The mechanism of beta-lactam resistance in MRSA is fundamentally different from that in beta-lactamase-producing organisms. MRSA resistance is mediated by:
- A Overproduction of beta-lactamase enzyme encoded on plasmid
- B Acquisition of mecA gene encoding PBP2a (PBP2'), which has very low affinity for all beta-lactams ✓
- C Efflux pump overexpression reducing intracellular beta-lactam concentration
- D Altered outer membrane porins preventing beta-lactam entry into the bacterial cell
Explanation
MRSA (methicillin-resistant Staphylococcus aureus) acquires the mecA gene (on a mobile genetic element called SCCmec) that encodes PBP2a (also called PBP2'), an altered penicillin-binding protein with extremely low affinity for all beta-lactam antibiotics. Transpeptidation can occur via PBP2a even when all other PBPs are inhibited, conferring pan-beta-lactam resistance. This is distinct from beta-lactamase production (plasmid-mediated enzymatic hydrolysis). Efflux and porin changes are Gram-negative resistance mechanisms, not typical of MRSA.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.