microbio 6 ch 9 antimicrobial chemotherapy part 3 (penicillin, ampicillin, antibiotics, toxicity, an

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microbio 6 ch 9 antimicrobial chemotherapy part 3 (penicillin, ampicillin, antibiotics, toxicity, an
2013-11-16 21:04:55
microbio antimicrobial chemotherapy part penicillin ampicillin antibiotics toxicity antibiotic resistance cephalosporin vancomycin

microbio ch 9 antimicrobial chemotherapy part 3 (penicillin, ampicillin, antibiotics, toxicity, antibiotic resistance, cephalosporin, vancomycin)
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  1. what are the two routes of administration of antibiotic?
    oral (recommended) and parenteral (any route other than oral)
  2. what are bacterial mechanisms to become resistant to antibiotics?
    1. The cell becomes impermeable to the antibiotic.

    • 2A. The bacterium has an enzyme that can modify the
    • structure of the antibiotic by addition of a small group such as phosphate or
    • methyl.  The modification prevents the
    • antibiotic from interacting with its target.

    2B. The antibiotic’s structure is disrupted.  ß-lactamase is a prime example.

    • 3. The target is modified. 
    • A well-known example is through target methylation.

    • 4. Multidrug Resistant Pumps.  These are known as efflux pumps and can
    • result in resistance to a multiplicity of antibiotics.  The drug can enter the cell, but is then
    • pumped out.
  3. what are antimetabolites?
    • The basis of the action of an antimetabolite is its
    • ability to outcompete a natural substrate for an enzyme. In other words, it blocks a metabolic pathway
  4. how do sulfonamides/sulfa drugs work?
    • The classic example for the action of n antmetabolite is the
    • synthesis of folic acid, which is needed as a cofactor for enzymes involved in
    • purine or pyrimidine synthesis.  The
    • synthesis of folic acid requires the incorporation of pABA.  Sulfonamide is an analog of pABA, but is
    • preferentially incorporated into the folic acid precursor instead of pABA.  Apparently sulfonamide binds more strongly to
    • the enzyme that normally incorporates pABA. 
    • This results in a pseudofolic acid that doesn’t function.
  5. what are factors that influence the effectiveness of antibiotics in vivo?
    • A. It must be able to reach the site of infection. If the
    • pathogen is in an abcess or a biofilm, it may be more difficult for the drug to
    • act on the bacterium.

    • B. If the antibiotic reaches the site of infection, the
    • concentration must be higher than the MIC.This depends on factors such as the
    • dose, the route of administration, the rate of uptake, and the rate of
    • elimination.

    • C. The pathogen must be sensitive to the antibiotic. It
    • can’t be genetically resistant or hiding in a biofilm.
  6. in order to create folic acid, ____ must be incorporated into the folic acid precursor
  7. what is folic acid needed for by a bacterial cell?
    it is needed as a cofactor in enzymes involved in purine and pyrimidine synthesis
  8. the enzyme that incorporates pABA into the folic acid precursor preferentially incorporates ____ into the folic acid precursor instead
  9. how can a bacterium develop resistance to an antimetabolite?
    1. The bacterium becomes impermeable to sulfonamide.

    • 2. The enzyme that binds pABA to sulfonamide is changed by
    • mutation.  Now it binds selectively to
    • pABA.

    • 3. The bacterium overproduces pABA which can then outcompete
    • sulfonamide.
  10. what is the name of the antiviral drug
  11. what is azidothymidine?
    it is an antiviral drug. it is an analog of the base thymine. it has an azide group at the 3' carbon of the ribose, so that when it is incorporated into DNA, DNA synthesis can no longer continue
  12. fungal diseases are called ____
  13. why is it more difficult to find effective therapeutic agents against fungi than it for bacteria?
    • A major barrier to this goal with eukaryotic microbes
    • is that we are eukaryotes, and consequently it is more difficult to find
    • exploitable differences between our cells and those of the fungi and yeast.
  14. what are two known differences between fungi and humans that can be exploited in order to target fungal infections?
    • One is sterols that are in the
    • plasma membrane. Our cells have cholesterol, but the eukaryotic microbes have
    • ergosterol. Consequently, compounds that selectively extract ergosterol from
    • the membrane of these organisms or selectively inhibit its synthesis are
    • effective antifungals.

    • Another unique target is the enzyme
    • chitin synthase, and chitin is an important component of the fungal cell wall.
    • Chitin is not found in animal cells.
  15. what are the three types of fungal infections?
    • superficial mycoses, subcutaneous mycoses and systemic
    • mycoses