Hepatitis A

Acute self-limiting viral hepatitis caused by hepatitis A virus (HAV), transmitted via faecal-oral route. Notifiable disease. No chronic state. Supportive management; prevention through vaccination and hygiene.

Key Facts

Faecal-oral transmission: contaminated food/water, close contact, MSM, travel to endemic areas Incubation period: 15-50 days (average 28 days); most infectious 2 weeks before to 1 week after jaundice onset Clinical: often subclinical in children; adults: prodromal illness → jaundice → recovery over 2-6 weeks; NO chronic hepatitis Diagnosis: anti-HAV IgM (acute infection); anti-HAV IgG (past infection/immunity) Fulminant hepatic failure: rare (<0.5% overall; higher in pre-existing liver disease and elderly — up to 1-2%) Prevention: HAV vaccine (Havrix/Vaqta — 2 doses, 0 and 6-12 months); post-exposure prophylaxis (vaccine within 14 days); notifiable disease in UK

Overview

Key Facts

Hepatitis A is an acute, self-limiting liver infection that does not cause chronic hepatitis. It is a notifiable disease in the UK. Prevention through vaccination and public health measures is the primary strategy.

Epidemiology

~350 cases per year in the UK (most travel-associated). Endemic in Sub-Saharan Africa, South/Southeast Asia, Central America. UK is low-endemicity — most adults are susceptible. Outbreaks occur in MSM communities, people who inject drugs, and institutional settings.

Aetiology

  • Hepatitis A virus (HAV): non-enveloped RNA virus (Picornaviridae family)
  • Transmission: faecal-oral — contaminated food (shellfish, salad), water, person-to-person (household, sexual contact), blood-borne (rare)
  • Risk groups: travellers to endemic areas, MSM, PWID, household contacts, occupational (sewage workers)

Pathophysiology

HAV replicates in hepatocytes. Liver damage is primarily immune-mediated (CD8+ T-cell response) rather than direct viral cytopathic effect. The inflammatory response causes hepatocyte necrosis and cholestasis. Viral shedding in stool begins 1-2 weeks before symptom onset and peaks around jaundice onset — hence transmission occurs before diagnosis. Complete viral clearance occurs and there is no chronic carrier state.

Clinical Presentation

Prodromal Phase (1-2 weeks)

  • Malaise, fatigue, anorexia, nausea
  • Low-grade fever, myalgia
  • RUQ discomfort

Icteric Phase (2-6 weeks)

  • Jaundice (dark urine, pale stools, pruritus)
  • Hepatomegaly (tender)
  • Prodromal symptoms often improve as jaundice appears
  • Splenomegaly (~15%)

Recovery Phase

  • Gradual resolution over weeks to months
  • Fatigue may persist for months

Atypical Presentations

  • Subclinical/anicteric: common in children (<6 years — 70% asymptomatic)
  • Cholestatic hepatitis: prolonged jaundice (>3 months) — good prognosis
  • Relapsing hepatitis: symptoms recur after apparent recovery (~10%)
  • Fulminant hepatic failure: rare (<0.5%) but potentially fatal; more common in elderly and those with pre-existing liver disease

Red Flags

  • Encephalopathy (confusion, asterixis) — fulminant failure
  • INR >1.5 with rising bilirubin
  • Rapidly shrinking liver size
  • Renal failure

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
Hepatitis B (acute)Risk factors (IVDU, sexual, endemic), HBsAgHBsAg, anti-HBc IgM
Hepatitis ESimilar presentation, UK autochthonous (pork)Anti-HEV IgM, HEV RNA
EBV hepatitisPharyngitis, lymphadenopathy, splenomegalyEBV VCA IgM, monospot
CMV hepatitisImmunosuppressed, or mononucleosis-like illnessCMV IgM, CMV PCR
Drug-induced liver injuryTemporal relationship to drugDrug history
Autoimmune hepatitisRaised IgG, autoantibodiesANA, SMA, IgG
Biliary obstructionObstructive LFT pattern, dilated ductsUSS, MRCP

Diagnosis / Investigation

Bedside

  • History: travel, food exposure, contacts, sexual history, occupation

Bloods

  • Anti-HAV IgM: diagnostic of acute infection (positive for up to 6 months)
  • Anti-HAV IgG: indicates past infection or vaccination (lifelong immunity)
  • LFTs: markedly raised ALT/AST (often >1000 IU/L); raised bilirubin; ALP variably raised
  • INR/PT: normal in most; raised in severe/fulminant disease (poor prognostic sign)
  • FBC: mild lymphopaenia, sometimes leucopaenia
  • U&Es: renal function (hepatorenal syndrome in fulminant)

Imaging

  • USS abdomen: exclude biliary obstruction; may show hepatomegaly

Special Tests

  • HAV RNA (PCR): confirms viraemia; rarely needed clinically (IgM sufficient)
  • Liver biopsy: NOT routinely indicated; shows portal and periportal inflammation with hepatocyte necrosis
  • King's College Criteria: for assessing need for liver transplant in fulminant failure

Management

Non-pharmacological

  • Supportive care: rest, adequate hydration, avoid alcohol, avoid hepatotoxic drugs
  • Infection control: handwashing, food hygiene; infectious until 7 days after jaundice onset
  • Notify PHE: HAV is a notifiable disease under the Health Protection (Notification) Regulations 2010
  • Contact tracing: household and sexual contacts

Pharmacological

  • No specific antiviral treatment for hepatitis A
  • Symptomatic relief: anti-emetics (cyclizine, ondansetron), cholestyramine for pruritus, paracetamol for pain (avoid if severe liver impairment)
  • Post-exposure prophylaxis: HAV vaccine within 14 days of exposure for close contacts (effective if given early); ± immunoglobulin (HNIG) if immunosuppressed or chronic liver disease

Surgical/Interventional

  • Liver transplantation: for fulminant hepatic failure meeting King's College Criteria (very rare)

Referral Criteria

  • Hepatology referral if: INR >1.5, encephalopathy, worsening liver function, prolonged cholestasis
  • Public health notification: mandatory for all cases
  • Liver transplant centre: if fulminant hepatitis

Prognosis

Hepatitis A is self-limiting in >99% of cases. No chronic hepatitis, no carrier state. Complete recovery with lifelong immunity. Fulminant hepatic failure occurs in <0.5% overall but ~1-2% in those >50 years or with pre-existing liver disease. Mortality from fulminant HAV is ~50% without transplant. Cholestatic and relapsing variants have good prognosis. Return to normal activities typically within 2-6 weeks.

Other Relevant Information

Hepatitis A Serology Interpretation

MarkerAcute InfectionPast Infection/ImmunityVaccinated
Anti-HAV IgMPositiveNegativeNegative
Anti-HAV IgGPositive (late)PositivePositive
HAV RNAPositiveNegativeNegative

HAV Vaccination

IndicationRegimen
Travel to endemic areasHavrix: 2 doses (0 and 6-12 months)
MSM2-dose schedule
Chronic liver disease2-dose schedule
PWID2-dose schedule
Post-exposure prophylaxisSingle dose within 14 days of exposure
Occupational (sewage workers)2-dose schedule