eMedicine Specialties > Gastroenterology > Liver

Hepatitis E

Author: Jonathan M Schwartz, MD, Assistant Professor, Department of Medicine, Division of Gastroenterology and Hepatology, Oregon Health and Sciences University
Coauthor(s): Kenneth Ingram, PAC, Assistant Professor, Department of Medicine, Division of Gastroenterology and Hepatology, Oregon Health Sciences University; Kenneth D Flora, MD, Adjunct Associate Professor of Medicine, Division of Gastroenterology and Hepatology, Oregon Health Sciences University; Consulting Staff, Department of Gastroenterology, The Oregon Clinic
Contributor Information and Disclosures

Updated: Nov 11, 2008

Introduction

Background

Hepatitis E virus (HEV) is an enterically transmitted infection that is typically self-limited. It is spread by fecally contaminated water within endemic areas. Outbreaks can be epidemic and individual. Hepatitis E has many similarities with hepatitis A. Hepatitis E infection has recently been associated with chronic hepatitis in solid organ-transplant recipients.1

HEV was discovered during electron microscopy of feces contaminated with enteric non-A, non-B hepatitis. The virus is icosahedral and nonenveloped. It has a diameter of approximately 34 nanometers, and it contains a single strand of RNA approximately 7.5 kilobases in length.

Hepatitis E is an RNA virus of the genus Hepevirus. Four hepatitis E genotypes exist, and genotype 1 causes human disease.

The most exciting recent advancement has been the development of a successful recombinant hepatitis E vaccine.2

Pathophysiology

The HEV genome contains 3 open reading frames (ORFs). The largest, ORF-1, codes for the nonstructural proteins responsible for viral replication. ORF-2 contains genes encoding the capsid. The function of ORF-3 is unknown, but the antibodies directed against ORF-3 epitopes have been identified.

Frequency

United States

The prevalence rate of anti-HEV antibodies is less than 2%. The route of exposure is unknown but generally is attributed to travel in endemic areas.

International

Hepatitis E has worldwide distribution, but predominating factors include tropical climates, inadequate sanitation, and poor personal hygiene. It is found most often in developing countries near the equator, in both the Eastern and Western hemispheres. Outbreaks are associated with rainy seasons, floods, and overcrowding. Water supply contamination with human feces is a frequent source of epidemics. The largest outbreak was reported in northeast China, with 100,000 people affected between 1986 and 1988. The reservoir of HEV is unknown, but it may be transmitted by animals.

Mortality/Morbidity

  • The overall case fatality rate is 4%.
  • The case fatality rate among pregnant women is 20%, which increases during the second and third trimesters. Reported causes of death include encephalopathy and disseminated intravascular coagulation.
  • The rate of fulminant hepatic failure in infected pregnant women is high.

Race

  • Infection has no apparent racial predilection.

Sex

  • Although predilection is unknown, pregnant women are prone to complications.

Age

  • Hepatitis E predominantly affects those aged 15-40 years.
  • It may affect younger age groups but generally is not recognized and may be subclinical.
  • No chronic cases have been described.

Clinical

History

The incubation period ranges from 15 days to 60 days, and the course of infection has 2 phases termed prodromal and icteric.

  • Prodromal-phase symptoms include the following:
    • Myalgia
    • Arthralgia
    • Fever with mild temperature elevations (25-97%)
    • Anorexia (66-100%)
    • Nausea/vomiting (30-100%)
    • Weight loss (typically 2-4 kg)
    • Dehydration
    • Right upper quadrant pain that increases with physical activity
  • Icteric-phase symptoms include the following:
    • Jaundice - May be difficult to see with some patients' natural skin color; serum bilirubin level is greater than 3 mg/dL; scleral icterus is present
    • Dark urine
    • Light-colored stools (20-40%)
    • Pruritus (50%)
  • Other features include the following:
    • Urticarial rash
    • Diarrhea
    • Rapidly increasing serum amino transferase (alanine aminotransferase [ALT], aspartate aminotransferase [AST]) levels that peak within 4-6 weeks of onset and gradually decrease to normal within 1-2 months
    • Viral excretion in stool persisting 14 days from onset
  • Symptoms of HEV are similar to other hepatitides and include the following:
    • Abdominal pain (35-80% of patients)
    • Jaundice
    • Anorexia
    • Hepatomegaly (10-85%)
    • Malaise (95-100%)
    • Vomiting
  • When or how long the patient is infectious cannot be determined, but infectivity may relate to the presence of the virus in the stool.

