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An acute infectious zoonotic disease caused by the bacterium Bacillus anthracis and primarily associated with herbivorous mammals. Carnivorous mammals, birds, reptiles, amphibians, fish, and insects are generally resistant to anthrax infection. However, carnivorous and omnivorous mammals often succumb after ingestion of infected meat containing the anthrax toxins, which can cause swelling in the throat and suffocation. Humans primarily present with cutaneous lesions, appearing as black scabs or eschars, after contact with infected animals, carcasses, or animal products.Zoonoses

Anthrax is responsible for the deaths of thousands of domesticated and wild herbivorous animals annually. Parts of Africa, Asia, southern Europe, and North and South America are subject to repeated outbreaks. In the Western Hemisphere, anthrax is well controlled in livestock.

Bacillus anthracis is a gram-positive, rod-shaped, endospore-forming bacterium, approximately 1.0–1.2 micrometers in diameter and 3–8 μm long. The spores resist drying, cold, heat, and disinfectants, and can remain viable for many years in soil, water, and animal hides and products. Bacillus anthracis possesses three virulence factors: lethal toxin, edema toxin, and a poly-d-glutamic acid capsule. Lethal toxin is composed of two proteins, lethal factor and protective antigen. The protective antigen is produced by the anthrax bacillus at a molecular weight of 83 kDa, but must be cleaved by either serum or target cell surface proteases to 63 kDa before it complexes with lethal factor to form lethal toxin. The edema toxin is composed of edema factor and protective antigen, and it is believed to complex in a manner similar to that seen for lethal toxin. Protective antigen plays a central role in that it is required for transport of lethal factor and edema factor into host target cells. The macrophage appears to be the primary host target cell for lethal toxin, whereas the neutrophil appears to be the target cell for edema toxin in addition to other cells involved in edema formation. The third virulence factor is the capsule, which inhibits phagocytosis through its negatively charged poly-d-glutamic acid composition. All three toxin components are encoded by a plasmid, pXO1, whereas the enzymes required for capsule synthesis are encoded for by the pXO2 plasmid. Strains lacking either or both plasmids are avirulent, such as the veterinary vaccine Sterne strain, which lacks the pXO2 plasmid.

Anthrax consists of two clinical forms, cutaneous and septicemic. The cutaneous form begins as a blisterlike lesion that eventually becomes an intensely dark, relatively painless, edematous lesion forming a black eschar. The lesions rapidly become sterile after antibiotic therapy and take several weeks to resolve, even with treatment. The cutaneous form is reported only in humans, rabbits, swine, and horses.

The septicemic form arises from various initial sites of infection, including cutaneous, oropharyngeal, gastrointestinal, or inhalational exposures. The course of septicemic disease depends on the exposure route and the susceptibility of the animal host. The vast majority of systemic anthrax cases in herbivorus animals occur from trauma to mucosal linings of the mouth and upper alimentary canal caused by ingested fibrous foods. Inhalation anthrax is believed to be initiated by phagocytosis of spores within the lungs by alveolar macrophages. Spore-laden macrophages pass through lymphatic channels to the sinuses of regional lymph nodes or migrate to the spleen, where the spores germinate within the macrophages, multiply, and overwhelm and escape the macrophages to invade the efferent lymphatics. For other portals of entry, mesenteric lymph nodes become involved. The bacilli move to the spleen, where they induce pronounced splenomegaly (enlargement of the spleen), and finally enter the bloodstream, where they induce secondary sites of infection, massive bacillemia, toxemia, and sudden death. Failure of the blood to clot, hemorrhages of skin, hemorrhagic meningitis, and reduced rigor mortis are frequently found in anthrax-infected carcasses. Exposure of contaminated body fluids to the lower atmospheric levels of carbon dioxide results in sporulation of the bacilli. Therefore, opening of infected carcasses should be avoided.

Besides its central role for binding the lethal and edema toxins to target cells, protective antigen plays an important role in the host's  protective immune response against anthrax, hence the term protective antigen. Vaccines lacking protective antigen are not protective. For United States and United Kingdom human anthrax vaccines, protective antigen bound to aluminum salts is the principal immunogen. However, veterinary vaccines are composed of viable spores of B. anthracis Sterne strain, a nonencapsulated toxigenic variant. Full protection against anthrax with the veterinary vaccine is afforded by primary and annual booster vaccinations. Infectious disease Medical bacteriology

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From McGraw-Hill Concise Encyclopedia of Environmental Science. The Content is a copyrighted work of McGraw-Hill and McGraw-Hill reserves all rights in and to the Content. The Work is © 2008 by The McGraw-Hill Companies, Inc.
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