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Pathogenic anaerobe gram positive bls 206

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  • 1. Corynebacterium Erysipelothrix & Listeria
  • 2. Pathogenic AnaerobicGram-Positive Bacilli
  • 3. 1. Corynebacteria (Genus Corynebacterium)Aerobic or facultatively anaerobicSmall, pleomorphic (club-shaped), gram-positivebacilli that appear in short chains (“V” or “Y”configurations) or in clumps resembling “Chineseletters”Cells contain metachromatic granules (visualizewith methylene blue stain)Lipid-rich cell wall contains meso-diaminopimelic acid, arabino-galactan polymers,and short-chain mycolic acidsLysogenic bacteriophage encodes for potentexotoxin in virulent strains
  • 4. Distinguishing Features of CMN Group Corynebacteriu Mycobacterium Nocardia  m
  • 5. Pathogenic Corynebacterial SpeciesCorynebacterium diphtheriaeCorynebacterium jeikeiumCorynebacterium urealyticum
  • 6. Corynebacterium urealyticumUrinary tract infections (UTI’s); rare butimportantUrease hydrolyzes urea; release of NH4+,increase in pH, alkaline urine, renal stones
  • 7. Corynebacterium diphtheriaeRespiratory diphtheria (pseudomembrane onpharynx) and cutaneous diphtheriaPrototype A-B exotoxin acts systemically • Toxoid in DPT and TD vaccinesDiphtheria toxin encoded by tox gene introducedby lysogenic bacteriophage (prophage)Selective media: cysteine-tellurite; serumtellurite; Loeffler’sGravis, intermedius, and mitis colonial morphology
  • 8. Epidemiology of Diphtheria
  • 9. Virulence Factors in Corynebacterium Species
  • 10. Diphtheria tox Gene in Beta Bacteriophage and Prophage
  • 11. See Handout on Exotoxins
  • 12. Mechanism of Action of Diphtheria Toxin: Inhibition of Protein Synthesis
  • 13. Molecular Structure of Diphtheria Toxin Catalytic Region A Subunit B Subunit Translocation Region Receptor-Binding Region
  • 14. Heparin-binding epidermal growth factor on heart & nerve surfaces
  • 15. Diagnostic Schick Skin TestImmune Status to C. diphtheriae and Sensitivity to Diphtheria Toxoid TOXIN TOXOID
  • 16. In vivo Detectionof Diphtheria Exotoxin
  • 17. 2. Genus Listeria
  • 18. 2.Listeria monocytogenes• Small, Gram +, nonsporing rod• End-over-end tumbling motility when grown at 20-25°C, not at 37°C• Facultative anaerobe, ß-hemolytic• CAMP Test positive (like Group B Streptococcus)
  • 19. Listeriosis• Humans, domestic animals described in ≥ 40 species of animals usually follows ingestion outbreaks, sporadic cases related to food asymptomatic fecal carriage common, especially for those in contact with domestic animals Incidence increases in summer, when outbreaks of food-borne disease are more common.
  • 20. ListeriosisNeonates, elderly & immunocompromisedGranulomatosis infantiseptica • Transmitted to fetus transplacentally • Early septicemic form: 1-5 days post-partum • Delayed meningitic form: 10-20 days following birthIntracellular pathogen • Cell-mediated and humoral immunity develop • Only cell-mediated immunity is protective
  • 21. Distribution of Listeria?Intestinal tract of mammals & birds (especially chickens)Persists in soilSoft cheeses & unwashed raw vegetablesRaw or undercooked food of animal origin  Luncheon meats  Hot dogsLarge scale food recalls have become common
  • 22. Epidemiology of Listeria Infections Natural Common Routes for Population atReservoirs Human Exposure Greatest Risk
  • 23. Virulence Factors and Pathogenesis - Motility• Actin-mediated motility (ActA) host cell actin polymerized growth of tail by actin polymerization at end of bacterium propels it through cytoplasm• Uptake: induced phagocytosis internalin similar to M protein of S. pyogenes (antiphagocytic), dissimilar functions
  • 24. Virulence Factors and Pathogenesis• After entry to epithelial cells escapes phagosome, multiplies in cytoplasm exocytosis from epithelial cell followed by phagocytosis by MØ, PMN multiplication followed by death of phagocytes, secondary phagocytosis systemic spread
  • 25. Virulence Factors and Pathogenesis - Listeriolysin• Major virulence factor: listeriolysin thiol-activated cytolysin, hemolysin mediates escape from phagocytic vesicle• LLO mutants: LD50 5 logs higher than WT, do not survive in MØ
  • 26. Virulence Factors and Pathogenesis• Bacteria encountering plasma membrane continue to move forward  produce protrusions extending into adjacent cell: listeriopods  escape listeriopod in double- membrane vesicle, enter cytoplasm of adjacent cell• Mediated by phospholipase
  • 27. Virulence Factors and Pathogenesis - Actin-based Motility• Bacteria in cytoplasm polymerize actin, form tails  hollow mesh forms on surface, left behind as bacterium moves forward  invade adjacent cells• Actin nucleating factor: ActA  ActA localized at one end of the bacterium, not found in tail
  • 28. Intracellular Survival & Replication of Listeria Phagocytosis Macrophag e Listeriolysin O? Macrophag e Intracellula Actin r Filaments Replication
  • 29. Immune Response• In infected mice, bacteria first appear in MØ, then invade hepatocytes  most replication probably occurs in liver  infection of MØ leads to presentation of antigens with MHC class I, stimulating cytotoxic T cell response  cytotoxic T cells (and NK cells) kill infected hepatocytes
  • 30. bacteria released from lysed host cells killed bv activated MØT cell-deficient mice survive infection: cytotoxic T-cell response helps clear hepatocytes, not essentialincreased susceptibility in mice unable to produce IFN-: suggests importance of activated MØ
  • 31. Erysipelothrix rhusopathiaeGram-positive non-motile bacillus; forms filamentsOccupational disease of meat and fish handlers,hunters, veterinarians  Preventable with protective gloves & clothingErysipeloid in humans; erysipelas in swine & turkeys  Organisms enter through break in skin  Nonsuppurative, self-limiting skin lesions with erythema and eruption  Peripheral spread may lead to generalized infection, septicemia and/or endocarditis  Organisms can be isolated from skin biopsy
  • 32. Epidemiology of Listeriosis
  • 33. Epidemiology of Listeria Infections Natural Common Routes for Population atReservoirs Human Exposure Greatest Risk
  • 34. ListeriosisNeonates, elderly & immunocompromisedGranulomatosis infantiseptica • Transmitted to fetus transplacentally • Early septicemic form: 1-5 days post-partum • Delayed meningitic form: 10-20 days following birthIntracellular pathogen • Cell-mediated and humoral immunity develop • Only cell-mediated immunity is protective
  • 35. Methods That Circumvent Phagocytic Killing See Chpt. 19
  • 36. Intracellular Survival & Replication of Listeria Phagocytosis Macrophage Listeriolysin O? Macrophage Intracellular Actin Replication Filaments
  • 37. 3. Erysipelothrix rhusopathiaeGram-positive non-motile bacillus; forms filamentsOccupational disease of meat and fish handlers,hunters, veterinarians  Preventable with protective gloves & clothingErysipeloid in humans; erysipelas in swine & turkeys  Organisms enter through break in skin  Nonsuppurative, self-limiting skin lesions with erythema and eruption  Peripheral spread may lead to generalized infection, septicemia and/or endocarditis  Organisms can be isolated from skin biopsy
  • 38. Epidemiology of Erysipelothrix Infection