Case Presentation:

A 49‐year‐old man presented with a 1‐day history of headache, drenching sweats, photophobia, and vomiting that prompted a CSF evaluation for meningitis. A lumbar puncture revealed protein of 105 mg/dL, a total of 214 nucleated cells/mL with 93% neutrophils, and glucose of 70 mg/dL (130 mg/dL in serum). Occasional myoclonic jerks, lip‐smacking behaviors, and apneic breathing spells without oxygen desaturation were observed. Fevers resolved completely within 24 hours of hospitalization, but severe headache proved difficult to control with non‐narcotic medications. A diagnosis of West Nile virus (WNV) encephalitis was made after considering a combination of the clinical syndrome, a positive IgM serum serology for WNV (which returned later in the clinical course), and experience with diagnosing another patient with WNV encephalitis just 1 week prior from the same rural county. Unfortunately, the patient remained encephalopathic with waxing‐and‐waning alertness and orientation after 72 hours (paradoxically, the previously diagnosed patient was much older but improved significantly in only 24 hours). With a lack of other disease‐modifying therapies, we started interferon alpha‐2b on hospital day 4, and astonishingly, the patient displayed remarkable improvement in mental status and alertness after 3 days of treatment. He was his baseline self after 5 days of treatment and was discharged home feeling well.


West Nile virus (WNV) is an arthropod‐borne flavivirus first recognized in the western hemisphere after an outbreak of meningitis and encephalitis in New York in 1999. A continuum of clinical syndromes is observed in WNV, ranging from no symptoms to pa‐ralysis and death. Many patients exhibit a self‐limited constellation of nonspecific symptoms that may include fever, headache, malaise, and rash. Others display signs of severe neuroinvasive disease with muscle weakness and flaccid paralysis. The mainstay of therapy remains supportive care, although the known in vitro activity against WNV of antiviral agents like ribavirin and interferon suggests a clinical utility.


To date, it has been reported that 5 patients improved and 1 patient showed no improvement and subsequently died after interferon alpha‐2b therapy for neuroinvasive WNV. Currently, 3 clinical treatment trials using agents like immunoglobulin and interferon are underway. Increased pharmacologic, biologic, educational, and epidemiologic research is needed into how to decrease the effects of the most significant epidemic cause of encephalitis in the western hemisphere. As seen here, neuroinvasive WNV can present nonspecifically, be frighteningly neurologically overwhelming, even to a young healthy host, and has no widely accepted treatment.

Author Disclosure:

A. Kamal, None; R. Orenstein, None.