Anthrax causes: Difference between revisions
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==Tropism== | ==Tropism== | ||
After entering the body (through the [[skin]], [[lungs]], [[gastrointestinal tract]] or by [[injection]]) [[B. anthracis]] [[spores]] are believed to germinate locally or be transported by [[phagocytic cells]] to the [[lymphatics]] and regional [[lymph nodes]], where they germinate.<ref name=CDC>{{cite web | title = Centers for Disease Control and Prevention Expert Panel Meetings on Prevention and Treatment of Anthrax in Adults | url = http://wwwnc.cdc.gov/eid/article/20/2/13-0687_article }}</ref><ref name="Ross1957">{{cite journal|last1=Ross|first1=Joan M.|title=The pathogenesis of anthrax following the administration of spores by the respiratory route|journal=The Journal of Pathology and Bacteriology|volume=73|issue=2|year=1957|pages=485–494|issn=0368-3494|doi=10.1002/path.1700730219}}</ref> Protective [[antigen]] (PA) and [[edema]] factor (EF) combine to form [[edema]] toxin (ET) and PA and lethal factor (LF) combine to form lethal toxin (LT). After binding to cell surface receptors, the PA portion of the complexes facilitates translocation of the [[toxins]] to the [[cytosol]] | After entering the body (through the [[skin]], [[lungs]], [[gastrointestinal tract]] or by [[injection]]) [[B. anthracis]] [[spores]] are believed to germinate locally or be transported by [[phagocytic cells]] to the [[lymphatics]] and regional [[lymph nodes]], where they germinate.<ref name=CDC>{{cite web | title = Centers for Disease Control and Prevention Expert Panel Meetings on Prevention and Treatment of Anthrax in Adults | url = http://wwwnc.cdc.gov/eid/article/20/2/13-0687_article }}</ref><ref name="Ross1957">{{cite journal|last1=Ross|first1=Joan M.|title=The pathogenesis of anthrax following the administration of spores by the respiratory route|journal=The Journal of Pathology and Bacteriology|volume=73|issue=2|year=1957|pages=485–494|issn=0368-3494|doi=10.1002/path.1700730219}}</ref> Protective [[antigen]] (PA) and [[edema]] factor (EF) combine to form [[edema]] toxin (ET) and PA and lethal factor (LF) combine to form lethal toxin (LT). After binding to cell surface receptors, the PA portion of the complexes facilitates translocation of the [[toxins]] to the [[cytosol]].<ref name="Moayeri2004">{{cite journal|last1=Moayeri|first1=M|title=The roles of anthrax toxin in pathogenesis|journal=Current Opinion in Microbiology|volume=7|issue=1|year=2004|pages=19–24|issn=13695274|doi=10.1016/j.mib.2003.12.001}}</ref><ref name=CDC>{{cite web | title = Centers for Disease Control and Prevention Expert Panel Meetings on Prevention and Treatment of Anthrax in Adults | url = http://wwwnc.cdc.gov/eid/article/20/2/13-0687_article }}</ref> | ||
==Natural Reservoir== | ==Natural Reservoir== |
Revision as of 14:02, 18 July 2014
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]
Overview
The causative agent of anthrax is B. anthracis, a nonmotile, Gram-positive, aerobic or facultatively anaerobic, endospore-forming, rod-shaped bacterium. The spores of B. anthracis, which can remain dormant in the environment for decades, are the infectious form, but vegetative B. anthracis rarely causes disease.[1] The Bacillus may enter the body through the skin, lungs, gastrointestinal system or by injection, after which it will travel to the lympathics and regional lymph nodes. There the virulence factors will facilitate the translocation of the toxins to the cytosol. The natural reservoirs of Bacillus anthracis includes humans, mammals, herbivores, reptiles, and birds.
