Hepatitis A

Virology And Epidemiology

Single-stranded RNA virus; Picornavirus family; heat stable.
Represents most common cause of acute viral hepatitis globally; accounts for 40-60% of pediatric cases in endemic regions.

Strict feco-oral transmission via person-to-person contact, contaminated food, or contaminated water.
Incubation period ranges 15-50 days (mean 3-4 weeks).
Highly contagious; peak fecal viral shedding occurs prior to symptom onset and ceases approximately 2 weeks post-jaundice onset.
Maternal-neonatal transmission absent; chronic infection state does not occur.

Young Children (<6 years): Frequently asymptomatic or anicteric; clinically indistinguishable from nonspecific viral gastroenteritis.
Older Children/Adolescents: Symptomatic acute febrile illness featuring abrupt onset.

Phase	Clinical Signatures
Prodrome	Low-grade fever, severe malaise, anorexia, nausea, vomiting.
Icteric Phase	Jaundice, dark urine, pale stools, tender hepatomegaly, splenomegaly, regional lymphadenopathy.
Convalescence	Spontaneous symptom resolution within 2-6 months; complete recovery customary.

Acute Liver Failure (ALF): Rare (<1% in developed nations, higher in endemic zones); features worsening encephalopathy (irritability, altered sleep), persistent anorexia, and uncorrectable coagulopathy.
Prolonged Cholestatic Syndrome: Waxes and wanes over several months; marked by severe pruritus and fat malabsorption without hepatic synthetic dysfunction.
Extrahepatic Complications:
- Hematologic: Bone marrow hypoplasia, aplastic anemia, autoimmune hemolytic anemia.
- Gastrointestinal: Acute pancreatitis, acalculous cholecystitis, intestinal ulceration.
- Systemic: Leukocytoclastic vasculitis, cryoglobulinemia, nephritis, reactive arthritis, myocarditis.

Significant elevation of Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST).
Conjugated hyperbilirubinemia; bilirubin peaks later and normalizes slower than transaminases.
Normal albumin and prothrombin time/INR (unless ALF develops).
Mild leukopenia featuring relative lymphocytosis.

Marker	Clinical Interpretation
Anti-HAV IgM	Diagnostic for acute infection. Peaks during acute illness; persists 4-6 months.
Anti-HAV IgG	Indicates past infection, recovery, and lifelong immunity. Appears during convalescence.
HAV RNA PCR	Detects viremia/fecal shedding; rarely required for routine clinical diagnosis.

Abdominal Ultrasonography: Mild hepatomegaly, increased hepatic echogenicity, marked edema of gallbladder wall, periportal lymphadenopathy.

Strict supportive care; specific antiviral pharmacotherapy unavailable.
Maintain hydration; intravenous crystalloid fluids indicated for intractable vomiting or clinical dehydration.
Prolonged Cholestasis: Administer antipruritic agents and fat-soluble vitamins (A, D, E, K).
Avoid hepatotoxic medications; enforced strict bed rest unnecessary.
Monitor serially for ALF (encephalopathy, worsening coagulopathy); refer immediately to transplant center if ALF suspected.

Mandate strict sanitation, safe drinking water, and rigorous handwashing hygiene.
Exclude infected children from school/childcare for 1 week post-jaundice onset.

Modality	Indication And Administration
Active Immunization	Inactivated vaccine. Recommended for all children >12 months. Two-dose intramuscular schedule (6-12 months apart). Seroconversion >95%; confers long-term protection.
Passive Immunization	Human Immunoglobulin (Ig). Utilized for post-exposure prophylaxis if administered within 2 weeks of known exposure. Indicated exclusively for infants <12 months or vaccine-allergic individuals.
Combination Therapy	Vaccine + Ig utilized for pre/post-exposure prophylaxis in immunocompromised hosts, older adults, or chronic liver disease patients.