The first description of hepatitis or “episodic jaundice” dates back to the time of Hippocrates, and the earliest outbreaks were reported in Europe in the seventeenth and eighteenth centuries [ 1 ].

During World War II the scientific details regarding this disease were obtained. Hepatitis A was epidemiologically differentiated from hepatitis B in 1940s but it was only in 1970s that serological tests were developed to definitively diagnose this disease.

Hepatitis A occurs worldwide but is endemic in Central, South America, Asia, the Middle East, and Africa. It is caused by hepatitis A virus (HAV) , a non-enveloped RNA virus belonging to the family of Picronaviridae . Humans are the only natural host. HAV is resistant to most organic solvents and detergents and can survive at a pH as low as 3 but can be inactivated by high temperature (>85 °C), chlorine, and formalin [ 2 ]. HAV infection is acquired through fecal-oral route either by person-person contact or through ingestion of contaminated food or water. The incubation period is approximately 28 days [ 3 ]. HAV replicates in the liver; infected persons shed the virus for 1–3 weeks and have a very high risk of transmission 1–2 weeks prior to the onset of symptoms. Risk factors for HAV infection include international traveling, men who have sex with men, intravenous drug users, and persons with chronic liver disease or with clotting disorders. The clinical features are similar to other types of acute viral hepatitis. HAV infection presents as an acute febrile illness with nausea, abdominal discom fort, and jaundice. Other atypical manifestations include vasculitis, cryoglobulinemia, and neurologic, renal, and immunologic reactions. HAV is a self-limited disease that does not produce chronic infection or chronic liver disease. Fatality from acute liver failure occurs in 0.5 % of those infected. Diagnosis is made on clinical, epidemiologic, and serologic basis. The antibody test for total anti- HAV measures both IgM-HAV and IgG-HAV. IgM becomes positive in acute HAV infection within 5–10 days before the onset of symptoms and can persist up to 5–6 months. IgG appears in the convalescent phase of the disease and confers lifelong protection.

In the prevaccine era, the only methods for prevention of hepatitis A were hygienic measures and use of protective immunoglobulins. Two inactivated whole-virus hepatitis A vaccines, VAQTA and HAVRIX [ 4 , 5 ], were licensed in 1995 in the USA and approved for use. The other vaccines used worldwide are AVAXIM, EPAXAL, and Heavile. All these vaccines are made from different strains of the HAV; VAQTA is based on strain CR326F, and HAVRIX is based on strain HM175 and contains a preservative unlike VAQTA. Both vac cines are highly immunogenic. ACIP recommends vaccination for all children at 12–23 months of age. Adults who are at increased risk of infection or complication from HAV infection should be routinely vaccinated. HAVRIX is administered intramuscularly as a single primary dose in children 1–18 years (0.5 ml) and adults above 19 years (1 ml) followed by a booster at 6–12 months. VAQTA is administered similarly to HAVRIX; however the booster is administered 6–18 months after primary dose. In 2001, Twinrix—a combi nation vaccine with adult dose of hepatitis B vaccine (Engerix-B) and pediatric dose of HAVRIX—was approved for adults greater than 18 years of age; it is given intramuscularly at 0, 1, and 6 months. Contraindications to the vaccine include allergic reactions or moderate-to-severe illness. Adverse reactions include pain at injection site but systemic side effects are rare. The wide use of vaccines has resulted in a sustained reduction of disease in most of the developed world; however hepatitis A infection remains an ongoing issue in the developing world.

[1] . Bachman L (1952) Infectious hepatitis in Europe. In: Rodenwalt E (ed) World Atlas of Epidemic Diseases. Falk-Verlag Hamburg, Germany

[2] Siegl G, Weitz M, Kronauer G (1984) Stability of hepatitis A virus. Intervirology 22:218–226

[3] Krugman S, Giles JP, Hammond J (1967) Infectious hepatitis: evidence of two distinctive clinical, epidemiological and immunological types of infection. JAMA 200: 365–373

[4] Peetermans J (1992) Production, quality control and characterization of an inactivated hepatitis A vaccine. Vaccine 10(Suppl 1): S99–S101

[5] Armstrong ME, Giesa PA, Davide JP et al (1993) Development of the formalin- inactivated hepatitis A vaccine, VAQTA from the live attenuated virus strain CR326F. J Hepatol 18(Suppl 2):S20–S26