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Antimicrobial Pharmacology: Mechanisms and Resistance MCQs

Notes · Pharm-D / Pharmacy · 28 practice questions

1. A urinary tract infection is treated with trimethoprim-sulfamethoxazole, which is bactericidal, even though neither trimethoprim nor sulfamethoxazole is bactericidal when used alone. What best explains this synergistic bactericidal effect?

  1. ASulfamethoxazole inhibits dihydrofolate reductase while trimethoprim inhibits dihydropteroate synthase, doubling the inhibition at one step
  2. BSulfamethoxazole is a suicide inhibitor that protects trimethoprim from bacterial degradation
  3. CThe two drugs act on sequential steps of the same folate synthesis pathway, more completely depleting tetrahydrofolate than either step alone
  4. DTrimethoprim enhances sulfamethoxazole's uptake by inhibiting bacterial efflux pumps
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C. The two drugs act on sequential steps of the same folate synthesis pathway, more completely depleting tetrahydrofolate than either step alone Sulfamethoxazole inhibits dihydropteroate synthase and trimethoprim inhibits dihydrofolate reductase—sequential steps in folate synthesis—so blocking both steps together more completely depletes tetrahydrofolate, producing bactericidal synergy despite each being only bacteriostatic alone.

2. A patient on long-term sertraline for depression is started on linezolid for a resistant Enterococcus infection. Which adverse effect should be most closely monitored given this drug combination?

  1. ASerotonin syndrome due to linezolid's monoamine oxidase inhibitory activity
  2. BQT prolongation from additive 50S ribosomal binding
  3. COtotoxicity from combined ribosomal effects
  4. DBone marrow deposition causing enamel hypoplasia
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A. Serotonin syndrome due to linezolid's monoamine oxidase inhibitory activity Linezolid inhibits monoamine oxidase, and combination with an SSRI like sertraline risks serotonin syndrome.

3. An Enterococcus faecium isolate shows a 1000-fold reduction in vancomycin binding affinity while remaining susceptible to ampicillin. Which structural modification best explains this resistance pattern?

  1. AProduction of a beta-lactamase-like enzyme that hydrolyzes the glycopeptide backbone
  2. BAcquisition of an altered penicillin-binding protein with low affinity for glycopeptides
  3. CUpregulation of an efflux pump that extrudes vancomycin from the cytoplasm
  4. DModification of the peptidoglycan precursor terminus from D-alanyl-D-alanine to D-alanyl-D-lactate
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D. Modification of the peptidoglycan precursor terminus from D-alanyl-D-alanine to D-alanyl-D-lactate VRE modifies the pentapeptide terminus to D-alanyl-D-lactate, which markedly reduces vancomycin's steric binding without necessarily affecting beta-lactam-PBP interactions.

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