ANTIBIOTICS-1 (only exam 1 material)

  1. Antibiotics produce what 2 effects?
    1- bacteriostatic

    2- bacteriocidal
  2. Antibiotics selectively inhibit the growth or survival of microorganisms at _____ concentrations.
  3. What is the purpose of the MIC (minimum inhibitory concentration) value?
    It is the lowest concentration where an antibiotic will produce a static or cidal effect
  4. What is the clinical dose of an antibiotic?
    It must have a plasma concentration of ~4-8 times the MIC value with minimum to no toxicity to the patient
  5. What is a bacteriostatic antibiotic?
    It stops the bacteria from dividing
  6. What is a bacteriocidal antibiotic?
    It kills the bacteria
  7. What 2 classes of antibiotics have a bacteriostatic effects?

  8. What 4 classes of antibiotics have bacteriocidal effects?
    • Penicillins
    • Aminoglycosides
    • Polypeptides
    • Quinolones
  9. True or false, you can predict whether or not an antibiotic is cidal or static based on the MOA.
  10. True or false, if a patient is immunocompromised they can take a static antibiotic.
    False, only immunocompetent patients can be prescribed static antibiotics
  11. Can all antibiotics exhibit a cidal effect?
    Yes if given at high concentrations
  12. Can all antibiotics exhibit both static and cidal effects?
    Yes, the majority of antibiotics have 2 doses (static and cidal)
  13. What 4 factors determine the effect (static or cidal) of an antibiotic?
    • 1- concentration
    • 2- MOA
    • 3- microbial susceptibility/resistance
    • 4- microbial species
  14. Can an antibiotic exhibit only a cidal effect regardless of concentration?
    Yes only 2 classes:

    • 1- beta-lactams
    • 2- polypeptides
  15. Can an antibiotic known to be cidal suddenly become static?
    Yes because of microbial resistance
  16. What is the purpose of using a narrow-spectrum antibiotic?
    It minimizes microbial resistance

    It is cheaper to use
  17. What is a broad-spectrum antibiotic?
    An antibiotic that is effective against a large number of bacterial strains and gram positive and negative bacteria
  18. What are the 3 advantages of using combination therapy?
    • 1- provide emiric(inital) therapy
    • 2- treat polymicrobial(mixed) infections
    • 3- obtain enhanced antimicrobial activity (synergism)
  19. What are the 4 disadvantages of using combination antimicrobial therapy?
    • 1- increased toxcicity
    • 2- increased cost
    • 3- antagonism
    • 4- microbial resistance
  20. What is synergisim?
    A four-fold or greater reduction in the MIC or MBC of each drug when used in combination vs. when used alone
  21. What is antagonism in combination therapy?
    When the combined effect of the drugs are less when used together vs. when they are used alone
  22. What is indifference in combination therapy?
    When the combined effect of the drugs is the same vs. when used alone
  23. What is the purpose of the FIC (fractional inhibitory concentration) index?
    It illustrates the interaction between 2 antimicrobial agents
  24. What is the FBC (fractional bactericidal concentration) index?
    When you substitute the MBC (min bactericidal concentration) for the MIC in the FIC Index equation
  25. Synergisim for combinations of 2 drugs requires an FIC or FBC index of _______
    0.5 or less
  26. Antagonism for combination of 2 drugs requires an FIC or FBC index of ________
    4 or more
  27. Indifference for combinations of 2 drugs requires and FIC or FBC index of ______
    0.5 to 4
  28. What are the 4 mechanisms of synergistic action?
    • 1- blockade of sequential steps in a metabolic sequence
    • 2- inhibition of enzymatic activation
    • 3- enhancement of antimicrobial agent uptake by bacterial cells
    • 4- binding enhancement
  29. What are the 2 mechanisms of antagonistic action?
    • 1- inhibition of cidal activity by static agents
    • 2- induction of enzymatic activation
  30. Microbes can aquire genes (including those for resistance) via _______ ________ from members from their own species or from an unrelated species.
    direct transfer
  31. What are the 4 mechansims for microbial resistance to antimicrobial therapy?
    • 1- drug inactivation via enzymes
    • 2- target modification
    • 3- alteration of target accessibility
    • 4- development of altered metabolic pathways
  32. What is target modification?
    Changing the chemistry of a binding site on a microbe so that the antibiotic cannot bind
  33. What are the 2 types genetic origin (r-factors) in microbial reisistance?
    • 1- chromosomal
    • 2- extrachromosomal
  34. What are the 2 origins of microbial resistance?
    • 1- non-genetic
    • 2- genetic
  35. True or false, chromosomal resistance contributes the most to microbial resistance?
    False, extra-chromosomal resistance contributes the most because the plasmid can be easily transferred
  36. What causes chromosomal resisitance?
    A spontaneous mutation
  37. What causes extrachromosomal resisitance?
    The transfer of R-factors (plasmids)
  38. Chromosomal mutations lead mainly to _____ _______ as the reisitance mechanism.
    target modification
  39. Transfer of R-factors leads mainly to _______________ as the resistance mechanism.
    drug inactivation by enzmyes
  40. What are the 4 mechanisms to transfer R-factors?
    • 1- transformation
    • 2- transduction
    • 3- conjugation
    • 4- transportation
  41. What is transformation?

    Does it contribute to the spread of resistance?
    Direct insertion of an R-factor into a bacterial cell

    It does NOT contribute to the spread of resistance
  42. What is transduction?
    When R-factors are transferred from 1 bacteria cell to another via a virus
  43. What is conjugation?
    When R-factors are transferred via mating
  44. What is the most important mechanism for transferring R-factors?
  45. What is transposition?
    Transfer of R-factors via transposons (jumping genes)

    *Leads to chromosomal resistance
Card Set
ANTIBIOTICS-1 (only exam 1 material)