Clinically, hepatitis type E was first identified in the early 1980s and described as "epidemic, non-A, non-B hepatitis." It was characterized as an infectious waterborne illness that was similar in many ways to HAV infection.[1,2]
Transmission of HEV occurs predominantly by the fecal-oral route, although the parenteral and perinatal routes have been implicated. HEV infection is prevalent in several developing countries where contamination of water supplies and lack of adequate sanitation are frequent.[1,2,8,9] In these areas, a large proportion of cases of acute viral hepatitis are due to infection with HEV genotype 1 or 2. The disease is considered to be infrequent in developed countries, where it occurs primarily in relation to travel to disease-endemic areas.
Locally acquired HEV infection has been documented, usually as genotype 3 and less commonly as genotype 4. The source of HEV infection acquired in nonendemic areas is unclear; however, HEV RNA has been detected in pork products, and there is a reported association between consumption of pork (often inadequately cooked) and hepatitis E.[8,9,10,11,12,13] HEV is therefore considered to be a zoonotic virus, with domestic swine and wild deer serving as reservoirs of HEV in nature.
For reasons that have not been defined, hepatitis E occurs more often and is more severe in pregnant women in endemic regions than in nonpregnant women, leading to a high mortality rate (10%-25%) and worse obstetric outcomes.[1,2,8,10]
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Cite this: William F. Balistreri. Thickening the Alphabet Soup: The Emergence of Hepatitis E - Medscape - Apr 25, 2013.