Bacillus Anthracis and Anthrax Infection

Bacillus Anthracis and Anthrax Infection
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What does anthrax look like?


In 1877, microbiologist Robert Koch first isolated the bacterium that causes anthrax in animals. The rod-shaped bacterium is quite large, gram-positive, aerobic, and endospore-forming. It usually thrives in the soil and could survive in dormancy for centuries. (At least 60 years have been observed experimentally). The reason behind its amazing survival is its ability to produce endospores prior to its death by desiccation or starvation. Endospores are durable, circular structures that contain the bacterial DNA and few organelles; these structures are the “resting cells” and will germinate to ordinary vegetative cells in the presence of water and nutrients needed for bacterial growth. (Read more about endospores here ). The bacterium that causes anthrax was eventually called Bacillus anthracis. Ruminants that ingest the endospores of the bacterium are infected and die within a few days because of fatal sepsis (Madigan 2006; Talaro 2008).

Anthrax Infection Risks

People who handle animals, wool, hides, and other imported animal products are at high risk of contracting anthrax. The endospores of B. anthracis attach to these animal products, where they are able to be transferred to people who used the products. Imported goat hair and handicrafts from the Middle East are repeated sources of infection in the U.S. (Ingraham 2002).

Anthrax Infection Pathology

B. anthracis infections are initiated by endospores. Immediately after introduction to the body, they are phagocytosed by macrophages but are not killed. Instead they start to multiply inside and eventually kill the macrophages through the lethal toxins they secrete. The bacterium produces two kinds of exotoxins: the edema toxin and the lethal toxin. Both of the exotoxins have a third toxic component, a cell-receptor-binding protein called the protective antigen; this toxin helps in binding the exotoxin to target cells of the host. The edema toxin causes local swelling (edema) and hinders the macrophages’ phagocytosis. The lethal toxin particularly targets and destroys macrophages, which halts an important defense mechanism of the host. What is very unusual with B. anthracis is the composition of its cell wall. Unlike other bacterial cell walls, which are composed of polysaccharide, the B. anthracis cell wall is composed of amino acid residues, which do not stimulate a defense mechanism of the host’s immune system. In the absence of an effective defense mechanism, the bacteria multiply exponentially in the bloodstream without any impediment. Bacterial count in the blood could reach tens of millions per milliliter! Calculate how many of them in a liter of blood! The large amount of toxins produced is enough to kill the patient by inducing septic shock (Madigan 2006; Talaro 2008).

Anthrax Infection References

  • Madigan, Michael. 2006. Brock Biology of Microorganisms. Upper Saddle River, N.J. : Prentice Hall/Pearson Education.
  • Talaro, Kathleen. 2008_. Foundations in microbiology: basic principles_. Boston: McGraw-Hill Higher Education.
  • Ingraham, John. 2002. Introduction to Microbiology. Pacific Grove, Calif.: Brooks/Cole Pub.
  • Photo from Wikipedia