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EPIDEMIOLOGY OF HEPATITIS B
AND C
Dr. Soumya Swaroop Sahoo
JR,Dept. of Community Medicine
PGIMS Rohtak
CONTENTS
 Introduction
 Global burden
 Problem statement in India
 Virus and transmission
 Clinical manifestations
 Treatment
 Prevention and control
 Vaccination
INTRODUTION
 Hepatitis B initially called as serum hepatitis is an acute
systemic illness with major pathology in liver.
 HBV infection is the 10th leading cause of death and
HBV related hepatocellular carcinoma(HCC ) is the 5th
most frequent cancer worldwide.
HEPATITIS- HISTORICAL PERSPECTIVE
A
“Serum”
Viral hepatitis
Enterically
transmitted
G
E
NANB
B D C Parenterally
transmitted
PROBLEM STATEMENT : WORLD
•2 billion people have been infected (1 out of 3 people).
•350 million people are chronically infected.
•10-30 million will become infected each year.
•An estimated 1 million people die each year from hepatitis B
and its complications.
•Approximately 2 people die each minute from hepatitis B.
Source-(WHO, hepb.org)
PREVALENCE OF CHRONIC HBV INFECTION, WORLDWIDE, 2006
 Source: CDC and Prevention. MMWR
2008;57(RR-8):1-20.
HBsAg Prevalence
>8% = High
2-7% = Intermediate
< 2% = Low
PROBLEM STATEMENT : INDIA
 India has over 40 million HBV carriers and accounts for
10–15% of the entire pool of HBV carriers of the world.
 Estimated 43-45 million new cases per year.
 100,000 death annually by disease related to HBV
infection.
 Of 25 million newborn annually, 1 million run lifetime
risk of HBV infection.
Source-1) API 2)World Health Organization (2012)
STUDIES IN HARYANA
 In Sirsa an outbreak of hepatitis B occured in
1997.
 54 cases of jaundice occurred in Dhottar village
(population 3096)
 8 (33·3%) of them died
 Virtually all fatal cases were adults and tested
positive for HBsAg.
 The results linked the outbreak to the use of
unnecessary therapeutic injections
Source-Journal of epidemiology and infection,2000(125) ,693-99
STUDIES IN HARYANA
 In a Study titled To Assess Trend In
Seroprevalence Of Hepatitis B Virus Infection
Among Blood Donors Of Southern Haryana,
 11,340 blood donors screened
 The overall seroprevalence of HBsAg was observed
to be 1.32%.
 According to the WHO classification, this southern
part of Haryana qualifies as a low prevalence area.
The Internet Journal of Pathology. 2012 Vol 13 (2)
ACUTE HEPATITIS B: CASE DEFINITION
 A clinical case of acute viral hepatitis is an
acute illness that includes
 discrete onset of symptoms and
 jaundice or elevated serum aminotransferase
levels (>2.5 times the upper limit of normal)
 A confirmed case of hepatitis B is a
suspected case that is laboratory confirmed:
 HBsAg positive or Anti-HBc-IgM positive and
 Anti-HAV-IgM negative.
AGENT
AGENT
• Hepatitis B virus belongs to hepadnavirdae family.
• Complex 42 nm. Double stranded
• Enveloped DNA virus (DNA polymerase with reverse
transcriptase activity)
• Known as “Dane” particle.
• Has affinity for liver and hepatocytes
AGENT FACTORS
Reservoir of infection
 Human beings are the only reservoir
 Infection spread by cases or carriers
 Carrier state defined as persistence of HBsAg > 6 months
Resistance of virus:
 Quite stable, can survive for days in environmental
conditions.
 Can be destroyed by sodium hypochlorite
 Also by autoclaving for 30 to 60 minutes
Period of communicability:
 From incubation period upto disappearance of HBsAg and
appearance of antibody.
HOST FACTORS
AGE:
 Acute Hepatitis B occurs in 1% perinatal, 10% early
childhood (1-5 yrs) and 30% in older children (>5 yrs age)
HBV infections.
 Outcome age dependent
 Development of chronic infection inversely related to age.
 Young children who become infected are most likely to
develop chronic infections:
 90% of infants infected during the first year of life develop
chronic infections;
 30–50% of children infected between one to four years of age
develop chronic infections.
HOST FACTORS
• 25% of adults who become chronically infected
during childhood die from hepatitis B-related liver
cancer or cirrhosis;
• 90% of healthy adults infected with HBV recover
and get completely rid of the virus within six
months.
• Globally, HBV causes 60 - 80% of the world’s
primary liver cancers.
