Epidemiology of Viral Hepatitis
Dr Shyam Ashtekar
SMBT Medical College Dhamangaon
Nashik Maharashtra
2nd march 2017
3/2/2017
Taxonomy
Viral Hepatitis
Feco-Oral transmitted
Hep A Hep E
Parentally transmitted
Hep B Hep C Hep D
Other viruses causing Hep
3/2/2017
Type of Hepatitis
A B C D E
Source of
virus
Feces Blood
Blood derived
Body fluids
Blood
Blood derived
Body fluids
Blood
Blood derived
Body fluids
Feces
Route of
Transmission
Feco-
oral
Percutaneous
Permucosal
Percutaneous
Permucosal
Percutaneous
Permucosal
Feco
oral
Chronic -
Infection
No Yes Yes Yes No
Prevention Pre /Post
Exposure
Immuniz
ation
Pre /Post
Exposure
Immunization
Blood donor
Screening
Blood donor
screening
Pre /Post
Exposure
Immunization
Ensure
Safe
Drinking
Water3/2/2017
Hepatitis A (HAV)Other names: Acute Infectious Hepatitis, Epidemic jaundice, Botkin’sdisease, MS1 Hepatitis, HBs-ve hepatitis.
3/2/2017
Feco-oral Transmission, food/water, fingers
Childhood infection, 90% infected by 10Y
Endemic or epidemic under insanitarayconditions
High proportion of mild & subclinical cases, espin childhood. Severe in adults
Heals completely, after-complications rare, with lifelong immunity
3/2/2017
Agent
Picarnovirus, non-
enveloped, four subtypes,
but only one is impOnly man is host,
thrives in hepatic cells
Infectivity : 2wk before
jaundice appears and one
week later. Feces is infective
Resistant to inactivation by
heat at 600 C for one hour,
ether & low pH
Not affected by anionic
detergents.
Survives prolonged storage
at 40 C or below.
Feces most infective, less so
semen, blood, breast milk,
sweat etc
Inactivated by
boiling for 1 minute,
1: 4,000 formaldehyde at
370 C for 72 hours
Susceptible to UV and 5
min of autoclaving, &
chlorine 1 ppm for 30
minutes.3/2/2017
Host
In India 90% infection happens among children-both sexes equal- by 10Yrs. But only about 8% infected children become icteric (jaundice)
10% infections happen to Adults,
30% of them become icteric.
The disease > severe in adults.
Lifelong immunity, with 5% chance of second attack
3/2/2017
Environment
Low sanitation countries have high endemicity,
but milder young age disease (>90% children infection) low mortality
Moderate endemicity
Perfect sanitation entails Low endemicity communities have sporadic but severe forms of adult
disease (mortality 0.3% to 2%)
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Clinicalpicture
Malaise
anorexia, nausea and vomiting,
fever, headachebodyache
Hepatic pain/tenderness
jaundice
hepatomegaly
Complete recovery in >98%
Rare-liver failure
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LAB.DIAGNOSIS
1. Urine-bile salts/pigments
2. Demonstration of Virus in feces:
By: Immunoelectron microscopy
2. Virus Isolation:
3. Detection of Antibody :By ELISA
4. Biochemical tests:
i) Alanine AminoTransferase (ALT)-liver specific enzyme
ii) Bilirubin
1
1
FecalHAV
Symptoms
0 1 2 3 4 5 6 12
24
Hepatitis A Infection
IgG anti-HAV
Titre ALT
IgM anti-HAV
Months after exposure
Typical Serological Course
Treatment/case management
• No treatment, antipyretics, fluids
• Absolute rest, simple diet
• Spread already happened. But use of 0.5% hypochlorite solution for disinfection of feces is effective.
• With jaundice, infectivity declines
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Prevention
Personal vaccination for high
risk individuals-
Personal measures such hand wash, avoid
unclean foods/raw foods
Sanitation and water safety (>1 ppm chlorine),boiling water in epidemics,
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Vaccines for HAV- for high risk individuals
Inactivated vaccine (NOT for infants)
Killed /inactivated vaccines
(1ml for adults, 0.5ml for children
IM injection on deltoid
2 doses 4-6 weeks apart
Booster dose after 6-12 months
Protective efficiency is 94%
15-25 years immunity
Live vaccine (BioVac)
• LIVE attenuated vaccine comes asa single dose, freeze dried
• Reconstituted with DW
• 0.5ml, deltoid area, subcutaneous
• No booster
• Used for both pre/post exposure prophylaxis (within 15 days). But role of Post-exposure uncertain.
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Hepatitis BOther names: Australia antigen hepatitis, serum hepatitis, Hippy hepatitis, serum jaundice, MS2 hepatitis, Tattoo jaundice e tc
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HBV-Global scene
Worldwide , especially tropical/subtropics. 66% of
world pop lives in HBV endemic regions
>2 billion are infected sometime.
>350 million chronic carriers
1 million deaths from liver
cirrhosis annually
Causes 60% of all liver cancers
>90% of infectedinfants become
carriers.
