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Transcript
Immune Evasion and Antimicrobial Resistance Evasion of ---/ Resistance Strategy Specific Mechanism Organism Notes Phagocytosis/ Macrophages Capsule S. Pneumo, H. Flu, N. Meningitidis, Klebsiella, Salmonella, Cryptococcus neoformans Inhibits phagocytosis Catalase Staph Break down H2O2 Phagolysosome fusion inhibited Mycobacteria, Legionella Escape phagosome Sialic Acid expression Listeria N. Meningitidis Using listeriolysin (forms pores) Inhibits C3, C5 convertase Coated w/ IgA N. Meningitidis IgA antibodies don’t activate complement M protein Strep Blocks C3 binding to organism and C3b binding to complement receptors by binding fibrin, fibrinogen to its surface Long O Antigen chains (LPS) Modified LPS “smooth” GNB (Salmonella, E. coli strains) Pseudomonas MAC prevented from accessing outer membrane; “rough” strains (little O antigen) not as virulent Resists action of peptide antibiotics Protein A S. aureus Binds Fc portion of IgG: camouflage IgAases N. gonorrhea, meningitidis, H. flu these extracell proteases that cleave IgA at hinge region, fragments ineffective IL-10 secretion EBV Inhibition of macrophage activation Soluble cytokine receptor production Poxviruses Immune modulator production Tapeworn (tenia) Slime layer Staph epidermidis Phase variation N.gonnorhea Complement Peptide Antibiotics (innate immunity) Antibody Response Immune Modulation Misc. Immune Evasion Block proteasomal activity EBV, CMV Can turn on/off exp of several Opa proteins (antigenic variants)/diff LPS genes by gain/loss of CTCTT repeats (shifts reading frame) Turn on/off fimbriae exp. (fimA) by inversion of DNA segment w/ promoter MHC class I affected Block in TAP transport HSV MHC I affected Remove class 1 from ER CMV MHC 1 affected E. coli Antigen Presentation (MHCs) Cysticerci produce paramyosin, taeniastatin- inhibit complement, bind antibody, interfere w/ CMI Exopolysaccharide secreted-resistance to phagocytes and adherence to plastics (entry) Antigenic Variation Vary Surface Antigens E. Coli N. gonorrhea Influenza HIV Trypanosomes Malaria Pilin genes Homologous recombo of pillin genes (Pil E exp, Pil S “silent”) Point mutations/genetic recombination of segemented RNA genome Hypervariable regions in nonconserved glycoproteins (ex. exposed regions of GP 120) VSGs (variant surface glycoproteins), clonal expansion of organisms coated by another VSG as immune resp develops, variation rate 10-2-10-6, over 1000 so “exhausts” immune sys Var (variety) gene family encoding PfEMP-1 proteins, every 10-6/10-7 organism shifts to diff var genes, takes ~18 months to run through family Display host antigens Schistisome Larvae S. pyogenes HIV Treponema pallidum Shed antigen coat Meninges Necrotic Tissue Modified peptidoglycan precursor B-lactamases Ameba N. meningitidis Clostridia Enterococci (VRE) Methicillin PBP2a (on mec A gene) S. Aureus (MRSA) Fluoroquinolones, tetracyclines, macrolides Aminoglycosides Efflux pumps GNB, pneumococcus Block transport Inactivating enzymes GNB (gram – bacteria) Staph Anatomic Sequestration Vancomycin Penicillin/ BLactams S. Aureus, et al Covered in host glycolipid, MHCs hyaluronic acid coat mimics host surface covered by polysacch side chains added by host enzy Cardiolipin, other major surf lipoproteins thought to derive from host D-ala-lactate not D-ala-D-ala PBP that “went wrong” Gram +: secrete extracell., resis cannot be overcome by giving more drug, Gram -: constitutive production, can overcome resis. w/ more drug Novel penicillin binding protein Inactivate active trans across membrane