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Introduction to Hepatitis AHepatitis A is the most common type of hepatitis reported in the United States. Hepatitis A was formerly called infectious hepatitis and was differentiated epidemiologically from hepatitis B in the 1940’s. In the 1970’s identification of the virus and the development of serologic tests for hepatitis B distinguished hepatitis A from other types of non-B hepatitis. The primary methods for prevention of hepatitis A were passive immunization with immune globulin (IG) that provided short-term protection and hygienic measures. The Hepatitis A vaccine was licensed in 1995 for use in children over the age of two and can provide long term protection up to 10 years. Hepatitis A is caused by infection with the hepatitis A virus (HAV), a non-enveloped RNA agent that is classified as a picornavirus. Humans are the only natural reservoir of the virus. A chronic HAV carrier state has not been reported and there are no insect or animal vectors. The Hepatitis A virus is stable at a low pH level and moderate temperatures below 185 degrees Fahrenheit , but can become inactivated by higher temperatures, formalin, and chlorine. The Hepatitis A virus replicates in the liver and approximately 10 to 12 weeks later, the virus is present in blood and is shed in feces. Peak titers occur during the 2 weeks before and 1 week after onset of the illness. Risk decreases and is minimal the week after the onset of jaundice. The modes of transmission of hepatitis A are the fecal-oral route with the virus being transmitted from person-to-person between household contact, sex partners, or by contaminated food or water. Blood-borne transmission of hepatitis A can occur, because the virus is present in serum during acute infection, but this mode of transmission has been reported infrequently.
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