HEPATITIS A DISEASE
Hepatitis A virus is the cause of what was formerly termed infectious hepatitis or short-incubation hepatitis. This virus is spread by the fecal–oral route, and out-breaks may be associated with contaminated food or water. The illness is subclini-cal in up to one half of infected adults. When symptomatic, there is usually fever and jaundice. Although fatal disease may occur, self-limited illness is the rule. Chronic hepatitis A rarely if ever occurs.
Humans appear to be the major natural hosts of hepatitis A virus. Several other primates (including chimpanzees and marmosets) are susceptible to experimental infection, and nat-ural infections of these animals may occur. The major mode of spread of hepatitis A is fecal–oral. Inoculation of infectious material intramuscularly can produce disease; trans-mission through blood transfusion, although possible, is not an important means of spread. While most cases of hepatitis A are not linked to a single contaminated source and occur sporadically, outbreaks have been described. The disease is common under conditions of crowding, and it occurs at high frequency in mental hospitals, schools for the retarded, and day-care centers. A chronic carrier state has not been observed with hepatitis A; perpetua-tion of the virus in nature presumably depends on sporadic subclinical infections and person-to-person transmission.
Outbreaks of hepatitis A have been linked to the ingestion of undercooked seafood, usually shellfish from waters contaminated with human feces. Common-source outbreaks related to other foods, including vegetables as well as con-taminated drinking water, have also been reported.
Hepatitis A is widespread but seroepidemiologic studies have shown marked variation in infection rates among various population groups. For example, rates are higher among those of lower socioeconomic status and among male homosexuals. Less than 50% of the general population of the United States now has serologic evidence of prior hepatitis A virus infection, and rates have been decreasing since 1970, apparently because of better sanitation and less crowding. In contrast, more than 90% of the adult population in many developing countries shows evidence of previous hepatitis A infection. The risk of clini-cally evident disease is much higher in infected adults than in children; travelers from developed countries who enter endemic areas are particularly susceptible. Patients are most contagious in the 1 to 2 weeks prior to the onset of clinical disease.
The virus is believed to replicate initially in the enteric mucosa. It can be demonstrated in feces by electron microscopy for 10 to 14 days before onset of disease. In most patients with symptoms of the disease, virus is no longer found in fecal specimens. Multiplication in the intestines is followed by a period of viremia with spread to the liver. The response to replication in the liver consists of lymphoid cell infiltration, necrosis of liver arenchymal cells, and proliferation of Kupffer cells. The extent of necrosis often coincides with the severity of disease. A variable degree of biliary stasis may be present. Detectable levels of IgG antibody to hepatitis A virus persist indefinitely in serum, and patients with anti–hepatitis A virus antibodies are immune to reinfection. Although virus-specific IgA has been demonstrated in stool, secretory immunity has not been shown to be important for hepatitis A.