Hepatitis A pathophysiology: Difference between revisions
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==Microscopic Pathology== | ==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]]. | [[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]]. | ||
Rarely, patients with acute viral [[hepatitis A]] develop features of [[cholestasis]]. | |||
Click on the arrow to view the pathologic findings in viral hepatitis: | Click on the arrow to view the pathologic findings in viral hepatitis: | ||
Revision as of 02:59, 29 July 2014
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Hepatitis A |
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Hepatitis A pathophysiology On the Web |
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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]
Overview
Pathogenesis
- Hepatitis A is a liver disease caused by the hepatitis A virus (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.
- Peak infectivity 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]
- 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.
- HAV can be inactivated by: chlorine treatment, formalin, peracetic acid, beta-propiolactone , and UV radiation.
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. Food-borne outbreaks are not uncommon,[5] and ingestion of shellfish cultivated in polluted water is associated with a high risk of infection.[6]
Common ways of acquiring Hepatitis A are:
- Direct transmission
- Eating food made by someone who has HAV 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. Cooked food can also cause hepatitis if 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.
Genetics
Associated Conditions
Gross Pathology
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.
Rarely, patients with acute viral hepatitis A develop features of cholestasis.
Click on the arrow to view the pathologic findings in viral hepatitis: {{#ev:youtube|_hXvbpSxFZw}}
References
- ↑ 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.
- ↑ 2.0 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) - ↑ 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.
- ↑ 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) - ↑ Brundage SC, Fitzpatrick AN (2006). "Hepatitis A". Am Fam Physician. 73 (12): 2162–8. PMID 16848078.
- ↑ 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.