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STREPTOCOCCUS & ENTEROCOCCUS

STREPTOCOCCUS & ENTEROCOCCUS. Cocos Gram-Positivos Streptococcus. Gênero Streptococcus. Fisiologia e Metabolismo Anaeróbios facultativos Exigentes nutricionalmente (fatores de crescimento) Capnofilia Catalase Negativa (2H 2 O 2 ---> O 2 + 2H 2 O)

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STREPTOCOCCUS & ENTEROCOCCUS

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  1. STREPTOCOCCUS & ENTEROCOCCUS

  2. Cocos Gram-Positivos Streptococcus

  3. Gênero Streptococcus Fisiologia e Metabolismo Anaeróbios facultativos Exigentes nutricionalmente (fatores de crescimento) Capnofilia Catalase Negativa (2H2O2 ---> O2 + 2H2O) Beta, Alfa, ou GamaHemolíticos em ágar sangue

  4. Gênero Streptococcus • Sistemas de classificação • Quanto à hemólise • Quanto ao determinante antigênico • Quanto à apresentação clínica • Quanto às provas bioquímicas • Rebecca Lancefield • Classificação de Streptococcus beta-hemolíticos pelo Carbohidrato da parede celular grupo-específico • Sorogrupos A a H e K a V • Grupos A, B, C, D, e G mais importantes

  5. Classificação de Lancefield - Streptococcus Beta-Hemolíticos • Grupo A Streptococci: • Streptococcus pyogenes • Um dos patógenos mais importantes • Doenças Supurativas: Faringite; Escarlatina; • Infecções cutâneas & de tecidos moles; doenças sistêmicas • Não-Supurativas:FRA,GNDA • Grupo B Streptococci: • Streptococcus agalactiae • Doenças sistêmicas, cutâneas, ITU • Doenças Neonatais • Complicações obstétricas REVIEW

  6. Streptococcus pyogenes (Contraste de fase)

  7. Streptococcus Pyogenes – Grupo A • Faringite eritemato-pultácea • Erisipela • Impetigo • Escarlatina • Síndrome do choque tóxico • Fascite necrosante, mionecrose, septicemia • Doenças não supurativas

  8. Erisipelas NOTE: • eritema • bolhas

  9. Determinantes de Patogenicidade • Fatores de Virulência Celulares • Cápsula • Antiphagocytic; Nonspecific adherence • Hyaluronic acid (polysaccharide) mimics animal tissue • Ácido Lipoteicoico • Cytotoxic for wide variety of cells • Adherence: Complexes with M protein (LTA-M) and binds to fibronectin on epithelial cells • Proteína M • LTA-M protein is adhesin • Antiphagocytic • Inhibitsalternate C’ pathway and opsonization • Proteínas M-like: bind IgM and IgG • Proteína F: mediates adherence

  10. Fatoresde VirulênciaExtracelulares • Exotoxinas: • Estreptolisina O (SLO): • Hemolytic and Cytolytic • Prototype of oxygen-labile and thiol-activated cytolytic exotoxins (e.g., Streptococcus, Bacillus, Clostridium, Listeria) • Lytic for variety of cells: bind to cholesterol-containing membranes and form arc- or ring- shaped oligomers that make cell leaky (RBC's, WBC’s, PMN's, platelets, etc.) • Causes sub-surface hemolysis on BAP • Stimulate release of lysosomal enzymes • SLO titer indicates recent infection (300-500 in pediatric populations)

  11. Fatoresde VirulênciaExtracelulares • Exotoxinas: • Estreptolisina S (SLS): • Hemolytic and Cytolytic • Oxygen stable, non-antigenic • Lytic for red and white blood cells and wall-less forms (protoplast, L- forms) • Causes surface hemolysis on BAP • Lisogenia: Lysogenized bacteriophages play key role in directing synthesis of various Group A streptococcal enzymes and toxins • Pyrogenic Exotoxin (erythrogenic toxin) • Phage-associated muralysins (lyse cell walls) produced by both Groups A and C

  12. Fatoresde VirulênciaExtracelulares • Exotoxinas: • ExotoxinasPirogênicas (Eritrogênicas) (A, B &C) • Produced by more than 90% of Grp A strep • Lysogeny: Structural gene is carried by temperate bacteriophage, as is the case with diphtheria toxin • Mediate pyrogenicity (fever) • Causes scarlet fever (scarletiniform) rash • Increase susceptibility to endotoxic shock • Type C toxin increases permeability of blood-brain barrier • Enhance DTH • Mitogenic for T lymphocytes (cause cell division), myocardial and hepatic necrosis, decrease in antibody synthesis • Immunomodulators (superantigens): stimulate T cells to release cytokines • Toxina Cardiohepática

