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HEPATITIS B
Introduction
• Hepatitis B infection is a major public health
problem in India and worldwide
• HBsAg prevalence rate is around 1.3-12.7 % in
children below 15 years of age in India
• It can cause acute, persistent or chronic infection
• Chronic infection are at risk of morbidity and
mortality associated with cirrhosis and HCC.
HBV structure
• HBV is DNA virus with a double shell
• Size is 42 nm in diameter
• Most infectious among all hepatitis viruses
• HBsAg (Australian antigen) – surface antigen
• HBcAg – hepatitis B core antigen
• HBeAg – integral part of core antigen, a marker of active
viral replication,so associated with high infectivity
• In a population with high prevalence of HBV,
infection is acquired early in life
• Man is the only reservoir
• An individual who is HBsAg positive for more than
6 months is called chronic carrier.
• Carriers may be asymptomatic or may have active
disease
• Virus is transmitted through blood , blood
products, body fluids, sexual contact ,mother to
newborn, needle injury, sharing of syringes
• Horizontal transmission – sexual contact (both
homosexual , heterosexual)
• Vertical transmission- mother to newborn is the
single most important factor for childhood
hepatitis B infection and chronic carrier state of
HBV.
• Risk of infection depends upon the HBeAg status
of the mother
• In HBeAg positive mother – risk is 60-90 %
• In HBeAg negative mother – risk is 2-15 %
• Other factors high viral DNA load , social status ,
type of delivery.
Clinical features
• Incubation period is 45-160 days
• Onset is insidious with loss of appetite, nausea,
vomiting, fever
• Acute hepatitis - clinical course is same as hepatitis A
• But fulminant hepatitis and complications are more
common in HBV infection
• Recovery occurs in 2-3 weeks
Extrahepatic manifestations are
• Aplastic anemia
• Arthritis
• Rash
• Urticaria
• Glomerulonephritis
• Pleural effusion
• Myocarditis, pericarditis
• Coombs positive hemolytic anemia
Chronic hepatitis
• out of all acute hepatitis B infection, 10%
becomes persistent HBsAg positive ,30% develop
chronic active hepatitis
• Chronically infected patients are at high risk for
developing chronic liver disease, cirrhosis ,
chronic active hepatitis, HCC.
• In perinatal infection 90% become carriers.
• Fulminant hepatitis development of hepatic
failure and encephalopathy with in 2 weeks of
onset of jaundice
• Sub fulminant hepatitis 2 weeks – 3 months
• Mortality is high and about 80 %
• HBV infection is the most common viral infection
leading to fulminant hepatitis
Investigations
HBsAg HBeAg
Anti
HBsAg
Anti
HBeAg
Anti
HBcAg
IgG
Acute
infection
+ + _ _ +
Chronic
infection
++ + _ _ +++
Recent HBV
infection
cured _ _ ++ + ++
Past HBV
infection
cured
_ _
+/ _
_
+/_
Healthy
carrier
+ _ _
+++
Recent HBV
vaccine
_ _ ++ _ _
Serological markers
Treatment
Acute hepatitis
• No specific therapy
• Supportive treatment
Chronic infection
• Aim is to decrease the viral replication to an
undetectable level
• Drugs – interferon α & lamivudine are used
maximally in children
• Adefovir a purine analog is used in more than 12
years
Prevention & control
• Universal precautions
• Prevent blood contamination
• Carefully use of needles and syringes
• Screening of blood and blood products
• Disinfection and sterilization of instruments
before reuse
• Public awareness about sexual transmission and
protected sex
• Immunization (both passive and active)
Hepatitis C
Hepatitis C
• HCV is a single stranded RNA virus
• Through blood, blood products, sexual contact,
perinatal transmission, needle injury, sharing of
syringes
• Incubation period is 2-24 weeks
• Clinical illness is insidious in onset and symptoms are
similar to hepatitis B but milder
• Extrahepatic manifestations are same
• 50-70% of infected persons develop chronic
infection
• They are at high risk of developing cirrhosis,
chronic liver disease , HCC
• Common cause of porphyria cutanea tarda
• Also causes small vessel vasculitis
Diagnosis & Treatment
• Detection of HCV RNA & anti HCV antibodies
• HCV RNA is gold standard
• HCV has six major genotypes
• Genotype 1 & 2 are more common worldwide
• DRUGS – Interferon α, Ribavirin
Pegylated interferon
• Treatment is usually given for 48 weeks
Hepatitis b & c

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Hepatitis b & c

  • 2. Introduction • Hepatitis B infection is a major public health problem in India and worldwide • HBsAg prevalence rate is around 1.3-12.7 % in children below 15 years of age in India • It can cause acute, persistent or chronic infection • Chronic infection are at risk of morbidity and mortality associated with cirrhosis and HCC.