• Motality from fulminant Hepatitis B -70%
HIGH RISK GROUPS
 Health care workers and laboratory personnel
 High risk sexual behaviour (homosexuals, prostitutes)
 Frequent blood transfusion recepient
 I.v. drug users
 Immunocompromised individuals
 Infants of HBV carrier mothers
 Recipients of solid organ transplants
ROUTES OF TRANSMISSION
1) Vertical transmission
2) Sexual
transmission
3) Parenteral transmission
Needle stick
injury
Househol
d contacts
VIRUS AND TRANSMISSION
 In developing countries, common routes of
transmission are:
 perinatal (from mother to baby at birth)
 early childhood infections (inapparent infection
through close interpersonal contact with infected
household contacts)
 unsafe injection practices
 unsafe blood transfusions
 unprotected sexual contact
 I.V. drug use
VIRUS AND TRANSMISSION
 In developed countries patterns of transmission are different from
those in developing countries.
 Majority of infections in developed countries are transmitted
during young adulthood by
 unsafe sexual practices
 I.V. drug use.
 The virus is not spread by contaminated food or water, and cannot
be spread casually in the workplace.
jaundice
fever
Abdominal pain
and
joint pain
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
IgM anti-HBc
Total anti-HBc
HBsAg
Acute
(6 months)
HBeAg
Chronic
(Years)
anti-HBe
0 4 8 12 16 20 24 28 32 36 52 Years
Weeks after Exposure
Titre
Progression to Chronic Hepatitis B Virus
Infection Typical Serologic Course
DIAGNOSIS
 HBsAg - used as a general marker of infection.
 HBsAb - used to document recovery and/or
immunity to HBV infection.
 anti-HBc IgM - marker of acute infection.
 anti-HBcIgG - past or chronic infection.
 HBeAg - indicates active replication of virus
 HBV-DNA - indicates active replication of virus,
more accurate than HBeAg. Used mainly for
monitoring response to therapy.
Acute hepatitis B infection
Asymptomati
c
Or
Subclinical
infection(33%
)
Clinical infection
-jaundice
-flu like
symptom(66%)
Fulminant
hepatitis
(0.5%)
Death
Chronic
Carrier
(5-10%)
Recovery
Immunity
(85-90%)
Minimal
liver
Disease
(70-90%)
Chronic
Hepatitis
(10-30%)
Primary
hepatocellul
ar carcinoma
cirrhosis
DEATH
Reactivation
HEPATITIS B AND HIV
 Around 10 percent of 40 million people infected with HIV are
coinfected with Hep B.
 HBV infection has minimal effect on progression of HIV.
 But HIV markedly increases the risk of developing cirrhosis and
hepatocellular CA.
 HIV treatment can be used safely and effectively if coinfected
with hepatitis B.
HEPATITIS B IN PREGNANCY
 Risk of transmission ranges from 10% in 1st trimester to about
90% in 3rd trimester.
 If a pregnant woman tests positive for hepatitis B, the newborn
must be given - the 1st dose of hepatitis B vaccine and one dose of
hepatitis B immune globulin (HBIG).
 Given within 12 hours of life, a newborn has 95% chance of
being protected against a lifelong hepatitis B infection.
 If not given in time - > 90% possibility that the baby will become
chronically infected.
 According to WHO, it is safe for an infected woman to breastfeed
her child since the benefits of breastfeeding outweigh the potential
risk of transmitting the virus through breast milk.
TREATMENT
 Acute : No medication available; best addressed
through supportive treatment
 Chronic hepatitis B:
• Antivirals: interferon-α-2a ,
interferon-α-2b,
Lamivudine,
Adefovir, Entecavir
 Immune-modulators: prednisone, interleukin, thymosin,
levamisole
 Liver cirrhosis and Hepatocellular CA: Liver
transplant
PREVENTION AND CONTROL
Goals of prevention:
 To decrease prevalence of chronic carrier and
chronic liver disease
 Prevention of acute hepatitis B infection
Strategies:
 Hepatitis B vaccination.
 Screening of blood, plasma and organ donor.
 Universal precautions.
HEPATITIS B VACCINATION
 Active immunization
 Passive immunization
ACTIVE IMMUNIZATION
 Two types of vaccine available
1. Plasma derived vaccine
2. Recombinant DNA vaccine
PLASMA DERIVED VACCINE:
 Based on HBsAg derived from plasma of human
carrier.
 Formalin inactivated
 Costlier
Recombinant DNA Vaccine
 Introduced in 1986 in USA.
 Has replaced plasma derived vaccine.