Taxonomy
Bacteria; Archaebacteria; Firmicutes; Bacilli; Bacillales; Bacillaceae; Bacillus; anthracis; Bacillus anthracis
Biology
B. anthracis, the causative agent of anthrax, is a nonmotile, Gram-positive, aerobic or facultatively anaerobic, endospore-forming, rod-shaped bacterium approximately 4 μm by 1 μm, although under the microscope it frequently appears in chains of cells. Like other Bacillus, Bacillus anthracis is saprophyte, being able to live in vegetations, air, water and soil.[4]
These bacterial cells may occur isolated, form groups of 2 or more cells in the body, or long chains in cultures.[4] In blood smears, smears of tissues or lesion fluid from diagnostic specimens, these chains are two to a few cells in length. In smears made from in vitro cultures, they can appear as endless strings of cells - responsible for the characteristic tackiness of the colonies and for the flocculating nature of broth cultures. Cell cultures appear as a large, grey and curled structure, resembling a "medusa head".[4]
B. anthracis have a characteristic square-ended appearance, traditionally associated with its vegetative state, although this may not always be very clear. In the presence of oxygen, mostly at 32 - 35 ºC, and towards the end of the exponential phase of growth, one ellipsoidal spore (approximately 2 μm by 1 μm in size) is formed in each cell.[5][4] The spores of B. anthracis, which can remain dormant in the environment for decades, being resistant to heat and disinfectants, are the infectious form, but vegetative B. anthracis rarely causes disease.[6][4]
In the absence of oxygen and under a high partial pressure of Co2, in the presence of bicarbonate, the vegetative cell secretes its polypeptide capsule, and it is one of the two established in vivo virulence factors of B. anthracis. The capsule is also a primary diagnostic aid.[5] Protective antigen (PA) and edema factor (EF) combine to form edema toxin (ET) and PA and lethal factor (LF) combine to form lethal toxin (LT).[7][8]
Origin
Anthrax is thought to have originated in Egypt and Mesopotamia. Many scholars think that in Moses’ time, during the 10 plagues of Egypt, anthrax may have caused what was known as the fifth plague, described as a sickness affecting horses, cattle, sheep, camels and oxen.
Tropism
After entering the body (through the skin, lungs, gastrointestinal tract or by injection) B. anthracis spores are believed to germinate locally or be transported by phagocytic cells to the lymphatics and regional lymph nodes, where they germinate.[8][9] Protective antigen (PA) and edema factor (EF) combine to form edema toxin (ET) and PA and lethal factor (LF) combine to form lethal toxin (LT). After binding to cell surface receptors, the PA portion of the complexes facilitates translocation of the toxins to the cytosol.[10][8]
Natural Reservoir
Natural reservoirs of Bacillus anthracis includes:[5][4][8]
- Humans
- Mammals
- Herbivores
- Reptiles
- Birds
References
- ↑ Sean V. Shadomy & Theresa L. Smith (2008). "Zoonosis update. Anthrax". Journal of the American Veterinary Medical Association. 233 (1): 63–72. doi:10.2460/javma.233.1.63. PMID 18593313. Unknown parameter
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ignored (help) - ↑ "http://phil.cdc.gov/phil/details.asp". External link in
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(help) - ↑ "http://phil.cdc.gov/phil/details.asp". External link in
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(help) - ↑ 4.0 4.1 4.2 4.3 4.4 4.5 Bhatnagar, Rakesh; Batra, Smriti (2001). "Anthrax Toxin". Critical Reviews in Microbiology. 27 (3): 167–200. doi:10.1080/20014091096738. ISSN 1040-841X.
- ↑ 5.0 5.1 5.2 "Anthrax in Humans and Animals" (PDF).
- ↑ Sean V. Shadomy & Theresa L. Smith (2008). "Zoonosis update. Anthrax". Journal of the American Veterinary Medical Association. 233 (1): 63–72. doi:10.2460/javma.233.1.63. PMID 18593313. Unknown parameter
|month=
ignored (help) - ↑ Mahtab Moayeri & Stephen H. Leppla (2004). "The roles of anthrax toxin in pathogenesis". Current opinion in microbiology. 7 (1): 19–24. doi:10.1016/j.mib.2003.12.001. PMID 15036135. Unknown parameter
|month=
ignored (help) - ↑ 8.0 8.1 8.2 8.3 "Centers for Disease Control and Prevention Expert Panel Meetings on Prevention and Treatment of Anthrax in Adults".
- ↑ Ross, Joan M. (1957). "The pathogenesis of anthrax following the administration of spores by the respiratory route". The Journal of Pathology and Bacteriology. 73 (2): 485–494. doi:10.1002/path.1700730219. ISSN 0368-3494.
- ↑ Moayeri, M (2004). "The roles of anthrax toxin in pathogenesis". Current Opinion in Microbiology. 7 (1): 19–24. doi:10.1016/j.mib.2003.12.001. ISSN 1369-5274.