Cultivation in vitro: The virus grows poorly in primate cellular cultures and loses virulence by in vitro passages.
Route of entry and Progress of infection: The virus is acquired by ingestion. It multiplies in the intestine and invades the blood, liver and saliva before any clinical manifestation of the disease appears. This period of incubation lasts an average of 4 (2-6) weeks. The virus disappears soon after the peak of serum transaminase is reached at which time the immune response and the hepatocellular damage start. This indicates that the damage is immunologically mediated. Indeed at this time NK (natural killer) cells, circulating or local in the liver (Pitt cells), are activated. CD8+ cytotoxic T lymphocytes that secrete gamma interferon infiltrate the field.
Clincal features: Most infections occur in children in whom the disease in most cases is either asymptomatic or symptomatic without jaundice. In adults, the infection is more severe with general symptoms malaise and jaundice; however hepatitis A is not very debilitating even in the presence of jaundice. Fever does not go above 39 degrees centigrade. Jaundice lasts for 7-10 days and the whole illness lasts about 4 weeks. Relapses however do occur especially in patients who resume drinking alcohol or exercise and may go on for 6 months. Typically all clincial forms with the exception of the lethal fulminant type resolve with complete liver regeneration without chronicity or long-term carrier state.
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Fig 88 - LABORATOR DIAGNOSIS (1):
1-Serum IgM antibody is present during the acute phase and disappears in 3 months. It may last up to 2 years in a few cases. The test is 100% sensitive and very specific. |
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Fig 89 - PORTAL AND PERIPORTAL INFLAMMATION:
Presence of both lobular and portal inflammation. This illustration shows marked protal and periportal inflammation with some hepatocellular ballooning degeneration.
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Fig 90 - LOBULAR INFLAMMATION:
Notice intralobular inflammatory cell, few shrinking apoptotic cells (Councilmann bodies), many swollen hepatocyte and binucleate hepatocytes indicating accelerated liver cell renewal.
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Fig 91 - CONFLUENT NECROSIS:
Death of adjacent groups of hepatocyte throughout the lobule. Confluence of many spotty necroses. Notice glycogen (red granules) depletion on damaged hepatocyte..
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Fig 92 - HEPATOCELLULAR DAMAGE:
Some hepatocytes are swollen and clear (hydropic degeneration). One is shrunken and dark with rests of nuclear disintegration (apoptotic cell, Councilmann body). There is a group of Kupffer cells with bile and lipofuscin granules in their function as scavenger cells.
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Fig 93 - CHOLESTATIC FORM OF VIRAL HEPATITIS A:
Marked cholestasis with intracytoplasmic yellow granules of bile and bile thrombi in canaliculi. Thes cholestatic changes are seen in cases of prolonged jaundice. (See cholestatic clinical form above in this chapter).
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Pre-exposure | A person preparing for travel or to contact an affected individual or a pregnant lady should first check serum IgG level for HAV immunity. If the test is positive, no immunoprophylaxis is necessary. The immunization is achieved with Serum Immunoglobulin (SIG) or with inactivated polio vaccine (the first one marketed by Smith Kline, Beecham Biologicals, Rixensart, Belgium, under the name of Havrix). |
Post-exposure | Serum immunoglobulin (SIG) must be administered within 2 weeks after exposure in the amount of 0.02 ml/Kg. Antibody level induced by this treatment is low and cannot be measured by standard methods. The main side effect of immunoglobulin injection is considerable soreness in the injection site. The cost is low. |