 Cost effective
 Available as monovalent or combined vaccine
Active substance:
-HBsAg derived from culture of yeast or mammalian cells
Adjuvant:
- Alum or thiomersal
Storage:
-2 to 8°C
- Freezing avoided
HEPATITIS B VACCINATION
Age :
 Ideal first dose at birth ( within 24 hours)
 Next 2 or 3 dose according to immunization schedule
No. of doses:
 3 or 4
 First at birth , second and third with DPT1 and DPT3.
 First at birth, second, third and fourth with DPT
 Adults 3 doses at 0, 1 month, 6 month
HEPATITIS B VACCINATION
 Neither pregnancy nor lactation is a contraindication for its use.
 Usually provides life long immunity
Adverse reactions:
 Infrequent and rare
 transient fever(1-5%) , local reaction(5%), soreness,
myalgia
 Very rarely anaphylactic reaction .
HEPATITIS B VACCINATION
PASSIVE IMMUNIZATION
 Hepatitis B immunoglobulin used for temporary post-exposure
prophylaxis.
 Combined active and passive vaccination is advised in following
cases:
- Newborn of HBsAg +ve mother
- Percutaneous exposure
- Sexual exposure
- After liver transplant in case of recurrent HBV infection
 Time :
within 6 hours of exposure and maximum upto 48 hours.
 Dose: 0.05 to 0.07 ml. / kg. body weight.
 Provides short term passive immunity for 3 months.
HEPATITIS B VACCINATION
HEPATITIS B VACCINATION
 As of July 2011, 179 countries have included hepatitis B as part of their
vaccination schedules – a major increase compared with 31 countries in
1992.
 Hep B3 coverage- 34% (WHO and UNICEF immunization coverage
2011)
 Catch up campaign for older age groups is important in intermediate and
low endemicity area.
 Catch up campaign for infants and young children is important in high
endemicity area.
Source - WHO
PREVENTION AND CONTROL
 For quality, safety and efficacy of blood
transfusion, the National Blood Policy, 2002
was formulated by the government.
 According to it each blood unit shall be
tested to be free from Hepatitis B surface
antigen and HCV antibody with the results
recorded on the label of the container.
SURVEILLANCE
 Hepatitis B and C are included in the IDSP
reporting format.
 Hepatitis B disease surveillance procedures should include
 Monitoring disease incidence
 Determination of sources of infection and modes of
transmission by epidemiological investigation
 Detection of outbreaks
 Spread containment
 Identification of contacts of cases for postexposure prophylaxis
HEPATITIS C
INTRODUCTION
 By the late 1970s it was apparent that HBV was not the only cause
of "serum" hepatitis, and that other "non-A-non-B" hepatitis
viruses existed.
 Houghton and colleagues cloned and expressed portions of a
RNA virus from the plasma of an infected chimpanzee in 1989.
 This virus, designated hepatitis C virus (HCV), is now known to
be a major cause of both transfusion-associated and sporadic non-
A-non-B hepatitis
INTRODUCTION
PROBLEM STATEMENT: WORLD
 According to WHO estimates
 3% of world population infected with HCV
 170 million are chronic carriers
 3–4 million new infections per year
 more than 350 000 people die every year from hepatitis C-related
liver diseases
 Highest – Egypt(15%)
 Most common cause of chronic liver disease
in the United States and the most common
indication for liver transplantation
PROBLEM STATEMENT:INDIA
 HCV prevalence-1.5%
 About 12 million chronic carriers
 HCV antibodies found in 2% of voluntary blood
donors.
 42% of patients with hepatocellular CA had markers
of HCV infection. Source-WHO, http://www.epidemic.org
HIGH RISK GROUPS
 Current or former i.v. drug users
 Recipients of clotting factor concentrates
 Recipients of blood transfusions or donated organs before July 1992
 Persons with known exposures to HCV (e.g., healthcare workers after
needlestick injuries)
 Infants born to infected mothers
 Long-term haemodialysis patients
ACUTE HEPATITIS C:
CASE DEFINITION
 Acute illness typically including acute jaundice, dark urine, anorexia,
malaise, extreme fatigue, and right upper quadrant tenderness.
 Biological signs include
 increased urine urobilinogen and
 >2.5 times the upper limit of serum alanine aminotransferase.
 Laboratory criteria for diagnosis:
 Hepatitis C: Positive for anti-HCV
 Confirmed Case: a suspected case that is laboratory confirmed.
AGENT
 HCV is a
 Small(55-65nm) enveloped,
 single-stranded, RNA virus
 Flaviviridae family
 Classified into 6 genotypes
 No resemblance to HBV or HDV.
