacking, and we must recognize that Galtier made cultures which showed the close relationship of his organisms to swine plague, and their lack of complete identity with those of the Lombriz.

Lienaux and Conte had pathogenic results in a limited number of animals only (rabbit, mouse, Guinea pig) illustrating the familiar truth of the variability in the pathogenesis of different specimens of septicæmic bacteria of the colon group.