Viral hepatitis a+e

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  • Viral hepatitis a+e

    1. 1. VIRAL HEPATITIS Dr Kamran Afzal Classified Microbiologist
    2. 2. HEPATITIS <ul><li>Hepatitis is defined as a widespread damage to the liver hepatocytes with inflammatory changes </li></ul><ul><li>In acute hepatitis liver damage is centrilobular or widespread and may either result in limited or massive necrosis of the liver parenchyma resulting in liver failure </li></ul><ul><li>A: Infective B: Non-infective </li></ul><ul><li>Direct cytotoxicity probably more important </li></ul><ul><li>In chronic hepatitis there is long standing inflammation and replacement of liver parenchyma by fibrous tissue with loss of function ultimately leading to cirrhosis </li></ul><ul><li>A: Infective B: Non-infective </li></ul><ul><li>Immune response probably more important </li></ul>
    3. 3. A “ Infectious” “ Serum” Viral hepatitis Enterically transmitted Parenterally transmitted F, G, TTV ? other E NANB B D C Viral Hepatitis - Historical Perspectives
    4. 4. <ul><li>Classification of Hepatitis Viruses </li></ul>*linear, single strand; ** circular, double strand; *** circular, single strand Virus HAV HBV HCV HDV HEV DNA or RNA RNA* DNA** RNA* RNA*** RNA* Family Picornaviridae Hepadnaviridae Flaviviridae Deltavirus (genus) ? Envelope no yes yes yes no (Previously classified as a calicivirus)
    5. 7. Basic Features of Hepatitis Viruses Virus A B C D E Incubation Period* 4 (2-6) 8-12 (6-24) 6-9 (2-24) ? (2-10) 4-5 (2-9) Transmission fecal-oral parenteral parenteral parenteral fecal-oral * Weeks Chronic Infection No Yes Yes Yes No
    6. 8. CAUSES OF ACUTE HEPATITIS <ul><li>Viral </li></ul><ul><ul><li>Hepatitis A virus </li></ul></ul><ul><ul><li>Hepatitis B virus </li></ul></ul><ul><ul><li>Hepatitis C virus </li></ul></ul><ul><ul><li>Hepatitis D virus </li></ul></ul><ul><ul><li>Hepatitis E virus </li></ul></ul><ul><ul><li>Hepatitis G virus </li></ul></ul><ul><ul><li>Cytomegalo (CMV) </li></ul></ul><ul><ul><li>Epstein-Barr (EBV) </li></ul></ul><ul><ul><li>Herpes simplex (HSV) </li></ul></ul><ul><ul><li>Yellow Fever viruses (YFV) </li></ul></ul>
    7. 9. <ul><li>Non-Viral infections </li></ul><ul><ul><li>Bacterial: Typhoid fever, Q fever, RMSF, Leptospirosis, sepsis </li></ul></ul><ul><ul><li>Parasitic: Amoebic, Toxocariasis, Liver flukes </li></ul></ul><ul><li>Drugs </li></ul><ul><ul><li>Acetaminophen, INH, rifampin, oral contraceptives, anti-seizure drugs, carbenicillin, sulfonamides </li></ul></ul><ul><li>Poisons </li></ul><ul><ul><li>Alcohol, Mushrooms, Carbon tetrachloride </li></ul></ul><ul><li>Metabolic </li></ul><ul><ul><li>Wilson’s disease, fatty change in pregnancy </li></ul></ul><ul><li>Autoimmune diseases </li></ul><ul><ul><li>Autoimmune hepatitis, SLE </li></ul></ul>
    8. 10. CAUSES OF CHRONIC HEPATITIS <ul><li>Viral: B,C,D,G? </li></ul><ul><li>Toxins: Alcohol, Drugs </li></ul><ul><li>Biliary obstruction </li></ul><ul><ul><li>Primary biliary cirrhosis </li></ul></ul><ul><ul><li>Secondary biliary cirrhosis: stricture, stone, neoplasms </li></ul></ul><ul><ul><li>Primary sclerosing cholangitis </li></ul></ul><ul><li>Metabolic diseases </li></ul><ul><ul><li>Heamochromatosis: Primary and secondary </li></ul></ul><ul><ul><li>Wilson’s disease </li></ul></ul><ul><ul><li>Alpha-1 antitrypsin deficiency </li></ul></ul><ul><li>Hepatic congestion </li></ul><ul><ul><li>Initially congestion then inflammatory swelling and then cirrhosis </li></ul></ul><ul><ul><li>Budd chiari syndrome, CCF, Venous congestion </li></ul></ul><ul><li>Unknown: Autoimmune, cryptogenic </li></ul>
