Hepatitis A, Acute
Hepatitis A is caused by an enterically transmitted RNA virus that, in older children and adults, causes typical symptoms of viral hepatitis, including anorexia, malaise, and jaundice. Young children may be asymptomatic. Fulminant hepatitis and death are rare. Chronic hepatitis does not occur. Diagnosis is by antibody testing. Treatment is supportive. Vaccination and previous infection are protective.
Hepatitis A virus (HAV) is a single-stranded RNA picornavirus. It is the most common cause of acute viral hepatitis and is particularly common among children and young adults.
In some countries, > 75% of adults have been exposed to HAV. In the US, an estimated 3000 cases occur annually—a decrease from 25,000 to 35,000 annual cases before the hepatitis A vaccine became available in 1995 (see CDC Hepatitis A FAQs).
HAV spreads primarily by fecal-oral contact and thus may occur in areas of poor hygiene. Waterborne and food-borne epidemics occur, especially in developing countries. Eating contaminated raw shellfish is sometimes responsible. Sporadic cases are also common, usually as a result of person-to-person contact.
Fecal shedding of the virus occurs before symptoms develop and usually ceases a few days after symptoms begin; thus, infectivity often has already ceased when hepatitis becomes clinically evident. HAV has no known chronic carrier state and does not cause chronic hepatitis or cirrhosis.
In children < 6 yr, 70% of hepatitis A infections are asymptomatic, and in children with symptoms, jaundice is rare. In contrast, most older children and adults have typical manifestations of viral hepatitis, including anorexia, malaise, fever, nausea, and vomiting; jaundice occurs in over 70%. Manifestations typically resolve after about 2 mo, but in some patients, symptoms continue or recur for up to 6 mo.
Recovery from acute hepatitis A is usually complete. Fulminant hepatitis rarely occurs.
In the initial diagnosis of acute hepatitis, viral hepatitis should be differentiated from other disorders causing jaundice (see Figure: Simplified diagnostic approach to possible acute viral hepatitis.). If acute viral hepatitis is suspected, the following tests are done to screen for hepatitis viruses A, B, and C:
If the IgM anti-HAV test is positive, acute hepatitis A is diagnosed. The IgG antibody to HAV (IgG anti-HAV) test is done (see Table: Hepatitis A Serology) to help distinguish acute from prior infection. A positive IgG anti-HAV test suggests prior HAV infection or acquired immunity. There is no further testing for hepatitis A.
HAV is present in serum only during acute infection and cannot be detected by clinically available tests.
IgM antibody typically develops early in the infection and peaks about 1 to 2 wk after the development of jaundice. It diminishes within several weeks, followed by the development of protective IgG antibody (IgG anti-HAV), which persists usually for life. Thus, IgM antibody is a marker of acute infection, whereas IgG anti-HAV indicates only previous exposure to HAV and immunity to recurrent infection.
No treatments attenuate acute viral hepatitis, including hepatitis A. Alcohol should be avoided because it can increase liver damage. Restrictions on diet or activity, including commonly prescribed bed rest, have no scientific basis.
Most patients may safely return to work after jaundice resolves, even if AST or ALT levels are slightly elevated.
For cholestatic hepatitis, cholestyramine 8 g po once/day or bid can relieve itching.
Viral hepatitis should be reported to the local or state health department.
Good personal hygiene helps prevent fecal-oral transmission of hepatitis A. Barrier protection is recommended, but isolation of patients does little to prevent spread of HAV.
Spills and contaminated surfaces in the home of patients can be cleaned with dilute household bleach.
Preexposure HAV vaccination (see Adult Immunization Schedule) should be provided for
Travelers to high or intermediate HAV endemicity
Diagnostic laboratory workers
Men who have sex with men
People who use injection or noninjection illicit drugs
People with chronic liver disorders (including chronic hepatitis C) because they have an increased risk of developing fulminant hepatitis due to HAV
People who receive clotting factor concentrates
People who anticipate close contact with an international adoptee during the first 60 days after arrival from a country with high or intermediate HAV endemicity
Preexposure HAV prophylaxis can be considered for day-care center employees and for military personnel.
Several vaccines against HAV are available, each with different doses and schedules; they are safe, provide protection within about 4 wk, and provide prolonged protection (probably for > 20 yr).
Previously, travelers were advised to get the hepatitis A vaccine ≥ 2 wk before travel; those leaving in < 2 wk should also be given standard immune globulin. Current evidence suggests immune globulin is necessary only for older travelers and travelers with chronic liver disease or another chronic disorder.
Postexposure prophylaxis should be given to family members and close contacts of patients with hepatitis A.
For healthy, unvaccinated patients aged 1 to 40 yr, a single dose of hepatitis A vaccine is given.
For other patients, particularly those > 75 yr, those with chronic liver disease, and immunocompromised patients, standard immune globulin (formerly immune serum globulin) prevents or decreases the severity of hepatitis A. A dose 0.02 mL/kg IM is generally recommended, but some experts advise 0.06 mL/kg (3 to 5 mL for adults). It can be given up to 2 wk after exposure, but the earlier, the better.
Hepatitis A virus is the most common cause of acute viral hepatitis; it is spread by the fecal-oral route.
Children < 6 yr may be asymptomatic; older children and adults have anorexia, malaise, and jaundice.
Fulminant hepatitis is rare, and chronic hepatitis, cirrhosis, and cancer do not occur.
Routine vaccination beginning at age 1 is recommended for all.
Vaccinate people at risk (eg, travelers to endemic areas, laboratory workers), and provide postexposure prophylaxis with standard immune globulin or, for some, vaccination.