CLINICAL COURSE
 Incubation period- mean 6-7 wks
 85% of individuals, the clinical course of the acute
infection is asymptomatic and easily missed
 Persistent infection and chronic hepatitis are the
hallmarks of HCV infection, despite the generally
asymptomatic nature of the acute illness.(75% to 85% of
cases)
 Immunity- no protective antibody response
ROUTES OF TRANSMISSION
1) Intravenous drug use:
sharing of needles and syringes
Reuse of contaminated needles2) Sexual transmission
3) Blood transfusion
4) Vertical transmission
5) Needlestick injury
fever
Nausea &
vomiting
fatigue
Muscle &
joint aches
Clay colored
Stools &
Dark urine
jaundice
SYMPTOMS OF ACUTE INFECTION
Symptoms
anti-HCV
ALT
Normal
0 1 2 3 4 5 6 1 2 3 4
Hepatitis C Virus Infection
Typical Serologic Course
Titre
Months Years
Time after
Exposure
DIAGNOSIS
 Diagnosis of acute infection is often missed because a
majority of infected people have no symptoms.
 Common methods of antibody detection cannot
differentiate between acute and chronic infection.
 The presence of antibodies against HCV indicates
infection.
 Recombinant immunoblot assay (RIBA) and hepatitis C
virus RNA testing are used to confirm the diagnosis.
 Chronic Hepatitis C- anti HCV> 6 months
NATURAL HISTORY OF HCV INFECTION
Exposure
(Acute Phase)
Chronic
Cirrhosis
HCC
Transplant
Death
Resolved
Stable
Slowly Progressive
85%(85)
80%(68) 20%(17)
25%(4)
75%(13)
15%(15)
HIV and
Alcohol
PROGRESSION OF HCV INFECTION
TREATMENT
 Acute :
 Antiviral (Ribavirin) and supportive treatment
 Chronic
 Regular monitoring for signs of liver disease progression;
 antiviral drugs – peginterferon
 Cirrhosis, liver cancer patients-
 liver transplant
PREVENTION
 Primary prevention
 There is no vaccine for hepatitis C.
 The risk of infection can be reduced by avoiding:
 unnecessary and unsafe injections;
 unsafe blood products;
 unsafe sharps waste collection and disposal;
 use of illicit drugs and sharing of injection equipment;
 unprotected sex with hepatitis C-infected people;
 sharing of sharp personal items that may be
contaminated with infected blood;
 tattoos, piercings and acupuncture performed with
contaminated equipment.
PREVENTION
 Secondary prevention:
 For people infected with the hepatitis C virus, WHO
recommends:
 education and counselling on options for care and
treatment;
 immunization with the hepatitis A and B vaccines to
prevent coinfection;
 early and appropriate medical management including
antiviral therapy ; and
 regular monitoring for early diagnosis of chronic liver
disease.
DIFFERENCE BETWEEN HEPATITIS B& C
Viral Hepatitis Type B Viral Hepatitis Type C
Incubation period 50-180 days (avg 60-90) 40-120 days
Principal age of
distribution
15-29 years Adults
Seasonal incidence Throughout the year Throughout the year
Route of infection Predominantly parenteral Predominantly parenteral
Occurrence of virus
Blood Months to years Months to years
Stool Absent Probably absent
Urine Absent Probably absent
Saliva ,semen Frequently present Unknown
Clinical &lab features
Onset Insidious Insidious
Fever >38oc (100.4 F) Less common Less common
Viral Hepatitis Type B Viral Hepatitis Type C
Duration of aminotransferase
elevation
1-6+ months 1-6+ months
Immunoglobulins (Ig M) Normal to slightly
elevated
Normal to slightly elevated
Complications Chronicity in 5-10%
cases
Chronicity in >50% cases
Mortality rate 1-2% 0.5-1%
HBs Ag Present Absent
Immunity
Homologous Yes ?
heterologous No No
Duration Probably lifetime ?
Immunoglobulins Prevents jaundice only if
immunoglobulin is of
sufficient potency against
HBV
 500 million people worldwide infected with either
Hepatitis C or Hepatitis B.
 Hepatitis B and C kill 1.5 million people a year.
 ONE in every 3 people in our planet exposed to either
or both virus.
 Most of the 500 million infected do not know.
 ONE in every 12 people worldwide are living with
either chronic Hepatitis B or Hepatitis C.
