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Western Equine Encephalitis Workup

  • Author: Mohan Nandalur, MD; Chief Editor: Burke A Cunha, MD  more...
 
Updated: Feb 29, 2016
 

Approach Considerations

Because of the large number of potential organisms that can be responsible for the signs and symptoms of Western equine encephalitis (WEE), diagnosis is often delayed and difficult. Laboratory confirmation is also difficult, because it requires either specific serologic findings or isolation of the virus in brain tissue or cerebrospinal fluid (CSF). However, isolation from either the blood or CSF is often difficult because of the low viremia associated with WEE.

The current guidelines from the Centers for Disease Control and Prevention (CDC) for diagnosis of an arbovirus infection require (1) an acute febrile illness with encephalitis during a time when transmission of the virus is likely and (2) one more of the following criteria:

  • A greater than 4-fold increase in the viral antibody titer between acute and convalescent sera (often 10 wk apart)
  • Viral isolation from the CSF, blood, or tissue
  • Immunoglobulin M (IgM) positive to the organism in the CSF

Presumptive positive diagnoses can be made based on the remaining biochemical assays (eg, hemagglutinin inhibition, immunofluorescence, neutralization, complement fixation).

A leukocytosis with a left shift often is present but is less than that observed in EEE. Otherwise, no prominent laboratory anomalies are unique to WEE.

Imaging studies

Encephalitis can be identified early with neuroimaging studies (eg, computed tomography [CT] scanning, magnetic resonance imaging [MRI]), which are routinely performed in patients with CNS symptoms.

Advances in imaging studies have shown that previous neuroradiographic manifestations of WEE were not precisely defined. Early studies revealed a predilection for the thalamic nuclei and the basal ganglia; however, these changes are also common with Japanese encephalitis, measles, mumps, echovirus-25 infection, Creutzfeldt-Jakob (CJ) disease, cyanide poisoning, and carbon monoxide poisoning and therefore are not entirely sensitive.

Of note, in patients who recover from WEE, most radiographic changes resolve.

Blood cultures

Blood cultures are unlikely to help in these situations but may be performed if suspicion of bacterial meningitis is high.

Throat swab

Occasionally, the virus can be recovered by throat swab.

Electroencephalography

Electroencephalography (EEG) often reveals generalized slowing and disorganization of the background. This is often followed by epileptiform activity that varies from isolated discharges to gross seizure activity.

Lumbar puncture

If suspicion is high, lumbar puncture is absolutely indicated as soon as possible. Assess the CSF for elevated opening pressures and send the CSF for a complete blood count (CBC) with differential; a Gram stain; glucose and protein levels; acid-fast bacillus; an India ink stain; a Venereal Disease Research Laboratory (VDRL) test; a herpes polymerase chain reaction (PCR) assay; and bacterial, viral, and fungal cultures.

Findings in CSF analysis (from lumbar puncture) include the following:

  • Increased protein and protein concentration in CSF - This is often present (approximately 90-110 mg/dL) and occurs with a high prevalence
  • Elevated CSF red blood cell (RBC) count
  • Elevated CSF white blood cell (WBC) count - Initial WBC count is 50-500/µL, with a median of 350/µL and a predominance of lymphocytes
  • No hypoglycorrhachia
  • Occasional viral isolation
  • Occasional IgM positivity, which can provide a presumptive diagnosis

Brain biopsies

Biopsies are not frequently performed anymore, and these procedures are often a last resort.

CNS histopathology

The perikaryon and dendrites are primarily affected and demonstrate evidence of cytoplasmic swelling, eosinophilia, and nuclear pyknosis. Occasionally, mature viral particles are present in extracellular spaces. The brain is grossly edematous, and evidence of inflammation parenchymally and perivascularly is present. Perivascular inflammation, vasculitis, thrombi, neurolysis (cell membrane rupture), neuronophagia, and demyelination may be observed. The areas primarily affected grossly are the thalamic nuclei and basal ganglia.

