HEPATITIS A DISEASE : CLINICAL ASPECTS
In hepatitis A virus infection, an incubation period of 10 to 50 days (mean, 25 days) is usu-ally followed by the onset of fever; anorexia (poor appetite); nausea; pain in the right up-per abdominal quadrant; and, within several days, jaundice. Dark urine and clay-colored stools may be noticed by the patient 1 to 5 days before the onset of clinical jaundice. The liver is enlarged and tender, and serum aminotransferase and bilirubin levels are elevated as a result of hepatic inflammation and damage. Recovery occurs in days to weeks.
Many persons who have serologic evidence of acute hepatitis A infection are asympto-matic or only mildly ill, without jaundice (anicteric hepatitis A). The infection-to-disease ratio is dependent on age; it may be as high as 20:1 in children and approximately 4:1 in older adults. Almost all cases (99%) of hepatitis A are self-limiting. Chronic hepatitis such as that seen with hepatitis B is very rare. In rare cases, fulminant fatal hepatitis associated with extensive liver necrosis may occur (~0.1%).
Antibody to hepatitis A virus can be detected during early illness, and most patients with symptoms or signs of acute hepatitis A already have detectable antibody in serum. Early antibody responses are predominantly IgM, which can be detected for several weeks or months. During convalescence, antibody of the IgG class predominates. The best method for documentation of acute hepatitis A virus infection is the demonstration of high titers of virus-specific IgM antibody in serum drawn during the acute phase of illness. Because IgG antibody persists indefinitely, its demonstration in a single serum sample is not indicative of recent infection; a rise in titer between acute and convalescent sera must be documented. Immune electron microscopic identification of the virus in fecal specimens and isolation of the virus in cell cultures remain research tools.
There is no specific treatment for patients with acute hepatitis A. Supportive measures in-clude adequate nutrition and rest. Avoidance of exposure to contaminated food or water are important measures to reduce the risk of hepatitis A infection.
Passive (ie, antibody) prophylaxis for hepatitis A has been available for many years. Immune serum globulin (ISG), manufactured from pools of plasma from large segments of the general population, is protective if given before or during the incubation period of the disease. It has been shown to be about 80 to 90% effective in preventing clinically apparent type A hepatitis. In some cases, infection occurs but disease is ameliorated; that is, patients develop anicteric, usually asymptomatic, hepatitis A. At present, ISG should be administered to household contacts of hepatitis A patients and those known to have eaten uncooked foods prepared or handled by an infected individual. Once clinical symp-toms have appeared, the host is already producing antibody, and administration of ISG is not indicated. Persons from areas of low endemicity traveling to areas with high infection rates may receive ISG before departure and at 3- to 4-month intervals as long as potential heavy exposure continues, but active immunization is preferable .
For hepatitis A, live attenuated vaccines have been evaluated but have demonstrated poor immunogenicity and have not been effective when given orally. Formalin-killed vaccines induce antibody titers similar to those of wild-virus infection and are almost 100% pro-tective. Use of this vaccine is preferable to passive prophylaxis for those with prolonged or repeated exposure to hepatitis A.
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