Elsevier

The Lancet

Volume 358, Issue 9278, 28 July 2001, Pages 261-264
The Lancet

Articles
Epidemic West Nile encephalitis, New York, 1999: results of a household-based seroepidemiological survey

https://doi.org/10.1016/S0140-6736(01)05480-0Get rights and content

Summary

Background

In the summer of 1999, West Nile virus was recognised in the western hemisphere for the first time when it caused an epidemic of encephalitis and meningitis in the metropolitan area of New York City, NY, USA. Intensive hospital-based surveillance identified 59 cases, including seven deaths in the region. We did a household-based seroepidemiological survey to assess more clearly the publichealth impact of the epidemic, its range of illness, and risk factors associated with infection.

Method

We used cluster sampling to select a representative sample of households in an area of about 7·3 km2 at the outbreak epicentre. All individuals aged 5 years or older were eligible for interviews and phlebotomy. Serum samples were tested for IgM and IgG antibodies specific for West Nile virus.

Findings

677 individuals from 459 households participated. 19 were seropositive (weighted seroprevalence 2·6% [95% CI 1·2–4·1). Six (32%) of the seropositive individuals reported a recent febrile illness compared with 70 of 648 (11%) seronegative participants (difference 21% [0–47]). A febrile syndrome with fatigue, headache, myalgia, and arthralgia was highly associated with seropositivity (prevalence ratio 7·4 [1·5–36·6]). By extrapolation from the 59 diagnosed meningoencephalitis cases, we conservatively estimated that the New York outbreak consisted of 8200 (range 3500–13 000) West Nile viral infections, including about 1700 febrile infections.

Interpretation

During the 1999 West Nile virus outbreak, thousands of symptomless and symptomatic West Nile viral infections probably occurred, with fewer than 1% resulting in severe neurological disease.

Introduction

West Nile virus is a mosquito-borne flavivirus that belongs to the Japanese encephalitis virus serocomplex, and which was first isolated from a woman with febrile illness in Uganda.1 Early reports described endemic and epidemic “West Nile fever” in Africa and the Middle East, which was characterised clinically by low-grade fever, headache, myalgia, and profound fatigue, sometimes with gastrointestinal symptoms, lymphadenopathy, or a diffuse roseolar rash.2, 3, 4 Neurological involvement with aseptic meningitis or encephalitis was thought to be rare, and mortality was negligible. More recent epidemics in northern Africa, Eastern Europe, and Russia, however, have been notable for a preponderance of West Nile meningoencephalitis, case-fatality rates of 4–13%, and no evidence of widespread mild illness.5, 6, 7

In the summer of 1999, West Nile virus was recognised in the western hemisphere for the first time when it caused an epidemic of encephalitis and aseptic meningitis in residents of greater New York City, NY, USA.8, 9, 10 Intensive hospital-based surveillance identified 59 patients who were admitted to hospital (seven of whom died) and three people with mild illness. The true extent of symptomless and mild infections was unknown. We did a householdbased seroepidemiological survey in the outbreak epicentre to assess more accurately the public-health impact of the New York epidemic, describe the clinical range of illness, and explore risk factors for infection.

Section snippets

Methods

The survey was carried out from Oct 2 to Oct 6, 1999— ie, about 6 weeks after the epidemic peak for West Nile encephalitis cases. The highest rates of illness occurred within an area of about 4·8 km2 (population 49 475 in 1990)11 of northern Queens in New York city. A multistage cluster design similar to that of the WHO Expanded Programme on Immunizations (EPI)12 was used to obtain a representative sample of households. Census blocks were sampled with probability proportional to the number of

Results

During evening hours and weekend days, 1861 households were visited. Residents were home and an adult was present in 1069 households; 470 (44%) agreed to participate. Of 1220 eligible residents, 700 (57%) were present and consented to interviews and phlebotomy. 23 individuals from 11 households were excluded because of inadequate specimens (n=14) or incorrect sampling (n=9). Of the 677 remaining survey participants, a smaller proportion were children or young adults compared with the 47 368

Discussion

Our study sheds light on the clinical manifestation and public-health importance of West Nile viral infection in immunologically naïve populations. By using a community-based design, we found evidence of a substantial, if undiagnosed, outbreak of West Nile fever that accompanied the outbreak of West Nile meningoencephalitis. The predominance of neurological illness described in recent outbreaks is probably due to hospital-based case finding, rather than the emergence of more pathogenic West

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