Hepatitis A Virus Infection

Infection with HAV, formerly known as infectious hepatitis, also occurs worldwide. The causative agent of hepatitis A is a small single-stranded RNA virus, similar to the enteroviruses, 27 nm in diameter . Viral particles are present in hepatocytes and in faeces during the late incubation period and early stage of clinical hepatitis. Unlike HBV, with HAV there is no persistent state of infection with prolonged viraemia, so transmission by blood or blood products via parenteral routes almost never occurs. Humans represent the only significant reservoir of infection. Faeces appear to be the only important source of virus and transmission occurs most often via the faecal-oral route, or via food or water contaminated by sewage. Shellfish such as clams, oysters and mussels concentrate the virus during filter feeding and are common sources of hepatitis A infection. High risk groups include male homosexuals, children and staff members in day care centres, and other populations living in crowded settings such as prisons, military facilities and certain schools. Infection in young children is usually asymptomatic; most recognized cases occur in household contacts of children. There is little evidence for sexual transmission between heterosexual partners. The highest attack rates are found in developing countries, where housing and sanitation are inadequate. In some developing countries more than 90% of young adults have serological evidence of prior infection, as compared with approximately 20% of adults in the United States. About one-half of acute viral hepatitis cases occurring in the United States are due to HAV.

The pattern of secondary infections in household contacts of patients with hepatitis A indicates that the patient is most infectious late in the incubation period or soon after the onset of symptoms, and this corresponds with the presence of the largest numbers of viral particles in the faeces. Faecal excretion of virus ends at about the time serum transaminases rise and jaundice appears in icteric cases. Although a transient viraemia may occur late in the incubation period, percutaneous transmission by blood or serum occurs very infrequently and is insignificant as a mode of HAV transmission.

Approximately 90% of cases of HAV infection are asymptomatic. In patients who become ill the clinical picture of the acute hepatitis is indistinguishable from that produced by HBV or by NANB viruses. The incubation period is usually from 2-6 weeks. Illness begins with fever, malaise, fatigue, headache, anorexia, nausea and vomiting, myalgias and epigastric or right upper quadrant pain. Diarrhoea, arthralgias, rash and respiratory symptoms of cough, coryza, and sore throat occur occasionally. Onset of symptoms may be more abrupt in hepatitis A than in hepatitis B, in which the illness usually develops gradually. As in hepatitis B, increased serum transaminases, dark urine and rising serum bilirubin precede the appearance of clinical jaundice. The illness usually lasts an average of two weeks, but in adults jaundice may last for one month or more. The histopathological findings are indistinguishable from those seen in acute hepatitis B. In contrast to hepatitis B, hepatitis A virus infection is not followed by chronic hepatitis.

Infection with HAV is followed by long-lasting immunity to reinfection. Serum IgG antibodies to HAV (anti-HAV)) appear during the convalescent stage and persist for years; IgM antibody is present during acute infection and disappears after 3-6 months. The best method of making a serological diagnosis of hepatitis A is by detection of anti-HAV IgM antibody during or shortly after the clinical illness; IgM antibody is not likely to be acquired passively via blood transfusion.

Careful attention to hand washing and proper disposal of infectious faeces and disposal or disinfection of contaminated objects can reduce the transmission of HAV infection. Household bleach diluted 1:32 can be used to disinfect objects or surfaces contaminated with HAV. Water can be rendered non-infectious by boiling for one minute or by adequate chlorination; the concentration of chlorine required depends upon the amount of organic matter in the water. Immunoglobulin can provide effective pre- or post-exposure passive protection against hepatitis A infection; it is recommended for household or sexual contacts, staff of day care centres, residents and staff of prisons or institutions for the mentally retarded, and for travellers to highly endemic areas. A single injection of immunoglobulin 0.02 ml/kg given intramuscularly within a few days of exposure to HAV reduces the attack rate of clinical hepatitis A by 80-90%; protection against further exposures lasts from 2-6 months. For travellers or residents in highly endemic settings, 0.06 ml/kg given intramuscularly provides protection for at least five months. The dose can be repeated every five months. A killed virus vaccine has been developed and appears to be immunogenic, but it is not yet available for general use.