1 / 43

Understanding Viral Hepatitis: Types, Epidemiology, and Prevention

Learn about the different types of viral hepatitis (A, B, C, D, E), their epidemiology, clinical features, and prevention strategies including vaccination and treatment options.

rcarruth
Download Presentation

Understanding Viral Hepatitis: Types, Epidemiology, and Prevention

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Epidemiology of Viral Hepatitis

  2. Introduction Viral hepatitis can be defined as an infection of liver caused by any of half dozen viruses i.e. Hepatitis A,B,C,D,E,G and Cytomegalovirus, Rubella virus, Yellow fever virus etc.

  3. Types of Viral Hepatitis A B C D E Source of feces blood/ blood/ blood/ feces infection blood-derived blood-derived blood-derived body fluids body fluids body fluids Parental, sexual, perinatal Mode of tra nsmission fecal-oral Parenteral Parental fecal-oral 15-45 days 6-7 wks Incubation Period 45-180 days 2-9 wks 2 wks before to 1 wk onset of Jaundice Period of communicability several month to years

  4. Hepatitis A Introduction It was formerly called as Epidemic Jaundice or Infectious Hepatitis Magnitude of problem • Epidemic in most developing countries • Globally,10-50 persons per 1,00,000 persons are affected annually • Very common in all SAARC countries • Responsible for 10-25% of total Hepatitis in > 10 years Children • 85-90% children of age > 10 years have been infected and immune to Hepatitis A • In Kathmandu, it occurred sporadically in past 30 years

  5. Source: International Travel and health,2009

  6. Geographic Distribution of HAV Infection

  7. Epidemiology Agent Factors Causative Agent:- Hepatitis A virus(RNA Enterovirus of Picornavirus family) Resistance:- Resistant to heat and not affected by chlorination in normal doses. Destroyed by formalin, UV rays, boiling for 5 minutes & autoclaving. Reservoir:- Human being

  8. Host factors- Age:-All, but more in children Sex:-Both Immunity:-Lifelong immunity after one attack, Only 5% have second attack Environmental factors • Throughout the year mainly during rainfall • Poor sanitation & hygiene • Overcrowding

  9. Mode of transmission • Faeco-oral, Parenteral, • Sexual contact, • Mother to child Clinical features 3Stages of clinical features Prodromal stage: • Fevers with perspiration, • nausea, Loose stool, Anorexia, Fatigue, Myalgia, • Restlessness, Discomfort in right hypochondriac region

  10. Contd… Icteric stage:- • Yellow sclera and nail, Pale stool, urine or body, • Loss of weight ,weakness • Fever, Bradicardia • Pain in right hypochondriac region, Hepatomegaly Recovery stage:- • In 2-4 weeks, signs and symptoms gradually disappear • Recovery

  11. Laboratory investigation • Urine routine:- Bile salt, bile pigment, protein urobilinogen • Serum test:- Increased SGPT • CBC:- CBC increase or sometimes decreases Complication:- • Cirrhosis of liver, • Aplastic anemia, • Acute hepatic failure, • Post hepatic syndrome

  12. Prevention Vaccination (pre-exposure) • Hepatitis A vaccine :-2 doses 6-8 months apart or • Combined vaccine:- with hepatitis B vaccine on 0,1,6 months schedule Human Immunoglobulin:- Within 1 -2 weeks of exposure Control of reservoir:- • Notification, • Complete bed rest

  13. Control of transmission • Good hygiene and sanitation • 1mg/L free residual chlorine destroys virus 30min at 8.5 PH Treatment: • Hepatitis A usually resolves on its own over several weeks. • Isolation, complete bed rest, high calorie diet • Complete avoidance of Alcohol, Smoking and Hepatotoxic drugs e.g. Rifampicin, Isoniazide • Low oily and spicious diet • Liv52/Livomin etc.

