West nile virus history and symptoms

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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 commonly 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 found in horses and vaccines are available for the disease in horses but not for human beings. The virus may also be transmitted through contact with other infected animals, their blood, or other tissues.A very small proportion of human infections have occurred through organ transplant, blood transfusions and breast milk. There is one reported case of transplacental (mother-to-child) WNV transmission. To date, no human-to-human transmission of WNV through casual contact has been documented, and no transmission of WNV to health care workers has been reported when standard infection control precautions have been put in place. Transmission of WNV to laboratory workers has been reported. 80% of the people infected with West Nile Virus are not aware that they are infected as it can be asymptomatic. West Nile fever can present with a variety of manifestation according to the severity of the diseases. It has three different effects on humans.

1) The first is an asymptomatic infection

2) The second is a mild febrile syndrome termed West Nile Fever;[2]

3) 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]

Symptoms

Asymptomatic variant

This is found in almost 80% of the people where the patients are asymptomatic and unaware that they have been infected.

West nile fever

The second, febrile stage has an incubation period of 3-8 days. The common symptoms found during this period in various systems are

Constitutional symptoms

Skin

  • Skin rash on the trunk of the body
  • Swelling of lymph nodes

GIT

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.

Severe form with neurovascular disease

The third effect is the most dangerous one with severe life threatening symptoms. It is called West Nile encephalitis or West Nile meningitis, depending on what part of the body is affected. 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. The major symptoms are

General

Neurological

It is the most severe form of the disease. They can present with a variety of manifestation in conjunction with fever like meningitis, flaccid paralysis, encephalitis or a combination of these . The most common neurological symptoms with their corresponding frequencies are tabulated below.

Symptom Percentage
Facial Palsy 13%
Dhyphagia 33%
Dysarthria 33%
Diplopia 33%
Tremor 22%
Parkinsonism 16%
Ataxia 31%
Motor seizures 5%
Myoclonus 31%
  • 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]

West nile meningitis

The main signs and symptoms are back pain, myalgia, rash , photophobia. Usually it is aseptic meningitis and resolves without major complications.

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.

Multiorgan abnormality

References

  1. 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).
  2. Olejnik E. "Infectious adenitis transmitted by Culex molestus." Bull. Res. Counc. Isr. 1952; 2: 210-211.
  3. Smithburn K C, Jacobs H R. "Neutralization-tests against neurotropic viruses with sera collected in central Africa." Journal of Immunology 1942; 44: 923.
  4. 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
  5. 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.
  6. 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.
  7. 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.
  8. Perelman A, Stern J. "Acute pancreatitis in West Nile Fever." American Journal of Tropical Medicine and Hygiene 1974; 23: 1150-1152.
  9. 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
  10. 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.


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