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
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, 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.
- Children may excrete virus longer than adults.
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).
Genetics
Associated Conditions
Gross Pathology
Microscopic Pathology
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.
- ↑ Rosenblum LS, Villarino ME, Nainan OV, Melish ME, Hadler SC, Pinsky PP, Jarvis WR, Ott CE, Margolis HS (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 2012-02-28. Unknown parameter
|month=ignored (help) - ↑ 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) - ↑ 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.
|access-date=requires|url=(help) - ↑ 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.
- ↑ 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.
- ↑ Insert footnote text Murray, P. r., Rosenthal, K. S., & Pfaller, M. A. (2005). Medical Microbiology," 5th ed., Elsevier Mosby.