GastroenterologyTier 1Disease (DEADMAN)

Hepatitis A

Description

Picornavirus, non-enveloped RNA virus; faecal-oral transmission
ACUTE ONLY - never chronic, no carrier state
Clinical course: prodrome -> icteric phase -> recovery
- Prodrome: anorexia, nausea/vomiting, abdominal pain, fever, malaise - lasts about 7-14 days
- Anicteric in most children <6 (>70%); icteric in most adults (>70%)
Severity increases with age - the defining epidemiological feature

Incubation 15-50 days (mean ~28)
Infectious from 2 weeks before to ~1 week after jaundice onset (peak shedding is PRE-symptomatic - the reason outbreaks spread)
Australia: low endemicity, ~200-300 notifications/yr
- Cases are travellers (South/South-East Asia), MSM, people who inject drugs, people experiencing homelessness
- Higher rates in remote Aboriginal and Torres Strait Islander communities before the 2005 targeted vaccination program
Case-fatality: <0.1% under 15; ~1.8% over 50
Food-borne outbreaks: frozen berries, shellfish, salad

Ingested -> replicates in hepatocytes -> excreted in bile -> faeces
*Hepatocyte injury is immune-mediated (CD8 T cells, NK cells), not cytopathic*
- -> explains why children (weaker immune response) have milder disease
No chronic infection: virus is cleared, lifelong immunity follows
Blood-borne transmission is possible but rare (short viraemia)

Anti-HAV IgM = acute infection (positive from symptom onset, persists 3-6 months)
- False positives occur in asymptomatic patients - do not use as a screening test
Anti-HAV IgG = past infection or vaccination -> immunity
ALT/AST often >1000, peaking before bilirubin
- Transaminase height does NOT predict outcome - INR and encephalopathy do
inc conjugated bilirubin, inc ALP (modest)
Check INR in every case - the only marker that identifies impending acute liver failure
HAV RNA (PCR) in stool/serum - outbreak investigation only
*Notifiable disease in all Australian jurisdictions*

1. Acute infection

Supportive - no specific antiviral
Avoid alcohol and hepatotoxins; paracetamol at reduced dose is acceptable and safer than NSAIDs
Monitor INR and mental state - admit if INR rising, encephalopathy, persistent vomiting, age >50, or chronic liver disease
Any encephalopathy + coagulopathy -> discuss with a liver transplant unit immediately
Exclude from work/school/childcare (food handlers, health-care and childcare workers) until 7 days after jaundice onset
Hand hygiene; notify public health

2. Post-exposure prophylaxis - within 14 days of exposure

Group	Prophylaxis
Healthy, 1-40 yr	HAV vaccine (preferred - gives durable immunity)
<1 yr, >40 yr, immunocompromised, chronic liver disease	Normal human immunoglobulin (+/- vaccine)

3. Vaccination - inactivated, highly effective

Travel to endemic regions; food-borne outbreaks (berries, shellfish)
MSM; people who inject drugs; homelessness; incarceration
Chronic liver disease - markedly worse outcome, hence vaccination
Childcare centres and institutions (faecal-oral spread)
Rare extrahepatic: reactive arthritis, cryoglobulinaemia, vasculitis, autoimmune haemolysis, Guillain-Barre

Complete recovery in >99% with lifelong immunity; no chronic infection and no cirrhosis
Complications
- Acute liver failure (fulminant hepatitis) - <1%, but rises steeply with age >50 and pre-existing chronic liver disease
- Prolonged cholestatic syndrome - jaundice and intense pruritus for up to 3-6 months; benign, self-limiting; steroids occasionally used
- Relapsing hepatitis - biphasic ALT rise in ~10%; still self-limiting
- Aplastic anaemia, autoimmune hepatitis triggered post-infection (rare)
*The exam trap: HAV in a patient with chronic hepatitis B/C or cirrhosis -> high risk of decompensation and death* - vaccinate them

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