Anthrax pathophysiology
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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
Genetics
Transmission
The route by which anthrax is transmitted allows for its classification, it includes:[1]
- Cutaneous anthrax - commonly requires a prior skin lesion as a prerequisite for infection
- Gastrointestinal anthrax - contracted following ingestion of contaminated food, primarily meat from an animal that died of the disease, or conceivably from ingestion of contaminated water
- Inhalational anthrax - from breathing in airborne anthrax spores
- Injection anthrax - from injection of a drug containing, or contaminated with Bacillus anthracis
Pathogenesis
B. anthracis, the causative agent of anthrax, is a spore-forming 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.[2] The bacterium causes disease through 2 mechanisms: toxemia and bacterial infection.[3] Spores introduced through the skin lead to cutaneous or injection anthrax; those introduced through the gastrointestinal tract lead to gastrointestinal anthrax; and those introduced through the lungs lead to inhalation anthrax. After entering a human or animal, B. anthracis spores are believed to germinate locally or be transported by phagocytic cells to the lymphatics and regional lymph nodes, where they germinate; or both.[4] B. anthracis begins producing toxins within hours of germination.[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). After binding to surface receptors, the PA portion of the complexes facilitates translocation of the toxins to the cytosol, in which EF and LF exert their toxic effects.[6]
Gross Pathology
Inhalation Anthrax
Gross pathologic lesions observed in non-human primates used in aerosol challenge models of inhalation anthrax include edema, congestion, hemorrhage and necrosis in the lungs and mediastinum. Splenitis and necrotizing or hemorrhagic lymphadenitis involving the mediastinal, tracheobronchial, and other lymph nodes are common.[7] Primary pulmonary lesions, including those of pneumonia, are occasionally observed. Meningeal involvement ranging from edema, congestion, hemorrhage, and necrosis to suppurative or hemorrhagic meningitis, usually secondary to hematogenous spread from other types of anthrax, occurs in ≤77% of animals studied.[8] Autopsy findings for persons who died from inhalation anthrax in Sverdlovsk and in the United States[9] are consistent with findings from the non-human primates studies. Persons who died had extensive amounts of serosanguinous fluid in pleural cavities and edema and hemorrhage of the mediastinum and surrounding soft tissues, and 48% had cerebral edema, 21% had ascites, 17% had pericardial effusions, and 14% had petechial rash. Mediastinal lymph nodes and spleen also showed hemorrhage and necrosis.[7][10]
Cutaneous Anthrax
Anthrax eschars are generally seen on exposed unprotected regions of the body, mostly on the face, neck, hands and wrists. Generally cutaneous lesions are single, but sometimes two or more lesions are present.
Microscopic Pathology
References
- ↑ "Anthrax in Humans and Animals" (PDF).
- ↑ Shadomy, Sean V.; Smith, Theresa L. (2008). "Anthrax". Journal of the American Veterinary Medical Association. 233 (1): 63–72. doi:10.2460/javma.233.1.63. ISSN 0003-1488.
- ↑ Liu, Shihui; Moayeri, Mahtab; Leppla, Stephen H. (2014). "Anthrax lethal and edema toxins in anthrax pathogenesis". Trends in Microbiology. 22 (6): 317–325. doi:10.1016/j.tim.2014.02.012. ISSN 0966-842X.
- ↑ 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.
- ↑ Hanna, Philip C.; Ireland, John A.W. (1999). "Understanding Bacillus anthracis pathogenesis". Trends in Microbiology. 7 (5): 180–182. doi:10.1016/S0966-842X(99)01507-3. ISSN 0966-842X.
- ↑ 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.
- ↑ 7.0 7.1 Guarner, Jeannette; Jernigan, John A.; Shieh, Wun-Ju; Tatti, Kathleen; Flannagan, Lisa M.; Stephens, David S.; Popovic, Tanja; Ashford, David A.; Perkins, Bradley A.; Zaki, Sherif R. (2003). "Pathology and Pathogenesis of Bioterrorism-Related Inhalational Anthrax". The American Journal of Pathology. 163 (2): 701–709. doi:10.1016/S0002-9440(10)63697-8. ISSN 0002-9440.
- ↑ Twenhafel, N. A. (2010). "Pathology of Inhalational Anthrax Animal Models". Veterinary Pathology. 47 (5): 819–830. doi:10.1177/0300985810378112. ISSN 0300-9858.
- ↑ A. A. Abramova & L. M. Grinberg (1993). "[Pathology of anthrax sepsis according to materials of the infectious outbreak in 1979 in Sverdlovsk (macroscopic changes)]". Arkhiv patologii. 55 (1): 12–17. PMID 7980032. Unknown parameter
|month=ignored (help) - ↑ A. A. Abramova & L. M. Grinberg (1993). "[Pathology of anthrax sepsis according to materials of the infectious outbreak in 1979 in Sverdlovsk (macroscopic changes)]". Arkhiv patologii. 55 (1): 12–17. PMID 7980032. Unknown parameter
|month=ignored (help)