West Nile Encephalitis Workup

Leukopenia

West Nile encephalitis (WNE), as with many viral illnesses, may manifest as mild leukopenia or a white blood cell (WBC) count that is borderline or in the low end of the reference range. Leukocytosis suggests a complication or superinfection.

In patients who present with acute encephalitis, leukocytosis should suggest eastern equine encephalitis (EEE), California encephalitis, or St. Louis encephalitis.

Lymphopenia

Although relative lymphopenia is not specific for WNE, it is a helpful diagnostic finding if present in a patient with aseptic meningitis, meningoencephalitis, or encephalitis of unknown cause.

Although patients with human immunodeficiency virus (HIV) or Venezuelan equine encephalitis often present with encephalitis and relative lymphopenia, lymphopenia with WNE is profound and prolonged, which should suggest the diagnosis.

Serum transaminases

Mild elevations of serum glutamic-oxaloacetic transaminase (SGOT) levels are not a feature of most encephalitides due to arboviral causes.

Mild elevations of the SGOT/serum glutamic-pyruvic transaminase (SGPT) level in a patient with encephalitis should suggest Epstein-Barr virus, Rocky Mountain spotted fever, ehrlichiosis, human herpesvirus type 6 infection, or Legionnaires disease, in addition to WNE. Serum amylase/lipase levels are increased in some cases of WNE.

Serum ferritin levels

Serum ferritin levels are highly elevated in WNE and not in other causes of encephalitis. The magnitude/duration of serum ferritin elevations also host prognostic importance.

Electroencephalography

This is the most sensitive method of making a presumptive diagnosis of HSV-1 encephalitis. Electroencephalography reveals an abnormal temporal lobe focus as early as the first few days of the disease.

The electroencephalogram in patients with WNE shows diffuse bilateral focal abnormalities in the temporal lobe.^[10]

Lumbar puncture

CSF reveals mild to moderate pleocytosis with a lymphocytic predominance in WNE.^{[11, 12]} CSF protein levels are variably elevated, and the CSF glucose level is not decreased.

The CSF lactic acid level is not elevated, and RBCs, excluding traumatic taps, are not present in WNE. CSF Gram stain and bacterial culture findings are negative.

Histologic findings

Brain biopsy findings exhibit diffuse encephalitis, which is nonspecific and nondiagnostic for WNE.

West Nile encephalopathy (WNE) may be cultured from the blood within the first 2 weeks of initial infection, but it is not usually culturable from CSF.

A specific diagnosis can be confirmed via serum testing. Various serologic methods are available, but the enzyme immunoassay (EIA) with plaque reduction neutralization test is the best test currently available. The polymerase chain reaction assay is also available at selected research centers. A highly elevated acute titer or a 4-fold or greater rise between acute and convalescent titer is diagnostic of WNE.

Since the differential diagnoses of WNE include HSV-1 meningoencephalitis and encephalitis, a head CT or MRI scan is helpful in excluding HSV-1 infection, the only treatable cause of viral encephalitis.

CT or MRI scans may exhibit changes in 1 temporal lobe, which is highly characteristic of HSV-1 encephalitis. Early CT scan and MRI findings are often negative. CT scans are less sensitive and may not reveal abnormalities if obtained very early in the disease process.

All other causes of aseptic meningitis, meningoencephalitis, or encephalitis, including systemic disorders with an encephalitic component, yield negative findings (nonfocal temporal lobe findings) on CT and MRI scans.

CNS lupus may be suggested by the diffuse uptake over the cerebral cortex, suggesting cerebritis.