Acute Viral Hepatitis A is an inflammation of liver with many kind degree of liver cells damage that be caused by Hepatitis A virus infection. Acute viral Hepatitis A frequent is found with incident rate high in areas which less environment sanitation. Main sources of infection are virus that can be found on feces at the end of incubation period until two weeks after onset of disease.

Approximately one per three of cases that be reported be found on child. Virus Hepatitis A is very easy to spread particularly with fecal – oral, direct or indirect. Spreading of acute viral Hepatitis A is related to inhabitant fully, bad personal hygiene, less sanitation, food and drink contamination, tight contact with patient, traveling to develop states and using intra vena forbidden drug. Acute Viral Hepatitis has been spread in whole world.

Parenteral transmission very seldom be occurred and this occur only on short viremia phase on incubation period of Acute Viral Hepatitis A.

Specific characteristic of Virus Hepatitis A (VHA) i.e.:

  • VHA be found on feces of patient with acute infection, and be transmitted by fecal-oral route.
  • Natural reservoir infection unknown yet
  • It is not found viremia with persistent infection
  • VHA is stable virus, exist persistent although on environment which is not benefit for virus itself.

By existence of environment sanitation and personal hygiene improvement will be happened change incident rate of Acute Viral Hepatitis A from younger ages to adult or elder ages. Of that because as prevention of Acute Viral Hepatitis A so anyone of younger ages must be given vaccination.

Etiology and Pathogenesis

As causer of acute viral Hepatitis A is viral hepatitis A. VHA shapes spherical, no envelope, by sizes 27 – 32 nm, its genome is RNA and be included family of picorna virus. VHA is stable extremely toward hot, cold box and acid conditions, by that cause virus resistant relatively to disinfectants.
Virus which be swallowed will create replication in small intestine and then migration through portal vena and in to liver. In liver cells be occurred replication again where then be excreted in to gallbladder and its finish will exit through feces. This condition goes continuous until appear clinical sign of hepatitis.

VHA doesn’t cause cytophatic effect in liver cells. When non specific immune system can not eliminate viral, specific immune system be stimulated to do it. Cytotoxic T lymphocytes (CTL) will play importance actor in virus elimination on liver cells which be infected, kill it’s by perforin mechanism ways, Fas legend and TNF-α (tumor necrosis factor).

Considering amount of liver cells 1000 times multiply or more than specific CTL in liver of patient, so viral cytolysis by CTL on liver cells which is infected only constitutes early step of liver cells damages. Macrophage, neutrophyl, and some type of cytokine so are participated in liver damaged next. Expansion of liver damages is established by host factor and viral. While immune respond work accordance with its character, so viral can be eliminated after acute attack of hepatitis.

But when immune respond work too strong can cause it’s occur fulminate hepatitis.
While viral infection start appear, non specific NK (Natural Killer) cell will recognize cell which be infected and then smash its. On time cells be infected by virus, will be stimulated production of interferon (IFN) α and β which will suppress viral replication. If infection can not be restrained at early stadium a while ago, so step by step will be stimulated production of neutralizing antibody and CTL which will as actor in viral elimination.
Neutralizing antibody will bundle specific viral particles in body fluids and will eliminate its, a moment CTL will recognize viral antigen which be expressed to cell infected surfaces and then attack cell and eliminated that viral.

Antibody production and activation along with CTL proliferation stay under control of T helper cells. T helper cells be activated at time they recognized existent of viral antigen which be presented by antigen presenting cells like as dendrite cell macrophage. While its be activated T helper cells type 1 (th1 cells) product interleukin (IL)-2 and IFN γ to accelerate activation and proliferation of CTL and NK cells. T helper cells type 2 (th2 cells) product IL-4, IL-5, IL-6 and IL-10 that promote β cells into antibody forming plasma cells and its cause proliferation of those cells.

Antigen presenting cells product IL-12 which be stimulated by activated T cells and this cytokine back to act on th1 cells, CTL and NK cells cause viral elimination and suppression viral replication. IL-10 which be produced by th2 cells to act on antigen presenting cells by decrease IL-12 production that suppress th1 cells activation, then will finish cellular immune respond toward virus.

The clinical picture of viral hepatitis A is extremely variable, ranging from asymptomatic infection without jaundice to fulminating disease. The clinical characteristics of the viral hepatitis A i.e. : infectious, faeca-oral transmission, incubation period 2 to 6 weeks, severity of acute illness mild to moderate, serology IgM-exposure, and immune prophylaxis normal Ig vaccine.


The key features for diagnosis are :

  • Prodrome of anorexia, nausea, vomiting, malaise, symptoms of upper respiratory infection of flu-like syndrome, aversion to smoking.
  • Fever, enlarged and tender liver, jaundice.
  • Abnormal liver tests, especially markedly elevated aminotransferases early in the course.
  • Liver biopsy will show characteristic hepatocellular necrosis and mononuclear infiltrate. This rarely indicated.

Differential Diagnosis

The overseas traveller presenting with jaundice may have :

  • Infection by any one of the viruses-hepatitis B, C, D or E. All are prevalent in deveploping countries, especially in south-eastern and eastern asia, some Pasific islands and Africa.
  • Other causes to consider are malaria, ascending cholangitis and drug induced hepatic damage due to, for example, the antimalarials, including mefloquine (larium) and Fansidar.


  • Bed rest. Advisible during the acute initial phase of the disease, when symptoms are most severe. Return to normal activity during the convalescent period should be gradual.
  • Fluids. If nausea and vomiting are pronounced or if oral intake is substantially decreased, intravenous administration of 10% glucose solution is indicated.
  • Diet. Dietary management consists of giving palatable meals as tolerated, without overfeeding. Patients should avoid alcohol, and hepatotoxic agents.
  • Corticosteroids. In control studies, corticosteroids have demonstrated no benefit in patients with viral hepatitis, including those with fulminant hepatitis. Treatment of patients with acute hepatitis C with alpha interveron appears to decrease the risk of chronic hepatitis.
  • Encephalophalopathy or serve coagulopathy. Suspect fulminant hepatic failure and hospitalization is mandatory.

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