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MICROBIOLOGY IRS. Gastroenteritis 1) Major cause of infantile death 2) Feacal-oral transmission 3) Gastroenteritis cause dehydration 4) 50 % of all causes.

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Presentation on theme: "MICROBIOLOGY IRS. Gastroenteritis 1) Major cause of infantile death 2) Feacal-oral transmission 3) Gastroenteritis cause dehydration 4) 50 % of all causes."— Presentation transcript:

1 MICROBIOLOGY IRS

2 Gastroenteritis 1) Major cause of infantile death 2) Feacal-oral transmission 3) Gastroenteritis cause dehydration 4) 50 % of all causes of diarrhea is ROTA ROTA is responsible for an estimated 1 million deaths each year among undernourished children

3 Viral agents of gastroenteritis 1) Reo=Respiratory and Enteric Orphans Most important Reo virus is ROTA ROTA means WHEEL in LATIN 2) Noro Norwalk, Astro, Calici 3) Adeno=adenovirus 40,41 (adeno is the only DNA virus on this page)

4 GENERAL info- Lab diagnosis of viruses! Electron Microscopy-Direct visualization Tissue culture- cytopathic effects PCR-Viral DNA/RNA detection ELISA/IF/LA etc- Antigen detection Serology- ELISA/IF/LA etc – IgG / IgM Antibody detection. (Disclaimer-some viruses have not yet been cultured, especially Hepatitis viruses and Enteritis viruses)

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6 KEY TO HEPATITIS VIRUSES Hepatitis virus named as A-E ( F,G AND OTHERS). RNA genome except HBV (DNA genome). Parenteral transmission- ( Except HAV and HEV - Enteric). Enveloped virus – ( Except HAV and HEV – non enveloped ). Chronic infections - HBV HCV and HDV. Oncogenic virus includes HBV and HCV. Vaccine availability –HAV and HBV. Defective / Dependent virus - HDV.

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8 Lab diagnosis of Hepatitis viruses Electron Microscopy Molecular Diagnosis SerologyAnimal tissue culture (ATC) Direct visualization PCR-Viral DNA/RNA detection ELISA/IF/LA Antigen detection Cytopathic effects (some virus not cultured)

9 Hepatitis A virus

10 Serologic Diagnosis Hepatitis A infection Specific antibody against HAV of the immunoglobulin (Ig) M type appears in blood at the onset of symptoms, The IgM response usually begins to decline in a few months and is followed by the appearance of IgG anti-HAV. IgG anti-HAV persists for years, perhaps for life

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14 Transmission of Hepatitis B virus

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16 Post Exposure prophylaxis PERINATALSEXUAL PERCUTANEOUS 0.5 ml, within 12 hrs of birth Boosters 1,6 months 0.06ml/kg, -within 14 days Non-Immunized- HBIG + 0,1,6 Immunized Test Anti-HB S level If inadequate HBIG +ONE BOOSTER)

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18 HBV-DNA by PCR also indicates active replication of the virus HBV replication = Disease (Acute or Chronic replicative phase)

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20 Anti-HBc IgM: Acute or present infection Anti-HBc IgG: Chronic or past infection

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26 Sequence of serologic markers for hepatitis C viral hepatitis demonstrating (A) acute infection with resolution and (B) progression to chronic relapsing infection.

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29 Genus: Hepevirus,Nonenveloped RNA Virus

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31 Hepatitis A virus (HAV) –Anti-HAV-IgM indicates active infection. –Anti-HAV-IgG indicates recovery from infection or vaccination.

32 Hepatitis E virus (HEV) Presence of anti-HEV-IgM indicates active infection. Anti-HEV-IgG indicates recovery (protective antibody).

33 Hepatitis D virus (HDV) –Presence of anti-HDV-IgM or IgG indicates active infection. –IgG is not a protective antibody. HCV, HDV: no protective antibodies

34 Hepatitis C virus (HCV) –Screen with enzyme immunoassay (EIA) (1) Presence of anti-HCV-IgG indicates active infection or recovery. Sensitivity > 97% (2) It does not differentiate among acute, chronic, or resolved infection. (3) It is not a protective antibody. –Confirmatory tests HCV testing: screen with EIA; confirm with RIBA and HCV RNA (1) Recombinant immunoblot assay (RIBA) (a) Supplemental test if EIA is positive (b) More specific but less sensitive than EIA (2) HCV RNA using polymerase chain reaction HCV RNA: gold standard test (a) Gold standard test for diagnosing HCV (b) Detects virus as early as 1 to 2 weeks after infection (c) Used to monitor patients on antiviral therapy (3) Positive RIBA and HCV RNA indicate active infection. (4) Positive RIBA and negative HCV RNA indicate recent recovery.

35 Hepatitis B virus (HBV) HBsAg: first antigen to arrive and last one to leave with recovery (2) Persists up to 4 months in acute hepatitis HBsAg longer than 6 months defines chronic HBV. –Hepatitis B e antigen (HBeAg) and HBV-DNA HBeAg and HBV-DNA: infective particles (1) Infective particles (2) Appear after HBsAg and disappear before HBsAg Anti-HBV core antibody IgM (anti-HBc-IgM) (1) Nonprotective antibody Remains positive in acute infections Anti-HBc-IgM: only marker present during window phase (2) Persists during "window phase" or "serologic gap" HBsAg, HBV DNA, and HBeAg are absent. (3) Converts entirely to anti-HBc-IgG by 6 months Anti-HBc-IgG: present after 6 months Anti-HBV surface antibody (anti-HBs) (1) Protective antibody (2) Marker of immunization after HBV vaccination Anti-HBs: protective antibody; immunization or recovery from past infection

36 Chronic HBV (1) Persistence of HBsAg longer than 6 months Anti-HBc-IgM converts to anti-HBc-IgG. HBsAg > 6 months defines chronic HBV (2) "Healthy" chronic carrier (a) Presence of HBsAg and anti-HBc-IgG (b) Absence of DNA and e antigen "Healthy" carrier: HBsAg, anti-HBc-IgG (c) Still contagious but at a much lower risk (3) Infective chronic carrier Infective carrier: HBsAg, HBeAg, HBV-DNA, anti-HBc-IgG (a) Presence of HBsAg, anti-HBc-IgG, and infective particles (DNA and e antigen) (b) Increased risk for postnecrotic cirrhosis and hepatocellular carcinoma


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