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Epidemiology of Viral Hepatitis2017
This document provides an overview of viral hepatitis, focusing on hepatitis A, B, C, D, and E. It discusses the taxonomy, transmission routes, clinical features, diagnosis, treatment, and prevention of each type of viral hepatitis. For hepatitis A, it summarizes the agent, host factors, environmental factors, clinical picture, laboratory diagnosis, treatment/management, and prevention including vaccines. For hepatitis B, it discusses global epidemiology, the structure and life cycle of HBV, transmission routes, the antigen-antibody response, interpretation of immunology tests, chronic infection treatment options, and vaccination schedules and programs. It also briefly summarizes hepatitis C, noting its milder clinical course but potential for chronic infection and liver
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Epidemiology of Viral Hepatitis2017
- 1. Epidemiology of Viral Hepatitis DrShyam Ashtekar SMBT Medical College Dhamangaon Nashik Maharashtra [email protected] 2nd march 2017 2/2017
- 2. Taxonomy Viral Hepatitis Feco-Oral transmitted Hep A HepE Parentally transmitted Hep B Hep C Hep D Other viruses causing Hep 2/2017
- 3. Type of Hepatitis AB C D E Source of virus Feces Blood Blood derived Body fluids Blood Blood derived Body fluids Blood Blood derived Body fluids Fece Route of ransmission 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 Ensur Safe Drinkin Wate 2/2017
- 4. Hepatitis A (HAV) Othernames: Acute Infectious Hepatitis, Epidemic jaundice, Botkin’s disease, MS1 Hepatitis, HBs-ve hepatitis. 2/2017
- 5. Feco-oral Transmission, food/water,fingers Childhood infection, 90% infected by 10Y Endemic or epidemic under insanitaray conditions High proportion of mild & subclinical cases, esp in childhood. Severe in adults Heals completely, after-complications rare, with lifelong immunity 2/2017
- 6. Agent Picarnovirus, non- enveloped, foursubtypes, but only one is imp Only 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. 2/2017
- 7. 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 2/2017
- 8. Environment Low sanitation countrieshave 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%) 2/2017
- 9. Clinical picture Malaise anorexia, nausea and vomiting, fever,headach bodyache Hepatic pain/tenderness jaundice hepatomegaly Complete recovery in >98% Rare-liver failure 2/2017
- 10. 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
- 11. 1 Fecal HAV Symptoms 0 1 23 4 5 6 1 2 2 4 Hepatitis A Infection IgG anti-HAV Titre ALT IgM anti-HAV Months after exposure Typical Serological Course
- 12. 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 2/2017 1
- 13. Prevention Personal vaccination for high riskindividuals- Personal measures such hand wash, avoid unclean foods/raw foods Sanitation and water safety (>1 ppm chlorine),boiling water in epidemics, 2/2017 1
- 14. Vaccines for HAV-for high risk individuals nactivated 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 a a single dose, freeze dried • Reconstituted with DW • 0.5ml, deltoid area, subcutaneou • No booster • Used for both pre/post exposure prophylaxis (within 15 days). But role of Post-exposure uncertain. 2/2017 1
- 15. Hepatitis B Other names:Australia antigen hepatitis, serum hepatitis, Hippy hepatitis, serum aundice, MS2 hepatitis, Tattoo jaundice e tc 2/2017 1
- 16. HBV-Global scene Worldwide ,especially pical/subtropics. 66% of d 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 infecte infants becom carriers. (5-10% of infect adults become ch 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 2/2017 1
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- 18. Natural History ofHepatitis B/HBV HBV Exposure (Is highly nfective) 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 Deat No infection (rare) 2/2017 1
- 19. India-HepB 30% infected, (Anti- HBsAgpositive) 2-7% of population is in carrier stage. Will remain a problem because of poor sanitation conditions 2/2017 1
- 20. Agent Double shelled DANEparticle 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 2/2017 2
- 21. Modes of transmissionof HBV Parenteral - IV drug abusers, health workers are at increased risk. Sexual - sex workers and homosexuals are particularly at risk. Perinatal (Vertical) – mother (HBeAg+) →infant. 2
- 22. The antigen- antibody story ofHBV 2/2017 2
- 23. 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 IgM and then as IgG • Anti-HBc will continue till infection is active, then decline 2/2017 2
- 24. 2 Viral Load • HBV-DNA- indicates active replication o virus, more accurate than HBeA especially in cases of escape mutant Used mainly for monitoring response t therapy.
- 25.
- 26. No Cure! Butcontrol of chronic viral nfection 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 vira 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. 2/2017 2
- 27. Prevention Universal precautions byhealth workers HBV vaccine-3 doses (IAP)OR 4 doses (UIP) after birth Awareness regarding risk behavior-needle stick injuries, STI, IDU, universal precautions 2/2017 2
- 28. Hep B vaccinationschedule-IAP & UIP ge Vaccine Hepatitis B vaccine** Scheme A Scheme B irth BCG, OPV 0 HB1 weeks DPT 1, OPV 1 HB 2 B 1 0 weeks DPT 2, OPV 2 (UIP gives HB3) HB 2 4 weeks DPT 3, OPV 3 HB 3 (UIP gives HB4) HB 3 months Measles Yellow fever* * 2/2017 2
- 29. Results of astudy 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. 2/2017 2
- 30. Two important issues Haveu taken all doses of HBV vaccine? Take universal precautions? • AVOID direct handling of body fluids, wounds, mucos etc—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 2/2017 3
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- 32. 3 OUTCOMES of HCVhepatitis
- 33. HCV in nutshell Lesscommon 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 2/2017 3