Phenotypic and genetic determinants of quinolone resistance in Escherichia coli at the human-swine interface of an agroecological farm.

Quinolone-resistant Escherichia coli are increasing in humans and livestock; however, their distribution and underlying mechanisms in shared environments remain incompletely characterized. We analyzed quinolone resistance in E. coli isolates from swine (n = 100) and humans (n = 65) associated with an agroecological farm in Morelos, Mexico. Antimicrobial susceptibility testing was performed for quinolones [nalidixic acid (NAL) and ciprofloxacin (CIP)], and the minimum inhibitory concentrations were determined. Phylogenetic grouping and genotypic analyses targeting gyrA mutations and plasmid-mediated quinolone resistance (PMQR) genes were conducted. High frequencies of NAL and moderate CIP resistance were observed in both swine (NAL, 79%; CIP, 23%) and human (NAL, 65%; CIP, 15%) isolates. The predominant phenotype was NAL-resistant/CIP-susceptible, particularly among commensals of phylogroups A and B1. High-level resistance to both antimicrobials was associated with double mutations in gyrA (S83L + D87N), whereas PMQR determinants, including qnr variants and aac(6')-Ib-cr, were widely distributed and linked to lower-level resistance. These findings indicate that quinolone resistance is shaped by the combined contribution of chromosomal mutations and plasmid-mediated mechanisms. The presence of PMQR determinants in isolates with reduced susceptibility highlights their potential role in the early stages of resistance development, emphasizing the urgent need for integrated surveillance of antimicrobial resistance in agricultural and community settings.