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25 Cards in this Set
- Front
- Back
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Normal flora is made up of what?
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symbionts and commensals.
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How are pathogens distinguished from non-pathogens?
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By the presence of virulence factors! (Ex: presence of ADP ribosylating toxin in certain serotypes of cholera is the key virulence factor for causing the disease.
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What is pathogenicity?
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The ability to cause diesease
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What is virulence?
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The degree of pathogenicity.
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Concerning virulence, it can be mediated by what
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direct tissue damage by the bacterial toxin or by host immune responses, inflammation, antigen antibody immune responses or cell mediated immunity.
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How is it proven that a particular bacterial gene product is important for virulence?
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Molecular version of Koch's postulate.
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What is Type Three Secretion system?
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It is an elaborate virulence system employed by pathogenic bacteria; gram negative protein secretion system; requires cell to cell contact; evolutionarily related to flagellar apparatus; effector molecules delivered vary.
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What is the TTSS composed of?
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an injectosome, proteins needed to assemble the injectosome, effector proteins that interfere or subvert the host response.
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Genetics of type three secretion system
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Locus on chromosome, indication of foreign origin due to differences in G+C content, borders often marked by repeat sequences.
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YopJ
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an effector protein of Yersinia TTSS, a deubiquinating enzyme, prevents release of of cytokines TNF so host cant mount immune response, does this by modifying MAPKK via MAPKKK (removes ubuquitin from signaling molecule)
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Sip A
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effector protein for Salmonella; required for entry into host hell; causes ruffling and rearrangement of the actin cytoskeleton; inhibits depolymerization of actin filaments causing extension of Salmonella ruffles helping bacterial uptake.
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Short version of SipA
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ruffles, actin cytoskeleton, Salmonella, facilitates bacterial uptake
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Tir
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effector protein of EPEC and EHEC; translocated tir in host membrane communicated with outermembrane proteins in E. coli allowing actin pedistal formation beneath bacteria.
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TLRs
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expressed on B cells and innate cells; type 1 transmembrane glycoprotein; diversity and specificity dependent on use of four intracellular adaptor molecules MyD88, Trif, Trap, Tram
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Trif, trap tram, myd88
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adaptor molecules, mediate proximal interactions with the intracellular domains of TLRs and create a platform to a cascade of kinases and transacting factors. like NFKB and interferon.
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Trif, trap tram, myd88
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create platform to kinase cascade for TLRs
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Two ways to evade TLRs
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Flagellin modification and LPS modification.
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C. jejuni, H. pylori and B. bacilliformis all require what and do what?
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flagellar motility and make flagellin molecules that are not recognized by TLR 5
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At mammalian body temp, Y. pestis synthesizes LPS with what
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poor TLR 4 stimulating activity. So immune system does not recognize it. This is a virulence factor.
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Some pathogens express proteins to
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recruit inactivating molecules of complement.
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Capsules, M protein and fibrin don't what (host evasion)
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bind adhesion molecules used by macrophages and neutrophils to phagocytose pathogens.
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peptidoglycan deacetylation confers what?
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resistance to lysozyme
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Some pathogens inhibit fusion of what (host evasion)
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fusion with lysosome and drop in pH or leave the phagosome. Example Mycobacterium and Chlamydia are taken up by cells but fusion of endocytic vacuole with the lysosome is blocked. The organisms therefore reside long terrm in an immature vacuole.
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Legionella (host evasion)
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alters vesicular trafficking and recruits ribosomes and ER
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Neisseria meningiditis and H. flu have proteases that can damage the hinge region of IgA1. What are two consequences of this?
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Agglutination and clearance is messed up, Fab still binds Ag and masks it so intact antibody won't bind it.
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