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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.
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
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
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