hepatitis A

hepatitis A
Name	Hepatitis A
Field	Infectious disease, Hepatology
Symptoms	Fever, fatigue, jaundice, nausea
Complications	Fulminant hepatic failure, relapsing hepatitis
Onset	2–6 weeks after exposure
Duration	Usually weeks to months
Causes	Hepatitis A virus (single-stranded RNA picornavirus)
Risks	Travel to endemic areas, contaminated food or water, close contact with infected persons
Diagnosis	Serology for IgM anti-HAV, liver function tests
Prevention	Vaccination, improved sanitation, hand hygiene
Treatment	Supportive care, rarely liver transplantation
Frequency	~1.5 million symptomatic cases estimated annually (historical)

hepatitis A Hepatitis A is an acute viral infection of the liver caused by the hepatitis A virus. It typically produces a self-limited illness characterized by systemic prodrome and cholestatic jaundice, with rare progression to fulminant hepatic failure. Outbreaks have been associated with contaminated food, travel, and close-contact settings.

Signs and symptoms

Typical presentation includes fever, malaise, anorexia, nausea, vomiting, abdominal pain, dark urine, pale stools, and jaundice. Symptoms usually follow a prodromal phase of systemic complaints and may include arthralgia and pruritus; conjugated hyperbilirubinemia and elevated aminotransferases are common. In children, infection is often subclinical or mild, whereas adults more commonly develop overt icteric disease. Rare complications include fulminant hepatic failure, relapsing hepatitis, and prolonged cholestatic hepatitis, which may necessitate liver transplantation in severe cases.

Cause and transmission

Hepatitis A virus is transmitted primarily via the fecal–oral route through ingestion of contaminated food or water. Outbreaks have been linked to shellfish harvested from sewage-contaminated waters, fresh produce irrigated with polluted water, and food handlers infected during the communicable period. Person-to-person spread occurs in households, daycare centers, correctional facilities, and among men who have sex with men; international travel to areas with higher endemicity increases risk. Transmission can also occur through blood exposure rarely, though routine transfusion-associated spread is uncommon because of donor screening practices.

Pathophysiology and virology

The causative agent is a nonenveloped, positive-sense single-stranded RNA virus of the Picornaviridae family. Following ingestion, the virus replicates in the oropharynx and gastrointestinal tract, then infects hepatocytes via bloodstream dissemination. Viral replication in hepatocytes provokes immune-mediated cytotoxicity principally by virus-specific cytotoxic T lymphocytes and natural killer cells, causing hepatocellular inflammation and necrosis. The nonenveloped virion confers environmental stability, enabling survival in seawater and on surfaces, which contributes to transmission through contaminated food and fomites. The incubation period is typically 15–50 days, reflecting the time required for viral amplification and immune response development.

Diagnosis

Diagnosis relies on serologic testing for anti-HAV antibodies: detection of IgM anti-HAV indicates acute or recent infection, whereas IgG anti-HAV signifies prior infection or successful immunization. Liver function tests show marked elevations of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) with a cholestatic pattern in many patients. Differential diagnoses include acute hepatitis caused by hepatitis B virus, hepatitis C virus, hepatitis E virus, Epstein–Barr virus, cytomegalovirus, drug-induced liver injury, and autoimmune hepatitis; appropriate serologic and molecular testing is used to exclude these causes. In outbreak investigations, molecular sequencing of viral RNA from stool or serum can link cases and identify sources.

Prevention and vaccination

Prevention centers on active immunization with inactivated hepatitis A vaccine and on improving sanitation and food safety. Vaccination strategies target infants in high-incidence countries, travelers to endemic regions, men who have sex with men, people with chronic liver disease, and other high-risk groups. Postexposure prophylaxis with hepatitis A vaccine or pooled human immunoglobulin is recommended for susceptible contacts within a defined window after exposure. Control of outbreaks also involves exclusion of infected food handlers during the infectious period, water treatment, and public health measures. The vaccine induces protective anti-HAV IgG within weeks and confers long-term immunity.

Treatment and prognosis

There is no specific antiviral therapy for hepatitis A; management is supportive, focusing on hydration, nutrition, avoidance of hepatotoxic agents, and monitoring for complications. Most immunocompetent patients recover fully without chronic sequelae, with normalization of liver enzymes over weeks to months. Mortality is low overall but increases with advancing age and preexisting chronic liver disease; fulminant hepatic failure, though rare, may require urgent liver transplantation. Immunization programs and improved sanitation have markedly reduced incidence in many regions.

Category:Viral hepatitis