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Hepatitis A

Last updated: April 28, 2021

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Hepatitis A infection is caused by the hepatotropic hepatitis A virus (HAV) and is usually transmitted via the fecal-oral route. About half of all cases of HAV infection that occur in the US are acquired during visits to countries that are endemic for HAV (e.g., tropical or subtropical regions). HAV infection results in acute hepatitis with a clinical course characterized by prodromal symptoms of fever and malaise, followed by jaundice. As in any other case of acute viral hepatitis, high levels of serum transaminase, and mixed hyperbilirubinemia are observed. Serological detection of anti-HAV IgM, which is elevated during acute infection, confirms the diagnosis. While prodromal symptoms resolve within a few weeks, jaundice usually resolves within 1–3 months. No chronic sequelae occur and acute hepatic failure occurs only in very rare cases. Therefore, supportive care is usually the only treatment required. As of 2006, routine immunization against hepatitis A is recommended for all children older than 12 months. Certain high-risk groups, such as tourists to areas where HAV is endemic, should also be immunized against HAV if they have not been vaccinated in the past.

An important differential diagnosis is another feco-orally transmitted viral infection caused by the hepatitis E virus (HEV). The clinical presentation of hepatitis E is almost identical to that of hepatitis A, with the exception that pregnant women are at a high risk of developing acute liver failure. Serological tests help to distinguish HEV from HAV.

  • Incidence (in the US): ∼ 2,000 cases per year (50% acquired during travels abroad) [1]
    • Hepatitis A virus is the second most common cause of acute hepatitis in the US.
    • Hepatitis A is very common in tropical and subtropical regions.
  • Age: Vaccination programs have made the disease fairly rare in children; infection is now more widespread in adults. [2]

Epidemiological data refers to the US, unless otherwise specified.

  • Pathogen: hepatitis A virus [2]
    • Belongs to the family of Picornaviridae and the genus Hepatoviridae
    • Small (27 nm in diameter), non-enveloped virus with single-stranded, positive-sense RNA
    • Resistant to denaturation by gastric acid, heat, and chemicals, and can remain viable for months in fresh and saltwater
    • Humans are the only reservoir for the hepatitis A virus. [3]
  • Route of transmission: fecal-oral [4]
    • Contaminated water and food (e.g., raw shellfish)
    • Risk groups: nursing home residents, international travelers, prison inmates, men who have sex with men, IV drug users.
  • Infectious period: 2 weeks before to 1 week after the onset of the illness [3]

When it comes to viral hepatitis, vowels (A and E) are bowels (transmitted feco-orally).

HAV is not cytopathic in itself; research suggests that liver damage is caused by cellular immunity (especially CD8+ T cells). [2]

HAV infection in children is typically asymptomatic. The risk of symptomatic disease increases with age and coinfection (e.g., with hepatitis B).

When it comes to viral hepatitis, vowels (A and E) cause only AcutE hepatitis while Consonants (B, C, and D) may have Chronic sequelae as well.

Positive IgG values indicate immunity against HAV due to prior infection or vaccination.

For an overview comparing the different types of viral hepatitis see “Differential diagnosis of viral hepatitis.”

Hepatitis E [9][10]

  • Pathogen: hepatitis E virus (HEV)
  • Epidemiology
    • Uncommon in the US
    • An important cause of endemic viral hepatitis in developing countries and equatorial regions (e.g., India, western and northern Africa, Middle East, and Mexico)
  • Route of transmission: fecal-oral (especially via contaminated water, food, or sources)
  • Pathophysiology: The degree of hepatic injury is usually mild and the patient may present with clinical features of acute hepatitis.
  • Clinical features: similar to those of hepatitis A (see “Clinical features” above). [2]
  • Diagnostics [2]
  • Treatment: supportive care
  • Prevention: no vaccine available

Women who are Expecting are FULly aware of the risks: pregnant women with hepatitis E can develop FULminant hepatitis.

A fulminant course is relatively common in pregnant women with HEV infection (occurring in up to 20% of cases) and is life-threatening for both the mother and fetus.

