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| {{Hepatitis A}}
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| {{CMG}}
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| ==Pathophysiology==
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| 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.
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| 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 <ref>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.</ref><ref name="pmid3014009">{{cite journal |author=Tassopoulos NC, Papaevangelou GJ, Ticehurst JR, Purcell RH |title=Fecal excretion of Greek strains of hepatitis A virus in patients with hepatitis A and in experimentally infected chimpanzees |journal=[[The Journal of Infectious Diseases]] |volume=154 |issue=2 |pages=231–7 |year=1986 |month=August |pmid=3014009 |doi= |url=http://www.jid.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=3014009 |accessdate=2012-02-28}}</ref>. The concentration of virus in stool declines after jaundice appears<ref>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.</ref><ref name="pmid3014009">{{cite journal |author=Tassopoulos NC, Papaevangelou GJ, Ticehurst JR, Purcell RH |title=Fecal excretion of Greek strains of hepatitis A virus in patients with hepatitis A and in experimentally infected chimpanzees |journal=[[The Journal of Infectious Diseases]] |volume=154 |issue=2 |pages=231–7 |year=1986 |month=August |pmid=3014009 |doi= |url=http://www.jid.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=3014009 |accessdate=2012-02-28}}</ref>. Children and infants can shed HAV for longer periods than adults, up to several months after the onset of clinical illness<ref name="pmid1651359">{{cite journal |author=Rosenblum LS, Villarino ME, Nainan OV, Melish ME, Hadler SC, Pinsky PP, Jarvis WR, Ott CE, Margolis HS |title=Hepatitis A outbreak in a neonatal intensive care unit: risk factors for transmission and evidence of prolonged viral excretion among preterm infants |journal=[[The Journal of Infectious Diseases]] |volume=164 |issue=3 |pages=476–82 |year=1991 |month=September |pmid=1651359 |doi= |url=http://www.jid.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=1651359 |accessdate=2012-02-28}}</ref>. Chronic shedding of HAV in feces does not occur; however, shedding can occur in persons who have relapsing illness<ref name="pmid3026213">{{cite journal |author=Sjogren MH, Tanno H, Fay O, Sileoni S, Cohen BD, Burke DS, Feighny RJ |title=Hepatitis A virus in stool during clinical relapse |journal=[[Annals of Internal Medicine]] |volume=106 |issue=2 |pages=221–6 |year=1987 |month=February |pmid=3026213 |doi= |url= |accessdate=2012-02-28}}</ref>. Viremia occurs soon after infection and persists through the period of liver enzyme elevation<ref name="pmid7831865">{{cite journal |author=Lemon SM |title=The natural history of hepatitis A: the potential for transmission by transfusion of blood or blood products |journal=[[Vox Sanguinis]] |volume=67 Suppl 4 |issue= |pages=19–23; discussion 24–6 |year=1994 |pmid=7831865 |doi= |url= |accessdate=2012-02-28}}</ref><ref>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.</ref>.
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| ===Transmission===
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| 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,<ref name="pmid16848078">{{cite journal
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| |author=Brundage SC, Fitzpatrick AN
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| |title=Hepatitis A
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| |journal=Am Fam Physician
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| |volume=73
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| |issue=12
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| |pages=2162–8
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| |year=2006
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| |pmid=16848078
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| }}</ref> and ingestion of shellfish cultivated in polluted water is associated with a high risk of infection.<ref name="pmid10946842">{{cite journal
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| |author=Lees D
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| |title=Viruses and bivalve shellfish
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| |journal=Int. J. Food Microbiol.
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| |volume=59
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| |issue=1-2
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| |pages=81–116
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| |year=2000
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| |pmid=10946842
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| |url=http://linkinghub.elsevier.com/retrieve/pii/S0168-1605(00)00248-8
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| |doi=10.1016/S0168-1605(00)00248-8}}</ref>
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| Approximately 40% of all acute viral hepatitis is caused by HAV.<ref>Insert footnote text Murray, P. r., Rosenthal, K. S., & Pfaller, M. A. (2005). ''Medical Microbiology," 5th ed., Elsevier Mosby.</ref> 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 60<sup>o</sup>C. 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%, 37<sup>o</sup>C, 72 hours), [[peracetic acid]] (2%, 4 hours), beta-propiolactone (0.25%, 1 hour), and [[UV radiation]] (2 μW/cm<sup>2</sup>/min).
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| ==Pathology==
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| Click on the arrow to view the pathologic findings in viral hepatitis:
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| {{#ev:youtube|_hXvbpSxFZw}}
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| ==References==
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| {{reflist|2}}
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| [[Category:Foodborne illnesses]]
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| [[Category:hepatitis|A]]
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| [[Category:Picornaviruses]]
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| [[Category:Viral diseases]]
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