Hepatitis a B15.9

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 24.06.2022

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Synonym(s)

A-hepatitis; HA; Hepatitis-A

Definition
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Hepatitis A is an acute liver inflammation transmitted by an enteric RNA virus that causes the typical symptoms of acute viral hepatitis in older children and adults. Young children may become ill asymptomatically. Fulminant hepatitis and death are rare. Chronic hepatitis does not occur. Diagnosis is made by antibody testing. Therapy is symptomatic. Vaccination and previous infection provide protection.

Suspected illness, illness and death from acute viral hepatitis must be reported by name.

Pathogen
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Hepatitis A virus (HAV), RNA enterovirus of the Hepeviridae family. The incubation period is 15-50 days. Transmission of the pathogen (route of infection) occurs by contact or smear infection (faecal-oral: infections in which pathogens excreted with the faeces (faecal) are ingested orally, e.g. through contaminated drinking water and/or contaminated food such as raw seafood, vegetables and salads fertilised with faeces). Parenteral infections through contaminated injection needles (intravenous drug abusers) or through anal-oral contacts are very rare.

As an unenveloped virus, the hepatitis A virus is stable against environmental influences. It "survives" freezing, alcohol influences of up to 60% and the acidic environment of the stomach passage.

Manifestation
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It occurs more frequently in children and young adults. Hepatitis A is one of the most common travel diseases. The risk groups are mainly travellers to (sub-) tropical regions (in some countries it is expected that > 75% of adults have been exposed to HAV), residents of community facilities, sewer workers and homosexuals. In Germany, about 10% of < 30 year olds are infected with the virus.

Clinical features
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In children <6 years of age, approximately 70% of hepatitis A infections are asymptomatic. Icterus is rare (<10%). Older children and adults usually present with the typical manifestations of viral hepatitis, including anorexia, malaise, fever, nausea, and vomiting (see also Hepatitis Acute); icterus occurs in about 45% of cases in 6-14 year olds and in about 75% of cases in adults.

Fulminant hepatitis A can develop in children with mutations in the IL18BP gene (interleukin 18 binding protein) (Belkaya S et al. 2019).

Laboratory
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Materials required: Blood serum (anti-HAV IgG, anti-HAV IgM); stool (HAV antigen). HAV antigen detection in blood or stool indicates a fresh hepatitis A infection in the incubation phase (detectable: 1-3 weeks before until 3-6 weeks after disease onset)

Anti-HAV IgM: indicative of fresh hepatitis A infection; antibodies are detectable from the onset of disease symptoms for 3-6 months

Anti-HAV IgG: indicates a fresh or expired infection or a vaccination; antibodies are detectable from the beginning of the disease symptoms, usually persist for life; serve as a parameter for the rate of infection.

Sequencing of the HAV genome - is only performed in special cases.

Pathologically elevated liver parameters: GPT, GOT, glutamate dehydrogenase (GLDH), gamma-glutamyl transferase (gamma-GT). Infectivity (HAV excretion) is present 2 weeks before and 2 weeks after the onset of the disease. For icterus: 1 week after the onset of the icterus.

General therapy
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Supportive treatment; no specific treatment necessary because not effective. Alcohol should be avoided. Restrictions in diet or physical activity including frequently prescribed bed rest are not based on scientific evidence.

After the icterus has subsided, most patients are able to work again, although the transaminases are still elevated.

In cholestatic hepatitis, the administration of colestyramine 8 g p.o. once or twice a day can reduce itching.

Progression/forecast
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The clinical symptoms typically subside completely after about 2 months; only in a few patients, the symptoms persist for a longer period of time or repeat up to 6 months. Fierce hepatitis rarely occurs (0.2% of cases); in HBV carriers up to 10%. In patients >50 years of age the lethality rate is about 3%. No chronic hepatitis. No permanent virus carriers.

Prophylaxis
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Good personal hygiene helps to avoid fecal-oral transmission of hepatits A. Protective measures are recommended, but isolation of the patient is of little help. Contaminated surfaces around the patient can be cleaned with virucidal disinfectants.

Vaccinations: Hepatitis A vaccine is recommended for all children beginning at 1 year of age, with a second dose 6 to 18 months after the first.

Pre-exposure HAV vaccination should be provided for:

  • Travelers with high or moderate HAV endemicity. Indication for travel is: "south of the Alps and east of the Oder".
  • Diagnostic laboratory workers
  • Men who have sex with men
  • People who use illegal drugs with or without injection
  • People with chronic liver disease (including chronic hepatitis C), as they are at increased risk of developing fulminant hepatitis due to HAV.
  • Individuals receiving blood clotting factor concentrates.
  • Pre-exposure HAV prophylaxis may be considered for nursery workers.

Note: HAV vaccines are safe and confer protective efficacy within approximately 4 weeks and also have long-term protective efficacy (probably > 20 years).

For basic immunization with monovalent hepatitis A vaccines, 2 doses are required at 6-12 month intervals. Depending on the manufacturer, booster vaccinations are only necessary after 20-30 years following basic immunisation.

Elderly travelers without vaccine protection who have received hepatitis A vaccination ≥ 2 weeks before travel to endemic areas should receive standard immunoglobulins.

Postexposure prophylaxis should be given to family members and close contacts of patients with hepatitis A.

In patients > 75 years of age with chronic liver disease and immunocompromised patients, standard immunoglobulin prevents hepatitis A infection or reduces the severity of the disease (dosage: 0.02 ml/kg i.m.). Immunoglobulins can be given up to 2 weeks after exposure.

Literature
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  1. Batts W et al. (2011) A novel member of the family Hepeviridae from cutthroat trout (Oncorhynchus clarkii). Virus Res 158: 116-123
  2. Belkaya S et al (2019) Inherited IL-18BP deficiency in human fulminant viral hepatitis. J Exp Med 216: 1777-1790.

  3. Bilic I et al (2009). Sequence analysis and comparison of avian hepatitis E viruses from Australia and Europe indicate the existence of different genotypes. J Gen Virol 90: 863-873.
  4. Fan J (2009). Open reading frame structure analysis as a novel genotyping tool for hepatitis E virus and the subsequent discovery of an inter-genotype recombinant. J Gen Virol 90: 1353-1358.
  5. Hsu I W-Y et al (2014). Avian hepatitis E virus in chickens, Taiwan Emerg Infect Dis 20: 149-151.
  6. Lu L et al (2006). Phylogenetic analysis of global hepatitis E virus sequences: genetic diversity, subtypes and zoonosis. Rev Med Virol 16: 5-36
  7. Smith DB et al (2014) Consensus proposals for classification of the family Hepeviridae. J Gen Virol. 95: 2223-2232.
  8. Takahashi M et al (2011). Analysis of the full-length genome of a hepatitis E virus isolate obtained from a wild boar in Japan that is classifiable into a novel genotype. J Gen Virol 92: 902-908.
  9. Zhao C et al (2009). A novel genotype of hepatitis E virus prevalent among farmed rabbits in China. J Med Virol 81: 1371-1379.

Disclaimer

Please ask your physician for a reliable diagnosis. This website is only meant as a reference.

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Last updated on: 24.06.2022