Hepatitis A infection, caused by an RNA virus in the picornavirus family, is the most common cause of hepatitis in the United States. It is transmitted mainly by the fecal-oral route and through contaminated foods. Transfusions are a rare source of hepatitis A. After ingestion, the virus is systemically absorbed and then replicates in the liver. The virus is shed in the biliary tract, making the stool of infected persons highly contagious. Stool virus concentrations are highest two weeks before symptoms develop, and transmission is most likely during this presymptomatic period. Most persons are no longer infectious about one week after jaundice begins. Infections in children younger than three years generally are asymptomatic, but most adolescents and adults develop symptoms. Children shed virus longer than adults, and young children, who also have poorer hygiene habits, are a frequent source of infection. Symptoms include malaise, fever, abdominal pain, and jaundice; illness lasts about two months. Fulminant hepatic failure is uncommon in children, and because a carrier state does not occur, cirrhosis and liver cancer do not result from hepatitis A infection. Leach reviewed the epidemiology and prevention of hepatitis A infection in children.
|Recommended in children two years and older living in areas where hepatitis A incidence is twice the U.S. average during 1987 to 1997 (i.e., approximately 20 cases per 100,000 persons). These areas are mostly in western states.|
|Recommended in persons with specific risk factors, such as travel to high-risk areas, men who have sex with men, illicit drug use, chronic liver disease, clotting factor disorders, and potential exposure to hepatitis A.|
|Consider in children two years and older in states with moderate infection rates (i.e., 10 to 20 cases per 100,000 persons).|
The number of reported cases of hepatitis A infection is decreasing, although it is unclear whether this decrease is a result of hepatitis A immunization. The highest infection rates occur in men 25 to 39 years of age who are members of a high-risk group such as American Indians, Alaskan natives, or Hispanics.
Prevention of hepatitis A infection includes active and passive measures, such as hand-washing, water sanitation, and food hygiene. Standard immunoglobulin IgG (0.02 mL per kg) is an effective secondary prevention when given within two weeks of exposure; it is protective for up to three months in travelers to high-risk regions. Higher dosages, up to 0.06 mL per kg, may protect travelers for up to five months. Persons with ongoing exposure risk should be vaccinated (see accompanying table). The vaccine and the IgG preparation can be given simultaneously, although there may be a slight, but not clinically significant, drop in eventual hepatitis A antibodies. IgG can interfere with response to live vaccines, so measles, mumps, rubella, and varicella vaccines should not be administered simultaneously with hepatitis A IgG.
Vaccine choices include two inactivated preparations with similar efficacy. One dose (0.5 mL for children two to 18 years of age; 1.0 mL for persons older than 18 years) is effective in about 97 percent of children and adolescents, and two doses provide virtually 100 percent immunity. Doses should be given six to 12 months apart. No serious adverse effects have been reported from the vaccines. Prevaccination serologic testing is not necessary in children but may be useful in adolescents and adults with a high likelihood of previous exposure. A postvaccination antibody check is not necessary. Hepatitis A vaccine is not approved for children younger than two years because response may be blunted by interference from maternal antibodies, but this age group is being studied. Protection appears to remain for 20 years or more.
The author concludes that future nationwide immunization of children for hepatitis A is inevitable. Immunization potentially could eliminate hepatitis A from the population, although this will require a preparation that is effective in infants.