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West Nile Encephalitis Workup

  • Author: Burke A Cunha, MD; Chief Editor: Michael Stuart Bronze, MD  more...
 
Updated: Oct 22, 2015
 

Approach Considerations

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 another diagnosis.

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 particularly encephalitis of unknown cause.

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

ESR/CRP ratio

An ESR/CRP ratio of less than 1 suggests WNE in adults with encephalitis.

Serum transaminases

Mild elevations of serum glutamic-pyruvic transaminase (SGPT) levels are not a feature of most arboviral encephalitides.

In addition to WNE, mild elevations of serum glutamic-oxaloacetic transaminase (SGOT)/SGPT levels in a patient with encephalitis should suggest Epstein-Barr virus, Rocky Mountain spotted fever, ehrlichiosis, HHV-6 infection, or Legionnaires disease.

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 has prognostic importance.

Electroencephalography

This is the most sensitive method of making a presumptive diagnosis of encephalitis. In 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, especially global slowing.[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.

CSF testing for immunoglobulin M (IgM) antibodies against West Nile virus should be performed (in addition to testing of the patient’s serum).

Histologic findings

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

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Serologic Testing

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-linked immunoassay (ELISA) is the best test currently available. Plaque reduction neutralization test (PRNT) can be performed through the CDC.

The polymerase chain reaction (PCR) assay is also available at selected centers.

Most centers start by testing serum and CSF for IgM antibody directed against West Nile virus. If the IgM serology is positive, no further diagnostic confirmation is required (ie, PRNT). Paired serologic testing of acute- and convalescent-phase specimens or PCR testing can be obtained in patients with an ELISA result that is unreactive for IgM. A highly elevated acute immunoglobulin G (IgG) titer or a 4-fold or greater rise between acute and convalescent IgM titer is diagnostic of WNE.

The CDC has established criteria for the laboratory diagnosis of West Nile virus infection.[13]

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CT Scanning and MRI

Since the differential diagnoses of WNE include HSV-1 meningoencephalitis and encephalitis, a head CT or MRI scan may be helpful in excluding HSV-1 infection after several days.

CT or MRI scans may exhibit changes in a 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 early in the disease process.

Most other causes of aseptic meningitis, meningoencephalitis, or encephalitis, including systemic disorders with an encephalitic component, have nonfocal temporal lobe findings on CT and MRI scans.

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Contributor Information and Disclosures
Author

Burke A Cunha, MD Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

John L Brusch, MD, FACP Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance

John L Brusch, MD, FACP is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Acknowledgements

Wesley W Emmons, MD, FACP Assistant Professor, Department of Medicine, Thomas Jefferson University; Consulting Staff, Infectious Diseases Section, Department of Internal Medicine, Christiana Care, Newark, DE

Wesley W Emmons, MD, FACP is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and International AIDS Society

Disclosure: Nothing to disclose.

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Common encephalitis associations.
Clinical features of arboviral encephalitis.
Differential diagnoses of meningoencephalitis.
The Culex mosquito, common in the eastern United States, is the primary vector responsible for infecting humans with West Nile virus. Prevention of West Nile virus is primarily directed at reducing the mosquito population from May to October and by taking precautions to limit human exposure during these months of high mosquito activity. Image courtesy of the Centers for Disease Control and Prevention.
The geographic distribution of the Japanese encephalitis servocomplex of the family Flaviridae, 2000. Image courtesy of the Centers for Disease Control and Prevention.
States reporting laboratory-positive West Nile virus infection in birds, mosquitoes, animals, or humans between January 1 and August 28, 2002. Image courtesy of the Centers for Disease Control and Prevention.
 
 
 
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