A clinical isolate of Streptococcus pneumoniae shows high-level penicillin resistance. The molecular mechanism responsible is:
- A Acquisition of blaZ gene encoding a broad-spectrum beta-lactamase
- B Alteration of penicillin-binding protein PBP2b reducing penicillin affinity ✓
- C Upregulation of AcrAB-TolC efflux pump expelling penicillin
- D Reduced outer membrane porins preventing penicillin entry
Explanation
S. pneumoniae resistance to penicillin arises exclusively through altered penicillin-binding proteins (PBPs), particularly PBP2b and PBP2x, which are acquired through horizontal transfer from closely related streptococci and have reduced affinity for beta-lactams. Unlike staphylococci, pneumococci do not produce beta-lactamases. Efflux pumps and porin changes are mechanisms seen in Gram-negative bacteria; pneumococci lack an outer membrane. This mechanism necessitates higher-dose amoxicillin or switching to ceftriaxone/respiratory fluoroquinolones for high-level resistance.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.