09 factors of_path_and_virulence_-_2_2_
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09 factors of_path_and_virulence_-_2_2_ 09 factors of_path_and_virulence_-_2_2_ Presentation Transcript

  • Institute for Microbiology, Medical Faculty of Masaryk University and St. Anna Faculty Hospital in Brno Miroslav Votava, Vladana Woznicová FACTORS OF PATHOGENICITY AND VIRULENCE – II Lecture for 2nd-year students April 20 th , 200 9
  • Ability to overcome the defence – A
    • A) Ability to overcome the innate immunity :
    • To resist complement to inhibit complement activation to protect one‘s own surface
    • To resist phagocytosis not to allow being engulfed to survive inside the phagocyte
    • To interfere with the cytokine function
  • Ability to resist complement
    • Inhibition of complement activation
    • capsule – shielding surface molecules (meningococci, pneumococci) activation inhibitors (gonococci – addition of sialic acid to terminal saccharides , many viruses, E. coli and S. pyogenes – production of regulation factor H, S. pyogenes and P. aeruginosa – enzymes splitting C3b a C5a)
    • Protection of the surface (salmonellae and E. coli in S phase, flagella of motile bacteria)
    • Ability to resist complement -> s eroresistance
  • http://inst.bact.wisc.edu
  • Ability to resist phagocytosis – I
    • 1. N ot to allow being engulfed
    • inhibitors of chemotaxis (bordetellae, vaginal anaerobes, pseudomonads)
    • leucocidins and lecithinase (staphylococci, streptococci, pseudomonads, clostridia)
    • injecting Yop (yersiniae)
    • formation of capsule ( most importan t! )
    • agents of meningitis and pneumonia ( N. meningitidis, H. influenzae, E. coli, S. pneumoniae, K. pneumoniae )
  • http://www.coll-outao.qc.ca
  • Ability to resist phagocytosis – II
    • 2. To survive inside the phagocyte
    • blockade of phagolysosome formation ( C hlamydia, M ycobacteri um , L egionella, T oxoplasma )
    • escape from phagosome ( R ickettsia, S higella, L isteria, L eishmania, T rypanosom a )
    • production of antioxidants
    • (staphylococci, gonococci, meningococci)
    • marked tenacity
    • ( C oxiell a , E hrlichia )
  • Ability to overcome the defence – B
    • B) Ability to overcome the acquired immunity:
    • Always an attempt to avoid antibodies or immune lymphocytes :
    • to reproduce quickly (respiratory viruses, diarrhoeal agents, malarial plasmodia)
    • attempt to deceive immune system
    • to hide itself
    • to change one‘s own antigens
    • to induce tolerance
    • attempt to suppress immune reaction
  • Ability to deceive the immune system – I
    • To hide itself in ganglions (HSV, VZV) on intracellular membranes (HIV, adenov.) in infectious focuses ( M. tbc , echinococci) in privileged sites (agents of mucosal infections, T. gondii in eye, retroviruses in cellular genome)
    • 2. To induce the immune tolerance
    • (CMV, rubella v., leishmaniae, cryptococci, maybe even HIV)
  • Ability to deceive the immune system – II
    • 3. To change antigens of one‘s own
    • antigenic mimicry ( S. pyogenes, T. pallidum, M. pneumoniae )
    • antigenic camouflage (schistosomes – blood proteins, staphylococci – protein A, streptococci – protein G, CMV – βmG)
    • antigenic variability (trypanosomes, borreliae, gonococci, influenza virus)
  • Ability to deceive the immune system – III
    • 4. To suppress immune reaction
    • invasion into the immune system (HIV, m easles virus) interference in cytokine formation ( M. leprae , protozoa) production of superantigens (staphylococci, streptococci) production of proteases (meningococci, gonococci, haemophili, pneumococci) binding Fc fragment of IgG (staphylococci, streptococci, HSV)
    • ? (influenza virus, HBV, EBV)
  • Toxicity – I
    • Damage by direct effect of infectious agent
    • Cellular death lysis by toxins, viruses, immune lymphocytes apoptosis (HSV, shigellae)
    • Metabolic injury – influence of exotoxins
    • Mechanical causes (schistosomal eggs, P. jirovecii , pseudomembranes in diphtheria)
    • The most frequent cause of death -> septic shock triggered by endotoxins G – : lipopolysaccharide G + : teichoic acid + peptidoglycan
  • Bacterial exotoxins
    • Spreading factors (hyase, DNase, elastase, collagenase)
    • Cytolysins (lecithinase, sfingomyelinase, hemolysins)
    • Inhibitors of proteosynthesis (diphtheria toxin)
    • Pharmacologically effective toxins (choleragen, E. coli thermolabile enterotoxin, pertussis toxin)
    • Neurotoxins (tetanotoxin, botulotoxin)
    • Superantigens (staphylococcal enterotoxin and exfoliatin, streptococcal pyrogenic toxin)
  • Toxicity – II
    • Damage as a result of defence reactions
    • a) Injuries caused by inflammatory reaction: calor, rubor, tumor, dolor, functio laesa = typical markers of inflammation = symptoms of disease
    • edema : encephalitis, epiglottitis inflammatory infiltrate: pneumonia suppuration: blennorrhoea neonatorum formation of connective tissue: scarring
  • Toxicity – III
    • Injury as a result of defence reactions
    • b) Injuries caused by specific immune reaction (immunopathological consequences of hypersensitivity )
    • 1st type: (IgE, anaphylaxis) helminthoses
    • 2nd type: (cytotoxicity) hepatitis B, febris rheumat.
    • 3rd type: (immunocomplexes) poststreptococcal nephritis, systemic reactions during sepsis
    • 4th type: (late, cellular) tbc, lepra, syphilis, actinomycosis, rash in measles
  • Recommended reading material
    • Paul de Kruif: Microbe Hunters
    • Paul de Kruif: Men against Death
    • Axel Munthe: The Story of San Michele
    • Sinclair Lewis: Arrowsmith
    • André Maurois: La vie de Sir Alexander Fleming
    • Hans Zinsser: Rats, Lice, and History
    • Michael Crichton: Andromeda Strain
    • Albert Camus: Peste
    • Victor Heisser: An American Doctor Odyssey