Hepatitis A pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: João André Alves Silva, M.D. [2]

Overview

Hepatitis A is a liver disease caused by the hepatitis A virus (HAV). HAV has fecal-oral transmission and its infectivity peaks about 2-weeks before the onset of jaundice. Gross observation of the liver may show an enlarged and erythematous liver, while microscopically it may reveal lymphocyte infiltration and inflammation of the portal tracts.

Pathogenesis

  • Hepatitis A is a liver disease caused by the HAV that can affect anyone.
  • HAV is acquired by mouth (through fecal-oral transmission) and replicates in the liver. After 10-12 days, the virus is present in blood and is excreted via the biliary system into the feces.
  • Peak titers occur during the 2 weeks before onset of illness. Although virus is present in serum, its concentration is several orders of magnitude less than in feces. Virus excretion begins to decline at the onset of clinical illness, and has decreased significantly by 7–10 days after onset of symptoms.
  • The concentration of virus in stool declines after jaundice appears.[3][2]
  • Most infected persons no longer excrete virus in the feces by the third week of illness.
  • Children may excrete virus longer than adults.
  • Chronic shedding of HAV in feces does not occur; however, shedding can occur in persons who have relapsing illness.[4]
  • The virus is resistant to detergent, acid, solvents, drying, and temperatures up to 60ºC. It can survive for months in salt water. Common-source outbreaks, such as water or restaurants are typical.

Transmission

The virus spreads by the fecal-oral route and infections often occur in conditions of poor sanitation. Hepatitis A can be transmitted by the parenteral route but very rarely by blood, and blood products. Today transmission of the virus through blood is rare, however, some risk groups such as IV drug users and their care takers are still infected by this route.[5]

Food-borne outbreaks are not uncommon,[6] and ingestion of shellfish cultivated in polluted water is associated with a high risk of infection.[7]

Direct Transmission

  • Eating food prepared by someone who has HAV and who did not properly wash their hands after using the bathroom
  • Having anal or oral sex with someone who has HAV
  • Not washing hands after changing a diaper (young children often are asymptomatic)

Indirect Transmission

  • Eating uncooked food that is HAV-contaminated
  • Eating cooked food that is not heated to 185°F (85°C) for 1 minute after being contaminated with HAV
  • Drinking contaminated water: This is a common route of infection in underdeveloped countries. Chlorinated water, such as tap water in developed countries, kills HAV

Gross Pathology

Gross observation of the liver with acute hepatitis A may include:

Microscopic Pathology

Virus-induced cytopathology may not be responsible for the pathologic changes seen in HAV infection, as liver disease may result primarily from immune mechanisms. Antigen-specific T-lymphocytes are responsible for the destruction of infected hepatocytes.[8]

Common histologic findings include:

  • Multifocal
  • Panacinar

Rarely, patients with acute viral hepatitis A develop features of cholestasis.[8]

Confluent hepatic necrosis may lead to fulminant hepatitis and death in 30-60% of cases. Death appears to be inevitable when necrosis involves more than 65-80% of the total hepatocyte fraction. In patients who survive an episode of acute fulminant hepatic failure, neither functional nor pathologic sequelae are common, despite the widespread necrosis.[8]

During the recovery stage, cell regeneration is prominent. The damaged hepatic tissue is usually restored within 8 to 12 weeks.[8]

Shown below is a video depicting the pathological findings in viral hepatitis. Click on the arrow to view the video.

References

  1. Skinh j P, Mathiesen LR, Kryger P, M ller AM. Faecal excretion of hepatitis A virus in patients with symptomatic hepatitis A infection. Scand J Gastroenterol 1981;16:1057-9.
  2. 2.0 2.1 Tassopoulos NC, Papaevangelou GJ, Ticehurst JR, Purcell RH (August 1986). "Fecal excretion of Greek strains of hepatitis A virus in patients with hepatitis A and in experimentally infected chimpanzees". The Journal of Infectious Diseases 154 (2): 231–7. PMID 3014009. Retrieved on 2012-02-28.
  3. Skinh j P, Mathiesen LR, Kryger P, M ller AM. Faecal excretion of hepatitis A virus in patients with symptomatic hepatitis A infection. Scand J Gastroenterol 1981;16:1057-9.
  4. Sjogren MH, Tanno H, Fay O, Sileoni S, Cohen BD, Burke DS, Feighny RJ (February 1987). "Hepatitis A virus in stool during clinical relapse". Annals of Internal Medicine 106 (2): 221–6. PMID 3026213. Retrieved on 2012-02-28.
  5. Melnick JL (1995). "History and epidemiology of hepatitis A virus.". J Infect Dis 171 Suppl 1: S2-8. PMID 7876643 [.
  6. Brundage SC, Fitzpatrick AN (2006). "Hepatitis A". Am Fam Physician 73 (12): 2162–8. PMID 16848078.
  7. Lees D (2000). "Viruses and bivalve shellfish". Int. J. Food Microbiol. 59 (1-2): 81–116. doi:10.1016/S0168-1605(00)00248-8. PMID 10946842.
  8. 8.0 8.1 8.2 8.3 Hepatitis A.

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