The differential diagnoses listed here are not exhaustive.

Disease is self-limiting; only supportive care is required.

Hepatitis A pre-exposure prophylaxis [3][13]

Hepatitis A post-exposure prophylaxis [3][4]

Post-exposure prophylaxis is indicated for all previously unvaccinated individuals who have been exposed to a serologically confirmed case of HAV infection. In order to be effective, post-exposure prophylaxis should be administered within two weeks of exposure.

  1. Lai M, Chopra S. Hepatitis A Virus Infection in Adults: An Overview. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/hepatitis-a-virus-infection-in-adults-an-overview.Last updated: October 17, 2016. Accessed: March 24, 2017.
  2. Kumar V, Abbas AK, Aster JC. Robbins & Cotran Pathologic Basis of Disease. Elsevier Saunders ; 2014
  3. Hepatitis A Questions and Answers for Health Professionals. https://www.cdc.gov/hepatitis/hav/havfaq.htm#B1. Updated: July 13, 2016. Accessed: March 24, 2017.
  4. Kasper DL, Fauci AS, Hauser SL, Longo DL, Lameson JL, Loscalzo J. Harrison's Principles of Internal Medicine. McGraw-Hill Education ; 2015
  5. Kim J-Y, Joung J-Y, Kang J-Y, Son C-G, Cho J-H. Acute Viral Hepatitis A with Cholestatic Hepatitis Treated with Traditional Korean Medicine: A Case Report. Journal of Korean Medicine. 2015; 36 (4): p.114-121. doi: 10.13048/jkm.15038 . | Open in Read by QxMD
  6. Watanabe H, Sekine H, Uruma T, et al. Increase of atypical lymphocytes expressing CD4+/CD45RO+ in an infectious mononucleosis-like syndrome associated with hepatitis A virus infection. Journal of Infection and Chemotherapy. 2009; 15 (3): p.187-190. doi: 10.1007/s10156-009-0677-9 . | Open in Read by QxMD
  7. De los Angeles Rodríguez Lay L, Larralde Díaz O, Martínez Casanueva R, Gutiérrez Moreno A. Anti-Hepatitis A Virus Immunoglobulin M Antibodies in Urine Samples for Rapid Diagnosis of Outbreaks. Clinical Diagnostic Laboratory Immunology. 2003; 10 (3): p.492-494. doi: 10.1128/cdli.10.3.492-494.2003 . | Open in Read by QxMD
  8. Matheny SC, Kingery JE. Hepatitis A.. Am Fam Physician. 2012; 86 (11): p.1027-34; quiz 1010-2.
  9. Hepatitis E. http://www.who.int/mediacentre/factsheets/fs280/en/. Updated: July 1, 2016. Accessed: March 24, 2017.
  10. Hepatitis E FAQs for Health Professionals. https://www.cdc.gov/hepatitis/hev/hevfaq.htm. Updated: May 31, 2015. Accessed: March 24, 2017.
  11. Park W-J, Park B-J, Ahn H-S, et al. Hepatitis E virus as an emerging zoonotic pathogen. Journal of Veterinary Science. 2016; 17 (1): p.1. doi: 10.4142/jvs.2016.17.1.1 . | Open in Read by QxMD
  12. Kamar N, Izopet J, Dalton HR. Chronic Hepatitis E Virus Infection and Treatment. Journal of Clinical and Experimental Hepatology. 2014; 3 (2): p.134-140. doi: 10.1016/j.jceh.2013.05.003 . | Open in Read by QxMD
  13. Chopra S, Lai M. Hepatitis A Virus Infection: Prevention. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/hepatitis-a-virus-infection-prevention.Last updated: November 2, 2016. Accessed: March 24, 2017.
  14. Herold G. Internal Medicine. Herold G ; 2014
  15. Umashanker R, Chopra S. Hepatitis E Virus Infection. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/hepatitis-e-virus-infection.Last updated: December 14, 2016. Accessed: March 24, 2017.