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Bacillus anthracis is a Gram-positive, rod-shaped, spore-forming bacterium that serves as the etiologic agent of anthrax, a severe zoonotic disease. Its pathogenicity is primarily governed by two virulence plasmids: pXO1, which encodes the tripartite anthrax toxin (Protective Antigen, Lethal Factor, and Edema Factor), and pXO2, which encodes a poly-D-glutamic acid capsule that allows the pathogen to evade host phagocytosis. The bacterium is characterized by its ability to form highly resilient endospores that persist in the environment for decades and germinate into vegetative cells upon entering a mammalian host. Treatment typically requires long-term administration of antibiotics such as ciprofloxacin or doxycycline to inhibit bacterial replication and protein synthesis. In advanced cases, monoclonal antibodies like raxibacumab are used to neutralize the Protective Antigen, preventing the toxins from entering host cells. Due to the rapid progression of inhalational anthrax and the stability of its spores, B. anthracis is classified as a Tier 1 select agent and is a major focus of biodefense and public health research.
Antibiotics inhibit bacterial DNA synthesis by targeting DNA gyrase and topoisomerase IV (fluoroquinolones), or inhibit protein synthesis by binding to ribosomal subunits (tetracyclines); monoclonal antibodies and immune globulins neutralize the Protective Antigen (PA) to block host cell receptor binding and subsequent intracellular delivery of Lethal Factor and Edema Factor.
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