Hepatitis A, an acute, self-limiting liver infection is transmitted through the fecal oral route by a picovnavirus, hepatitis A Virus(HAV) (1). It is the major cause of acute viral hepatitis in children (2). HAV cause asymptomatic infection in young children and symptomatic infection in adults (3). A study shows symptomatic infection in 4-16% of children as compared to 75-95% of adults (1). The symptoms include jaundice, fever, abdominal pain, malaise, anorexia which resolve after onset within 1-2 months. Lifelong immunity is seen after acute infection (3). Endemicity of HAV infection depends upon hygiene, sanitary conditions, socio-economic level and other development indications (1).
In the last five years, a decrease seroprevalance was seen in Southern Asia, America, and Europe due to improved hygiene and sanitation and decrease exposure of children to contaminated water and food. In India, seroprevalance of HAV antibody is reported in >90% of adults (2). The consumption of contaminated raw seafood, partially cooked shellfish has been reported as a risk factor in Sardinia. Local health services have also reported that an outbreak occurred in Sardinia due to consumption of raw shellfish in which 94% were young adults. Other risk factors include use of intravenous drugs, occupational exposures, homosexual practices, etc. HAV risk is also associated with importing food from countries with lower standards of environmental hygiene and higher levels of HAV. This can lead to spread of HAV infections from endemic to nonendemic areas which can pose a serious risk of an HAV outbreak in a population with no herd immunity (1).
In order to assess hepatitis A vaccine, serologic testing is not recommended, because protective anti-HAV concentration is below the limit of detection after vaccination for commercially available anti-HAV assays. Similarly testing for IgM anti-HAV cannot be used to assess response to vaccination or to screen asymptomatic persons with no known recent exposure to HAV.The positive anti-HAV test results can lead to irrelevant and unnecessary concerns, also adds cost to patients and health care providers can misdiagnose it. In order to reduce inappropriate testing, there should be separate panels of tests for determining immunity to HAV and for diagnosing acute hepatitis (3).
In the studies conducted in Italy and European countries it was observed that anti-HAV seroprevalence was high in age >40 years and low in younger subjects of age <40 years. This different seroprevalence picture suggests that the preventive strategies must be done based on specific risk assessments. In order to reduce the risk of HAV infections, household contacts of sporadic cases and individuals at higher risk of infection or at risk of complications of HAV hepatitis need to be vaccinated (1). It is recommended to give mass HAV vaccine to children in regions of low endimicity (2).
References:
1.Campagna M, Siddu A, Meloni A, Basciu C, Ferrai L, Pettinau A, et al. Changing pattern of hepatitis a virus epidemiology in an area of high endemicity. Hepatitis monthly. 2012;12(6):382-5. Epub 2012/08/11.
2.Batra Y, Bhatkal B, Ojha B, Kaur K, Saraya A, Panda SK, et al. Vaccination against hepatitis A virus may not be required for schoolchildren in northern India: results of a seroepidemiological survey. Bulletin of the World Health Organization. 2002;80(9):728-31. Epub 2002/10/16.
3.Castrodale L, Fiore A, Schmidt T. Detection of immunoglobulin M antibody to hepatitis A virus in Alaska residents without other evidence of hepatitis. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2005;41(9):e86-8. Epub 2005/10/06.
ARTICLE BY,
Geetika Kainthla
(M.sc biotechnology)
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