    9. 11. <ul><li>LABORATORY FINDINGS IN AVH </li></ul><ul><li>Laboratory indicators of liver pathology </li></ul><ul><ul><li>Elevated ALT (SGPT) and AST (SGOT) </li></ul></ul><ul><ul><li>Elevated bilirubin </li></ul></ul><ul><ul><li>Elevated alkaline phosphatase </li></ul></ul><ul><li>Laboratory indicators of infection </li></ul><ul><ul><li>Increased WBC </li></ul></ul><ul><ul><li>Detection of IgM antibodies in acute infection </li></ul></ul><ul><ul><li>Four fold rise in the antibody titer </li></ul></ul><ul><li>Isolation of the virus in cell culture </li></ul><ul><li>Total immune globulin (Total Ig) </li></ul><ul><ul><li>Combination of IgM and IgG </li></ul></ul><ul><ul><li>Early infection - primarily IgM </li></ul></ul><ul><ul><li>Late infection - primarily IgG </li></ul></ul>
    10. 12. HEPATITIS A
    11. 13. NATURE OF HAV <ul><li>Enterovirus included in the family Picornaviridae </li></ul><ul><li>HAV is a 27 – 30 nm spherical particle with cubic symmetry </li></ul><ul><li>Contain linear ss-RNA genome </li></ul><ul><li>Non-enveloped RNA virus </li></ul><ul><li>Replicates in the cytoplasm of the cells </li></ul><ul><li>Only one serotype </li></ul>
    12. 14. HAV CHARACTERS <ul><li>HAV are stable to treatment with 20% ether, acid and heat at 60 0 C for 1 hour </li></ul><ul><li>The virus are destroyed by </li></ul><ul><ul><li>Autoclaving at 121 0 C for 20 minutes </li></ul></ul><ul><ul><li>Boiling in water for 5 minutes </li></ul></ul><ul><ul><li>Treatment with chlorine 1 ppm for 30 minutes </li></ul></ul><ul><ul><li>Heating food > 85 0 C for 1 minute </li></ul></ul>
    13. 15. EPIDEMIOLOGY <ul><li>A major communicable disease in the developing world </li></ul><ul><li>Community hygiene is important in schools, hostels and jails, as overcrowding and poor sanitation favour the spread </li></ul><ul><li>Well cooked food and sanitary water supply will protect </li></ul><ul><li>Many cases occur in community-wide outbreaks </li></ul><ul><ul><li>highest attack rates in 5-14 year olds </li></ul></ul><ul><ul><li>children serve as reservoir of infection </li></ul></ul><ul><li>Persons at increased risk of infection </li></ul><ul><ul><li>travelers </li></ul></ul><ul><ul><li>homosexual men </li></ul></ul><ul><ul><li>injecting drug users </li></ul></ul>
    14. 17. TRANSMISSION <ul><li>Transmitted by fecal-oral route </li></ul><ul><li>Ingestion of food or water contaminated, even in microscopic amounts </li></ul><ul><li>Virus appears in the feces about 2 weeks before the appearance of symptoms </li></ul><ul><li>Virus present in blood and feces 10-12 days after infection </li></ul><ul><li>Level of viremia is low, chronic infection does not occur hence rarely transmitted through blood </li></ul>
    15. 18. <ul><li>Close personal contact </li></ul><ul><ul><li>Household contact, child day care centers </li></ul></ul><ul><li>Contaminated food or water with fecal matter </li></ul><ul><ul><li>Infected food handlers, raw shellfish </li></ul></ul><ul><li>Blood exposure (rare) </li></ul><ul><ul><li>Injecting drug use, transfusion </li></ul></ul><ul><li>Not transmitted by Transplacental route </li></ul>
