Pharmacology · Antimicrobials (Cell Wall Inhibitors, Protein Synthesis Inhibitors, Fluoroquinolones)

A surgeon notices that a patient receiving cefazolin prophylaxis develops a wound infection caused by methicillin-resistant Staphylococcus aureus (MRSA). The resistance mechanism in MRSA involves:

  • A Production of beta-lactamase that hydrolyzes all cephalosporins and carbapenems
  • B Overexpression of efflux pumps that expel cephalosporins from the cell
  • C Acquisition of mecA gene encoding a modified penicillin-binding protein (PBP2a) with low beta-lactam affinity
  • D Loss of outer membrane porins preventing drug entry into the peptidoglycan space
Correct answer: C. Acquisition of mecA gene encoding a modified penicillin-binding protein (PBP2a) with low beta-lactam affinity

Explanation

MRSA resistance is mediated by the mecA gene (carried on SCCmec), which encodes PBP2a (also called PBP2'), a transpeptidase with greatly reduced affinity for virtually all beta-lactam antibiotics. Since PBP2a can perform transpeptidation even when all other PBPs are inhibited, cell wall synthesis continues despite beta-lactam presence. Beta-lactamase production is the primary mechanism in methicillin-sensitive strains but is insufficient to explain MRSA resistance to newer beta-lactam-stable antibiotics.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.

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