An isolate of Neisseria gonorrhoeae shows a high ceftriaxone MIC with a wild-type beta-lactamase-negative profile. Molecular analysis reveals a mosaic penA gene. The resistance mechanism demonstrated here involves:

• A Plasmid-encoded TEM-1 beta-lactamase hydrolyzing cephalosporins
• B Efflux pump overexpression encoded by tetM determinants
• C Altered penicillin-binding protein 2 acquired by recombination from commensal Neisseria species ✓
• D Mutation of the 23S rRNA gene reducing drug binding

Explanation

Reduced susceptibility to third-generation cephalosporins in gonococci is chromosomal and driven by mosaic penA alleles encoding an altered PBP2 with reduced affinity for ceftriaxone and cefixime; these mosaics arose by horizontal recombination with commensal Neisseria species such as N. flavescens and N. cinerea. Plasmid TEM-1 enzyme accounts for penicillin resistance in PPNG strains but does not explain cephalosporin resistance. Efflux (mtrCDE) contributes modestly, and 23S rRNA mutations underlie macrolide resistance, not cephalosporin resistance.

Reference: Harrison's Principles of Internal Medicine, 21st ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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