Case Presentation: A 35-year-old woman with no significant medical history presented with severe headache, neck pain, photophobia, fevers, nausea, vomiting, and petechial rash for 5 days. She had recently attended a large outdoor wedding in rural Iowa. On exam her vital signs were within normal limits and neurologic exam was without focal deficits or meningeal signs. The patient was admitted for symptomatic treatment of her intractable headache and infectious workup. However, three days into admission, the patient developed flattening of the left nasolabial fold and asymmetric upper extremity weakness. Magnetic resonance imaging (MRI) of the brain showed subtle T2/FLAIR hyperintensity involving bilateral caudate nuclei and putamina. Acyclovir was empirically started for suspicion of viral encephalitis as well as doxycycline for possible ehrlichiosis, anaplasmosis or borreliosis. Lumbar puncture revealed an opening pressure of 31 cm H2O, low normal glucose (48 mg/dL), and elevated protein (100.9 mg/dL). CSF Gram stain showed lymphocytic pleocytosis without organisms. While awaiting results of CSF testing, the patient developed sudden onset central right eye blindness. Dilated eye exam which revealed intraretinal hemorrhages in the right macula. CSF tested positive for West Nile Virus (WNV) IgM and IgG antibodies. Serum WNV resulted as IgM positive and IgG negative. Acyclovir and doxycycline were discontinued. The patient’s symptoms gradually improved, and she was discharged home in stable condition.
Discussion: West Nile Virus is a member of the Flaviviridae family and is transmitted to humans via mosquito bites. Since WNV first appeared in the United States in 1999 it has become one of the leading causes of viral encephalitis. The incidence rate of WNV is highest in the Great Plains region and peaks during summer months. Most people infected with WNV are asymptomatic or have a mild febrile illness. WNV Neuroinvasive disease is rare, occurring in less than 1 % of cases and can manifest as aseptic meningitis/encephalitis, acute flaccid paralysis, or cranial nerve palsies. Acute flaccid paralysis presents as asymmetric limb weakness and is caused by a poliomyelitis syndrome with involvement of the anterior horn cells of the spinal cord. WNV-associated cranial nerve palsies can cause facial weakness, vertigo, diplopia, dysarthria, or cerebellar ataxia. Risk factors for developing these conditions include older age or an immunocompromised state. Neuroinvasive disease is underdiagnosed because only a third of adults with meningitis or encephalitis get tested for WNV. Chorioretinitis and retinal hemorrhage are two unique ocular complications of WNV that can help distinguish it from other infections. The mainstay of treatment for WNV meningoencephalitis is supportive care with a focus on pain management.
Conclusions: Meningitis is a potentially life-threatening condition commonly encountered on a hospitalist service. Most clinicians are familiar with the classic features of meningitis but m ay be less comfortable identifying the signs and symptoms unique to specific viral, bacterial, or fungal causes of meningitis. We present this case to spread awareness of the unique manifestations of WNV meningoencephalitis and encourage clinicians to have a low threshold to test for WNV, especially if a patient presents during the summer months or has a history of travel to a high-incidence area.