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“Infectious” A Enterically
E
transmitted
Hepatitis A-E Viruses
Viral hepatitis NANB
An Overview
Parenterall
“Serum” B D C y
transmitted
F, G, TTV
? other
1 | PEDIA-VIRO
Hepatitis A ‐ Clinical Features Clinical Manifestations
Asymptomatic or mild, nonspecific illness‐ majority
below 5 yo
Incubation period: Average 30 days
Symptomatic
Range 15‐50 days
Jaundice by <6 yrs, <10% Pre‐icteric‐fever,vomiting,profound anorexia &
age group: 6‐14 yrs, 40%‐50% abdominal discomfort.Mild & unnoticed in infants &
>14 yrs, 70%‐80% young children.(+)Diarrhea in children, constipation
Complications: Fulminant hepatitis 0.15% in adults
Relapsing hepatitis 3‐20%
Icteric phase‐ jaundice/dark urine after systemic
Chronic sequelae: None symptoms x a week. Subtle & unnoticed in young
kids. Appetite.Well‐being gradually return to normal
Extrahepatic‐ none
0 1 2 3 4 5 6 12 24
Months after exposure
Prevention Hepatitis B
Postexposure Immunization:
2 | PEDIA-VIRO
Hepatitis B - Clinical Features Clinical manifestations
Anicteric‐majority of cases including children
Incubation period: Average 60‐90 days Icteric Phase‐similar to hepatitis A or C, maybe more severe
Range 45‐180 days Extrahepatic manifestations‐occur early; may precede jaundice
Clinical illness (jaundice): <5 yrs, <10% as arthralgia, arthritis, macular rashes, thrombocytopenia,
5 yrs, 30%‐50% papular acrodermatitis,(Gianotti‐Crosti syndrome),
Acute case‐fatality rate: 0.5%‐1% glomerulonephritis, aplastic anemia
Chronic infection: <5 yrs, 30%‐90% Chronic infection‐
5 yrs, 2%‐10% perinatal transmission‐ >90% risk of chronic infection
Premature mortality from
1‐5 years old‐ 25‐50%
chronic liver disease: 15%‐25% older children/adult‐ 6‐10%
* ~25% on infants and children with chronic hepatitis B will
eventually develop HBV related hepatocellular Ca or cirrhosis
Symptoms
1. Chronic Persistent Hepatitis ‐ asymptomatic
HBeAg anti-HBe
2. Chronic Active Hepatitis ‐ symptomatic
Total anti-HBc
exacerbations of hepatitis
Titre
3. Cirrhosis of Liver
HBsAg IgM anti-HBc anti-HBs
4. Hepatocellular Carcinoma
0 4 8 12 16 20 24 28 32 36 52 100
IgM anti-HBc 20 20
Symptomatic Infection
0 0
Birth 1-6 months 7-12 months 1-4 years Older Children
0 4 8 12 16 20 24 28 32 36 52 Years and Adults
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Concentration of Hepatitis B Virus in Hepatitis B Virus
Various Body Fluids Modes of Transmission
Diagnosis Treatment
• HBsAg ‐ general marker of infection. • Interferon ‐ for HBeAg (+) carriers with chronic
• HBsAb ‐ recovery &/or immunity to HBV infection. active hepatitis. Response rate is 30 to 40%.
• anti‐HBc IgM ‐ marker of acute infection.
• Lamivudine ‐ a nucleoside analogue reverse
• anti‐HBc IgG ‐ past or chronic infection. transcriptase inhibitor. Well tolerated, most
• HBeAg ‐ active replication of virus ; infectiveness. patients will respond favorably; tendency to
• Anti‐Hbe ‐ virus no longer replicating; the patient can relapse on cessation of Tx; rapid emergence of
still be (+) for HBsAg made by integrated HBV. drug resistance.
• HBV‐DNA ‐ active replication , more accurate than
HBeAg especially in escape mutants; for monitoring
• Successful response to Tx: disappearance of
response to therapy. HBsAg, HBV‐DNA, and seroconversion
4 | PEDIA-VIRO
Hepatitis C Hepatitis C ‐ Clinical Features
Degree of Seroprevalence • Transmission : blood or body fluid
exposure
• Parenteral exposure to HCV‐
Large,repeated 60=90%
infected blood: primary route; Incubation period: Average 6‐7 wks
seroprevalence depend on
exposure(IV drug
degree of exposure Range 2‐26 wks
users,hemophiliacs
before 1987 Clinical manifestations:
Frequent ,smaller 10-20%
exposure(hemodialy
sis pt)
Asymptomatic illness‐ majority of cases
Inapparent 1-10% Symptomatic illness: mimics hepatitis A or B
percutaneous
exposure(sex • Perinatal transmission is Extrahepatic manifestations: essential mixed
worker) uncommon(5‐6%)
Sporadic exposure 1% cryoglobulinemia,cutaneous vasculitis,peripheral neuropathy,
glomerulonephritis,etc.
Risk Factors Associated with
Chronic Hepatitis C Infection
Transmission of HCV
• HCV most likely to cause chronic infection;~85% become
chronic Transfusion or transplant from infected donor
• After ~20‐30 years, about 25% ultimately progress to Injecting drug use
cirrhosis, liver failure & occasionally
primary hepatoCa
Hemodialysis (yrs on treatment)
• Hepatocellular Ca associated with HCV, which is less effective Accidental injuries with needles/sharps
than HBV in causing primary hepatoCa almost always occurs
Sexual/household exposure to anti‐HCV‐positive
with cirrhosis; results from chronic inflammation & necrosis
rather than oncogenic effect of virus contact
Multiple sex partners
Birth to HCV‐infected mother
Laboratory Diagnosis Treatment
• HCV antibody ‐ Not useful in the acute phase ; • Interferon ‐ considered for chronic active
at least 4 weeks after infection before (+) hepatitis;response rate ~ 50% but 50% of
• HCV‐RNA ‐ PCR and branched DNA; useful in responders will relapse upon withdrawal of Tx.
the acute phase; used mainly in monitoring • Ribavirin ‐ recent studies suggest that a
response to antiviral therapy.
combination of interferon and ribavirin is
• HCV‐antigen ‐ by EIA , much easier procedure more effective than interferon alone.
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Prevention of Hepatitis C Hepatitis D (Delta) Virus
antigen HBsAg
Screening of blood, organ, tissue donors
High‐risk behavior modification
Blood and body fluid precautions
RNA
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Hepatitis E Virus
Hepatitis E ‐ Clinical Features
• enteric non‐A, non‐B hepatitis
Incubation period: Average 40 days
Range 15‐60 days
Case‐fatality rate: Overall, 1%‐3%
Pregnant women,
15%‐25%
Illness severity: Increased with age
Chronic sequelae: None identified
Virus in stool
0 1 2 3 4 5 6 7 8 9 10 11 12 13
Hepatitis G (HGV)
‐RNA virus, flaviviridae family, 27% homology to HCV
‐reported in adults and children
‐seen in HIV pts and in 10‐20% of adults with chronic hepatitis B
and hepatits C
‐primary source: transfusion; organ transplant, IV drug use,
THE END
hemodialysis, sexual transmission
‐ accounts for only small proportion of cases of non‐A‐E
•
hepatitis
‐most infection not associated with hepatic inflammation
;doesn’t seem to worsen coinfection with hepatitis B or C
‐diagnosis: HGV RNA PCR
‐prevention: none
Edited by KDE
7 | PEDIA-VIRO