    16. 20. PATHOGENESIS <ul><li>Entry from mouth </li></ul><ul><li>The virus replicates in the gastrointestinal tract and spreads to the liver via blood, viral replication in the liver </li></ul><ul><li>Hepatocytes are infected but no cytopathic effect on hepatocytes has been observed </li></ul><ul><li>Cytotoxic T cells produced during the immunological reaction cause the damage which is repaired, infection clears and no chronicity develops </li></ul><ul><li>In acute phase of the disease IgM antibodies appear- diagnostic, followed by the appearance of IgG antibodies – make the person immune to further infection </li></ul>
    17. 21. PATHOLOGY <ul><li>Microscopically there is spotty parenchymal cell degeneration, with necrosis of Hepatocytes and disruption of liver cell cords </li></ul><ul><li>The parenchymal changes are accompanied by Reticuloendothelial (KUPFFER) cell hyperplasia, peri-portal infiltration by monoculear cells and cell degeneration </li></ul><ul><li>Localised areas of necrosis are frequently observed </li></ul><ul><li>Later, accumulation of macrophages near degenerating Hepatocytes </li></ul>
    18. 22. CLINICAL FINDINGS <ul><li>Incubation period is 2-4 weeks -> short incubation hepatitis </li></ul><ul><li>Fever, anorexia, nausea, vomiting, jaundice, liver tenderness </li></ul><ul><li>Dark urine, pale feces </li></ul><ul><li>Most HAV infections are asymptomatic, detected only by the presence of antibodies </li></ul><ul><li>No chronic carrier state, no chronic hepatitis, no predisposition to hepatocellular carcinoma </li></ul><ul><li>Recovery in 4-6 weeks </li></ul><ul><li>Complications </li></ul><ul><ul><li>Fulminant hepatitis, Cholestatic hepatitis, Relapsing hepatitis </li></ul></ul><ul><li>Mortality 0.1 – 1 % </li></ul>
    19. 23. LABORATORY DIAGNOSIS <ul><li>Acute infection is diagnosed by the detection of HAV-IgM in serum </li></ul><ul><ul><li>EIA </li></ul></ul><ul><li>Past Infection - immunity is determined by the detection of HAV-IgG </li></ul><ul><ul><li>EIA </li></ul></ul><ul><li>Cell culture </li></ul><ul><ul><li>Difficult and takes up to 4 weeks, not routinely performed </li></ul></ul><ul><li>Direct Detection </li></ul><ul><ul><li>EM, PCR of HAV in faeces </li></ul></ul><ul><ul><li>Can detect illness earlier than serology but rarely performed </li></ul></ul>
    20. 24. Fecal HAV Symptoms 0 1 2 3 4 5 6 12 24 Hepatitis A Infection Total anti-HAV Titer ALT IgM anti-HAV Months after exposure Typical Serological Course IgG anti-HAV
    21. 25. TREATMENT <ul><li>No antiviral therapy is available </li></ul><ul><li>Bed rest </li></ul><ul><li>During the period of anorexia, the patient should receive frequent small IV fluids with glucose </li></ul><ul><li>Advise patient to avoid substances that may affect liver function </li></ul><ul><ul><li>Medication such as acetaminophen, herbs, illicit drugs and toxins </li></ul></ul><ul><li>Be very careful about personal hygiene to avoid fecal-oral transmission to other members of the household </li></ul>
    22. 26. PREVENTION <ul><li>Active immunization with vaccine containing inactivated HAV </li></ul><ul><li>Passive immunization with immune serum globulin if given prior to infection or within 14 days after exposure to infection can prevent the disease </li></ul>
    23. 27. VACCINATION <ul><li>Hepatitis A vaccination is recommended for all children starting at age 1 year, travellers to certain countries, and others at risk </li></ul><ul><li>A safe and effective formalin inactivated vaccine containing HAV grown in human diploid cell culture is available </li></ul><ul><li>A full course containing two intramuscular injections of the vaccine </li></ul><ul><ul><li>1 dose </li></ul></ul><ul><ul><li>booster dose 6-18 months after first dose </li></ul></ul><ul><li>Protection starts after 4 weeks after injection and lasts for 10 – 20 years </li></ul>
