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Viral hepatitis a+e

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