During surveillance of a tertiary care ICU, several Klebsiella pneumoniae and E. coli isolates show transferable colistin resistance even between unrelated species. The genetic element and mechanism most consistent with this finding are:
- A Plasmid-borne mcr-1 encoding a phosphoethanolamine transferase that modifies lipid A ✓
- B Chromosomal pmrAB mutations modifying lipid A with 4-aminoarabinose
- C Plasmid-borne armA conferring 16S rRNA methylation
- D Chromosomal mgrB loss activating the PhoPQ pathway
Explanation
mcr-1, first described in China in food animals, is carried on conjugative plasmids and encodes a phosphoethanolamine transferase that adds phosphoethanolamine to lipid B, reducing polymyxin binding. It is the key horizontally transmissible colistin resistance determinant. pmrAB and mgrB alterations also cause polymyxin resistance but are chromosomal and non-transferable; armA mediates aminoglycoside resistance by ribosomal methylation.
Reference: Koneman's Color Atlas and Textbook of Diagnostic Microbiology, 7th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.