REFERENCES
 Park’s Textbook of preventive and social medicine, 21st edition
 World Health Organisation(WHO) www.who.org
 Hepatitis B foundation, www.hepb.org
 Robbins Textbook of Pathology, 8th edition
 Centre for Disease Control and Prevention(CDC)
www.cdc.gov_hepatitis_hbv_pdfs_hepbgeneralfactsheet
 Virology Journal, An overview of molecular epidemiology of hepatitis
B virus (HBV) in India
 Association of Physicians of India: Indian Guidelines and Protocols:
Hepatitis B
WORLD HEPATITS DAY- 2012

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EPIDEMIOLOGY OF HEPATITIS B AND C

  • 1. EPIDEMIOLOGY OF HEPATITIS B AND C Dr. Soumya Swaroop Sahoo JR,Dept. of Community Medicine PGIMS Rohtak
  • 2. CONTENTS  Introduction  Global burden  Problem statement in India  Virus and transmission  Clinical manifestations  Treatment  Prevention and control  Vaccination
  • 3. INTRODUTION  Hepatitis B initially called as serum hepatitis is an acute systemic illness with major pathology in liver.  HBV infection is the 10th leading cause of death and HBV related hepatocellular carcinoma(HCC ) is the 5th most frequent cancer worldwide.
  • 4. HEPATITIS- HISTORICAL PERSPECTIVE A “Serum” Viral hepatitis Enterically transmitted G E NANB B D C Parenterally transmitted
  • 5. PROBLEM STATEMENT : WORLD •2 billion people have been infected (1 out of 3 people). •350 million people are chronically infected. •10-30 million will become infected each year. •An estimated 1 million people die each year from hepatitis B and its complications. •Approximately 2 people die each minute from hepatitis B. Source-(WHO, hepb.org)
  • 6. PREVALENCE OF CHRONIC HBV INFECTION, WORLDWIDE, 2006  Source: CDC and Prevention. MMWR 2008;57(RR-8):1-20. HBsAg Prevalence >8% = High 2-7% = Intermediate < 2% = Low
  • 7. PROBLEM STATEMENT : INDIA  India has over 40 million HBV carriers and accounts for 10–15% of the entire pool of HBV carriers of the world.  Estimated 43-45 million new cases per year.  100,000 death annually by disease related to HBV infection.  Of 25 million newborn annually, 1 million run lifetime risk of HBV infection. Source-1) API 2)World Health Organization (2012)
  • 8. STUDIES IN HARYANA  In Sirsa an outbreak of hepatitis B occured in 1997.  54 cases of jaundice occurred in Dhottar village (population 3096)  8 (33·3%) of them died  Virtually all fatal cases were adults and tested positive for HBsAg.  The results linked the outbreak to the use of unnecessary therapeutic injections Source-Journal of epidemiology and infection,2000(125) ,693-99
  • 9. STUDIES IN HARYANA  In a Study titled To Assess Trend In Seroprevalence Of Hepatitis B Virus Infection Among Blood Donors Of Southern Haryana,  11,340 blood donors screened  The overall seroprevalence of HBsAg was observed to be 1.32%.  According to the WHO classification, this southern part of Haryana qualifies as a low prevalence area. The Internet Journal of Pathology. 2012 Vol 13 (2)
  • 10. ACUTE HEPATITIS B: CASE DEFINITION  A clinical case of acute viral hepatitis is an acute illness that includes  discrete onset of symptoms and  jaundice or elevated serum aminotransferase levels (>2.5 times the upper limit of normal)  A confirmed case of hepatitis B is a suspected case that is laboratory confirmed:  HBsAg positive or Anti-HBc-IgM positive and  Anti-HAV-IgM negative.
  • 11. AGENT AGENT • Hepatitis B virus belongs to hepadnavirdae family. • Complex 42 nm. Double stranded • Enveloped DNA virus (DNA polymerase with reverse transcriptase activity) • Known as “Dane” particle. • Has affinity for liver and hepatocytes
  • 12. AGENT FACTORS Reservoir of infection  Human beings are the only reservoir  Infection spread by cases or carriers  Carrier state defined as persistence of HBsAg > 6 months Resistance of virus:  Quite stable, can survive for days in environmental conditions.  Can be destroyed by sodium hypochlorite  Also by autoclaving for 30 to 60 minutes Period of communicability:  From incubation period upto disappearance of HBsAg and appearance of antibody.
  • 13. HOST FACTORS AGE:  Acute Hepatitis B occurs in 1% perinatal, 10% early childhood (1-5 yrs) and 30% in older children (>5 yrs age) HBV infections.  Outcome age dependent  Development of chronic infection inversely related to age.  Young children who become infected are most likely to develop chronic infections:  90% of infants infected during the first year of life develop chronic infections;  30–50% of children infected between one to four years of age develop chronic infections.
