Enterically transmitted viral hepatitis can be caused by either hepatitis A or E viruses. The former which is the predominant form in the United States, is a 27 nm picornavirus. This virus is endemic throughout the world and the most common form of epidemic hepatitis. Hepatitis E virus is a recently discovered agent also capable of causing enterically transmitted hepatitis. This virus, classified as a calicivirus, is endemic in Asia, Northern and Western parts of Africa, and Mexico. Morphologically, it is a 27-38 nm virus that shares features with picornavirus.

The clinical diseases resulting from both viral infections are similar. Both are transmitted primarily by the fecal-oral routes and are particularly common in low socio-economic areas, especially those with inadequate water and sewage treatment facilities. Other factors that are associated with high prevalence rates include overcrowding and low personal hygiene standards. Although rare cases have been associated with parenteral transmission or sexual exposure, these are uncommon routes of transmission. Clinically, both viruses can cause acute hepatitis which rarely can lead to fulminant hepatic failure. However, neither hepatitis A or E viruses cause chronic liver disease and infection results in lifetime immunity.

In countries with high levels of sanitation, epidemics of hepatitis A are usually limited to homes for the disabled and day care facilities. In 1991, a total of 249 cases of hepatitis A infection were reported to the Pennsylvania Department of Health. Risk factors included contacts with known cases of hepatitis A (31%), users of day care facilities (10%, foreign travel (9%), ingestion of raw shellfish (8%), and IV drug use (3.5%). Epidemic outbreaks accounted for 3.8% of cases.

Clinically, the incubation period for hepatitis A is between 15-50 days. Most cases occur in either

children or young adults. It is of note that, by the age of 40, approximately 50% of the population in developed countries have antibodies to hepatitis A virus (HAV). A majority of these individuals do not relate a history suggestive of hepatitis suggesting that many infections are asymptomatic. It appears that this is particularly common in children. In those who develop overt hepatitis, the major symptoms include fever, malaise, anorexia, nausea, abdominal pain and jaundice. The acute disease is characterized by marked elevations of hepatic enzymes, particularly the ALT. Fulminant hepatitis is rare; the mortality rate in those with overt hepatitis is 0.6%. There are no long term sequelae resulting from hepatitis A infections.

Hepatitis A prophylaxis consists of the administration of immune globulin. This provides passive protection and is primarily indicated for individuals traveling in endemic areas or those who have close exposure to a person with acute hepatitis. Immune globulin is effective if administered within two weeks of an exposure. A single dose of 0.02 ml/kg provides up to three months protection.

Hepatitis E virus infections should be suspected in persons with clinical evidence of acute viral hepatitis that is not supported by serological tests for hepatitis A, B, or C. The incubation period is 2-9 weeks (mean 6 weeks). Symptoms are similar to those of hepatitis A. It appears that 15-40 year olds are the most susceptible population. Complete recovery is seen in over 98% of the cases; the major exception is pregnant females (particularly those in the third trimester) in which there may a 20% fatality rate.

Although these are major causes of hepatitis in the U.S., fecal-oral transmission plays a minor role, if any, in their incidence. Hepatitis B infection is transmitted sexually, parenterally, and perinatally. Hepatitis C is almost exclusively transmitted by parenteral routes; sexual transmission and perinatal infections are extremely uncommon. Unlike hepatitis A and E, infections with either hepatitis B or C may result in chronic liver disease.