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Hepatitis viruses

Hepatitis viruses. Gehan J. Panagoda. A systemic diseases where inflammation of the liver takes place There are microbial and non-microbial agents involve in the inflammation Viruses are the most important agents as part of a generalized infection of yellow fever CMV EBV.

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Hepatitis viruses

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  1. Hepatitis viruses Gehan J. Panagoda

  2. A systemic diseases where inflammation of the liver takes place • There are microbial and non-microbial agents involve in the inflammation • Viruses are the most important agents • as part of a generalized infection of yellow fever CMV EBV

  3. Classification • 7 types • A, B, C, D, E, F, G • Mostly caused by A, B and C • Except B others contain RNA, B contains DNA • A has a short IP (15-40 Days) • B IP is 40-200 days

  4. A known as infectious hepatitis • B serum hepatitis • C in transfusion • D causes only in the presence of B and transmitted parenterally • E involves in epidemics in Asia and Africa, transmitted by faeco-oral route

  5. Enterovirus 72 No envelope Single stranded RNA

  6. Resistance • Stable to treatment with 20% ether, PH 2.4 • Destroyed by boiling for 5 min/autoclaving/ dry heat/UV/formalin

  7. Viral in blood (2.5-4.3 weeks) Virus in faces (2-6.3 weeks) Transmission (3-8 weeks) Jaundice (4-7 weeks)

  8. Lab diagnosis • Only one type of antigens (HAV) • Isolation - it is not possible to isolate routenley from the faces • Immunofluorescence - HAV of faces during excretion of stools • HAV antibody - Ig M - a recent infection (up to 2-6 months) • IgG appears during convalescence stage

  9. Prevention 1. Improved sanitation 2. Passive prophylaxix with human IgG before or within 1-2 weeks of exposure 3. Disinfection of water with sodium hypochlorite 4. Single attack give life long immunity no effective vaccine

  10. Hepatitis B • Hepadna viruses - Hep B - Pekin duck - Ground squirrel • Transmission - artificial inoculation blood and its products - sexual activity • Onset is slow but severe and protracted than Hep A

  11. Extrahepatic manifestations - Immune complexes - HBV antigens and IgM serum sickness polyartertis nodosa glomerulonephritis • There will be one of the three forms • Acute • Chronic • Asymptomatic

  12. Exposure Infection • Deaths 1% Recovery Persistent infection (HbsAg> 6months) Fulminant hep 90-95% Asymptomatic Chronic Clearance Chronic active Immune Hepatitis Cirrhosis Hepatocellular carcinoma • Persist in 5-10% adults/30% children/90% new born/Immunocompromised are more prone to infection

  13. Enveloped Icosahedral

  14. Antigenic structure • HBsAg -envelope proteins • HBcAg - in the nucleocapsid • HBeAg - Hidden in the core it is soluble disappears in few weeks

  15. Subtypes HBsAg - is complex with four antigenic types - adw - in Europe - adr - ayw - in west Asia - ayr

  16. Not protective Protective

  17. Hep B carriers Super carriers - with HBeAg, are highly infectious/ 0.0001ml of plasma can infect Simple carriers - Do not have HBeAg but low titre of HBsAg antigens/

  18. Hepatitis B monitoring panels When a patient is tested for acute hep B (+ve HBsAg/anti-HBcIgM) To monitor the patient progress Check the following four markers HBsAg HBeAg anti-HBe anti-HBs WHY ?

  19. Why do you want to check for these markers 1. To find out whether patient is developing chronic hep (persistence HBsAg) 2. Find out relative infectivity (HBeAg) 3. To monitor sero-conversion (HBeAg to anti-HBe- resolution of the disease) 4. To monitor sero-conversion to anti-HBs (resolution of the disease and immunity)

  20. If a person is highly infectious • advice the person about the transmission • clinical course and out come of the disease • about donation of blood • patient should attend the clinic monthly to monitor the progress of the diseases

  21. Testing to determine the immunity -anti-HBs 1. This is the only marker to determine the immunity 2. Normal lever enzymes and -ve HBsAg also indicate the recovery

  22. Prevention /Prophylaxix • 1. Worldwide screening blood and blood products • Destruction of disposable needles/ adequate sterilization - surgical and dental instruments • Effective use of universal precautions • education - inadequate/unsterilized equipment • H-BIG

  23. Pre-vaccination testing 1. Anti-HBc (IgG and IgM) - current or previous infection 2. Anti-HBc and ant-HBs - indicate prior natural infection

  24. Prevention against hepatitis B • 1. HBsAg vaccine - with 22 nm particles - inactivated with formalin/urea/heat 2. Hep B vaccine - recombinant DNA in yeast or continuous mammalian cell lines (HBsAg gene has been incorporated to yeast genome)

  25. Immunity to Hep B is dependent on a highly individual response to the vaccine The following personnel should be checked following vaccine series 1. Health care workers 2. Babies born to HBV infected mothers 3. Sex partners 4. Immunocompromised individuals

  26. Non-A Non-B • The rest of the viruses other than A and B • C/D/E/F/G

  27. 90% of transfusion hepatitis is caused by Hep C • 30-60 nm • Among IV drug abusers • Heterosexual transmossion

  28. Route of transmission Percutaneous Contaminated needle stick Haemodialysis Human bite (In Sri Lanka may be in the ?) Transplant or transfusion Acupunture/tattooing etc Permucosal Sexual Perinatal - infants born to HCV mothers

  29. Individuals at risk Injecting drug users Persons occupationally exposed to blood Haemodialysis patients Transplant and transfusion patients

  30. Therapy No post exposure prophylaxis is available Control measure should be taken

  31. Individuals at risk 1. Who are with HBV 2. Any one at risk for HBV 3. Injecting drug users 4. Homosexual men 5. Who are having multiple sex partners

  32. Prevention No vaccine Control HBV Therapy Follow HBV therapy

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