Bacillus anthracis is the pathogen of the anthrax acute disease. It is a Gram-positive, spore-forming, rod-shaped bacterium, with a width of 1-1.2µm and a length of 3-5µm. It can be grown in an ordinary nutrient medium under aerobic or anaerobic conditions.
It is one of few bacteria known to synthesize a protein capsule (D-glutamate). Like Bordetella pertussis, it forms a calmodulin-dependent adenylate cyclase exotoxin known as (edema factor), along with lethal factor. It bears close genotypical and phenotypical resemblance to Bacillus cereus and Bacillus thuringiensis. All three species share cellular dimensions and morphology. All form oval spores located centrally in an unswollen sporangium. Bacillus anthracis spores in particular are highly resilient, surviving extremes of temperature, low-nutrient environments, and harsh chemical treatment over decades or centuries.
Casimir Davaine demonstrated the symptoms of anthrax were invariably accompanied by the microbe B. anthracis. Aloys Pollender is also credited for this discovery. B. anthracis was the first bacterium conclusively demonstrated to cause disease, by Robert Koch in 1876. The species name anthracis is from the Greek anthrakis (ἄνθραξ), meaning "coal" and referring to the most common form of the disease, cutaneous anthrax, in which large, black skin lesions are formed.
Three forms of anthrax disease are recognized based on their form of inoculation.
- Cutaneous, the most common form (95%), causes a localized, inflammatory, black, necrotic lesion (eschar).
- Pulmonary, the highly fatal form, is characterized by sudden, massive chest edema followed by cardiovascular shock.
- Gastrointestinal, a rare but also fatal (causes death to 25%) type, results from ingestion of spores.
Infections with B. anthracis can be treated with β-lactam antibiotics such as penicillin, and others which are active against Gram-positive bacteria. Penicillin-resistant B. anthracis can be treated with fluoroquinolones such as ciprofloxacin or tetracycline antibiotics such as doxycycline.
Components of tea, such as polyphenols, have the ability to inhibit the activity both of Bacillus anthracis and its toxin considerably; spores, however, are not affected. The addition of milk to the tea completely inhibits its antibacterial activity against anthrax. Activity against the B. athracis in the laboratory does not prove that drinking tea affects the course of an infection, since it is unknown how these polyphenols are absorbed and distributed within the body.
As with most other pathogenic bacteria, B. anthracis must acquire iron to grow and proliferate in its host environment. The most readily available iron sources for pathogenic bacteria are the heme groups used by the host in the transport of oxygen. To scavenge heme from host hemoglobin and myoglobin, B. anthracis uses two secretory siderophore proteins, IsdX1 and IsdX2. These proteins can separate heme from hemoglobin, allowing surface proteins of B. anthracis to transport it into the cell.
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- ^ Koch, R. (1876) "Untersuchungen über Bakterien: V. Die Ätiologie der Milzbrand-Krankheit, begründet auf die Entwicklungsgeschichte des Bacillus anthracis" (Investigations into bacteria: V. The etiology of anthrax, based on the ontogenesis of Bacillus anthracis), Cohns Beitrage zur Biologie der Pflanzen, vol. 2, no. 2, pages 277-310.
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- ^ "Anthrax and tea". Society for Applied Microbiology. 2011-12-21. http://web.archive.org/web/20090213231226/http://www.sfam.org.uk/newsarticle.php?214&2. Retrieved 2011-12-21.
- ^ Maresso AW, Garufi G, Schneewind O (2008). "Bacillus anthracis Secretes Proteins That Mediate Heme Acquisition from Hemoglobin". PLOS Pathogens 4(8): e1000132.