qnrS — Plasmid-mediated quinolone resistance

Mechanism

A Qnr protein that protects DNA gyrase and topoisomerase IV from quinolones.

What it removes from the grid

Fluoroquinolones are downgraded.

What it spares

Other classes are unaffected.

A multiplex panel can't say which organism in a mixed specimen carries a detected gene. CORE-ABR applies qnrS only to organisms known to carry it, and only to the agents its mechanism defeats — so a detected gene moves the right cells and spares the rest.

Organisms it is applied to

Escherichia coliThe most common cause of urinary tract infection, and a frequent organism in wound and intra-abdominal specimens.Gram-negative bacteria · UTI · Wound Klebsiella pneumoniae / oxytocaCommon uropathogens and a leading host of ESBL and KPC carbapenemase genes.Gram-negative bacteria · UTI · Wound · STI Pseudomonas aeruginosaA non-fermenting gram-negative bacillus common in chronic wounds and complicated UTI, with a long list of intrinsic resi…Gram-negative bacteria · UTI · Wound · STI

Coding

Z16.23 (resistance to quinolones and fluoroquinolones), as documentation supports. CORE-ABR adds resistance findings as supporting codes, not primary, and prints the rationale on the report.

Tagged

Decision support only. The treating clinician decides. Molecular genotype does not replace phenotypic susceptibility testing, culture, or public-health reporting. Absence of a detected resistance gene does not establish susceptibility. Organism targets vary by panel; CORE-ABR is configured to the assay each laboratory runs.