Epidemiology of Viral Hepatitis

Dr Shyam Ashtekar

SMBT Medical College Dhamangaon

Nashik Maharashtra

Ashtekar.shyam@gmail.com

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.

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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

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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

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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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