  14. Hepatitis B ( Formerly known as Serum Hepatitis) Magnitude of problem:- Globally • Endemic in tropical and developing countries • 30%(>2 billion) people are seropositive • 350 million have chronic infection • An estimated 6,20,000 death annually • Cause of 60-80% liver cancer

  15. SEAR • More than 1/3rd of total population have been infected & 80 million(6%) lifelong carrier • Approximately14-16 million people are infected & Approx. 2 lakh death annually • In Bhutan, India, Maldives carrier rate is; 5-7%; In Bangladesh, DPR Korea, Manmar, Thailand, it is 9-12% Nepal • Low endemicity with carrier rate 0.9-1% • Prevalence of chronic infection in 2%

  16. Source: International Travel and Health,2009

  17. HBsAg Prevalence ³8% - High 2-7% - Intermediate <2% - Low Geographic Distribution of Chronic Hepatitis-B Infection

  18. Epidemiology Agent factor Causative Agent:- Hepatitis B virus(DNA Hepadnavirus) • 3 antigens- Surface antigen-HBsAg(first to appear),) E antigen-HBeAg(marker of replication) and Core-antigen(HBcAg) • Corresponding antibodies are- Anti-HBs, Anti-HBc, Anti-HBe • Antibodies- first anti c, then e antibody & last anti s • Seroconversion for e good prognosis • Anti HBs indicate recovery Resistance:- Stable, destroyed by sod. Hypochlorite, Autoclaving

  19. Source of infection:- Blood, body secretions e.g. saliva, semen, vaginal secretions Period of communicability: Several months to years Host factors:- Age:- commonly 20-40 years Sex:- Both High risk groups:- • Surgeons, laboratory workers, physicians • Sex workers, clients of sex workers • Injection drug users • Hemodialysis patients, recipient of blood transfusion

  20. Infants to HBV carrier mothers • International travelers, children of immigrants from disease-endemic areas • In carriers there is no seroconversion for HBe for years Persistent carriers- Defined as if HBsAg for more than 9 months Incubation period:Average 60-90 days Range 45-180 days

  21. Symptoms HBeAg anti-HBe Total anti-HBc Titer IgM anti-HBc anti-HBs HBsAg 0 4 8 12 16 24 28 32 52 100 20 36 Weeks after Exposure Acute Hepatitis B Virus Infection with Recovery Typical Serologic Course

  22. Acute (6 months) Chronic (Years) HBeAg Anti-HBe HBsAg Total anti-HBc Titer IgM anti-HBc 0 4 8 16 20 24 28 36 12 32 52 Weeks after Exposure Progression to Chronic Hepatitis B Virus Infection Typical Serologic Course

  23. Modes of Transmission • Sexual • Parenteral • Perinatal-40 % • Child to child i.e. horizontal • Others Clinical features • Yellowing of skin, and eyes(Jaundice) • Nausea, vomiting, fatigue • Abdominal pain • May cause chronic disease which may lead to cirrhosis of liver or liver cancer

  24. Concentration of HBV in Various Body Fluids Some features of Hepatitis B • Clinical illness <5 yrs, <10%(jaundice): >5 yrs, 30%-50% • Acute case-fatality rate: 0.5%-1% • Chronic infection: <5 yrs, 30%-90% >5 yrs, 2%-10% • Premature mortality fromchronic liver disease:15%-25%

  25. Outcome of HBV Infection

  26. Fulminent Exposure Acute Hepatitis B Infection 66% 0-5% 33% Clinical Infection Jaundice, Flu-like Sub-clinical Infection -Asymptomatic 5-10% 85.90% 70-90% Chronic carrier 10.30% Minimal Liver Disease Recovery Immunity Chronic Hepatitis Reactivation Primary Liver Cancer Cirrhosis Death

  27. Prevention 1.Vaccination For infants:-DPT-Hep-B-Hib vaccine 0.5 ml IM at 6,10 &14 weeks For children below 10 years:-Plasma derived Vaccine- formalin inactivated subunit viral vaccine 0.5ml IM Schedule:- 0,1,6 months, booster at 5 years/ For adults:- • Hepatitis vaccine 1ml IM 3 doses(2nd dose after 1 months of 1st dose & 3rd dose after 6 months of 2nd dose) • RDNA yeast derived vaccine

  28. 2.Immunoglobulin • Those acutely exposed eg. Health personnel, newborn, sexual contact, • Ideally within 6 hrs not more than 24 hrs • 0.05 to 0.07ml/kg body weight; 2doses 30 days apart 3. Simultaneous Immunoglobulin and vaccination 4. Other measures:- • Screening in blood donors • Adequate sterilization • Surveillance

  29. Treatment • For chronic hepatitis B: Drug treatment with Alpha-interferon, Peginterferon, Lamivudine, Adefovir or Dipivoxil. • Acute hepatitis B usually resolves on its own. Very severe cases can be treated with Lamivudine • Complete avoidance of Alcohol, Smoking and Hepatotoxic drugs e.g. Rifampicin, Isoniazide • Low oily and spicious diet • Liv52/Livomin etc.

