A Staphylococcus aureus isolate from a wound is resistant to erythromycin. When tested against clindamycin using the D-test, flattening of the clindamycin zone around the erythromycin disc indicates inducible resistance. The molecular basis shared by all drugs in the affected group is:
- A Mutations in ribosomal protein L22 altering the peptide exit tunnel
- B Plasmid-mediated acetyltransferase modification of the drug
- C erm-encoded methylation of 23S rRNA at the ribosomal binding site ✓
- D Active efflux driven by the mef transporter alone
Explanation
Macrolides, lincosamides, and streptogramin B antibiotics share overlapping binding sites on the 23S rRNA of the 50S subunit. Methylation of adenine residues in 23S rRNA encoded by erm genes sterically blocks binding of all three groups, producing the MLSB phenotype. The D-test demonstrates inducible expression of this methylase. Efflux via mef pumps affects mainly macrolides, and L22 mutations alter exit tunnel geometry without conferring lincosamide resistance.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.