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AUTHOR AND EDITOR INFORMATION

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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 is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America

Editors: 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; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; John L Brusch, MD, FACP, Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance; Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital; Michael Stuart Bronze, MD, Professor, Stewart G Wolf Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center

Author and Editor Disclosure

Synonyms and related keywords: West Nile encephalitis, WNE, West Nile virus encephalitis, WNVE, West Nile virus, viral encephalitis, western equine encephalitis, WEE, eastern equine encephalitis, EEE, Japanese encephalitis, Venezuelan encephalitis


INTRODUCTION

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Background

West Nile encephalitis (WNE) is distinguished from other arthropod-borne causes of viral encephalitis (eg, western equine encephalitis, eastern equine encephalitis [EEE], Japanese encephalitis, Venezuelan encephalitis) based on its geographic distribution, clinical features, and laboratory findings.

WNE is endemic in the Middle East, Africa, and Asia. In North America, WNE first occurred in the northeast United States along the eastern seaboard and now extends nationwide. WNE may have existed in antiquity in the Middle East. Some have suggested that Alexander the Great may have died from WNE.1, 2

Seventeen species of wild birds transmit WNE to humans via the Culex, Aedes, and Anopheles mosquitoes. WNE first causes symptomatic or asymptomatic illness in wild migratory birds that act as viral replication factories. Wild birds infected with WNE contain high titers of the virus and remain viremic for 1-2 weeks, making them ideal hosts to perpetuate the disease. Mosquitoes transmit WNE from birds to humans. Horses, dogs, and other small animals may harbor WNE after being bitten; however, they are inefficient transmitters because viral titers are relatively low, and WNE viremia is short-lived in these animals.

Pathophysiology

WNE, as with other arthropod-borne viral encephalitides, traverses the blood-brain barrier and infects the brain parenchyma, clinically manifesting as viral encephalitis. WNE may also affect the leptomeninges, resulting in a clinical presentation of aseptic meningitis (viral meningitis). Patients with WNE may present with features of both encephalitis and aseptic meningitis (meningoencephalitis).

Frequency

United States

Cases of WNE in the United States initially occurred mostly in the greater New York area, but cases have now occurred in western states. Wild birds with West Nile virus have been found in various states and Canada.

Furthermore, the cluster of recent outbreaks in Romania, Russia, the Congo, and the United States is characterized by a low frequency of classic WNE features but a high rate of encephalitis and death.

Most exposures to West Nile virus result in asymptomatic seroconversion.

International

Approximately 50% of children in Egypt have West Nile virus seropositivity. WNE is the most common cause of viral aseptic meningitis or encephalitis in patients presenting to emergency departments in Cairo. WNE is common in the Middle East, Asia, and Africa.

Mortality/Morbidity

Most children with WNE in Asia and Africa have a benign course and only rarely die of the disease. In the United States, most fatal cases have occurred in elderly patients.

Race

WNE has no racial predisposition.

Sex

WNE is equally common in males and females.

Age

Most US cases occur in elderly patients. Worldwide, most cases occur in young children or young adults; however, elderly patients are affected more severely.


CLINICAL

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History

  • Mosquito bites: Patients may not provide a mosquito bite history. The incubation period of West Nile encephalitis (WNE) is 1-6 days, perhaps as long as 14 days in immunosuppressed patients.
  • Symptoms
    • Most people who are infected (at least most children) are asymptomatic or have a flulike illness. A minority of people develop neurologic disease.
    • Many patients describe prominent GI symptoms, especially vomiting and diarrhea.
    • Nonspecific symptoms may include sore throat, backache, myalgias, and arthralgias.
    • Most patients with WNE present with features of encephalitis, aseptic meningitis (meningoencephalitis), or both.
    • Symptoms include a mild febrile illness accompanied by headache, mental confusion, tremors, or flaccid paralysis.
    • Symptoms are most prominent in very young and very old people.

