Anthrax
Abstract
Anthrax is a virulent, contagious, and potentially fatal disease. The first accounts of anthrax infection were written by the Roman poet Vergil in early antiquity. While its lethal effects were ascribed to the actions of an exotoxin over a half century ago, the pathogenesis and mechanism of anthrax toxicity continue to be refined. Depending on the route of exposure, anthrax can cause a different disease, including inhalational, cutaneous, and oral/ingestional forms. Anthrax infection involves a complex set of steps in its pathogenesis from spore uptake by immune cells, germination, transport to local lymph nodes, production of deadly toxins, systemic spread, and ultimately death of the host. The details of each step are continually being debated. Even today debate ensues regarding the mechanisms of macrophage killing by the toxins and the importance of other cell types involved in toxin-induced fatality. While anthrax infection causes high numbers of bacilli and overt septicemia, it is the exotoxins which are responsible for the intoxicating symptoms and death. Birth of the molecular age in modem research led to the identification and enzymatic characterization of three proteins that constitute two anthrax exotoxins. These are the protective antigen (PA), edema factor (EF), and lethal factor (LF). A better understanding of the precise mechanisms of toxicity initiated by anthrax toxins will uncover many of the unsolved mysteries surrounding Bacillus anthracis infection. Moreover, nature's clever engineering will be evident from the sometimes contradictory actions of the spore form, vegetative bacilli, and bacterial toxins.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jan 01, 2009
- Accession Number
- ADA539687
Entities
People
- Alexandre M. Katos
- Corey J. Hilmas
- Jaime Anderson
- Patrick T. Williams
Organizations
- United States Army Medical Research Institute of Chemical Defense