The likelihood of symptomatic illness from HAV infection is directly related to age. ![]() Fulminant hepatic failure occurs in less than 1% of cases. Symptomatic hepatitis A infection is clinically indistinguishable from other types of acute viral hepatitis, but is usually mild and self-limited. The mean incubation period of hepatitis A is approximately 28 days (range 15–50 days). Infected children and infants may excrete virus longer than adults. Although virus is present in serum of an infected person, its concentration is several orders of magnitude less than in feces. Most persons cease to be infectious 1 week after jaundice appears. Peak infectivity occurs during the 2 weeks prior to onset of clinical signs and symptoms (jaundice or elevated liver enzymes). HAV replicates in the liver, is excreted in bile, and is shed in the stool of infected people in high concentrations 2–3 weeks before and 1 week after onset of illness. Hepatitis A is typically acquired through fecal-oral transmission, either from direct person-to-person contact or consumption of contaminated food or water. The virus is relatively stable at low pH levels and freezing to moderate temperatures, but can be inactivated by high temperature (185☏ or higher for 1 minute) or through disinfection of surfaces with a 1:100 dilution of sodium hypochlorite in water. Depending on conditions, HAV can be stable in the environment for months. Humans are the only natural host, although several nonhuman primate species have been infected in laboratory settings. HAV was first identified by immune electron microscopy in 1973 and initially replicated in mammalian cell culture in 1979. Hepatitis A is caused by infection with hepatitis A virus (HAV), a non-enveloped RNA virus that is classified as a picornavirus. ![]() Monina Klevens, DDS, MPH Noele Nelson, MD, PhD, MPH Disease Description Manual for the Surveillance of Vaccine-Preventable DiseasesĪuthors: Megan G.
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