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
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.