  • 14. HOST FACTORS • 25% of adults who become chronically infected during childhood die from hepatitis B-related liver cancer or cirrhosis; • 90% of healthy adults infected with HBV recover and get completely rid of the virus within six months. • Globally, HBV causes 60 - 80% of the world’s primary liver cancers. • Motality from fulminant Hepatitis B -70%
  • 15. HIGH RISK GROUPS  Health care workers and laboratory personnel  High risk sexual behaviour (homosexuals, prostitutes)  Frequent blood transfusion recepient  I.v. drug users  Immunocompromised individuals  Infants of HBV carrier mothers  Recipients of solid organ transplants
  • 16. ROUTES OF TRANSMISSION 1) Vertical transmission 2) Sexual transmission 3) Parenteral transmission Needle stick injury Househol d contacts
  • 17. VIRUS AND TRANSMISSION  In developing countries, common routes of transmission are:  perinatal (from mother to baby at birth)  early childhood infections (inapparent infection through close interpersonal contact with infected household contacts)  unsafe injection practices  unsafe blood transfusions  unprotected sexual contact  I.V. drug use
  • 18. VIRUS AND TRANSMISSION  In developed countries patterns of transmission are different from those in developing countries.  Majority of infections in developed countries are transmitted during young adulthood by  unsafe sexual practices  I.V. drug use.  The virus is not spread by contaminated food or water, and cannot be spread casually in the workplace.
  • 20. 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
  • 21. IgM anti-HBc Total anti-HBc HBsAg Acute (6 months) HBeAg Chronic (Years) anti-HBe 0 4 8 12 16 20 24 28 32 36 52 Years Weeks after Exposure Titre Progression to Chronic Hepatitis B Virus Infection Typical Serologic Course
  • 22. DIAGNOSIS  HBsAg - used as a general marker of infection.  HBsAb - used to document recovery and/or immunity to HBV infection.  anti-HBc IgM - marker of acute infection.  anti-HBcIgG - past or chronic infection.  HBeAg - indicates active replication of virus  HBV-DNA - indicates active replication of virus, more accurate than HBeAg. Used mainly for monitoring response to therapy.
  • 23. Acute hepatitis B infection Asymptomati c Or Subclinical infection(33% ) Clinical infection -jaundice -flu like symptom(66%) Fulminant hepatitis (0.5%) Death Chronic Carrier (5-10%) Recovery Immunity (85-90%) Minimal liver Disease (70-90%) Chronic Hepatitis (10-30%) Primary hepatocellul ar carcinoma cirrhosis DEATH Reactivation
  • 24. HEPATITIS B AND HIV  Around 10 percent of 40 million people infected with HIV are coinfected with Hep B.  HBV infection has minimal effect on progression of HIV.  But HIV markedly increases the risk of developing cirrhosis and hepatocellular CA.  HIV treatment can be used safely and effectively if coinfected with hepatitis B.
  • 25. HEPATITIS B IN PREGNANCY  Risk of transmission ranges from 10% in 1st trimester to about 90% in 3rd trimester.  If a pregnant woman tests positive for hepatitis B, the newborn must be given - the 1st dose of hepatitis B vaccine and one dose of hepatitis B immune globulin (HBIG).  Given within 12 hours of life, a newborn has 95% chance of being protected against a lifelong hepatitis B infection.  If not given in time - > 90% possibility that the baby will become chronically infected.  According to WHO, it is safe for an infected woman to breastfeed her child since the benefits of breastfeeding outweigh the potential risk of transmitting the virus through breast milk.
  • 26. TREATMENT  Acute : No medication available; best addressed through supportive treatment  Chronic hepatitis B: • Antivirals: interferon-α-2a , interferon-α-2b, Lamivudine, Adefovir, Entecavir  Immune-modulators: prednisone, interleukin, thymosin, levamisole  Liver cirrhosis and Hepatocellular CA: Liver transplant
  • 27. PREVENTION AND CONTROL Goals of prevention:  To decrease prevalence of chronic carrier and chronic liver disease  Prevention of acute hepatitis B infection Strategies:  Hepatitis B vaccination.  Screening of blood, plasma and organ donor.  Universal precautions.
