Hepatitis A: Difference between revisions
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[[File:Jaundice eye new.jpg|thumb|300px|right|Jaundice: yellowing of the sclera in a patient with viral hepatitis A]] | [[File:Jaundice eye new.jpg|thumb|300px|right|Jaundice: yellowing of the sclera in a patient with viral hepatitis A]] | ||
</noinclude> | </noinclude> | ||
The causative agent is HAV, which is an [[RNA]] | The causative agent is HAV, which is an [[RNA - types, structure and function|RNA]] virus from the Picornaviridae family (Enteroviridae, Enterovirus 72), that acts directly cytolytically. HAV is a small virus (27-30nm), genetically homogenous, resistant to the external environment. It is exclusively human pathogen. | ||
<ref name="zampachova"> | <ref name="zampachova"> | ||
{{Cite | {{Cite | ||
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=== The course of infection === | === The course of infection === | ||
The incubation period is 15-48 days.<ref name="muntau" /> First, the prodromal (“preicteric”) stage begins (dyspepsia, fatigue, fever, weight loss). This is followed by the symptomatic stage (“icteric”) - the leading symptoms are jaundice, dark urine and acholic stool. The course is milder and shorter than in VHB. Cholestatic symptoms are rare and may occur fulminantly. HAV does not cause chronic infections. .<ref name="zampachova" /> | |||
===Diagnostics=== | ===Diagnostics=== | ||
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;Detection of antibodies | ;Detection of antibodies | ||
Diagnostics is done using anti-HAV antibodies. We perform '''the examination of specific | Diagnostics is done using anti-HAV antibodies. We perform '''the examination of specific IgM in serum''' (anti-HAV-IgM), the increase in transaminases and bilirubin and the slight increase in ALP. Negative test in immunocompetent individuals excludes infection. IgM persists in serum for 3-6 months after infection, IgG persists long-term. The infection leaves a long-term to lifelong immunity. The main diagnostic marker. | ||
;Electron-microscopic detection of virus in faeces <ref name="zampachova" /> | ;Electron-microscopic detection of virus in faeces <ref name="zampachova" /> | ||
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===Therapy=== | ===Therapy=== | ||
Treatment is symptomatic - rest, no alcohol, diet with carbohydrates (possibly | Treatment is symptomatic - rest, no alcohol, diet with carbohydrates (possibly glucose) and fat reduction. Corticosteroids only in fulminant forms. | ||
===Complications=== | ===Complications=== | ||
The severity of the infection increases with age (90% are asymptomatic in young children). In 10%, it is a prolonged form, which, however, does not lead to chronicity. Chronic infection and carriers do not exist. | The severity of the infection increases with age (90% are asymptomatic in young children). In 10%, it is a prolonged form, which, however, does not lead to chronicity. Chronic infection and carriers do not exist. | ||
Complications: fulminant [[liver failure]] (rare), [[myocarditis]], [[encefalopathy]], | Complications: fulminant [[Liver Failure|liver failure]] (rare), [[myocarditis]], [[Encephalopathy|encefalopathy]], cryoglobulinemia, bone marrow hypoplasia, spleen rupture, [[Acute pancreatitis (diagnostic tests)|pancreatitis]], Guillain-Barré syndrome.<ref name="muntau" /> | ||
===Prevention=== | ===Prevention=== | ||
Vaccination with an attenuated vaccine, increased health surveillance at the site of the outbreak. By clinical examination and liver function monitoring, new cases of infections are identified. Immunolactively administered | Vaccination with an attenuated vaccine, increased health surveillance at the site of the outbreak. By clinical examination and liver function monitoring, new cases of infections are identified. Immunolactively administered imunoglobulin (NORGA) is administered to the exposed.<noinclude> | ||
==Links== | ==Links== | ||
===Related articles=== | ===Related articles=== | ||
*[[ | *[[Viral hepatitis]] | ||
===References=== | ===References=== | ||
<references /> | <references /> | ||
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|surname1 = Beneš | |surname1 = Beneš | ||
|name1 = Jiří | |name1 = Jiří | ||
|source_name = | |source_name = Study materials | ||
|year = | |year = | ||
|cited = 2010 | |cited = 2010 | ||
Revision as of 20:53, 30 November 2021
The causative agent is HAV, which is an RNA virus from the Picornaviridae family (Enteroviridae, Enterovirus 72), that acts directly cytolytically. HAV is a small virus (27-30nm), genetically homogenous, resistant to the external environment. It is exclusively human pathogen. [1] It spreads by the faecal-oral route (“dirty hand disease”), often by contaminated food and water, rarely parenterally. The entrance gate is the digestive tract and it is excreted in faeces. Transplacental transmission is not possible.[2] The virus is highly resistant to external influences. It is excreted in faeces as early as 2 weeks before the onset of symptoms and continues for about a week (up to 2 weeks)[2] after the symptoms stop. The patient is the most contagious before the end of the incubation period.
