Week 3: Antibiotic Resistance

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Week 3: Antibiotic Resistance
2014-01-27 23:05:11
antibiotic resistance
Micro Week 3 Lecture
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  1. 4 Mech. of Antibiotic Resistance
    • 1. Reduced drug accumulation
    • 2. Drug inactivation or modification
    • 3. Alteration of drug target site
    • 4. Alteration of biosynthesis (metabolic) pathway
  2. Reduced drug accumulation:

    - mode of action
    •by decreasing permeability (e.g., altered porin channel)

    •by increasing drug efflux (e.g., activated or overexpressed efflux pump; MDR, multiple drug resistant)
  3. Drug inactivation or modification:

    - mode of action
    b-lactamases, aminoglycosides-modifying enzymes
  4. Alteration of drug target site:

    - mode of action

    •Alteration of PBPs, gyrase, ribosome, RNA polymerase
  5. Alteration of biosynthesis (metabolic) pathway:

    • Some sulfonamide-resistant bacteria
  6. Origin of antibiotic resistance

    2 groups
    • 1) Inherent (natural, intrinsic) resistance
    • - some species are naturally resistant

    2) Acquired resistance: driven by four genetic processes

      (1) Transformation

      (2) Conjugation

      (3) Transduction

      (4) Spontaneous mutation
  7. Mechanisms of b-lactams resistance
    • Production of b-lactamase enzymes
    • (penicillinase, Cephalosporinase)

    –hydrolyze b-lactam ring causing inactivation

    –mostly carried by plasmid

    Alteration in penicillin-binding proteins (PBPs) leading to decreased binding affinity

    –caused by gene mutations

    –caused by overproduction of PBPs (gene duplication, alteration of gene regulation)
  8. Mechanisms of vancomycin resistance
    •Inactive against gram negative bacteria (too big to pass through the outer membrane)

    •Production of non-compatible tetrapeptide terminus which does not bind to vancomycin
  9. Relationship between normal flora and host (symbiotic relationship)
    • 1. Commensalism
    • -  Neither party benefits or harmed from the association

    • 2. Mutualism
    • -   Both parties benefit from the association

    • 3. Opportunism
    • - Potential pathogens (opportunistic pathogens)

    - Normal flora becomes pathogenic when inoculated into wrong places or when the host becomes weakened and immunologically compromised (AIDS)
  10. Normal Flora:  Tissue specificity
    Most members of the normal bacterial flora prefer to colonize certain tissues and not others.

    This "tissue specificity" is usually due to properties of both the host and the bacterium.

    • - tissue tropism
    • - specific adherence
  11. Tissue tropism
    – different factors for bacterial growth, e.g., temperature, pH, oxygen, essential nutrients
  12. Specific adherence
    - surface molecules (adhesions or ligands) on a bacterium bind specifically to complementary surface receptors on cells of certain host tissues
  13. Benefits of Normal Flora
    •synthesize and excrete vitamins (e.g., Vitamins K and B12 are produced by certain intestinal bacteria)

    •prevent colonization of pathogens (by competing for attachment sites or nutrients)

    •produce substances that can inhibit or kill pathogens

    •stimulate the development of certain tissues (e.g., caecum and Peyer's patches in the GI tract)

    •stimulation of immune system