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* Deep tendon reflexes are hyperactive at first, later diminished. There are also [[extrapyramidal disorder]]s. 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.<ref>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.</ref> WNV-associated [[Guillain-Barré syndrome]] has been identified<ref>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.</ref> | * Deep tendon reflexes are hyperactive at first, later diminished. There are also [[extrapyramidal disorder]]s. 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.<ref>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.</ref> WNV-associated [[Guillain-Barré syndrome]] has been identified<ref>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.</ref> | ||
====West Nile Meningoencephalitis==== | |||
It is the most common form of severe disease presenting as behavioual changes like confusion, irritability, disorientation along with focal signs like tremor, ataxia , bulbar dysfunction, or focal weakness. | |||
====Acute Flaccid Paralysis==== | |||
It usually occurs in the subclinical phase presenting as lower limb weakness with flaccid tone, areflexia or hyporeflexia. | |||
Revision as of 05:00, 11 September 2014
West Nile fever infection can present with a variety of manifestation according to the severity of the diseases. West Nile fever infection has three different clinical presentations in humans.
- Asymptomatic infection
- Mild febrile syndrome termed West Nile Fever (febrile stage has an incubation period of 3-8 days). 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.[1]
- Neuroinvasive disease termed West Nile meningitis or encephalitis.[2]
In infected individuals the ratio between the three states is roughly 110:30:1.[3]
It is estimated that approximately 1 in 150 persons infected with the West Nile virus will develop a more severe form of disease. Serious illness can occur in people of any age, however people over the age of 50 and some immunocompromised persons (for example, transplant patients) are at the highest risk for getting severely ill when infected with WNV. The incubation period is usually 3 to 14 days.
- 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.[4] WNV-associated Guillain-Barré syndrome has been identified[5]
West Nile Meningoencephalitis
It is the most common form of severe disease presenting as behavioual changes like confusion, irritability, disorientation along with focal signs like tremor, ataxia , bulbar dysfunction, or focal weakness.
Acute Flaccid Paralysis
It usually occurs in the subclinical phase presenting as lower limb weakness with flaccid tone, areflexia or hyporeflexia.
- ↑ 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.