  • 28. HEPATITIS B VACCINATION  Active immunization  Passive immunization ACTIVE IMMUNIZATION  Two types of vaccine available 1. Plasma derived vaccine 2. Recombinant DNA vaccine PLASMA DERIVED VACCINE:  Based on HBsAg derived from plasma of human carrier.  Formalin inactivated  Costlier
  • 29. Recombinant DNA Vaccine  Introduced in 1986 in USA.  Has replaced plasma derived vaccine.  Cost effective  Available as monovalent or combined vaccine Active substance: -HBsAg derived from culture of yeast or mammalian cells Adjuvant: - Alum or thiomersal Storage: -2 to 8°C - Freezing avoided HEPATITIS B VACCINATION
  • 30. Age :  Ideal first dose at birth ( within 24 hours)  Next 2 or 3 dose according to immunization schedule No. of doses:  3 or 4  First at birth , second and third with DPT1 and DPT3.  First at birth, second, third and fourth with DPT  Adults 3 doses at 0, 1 month, 6 month HEPATITIS B VACCINATION
  • 31.  Neither pregnancy nor lactation is a contraindication for its use.  Usually provides life long immunity Adverse reactions:  Infrequent and rare  transient fever(1-5%) , local reaction(5%), soreness, myalgia  Very rarely anaphylactic reaction . HEPATITIS B VACCINATION
  • 32. PASSIVE IMMUNIZATION  Hepatitis B immunoglobulin used for temporary post-exposure prophylaxis.  Combined active and passive vaccination is advised in following cases: - Newborn of HBsAg +ve mother - Percutaneous exposure - Sexual exposure - After liver transplant in case of recurrent HBV infection  Time : within 6 hours of exposure and maximum upto 48 hours.  Dose: 0.05 to 0.07 ml. / kg. body weight.  Provides short term passive immunity for 3 months. HEPATITIS B VACCINATION
  • 33. HEPATITIS B VACCINATION  As of July 2011, 179 countries have included hepatitis B as part of their vaccination schedules – a major increase compared with 31 countries in 1992.  Hep B3 coverage- 34% (WHO and UNICEF immunization coverage 2011)  Catch up campaign for older age groups is important in intermediate and low endemicity area.  Catch up campaign for infants and young children is important in high endemicity area. Source - WHO
  • 34.
  • 35. PREVENTION AND CONTROL  For quality, safety and efficacy of blood transfusion, the National Blood Policy, 2002 was formulated by the government.  According to it each blood unit shall be tested to be free from Hepatitis B surface antigen and HCV antibody with the results recorded on the label of the container.
  • 36. SURVEILLANCE  Hepatitis B and C are included in the IDSP reporting format.  Hepatitis B disease surveillance procedures should include  Monitoring disease incidence  Determination of sources of infection and modes of transmission by epidemiological investigation  Detection of outbreaks  Spread containment  Identification of contacts of cases for postexposure prophylaxis
  • 38. INTRODUCTION  By the late 1970s it was apparent that HBV was not the only cause of "serum" hepatitis, and that other "non-A-non-B" hepatitis viruses existed.  Houghton and colleagues cloned and expressed portions of a RNA virus from the plasma of an infected chimpanzee in 1989.  This virus, designated hepatitis C virus (HCV), is now known to be a major cause of both transfusion-associated and sporadic non- A-non-B hepatitis
  • 40. PROBLEM STATEMENT: WORLD  According to WHO estimates  3% of world population infected with HCV  170 million are chronic carriers  3–4 million new infections per year  more than 350 000 people die every year from hepatitis C-related liver diseases  Highest – Egypt(15%)  Most common cause of chronic liver disease in the United States and the most common indication for liver transplantation
  • 41.
  • 42. PROBLEM STATEMENT:INDIA  HCV prevalence-1.5%  About 12 million chronic carriers  HCV antibodies found in 2% of voluntary blood donors.  42% of patients with hepatocellular CA had markers of HCV infection. Source-WHO, http://www.epidemic.org
  • 43. HIGH RISK GROUPS  Current or former i.v. drug users  Recipients of clotting factor concentrates  Recipients of blood transfusions or donated organs before July 1992  Persons with known exposures to HCV (e.g., healthcare workers after needlestick injuries)  Infants born to infected mothers  Long-term haemodialysis patients
  • 44. ACUTE HEPATITIS C: CASE DEFINITION  Acute illness typically including acute jaundice, dark urine, anorexia, malaise, extreme fatigue, and right upper quadrant tenderness.  Biological signs include  increased urine urobilinogen and  >2.5 times the upper limit of serum alanine aminotransferase.  Laboratory criteria for diagnosis:  Hepatitis C: Positive for anti-HCV  Confirmed Case: a suspected case that is laboratory confirmed.
  • 45. AGENT  HCV is a  Small(55-65nm) enveloped,  single-stranded, RNA virus  Flaviviridae family  Classified into 6 genotypes  No resemblance to HBV or HDV.