    24. 28. Vaccine Recommendations <ul><li>International travelers </li></ul><ul><li>Homosexual men </li></ul><ul><li>IDUs </li></ul><ul><li>Persons with occupational risk </li></ul><ul><li>People with impaired immune systems or CLD </li></ul><ul><li>People with blood-clotting disorders who receive clotting factors </li></ul><ul><li>Healthcare workers </li></ul><ul><li>Child care centers not routinely recommended </li></ul><ul><li>Sewer workers or plumbers </li></ul><ul><li>Food handlers: may be considered based on local circumstances </li></ul>
    25. 29. HEPATITIS E
    26. 30. HEPATITIS E VIRUS <ul><li>Calicivirus-like viruses </li></ul><ul><li>Non-enveloped RNA virus, 32-37nm in diameter </li></ul><ul><li>Single stranded RNA genome </li></ul><ul><li>Very labile and sensitive </li></ul><ul><li>Can only be cultured recently </li></ul>
    27. 31. <ul><li>Most outbreaks and epidemics associated with fecally contaminated drinking water </li></ul><ul><li>Several other large epidemics have occurred in the Indian subcontinent, the USSR, China, Africa and Mexico </li></ul><ul><li>In the United States and other nonendemic areas, where outbreaks of hepatitis E have not been documented to occur, a low prevalence of anti-HEV (<2%) has been found in healthy populations </li></ul><ul><li>Minimal person-to-person transmission </li></ul>EPIDEMIOLOGY
    28. 33. TRANSMISSION <ul><li>HEV is found in the stool of persons with hepatitis E </li></ul><ul><li>HEV is spread by eating or drinking contaminated food or water </li></ul><ul><li>Transmission from person to person occurs less commonly than with hepatitis A virus </li></ul><ul><li>Most outbreaks in developing countries have been associated with contaminated drinking water </li></ul><ul><li>Pregnant women are more prone to develop HEV infection </li></ul>
    29. 35. <ul><li>Incubation period Average 40 days </li></ul><ul><li>(Range 15-60 days) </li></ul><ul><li>Case-fatality rate Overall 1-3% Pregnant women 15-25%, a high incidence of fetal wastage or perinatal morbidity and mortality </li></ul><ul><li>Illness severity Increased with age </li></ul><ul><li>Chronic sequelae None identified </li></ul><ul><li>Jaundice, fatigue, abdominal pain, loss of appetite, nausea, vomiting, dark (tea colored) urine </li></ul>CLINICAL FEATURES
    30. 36. Symptoms ALT IgG anti-HEV IgM anti-HEV Virus in stool 0 1 2 3 4 5 6 7 8 9 10 11 12 13 Hepatitis E Virus Infection Typical Serologic Course Titer Weeks after Exposure
    31. 38. LABORATORY DIAGNOSIS <ul><li>Acute infection is diagnosed by the detection of HEV-IgM in serum </li></ul><ul><ul><li>EIA </li></ul></ul><ul><ul><li>Four fold rise in antibodiy titer </li></ul></ul><ul><li>Past Infection - immunity is determined by the detection of HEV-IgG </li></ul><ul><ul><li>EIA </li></ul></ul><ul><li>Cell culture </li></ul><ul><ul><li>Difficult and takes up to 4 weeks, not routinely performed </li></ul></ul><ul><li>Direct Detection </li></ul><ul><ul><li>EM, PCR of HEV in faeces </li></ul></ul>
    32. 39. <ul><li>No vaccine available for the HEV </li></ul><ul><li>Unknown efficacy of IG prepared from donors in endemic areas </li></ul><ul><li>Being a waterborne disease with feco-oral transmission, the steps and measures as discussed under HAV prevention are also useful for HEV prevention </li></ul>PREVENTION AND CONTROL MEASURES