Physical

  • Right upper quadrant tenderness
  • Possible enlarged liver (palpable edges)
  • Possible splenomegaly
  • Possible transient spider angiomata

Causes

  • HEV is spread by fecally contaminated water within endemic areas. See Background.

More on Hepatitis E

Overview: Hepatitis E
Differential Diagnoses & Workup: Hepatitis E
Treatment & Medication: Hepatitis E
Follow-up: Hepatitis E
References
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References

  1. Kamar N, Selves J, Mansuy JM, et al. Hepatitis E virus and chronic hepatitis in organ-transplant recipients. N Engl J Med. Feb 21 2008;358(8):811-7. [Medline].

  2. Shrestha MP, Scott RM, Joshi DM, et al. Safety and efficacy of a recombinant hepatitis E vaccine. N Engl J Med. Mar 1 2007;356(9):895-903. [Medline].

  3. Favorov MO, Fields HA, Purdy MA, et al. Serologic identification of hepatitis E virus infections in epidemic and endemic settings. J Med Virol. Apr 1992;36(4):246-50. [Medline].

  4. Fields HA, Favorov MO, Margolis HS. Hepatitis E virus: a review. J Clin Immunoassay. 1993;16:215-23.

  5. Ghabrah TM, Tsarev S, Yarbough PO, et al. Comparison of tests for antibody to hepatitis E virus. J Med Virol. Jun 1998;55(2):134-7. [Medline].

  6. Harrison TJ. Hepatitis E virus -- an update. Liver. Jun 1999;19(3):171-6. [Medline].

  7. Mast EE, Krawczynski K. Hepatitis E: an overview. Annu Rev Med. 1996;47:257-66. [Medline].

  8. Purdy MA, Krawczynski K. Hepatitis E. Gastroenterol Clin North Am. Sep 1994;23(3):537-46. [Medline].

  9. Skidmore SJ. Factors in spread of hepatitis E. Lancet. Sep 25 1999;354(9184):1049-50. [Medline].

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Further Reading

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Keywords

hepatitis E, hepatitis E virus, HEV, Caliciviridae family, anti-HEV antibodies

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Contributor Information and Disclosures

Author

Jonathan M Schwartz, MD, Assistant Professor, Department of Medicine, Division of Gastroenterology and Hepatology, Oregon Health and Sciences University
Jonathan M Schwartz, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, and American Hepato-Pancreato-Biliary Association
Disclosure: Nothing to disclose.

Coauthor(s)

Kenneth Ingram, PAC, Assistant Professor, Department of Medicine, Division of Gastroenterology and Hepatology, Oregon Health Sciences University
Disclosure: Nothing to disclose.

Kenneth D Flora, MD, Adjunct Associate Professor of Medicine, Division of Gastroenterology and Hepatology, Oregon Health Sciences University; Consulting Staff, Department of Gastroenterology, The Oregon Clinic
Kenneth D Flora, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, and American Gastroenterological Association
Disclosure: Nothing to disclose.

Medical Editor

David Eric Bernstein, MD, Chief, Section of Hepatology, North Shore University Hospital, Director, Associate Professor, Department of Internal Medicine, Division of Hepatology, New York University School of Medicine
David Eric Bernstein, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Oscar S Brann, MD, FACP, Associate Clinical Professor, Department of Medicine, University of California at San Diego; Consulting Staff, Mecklenburg Medical Group
Oscar S Brann, MD, FACP is a member of the following medical societies: American Gastroenterological Association
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
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