  • 46. CLINICAL COURSE  Incubation period- mean 6-7 wks  85% of individuals, the clinical course of the acute infection is asymptomatic and easily missed  Persistent infection and chronic hepatitis are the hallmarks of HCV infection, despite the generally asymptomatic nature of the acute illness.(75% to 85% of cases)  Immunity- no protective antibody response
  • 47. ROUTES OF TRANSMISSION 1) Intravenous drug use: sharing of needles and syringes Reuse of contaminated needles2) Sexual transmission 3) Blood transfusion 4) Vertical transmission 5) Needlestick injury
  • 48. fever Nausea & vomiting fatigue Muscle & joint aches Clay colored Stools & Dark urine jaundice SYMPTOMS OF ACUTE INFECTION
  • 49. Symptoms anti-HCV ALT Normal 0 1 2 3 4 5 6 1 2 3 4 Hepatitis C Virus Infection Typical Serologic Course Titre Months Years Time after Exposure
  • 50. DIAGNOSIS  Diagnosis of acute infection is often missed because a majority of infected people have no symptoms.  Common methods of antibody detection cannot differentiate between acute and chronic infection.  The presence of antibodies against HCV indicates infection.  Recombinant immunoblot assay (RIBA) and hepatitis C virus RNA testing are used to confirm the diagnosis.  Chronic Hepatitis C- anti HCV> 6 months
  • 51. NATURAL HISTORY OF HCV INFECTION Exposure (Acute Phase) Chronic Cirrhosis HCC Transplant Death Resolved Stable Slowly Progressive 85%(85) 80%(68) 20%(17) 25%(4) 75%(13) 15%(15) HIV and Alcohol
  • 52. PROGRESSION OF HCV INFECTION
  • 53. TREATMENT  Acute :  Antiviral (Ribavirin) and supportive treatment  Chronic  Regular monitoring for signs of liver disease progression;  antiviral drugs – peginterferon  Cirrhosis, liver cancer patients-  liver transplant
  • 54. PREVENTION  Primary prevention  There is no vaccine for hepatitis C.  The risk of infection can be reduced by avoiding:  unnecessary and unsafe injections;  unsafe blood products;  unsafe sharps waste collection and disposal;  use of illicit drugs and sharing of injection equipment;  unprotected sex with hepatitis C-infected people;  sharing of sharp personal items that may be contaminated with infected blood;  tattoos, piercings and acupuncture performed with contaminated equipment.
  • 55. PREVENTION  Secondary prevention:  For people infected with the hepatitis C virus, WHO recommends:  education and counselling on options for care and treatment;  immunization with the hepatitis A and B vaccines to prevent coinfection;  early and appropriate medical management including antiviral therapy ; and  regular monitoring for early diagnosis of chronic liver disease.
  • 56. DIFFERENCE BETWEEN HEPATITIS B& C Viral Hepatitis Type B Viral Hepatitis Type C Incubation period 50-180 days (avg 60-90) 40-120 days Principal age of distribution 15-29 years Adults Seasonal incidence Throughout the year Throughout the year Route of infection Predominantly parenteral Predominantly parenteral Occurrence of virus Blood Months to years Months to years Stool Absent Probably absent Urine Absent Probably absent Saliva ,semen Frequently present Unknown Clinical &lab features Onset Insidious Insidious Fever >38oc (100.4 F) Less common Less common
  • 57. Viral Hepatitis Type B Viral Hepatitis Type C Duration of aminotransferase elevation 1-6+ months 1-6+ months Immunoglobulins (Ig M) Normal to slightly elevated Normal to slightly elevated Complications Chronicity in 5-10% cases Chronicity in >50% cases Mortality rate 1-2% 0.5-1% HBs Ag Present Absent Immunity Homologous Yes ? heterologous No No Duration Probably lifetime ? Immunoglobulins Prevents jaundice only if immunoglobulin is of sufficient potency against HBV
  • 58.  500 million people worldwide infected with either Hepatitis C or Hepatitis B.  Hepatitis B and C kill 1.5 million people a year.  ONE in every 3 people in our planet exposed to either or both virus.  Most of the 500 million infected do not know.  ONE in every 12 people worldwide are living with either chronic Hepatitis B or Hepatitis C.
  • 59. REFERENCES  Park’s Textbook of preventive and social medicine, 21st edition  World Health Organisation(WHO) www.who.org  Hepatitis B foundation, www.hepb.org  Robbins Textbook of Pathology, 8th edition  Centre for Disease Control and Prevention(CDC) www.cdc.gov_hepatitis_hbv_pdfs_hepbgeneralfactsheet  Virology Journal, An overview of molecular epidemiology of hepatitis B virus (HBV) in India  Association of Physicians of India: Indian Guidelines and Protocols: Hepatitis B

Notas del editor

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