MRSA strains are resistant to all beta-lactam antibiotics. The mechanism of this resistance is best described as:
- A Acquisition of mecA gene encoding penicillin-binding protein 2a (PBP2a) with low affinity for beta-lactams ✓
- B Hyperproduction of beta-lactamase enzyme
- C Efflux pump overexpression reducing intracellular antibiotic concentration
- D Altered outer membrane porins reducing drug entry
Explanation
MRSA resistance to all beta-lactams (including cephalosporins and carbapenems) is mediated by the mecA gene (carried on SCCmec), which encodes PBP2a — a penicillin-binding protein with very low affinity for beta-lactam antibiotics, allowing cell wall synthesis to continue even in their presence. Beta-lactamase hyperproduction (BLNAR) causes narrow-spectrum resistance, not pan-beta-lactam resistance. Efflux pumps and porin changes are relevant in Gram-negative resistance, not S. aureus. Vancomycin (or linezolid/daptomycin) is used to treat MRSA.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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