Hepatitis A pathophysiology

Jump to navigation Jump to search

Hepatitis Main Page

Hepatitis A


Patient Information


Historical Perspective



Differentiating Hepatitis A from other Diseases

Epidemiology and Demographics

Risk Factors


Natural History, Complications and Prognosis


History and Symptoms

Physical Examination

Laboratory Findings




Medical Therapy


Primary Prevention

Secondary Prevention

Case Studies

Case #1

Hepatitis A pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides


American Roentgen Ray Society Images of Hepatitis A pathophysiology

All Images
Echo & Ultrasound
CT Images

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Hepatitis A pathophysiology

CDC on Hepatitis A pathophysiology

Hepatitis A pathophysiology in the news

Blogs on Hepatitis A pathophysiology

Directions to Hospitals Treating Hepatitis A

Risk calculators and risk factors for Hepatitis A pathophysiology

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


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.


  • 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]
  • 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.


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. {{#ev:youtube|_hXvbpSxFZw}}


  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 (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 2012-02-28. Unknown parameter |month= ignored (help)
  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 (1987). "Hepatitis A virus in stool during clinical relapse". Annals of Internal Medicine. 106 (2): 221–6. PMID 3026213. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  5. Melnick JL (1995). "History and epidemiology of hepatitis A virus". J Infect Dis. 171 Suppl 1: S2–8. PMID [ 7876643 [ Check |pmid= value (help).
  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" (PDF).

Template:WH Template:WS