Pathogenesis of Anthrax

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There are two main factors that are important for an anthrax infection: bacterial proliferation (growth) and invasion of organ systems and the “…cytotoxic effect of anthrax toxin, with eventual organ failure and death” (Karginov). The first factor occurs once the host has been infected. This infection will never be reached if it were not for a very important characteristic of the bacterium: its ability to form spores. Sporulation occurs in the soil and on culture media but “…not in living tissue, unless exposed to air” (Sakarya). These spores are formed by B. anthracis in soil when the environment becomes inhospitable to growth due to a variety of factors including drought, excessive heat, lack of nutrients, or presence of harsh chemicals. The formation of a spore begins when a bacterium replicates its chromosome and places it within a hard shell. Once the outer cell wall dissolves, the endospore (“inner spore”) is released. This spore can lie dormant in its environment for a long period of time and survive many harsh conditions. Once the environment is favorable for growth, “…the spore will rehydrate to form a vegetative bacterium” (Campbell). Endospores are highly resistant to UV light, temperature extremes, high pH, drying, high salinity (salt) levels, different types of disinfection, and even time. An experiment conducted at Iowa State University in 1978, “…showed that a 50-year old vial of anthrax spores could still give rise to live bacteria” (Boyer). The two main methods for killing spores are incineration and high-pressure steam. The temperature required by these methods that will result in spore death is 240?F. Most laboratories and hospitals use similar conditions to sterilize instruments in an autoclave. Without the help of these spores, the chance for infection by B. anthracis would decrease dramatically. Once a host is infected by the spores and germinates, production of a capsule and three toxin proteins takes place. This leads to an important factor of anthrax infection involving the three toxin proteins: protective antigen (PA), edema factor (EF) and lethal factor (LF). To produce “…active toxins, PA must bind to cellular receptors and then to either EF or LF”(Joellenbeck). Binding of the protective antigen to either of the other two toxin proteins will form “…complexes which penetrate the patient’s cells to cause massive cell swelling and rapid cardiovascular collapse” (Hersack). These complexes will contribute to causing the disease. The edema toxin forms edema, which might “increase host susceptibility to infection with B.

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