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Vishal L. Kulkarni
Dept. of Microbiology
Hepatitis B & C
Hepatitis B
 It is a liver disease caused by the hepatitis B virus
(HBV).
 It ranges in severity from a mild illness, lasting a few
weeks (acute), to a serious long-term (chronic)
illness that can lead to liver disease or liver cancer.
Hepatitis B is Serious – Global
Impact
 It’s a common disease!
 Over 350 million people in the world have chronic
hepatitis B
HBV classification and morphology :
 Family -Hepadnaviridae.
 Genus- Orthohepadnavirus
 42 nm DNA virus with outer envelope and inner
core.
 Blumberg in 1965 discovered , named as Australia
antigen.
 Later it was found to be surface component of HBV.
Morphology ….
 Spherical particles 22 nm in diam.
 Filamentous or tubular 22 nm
with varying length
 Called as HBs Ag surface components which are
produced in excess.
 Third type double walled spherical structure 42 nm diameter
called as Dane particle
HBV structure
Hepatitis B virus
Epidemiology:
 Natural infection occurs only in humans.
 No animal reservoir.
 Virus is maintained in large pools of carrier.
 Usually occur as sporadics.
 Occasional outbreaks occur in hospitals, orphanages
and institutions for mentally handicapped.
 India falls in intermediate group: carrier rate 2-7%.
High in southern part of India .
Carrier :
- Person with detectable HBsAg in blood for more than
six months.
Super carrier:
- High titres of HBsAg+HBeAg+ DNA polymerase
+HBV in circulation.
- Elevated transaminases. Highly infectious.
Simple carrier:
- Low titres of HBsAg
- Negative for HBeAg, DNA polymerase ,HBV. Low
infectivity
Modes of
transmission
:
Parenteral
Perinatal
Sexual
Parenteral:
 Blood and blood products of carrier and patients.
 HBV is highly infectious than HIV.
 0.00001 ml can be infectious..!
 Objects like shared syringes, needles, sharp items,
endoscopes, razors, nail clippers ,combs,
accupunture, ritual circumcision.
 Direct contact with skin lesions like eczema,
pyoderma and scratches.
How the HBV is transmitted
Perinatal:
 Quite common from carrier mother to baby.
 If mother HBeAg positive – high risk (60-90%)
 If mother HBeAg negative- low risk (5-15%)
 Infection usually acquired during birth.
Sexual:
 more common in developed countries, particularly in
promiscuous homosexuals.
 Can also occur by artificial insemination.
 Saliva ,breast milk, semen, vaginal secretion ,urine,
bile and feces also contains virus.
High Moderate
Low/Not
Detectable
blood semen urine
serum vaginal fluid feces
wound exudates saliva sweat
tears
breastmilk
Concentration of Hepatitis B Virus
in Various Body Fluids
High risk occupational groups:
 Medical and paramedical personnel.
 Staff of blood bank
 Dialysis units
 Medical laboratories
 Mental health institutions
 Barbers and Sex workers
LAB DIAGNOSIS:
Serological demonstration of viral markers :
HBsAg :
 first marker to appear in the blood.
 Being detectable in blood even before onset of
clinical illness.
 Disappears in 2 months.
 Then anti-HBs appears.
 Presence of anti-HBsAg alone indicates vaccination
Symptoms
HBeAg anti-HBe
Total anti-HBc
IgM anti-HBc anti-HBsHBsAg
0 4 8 12 16 20 24 28 32 36 52 100
Acute Hepatitis B Virus Infection with Recovery
Typical Serologic Course
Weeks after Exposure
Titre
18
HBcAg:
 Not demonstrable in circulation.
 Antibody appears after 1-2 wk of appearance HBsAg.
 Earliest antibody marker to be seen in blood.
IgM anti- HBc: acute infection
IgG anti- HBc: remote infection
HBeAg:
 Appears concurrently with HBsAg.
 Indicator of active intrahepatic viral replication.
 Its presence denotes high infectivity.
Prophylaxis :
 Avoiding risky practices like promiscuous
sex, injectable drug abuse, direct or indirect
contact with blood, semen or other body fluids of patients
and carrier.
 Use of disposable syringes, needles.
 Screening of blood, semen and organ donors.
 Health education
 Immunization : Best method
 Passive Immunisation-
 HBIG (0.5 ml IM)
 Active Immunisation-
 HBsAg Vaccine (0.5 ml IM ; 0, 1 and 6 month)
 Post exposure prophylaxis-
 HBIG 300-500IU, within 48 hrs
 Full course of vaccination
Hepatitis C Virus
 HCV is small (50-60 nm) virus with single stranded
RNA.
 Enveloped virus- carrying
glycoprotein spikes
 Shows considerable genetic and
antigenic diversity.
 Has not been grown in culture, but cloned in E.coli.
How infection occurs
 Source of infection- carriers
 Mode-
Lab diagnosis
 Detection of viral antigen-
 IF of blood and biopsy specimen
 Detection of nucleic acid –HCV RNA by RT-
PCR
Immunoblotting
 Detection of specific antibodies
 ELISA
 Recombinant immunoblot techniques
RT PCR
 Prophylaxis-
 No vaccine available
 General measures-
- blood screening, safe blood and safe injection
practices.