  13. Fatoresde VirulênciaExtracelulares • Enzimas: • Nucleases:Four antigenic types (A,B,C,D) • Facilitate liquefication of pus generating growth substrates • Nucleases A, C have DNase activity • Nucleases B, D also have RNase activity • Estreptoquinases: Two different forms • Lyse blood clots: catalyze conversion of plasminogen to plasmin, leading to digestion of fibrin • C5a Peptidase: destroys C’ chemotactic signals (C5a) • Hialuronidase: hydrolyzes hyaluronic acid • Others:Proteinase, NADase, ATPase, phosphatase, etc.

  14. Nonsuppurative Sequelae of Acute Group A Streptococcal Infection • Acute Rheumatic Fever (ARF) • Inflammatory reaction characterized by arthritis, carditis, chorea (disorder of CNS with involuntary spastic movements), erythema marginatum (skin redness with defined margin), or subcutaneous nodules • Within 2-3 weeks followingpharyngitis • Epidemic pharyngitis: ARF in as many as 3% • Sporadic pharyngitis: ARF in 1 per 1000 • Morbidity & mortality linked to subsequent disease of heart valve (Rheumatic Heart Disease) • Poorly understood pathogenesis with several proposed theories including cross-reactivity of heart tissues & strep AGNs • ?? (Type ??hypersensitivity, exotoxins, direct invasion) II REVIEW

  15. NonsuppurativeSequelae of Acute Group A Streptococcal Infection (cont.) • Acute Glomerulonephritis • Follows either respiratory (pharyngitis) or cutaneous(pyoderma) streptococcal infection • Associated with well-defined group of M-types • Incidence varies from <1% to 10-15% • Most often seen in children manifesting as dark, smoky urine with RBC's, RBC casts, white blood cells, depressed serum complement, decreased glomerular filtration rate • Latent period: 1-2 weeks after skin infection and 2-3 weeks after pharyngitis • Granular accumulations of immunoglobulin due to deposition of immune complexes within the kidney • (Type ?? Hypersensitivity) III REVIEW

  16. Group B Streptococcus • Streptococcus agalactiae

  17. Streptococcus agalactiae

  18. Group B Streptococcal Infections

  19. Grp B Streptococcal Infections (cont.)

  20. Age-Specific Attack Rates of Group B Streptococcal Disease

  21. Epidemiology of Neonatal Group B Streptococcal Disease

  22. Group B Streptococcus S. agalactiae • Diagnostic Laboratory Tests • CAMP factor positive • Hippurase positive

  23. CAMP Factor Test S. aureus (Spingomyelinase C) Group B Streptococcus (CAMP Factor) Group A Streptococcus Enhanced Zone of Hemolysis

  24. Hippurase NEG

  25. Grp B Streptococci and Campylobacter Hippurase POS

  26. Streptococcus pneumoniae • Também chamado de pneumococcus

  27. Streptococcus pneumoniae Infections

  28. Pneumococcal Infections (cont.) Epidemiology (cont.)

  29. S. pneumoniae • Diplococcus

  30. S. pneumoniae: lancet-shaped diplococcus

  31. S. pneumoniae Virulence Factors

  32. S. pneumoniae Seasonal Incidence

  33. Comparison of Morbidity & Mortality for Bacterial Meningitis

  34. Genetic Variation (Mutation)

  35. Beginning of Molecular Genetics

  36. Transformation (In vivo) (Griffith)

  37. Streptococcus pneumoniae • Diagnostic Laboratory Tests • Optochin sensitivity (Taxo P disc)

  38. Optochin Sensitivity Taxo P Streptococcus pneumoniae

  39. Enterococcus faecalis Enterococcus faecium • GI tract of humans and animals • Group D carbohydrate cell wall antigen • Formerly Streptococcus

  40. Enterococcal Infections

  41. Enterococcal Infections (cont.)

  42. Important nosocomial pathogen • Vancomycin resistant Enterococcus (VRE)

  43. Enterococcus • Diagnostic Laboratory Tests • Resistant to bile • Esculin hydrolysis • BEA media

  44. Enterococcus Group D Streptococcus Bile Esculin Agar POS Bile Esculin Agar NEG

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