| Summary: | Fluoroquinolone resistance and the associated genetic mechanisms were assessed by antimicrobial susceptibility and whole genome sequencing in 56 <i>Pseudomonas aeruginosa</i> strains from human, animal, food and environmental origins. <i>P. aeruginosa</i> PAO1, PA7 and PA14 reference strains were also included in the study. Twenty-two strains (37%) were resistant to, at least, one fluoroquinolone agent. Correlation between the number of changes in GyrA and ParC proteins and the level of fluoroquinolone resistance was observed. Mutations or absence of genes, such as <i>mexZ</i>, <i>mvaT</i> and <i>nalD</i> encoding efflux pumps regulators, were also found in resistant strains. The <i>crpP</i> gene was detected in 43 strains (72.9%; 17 of them non-clinical strains), and coded seven different CrpP variants, including a novel one (CrpP-7). The <i>crpP</i> gene was located in 23 different chromosomal mobile integrative and conjugative elements (ICEs), inserted in two tRNAs integration sites. A great variety of structures was detected in the <i>crpP</i>-ICEs elements, e.g., the fimbriae related <i>cup</i> clusters, the mercury resistance <i>mer</i> operon, the pyocin S5 or S8 bacteriocin encoding genes, and mobilization genes. The location of <i>crpP</i>-like genes in mobilizable ICEs and linked to heavy metal resistance and virulence factors is of significant concern in <i>P. aeruginosa</i>. This work provides a genetic explanation of the fluoroquinolone resistance and <i>crpP</i>-associated pathogenesis of <i>P. aeruginosa</i> from a One-Health approach.
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