An isolate of Staphylococcus aureus from a patient failing azithromycin therapy shows resistance to erythromycin, clarithromycin, and clindamycin on routine testing. The single molecular event that best explains this combined pattern is:
- A Methylation of the 23S ribosomal RNA adenine residue encoded by erm genes ✓
- B Efflux pump overexpression encoded by mef genes
- C Mutation of the L4 and L22 ribosomal proteins
- D Acquisition of a plasmid-encoded macrolide hydrolase
Explanation
erm-encoded ribosomal RNA methylase modifies an adenine residue in 23S rRNA near the peptidyl transferase center, blocking binding of macrolides, lincosamides, and streptogramins A alike. This produces the constitutive or inducible MLSb phenotype explaining simultaneous resistance to azithromycin and clindamycin. mef-encoded efflux pumps confer resistance only to 14- and 15-membered macrolides and leave clindamycin susceptible. Ribosomal protein mutations occur but cause low-level, narrow resistance and are uncommon in staphylococci.
Reference: Goodman and Gilman's The Pharmacological Basis of Therapeutics, 14th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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