Morphology and Cultural Characteristics
B. anthracis is a large Gram-positive bacillus. In infected tissues, the microorganism appears singly, in pairs, or in short chains. On artificial nutrient media, the bacteria form long filaments visually resembling a 'bamboo cane'.
To evade the immune system inside the host, the pathogen produces a capsule. Upon release into the external environment in the presence of oxygen, the bacillus forms a centrally located spore that does not exceed the cell diameter. Spores exhibit extreme resistance: they withstand boiling and exposure to liquid nitrogen, and persist in water bodies for years.
The bacterium is an aerobe or facultative anaerobe, growing readily on simple media (pH 7.2–7.6, temperature 35–37 °C). On solid meat-peptone agar, colonies grow large, matt, with irregular edges (microscopically demonstrating the 'lion's mane' or 'Medusa head' phenomenon). In liquid broth, the pathogen produces a characteristic sediment resembling cotton flakes while leaving the medium clear. A specific identification test involves culturing on penicillin-containing media: cells transform into spheroplasts and align in chains, forming the 'pearl necklace' phenomenon.
Pathogenicity Factors
The virulence of Bacillus anthracis is based on two main components: the capsule and a potent exotoxin.
The capsule is composed of a D-glutamic acid polypeptide. It is non-immunogenic but performs a critical antiphagocytic function, preventing uptake by immune cells and facilitating tissue adhesion.
The exotoxin is synthesized exclusively within the host (or on media containing animal proteins) and is encoded by plasmids. Its toxic effect requires the synergistic action of three components:
- Protective antigen (PA) — serves a transport function, binding and translocating the other two factors into the cell (it is responsible for inducing protective antibodies).
- Lethal factor (LF) — a zinc-dependent metalloprotease that inactivates protein kinases and selectively destroys macrophages.
- Edema factor (EF) — a calmodulin-dependent adenylate cyclase that dramatically increases intracellular cAMP levels, disrupting membrane permeability and causing massive edema.
Epidemiology and Pathogenesis
Anthrax is a globally distributed infection linked to livestock-raising regions. The source of infection includes sick animals (cattle, small ruminants, horses, pigs), with infected soil serving as the reservoir. Humans represent a biological dead-end, as they do not transmit the infection further.
Main transmission routes include: contact (handling hides, wool, bones), alimentary (ingesting contaminated meat), airborne dust (inhaling spores), and rarely vector-borne (insect bites).
Upon entering the body through damaged skin or mucous membranes, spores are engulfed by macrophages and germinate into encapsulated vegetative forms. Toxin release leads to serous-hemorrhagic inflammation and necrosis. Bacilli then multiply in lymph nodes, break into the bloodstream (bacteremia), and cause generalized sepsis. Toxin accumulation in the blood leads to toxic shock and death.
Clinical Forms and Diagnostics
Depending on the portal of entry, three main clinical forms are distinguished:
- Cutaneous — the most common form. Characterized by the formation of a firm black eschar (carbuncle) with serous-hemorrhagic exudate. Pathognomonic sign: complete absence of pain in the necrotic zone despite marked surrounding edema.
- Pulmonary — develops via spore inhalation (potential bioweapon). It follows a severe course with rust-colored sputum and rapid death from shock.
- Gastrointestinal — accompanied by lesions in the intestinal lymphoid tissue, bloody diarrhea, and ileus.
Diagnosis utilizes microscopy (Gram stain and capsule visualization), culture, PCR, and direct immunofluorescence. For early diagnosis, an intradermal allergic skin test with anthraxin is effective. For post-mortem examination or old animal hides where live cultures cannot be isolated, Ascoli's thermoprecipitation test is used to detect the heat-stable somatic antigen.