RESEARCH Acute Flaccid Paralysis and West Nile Virus Infection James J. Sejvar,* A. Arturo Leis,† Dobrivoje S. Stokic,† Jay A. Van Gerpen,‡ Anthony A. Marfin,* Risa Webb,§ Maryam B. Haddad,* Bruce C. Tierney,* Sally A. Slavinski,§ Jo Lynn Polk,† Victor Dostrow,† Michael Winkelmann,† and Lyle R. Petersen* Acute weakness associated with West Nile virus (WNV) infection has previously been attributed to a periph- eral demyelinating process (Guillain-Barré syndrome); however, the exact etiology of this acute flaccid paralysis has not been systematically assessed. To thoroughly describe the clinical, laboratory, and electrodiagnostic fea- tures of this paralysis syndrome, we evaluated acute flac- cid paralysis that developed in seven patients in the setting of acute WNV infection, consecutively identified in four hos- pitals in St. Tammany Parish and New Orleans, Louisiana, and Jackson, Mississippi. All patients had acute onset of asymmetric weakness and areflexia but no sensory abnor- malities. Clinical and electrodiagnostic data suggested the involvement of spinal anterior horn cells, resulting in a poliomyelitis-like syndrome. In areas in which transmission is occurring, WNV infection should be considered in patients with acute flaccid paralysis. Recognition that such weakness may be of spinal origin may prevent inappropri- ate treatment and diagnostic testing. Mflavivirus within the Japanese encephalitis virus ost human infections with West Nile virus (WNV), a antigenic complex, are clinically inapparent (1,2). Mild febrile illness develops in approximately 1 in 5 infected persons; more severe neurologic disease, mostly meningi- tis or encephalitis, occurs in and 1 in 150 (1–4). Less fre- quently, acute WNV infection has been associated with acute flaccid paralysis, which has been attributed to Guillain-Barré syndrome, motor axonopathy, or axonal polyneuropathy (4–6). However, these reports describe clinical and laboratory features that seem inconsistent with such diagnoses, and the exact cause of acute flaccid paral- ysis has not been thoroughly assessed with rigorous elec- trophysiologic, laboratory, and neuroimaging data. Brief descriptions of six patients have suggested that this flaccid paralysis is due to anterior horn cell involvement with a resultant poliomyelitis-like syndrome (7–9). Because *Centers for Disease Control and Prevention, Atlanta, Georgia, USA; †Methodist Rehabilitation Center, Jackson, Mississippi, USA; ‡Ochsner Clinic, New Orleans, Louisiana, USA; and §Mississippi State Department of Health, Jackson, Mississippi, USA understanding the clinical characteristics and underlying etiology of WNV-induced acute flaccid paralysis is critical for therapeutic decisions as well as prognosis, we describe the detailed clinical, laboratory, and electrophysiologic findings from these six patients and from one additional patient. Patients and Methods Seven patients were detected through WNV surveil- lance conducted by the Mississippi Department of Health and the Louisiana Office of Public Health. For each patient, a standardized questionnaire, including demo- graphics, medical history, initial signs and symptoms, risk factors, and treatment, was completed; a standardized neu- rologic examination was performed by a single neurologist (JJS). Electrodiagnostic studies were performed by neurol- ogists (AAL and JAVG) specializing in electrodiagnostic medicine. Cerebrospinal fluid (CSF) and acute- or convalescent- phase serum specimens (or both) from each patient were tested for antibody to WNV by immunoglobulin (Ig) M antibody-capture enzyme immunoassay (10) or plaque reduction neutralization assay (11). The initial specimen for one patient (patient 5, Table 1) was tested with a slight- ly modified IgM antibody assay at a commercial laborato- ry (12). IgM assays were considered positive if the optical density ratio of the patient and negative control samples (P/N ratio) was greater than three. For patient samples, a P/N ratio for WNV at least three times that for St. Louis encephalitis virus indicated WNV infection (13). A plaque reduction neutralization test result of at least 10 was con- sidered positive. All seven patients had serologic evidence of WNV infec- tion (Table 1). On the basis of serologic data, three of the patients were classified as confirmed case-patients (patients 4, 6, and 7) and four as probable case-patients (patients 1–3, 5), according to the national case definition (14). Case 1 On July 1, 2002, a previously healthy, 56-year-old, male Mississippi resident was hospitalized with a 1-week 788 Emerging Infectious Diseases • Vol. 9, No. 7, July 2003