West Nile Encephalitis 

  • Author: Burke A Cunha, MD; Chief Editor: Michael Stuart Bronze, MD   more...
 
Updated: Jun 17, 2011
 

Background

West Nile encephalitis (WNE) is distinguished from other arthropod-borne causes of viral encephalitis (eg, western equine encephalitis, eastern equine encephalitis [EEE], Japanese encephalitis, Venezuelan encephalitis) based on its geographic distribution, clinical features, and laboratory findings. (See Etiology, Differentials, and Workup.)

WNE is endemic in the Middle East, Africa, and Asia. In North America, WNE first occurred in the northeast United States along the eastern seaboard and now extends nationwide. WNE may have existed in antiquity in the Middle East. (Some have suggested that Alexander the Great may have died from WNE.)(See Epidemiology.)[1, 2]

In 1999, a late summer outbreak of West Nile encephalitis (WNE), not found previously in the United States, was implicated in several deaths in New York. By late summer 2002, West Nile virus has been identified throughout the eastern and southeastern United States. Following bird migration, the virus is presently extending westward, and by April 2003, virus activity had been detected in 46 states and the District of Columbia.

Throughout the world, outbreaks of WNE have been associated with severe neurologic disease,[3] although in general, only 1 in 150 affected patients develops symptomatic WNE. (See History.)

For more information, see the CDC fact sheet on West Nile virus, links to state and local government web sites on West Nile virus, and the Environmental Protection Agency (EPA) article on mosquito control.

For clinical information on the Internet, see West Nile Virus: A Primer for the Clinician from the August 6, 2002, issue of the Annals of Internal Medicine, which is available online in Adobe PDF format.[4] The Canadian equivalent, West Nile Virus: Primer for Family Physicians, was published June 10, 2005 in Canadian Family Physician.[3]

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Prognosis

Prognosis is excellent in all patients except those who are elderly or debilitated.[5]

Severe cases may result in death or neurologic sequelae; however, recovery is usually complete. Most children with WNE in Asia and Africa have a benign course and only rarely die of the disease. In the United States, most fatal cases have occurred in elderly patients.

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Etiology and Pathophysiology

Mosquito bites, which are particularly likely during feeding times (dawn and dusk) in the summer months, transmit West Nile virus. Prolonged contact or multiple mosquito bites enhance the risk.

Seventeen species of wild birds transmit West Nile encephalitis (WNE) to humans via the Culex, Aedes, and Anopheles mosquitoes. (See the image below.) WNE first causes symptomatic or asymptomatic illness in wild migratory birds that act as viral replication factories. Wild birds infected with WNE contain high titers of the virus and remain viremic for 1-2 weeks, making them ideal hosts to perpetuate the disease. Mosquitoes transmit WNE from birds to humans. Horses, dogs, and other small animals may harbor WNE after being bitten; however, they are inefficient transmitters because viral titers are relatively low, and WNE viremia is short-lived in these animals.

The Culex mosquito, common in the eastern United SThe Culex mosquito, common in the eastern United States, is the primary vector responsible for infecting humans with West Nile virus. Prevention of West Nile virus is primarily directed at reducing the mosquito population from May to October and by taking precautions to limit human exposure during these months of high mosquito activity. Image courtesy of the Centers for Disease Control and Prevention.

WNE, like other arthropod-borne viral encephalitides, traverses the blood-brain barrier and infects the brain parenchyma, clinically manifesting as viral encephalitis. WNE may also affect the leptomeninges, resulting in a clinical presentation of aseptic meningitis (viral meningitis). Patients with WNE may present with features of encephalitis and aseptic meningitis (meningoencephalitis).

West Nile virus may also be transmitted in organ transplants and has been found in breast milk.[6]

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Epidemiology

In North America, as previously stated, WNE first occurred in the northeast United States along the eastern seaboard and now extends nationwide.

Approximately 50% of children in Egypt have West Nile virus seropositivity. West Nile encephalitis (WNE) is the most common cause of viral aseptic meningitis or encephalitis in patients presenting to emergency departments in Cairo. WNE is common in the Middle East, Asia, and Africa.

WNE usually occurs in the summer, when mosquitoes, wild migratory birds, and humans are in close proximity outdoors. Most US cases occur in elderly patients. Worldwide, most cases occur in young children or young adults; however, elderly patients are affected more severely.

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Patient Education

Avoid exposure, particularly from dawn to dusk, in areas where mosquitoes and West Nile encephalitis (WNE) are present. Mosquito netting and mosquito repellents may also be used.

Avoid wearing bright colors and highly aromatic perfumes, deodorants, and hair products that attract mosquitoes. Avoid handling dead or diseased wild birds without proper aseptic precautions.

For patient education information, see the Brain and Nervous System Center and the Infections Center, as well as West Nile Virus and Encephalitis.

