Hepatitis A pathophysiology: Difference between revisions

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==Overview==
==Overview==
[[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.


==Pathogenesis==
==Pathogenesis==
* Hepatitis A is a liver disease caused by the [[hepatitis A virus]] ([[HAV]]), that can affect anyone.
* 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, [[virus]] is present in [[blood]] and is excreted via the [[biliary system]] into the [[feces]].
* 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 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. <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>


* Most [[infected]] persons no longer excrete [[virus]] in the [[feces]] by the third week of illness.
* Most [[infected]] persons no longer excrete [[virus]] in the [[feces]] by the third week of illness.
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* Children may excrete [[virus]] longer than adults.
* 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.<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>


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>
* 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.
{{#widget:SchemaSnippet}}


* HAV can be inactivated by [[chlorine]] treatment, [[formalin]], [[peracetic acid]], beta-propiolactone, and [[UV radiation]].


===Transmission===
===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,<ref name="pmid16848078">{{cite journal
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.<ref name="pmid7876643    [">{{cite journal| author=Melnick JL| title=History and epidemiology of hepatitis A virus. | journal=J Infect Dis | year= 1995 | volume= 171 Suppl 1 | issue=  | pages= S2-8 | pmid=7876643    [ | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7876643  }} </ref>
|author=Brundage SC, Fitzpatrick AN
 
|title=Hepatitis A
Food-borne outbreaks are not uncommon,<ref name="pmid16848078">{{cite journal|author=Brundage SC, Fitzpatrick AN|title=Hepatitis A|journal=Am Fam Physician|volume=73|issue=12|pages=2162–8|year=2006|pmid=16848078}}</ref> and ingestion of shellfish cultivated in polluted water is associated with a high risk of [[infection]].<ref name="pmid10946842">{{cite journal|author=Lees D|title=Viruses and bivalve shellfish|journal=Int. J. Food Microbiol.|volume=59
|journal=Am Fam Physician
|issue=1-2|pages=81–116|year=2000|pmid=10946842|url=http://linkinghub.elsevier.com/retrieve/pii/S0168-1605(00)00248-8|doi=10.1016/S0168-1605(00)00248-8}}</ref>
|volume=73
 
|issue=12
====Direct Transmission====
|pages=2162–8
* Eating food prepared by someone who has HAV and who did not properly wash their hands after using the bathroom
|year=2006
* Having anal or oral sex with someone who has HAV
|pmid=16848078
* Not washing hands after changing a diaper (young children often are asymptomatic)
}}</ref> and ingestion of shellfish cultivated in polluted water is associated with a high risk of infection.<ref name="pmid10946842">{{cite journal
|author=Lees D
|title=Viruses and bivalve shellfish
|journal=Int. J. Food Microbiol.
|volume=59
|issue=1-2
|pages=81–116
|year=2000
|pmid=10946842
|url=http://linkinghub.elsevier.com/retrieve/pii/S0168-1605(00)00248-8


|doi=10.1016/S0168-1605(00)00248-8}}</ref>
====Indirect Transmission====
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).
* 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:
* Enlarged [[liver]]
* [[Erythematous]] surface


<!--
==Microscopic Pathology==
Hepatitis A is spread through ingesting food or water contaminated by the feces of an infected person. People with HAV are infectious from the beginning of the incubation period (about a month before symptoms) until one week after they become jaundiced.  
[[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]].<ref name=WHO>{{cite web | title = Hepatitis A | url = http://www.who.int/csr/disease/hepatitis/HepatitisA_whocdscsredc2000_7.pdf }}</ref>
Common ways of acquiring Hepatitis A are:
* Direct Person-to-person 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.
If you have HAV or you live with someone who has HAV, to prevent spreading one with HAV should:
*Always wash hands thoroughly after going to the bathroom.
*Clean bathrooms often, paying attention to commonly-touched surfaces (toilet seats, faucet taps, etc.).
*Not prepare food for other people.
*Not share utensils.
*Not share any personal items that can spread HAV (toothbrushes, towels, etc.).
It is recommended that all people with Hepatitis A not work for 1 week after they become jaundiced to prevent spreading.


-->
Common [[histologic]] findings include:
* [[Inflammatory]] infiltrates ([[lymphocytes]])
* [[Necrosis]] and [[apoptosis]] of [[hepatocytes]]
* The [[hepatocyte]] [[inflammation]] may have the following patterns:
:* Multifocal
:* Panacinar
* [[Inflammation]] of portal tracts


==Genetics==
Rarely, patients with acute viral [[hepatitis A]] develop features of [[cholestasis]].<ref name=WHO>{{cite web | title = Hepatitis A | url = http://www.who.int/csr/disease/hepatitis/HepatitisA_whocdscsredc2000_7.pdf }}</ref>


==Associated Conditions==
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.<ref name=WHO>{{cite web | title = Hepatitis A | url = http://www.who.int/csr/disease/hepatitis/HepatitisA_whocdscsredc2000_7.pdf }}</ref>


==Gross Pathology==
During the recovery stage, cell [[regeneration]] is prominent. The damaged hepatic tissue is usually restored within 8 to 12 weeks.<ref name=WHO>{{cite web | title = Hepatitis A | url = http://www.who.int/csr/disease/hepatitis/HepatitisA_whocdscsredc2000_7.pdf }}</ref>


==Microscopic Pathology==
Shown below is a video depicting the pathological findings in viral hepatitis.  Click on the arrow to view the video.
Click on the arrow to view the pathologic findings in viral hepatitis:
{{#ev:youtube|_hXvbpSxFZw}}
{{#ev:youtube|_hXvbpSxFZw}}


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Latest revision as of 22:04, 29 July 2020

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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

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.

Pathogenesis

  • 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.

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. 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}}

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 (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).

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