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West Nile Virus Infection

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  • Author: James J. Sejvar1
  • Editors: W. Michael Scheld2, James M. Hughes3, Richard J. Whitley4
  • VIEW AFFILIATIONS HIDE AFFILIATIONS
    Affiliations: 1: Division of High-Consequence Pathogens and Pathology, National Center for Emerging and Zoonotic Infectious Diseases (NCEZID), Centers for Disease Control and Prevention (CDC), Atlanta, GA 30333; 2: Department of Infectious Diseases, University of Virginia Health System, Charlottesville, VA; 3: Division of Infectious Diseases, Department of Medicine, Emory University School of Medicine, Atlanta, GA; 4: Department of Pediatrics, University of Alabama at Birmingham, Birmingham, AL
  • Source: microbiolspec May 2016 vol. 4 no. 3 doi:10.1128/microbiolspec.EI10-0021-2016
  • Received 24 March 2016 Accepted 25 March 2016 Published 27 May 2016
  • James J. Sejvar, zea3@cdc.gov
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  • Abstract:

    Although long recognized as a human pathogen, West Nile virus (WNV) emerged as a significant public health problem following its introduction and spread across North America. Subsequent years have seen a greater understanding of all aspects of this viral infection. The North American epidemic resulted in a further understanding of the virology, pathogenesis, clinical features, and epidemiology of WNV infection. Approximately 80% of human WNV infections are asymptomatic. Most symptomatic people experience an acute systemic febrile illness; less than 1% of infected people develop neuroinvasive disease, which typically manifests as meningitis, encephalitis, or anterior myelitis resulting in acute flaccid paralysis. Older age is associated with more severe illness and higher mortality; other risk factors for poor outcome have been challenging to identify. In addition to natural infection through mosquito bites, transfusion- and organ transplant–associated infections have occurred. Since there is no definitive treatment for WNV infection, protection from mosquito bites and other preventative measures are critical. WNV has reached an endemic pattern in North America, but the future epidemiologic pattern is uncertain.

  • Citation: Sejvar J. 2016. West Nile Virus Infection. Microbiol Spectrum 4(3):EI10-0021-2016. doi:10.1128/microbiolspec.EI10-0021-2016.

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/content/journal/microbiolspec/10.1128/microbiolspec.EI10-0021-2016
2016-05-27
2017-11-25

Abstract:

Although long recognized as a human pathogen, West Nile virus (WNV) emerged as a significant public health problem following its introduction and spread across North America. Subsequent years have seen a greater understanding of all aspects of this viral infection. The North American epidemic resulted in a further understanding of the virology, pathogenesis, clinical features, and epidemiology of WNV infection. Approximately 80% of human WNV infections are asymptomatic. Most symptomatic people experience an acute systemic febrile illness; less than 1% of infected people develop neuroinvasive disease, which typically manifests as meningitis, encephalitis, or anterior myelitis resulting in acute flaccid paralysis. Older age is associated with more severe illness and higher mortality; other risk factors for poor outcome have been challenging to identify. In addition to natural infection through mosquito bites, transfusion- and organ transplant–associated infections have occurred. Since there is no definitive treatment for WNV infection, protection from mosquito bites and other preventative measures are critical. WNV has reached an endemic pattern in North America, but the future epidemiologic pattern is uncertain.

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Image of FIGURE 1
FIGURE 1

West Nile virus neuroinvasive disease incidence reported to the CDC by year, 1999–2014.

Source: microbiolspec May 2016 vol. 4 no. 3 doi:10.1128/microbiolspec.EI10-0021-2016
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Image of FIGURE 2
FIGURE 2

Average annual incidence of West Nile virus neuroinvasive disease reported to the CDC by county, 1999–2014.

Source: microbiolspec May 2016 vol. 4 no. 3 doi:10.1128/microbiolspec.EI10-0021-2016
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FIGURE 3

Fluid-attenuated inversion recovery magnetic resonance imaging sequence of the brain of a patient with West Nile virus encephalitis with associated parkinsonism and tremor, displaying signal abnormality in the substantia nigra (short arrow), the mesial temporal lobe (long arrow), and right posterior thalamus (thick arrow).

Source: microbiolspec May 2016 vol. 4 no. 3 doi:10.1128/microbiolspec.EI10-0021-2016
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Image of FIGURE 4
FIGURE 4

Sagittal and axial T2-weighted magnetic resonance imaging of the cervical spinal cord of a patient with bilateral upper extremity paralysis and respiratory failure from West Nile poliomyelitis, displaying increased signal in the anterior spinal cord (circle and arrow).

Source: microbiolspec May 2016 vol. 4 no. 3 doi:10.1128/microbiolspec.EI10-0021-2016
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Tables

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TABLE 1

Reported West Nile virus disease cases in humans, United States, 1999–2014

Source: microbiolspec May 2016 vol. 4 no. 3 doi:10.1128/microbiolspec.EI10-0021-2016
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TABLE 2

Clinical and electrodiagnostic features of West Nile virus–associated acute flaccid paralysis

Source: microbiolspec May 2016 vol. 4 no. 3 doi:10.1128/microbiolspec.EI10-0021-2016

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