Bacillus anthracis

Bacillus anthracis

Organism

Bacillus anthracis is a large gram-positive, endospore-producing bacillus. In clinical specimans it typically appears singly or in pairs; in culture it appears as a streptobacillus.
While endospores appear in culture, they are not seen in clinical specimans.
A facultative anaerobe (def).

Habitat

B. anthracis primarily infects herbivores.

Source

Contact with infected animals, animal materials, infected soil, or B. anthracis endospores used as a bioweapon.

Epidemiology

B. anthracis primarily infects herbivores (def); humans are usually accidental hosts.
Rare in developed countries but more prevalent in underdeveloped countries where animals are vaccinated against anthrax.
There are three forms of anthrax: cutaneous, inhalation, and gastrointestinal. Around 95% of human anthax infections in nature are the cutaneous form as a result of B. anthracis endospores entering exposed skin.

Clinical Disease

Cutaneous anthrax first appears as a painless papule (def) at the site of infection and rapidly progresses to an ulcer (def) surrounded by vesicles (def) and finally a necrotic eschar (def). The mortality rate from untreated cutaneous anthrax is approximately 20%.
Inhalation anthrax may initially have an asymptomatic latent period of two months or more. Typically, alveolar macrophages (def) engulf the inhaled endospores of B. anthracis and transport them to the mediastinal lymph nodes (def) where they can germinate. Initial symptoms are nonspecific and include coughing, headache, fever, chills, vomiting, and chest and abdominal pain. This rapidly worsens and presents as worsening fever, edema, and massive enlargement if the mediastinum (def). About half of infected individuals have symptoms of meningitis (def). Almost all cases progress to shock (def) and death within about three days of the initial symptoms. This is the most deadly form of anthrax.
Gastrointestinal anthrax as a result of ingestion of B. anthracis can appear two ways: ulceration of the mouth and esophagus (def) followed by localized lymphadenopathy (def), edema (def), and sepsis (def) if the bacterium invades the upper intestinal tract; and nausea, vomiting, and malaise (def) rapidly progressing to sepsis if the bacterium invades the large intestines. Commonly fatal.

Pathogenicity

Bacillus anthracis produces three toxins: two different A-components known as lethal factor (LF) and edema factor (EF), both of which can share a common B-component known as protective antigen (PA). Protective antigen, the B-component, first binds to receptors on host cells and is cleaved by a protease creating a binding site for either lethal factor or edema factor.
Lethal factor is a protease that inhibits mitogen-activated kinase-kinase. At low levels, LF inhibits the release of proinflammatory cytokines such as interleukin-1 (IL-1), tumor necrosis factor-alpha, (TNF-alpha), and NO. This may initially reduce immune responses against the organism and its toxins. But at high levels, LF is cytolytic for macrophages, causing release of high levels of interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-alpha), and NO. Excessive release of these cytokines can lead to a massive inflammatory response and the shock cascade, similar to septic shock.
Edema factor is an adenylate cyclase that generates cyclic AMP in host cells, impairs phagocytosis, and inhibits production of TNF and interleukin-6 (IL-6) by monocytes. This most likely impairs host defenses and is responsible for the fluid accumulation seen in anthrax.
A polypeptide capsule blocks phagocytosis.
Endospores enable the bacterium to survive indefinitely in soils and other environments.

Treatment

Ciprofloxacin the antibiotic of choice; doxycline, penicillin, and erythromycin can be used on susceptible strains* (see antibiotic table)
Prevention of anthax in animals is achieved through active immunization (def) with protective antigen (PA). This stimulates the body to make neutralizing antibodies against the binding component used by both lethal factor (LF) and edema factor (EF). Once the antibody binds to the PA, the toxins can no longer bind to the receptors on the host cell membrane.

*Drugs may change with time.

For a more detailed article on anthrax, see Anthrax, by Burke A Cunha, MD, Professor of Medicine, State University of New York at Stony Brook School of Medicine; Chief, Infectious Disease Division, Vice-Chair, Department of Internal Medicine, Winthrop-University Hospital.