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CDC Health Information for International Travel 2008

Chapter 4
Prevention of Specific Infectious Diseases

Hepatitis, Viral, Type E

Description

Hepatitis E, which is caused by the hepatitis E virus (HEV), cannot be distinguished reliably from other forms of acute viral hepatitis except by specific serologic testing.

Occurrence

HEV, which is transmitted by the fecal-oral route, occurs both in epidemic and sporadic forms. Transmission is associated primarily with ingestion of fecally contaminated drinking water. The potential for HEV transmission from contaminated food is still under investigation, and there is no evidence of transmission by percutaneous or sexual exposures (1,2).

Hepatitis E occurs primarily in adults. The highest rates of symptomatic disease (jaundice) have been reported in young to middle-aged adults. Lower disease rates in younger age groups may be the result of subclinical HEV infection. Chronic infection does not occur (1).

Epidemics and sporadic cases of hepatitis E have been reported from areas of Asia (Afghanistan, Bangladesh, Burma [Myanmar], China, India, Indonesia, Kazakhstan, Kyrgyzstan, Malaysia, Mongolia, Nepal, Pakistan, Tajikistan, Turkmenistan, and Uzbekistan), Mexico, the Middle East, Northern Africa, and sub-Saharan Africa. No outbreaks have been recognized in Europe, the United States, Australia, or South America (1). Hepatitis E usually occurs in persons who travel to or live in an endemic area. However, five cases have been identified in U.S. residents who had no history of recent international travel (3). Studies are in progress to determine if hepatitis E is an endemic disease in the United States.

Risk for Travelers

The incidence of hepatitis E among travelers is unknown but likely low. As with hepatitis A, risk for infection is highest for those who frequently eat or drink in settings of poor sanitation (4,5).

Clinical Presentation

The incubation period averages 40 days (range 15-60 days). Signs and symptoms, if they occur, include fatigue, loss of appetite, nausea, abdominal pain, and fever. Most patients with hepatitis E have a self-limiting course. Hepatitis E has a low (0.5%-4.0%) case-fatality rate in the general population. Fulminant hepatitis, however, is more commonly associated with hepatitis E than with other types of viral hepatitis, particularly among pregnant women in the second or third trimester. Fetal loss is common. Case-fatality rates as high as 15%-25% have been reported among pregnant women. Perinatal transmission of HEV has also been reported (1).

No FDA-approved diagnostic test is available, although some U.S. commercial laboratories offer serologic tests for HEV infection. Several of these tests have been shown to perform well in detecting anti-HEV in known positive sera, such as from travelers to an HEV-endemic country who develop acute hepatitis but have negative test results for other potential infectious and noninfectious causes of hepatitis. However, these tests provide highly discordant results when used on panels of U.S. blood donor sera, indicating that use of currently available serologic tests in persons without signs or symptoms of hepatitis and recent travel to an endemic country is unreliable, and results in this setting should be interpreted with caution (2,6,7).

Prevention

Vaccines to prevent hepatitis E are being developed, but none are yet available. Immune globulin prepared from plasma collected in HEV- endemic areas has not been effective in preventing clinical disease during HEV outbreaks. IG prepared from plasma collected from parts of the world where HEV is not an endemic disease such as the US is unlikely to be effective (5). The best prevention of infection is to avoid potentially contaminated water and food and use measures recommended to prevent hepatitis A and other enteric infections.

Treatment

No specific treatment is available for hepatitis E. Treatment is supportive.

References

  1. Labrique AB, Thomas DL, Stoszek SK, Nelson KE. Hepatitis E: an emerging infectious disease. Epidemiol Rev. 1999;21:162-79.
  2. Emerson SU, Purcell RH. Hepatitis E virus. Rev Med Virol. 2003;13:145-54.
  3. Amon JJ, Drobeniuc J, Bower WA, Magana JC, Escobedo MA, Williams IT, et al. Locally acquired hepatitis E virus infection, El Paso, Texas. J Med Virol. 2006;78:741-6.
  4. CDC. Hepatitis E among U.S. travelers, 1989-1992. MMWR Morbid Mortal Wkly Rep. 1993;42:1-4.
  5. Schwartz E, Jenks NP, Van Damme P, Galun E. Hepatitis E virus infection in travelers. Clin Infect Dis. 1999;29:1312-4.
  6. Mast EE, Alter MJ, Holland PV, Purcell RH. Evaluation of assays for antibody to hepatitis E virus by a serum panel. Hepatology. 1998;27:857-61.
  7. Mast EE, Kuramoto IK, Favorov MO, Schoening VR, Burkholder BT, Shapiro CN, et al. Prevalence of and risk factors for antibody to hepatitis E virus seroreactivity among blood donors in Northern California. J Infect Dis. 1997;176:34-40.
ANTHONY FIORE, BETH BELL

  • Page last updated: January 07, 2009
  • Content source:
    Division of Global Migration and Quarantine
    National Center for Preparedness, Detection, and Control of Infectious Diseases
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