A microbiologist notes that a clinical isolate of Streptococcus pneumoniae has markedly altered penicillin-binding proteins (PBPs) with reduced affinity for beta-lactams. This resistance mechanism differs from beta-lactamase production in that it:
- A Can be overcome by adding beta-lactamase inhibitors such as clavulanate
- B Cannot be overcome by beta-lactamase inhibitors and requires higher doses or alternative antibiotics ✓
- C Is encoded on transferable plasmids and can spread by conjugation
- D Only affects penicillin G and not extended-spectrum cephalosporins
Explanation
Altered PBPs represent intrinsic resistance through chromosomal gene recombination (as in PRSP and MRSA with PBP2a), and the drug-target affinity is reduced. Beta-lactamase inhibitors protect beta-lactams from enzymatic hydrolysis, not from poor PBP binding; therefore adding clavulanate does not restore activity against organisms with altered PBPs. Treatment requires higher antibiotic doses, newer cephalosporins such as ceftriaxone (for PRSP), or entirely different antibiotic classes.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.