(5-10% of infecteadults become chro
carriers)
TYPING of COUNTRIES by prevalence
Low endemic (<2%)
High endemic (>8%)
Intermediate 2-8%
Country Categories by Carrier rate
Type1: <1% carrier rate-Nepal, Srilanka
Type2: 5-7% India, Indonesia
Type3: >9% : Korea, Bangladesh Bhutan etc
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1
HBV : Structure
Natural History of Hepatitis B/HBV
HBV Exposure
(Is highly infective)
30% clinical
cases, 70% subclinical
cases
90% recover, & immunity
10% become chronic carriers
30% minimum
liver disease
70% Chronic hepatitis
Primary
Liver
cancer OR
Cirrhosis
Death
No infection (rare)
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India-HepB
30% infected, (Anti-HBsAg positive)
2-7% of population is in carrier stage.
Will remain a problem because of poor sanitation conditions
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Agent
Double shelled DANE particle
Three forms are circulating-Small antigenic particles (HBsAg), Tubules, DANE particles
Only DANE particle is infectious, CONTAMINATED blood/body fluids main source , infective a month before jaundice
Man is the only host--only reservoir (cases and carriers)
The virus can stay in environment for 7 days..but susceptible to sodium hypochlorite/autoclaving for 30 min
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Modes of transmission of HBV
�Parenteral - IV drug abusers,health workers are atincreased risk.
�Sexual - sex workers andhomosexuals are particularlyat risk.
�Perinatal (Vertical) – mother(HBeAg+) →infant.
2
The antigen-antibody story of HBV
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Immunology of HBV
HBsAg (surface)
• Appears early and usually declines within 6 months
• Produces Anti-HBsAg-continues lifelong
• HBs-Ag will continue in chronic case
HBeAg (Envelope)
• Appears within 3-4 days of HBsAg
• The anti-HBe will appear within 2nd
month. It indicates viral replication
HBcAg (core)
• HBcAg will can not be detected in blood
• But anti-HBcAg will appear in second month, first as IgMand then as IgG
• Anti-HBc will continue till infection is active, then decline
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2
Viral Load• HBV-DNA - indicates active replication o
virus, more accurate than HBeAespecially in cases of escape mutantsUsed mainly for monitoring response ttherapy.
Interpretation of HBV immunology
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No Cure! But control of chronic viral infection
Drugs
Pegylated interferon (may cure in 35% cases,
Has side effects
May lead to mutants
ORAL DRUGS
Lamuvidine-may lead to mutants
Tenofovir-95% success rate
Entacavir-95% success rate
Goal of treatment
• Control of viral load is most important
• With successful treatment, the viral load (DNA PCR) is untectable
• Small possibility of mutants with tenofovir/entacavir
• The liver cirrhosis may take years to develop..death may be due to other causes.
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Prevention
Universal precautions by health workers
HBV vaccine-3 doses (IAP)OR
4 doses (UIP) after birth
Awareness regarding risk behavior-needle stick injuries, STI, IDU, universal precautions
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Hep B vaccination schedule-IAP & UIP
Age Vaccine Hepatitis B vaccine**
Scheme A Scheme B
Birth BCG, OPV 0 HB1
6 weeks DPT 1, OPV 1 HB 2 B 1
10 weeks DPT 2, OPV 2 (UIP gives HB3) HB 2
14 weeks DPT 3, OPV 3 HB 3 (UIP gives HB4) HB 3
9 monthsMeasles Yellow
fever* *
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Results of a study on HBV vaccine in UIP India (2013)
Coverage with three doses of Hep B vaccine was lower than similarly timed three doses of DPT vaccine.
Poor stock management ("stock outs or nil stocks" at various levels),
Incomplete recording and reporting, perceived high cost & related fear of wastage of vaccine in 10 dose vial,
Incomplete knowledge amongst health functionaries about vaccination schedule were the main reasons cited for reported lower coverage.
Hep B vaccine birth dose was introduced in only 3 of 5 states evaluated.
Lack of knowledge amongst Health Workers about birth dose administration, no mechanism for recording birth dose, and insufficient trainings, official communications, and coordination at various levels.
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Two important issues
Have u taken all doses of HBV vaccine? Take universal precautions?
• AVOID direct handling of body fluids, wounds, mucosaetc—potential exposure
• Wear protective Masks,
• Wear gowns if necessary
• Eye protection-glasses
• Good Hand-wash (before &) after procedure
• Always Gloves, if necessary double gloves.
• Avoid needle stick injuries, avoid recappping the needle.
• Never walk barefeet in OT, labour room, wards, lab. Always use proper footware in these situations.
• AND follow Bio-waste management
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Hepatitis C
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3
OUTCOMES of HCV hepatitis
HCV in nutshell
Less common infection, mild clinically
Ten times less infective than HBV
But 80% cases become carriers
May lead to Liver cirrhosis/hepatic cancer
No active or passive immunization possible
Diagnosis with viral particles (DNA PCR)
Drugs-Interferon, ribavirin
Now addition of Telaprevir/Boceprevir
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