Epidemiology and pathogenesis
The source of infection is most commonly individuals with asymptomatic or mild forms of the disease. About 80% of all cases occur in children under 15 years of age, and a seasonal rise in incidence is traditionally registered in the summer-autumn period.
The infectious process develops in stages:
- Penetration: the virus enters the bloodstream via the intestine and is carried to the liver.
- Fixation: the pathogen binds to specific hepatocyte receptors and enters the cell for replication.
- Elimination: new virions return to the intestine via the bile canaliculi and are excreted into the external environment.
- Damage: the virus itself does not have a direct cytopathic effect. The main damage to hepatocytes is caused by immune mechanisms — interferons, NK cells, and antibodies.
Clinical presentation and forms
The manifest course of the infection includes four successive periods: incubation (from 2 to 26 weeks), prodromal (pre-icteric with non-specific symptoms), full-blown icteric, and convalescence.
Clinical manifestations are polymorphic:
- Typical course: mild, cyclic, accompanied by mild jaundice, dark urine (choluria), and pale stools (acholia).
- Non-specific syndromes: toxic, flu-like, dyspeptic, and asthenovegetative.
- Clinical and morphological forms: anicteric and subclinical variants predominate in most people. Rarely (in 0.1% of cases), a fulminant form develops with massive hepatic cell necrosis.
Pathological anatomy and diagnostics
At the peak of the disease, characteristic morphological changes are detected in the liver tissue:
- Degeneration: pronounced hydropic degeneration of hepatocytes.
- Inflammation: lymphomacrophagic infiltrates located predominantly in the periportal zone of the lobules and portal tracts.
- Alteration: coagulation and colliquative necrosis, as well as the formation of apoptotic bodies.
- Outcomes: focal intralobular sclerosis and portal tract sclerosis may form at the site of destroyed cells.
To confirm the diagnosis, laboratory methods are used: detection of specific anti-HAV IgM antibodies using enzyme-linked immunosorbent assay (ELISA) and detection of viral RNA by molecular biological methods.
Complications, outcomes, and prevention
In 90% of cases, the disease ends favorably with complete recovery and the development of lifelong post-infection immunity, which is mediated by anti-HAV IgG.
Residual symptoms may occur in the remaining patients:
- Asthenovegetative (post-hepatitis) syndrome;
- Liver sclerosis and biliary system disorders (dyskinesia, cholecystitis), with liver function tests remaining normal;
- Relapses, exacerbations, and concomitant biliary tract disorders.
Preventive measures include sanitary and hygienic measures, passive immunization with donor immunoglobulin for close contacts, and active vaccination using inactivated monovaccines and combination vaccines.
Briefly: answers to topical questions
What is the macroscopic appearance of the liver in the typical course of acute viral hepatitis A?
In the typical course of acute viral hepatitis A, the sources indicate the following morphological changes:
- Degeneration — hydropic degeneration of hepatocytes; ballooning degeneration is also described.
- Necrosis — necrobiotic processes (coagulation and colliquative necrosis), formation of apoptotic bodies; patchy necrosis and Councilman bodies are described.
- Inflammation — lymphomacrophagic infiltrates predominantly in the periportal zone of the lobules and portal tracts.
Macroscopically, the source indicates a large red liver, although the sign of congestion is not directly cited.
What morphological picture is characteristic of the fulminant form of viral hepatitis A?
The fulminant form of viral hepatitis is characterized by massive progressive necrosis with rapid disintegration of hepatocytes.
Macroscopic appearance:
- Size and capsule — the organ is reduced in size, the capsule is wrinkled.
- Consistency — the liver is flabby (the tissue "collapses").
- Color on cross-section — mottled, initially yellow (stage of yellow atrophy), then red.
Microscopic appearance:
- 2nd and 3rd zones of the acinus — submassive hepatocyte necrosis, formation of fat-protein detritus, infiltration by segmented neutrophils and macrophages.
- 1st zone of the acinus — hepatocytes contain large optically empty vacuoles.
How does acute viral hepatitis A morphologically differ from acute viral hepatitis B?
Sources for viral hepatitis B describe specific morphological features: ground-glass hepatocytes due to HBsAg accumulation in the endoplasmic reticulum and " sanded" nuclei associated with the presence of HBcAg. For viral hepatitis A, hydropic degeneration of hepatocytes is described, as well as lymphomacrophagic infiltrates predominantly in the periportal zone of the lobules and portal tracts.
Sources do not state that specific markers of virus B are found exclusively in HBV or absent in HAV, and do not provide a separate comparison of acute HAV with acute HBV.
A stands for Autonomous: hepatitis A is completely reversible, does not become chronic, confers lifelong immunity, and is transmitted via unwashed hands (fecal-oral).
Class and exam questions
Does a chronic carrier state develop in viral hepatitis A?
No, viral hepatitis A has a completely reversible course. Carrier state and chronic hepatitis do not develop with this infection.
What is the main mechanism of liver cell damage in HAV?
Hepatocyte damage is caused not by the direct action of the virus, but by immunopathological reactions involving interferons, NK cells, and antibodies.
Which antibodies confirm an acute process in laboratory diagnostics?
To diagnose the acute period, the detection of specific IgM antibodies — anti-HAV IgM — is used.
What type of immunity remains after recovering from hepatitis A?
After the infection, lifelong post-infection immunity is established, which is provided by anti-HAV IgG antibodies.
What else to study on this topic
- General characteristics and classification of all hepatotropic viruses (B, C, D, E)
- Pathogenetic differences between enteral and parenteral hepatitis
- Morphological features of the fulminant form of viral hepatitis
- The role of immunopathological mechanisms in hepatocyte damage
- Principles of active and passive specific prevention of viral hepatitis A
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