The course of infection
The incubation period is 15-48 days.[2] First, the prodromal (“preicteric”) stage begins (dyspepsia, fatigue, fever, weight loss). This is followed by the symptomatic stage (“icteric”) - the leading symptoms are jaundice, dark urine and acholic stool. The course is milder and shorter than in VHB. Cholestatic symptoms are rare and may occur fulminantly. HAV does not cause chronic infections. .[1]
Diagnostics
- Detection of antibodies
Diagnostics is done using anti-HAV antibodies. We perform the examination of specific IgM in serum (anti-HAV-IgM), the increase in transaminases and bilirubin and the slight increase in ALP. Negative test in immunocompetent individuals excludes infection. IgM persists in serum for 3-6 months after infection, IgG persists long-term. The infection leaves a long-term to lifelong immunity. The main diagnostic marker.
- Electron-microscopic detection of virus in faeces [1]
It can be detected in the second half of the incubation period and shortly after the onset of clinical symptoms.
- Detection of antigen and RNA [1]
In stool, similar to microscopy.
Therapy
Treatment is symptomatic - rest, no alcohol, diet with carbohydrates (possibly glucose) and fat reduction. Corticosteroids only in fulminant forms.
Complications
The severity of the infection increases with age (90% are asymptomatic in young children). In 10%, it is a prolonged form, which, however, does not lead to chronicity. Chronic infection and carriers do not exist.
Complications: fulminant liver failure (rare), myocarditis, encefalopathy, cryoglobulinemia, bone marrow hypoplasia, spleen rupture, pancreatitis, Guillain-Barré syndrome.[2]
Prevention
Vaccination with an attenuated vaccine, increased health surveillance at the site of the outbreak. By clinical examination and liver function monitoring, new cases of infections are identified. Immunolactively administered imunoglobulin (NORGA) is administered to the exposed.
Links
Related articles
References
- ↑ Jump up to: a b c d ŽAMPACHOVÁ, Eva. Downloadable lectures and materials from dr. Žampachová [online]. [cit. 2012-01-12]. <http://mujweb.cz/zampach/motol/?redirected=1521314685>.
- ↑ Jump up to: a b c d MUNTAU, Ania Carolina. Pediatrie. 4. edition. Prague : Grada, 2009. pp. 393-394. ISBN 978-80-247-2525-3.
Sources
- PASTOR, Jan. Langenbeck's medical web page [online]. [cit. 2010]. <http://langenbeck.webs.com>.
- BENEŠ, Jiří. Study materials [online]. [cit. 2010]. <http://jirben.wz.cz>.
Literature used
- HAVLÍK,. Infektologie. 2. edition. Prague : Avicenum, 1990. 393 pp. ISBN 80-201-0062-8.
- LOBOVSKÁ,. Infekční nemoci. 1. edition. Prague : Karolinum, 2001. 263 pp. ISBN 80-246-0116-8.