    33. 40. HEALTH EDUCATION MESSAGES <ul><li>Always wash your hands with soap and water after using the bathroom, changing a diaper, and before preparing and eating food </li></ul><ul><li>Avoid drinking water (and beverages with ice) of unknown purity, uncooked shellfish, and uncooked fruits or vegetables that are not peeled or prepared properly </li></ul><ul><li>Transmission from person to person occurs less commonly in Hepatitis E than with Hepatitis A virus </li></ul><ul><li>As Hepatitis E is more severe among pregnant women, especially in third trimester, therefore special precautions, health education and hygienic measures are required in this group </li></ul>
    34. 41. <ul><li>All of the following can cause primary viral diarrhea EXCEPT: </li></ul><ul><li>A. Rotavirus </li></ul><ul><li>B. Norwalk virus </li></ul><ul><li>C. Adenovirus </li></ul><ul><li>D. Epstein-Barr virus </li></ul><ul><li>E. Hepatitis A virus </li></ul>
    35. 42. <ul><li>All of the following can cause primary viral diarrhea EXCEPT: </li></ul><ul><li>A. Rotavirus </li></ul><ul><li>B. Norwalk virus </li></ul><ul><li>C. Adenovirus </li></ul><ul><li>D. Epstein-Barr virus </li></ul><ul><li>E. Hepatitis A virus </li></ul>
    36. 43. <ul><li>All the following statements about viral hepatitis are true, EXCEPT: </li></ul><ul><li>A. Hepatitis A and hepatitis E are transmitted primarily via the fecal-oral route </li></ul><ul><li>B. Hepatitis B is no longer an important cause of post- transfusion hepatitis </li></ul><ul><li>C. Hepatitis A virus produces acute but not chronic hepatitis </li></ul><ul><li>D. Hepatitis D can only affect persons co-infected with hepatitis B </li></ul><ul><li>E. An effective, killed vaccine is available for hepatitis C </li></ul>
    37. 44. <ul><li>All the following statements about viral hepatitis are true, EXCEPT: </li></ul><ul><li>A. Hepatitis A and hepatitis E are transmitted primarily via the fecal-oral route </li></ul><ul><li>B. Hepatitis B is no longer an important cause of post- transfusion hepatitis </li></ul><ul><li>C. Hepatitis A virus produces acute but not chronic hepatitis </li></ul><ul><li>D. Hepatitis D can only affect persons co-infected with hepatitis B </li></ul><ul><li>E. An effective, killed vaccine is available for hepatitis C </li></ul>
    38. 45. <ul><li>The following viruses are associated with gastroenteritis </li></ul><ul><li>A. Astroviruses </li></ul><ul><li>B. Norwalk-like viruses </li></ul><ul><li>C. Picornaviruses </li></ul><ul><li>D. Adenoviruses </li></ul><ul><li>E. Rotaviruses </li></ul>
    39. 46. <ul><li>The following viruses are associated with gastroenteritis </li></ul><ul><li>A. Astroviruses </li></ul><ul><li>B. Norwalk-like viruses </li></ul><ul><li>C. Picornaviruses </li></ul><ul><li>D. Adenoviruses </li></ul><ul><li>E. Rotaviruses </li></ul>
    40. 47. <ul><li>The most likely infecting virus for an outbreak of diarrhea in a class of medical students </li></ul><ul><li>A. Hantavirus </li></ul><ul><li>B. Coxsackie virus </li></ul><ul><li>C. Rota virus </li></ul><ul><li>D. Hepatitis A virus </li></ul><ul><li>E. Norwalk virus </li></ul>
    41. 48. <ul><li>The most likely infecting virus for an outbreak of diarrhea in a class of medical students </li></ul><ul><li>A. Hantavirus </li></ul><ul><li>B. Coxsackie virus </li></ul><ul><li>C. Rota virus </li></ul><ul><li>D. Hepatitis A virus </li></ul><ul><li>E. Norwalk virus </li></ul>

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