Lecture 10 - Hepatitis A

Lecture 10 - Hepatitis A - Hepatitis A Hepatitis A The...

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14 Hepatitis A The first descriptions of hepatitis (epidemic jaundice) are generally attributed to Hippocrates. Outbreaks of jaundice, probably hepatitis A, were reported in the 17th and 18th centuries, particularly in association with military campaigns. Hepatitis A (formerly called infectious hepatitis) was first differentiated epidemiologically from hepatitis B, which has a long incubation period, in the 1940s. .Development of serologic tests allowed definitive diagnosis of hepatitis B. In the 1970s, identification of the virus, and development of serologic tests helped differentiate hepatitis A from other types of non-B hepatitis. Until 2004, hepatitis A was the most frequently reported type of hepatitis in the United States. In the prevaccine era, the primary methods used for preventing hepatitis A were hygienic measures and passive protection with immune globulin (IG). Hepatitis A vaccines were licensed in 1995 and 1996. These vaccines provide long-term protection against hepatitis A virus (HAV) infection. The similarities between the epidemiology of hepatitis A and poliomyelitis suggest that widespread vaccination of appropriate susceptible populations can substantially lower disease incidence, eliminate virus transmission, and ultimately, eliminate HAV infection. Hepatitis A Virus Hepatitis A is caused by infection with HAV, a nonenveloped RNA virus that is classified as a picornavirus. It was first isolated in 1979. Humans are the only natural host, although several nonhuman primates have been infected in laboratory conditions. Depending on conditions, HAV can be stable in the environment for months. The virus is relatively stable at low pH levels and moderate temperatures but can be inactivated by high temperature (185°F [85°C] or higher), formalin, and chlorine. Pathogenesis HAV is acquired by mouth (through fecal-oral transmission) and replicates in the liver. After 10–12 days, virus is present in blood and is excreted via the biliary system into the feces. Peak titers occur during the 2 weeks before onset of illness. Although virus is present in serum, its concentration is several orders of magnitude less than in feces. Virus excretion begins to decline at the onset of clinical illness, and has decreased significantly by 7–10 days after onset of symptoms. Most infected persons no longer excrete virus in the feces by the third week of illness. Children may excrete virus longer than adults. Hepatitis A 193
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14 Clinical Features The incubation period of hepatitis A is approximately 28 days (range 15–50 days). The clinical course of acute hepatitis A is indistinguishable from that of other types of acute viral hepatitis. The illness typically has an abrupt onset of fever, malaise, anorexia, nausea, abdominal discomfort, dark urine and jaundice. Clinical illness usually does not last longer than 2 months, although 10%–15% of persons have prolonged or relapsing signs and symptoms for up to 6 months. Virus may be excreted during a relapse.
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This note was uploaded on 04/29/2009 for the course BIOL 420 taught by Professor Edwardsoaks during the Fall '08 term at George Mason.

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Lecture 10 - Hepatitis A - Hepatitis A Hepatitis A The...

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