JC54 (Medicine) - Acute hepatitis - HAV and HEV Flashcards

1
Q

Compare Hepatitis viruses

  • Family
  • Genome and envelop structure
  • Endemic or epidemic
  • Transmission
A
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2
Q

Compare Hepatitis viruses
- Incubation period and Chronicity

A

A: 2-4 weeks, never chronic
E: 2-7 weeks, never chronic except in transplant patients

B: 4-24 weeks, Chronic
C: 2-25 weeks, Chronic
D: Depends on Hep. B co-infection

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3
Q

Hepatitis infections

  • General Clinical phase
  • S/S in each phase
  • Total time span
A

Usually lasts for 1-2w, rarely beyond 3-6w

Pre-icteric phase: a few days to 2w before development of jaundice
Viral syndrome: low-grade fever (usually <39oC), severe anorexia (typical), severe fatigue and myalgia
GI upset: diarrhoea and N/V
Liver symptoms:
- RUQ pain: characteristically NOT severe(due to liver capsule distension)
- Cholestasis: darkened urine, pale stools, transient pruritis (due to bile canaliculi compression)

Icteric phase: jaundice

Convalescent phase

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4
Q

HAV

Transmission route

Window of transmission

Mode/ vector of transmission

A

Faeco-oral transmission:
→ Window: faecal viral shedding from incubation (2-4w) to 7-10d after onset of jaundice
→ Usually via
- Undercooked shellfish from infected water, esp clams, oyster, mussels
- Ingestion of infected water, eg. from uncooked vegetable
- Faecal contamination in children, by anal sex or in healthcare workers

Parenteral transmission: RARE
→ Window: transient viraemia during incubation phase
→ Usually via
- Transfusion
- Acupuncture and tattooing

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5
Q

HAV

Clinical manifestations

Recovery time

A

□ Clinical symptoms of acute viral hepatitis:
→ Anicteric/ mildly symptomatic in children
→ Icteric in small proportion of adults, mostly asymptomatic

□ Diarrhoea common in early stages

□ Recovery usually occurs within 4-6 weeks

□ Fulminant hepatitis (<1%) esp in patients >50y or with other liver disease (eg. chronic hep B)

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6
Q

Complications of HAV infection

A

Cholestatic hepatitis (prolonged cholestasis) (<5%)

Relapsing hepatitis (6-10%)

Extrahepatic manifestations (<15%)

Type I autoimmune hepatitis (rare)

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7
Q

Cholestatic hepatitis

S/S

Biochemistry

Histology of liver parenchyma

Management

A

S/S: prolonged jaundice and pruritus for up to 12-24w

Biochemistry: characterized by high bilirubin (10× ULN) but with decreasing AST/ALT

Histology: centrilobular cholestasis with periportal inflammation (may mimic chronic active hepatitis)

Mx: ALWAYS complete resolution
- Steroids: quickly ‘whitewashes’ the cholestatic picture but increase relapse → NOT used!

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8
Q

Relapsing hepatitis A

S/S

Relapse Course and duraton

Mechanism

Biochemistry

Management

A

→ S/S: apparent clinical recovery followed by biochemical ± clinical relapse

→ Course: biphasic or polyphasic, may last 3-12 months

→ Mechanism: related to immune reaction towards HAV, unlikely reintroduction of virus

→ Biochemistry: AST/ALT >1000IU/L, with IgM anti-HAV remaining positive

HAV identified in stools and HAV RNA in serum

→ Mx: ALWAYS complete resolution (steroids can ↑relapse)

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9
Q

Extra-hepatic manifestations of HAV infection

Cause

Manifestations

A

Cause: prolonged diseases, eg. relapsing hepatitis, prolonged cholestasis

S/S: characterized by immune complex-mediated disease

  • Purpuric rash due to leukocytoclastic vasculitis
  • Arthralgia due to arthritis
  • Cryoglobulinaemia
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10
Q

Serological diagnosis of HAV

Time course

A

IgM anti-HAV for acute infection
→ Detected: 1-2w after jaundice, 2-3w after ↑AST/ALT
→ Peak: acute stage or early convalescence
→ Persist: usually 3-4mo, rarely >12mo

IgG anti-HAV for immunity (or previous HAV infection)
→ Time: persists for decades

NO DIAGNOSTIC USE as prior hepatitis A infection common in population

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11
Q

Prevention of HAV infection

A

Careful cooking of shelled seafood (Dry heat at 100oC in 1min, Wet heat at 100oC in 5-10min)

Chlorination of drinking water

Passive immunization by IVIg - e.g. urgent travelling to endemic regions

Active immunization by inactivated whole virus vaccine

2 doses Intra-Muscular injection with 6mo in between, protection within 3-4 weeks

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12
Q

HEV

Trend of infection rate and demographiucs

Transmission pattern and vector of transmission

A

Demographics:

  • ↑trend (similar to hepatitis A)
  • adults in 3rd decade of life

Transmission:

Waterborne transmission for genotypes 1 and 2

  • Transmitted human-to-human by contaminated water
  • Endemic in resource-limited countries with poor sanitation

Zoonotic transmission for genotypes 3 and 4

  • Transmitted from animals, esp pigs and filter feeder shellfish, to humans
  • consumption of pork liver or blood
  • rats
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13
Q

Difference between immunogenicity and protective efficacy

A

Immunogenicity: development of antibody (high or low)

Protective efficacy: effect of antibody production to protect against infection

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14
Q

Compare and contrast HAV with HEV infection (6)

A

Clinical features: self-limited acute infection almost identical to hepatitis A except

□ Incubation period: 2-7 weeks (cf 2-4w in hepatitis A)

□ High proportion with prominent cholestasis: ~20% (cf <5% in hepatitis A)

□ No permanent protection against re-infection (cf lifelong protection in hepatitis A)

□ Higher mortality: 1-2% for normal patients (cf 0.2% for hepatitis A)

□ Risk of fulminant hepatitis in pregnant women: up to 20% mortality

□ Possibility of causing chronicity in transplant recipients (cf NEVER in hepatitis A)

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15
Q

Pathophysiology of high pregnancy mortality rate in HEV infection

A

Reason: HEV causes Kupffer cell damage → allows endotoxin damage to liver, pregnant women more sensitive to endotoxin effects

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16
Q

Serological Diagnosis of HEV

What markers and time course

A

IgM anti-HEV: appear in >90% of pts
→ Appear during early phases of clinical illness and coincides with symptoms (cf delayed for 1-2w after jaundice in hep A)
→ Persists for ~3mo

IgG anti-HEV:
→ Rises after anti-HEV IgM
→ ↑titres in acute and convalescent phase
→ Persists for several years

PCR for HEV RNA: for chronic carriers

17
Q

Management of HEV infection

A

Supportive Treatment

Consider transplantation if fulminant hepatitis

Reduce immunosuppression + antivirals for chronic hepatitis E infection

  • E.g. reduce dose of Tacrolimus + Add Ribavirin
  • Aim: sustained virologic response (SVR), i.e. undetectable HEV RNA for 12w after Tx
18
Q

Prevention of HEV

A

□ Better sanitation: avoid dirty water/food, raw or undercooked seafood and pork

□ Passive immunization by immunoglobulin (unknown efficacy)

□ Active immunization by recombinant vaccine × 3 doses

  • Recombinant vaccine containing genotypes 1,4
  • 3 doses at 0,1,6 months