Hepatitis A pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Pathophysiology

Hepatitis A is a liver disease caused by the hepatitis A virus (HAV). Hepatitis A can affect anyone. In the United States, hepatitis A can occur in situations ranging from isolated cases of disease to widespread epidemics.

In infected persons, HAV replicates in the liver, is excreted in bile, and is shed in the stool. Peak infectivity of infected persons occurs during the 2-week period before onset of jaundice or elevation of liver enzymes, when the concentration of virus in stool is highest. [1][2] The concentration of virus in stool declines after jaundice appears.[3][2] Children and infants can shed HAV for longer periods than adults, up to several months after the onset of clinical illness.[4] Chronic shedding of HAV in feces does not occur; however, shedding can occur in persons who have relapsing illness.[5] Viremia occurs soon after infection and persists through the period of liver enzyme elevation.[6][7]

Transmission

The virus spreads by the fecal-oral route and infections often occur in conditions of poor sanitation and overcrowding. Hepatitis A can be transmitted by the parenteral route but very rarely by blood and blood products. Food-borne outbreaks are not uncommon,[8] and ingestion of shellfish cultivated in polluted water is associated with a high risk of infection.[9] Approximately 40% of all acute viral hepatitis is caused by HAV.[10] Infected individuals are infectious prior to onset of symptoms, roughly 10 days following infection. The virus is resistant to detergent, acid (pH 1), solvents (e.g., ether, chloroform), drying, and temperatures up to 60oC. It can survive for months in fresh and salt water. Common-source (e.g., water, restaurant) outbreaks are typical. Infection is common in children in developing countries, reaching 100% incidence, but following infection there is life-long immunity. HAV can be inactivated by: chlorine treatment (drinking water), formalin (0.35%, 37oC, 72 hours), peracetic acid (2%, 4 hours), beta-propiolactone (0.25%, 1 hour), and UV radiation (2 μW/cm2/min).

Microscopic Pathology

Click on the arrow to view the pathologic findings in viral hepatitis:

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. Rosenblum LS, Villarino ME, Nainan OV, Melish ME, Hadler SC, Pinsky PP, Jarvis WR, Ott CE, Margolis HS (September 1991). "Hepatitis A outbreak in a neonatal intensive care unit: risk factors for transmission and evidence of prolonged viral excretion among preterm infants". The Journal of Infectious Diseases 164 (3): 476–82. PMID 1651359. Retrieved on 2012-02-28.
  5. 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.
  6. Lemon SM (1994). "The natural history of hepatitis A: the potential for transmission by transfusion of blood or blood products". Vox Sanguinis 67 Suppl 4: 19–23; discussion 24–6. PMID 7831865. Retrieved on 2012-02-28.
  7. Bower WA, Nainan OV, Margolis HS. Duration of viremia in naturally-acquired hepatitis A viral infections. [Abstract 103] In: Abstracts of the Infectious Diseases Society of America 35th Annual Meeting. Alexandria, VA: Infectious Diseases Society of America, 1997.
  8. Brundage SC, Fitzpatrick AN (2006). "Hepatitis A". Am Fam Physician 73 (12): 2162–8. PMID 16848078.
  9. 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.
  10. Insert footnote text Murray, P. r., Rosenthal, K. S., & Pfaller, M. A. (2005). Medical Microbiology," 5th ed., Elsevier Mosby.

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