West nile
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
History and Symptoms
West Nile Fever is caused by Flavivirus . Birds are the natural reservoir of the virus and the virus is most commony is trasmitted by mosquitoes. It is transmitted by many types of mosquitoes especially Culex mosquitoes. They carry the highest amount of risk of transmission in early fall and so the rate of disease is highest in late August to early September. After that the rate decreases as the mosquitoes cannot tolerate the cold. [1] It is also foundn in horses and vaccines are avaliable for the disease in horses but not for human beings. 80 % of the people infected with West Nile Virus are not aware that they ar infected as it can be asymptomatic. has three different effects on humans. The first is an asymptomatic infection; the second is a mild febrile syndrome termed West Nile Fever;[2] the third is a neuroinvasive disease termed West Nile meningitis or encephalitis.[3] In infected individuals the ratio between the three states is roughly 110:30:1.[4]
The second, febrile stage has an incubation period of 3-8 days followed by fever, headache, chills, diaphoresis, weakness, lymphadenopathy, and drowsiness. Occasionally there is a short-lived truncal rash and some patients experience gastrointestinal symptoms including nausea, vomiting, loss of appetite, or diarrhea. All symptoms are resolved within 7-10 days, although fatigue can last for some weeks and lymphadenopathy can take up to two months to resolve.
The more dangerous encephalitis is characterized by similar early symptoms but also a decreased level of consciousness, sometimes approaching near-coma. Deep tendon reflexes are hyperactive at first, later diminished. There are also extrapyramidal disorders. Recovery is marked by a long convalescence with fatigue.
More recent outbreaks have resulted in a deeper study of the disease and other, rarer, outcomes have been identified.The spinal cord may be infected, marked by anterior myelitis with or without encephalitis.[5] WNV-associated Guillain-Barré syndrome has been identified[6] and other rare effects include multifocal chorioretinitis (which has 100% specificity for identifying WNV infection in patients with possible WNV encephalitis)[7] hepatitis, myocarditis, nephritis, pancreatitis, and splenomegaly.[8][9][10]
References
- ↑ Kantrowitz ER, Lipscomb WN (1976). "An essential residue at the active site of aspartate transcarbamylase". J Biol Chem. 251 (9): 2688–95. PMID PMH0004457 Check
|pmid=value (help). - ↑ Olejnik E. "Infectious adenitis transmitted by Culex molestus." Bull. Res. Counc. Isr. 1952; 2: 210-211.
- ↑ Smithburn K C, Jacobs H R. "Neutralization-tests against neurotropic viruses with sera collected in central Africa." Journal of Immunology 1942; 44: 923.
- ↑ Tsai T F, Popovici F, Cernescu C, Campbell G L, Nedelcu N I. "West Nile encephalitis epidemic in south eastern Romania." Lancet 1998; 352: 767-771
- ↑ Sejvar J J, Haddad M B, Tierney B C, Campbell G L, Marfin A A, VanGerpen J A, Fleischauer A, Leis A A, Stokic D S, Petersen L R. "Neurologic manifestations and outcome of West Nile virus infection." JAMA 2003; 290: 511-515.
- ↑ Ahmed S, Libman R, Wesson K, Ahmed F, Einberg K. "Guillain-Barre syndrome: an unusual presentation of West Nile virus infection." Neurology 2000; 55: 144-146.
- ↑ Abroug F, Ouanes-Besbes L, Letaief M, Ben Romdhane F, Khairallah M, Triki H, Bouzouiaia N. "A cluster study of predictors of severe West Nile virus infection." Mayo Clinic Proceedings 2006; 81: 12-16.
- ↑ Perelman A, Stern J. "Acute pancreatitis in West Nile Fever." American Journal of Tropical Medicine and Hygiene 1974; 23: 1150-1152.
- ↑ Omalu B I, Shakir A A, Wang G, Lipkin W I, Wiley C A. "Fatal fulminant pan-meningo-polioencephalitis due to West Nile virus." Brain Pathology 2003; 13: 465-472
- ↑ Mathiot C C, Georges A J, Deubel V. "Comparative analysis of West Nile virus strains isolated from human and animal hosts using monoclonal antibodies and cDNA restriction digest profiles." Res Virol 1990; 141: 533-543.