GI - HAV and HEV (refer to Summary) Flashcards
Compare Hepatitis viruses
- Family
- Genome and envelop structure
- Endemic or epidemic
- Transmission
Compare Hepatitis viruses
- Incubation period and Chronicity
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
Hepatitis infections
- General Clinical phase
- S/S in each phase
- Total time span
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
HAV
Transmission route
Window of transmission
Mode/ vector of transmission
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
HAV
Clinical manifestations
Recovery time
□ 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)
Complications of HAV infection
Cholestatic hepatitis (prolonged cholestasis) (<5%)
Relapsing hepatitis (6-10%)
Extrahepatic manifestations (<15%)
Type I autoimmune hepatitis (rare)
Cholestatic hepatitis
S/S
Biochemistry
Histology of liver parenchyma
Management
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!
Relapsing hepatitis A
S/S
Relapse Course and duraton
Mechanism
Biochemistry
Management
→ 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)
Extra-hepatic manifestations of HAV infection
Cause
Manifestations
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
Serological diagnosis of HAV
Time course
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
Prevention of HAV infection
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
HEV
Trend of infection rate and demographiucs
Transmission pattern and vector of transmission
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
Difference between immunogenicity and protective efficacy
Immunogenicity: development of antibody (high or low)
Protective efficacy: effect of antibody production to protect against infection
Compare and contrast HAV with HEV infection (6)
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)
Pathophysiology of high pregnancy mortality rate in HEV infection
Reason: HEV causes Kupffer cell damage → allows endotoxin damage to liver, pregnant women more sensitive to endotoxin effects
