Within the living animal body the development never goes aside from these forms. The growth appears limited to micrococcus and bacillus rods, while spores or bacillus threads are never found. This finds its counterpart in the micrococcus poisoning caused by the inoculation with the spores of common moulds (Grawitz); and in septicæmia also micrococcus and bacillus forms only are found, the filamentous never.
When grown in organic infusions out of the animal body the anthrax-germ develops from micrococcus or bacillus into a long, branching, filamentous product, which in the presence of oxygen develops into spores. Apart from oxygen or when the proper nourishment of the bacillus is exhausted the protoplasmic elements within the filamentous sheath undergo granular degeneration, and finally the empty envelope disintegrates and disappears. The spores appear at intervals in the protoplasm of the filament as clear, brightly refrangent bodies, at first spheroidal, afterward larger and oblong. Unlike the micrococcus and bacillus, they do not stain. Under favorable circumstances the primary cell is capable of forming one, or if extra long, two spores (Koch, Klein). Cossar-Ewart claims to have seen the formation of motile flagellate organisms aggregating themselves into zooglæa masses, but as these were not found in the carefully-conducted cultures of Koch and Klein, they are supposed to have been aërial microphytes accidentally introduced.
The great tenacity of life in the spores in heat and cold, dryness and wet, excluded from air and under several atmospheres of oxygen, in the midst of putrefaction and in pure watery fluids, well accounts for the persistence of infection in buildings and localities where the poison has gained a foothold. In order to their destruction in a natural manner it seems necessary that they should germinate and develop into the anthrax micrococcus, bacillus, or mycelium. This germination may take place in the presence of moisture, oxygen, and suitable nourishment, whether in the soil, the animal body, or elsewhere, and then the exhaustion of the aliment, the exclusion of the oxygen by putrefaction, the submergence in a medium unfavorable to development, or exposure to a very high temperature, may suddenly destroy the poison.
There is reason to believe that a too free exposure to oxygen proves destructive to the virulence, if not to the life, of the poison, and thus in all porous, well-drained soils the anthrax poison, even when introduced from without and concentrated by the death and burial of many victims, soon disappears. This feature, which is common to many zymotic diseases the germs of which live and multiply outside the animal body (typhoid, yellow fever, tuberculosis, swine plague, chicken cholera, diphtheria, etc.), offers countenance to the claims of Buchner that he had by prolonged culture, in the presence of air, metamorphosed the bacillus anthracis into a harmless mycrophyte, and that, conversely, by continuous cultivation under the surface of a suitable beef infusion he had changed the harmless bacillus subtilis of hay into the deadly bacillus anthracis. Koch, Klein, and others have discredited Buchner's results, on the ground that he had not, in their opinion, taken due precautions against impure cultures, and that his alleged transitions took place too abruptly; yet further observation must determine whether he has been condemned too hastily. The diminished virulence of Pasteur's attenuated virus, which is unaffected by the next subsequent culture or by the formation of spores, shows plainly enough that the bacillus anthracis is capable of physiological changes under the influence of varying conditions of growth, and that such changes are not at once undone by a return of the former conditions.
How anthrax-germs enter the body is partly known and partly conjectured. Direct inoculation on a sore by contact, by insects, by harness, by accidents, etc. is an undoubted method. The sound cuticle is probably an efficient barrier, since bacteria habitually inhabit, without hurt, the surface and gland-ducts of the skin; yet the entrance of these saprophytes through the shell and membranes of the egg leaves a doubt as to the efficiency of the cuticular obstacle. The mucous membranes are manifestly frequently penetrated by the parasite. Hence the local affections in the mouth and throat (glossanthrax, anthrax angina) and in the lungs (pulmonary anthrax). Cohn claims that the gastric juice of Carnivora especially is destructive to the anthrax poison, yet the constant recurrence of intestinal anthrax (mycosis) seems to imply that the germs often escape destruction in the stomach. Pasteur supposes that anthrax-infected food is only injurious when there are inoculable sores in the mouth or pharynx, but it seems as if in that case the disease would be first shown at these points and in the nearest lymphatic glands rather than in the bowels, the rule for the inoculated anthrax being to develop first in the tissues and thence to reach the blood-vessels through the lymphatics.
The anthrax poison expends its fatal energy especially on the blood and blood-vessels. The bacilli in the blood use up the available oxygen, so that the circulating liquid becomes venous, dark, and unfitted for the maintenance of the normal functions of life. What is even worse, the ability of the blood to absorb oxygen is greatly impaired. In men and dogs suffering from anthrax the consumption of oxygen was found to be reduced in one instance even by two-thirds, probably in part by reason of the action of the chemical products of the bacillus. A third condition constantly found is embolism of the capillaries by the bacillus and the occurrence of local gangrene.
SYMPTOMS.—Anthrax shows itself in three principal forms: 1st, the apoplectiform; 2d, anthrax fever without local external lesions; and 3d, external localized anthrax. The two last forms correspond in the main to the acute and subacute forms.
The period of incubation varies according to the dose of the poison and the receptivity of the animal. In some cases infection is at once followed by illness. In these it is probably the chemical products that produce the first effect, while the disease caused by the propagation of the bacillus appears later should the animal survive. Such incubation is shortest for the smaller animals (mice, rabbits, guinea-pigs, cats), in which illness usually sets in in from twenty-four to forty-eight hours. In sheep and goats incubation may be extended to three or four days, while in horses and cattle it may last a day longer.
The apoplectiform type attacks animals which a few minutes before seemed in fine health, appetite, and spirits, striking them down as if by lightning, and the victims struggle convulsively for some minutes, expel blood perhaps by the nose or anus, and expire. In the less suddenly fatal cases there may be muscular trembling, unsteady gait, excited breathing, accelerated pulse, tumultuous heart's action, bleeding from some natural orifice, and death in from one to several hours. Occurring as these cases often do in summer, the sudden death is probably hastened by insolation.
In anthrax fever or acute internal anthrax there is loss of appetite, and, in ruminants, of rumination, suppression of milk, dulness, languor, staring coat, or even a rigor, and thirst. Then follows the hot stage, in which the temperature may rise to 106° or 107° F.; there are acceleration of pulse and breathing, petechiæ or a brown or yellowish tinge of the mucous membranes and white parts of the skin, tenderness of the spine, often jerking or clonic spasms of the muscles of the extremities, and much prostration and weakness, the patient hanging back on the halter, leaning against a wall, or swaying when made to move. The feces are usually more or less mingled with blood-clots, or may be at once liquid and bloody. Bloody urine and the discharge of blood from other natural channels are frequent. Some cases are manifestly delirious, and in others the skin crackles on being handled. Remissions are not uncommon, during which the animal remains dull and prostrate. As the disease advances and the blood is robbed of its oxygen, the temperature descends below the natural standard, great weakness and stupor set in, the pupils are widely dilated, and death from asphyxia occurs in one or two days from the onset.