Anthrax causes: Difference between revisions
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==Biology== | ==Biology== | ||
[[Image:Anthrax - inhalational.jpg|thumb|left|250px|Inhalational anthrax - [[mediastinum|Mediastinal]] widening]] | |||
''Bacillus anthracis'' is a rod-shaped [[Gram-positive]] bacterium, about 1 by 9 micrometers in size. It was shown to cause disease by [[Robert Koch]] in 1877. [http://german.about.com/library/blerf_koch.htm] The bacterium normally rests in [[endospore]] form in the soil, and can survive for decades in this state. Once ingested by a ruminant or placed in an open cut, the bacterium begins multiplying inside the animal or human and in a few days to a month kills it. Veterinarians can often tell a possible anthrax induced death by its sudden occurrence and by the blood and bloody fluids that oozed from the body orifices. Most anthrax bacteria inside the body are destroyed by anaerobic bacteria that can grow without oxygen. The greater danger lies in the bodily fluids and blood that spills from the body and spill into the soil where the anthrax bacteria turn into a dormant protective spore form. Once formed the spores are very hard to eradicate. | |||
The infection of ruminants (and occasionally humans) normally proceeds as follows: once the spores are inhaled they are transported through the air passages into the tiny air sacs (alveoli) in the lungs. The spores are then picked up by scavenger cells (macrophages) in the lungs and are transported through small vessels (lymphatics) to the glands (lymph nodes) in the central chest cavity (mediastinum). Damage caused by the anthrax spores and bacilli to the central chest cavity lungs can cause chest pain and difficulty breathing. Once in the lymph glands, the spores germinate into active bacillus, that multiplies, and eventually bursts the macrophage cell, releasing many more bacilli into the bloodstream which are transferred to the entire body. Once in the blood stream these bacilli release a tripartite toxin (composed of lethal factor, edema factor and protective antigen) which is known to be the primary agents of tissue destruction, bleeding, and death. If antibiotics are given too late, even if the antibiotics eradicate the bacteria, some people still will die because the toxins produced by the bacilli still remain in their system at lethal dose levels. | |||
In order to enter the cells, the toxins use another protein produced by ''B. anthracis'', protective antigen. Edema factor inactivates [[neutrophil]]s (a type of phagocytic cell) so that they cannot phagocytose bacteria. Historically, it was believed that lethal factor caused macrophages to make [[TNF-alpha]] and [[IL1B|interleukin 1, beta]] (IL1B), both normal components of the immune system used to induce an inflammatory reaction, ultimately leading to [[septic shock]] and death. However, recent evidence indicates that anthrax also targets endothelial cells (cells that lines serous cavities, lymph vessels, and blood vessels), causing vascular leakage (similar to hemorrhagic bleeding), and ultimately [[hypovolemic shock]] (low blood volume), and not only septic shock. In other words the patient bleeds to death internally. | |||
The virulence of a strain of anthrax is dependent on multiple factors, primarily the poly-D-glutamic acid capsule that protects the bacterium from phagocytosis by host neutrophils and its [[anthrax toxin|toxins]], edema toxin and lethal toxin. | |||
==Origin== | ==Origin== | ||
Revision as of 18:05, 16 July 2014
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Taxonomy
Bacteria; Archaebacteria; Firmicutes; Bacilli; Bacillales; Bacillaceae; Bacillus; anthracis; Bacillus anthracis
Biology
Bacillus anthracis is a rod-shaped Gram-positive bacterium, about 1 by 9 micrometers in size. It was shown to cause disease by Robert Koch in 1877. [2] The bacterium normally rests in endospore form in the soil, and can survive for decades in this state. Once ingested by a ruminant or placed in an open cut, the bacterium begins multiplying inside the animal or human and in a few days to a month kills it. Veterinarians can often tell a possible anthrax induced death by its sudden occurrence and by the blood and bloody fluids that oozed from the body orifices. Most anthrax bacteria inside the body are destroyed by anaerobic bacteria that can grow without oxygen. The greater danger lies in the bodily fluids and blood that spills from the body and spill into the soil where the anthrax bacteria turn into a dormant protective spore form. Once formed the spores are very hard to eradicate.
The infection of ruminants (and occasionally humans) normally proceeds as follows: once the spores are inhaled they are transported through the air passages into the tiny air sacs (alveoli) in the lungs. The spores are then picked up by scavenger cells (macrophages) in the lungs and are transported through small vessels (lymphatics) to the glands (lymph nodes) in the central chest cavity (mediastinum). Damage caused by the anthrax spores and bacilli to the central chest cavity lungs can cause chest pain and difficulty breathing. Once in the lymph glands, the spores germinate into active bacillus, that multiplies, and eventually bursts the macrophage cell, releasing many more bacilli into the bloodstream which are transferred to the entire body. Once in the blood stream these bacilli release a tripartite toxin (composed of lethal factor, edema factor and protective antigen) which is known to be the primary agents of tissue destruction, bleeding, and death. If antibiotics are given too late, even if the antibiotics eradicate the bacteria, some people still will die because the toxins produced by the bacilli still remain in their system at lethal dose levels.
In order to enter the cells, the toxins use another protein produced by B. anthracis, protective antigen. Edema factor inactivates neutrophils (a type of phagocytic cell) so that they cannot phagocytose bacteria. Historically, it was believed that lethal factor caused macrophages to make TNF-alpha and interleukin 1, beta (IL1B), both normal components of the immune system used to induce an inflammatory reaction, ultimately leading to septic shock and death. However, recent evidence indicates that anthrax also targets endothelial cells (cells that lines serous cavities, lymph vessels, and blood vessels), causing vascular leakage (similar to hemorrhagic bleeding), and ultimately hypovolemic shock (low blood volume), and not only septic shock. In other words the patient bleeds to death internally.
The virulence of a strain of anthrax is dependent on multiple factors, primarily the poly-D-glutamic acid capsule that protects the bacterium from phagocytosis by host neutrophils and its toxins, edema toxin and lethal toxin.