An erythromycin-resistant isolate of Streptococcus pyogenes is found to also show resistance to clarithromycin, azithromycin, clindamycin, and streptogramins. The single molecular mechanism that best explains this combined phenotype is:

• A Efflux of all these drugs through a common transporter
• B Production of a phosphotransferase that inactivates macrolides
• C Methylation of adenine in 23S rRNA encoded by erm genes, reducing ribosomal binding ✓
• D Mutation of the L4 ribosomal protein altering the peptide exit tunnel

Explanation

erm-encoded ribosomal methylase methylates an adenine residue of 23S rRNA at or near the peptidyl transferase center. Because erythromycin, clindamycin, streptogramin C, and related drugs share this overlapping binding region, methylation produces cross-resistance to the whole MLSb group. Efflux encoded by mef genes covers macrolides only, which kills option A, and enzymatic inactivation does not explain clindamycin resistance.

Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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