The bacillus anthracis as found in the blood is a nonmotile rod-shaped organism, 5 to 20μ long by 1 to 1.5μ broad with ends apparently square, but really slightly cup shaped as seen in the stained specimens when two have remained connected end to end. Under favorable conditions a clear hyaline envelope may be seen around the bacillus. Though usually isolated in the living blood, yet in bouillon cultures the bacilli grow out into long flexible filaments, made up of separate segments which are easily distinguished in the stained specimen. In all cultures out of the living animal body, in the presence of air and at a suitable temperature spores form endogenously in the bacilli and are set free by the granular degeneration of the latter. In peptonized bouillon this may occur in four days at 14° C., or in eight hours at 37° to 40° C., but not above 42° C. (Schreiber. Centr. S. Bact. 1896). Sporulation never occurs in the living animal body.
The bacillus is ærobic, yet it will grow at the bottom of a stick culture in solid media. It fails to grow in an atmosphere of CO2, H, or N. It stains readily in aniline colors, and also by Gram’s method. It grows freely on a variety of culture media (blood serum, aqueous humor, urine, vegetable infusions, milk, meat bouillon, peptonized gelatine, potatoes, etc.) at a temperature of 20° to 38° C. Growth ceases below 12° C., and above 45° C. Growth is most active in neutral or slightly alkaline media, and is arrested by that which is decidedly acid.
Action of physical and chemical agents on the bacillus anthracis. The bacilli survive a temperature of −45° C. (−49° F.), but they perish in 10 minutes at a temperature of 100° C. (212° F). A temperature of 55° C. (131° F.), proves fatal if sufficiently prolonged. The spores are much more resistant. They have survived −130° C. (−202° F.) and though they may die in 10 minutes in liquid media kept at 95° C. (203° F.), yet when old and dry it may require several hours at 140° C. (282° F.) to sterilize them.
Even the bacilli are comparatively resistant to ordinary disinfectants, and, as spores form in the body very rapidly after death, and in virulent products, it is always best to assume their presence. In a moist medium Cl. 44.7% destroyed the spores in 3 hours: HCl (1:1100) in 2 hours: HgCl (1:1000) in a few minutes: HgI2 (1:20000) in 2 hours: Malachite green (1:40,000) in 2 hours: Methyl violet (1:5000) in 2 hours: Aseptol (1:10) in 10 minutes: Carbolic acid (4:100) with HCl (2:100) in 1 hour.
Action of septic ferments on the bacillus anthracis. Rapid putrefaction in the anthrax carcass which has not been opened tends to speedy granular degeneration and death of the bacillus anthracis, so that the blood and tissues may be no longer infecting after six days in summer. In such cases the irrespirable gaseous products of decomposition drive out the oxygen without which the bacillus cannot live. If, however, spores have already formed or if air is freely admitted the infection survives in spite of decomposition. The search for the bacilli may thus be fruitless as soon as decomposition is well advanced and the material can only be virulent through any spores that may have formed. Eventration serves to retard sepsis and admit air to form spores, and salting operates in a similar manner.
The infected hides, the nasal, buccal, kidney and bowel discharges, and spilt blood and exudates mingling freely with the air tend to form spores and to preserve and propagate the contagion. On the contrary prompt and deep burial, without opening the carcass and before spores can have formed will usually ensure its destruction. The main danger in such cases comes from infecting matter (adherent to the surface of the body) which sporulates easily. This serves to explain the great danger of working in anthrax hides, leather, horn, wool, hairs and bristles. It also explains sporulation and preservation of infection when the virulent excretions, blood, etc., mix with the surface layers of soil. This may happen at a greater depth (3 or 4 feet) in a very porous soil and where the temperature is sufficiently elevated (above 14° C.) It may even occur in water. The dried spores are mostly carried in dust, hay, fodder, and running streams.
Since 1892 anthrax has prevailed along the banks of the Delaware river for a distance of 40 miles in N. J. and Del., destroying from 70 to 80 per cent of the farm stock. The great morocco industry on this river draws infected hides from India, China, Russia, Africa and South America, and the spores are carried and distributed by the tides.
Infection-Atria. Infection may occur by a variety of channels as: 1st, by ingestion, giving rise most commonly to anthrax of the mouth, throat or intestines; 2d, by inhalation, giving rise to pulmonary anthrax (wool-sorter’s disease): 3d, by inoculation through contact of abrasions, wounds, etc., with infecting bodies, including surgical instruments: 4th, by flies and other insects: and 5th, by transmission to the fœtus in utero. This last form is very rare in the larger animals, but has been repeatedly seen in Guinea pigs, rabbits, goats and even in one case (Pangalli) in man.
