Yellow fever pathophysiology
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Yellow fever Microchapters |
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Yellow fever pathophysiology On the Web |
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Risk calculators and risk factors for Yellow fever pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology
Yellow fever is caused by an arbovirus of the family Flaviviridae, a positive single-stranded RNA virus. Human infection begins after deposition of viral particles through the skin in infected arthropod saliva. The mosquitos involved are Aedes simpsaloni, A. africanus, and A. aegypti in Africa, the Haemagogus genus in South America, and the Sasbethes genera in France. Yellow fever is frequently severe but more moderate cases may occur as the result of previous infection by another flavivirus. After infection the virus first replicates locally, followed by transportation to the rest of the body via the lymphatic system.Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed. ed.). McGraw Hill. ISBN 0-8385-8529-9. Following systemic lymphatic infection the virus proceeds to establish itself throughout organ systems, including the heart, kidneys, adrenal glands, and the parenchyma of the liver; high viral loads are also present in the blood. Necrotic masses (Councilman bodies) appear in the cytoplasm of hepatocytes.,[1] There is a difference between disease outbreaks in rural or forest areas and in towns. Disease outbreaks in towns and non-native people are usually more serious.
References
- ↑ Quaresma JA, Barros VL, Pagliari C, Fernandes ER, Guedes F, Takakura CF, Andrade HF Jr, Vasconcelos PF, Duarte MI (2006). "Revisiting the liver in human yellow fever: virus-induced apoptosis in hepatocytes associated with TGF-beta, TNF-alpha and NK cells activity". Virology. 345 (1): 22–30. PMID 16278000.