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Background and Aim: The prevalence of fluoroquinolone resistance among Pseudomonas aeruginosa isolates, particularly in burn wound infections, has been increasing. The primary cause of ciprofloxacin resistance is attributed to genetic alterations in the quinolone resistance determinant region (QRDR). In this study, we evaluated the antimicrobial resistance profile and QRDR gene mutations in both ciprofloxacin-resistant and non-resistant strains of P. aeruginosa derived from burn wound patients. Materials and Methods: A total of 300 samples were collected from patients with burn wound infections in Guilan, Iran. The isolates were identified as P. aeruginosa, and drug susceptibility tests were conducted using the agar disk diffusion method. DNA extraction and polymerase chain reaction (PCR) analysis were performed for the amplification and sequencing of gyrA, gyrB, parC, and parE genes in the QRDR region. Results: Resistance to Tobramycin, Gentamicin, Piperacillin, Ciprofloxacin, Ceftazidime, and Amikacin was observed in 59.32%, 55.08%, 51.69%, 50.84%, 30.50%, and 26.27% of the isolates, respectively. Forty-two (35.59%) isolates were multidrug- resistant (MDR). The sequencing results in the QRDR region showed that the majority of mutations were in the gyrA gene, with 85.71% of these mutations being the substitution of threonine with isoleucine (Thr-83 Ile) in ciprofloxacinresistant strains. Conclusion: The results of this study indicate that mutations in the gyrA (gyrase gene) are a significant mechanism of resistance to fluoroquinolones. Identifying these mutations can aid in the detection of fluoroquinolone-resistant isolates and simplify treatment challenges by selecting the appropriate antibiotic. [ABSTRACT FROM AUTHOR]

The global dissemination of multidrug-resistant Escherichia coli lineages belonging to high- risk clones poses a significant public health threat. Herein we report the identification and genomic profiling of two multidrug-resistant E. coli strains [BL-II-03(2) and BL-II-11(3)] belonging to the O15:H1-D-ST393 (clonal complex 31) worldwide spread clone, isolated from fecal samples of indigenous peoples belonging to two different ethnic groups of remote communities of Brazilian Amazon. Genomic analysis revealed genes and mutations conferring resistance to β-lactams bla TEM-1 , aminoglycosides aadA5 , aph(3″)-Ib , aph(6)-Id , tetracyclines tetB , sulfamethoxazole/trimethoprim sul1 , sul2 , dfrA17 , and fluoroquinolones gyrA (D87N, S83L), parC (S80I, S57T), parE (L416F)]; and presence of IncQ1, IncFIA, and IncFIB(pB171) plasmids. On the other hand, phylogenomics of globally reported E. coli ST393 assigned E. coli strains BL-II-03(2) and BL-II-11(3) to a cluster comprising human isolates from Australia, Canada, China, Sweden, and United States of America. These results might provide valuable information for understanding dissemination of intercontinental multidrug-resistant clones in remote communities with low levels of antibiotic exposure. • Occurrence of MDR Enterobacterales in remote communities of Amazon was investigated. • Fluoroquinolone-resistant E. coli were identified in fecal samples of indigenous peoples. • Genomic data revealed the presence of the international high-risk clone O15:H1-D-ST393. • Wide resistome and gyrA , parC and parE mutations were responsible for MDR phenotype. • Emergence of international MDR E. coli clones in remote communities is discussed. [ABSTRACT FROM AUTHOR]