Forms of Anthrax in Domestic Animals. In the lower animals anthrax manifests itself differently according to the seat of invasion and the amount of the virus. The worst forms, seen especially in cattle and sheep, are so sudden that they have been called apoplectic or fulminant. Without premonitory symptoms there is sudden loss of appetite, trembling, haggard expression of face, uneasy shifting of the feet, irregular movements backward or to one side, dyspnœa, cyanosis, plaintive cries, convulsions, ejection of blood by the nose or with urine or fæces, and death in a time varying from a few minutes to four hours. The second type is the anthrax fever, known also as splenic fever, splenic apoplexy, or internal anthrax. In this form there may be prodromata, especially in sheep, excitability, restlessness, and above all, a rise of temperature of often 3° or 4°. There may be distillation of drops of blood from the nose, eyes or ears, the mucosæ become congested, and in sheep this may show on the finer parts of the skin, as inside the forearm or thigh. Tremors, erection of the hairs, dulness, prostration, lagging behind the flock or herd, insensibility of the loins to pinching, inappetence, ardent thirst, grinding of the teeth, colics, tympany, mucus coated, bloody or liquid fæces, bloody urine, tumultuous heart beats, dyspnœa, dark, congested mucosæ, amounting to cyanosis, and spasmodic contractions of the muscles of the back, neck or eyes. If blood is drawn it may appear abnormally dark in color and very slow to brighten under the action of the air, it may have a thick, tarry appearance, and form a very loose clot. Death, (usually in coma or convulsions) will supervene, in sheep under 24 hours, in cattle in 2 to 5 days, and in horses in 1 to 6 days. The third type is the local or external anthrax, assuming in cattle the special forms of gloss-anthrax, pharyngeal anthrax, hœmorrhoidal anthrax, cutaneous and subcutaneous anthrax. In horses most of the same forms appear, in the tongue, throat, neck, shoulders, withers, flank or thigh. These swellings have a firm or doughy feeling, are comparatively and sometimes wholly insensible and show a marked tendency to necrotic changes. When incised they show extensive blood extravasation, or a pale, straw-colored exudate mixed with sanguineous lines or patches, and manifest no tendency to suppuration, nor to emphysematous crepitation. These features distinguish them from phlegmon and emphysematous anthrax. When suppuration ensues it is tardy and indolent and is, on the whole, a favorable indication. In all cases the bacillus may be found on microscopic examination of the exudate.
Lesions. Putrefaction of the carcass is usually rapid. In the very rapidly fatal cases the changes in the blood and tissues are often little marked, and after the removal of the enlarged, engorged spleen and infiltrated internal organs, the carcass might often be placed on the market without much suspicion. In more prolonged cases the blood is profoundly changed, being very dark, not subject to rapid æration, and incapable of coagulating firmly or at all. The red globules are crenated or otherwise distorted, adhere to each other in irregular masses, and have parted with much of their hæmoglobin which diffused in the serum stains the intima of the blood vessels and other white tissues. The leucocytes are relatively very much encreased. The bacteria are easily found in the intervals between the globules. The heart is often soft, discolored, as it were parboiled, with the endocardium deeply stained and the contained blood dark and diffluent or liquid. The liver is usually enlarged, softened, friable, and as if parboiled, with many hæmorrhagic patches. The spleen is materially, often enormously enlarged, irregular in outline from extreme engorgement with blood, and in exceptional cases even ruptured. An encrease to two or three times the normal is common. The bacilli are present in great numbers in the spleen, alike in the pulp, in the blood vessels and in the trabeculæ. The lymph glands are almost always hyperæmic, hypertrophied, and softened, especially in the vicinity of the localizations of the tissue lesions. They may be merely petechiated, or they may seem like a mass of black blood, and under pressure may break down readily into a sanguineous pulpy mass. Like the spleen they are favorite centres for the accumulation of the bacilli. The marked alterations in these glands will often indicate the channel by which the infection entered the body. The serosæ are usually hyperæmic, with many hæmorrhagic points and even extensive exudations, and they often enclose a sanguineous liquid. The hyperæmia and points or patches of extravasation are to be found in any part of the body in which the bacilli have been colonized, thus they are common in the tongue, the throat, the lungs, the stomach or bowels, the mesentery, the omentum, the skin, the connective tissue, or the muscular system. There may be bloody or gelatinoid exudation, but there are always the capillary embolisms by irregular masses of blood globules, and bacilli. These embolisms, the arrest of hæmatosis and the destructive action of the toxins on the red globules go far to account for the extreme fatality of the disease.