  30. Hepatitis C Introduction It was identified in 1989 and previously all other Hepatitis than A & B Magnitude of problem Globally • Estimated 3% global population is infected with Hepatitis C • Around 3,00,000 new infections and 8,000- 10,000 deaths annually • 170 millions are chronic carriers and at risk of developing liver cancer and cirrhosis

  31. Epidemiology Agent factor Causative Agent :- Hepatitis C virus(Single stranded RNA virus, Hepasivirus of flavivirus family) Mode of Transmission:- • Blood or blood product transfusion • Infected needles • less commonly through sexual contact and childbirth. Incubation period: Average 6 - 7 wks, Range 2 - 26 wks Diagnosis:-Immunoassay

  32. Clinical Features • Acute illness (jaundice) Mild (≤20%) • Case fatality rate Low • Chronic infection 60%-85% • Chronic hepatitis 70% • Cirrhosis 5%-20% • Mortality from CLD 3% People at Risk • Injection drug users, • Sexual contact with an infected person, • people who have multiple sex partners, • Health care workers, • Infants born to infected women, • Hemodialysis patients, recipient of blood transfusion or blood products

  33. Prevention • No vaccine available for hepatitis C • Screening of blood donors • Reduction of risk of exposure to the virus. • Health Education Treatment • Chronic hepatitis C: Drug treatment with Peginterferon alone or combination treatment with Peginterferon and the drug Ribavirin. • Acute hepatitis C: Treatment is recommended if it does not resolve within 2 to 3 months.

  34. Hepatitis D Introduction:- It is new form of Hepatitis and it occurs always in association with Hepatitis B virus and can't occur alone due to absence of its surface antigen Epidemiology Causative Agent:- Hepatitis D virus Modes of Transmission:-Blood Contact Diagnosis:-Detection of delta antigen in acute case

  35. People at Risk:-Anyone infected with Hepatitis B Prevention • Immunization against hepatitis B for those not already infected; • Avoiding exposure to infected blood, contaminated needles, infected person's personal items (toothbrush, razor, nail clippers). Treatment:- Chronic hepatitis D: drug treatment with Alpha interferon

  36. Hepatitis E Introduction It was discovered in 1990 and formerly termed as Enterically transmitted hepatitis non-A, non-B Magnitude of problem • After Yamuna flood, 30,000 jaundice cases in Delhi were supposed to be due to Hepatitis E in 1995-96 • China reported 1,00,000 cases in 1986-88 • Out breaks have been reported from Borno, India,Indonesia,Mexico, Nepal, Pakistan Epidemiology Causative Agent:- Hepatitis E virus(Calicivirus) Modes of Transmission:- Through food or water contaminated with feces

  37. People at Risk:- • Mainly young adults 15-40 years • International travelers • Can produce fulminating form particularly in pregnant women • Mortality in fulminant form- up to 80% • Risk of abortions, Perinatal mortality and morbidity Prevention • No vaccine available for hepatitis E • Only way of prevention is reduction of risk of exposure Treatment:- Usually resolves on own over several weeks to months

  38. Hepatitis G Introduction It has been Recently discovered in 1996 and its Prevalence is still unknown Causative Agent:- Hepatitis G virus(flavivirus)

  39. Data as of BPKIHS from Jan.2009-Nov 2010 Source: BPKIHS, Recording Section

  40. References • Park. K,Textbook of Preventive and social Medicine.20th edition, BanarasidasBhanot Publishers, Jabalpur-India • K.C. Saroj, Applied Epidemiology in Nepalese Context; A.K. Books & Educational Enterprises, Nepal 2007 • Annual Report;Department of Health Services, 1995/96- 2008/9 • The contributions of hepatitis B virus and hepatitis C virus infections to cirrhosis and primary liver cancer worldwide,Journal of Hepatology 45 (2006) 529–538 • GIDEON, • Recording Section,BPKIHS; Dharan • International Travel and Health, 2009 • http://www.who.int • http:// www.searo.who.int

  41. Feedback and Suggestion are welcome

  42. Thank you

More Related