Physical

  • The extent and severity of CNS viral invasion determine the clinical expression of WNE.
  • Most patients are febrile or have low-grade fevers.
  • Patients who present with encephalitis have mental confusion or disorientation and may have decreased consciousness. Patients with severe cases of WNE may present with stupor or coma.
  • Multifocal chorioretinitis is the most common ophthalmologic manifestation of WNE.
  • Ten percent of patients with WNE have an enlarged liver. Approximately 20% have splenomegaly.
  • CNS findings include a stiff neck with meningeal signs, including positive Kernig or Brudzinski signs in patients with aseptic meningitis or meningoencephalitis.
  • Some cases of WNE are accompanied by mild nonexudative pharyngitis.
  • In a 2001 study, approximately 20% of patients infected with West Nile virus in New York City presented with truncal maculopapular rash.3 
  • Generalized adenopathy and an enlarged submental node are uncommon (1%).3
  • Consider WNE in patients who have encephalitis and otherwise unexplained extremity weakness and/or paralysis.

Causes

  • WNE usually occurs in the summer, when mosquitoes, wild migratory birds, and humans are in close proximity outdoors.
  • Mosquito bites, which are particularly likely during feeding times (dawn and dusk) in the summer months, transmit West Nile virus.
  • Prolonged contact or multiple mosquito bites enhances the risk.
  • West Nile virus may be transmitted in organ transplants.
  • West Nile virus has been found in breast milk.


DIFFERENTIALS

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Encephalopathy, Hypertensive
Epidural Abscess

Other Problems to be Considered

Encephalopathy due to systemic illnesses

Encephalopathy is a feature of many systemic illnesses that the clinician should consider in patients presenting with encephalitis. Most of these patients have extra-CNS findings that suggest the underlying disease process. Common disorders with CNS manifestations that may mimic West Nile encephalitis (WNE) include subacute bacterial endocarditis, Legionnaires disease, Rocky Mountain spotted fever, Epstein-Barr virus infectious mononucleosis, human herpesvirus type 6 infection, and systemic lupus erythematosus cerebritis.

Other arthropod-borne viral encephalitides

The clinical presentation of WNE is not dissimilar from other causes of arthropod-borne viral encephalitis (eg, Japanese equine encephalitis, St. Louis encephalitis), including mental confusion, stupor, or coma. However, the clinical presentation of arthropod-borne viral encephalitis is characterized by rapid onset and severe headache. Arthropod-borne viral encephalitis has some distinctive features that indicate a prospective clinical diagnosis (see Images 1-2).

The differential diagnoses for aseptic meningitis is extensive but may be reduced to 2 common clinical entities.

Enteroviral aseptic meningitis

The most common cause of aseptic meningitis encountered during the summer months is enteroviral meningitis. Enteroviral aseptic meningitis is most commonly due to coxsackieviruses but may also be due to enterocytopathogenic human orphan virus or nonparalytic strains of poliovirus. Enteroviral meningitis may occur after water exposure in swimming pools, lakes, streams, or oceans as well as after contact with infected individuals.

Acute enteroviral CNS infections usually manifest as aseptic meningitis, uncommonly as meningoencephalitis, or rarely as encephalitis. Nonexudative pharyngitis, maculopapular extremity rash, loose stools, and even diarrhea often accompany enteroviral aseptic meningitis, which provides clues to its presence.

Enteroviral meningitis is not accompanied by paralysis or prolonged and/or profound lymphopenia.

Herpesvirus type 1 encephalitis

Herpes simplex virus encephalitis due to herpesvirus type 1 (HSV-1) is the most common cause of non–arthropod-borne (nonseasonal) encephalitis in the United States. HSV-1 infection usually manifests as encephalitis, uncommonly as meningoencephalitis, or rarely as aseptic meningitis (see Image 3).

Nonsteroidal anti-inflammatory drugs

In patients who present with aseptic meningitis, consider drug-induced aseptic meningitis, most commonly due to nonsteroidal anti-inflammatory drugs (NSAIDs). A patient presenting with aseptic meningitis with no predisposing risk factors may have recently been taking NSAIDs or may be currently taking NSAIDs.


WORKUP

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Lab Studies

  • Leukopenia
    • West Nile encephalitis (WNE), as with many viral illnesses, may manifest as mild leukopenia or a 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 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 HIV or Venezuelan equine encephalitis often present with encephalitis and 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.
  • Serologic testing
    • WNE may be cultured from the blood within the first 2 weeks of initial infection, but it is not usually culturable from cerebrospinal fluid (CSF).
    • A specific diagnosis can be confirmed via serum testing. Various serologic methods are available, but enzyme immunoassay (EIA) with plaque reduction neutralization test is the best test currently available. Polymerase chain reaction 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.

