- Clinical science
Hepatitis A infection is caused by the hepatotropic hepatitis A virus (HAV) and is usually transmitted via the fecal-oral route. About half of all cases of HAV infection that occur in the US are acquired during visits to countries that are endemic for HAV (e.g., tropical or subtropical regions). HAV infection results in acute hepatitis with a clinical course characterized by prodromal symptoms of fever and malaise, followed by jaundice. As in any other case of acute viral hepatitis, high levels of serum transaminase and mixed hyperbilirubinemia are observed. Serological detection of anti-HAV IgM, which is elevated during an acute infection, confirms the diagnosis. While prodromal symptoms resolve within a few weeks, jaundice usually resolves within 1–3 months. No chronic sequelae occur and acute hepatic failure occurs only in very rare cases. Therefore, supportive care is usually the only treatment required. As of 2006, routine immunization against hepatitis A is recommended for all children older than 12 months. Certain high-risk groups, such as tourists to areas where HAV is endemic, should also be immunized against HAV if they have not been vaccinated in the past.
An important differential diagnosis is another feco-orally transmitted viral infection: hepatitis E (HEV). The clinical presentation of HEV is almost identical to that of HAV, with the exception that pregnant women are at a high risk of developing acute liver failure. Serological tests help to distinguish HEV from HAV.
- Hepatitis A infection is the second most common cause of acute hepatitis in the US.
- Hepatitis A is very common in tropical and subtropical regions.
- Incidence: (in the US): 2,000 cases per year (50% acquired during travels abroad)
- Average age of infected persons: vaccination programs have made the disease fairly rare in children; infection is now more widespread in adults.
Epidemiological data refers to the US, unless otherwise specified.
Pathogen: hepatitis A virus
- Belongs to the family of Picornaviridae and the genus Hepatoviridae; . It is a small (27 nm in diameter), non-enveloped virus with single-stranded, positive-sense RNA
- Humans are the only reservoir for the hepatitis A virus.
- Extremely resistant to denaturation by heat and chemicals and can remain viable for many years
Route of transmission: fecal-oral
- Contaminated food, e.g., raw shellfish
- Risk groups: children, employees of day care centers, convicts, men who have sex with men
- Infectious period: 2 weeks before to 1 week after the onset of the illness
When it comes to viral hepatitis, vowels (A and E) are bowels (i.e., transmitted feco-orally)!
- Incubation period: 2–6 weeks
- HAV infection in children is typically asymptomatic. The risk of symptomatic infection increases with age and coinfection (e.g., with hepatitis B).
- Acute viral hepatitis: three phases
- Potential complications: cholestasis, relapsing HAV infection
- The mortality rate is 0.1–0.3% because few patients progress to acute liver failure.
- Patients do not become carriers nor develop chronic hepatitis (unlike in hepatitis B and C).
When it comes to viral hepatitis, vowels (A and E) cause only AcutE hepatitis while consonants (B, C, and D) may have chronic sequelae as well!
- ↑↑ Serum transaminase (AST, ALT) Serum transaminase levels return to the baseline within 5–20 weeks.
- Mixed hyperbilirubinemia (direct bilirubin makes up 20–50% of total bilirubin)
- Possibly ↑ ALP, ↑ γ-GT
- Urine analysis: ↑ urine bilirubin, ↑ urobilinogen
- Atypical lymphocytosis, which may be preceded by transient neutropenia and lymphopenia
- Measurement of prothrombin time: to rule out hepatic necrosis
- ↑ Anti-HAV IgM: active infection (Anti-HAV IgM antibody levels begin to rise 1 week after the onset of the illness and peak at around 3 weeks, after which point they decline. Anti-HAV IgM can be found in serum 3–6 months after the infection.) In the case of relapsing HAV infection, IgM levels remain high even after 6 months.
- ↑ Anti-HAV IgG: past infection or vaccination
- HAV RNA can be detected by PCR in stool and serum samples.
- Liver biopsy (not normally necessary): Periportal inflammation, ballooning degeneration, bridging necrosis, and Councilman bodies (apoptotic hepatocytes)
For an overview comparing the different types of viral hepatitis: see .
Pathogen: hepatitis E virus (HEV)
- The hepatitis E virus, which belongs to the family of Hepeviridae and the genus Orthohepeviridae; , is a small (34 nm in diameter), non-enveloped virus with single-stranded, positive-sense RNA.
- HEV genotypes 1 and 2 are found only in humans, but genotypes 3 and 4 are zoonotic diseases with reservoirs in both humans and animals (e.g., pigs, monkeys, and dogs).
- Epidemiology: HEV is not common in the US.
- Route of transmission: fecal-oral
- Pathophysiology: the degree of hepatic injury is usually mild and the patient may present with clinical features of acute hepatitis
- Incubation period: 2–8 weeks
- Clinical features are similar to those of hepatitis A (see “Symptoms/clinical findings” above).
- In the majority of cases, the disease is self-limiting with complete recovery.
- Fulminant hepatitis among pregnant women
- Patients do not become carriers nor develop chronic hepatitis (unlike in hepatitis B and C). However, chronic hepatitis E infection has been reported in immunosuppressed individuals (e.g., following transplantation, or in pateints with AIDS).
Treatment: supportive care
- No specific antiviral therapy
- Prevention: no vaccine available
Fulminant hepatitis due to HEV is relatively common among pregnant women (occurring in up to 20% of cases) and is life-threatening for both the mother and fetus!
The differential diagnoses listed here are not exhaustive.
- Disease is self-limiting → supportive care.
- Travelers should be advised to follow primary preventive measures such as hand-washing and following proper
- Routine active immunization is now recommended for all children over 12 months consisting of a first IM dose of hepatitis A vaccine followed by a booster dose after 6 months (see also “”)
- Active immunization is also recommended for certain high-risk groups who have not been immunized in the past:
Post-exposure prophylaxis; is indicated for all previously unvaccinated individuals; who have been exposed to a serologically confirmed case of HAV infection. In order to be effective, post-exposure prophylaxis should be administered within two weeks of exposure.
- Healthy individuals aged 1–40 years: active immunization with hepatitis A vaccine
- Infants, individuals older than 40 years, patients with chronic liver disease and/or immunosuppression: passive immunization with anti-HAV immunoglobulins (0.20 mL/kg)
- Hepatitis A is a notifiable disease.