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Kenneth L. Tyler, MD

Arch Neurol. 2004;61:1190-1195.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

INTRODUCTION

West Nile virus (WNV), an arthropod-borne flavivirus belonging to the Japanese encephalitis virus antigenic complex, first appeared as a cause of naturally acquired meningitis and encephalitis in the United States in the New York City area in the summer of 1999.¹ During succeeding years, the virus has spread rapidly throughout North America, becoming enzootic in bird and mosquito populations throughout much of the continental United States. In 2003, WNV was responsible for one of the largest arboviral encephalitis epidemics in US history (9858 cases; 2863 with meningoencephalitis and 262 deaths) and one of the largest WNV meningoencephalitis epidemics yet recorded.²

EPIDEMIOLOGY AND ECOLOGY

The vast majority of human infections are caused by the bite of an infected mosquito, typically of the Culex genus. Human infection occurs predominantly between June and November, with a peak between mid-July and mid-September, reflecting the seasonal activity cycle of mosquito vectors. Wild birds serve . . . [Full Text of this Article]

SEROLOGY AND DIAGNOSIS

CSF, NEUROIMAGING, AND ELECTROENCEPHALOGRAPHY

NEUROLOGICAL ILLNESS

MENINGITIS AND CRANIAL NERVE PALSIES

ENCEPHALITIS

ACUTE FLACCID PARALYSIS

PREVENTION AND TREATMENT

SEQUELAE AND OUTCOME

NEUROPATHOLOGY

AUTHOR INFORMATION

Author Affiliation: Department of Neurology, University of Colorado Health Sciences Center and the Denver VA Medical Center, Denver.

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