Imaging Studies

  • CT scanning and MRI
    • Since the differential diagnoses of WNE include HSV-1 meningoencephalitis or encephalitis, a head CT scan or MRI is helpful to exclude HSV-1 infection, the only treatable cause of viral encephalitis.
    • CT scan or MRI may exhibit changes in one 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 scan and MRI.
    • CNS lupus may be suggested by the diffuse uptake over the cerebral cortex, suggesting cerebritis.

Other Tests

  • Electroencephalography
    • This is the most sensitive method of making a presumptive diagnosis of HSV-1 encephalitis. EEG reveals an abnormal temporal lobe focus as early as the first few days of the disease.
    • The EEG in patients with WNE shows diffuse bilateral focal abnormalities in the temporal lobe.

Procedures

  • Lumbar puncture
    • CSF reveals mild-to-moderate pleocytosis with a lymphocytic predominance in WNE. 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.


TREATMENT

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Medical Care

  • Provide supportive care to minimize the potential for cerebral edema.
  • In comatose patients, pay special attention to maintaining a clear airway.
  • Replace fluids and electrolytes, as they are lost through insensible losses due to fever and decreased or absent intake.

Surgical Care

  • No surgical care is necessary.

Consultations

  • Consult an infectious disease specialist.
  • Consult a neurologist.

Diet

  • A normal diet, as tolerated by the patient, is acceptable.

Activity

  • Normal activity, as tolerated by the patient, is acceptable.
  • Many patients recover quickly, but some experience prolonged malaise.


MEDICATION

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No specific drug treatment exists for West Nile encephalitis (WNE).


FOLLOW-UP

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Further Inpatient Care

  • In patients with West Nile encephalitis (WNE), repeat testing for lymphopenia or increased serum transaminases until levels return to normal.
  • A repeat lumbar puncture is usually unnecessary.
  • Patients who are unconscious may need ventilation support in an intensive care unit (ICU) until consciousness is restored.

Further Outpatient Care

  • Further outpatient care is usually unnecessary.

In/Out Patient Meds

  • No medications are indicated.

Transfer

  • Transfer is usually unnecessary.

Deterrence/Prevention

  • Avoid exposure to mosquitoes.

Complications

  • Severe cases may result in death; however, recovery is usually complete and does not result in neurologic sequelae.

Prognosis

  • Prognosis is excellent in all patients except those who are elderly or debilitated.

Patient Education

  • Avoid exposure, particularly from dawn to dusk, in areas where mosquitoes and WNE are present.
  • Mosquito netting and mosquito repellents may also be used.
  • Avoid wearing bright colors and highly aromatic perfumes, deodorants, and hair products that attract mosquitoes.
  • Avoid handling dead or diseased wild birds without proper aseptic precautions.
  • For excellent patient education resources, visit eMedicine's Brain and Nervous System Center and Bacterial and Viral Infections Center. Also, see eMedicine's patient education articles West Nile Virus and Encephalitis.


MISCELLANEOUS

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Medical/Legal Pitfalls

  • Excluding systemic illnesses (eg, subacute bacterial endocarditis, Legionnaires disease) with encephalopathy is important so that the underlying infection or disorder may be treated properly.
  • Specifically question patients presenting with aseptic meningitis about NSAIDs, which may cause symptoms similar to those of West Nile encephalitis (WNE). Discontinue NSAIDs if the patient is taking them.
  • The most important infection to exclude in the differential is HSV-1 encephalitis because it is the only treatable viral encephalitis. HSV-1 encephalitis is suggested by temporal lobe abnormalities on EEG and later on CT scans and MRI.
  • Early in the course of HSV-1 encephalitis, CSF may initially show a polymorphonuclear predominance, frequently has RBCs, and may be associated with a decreased CSF glucose level in contrast to the CSF in WNE, which does not have any of these features.


MULTIMEDIA

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Media file 1:  Common encephalitis associations.
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Media file 2:  Clinical features of arboviral encephalitis.
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Media file 3:  Differential diagnoses of meningoencephalitis.
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Media file 4:  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.
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Media type:  Image

Media file 5:  The geographic distribution of the Japanese encephalitis servocomplex of the family Flaviridae, 2000. Image courtesy of the Centers for Disease Control and Prevention.
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Media file 6:  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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Media type:  Image


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West Nile Encephalitis excerpt

Article Last Updated: Aug 1, 2008