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14, 15, 16_Alice - TOPICS 14 AND 15 1 A Microbiology of C...

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TOPICS 14 AND 15 1. A. Microbiology of C. diphtheriae: Gram positive, nonsporeforming, nonmotile rods. Must be grown on Tellurite medium or Loeffler’s coagulated blood serum , grows in mitis, intermedius, or gravis . B. Epidemiology of C. diphtheriae : Humans are the only known reservoir, transmission through droplets, contact with cutaneous lesions, or fomites. Diphtheria outbreak in the newly independent states of the former Soviet Union. C. Clinical findings of respiratory diphtheria: Pseudomembrane formation beginning in the tonsils, soft palate, and/or uvula and extending into the nasopharynx, oropharynx, and/or larynx. The extent of pseudomembrane formation correlates with the severity of symptoms. The pseudomembrane is made of fibrin, dead epithelial cells, RBCs, and WBCs, and will tear the capillaries and cause bleeding if dislodged. Cervical lymph nodes will swell and produce a “bullneck appearance”. The diphtheria toxin can spread systemically and especially targets heart, nerve, and kidney cells, leading to myocarditis, neuropathy, and muscle group paralysis. D. Infectious steps for C. diphtheriae: i) Transmission via infectious aerosols, from human-to-human contact ii) Entry into host via respiratory route iii) Overcomes innate defenses at the mucous membranes: a. sIgA in mucin layer, viscosity of mucin layer c. M cells, basolateral pockets, tight junctions d. MALT, macrophages, dendritic cells e. Mucociliary escalator, goblet cells iv) Attachment and colonization- pathogen remains localized, toxin acts both locally and systemically v) Acute inflammatory response a. Vasodilation b. Increased vasopermeability- leakage of exudate and complement proteins c. Emigration of phagocytes- margination and diapedesis d. Chemotaxis- active migration to site of injury via chemokine signals (released by injured cells), cytokine signals (released by tissue macrophages), and anaphylotoxins and chemotaxins (C3a and C5a) e. Phagocytosis f. Formation of fibrin strands vi) Disease is produced!!
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a. DT produced locally and acts both locally and systemically b. Direct damage to cells due to multiplication of organisms as well as DT c. Immunopathology by the acute inflammatory response vii) Adaptive immune response against DT viii)Exit from host via aerosols E. Virulence factors for C. diphtheriae : DT i) AB exotoxin- the A fragment is an enzyme which catalyzes the toxic activity, the B fragment mediates receptor binding ii) Secreted as single polypeptide proenzyme, must be cleaved into two fragments connected by a disulfide bond. The disulfide bond must be reduced to yield the active A fragment, probably during membrane translocation into the cytoplasm iii) Steps in DT action: a. B fragment binds Heparin-Binding Epithelial Growth Factor receptor (most common on heart and nerve cells), taken into endocytic vesicle b. Decreased pH conformational changes in A and B chains c. Translocation of A fragment into cytoplasm d. A fragment ADP-ribosylates Elongation Factor 2 at diphthamide location, stopping protein synthesis iv) Regulation of DT: a. Nontoxigenic v. toxigenic strains
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