Bacillus anthracis (B. anthracis) is an aerobic, spore-forming, gram-positive bacterium[1]. The organism exists in two physical forms, the biologically active vegetative form and the biologically inert spore form. It is the vegetative form which is found in the tissue of infected individuals and is responsible for the pathology associated with the disease. As the animal succumbs to infection, the vegetative form converts into inert, resistant spores which provide a lifeboat for the organism until it is able to infect a new host. The relative resistance of B. anthracis spores to environmental conditions such as drought, heat, rain, cold, radiation and disinfectants is one of the reasons why this organism has been be explored as a potential biowarfare agent[2].
Humans generally acquire anthrax through contact with infected animals or from occupational or nutritional exposure to contaminated animal products such as meat, hair or skin[3, 4]. In humans, there are three main routes of anthrax infection: cutaneous, respiratory, and gastrointestinal. Cutaneous anthrax is the most common manifestation of human B. anthracis infection, representing >95% of cases[5]. Cutaneous anthrax, while potentially fatal, is often self-limiting when left untreated; Acute inhalation anthrax is usually diagnosed post-mortem fatal, with mediastinal widening described as a typical finding; Enteric anthrax, usually from the consumption of poorly cooked infected meat, is more likely to be lethal, although this is not easily evaluated.
B. anthracis is best distinguished from related species by its ability to synthesize the anthrax toxin proteins and the poly-d-glutamic acid capsule[6]. The major pathogenicity factors are coded by genes located on the virulence plasmids pXO1 and pXO2, respectively. The anthrax toxins consist of three synergistically acting proteins: protective antigen (PA), edema factor (EF), and lethal factor (LF). PA in combination with EF forms the edema toxin, and PA in combination with LF forms the lethal toxin. The role of PA is to transport LF and EF inside target cells, where they interact with essential cellular pathways. The toxins are responsible for the characteristic signs and clinical symptoms of the disease, whereas the poly-D-glutamic acid capsule protects the bacterium from phagocytosis[7].
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[2] Doganay M. Anthrax. Infectious Diseases. 4th ed[M]. The Netherlands: Elsevier; Amsterdam, 2017.
[3] Pilo P, Frey J. Pathogenicity, population genetics and dissemination of Bacillus anthracis[J]. Infect Genet Evol, 2018, 64: 115-125.
[4] Zasada A A. Detection and Identification of Bacillus anthracis: From Conventional to Molecular Microbiology Methods[J]. Microorganisms, 2020, 8(1): 125.
[5] Chateau A, Van der Verren S E, Remaut H, et al. The Bacillus anthracis Cell Envelope: Composition, Physiological Role, and Clinical Relevance[J]. Microorganisms, 2020, 8(12): 1864.
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[7] Zasada A A. Detection and Identification of Bacillus anthracis: From Conventional to Molecular Microbiology Methods[J]. Microorganisms, 2020, 8(1): 125.