  • 3. HBV structure • HBV is DNA virus with a double shell • Size is 42 nm in diameter • Most infectious among all hepatitis viruses • HBsAg (Australian antigen) – surface antigen • HBcAg – hepatitis B core antigen • HBeAg – integral part of core antigen, a marker of active viral replication,so associated with high infectivity
  • 4. • In a population with high prevalence of HBV, infection is acquired early in life • Man is the only reservoir • An individual who is HBsAg positive for more than 6 months is called chronic carrier. • Carriers may be asymptomatic or may have active disease
  • 5. • Virus is transmitted through blood , blood products, body fluids, sexual contact ,mother to newborn, needle injury, sharing of syringes • Horizontal transmission – sexual contact (both homosexual , heterosexual) • Vertical transmission- mother to newborn is the single most important factor for childhood hepatitis B infection and chronic carrier state of HBV.
  • 6. • Risk of infection depends upon the HBeAg status of the mother • In HBeAg positive mother – risk is 60-90 % • In HBeAg negative mother – risk is 2-15 % • Other factors high viral DNA load , social status , type of delivery.
  • 7. Clinical features • Incubation period is 45-160 days • Onset is insidious with loss of appetite, nausea, vomiting, fever • Acute hepatitis - clinical course is same as hepatitis A • But fulminant hepatitis and complications are more common in HBV infection • Recovery occurs in 2-3 weeks
  • 8. Extrahepatic manifestations are • Aplastic anemia • Arthritis • Rash • Urticaria • Glomerulonephritis • Pleural effusion • Myocarditis, pericarditis • Coombs positive hemolytic anemia
  • 9. Chronic hepatitis • out of all acute hepatitis B infection, 10% becomes persistent HBsAg positive ,30% develop chronic active hepatitis • Chronically infected patients are at high risk for developing chronic liver disease, cirrhosis , chronic active hepatitis, HCC. • In perinatal infection 90% become carriers.
  • 10. • Fulminant hepatitis development of hepatic failure and encephalopathy with in 2 weeks of onset of jaundice • Sub fulminant hepatitis 2 weeks – 3 months • Mortality is high and about 80 % • HBV infection is the most common viral infection leading to fulminant hepatitis
  • 12. HBsAg HBeAg Anti HBsAg Anti HBeAg Anti HBcAg IgG Acute infection + + _ _ + Chronic infection ++ + _ _ +++ Recent HBV infection cured _ _ ++ + ++ Past HBV infection cured _ _ +/ _ _ +/_ Healthy carrier + _ _ +++ Recent HBV vaccine _ _ ++ _ _ Serological markers
  • 13. Treatment Acute hepatitis • No specific therapy • Supportive treatment Chronic infection • Aim is to decrease the viral replication to an undetectable level • Drugs – interferon α & lamivudine are used maximally in children • Adefovir a purine analog is used in more than 12 years
  • 14. Prevention & control • Universal precautions • Prevent blood contamination • Carefully use of needles and syringes • Screening of blood and blood products • Disinfection and sterilization of instruments before reuse • Public awareness about sexual transmission and protected sex • Immunization (both passive and active)
  • 16. Hepatitis C • HCV is a single stranded RNA virus • Through blood, blood products, sexual contact, perinatal transmission, needle injury, sharing of syringes • Incubation period is 2-24 weeks • Clinical illness is insidious in onset and symptoms are similar to hepatitis B but milder • Extrahepatic manifestations are same
  • 17. • 50-70% of infected persons develop chronic infection • They are at high risk of developing cirrhosis, chronic liver disease , HCC • Common cause of porphyria cutanea tarda • Also causes small vessel vasculitis
  • 18. Diagnosis & Treatment • Detection of HCV RNA & anti HCV antibodies • HCV RNA is gold standard • HCV has six major genotypes • Genotype 1 & 2 are more common worldwide • DRUGS – Interferon α, Ribavirin Pegylated interferon • Treatment is usually given for 48 weeks