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
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
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