Abstract
The Houston West Nile Cohort (HWNC) was founded in 2002 when West Nile virus (WNV) reached Houston, TX. The long-term outcomes following WNV infection are still mostly unknown, though neurological abnormalities up to 1 year postinfection have been documented. We report an observational study of neurological abnormalities at 1–3 and 8–11 years following WNV infection in the HWNC. We conducted standard neurological examinations at two separate time points to assess changes in neurological status over time. The majority of patients (86%, 30/35) with encephalitis had abnormal neurological exam findings at the time of the first assessment compared with uncomplicated fever (27%, 3/11) and meningitis (36%, 5/14) cases. At the time of the second assessment, 57% (4/7) of West Nile fever (WNF), 33% (2/6) of West Nile meningitis (WNM), and 36% (5/14) of West Nile encephalitis (WNE) had developed new neurological complications. The most common abnormalities noted were tandem gait, hearing loss, abnormal reflexes, and muscle weakness. Long-term neurological abnormalities were most commonly found in patients who experienced primary WNV encephalitis. New abnormalities may develop over time regardless of initial clinical infection. Future studies should aim to differentiate neurological consequences due to WNV neuroinvasive infection versus neurological decline related to comorbid conditions.
Highlights
The first outbreak of West Nile virus (WNV) in the Western Hemisphere occurred in New York City in 1999.1 Subsequently, the virus spread rapidly south and westward throughout the United States reaching Harris County, Texas in 2002
The median age in years was older in the West Nile encephalitis (WNE) compared with West Nile meningitis (WNM) and West Nile fever (WNF) groups (68 years versus 46 and 54 years, respectively)
We found that patients who initially presented with acute WNE have high rates of persistent neurological abnormalities over time compared with those who presented with acute WNF or WNM
Summary
The first outbreak of West Nile virus (WNV) in the Western Hemisphere occurred in New York City in 1999.1 Subsequently, the virus spread rapidly south and westward throughout the United States reaching Harris County, Texas in 2002. WNV infection is most commonly asymptomatic with approximately 20% infected persons found to have clinically apparent disease.[5,6,7] The majority of people with symptoms present with fatigue, fever, and headache and less commonly with myalgia, muscle weakness, rash, difficulty concentrating, neck pain, arthralgia, vomiting, diarrhea, and sensitivity to light.[8,9] West Nile neuroinvasive disease (WNND), characterized as meningitis, encephalitis, and/or acute flaccid paralysis, occurs in as few as 1 in 150 infected persons.[6] WNV meningitis is defined clinically as fever, pleocytosis in the cerebrospinal fluid (CSF), and clinical evidence of meningeal inflammation (nuchal rigidity, photophobia, and nausea/vomiting). WNV encephalitis further requires the presence of prolonged altered mental status (> 24 hours), seizures, or focal neurological abnormalities.[10,11] Among the patients who meet clinical criteria for WNND, acute case fatality is approximately 10%.1. Patients presenting with clinically compatible symptoms are typically diagnosed with WNV infection by detection of antiWNV IgM using monoclonal antibody capture enzyme-linked immunosorbent assay (MAC-ELISA) in the serum or CSF.[5,12] WNV encephalitis further requires the presence of prolonged altered mental status (> 24 hours), seizures, or focal neurological abnormalities.[10,11] Among the patients who meet clinical criteria for WNND, acute case fatality is approximately 10%.1 Patients presenting with clinically compatible symptoms are typically diagnosed with WNV infection by detection of antiWNV IgM using monoclonal antibody capture enzyme-linked immunosorbent assay (MAC-ELISA) in the serum or CSF.[5,12]
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