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1 June 2006

Volume 42, Number 11
Clinical Infectious Diseases 2006;42:1527–1535
© 2006 by the Infectious Diseases Society of America. All rights reserved.
1058-4838/2006/4211-0004$15.00
DOI: 10.1086/503841
MAJOR ARTICLE

Fatal Hemorrhagic Fever Caused by West Nile Virus in the United States

Christopher D. Paddock,1

William L. Nicholson,2

Julu Bhatnagar,1

Cynthia S. Goldsmith,1

Patricia W. Greer,1

Edward B. Hayes,3

Joseph A. Risko,4

Corey Henderson,4

Carina G. Blackmore,5

Robert S. Lanciotti,3

Grant L. Campbell,3 and

Sherif R. Zaki1

1Infectious Disease Pathology Activity and 2Viral and Rickettsial Zoonoses Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia; 3Arboviral Diseases Branch, Division of Vector‐Borne Infectious Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Fort Collins, Colorado; 4Florida Hospital Waterman, Tavares, and 5Florida Department of Health, Tallahassee

Background.Most West Nile virus (WNV) infections in humans are asymptomatic; severe disease occurs in relatively few patients and typically manifests as encephalitis, meningitis, or acute flaccid paralysis. A few cases of life‐threatening disease with diffuse hemorrhagic manifestations have been reported in Africa; however, this clinical presentation has not been documented for any of the >16,700 cases of WNV disease reported in the United States during 1999–2004. We describe a case of fulminant WNV infection in a 59‐year‐old Florida man who died following a brief illness that resembled hemorrhagic disease caused by Rickettsia rickettsii, dengue virus or yellow fever virus.

Methods.Traditional and contemporary diagnostic assays, including culture isolation, electron microscopic examination, reverse‐transcriptase polymerase chain reaction amplification, and immunohistochemical stains, were used to confirm systemic WNV infection in the patient.

Results.WNV was isolated in a cell culture from a skin biopsy specimen obtained from the patient shortly prior to death. Electron microscopic examination identified the isolate as a flavivirus, and reverse‐transcriptase polymerase chain reaction amplified specific WNV sequences from the isolate and patient tissue. Quantitative polymerase chain reaction identified approximately viral copies/mL in the patient’s serum. WNV antigens were detected by immunohistochemical stains in intravascular mononuclear cells and endothelium in skin, lung, liver, kidney, spleen, bone marrow, and central nervous system; no viral antigens were identified in neurons or glial cells of the central nervous system.

Conclusions.Although hemorrhagic disease is a rare manifestation of WNV infection, the findings provided by this report may offer new insights regarding the clinical spectrum and pathogenesis of WNV disease in humans.

Received 9 November 2005; accepted 24 January 2006; electronically published 27 April 2006.

Reprints or correspondence: Dr. Christopher D. Paddock, Infectious Disease Pathology Activity, G‐32, Centers for Disease Control and Prevention, 1600 Clifton Rd., Atlanta, GA 30333 ().

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  • The findings and conclusions in this article are those of the authors and do not necessarily reflect the views of the U.S. Department of Health and Human Services.

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