Thank You…

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Hepatitis b & c

  • 1. Vishal L. Kulkarni Dept. of Microbiology Hepatitis B & C
  • 2. Hepatitis B  It is a liver disease caused by the hepatitis B virus (HBV).  It ranges in severity from a mild illness, lasting a few weeks (acute), to a serious long-term (chronic) illness that can lead to liver disease or liver cancer.
  • 3. Hepatitis B is Serious – Global Impact  It’s a common disease!  Over 350 million people in the world have chronic hepatitis B
  • 4. HBV classification and morphology :  Family -Hepadnaviridae.  Genus- Orthohepadnavirus  42 nm DNA virus with outer envelope and inner core.  Blumberg in 1965 discovered , named as Australia antigen.  Later it was found to be surface component of HBV.
  • 5. Morphology ….  Spherical particles 22 nm in diam.  Filamentous or tubular 22 nm with varying length  Called as HBs Ag surface components which are produced in excess.  Third type double walled spherical structure 42 nm diameter called as Dane particle
  • 8. Epidemiology:  Natural infection occurs only in humans.  No animal reservoir.  Virus is maintained in large pools of carrier.  Usually occur as sporadics.  Occasional outbreaks occur in hospitals, orphanages and institutions for mentally handicapped.  India falls in intermediate group: carrier rate 2-7%. High in southern part of India .
  • 9. Carrier : - Person with detectable HBsAg in blood for more than six months. Super carrier: - High titres of HBsAg+HBeAg+ DNA polymerase +HBV in circulation. - Elevated transaminases. Highly infectious. Simple carrier: - Low titres of HBsAg - Negative for HBeAg, DNA polymerase ,HBV. Low infectivity
  • 11. Parenteral:  Blood and blood products of carrier and patients.  HBV is highly infectious than HIV.  0.00001 ml can be infectious..!  Objects like shared syringes, needles, sharp items, endoscopes, razors, nail clippers ,combs, accupunture, ritual circumcision.  Direct contact with skin lesions like eczema, pyoderma and scratches.
  • 12. How the HBV is transmitted
  • 13. Perinatal:  Quite common from carrier mother to baby.  If mother HBeAg positive – high risk (60-90%)  If mother HBeAg negative- low risk (5-15%)  Infection usually acquired during birth.
  • 14. Sexual:  more common in developed countries, particularly in promiscuous homosexuals.  Can also occur by artificial insemination.  Saliva ,breast milk, semen, vaginal secretion ,urine, bile and feces also contains virus.
  • 15. High Moderate Low/Not Detectable blood semen urine serum vaginal fluid feces wound exudates saliva sweat tears breastmilk Concentration of Hepatitis B Virus in Various Body Fluids
  • 16. High risk occupational groups:  Medical and paramedical personnel.  Staff of blood bank  Dialysis units  Medical laboratories  Mental health institutions  Barbers and Sex workers
  • 17. LAB DIAGNOSIS: Serological demonstration of viral markers : HBsAg :  first marker to appear in the blood.  Being detectable in blood even before onset of clinical illness.  Disappears in 2 months.  Then anti-HBs appears.  Presence of anti-HBsAg alone indicates vaccination
  • 18. Symptoms HBeAg anti-HBe Total anti-HBc IgM anti-HBc anti-HBsHBsAg 0 4 8 12 16 20 24 28 32 36 52 100 Acute Hepatitis B Virus Infection with Recovery Typical Serologic Course Weeks after Exposure Titre 18
  • 19. HBcAg:  Not demonstrable in circulation.  Antibody appears after 1-2 wk of appearance HBsAg.  Earliest antibody marker to be seen in blood. IgM anti- HBc: acute infection IgG anti- HBc: remote infection HBeAg:  Appears concurrently with HBsAg.  Indicator of active intrahepatic viral replication.  Its presence denotes high infectivity.
  • 20. Prophylaxis :  Avoiding risky practices like promiscuous sex, injectable drug abuse, direct or indirect contact with blood, semen or other body fluids of patients and carrier.  Use of disposable syringes, needles.  Screening of blood, semen and organ donors.  Health education  Immunization : Best method
  • 21.  Passive Immunisation-  HBIG (0.5 ml IM)  Active Immunisation-  HBsAg Vaccine (0.5 ml IM ; 0, 1 and 6 month)  Post exposure prophylaxis-  HBIG 300-500IU, within 48 hrs  Full course of vaccination
  • 22. Hepatitis C Virus  HCV is small (50-60 nm) virus with single stranded RNA.  Enveloped virus- carrying glycoprotein spikes  Shows considerable genetic and antigenic diversity.  Has not been grown in culture, but cloned in E.coli.
  • 23. How infection occurs  Source of infection- carriers  Mode-
  • 24. Lab diagnosis  Detection of viral antigen-  IF of blood and biopsy specimen  Detection of nucleic acid –HCV RNA by RT- PCR
  • 25. Immunoblotting  Detection of specific antibodies  ELISA  Recombinant immunoblot techniques RT PCR
  • 26.  Prophylaxis-  No vaccine available  General measures- - blood screening, safe blood and safe injection practices.