Infants who die of WEE or neonates infected in utero often have massive neuroparenchymal destruction. Of those who survive, most have a normal brain grossly, but some cysts may be present.

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Biochemical Assays

The use of biochemical assays is most valuable for diagnosis. Obtain sera at 2- to 3-day intervals to assess for a potential outcome upon early suspicion. The potential drawbacks include an inability to rapidly receive the results of these tests.

Enzyme-linked immunosorbent assay (ELISA) is used to detect IgM, primarily during convalescent stages or prolonged courses, and is virus-specific.

ELISA may also reveal antiarboviral immunoglobulin G (IgG) and yields results similar to those of the neutralization assay. The current use of this assay is primarily as an adjunct to the IgM ELISA.[6]

A serum hemagglutinin inhibition titer of at least 1:320 is used most commonly and allows differentiation among EEE, WEE, and VEE.

A complement fixation titer of at least 1:128 is found primarily in convalescing patients.

An immunofluorescence titer of at least 1:256 is uncommon.

A neutralization assay titer of at least 1:160 is common.

Clinicians may document the presence of WEE in a specimen by inoculating mice or embryonated eggs (Vero cell plaque assay).

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Polymerase Chain Reaction

A final alternative study, which should provide rapid diagnosis in the future, is PCR analysis of the various organisms known to cause encephalitis. PCR analysis has been performed in WEE since 1996, but initial uses were primarily to differentiate between various cross-species of the virus.

Studies, however, indicate that PCR is much more accurate than the 10% likelihood of serologic diagnostics yielding positive results. Other advantages of PCR include the ability to target antiviral therapy, to reduce the need for brain biopsy, and to increase the speed of diagnosis (ie, the panel can often be run in 72 h). The current limitation of PCR is that it will likely require a state or national effort, which may not be available for WEE. The currently used assay is the TaqMan reverse transcriptase PCR assay.

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CT Scanning and MRI

CT scanning

This is an excellent modality for either monitoring the evolution of lesions or determining primary areas of disease.

The most common finding is a lesion of the basal ganglia. Lesions vary in size and may exhibit secondary mass effect with edema.

A CT scan may reveal areas of punctate hemorrhage, focal edema with mass effect, poorly marginated lesions, or interventricular hemorrhage.

In elderly patients, the findings could mimic early infarction or nonspecific common findings.

Occasionally, meningeal enhancement may also be observed and may indicate a subarachnoid hemorrhage or meningitis.

MRI

MRI is often sensitive to early changes secondary to EEE, but no studies have been completed with WEE. In EEE, MRI was more sensitive and revealed more abnormalities with increased detail compared with CT scan; these findings probably would be the same in studies of WEE.

The lesions are best observed with T2-weighted images and appear as areas of increased signal intensity.

The most commonly affected areas of the CNS include the basal ganglia (ie, unilateral or asymmetrical, with occasional internal capsule involvement) and thalamic nuclei. Other areas include the brain stem (often the midbrain), periventricular white matter, and cortex (most often temporally).

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Contributor Information and Disclosures
Author

Mohan Nandalur, MD Staff Physician, Department of Internal Medicine, Section of Cardiovascular Medicine, Washington Hospital Center

Mohan Nandalur, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians-American Society of Internal Medicine, Phi Beta Kappa

Disclosure: Nothing to disclose.

Coauthor(s)

Andrew W Urban, MD Chief, Section of Infectious Diseases, Middleton Memorial Veterans Hospital; Clinical Assistant Professor, Department of Internal Medicine, University of Wisconsin at Madison School of Medicine and Public Health

Andrew W Urban, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine

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

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.

Acknowledgements

Kenneth C Earhart, MD Deputy Head, Disease Surveillance Program, United States Naval Medical Research Unit #3

Kenneth C Earhart, MD is a member of the following medical societies: American College of Physicians, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and Undersea and Hyperbaric Medical Society

Disclosure: Nothing to disclose.

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