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Biology : Hepatitis A - Research Paper Example

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Hepatitis A HEPATITIS A INTRODUCTION Hepatitis or inflammation of the liver caused by hepatitis A can be a sudden illness with a mild to moderate presentation followed by complete resolution. The heapatitis A virus belongs to the Heparna genus of the Picorna family and is a non-enveloped, icosahedral virus with positive single stranded RNA nucleic acids…
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Biology Research: Hepatitis A
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"Biology : Hepatitis A"

Download file to see previous pages In the past infection from this virus has also been named catarrhal jaundice, epidemic jaundice and campaign jaundice. Currently four distinct genotype of hepatitis A virus have been identified which all belong to the same serotype. (Gerety Hepatitis A, 1984) EPIDEMIOLOGY Hepatitis A virus (HAV) infection occurs throughout the world although presently its incidence has been greatly reduced since the development of a vaccine. In the United States alone the occurrence of hepatitis caused by HAV has reduced by 92 percent from 1995 to 2007. Previously the incidence rate was 12 in 100,000 people which have declined to 1 person now. Presently the major sources of infection in the United States are the international travellers. Since HAV follows a fecal oral route for transmission it has great potential to cause epidemics especially in areas with poor hygienic conditions. Apart from poor hygienic conditions other risk factors for this virus include homo sexuality in men, intra venous injection use and contact with already infected individuals. Globally the incidence of Hepatitis A has also reduced because of the improving socio-economic conditions and herd immunity. Herd immunity provides a protective effect due to the large population that has anti bodies against the virus present in their serum. (Daniels D, 2009 May 22) PATHOGENESIS The pathogenesis of HAV involves an incubation period of twenty to forty days during which the virus replicates in the cytoplasm of hepatocytes. Although the virus does not have a direct cytopathic effect on the liver cells it causes the release of numerous cytokines which mediate the response of natural killer cells and HAV-specific CD 8+ T lymphocytes. The lymphocyte response then causes hepatocellular damage. At the same time interferon gamma is proposed to play a significant part in clearance of infected liver cell. The severity if infection is dependent upon the extent of host immune response. Clinically a patient may present with any of the following; jaundice, right hypochondrial pain, fatigue, malaise, fever, anorexia, hepatosplenomegaly, thrombocytopenia, arthritis, lymphadenopathy, nausea and vomiting. Generally the symptoms are less severe in children as compared to adults. The laboratory findings of an individual with hepatitis cause by HAV include raised liver function enzymes e.g. AST, ALT and alkaline phosphatase and increased total and direct bilirubin which is the cause of jaundice. Normally the bilirubin surge is seen after an increase in amino transfreases (AST and ALT). Other findings include those of normal inflammation e.g. raised erythrocyte sedimentation rate and increase in acute phase reactants. (Catherine P Cheney, 19 May 2011) DIAGNOSIS Diagnosis is made mostly on clinical grounds. Anti HAV antibodies are diagnostic in case of suspicion. The presence of anti- HAV antibodies positive in cases where there is no clinical suspicion can be misleading. It can be positive in patients who have previously had an HAV infection and have a prolonged immunological response to it. In these patients anti HAV can be elevated for extended periods of time. False positive results could be another possibility in such cases. Asymptomatic infection is likely in patients younger than 6 years of age. Anti HAV is elevated in cases of acute infection and remains elevated for ...Download file to see next pagesRead More
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