Hepatitis A Prevention Through Immunization : Diagnosis, Disease Patterns

by CDC

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Diagnosis

Hepatitis A cannot be differentiated from other types of viral hepatitis on the basis of clinical or epidemiologic features alone. Serologic testing to detect immunoglobulin M (IgM) antibody to the capsid proteins of HAV (IgM anti-HAV) is required to confirm a diagnosis of acute HAV infection. Sensitive tests for IgM and immunoglobulin G (IgG) anti-HAV in saliva have been developed but are not licensed in the United States. In the majority of persons, serum IgM anti-HAV becomes detectable 5 - 10 days before onset of symptoms. IgG anti-HAV, which appears early in the course of infection, remains detectable for the person's lifetime and provides lifelong protection against the disease. Two serologic tests are licensed for the detection of antibodies to HAV: 1) IgM anti-HAV and 2) total anti-HAV (i.e., IgM and IgG anti-HAV, referred to in this report as anti-HAV). In the majority of patients, IgM anti-HAV declines to undetectable levels <6 months after infection. However, persons who test positive for IgM anti-HAV >1 year after infection have been reported, as have likely false-positive tests in persons without evidence of recent HAV infection. Total anti-HAV testing is used in epidemiologic studies to measure the prevalence of previous infection or by clinicians to determine whether a person with an indication for pre-exposure prophylaxis is already immune.

HAV RNA can be detected in the blood and stool of the majority of persons during the acute phase of infection by using nucleic acid amplification methods, and nucleic acid sequencing has been used to determine the relatedness of HAV isolates for epidemiologic investigations. However, only a limited number of research laboratories have the capacity to use these methods.

Epidemiology of Hepatitis A

Modes of Transmission

Person-to-person transmission through the fecal-oral route is the primary means of HAV transmission in the United States. Transmission occurs most frequently among close contacts, especially in households and extended family settings. Because the majority of children have asymptomatic or unrecognized infections, they play a key role in HAV transmission and serve as a source of infection for others. In one study of adults without an identified source, 52% of their households included a child aged <6 years, and the presence of a young child was associated with HAV transmission in the household. In studies in which serologic testing of the household contacts of adults without an identified source of infection was performed, 25% - 40% of contacts aged <6 years had serologic evidence of acute HAV infection (IgM anti-HAV).

Common-source outbreaks and sporadic cases also can occur from exposure to fecally contaminated food or water. Uncooked foods have been recognized frequently as a source of outbreaks. Cooked foods also can transmit HAV if cooking is inadequate to kill the virus or if food is contaminated after cooking, as occurs commonly in outbreaks associated with infected food handlers. Waterborne outbreaks of hepatitis A are infrequent in developed countries with well-maintained sanitation and water supplies. The majority of waterborne outbreaks are associated with sewage-contaminated or inadequately treated water. Outbreaks in the context of floods or other natural disasters (e.g., hurricanes) have not been reported in the United States.

Depending on conditions, HAV can be stable in the environment for months. Heating foods at temperatures >185°F (>85°C) for 1 minute or disinfecting surfaces with a 1:100 dilution of sodium hypochlorite (i.e., household bleach) in tap water is necessary to inactivate HAV.

On rare occasions, HAV infection has been transmitted by transfusion of blood or blood products collected from donors during the viremic phase of their infection. Since 2002, nucleic acid amplification tests such as polymerase chain reaction (PCR) have been applied to the screening of source plasma used for the manufacture of plasma-derived products.

In experimentally infected nonhuman primates, HAV has been detected in saliva during the incubation period. However, transmission by saliva has not been demonstrated.

Disease Patterns

Prevaccine Era

Hepatitis A epidemiology in the United States has fundamentally changed with licensure of hepatitis A vaccine and implementation of national ACIP recommendations for its use. Before vaccine licensure during 1995 - 1996, hepatitis A incidence was primarily cyclic, with peaks occurring every 10 - 15 years. In the United States, during 1980 - 1995, approximately 22,000 - 36,000 hepatitis A cases were reported annually to CDC (rate: 9.0 - 14.5 cases per 100,000 population), but incidence models indicate that the number of infections was substantially higher. One such analysis estimated an average of 271,000 infections per year during 1980 - 1999, representing 10.4 times the reported number of cases. Each year in the United States, an estimated 100 persons died as a result of acute liver failure attributed to hepatitis A.

The costs associated with hepatitis A are substantial. Surveillance data indicate that 11% - 22% of persons with hepatitis A are hospitalized. The average duration of work loss for adults who become ill has been estimated at 15.5 days for nonhospitalized patients and 33.2 days for hospitalized patients. Estimates of the annual direct and indirect costs of hepatitis A in the United States have ranged from $300 million to $488.8 million in 1997 dollars. A recent Markov model analysis estimated economic costs of $133.5 million during the lifetime of a single age cohort of children born in 2005, in the absence of vaccination.

Variation by Age, Race/Ethnicity, and Region. During the prevaccine era, the reported incidence of hepatitis A was highest among children aged 5 - 14 years, with approximately one third of reported cases involving children aged <15 years. Because young children frequently have unrecognized or asymptomatic infection, a relatively smaller proportion of infections among children than adults are detected by routine disease surveillance. Incidence models indicate that during 1980 - 1999, the majority of HAV infections occurred among children aged <10 years, and the highest incidence was among those aged 0 - 4 years. Before the use of hepatitis A vaccine, rates among American Indians and Alaska Natives were more than five times higher than rates in other racial/ethnic populations, and rates among Hispanics were approximately three times higher than rates among non-Hispanics.

About the Author

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