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Contributor Information and Disclosures
Author

Burke A Cunha, MD  Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Specialty Editor Board

Wesley W Emmons, MD, FACP  Assistant Professor, Department of Medicine, Thomas Jefferson University; Consulting Staff, Infectious Diseases Section, Department of Internal Medicine, Christiana Care, Newark, DE

Wesley W Emmons, MD, FACP is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and International AIDS Society

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

John L Brusch, MD, FACP  Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance

John L Brusch, MD, FACP is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD  Professor, Stewart G Wolf Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physician Executives, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, Association of Professors of Medicine, Association of Program Directors in Internal Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

References
  1. Cunha BA. Alexander the Great and West Nile virus encephalitis. Emerg Infect Dis. Jul 2004;10(7):1328-9; author reply 1332-3. [Medline].

  2. Oldach D, Benitez RM, Mackowiak PA. Alexander the Great and West Nile virus encephalitis. Emerg Infect Dis. Jul 2004;10(7):1329-30; author reply 1332-3. [Medline].

  3. MacDonald RD, Krym VF. West Nile virus. Primer for family physicians. Can Fam Physician. Jun 2005;51:833-7. [Medline]. [Full Text].

  4. Petersen LR, Marfin AA. West Nile virus: a primer for the clinician. Ann Intern Med. Aug 6 2002;137(3):173-9. [Medline].

  5. Murray K, Baraniuk S, Resnick M, Arafat R, Kilborn C, Cain K, et al. Risk factors for encephalitis and death from West Nile virus infection. Epidemiol Infect. Dec 2006;134(6):1325-32. [Medline]. [Full Text].

  6. Wadei H, Alangaden GJ, Sillix DH, et al. West Nile virus encephalitis: an emerging disease in renal transplant recipients. Clin Transplant. Dec 2004;18(6):753-8. [Medline].

  7. Zou S, Foster GA, Dodd RY, Petersen LR, Stramer SL. West Nile fever characteristics among viremic persons identified through blood donor screening. J Infect Dis. Nov 1 2010;202(9):1354-61. [Medline].

  8. Abroug F, Ouanes-Besbes L, Letaief M, et al. A cluster study of predictors of severe West Nile virus infection. Mayo Clin Proc. Jan 2006;81(1):12-6. [Medline]. [Full Text].

  9. Nash D, Mostashari F, Fine A, et al. The outbreak of West Nile virus infection in the New York City area in 1999. N Engl J Med. Jun 14 2001;344(24):1807-14. [Medline].

  10. Rodriguez AJ, Westmoreland BF. Electroencephalographic characteristics of patients infected with west nile virus. J Clin Neurophysiol. Oct 2007;24(5):386-9. [Medline].

  11. Rawal A, Gavin PJ, Sturgis CD. Cerebrospinal fluid cytology in seasonal epidemic West Nile virus meningo-encephalitis. Diagn Cytopathol. Feb 2006;34(2):127-9. [Medline].

  12. Tyler KL, Pape J, Goody RJ, et al. CSF findings in 250 patients with serologically confirmed West Nile virus meningitis and encephalitis. Neurology. Feb 14 2006;66(3):361-5. [Medline].

  13. Murray KO, Resnick M, Miller V. Depression after infection with West Nile virus. Emerg Infect Dis. Mar 2007;13(3):479-81. [Medline]. [Full Text].

  14. Ou AC, Ratard RC. One-year sequelae in patients with West Nile Virus encephalitis and meningitis in Louisiana. J La State Med Soc. Jan-Feb 2005;157(1):42-6. [Medline].

  15. Sejvar JJ. The long-term outcomes of human West Nile virus infection. Clin Infect Dis. Jun 15 2007;44(12):1617-24. [Medline].

  16. Cunha BA. Differential diagnosis of West Nile encephalitis. Curr Opin Infect Dis. Oct 2004;17(5):413-20. [Medline].

  17. Cunha BA, Minnaganti V, Johnson DH, Klein NC. Profound and prolonged lymphocytopenia with West Nile encephalitis. Clin Infect Dis. Oct 2000;31(4):1116-7. [Medline].

  18. Cunha BA, Sachdev B, Canario D. Serum ferritin levels in West Nile encephalitis. Clin Microbiol Infect. Feb 2004;10(2):184-6. [Medline].

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Common encephalitis associations.
Clinical features of arboviral encephalitis.
Differential diagnoses of meningoencephalitis.
The Culex mosquito, common in the eastern United States, is the primary vector responsible for infecting humans with West Nile virus. Prevention of West Nile virus is primarily directed at reducing the mosquito population from May to October and by taking precautions to limit human exposure during these months of high mosquito activity. Image courtesy of the Centers for Disease Control and Prevention.
The geographic distribution of the Japanese encephalitis servocomplex of the family Flaviridae, 2000. Image courtesy of the Centers for Disease Control and Prevention.
States reporting laboratory-positive West Nile virus infection in birds, mosquitoes, animals, or humans between January 1 and August 28, 2002. Image courtesy of the Centers for Disease Control and Prevention.
 
 
 
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