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Viral hepatitis

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viral hepatitis

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Viral hepatitis

  1. 1. VIRAL HEPATITiS ANGEL DAS Y.L ROLL NO: 17
  2. 2. What is viral hepatitis?  Infection of liver caused by hepatotropic viruses (hepatitis viruses A, B, C, D, and E)  other viruses that can also cause liver inflammation include Cytomegalovirus, Epstein–Barr virus, or Yellow fever.
  3. 3. 5 Main varieties of viruses Hep A –> feco-orally Hep B-> parenterally Hep C-> mainly transfusion Hep D-> associated as super infection with HBV Hep E-> feco-orally
  4. 4. ETIOLOGIC CLASSIFICATION Viral Hepatitis Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E Hepatitis G
  5. 5. Benign, self limiting disease Responsible for 20-25% of clinical acute hepatitis Incubation period 2-6 weeks Affected age group 5-14 years Transmission feco-oral route Shed in stool 2-3 weeks before & 1 week after the onset of jaundice
  6. 6. Hepatitis A virus  Small,icosahedral non-enveloped virus  ss RNA virus Serological Diagnosis Anti HAV antibody IgM-onset of acute hepatitis IgG- after acute illness & provide life-long immunity
  7. 7. Caused by HBV Incubation period 4-26 weeks(1-4months) Transmission:  exposure to infectious blood or body fluids.  Possible forms of transmission include: sexual contact blood transfusion reuse of contaminated syringe vertical transmission
  8. 8. Hep B produces Acute Hepatitis Chronic Hepatitis Fulminant Hepatitis Asymptomatic carrier stage Role in development of hepatocellular Carcinoma
  9. 9. MORPHOLOGY - HBV  Partially ds DNA virus a) HBV occurs in 3 morphology form in serum: o Small particles – 2 forms 22nm diameter exist as tubules spheres o Large particles – 42 nm diameter also called as “Dane particles” double shelled spherical particles
  10. 10. HBV evokes  Humoral immunity  Cell mediated immunity  Hepatocyte damage – attack of virus infected cells by CD8+ cytotoxic T cells HBsAg anti -HBsAg HBcAg anti -HBcAg HBeAg anti -HBeAg Serological Diagnosis
  11. 11. HBsAg before the onset of symptoms appears after 6 week of infection declines in 3-6 months >6 months carrier state Anti HBs Ab appears late – 3 months after the onset HBeAg soon after HBsAg, present transiently 3-6 weeks indicator of continued viral replication , infectivity >10 weeks - development of CLD & carrier state Anti HBe ab prognostic sign for resolution of infection HBc Ag cannot be detected in blood demonstrated in nuclei of hepatocyte in chronic hepatitis & carrier state Anti –HBc ab 1st ab appears in serum, before the onset of symptoms
  12. 12.  Major cause of chronic liver disease(80%)  Key features-Persistence of infection & chronic hepatitis  Late consequence – cirrhosis & hepatocellular carcinoma Mode of transmission: 1. Parental: inoculations and blood transfusion 2. Vertical transmission 3. Close personal contact – sexual contact Type of virus:  -HCV is a small-enveloped virus  -ssRNA  Incubation period : 2 – 26 weeks(mean : 6-12 weeks)
  13. 13. Serological Diagnosis HCV RNA – few days after exposure Anti HCV ab – within weeks to few months S. Aminotransferase- 2- 12 weeks
  14. 14. 19 HBsAg RNA  antigenDefective virus,cause infection only in presence of HBV Small, ssRNA particle Double shelled outer shell- HBsAg inner shell-  Ag
  15. 15.  Enterically transmitted virus  By contamination of water supplies  Usually affects young or middle aged individuals  High mortality in pregnant women otherwise self limited disease  Not associated with chronic liver disease

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