Bacillus Anthracis
The bacteria Bacillus anthracis, the etiologic agent of Anthrax, is a large, gram positive, sporulating rod. Approximately 2-6 µm in length, this bacterium can be cultivated in ordinary nutrient medium under aerobic or anaerobic conditions. More commonly recognized by the name Anthrax, this bacterial pathogen is primarily a disease of domesticated and wild animals, particularly herbivorous animals, such as cattle, sheep, horses, mules, and goats. Humans become infected incidentally when brought into contact with diseased animals, which includes their flesh, bones, hides, hair and excrement. Recent bio-terrorism events in history dictate the necessity for a complete understanding of Anthrax and its infectious abilities. Unfortunately, the road to such discovery is long and arduous. The virulence of Anthrax depends on two factors: the bacterial capsule and the toxin complex. All virulent strains of B. anthracis form a single antigenic type of capsule consisting of a poly-D-glutamate polypeptide. The unusual poly-D-glutamyl acid capsule is itself nontoxic, but functions to protect the organism against the bactericidal components of serum and phagocytes and against phagocytic engulfment. Capsule production depends on a 60-m
Production of the Anthrax toxin is mediated by a temperature-sensitive plasmid, pX01, of 110 megadaltons. The toxin complex is then transported to the cytosol where edema toxin acts by converting adenosine triphosphate to cyclic adenosine monophosphate. Cellular cyclic adenosine monophosphate levels are increased, leading to the edema characteristic of disease. All RAW264.7 murine macrophages that were treated with high levels of toxin released large amounts of superoxide anion, in correlation with the onset of cytolysis. It was found that cytolysis could be blocked with various exogenous antioxidants or with N-acetyl-L-cysteine and methionine, which promote production of the endogenous antioxidant, glutathione, which in turn helps to reduce free-radical damage inside our cells. Mutant murine macrophage lines deficient in production of reactive oxygen intermediates (ROIs) were relatively insensitive to the lytic effects of the toxin, whereas a line with increased oxidative burst potential showed elevated sensitivity. Also, cultured blood monocyte-derived macrophages from a patient with Chronic Granulomatous Disease, a disorder in which the phagocyte's oxidative burst is disabled, were totally resistant to toxin, in contrast to control monocytes. While the exact mechanism of action of lethal factor is unknown, death is apparently due to oxygen depletion, secondary shock, increased vascular permeability, respiratory failure and cardiac failure. Death from Anthrax in humans or animals frequently occurs suddenly and unexpectedly. The level of the lethal toxin in the circulation increases rapidly quite late in the disease, and it closely parallels the concentration of organisms in the blood. It has been observed, however, that high levels of the toxin are cytolytic to macrophages, whereas low levels stimulate these cells to produce cytokines such as interleukin-1 beta (IL-1a) and tumor necrosis factor-alpha (TNF-a), which induce systemic s
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