| dc.description.abstract | Background: Despite intensive care and treatment strategies, the development of antibiotic resistance to empirical drugs is concerning. Objectives: The aim of this study was to characterize extended-spectrum?-lactamase (ESBL)-producing Escherichia coli and Klebsiella pneumoniae for integron-mediated quinolone resistance and multidrug resistance (MDR). Methods: In this cross-sectional study, 71 E. coli and 63 K. pneumoniae clinical isolates underwent antibiotic susceptibility testing with the Kirby-Bauer method, followed by ESBL phenotypic screening with the combination disc method. The isolates were then genotypically characterized with PCR for the presence of integrons and the gyrA, parC, blaCTX-M-3, blaTEM, and blaSHV genes. Resistance to antibiotics was confirmed by sequencing. Results: K. pneumoniae was a potent ESBL producer (71.4%) in comparison to E. coli (57.7%). The predominant ESBL genotypes in E. coli and K. pneumoniae confirmed by sequencing were blaCTX-M-15 (67.60%) and blaSHV-1 (80.95%), respectively. Imipenem was the only antibiotic active against the ESBL-producing isolates. Approximately 54% of the isolates exhibited MDR patterns. MDR was more frequently related to the presence of blaCTX-M-3 in comparison to other genotypes. The prevalence of class 1 integrons was 15 (45.4%) and 22 (66.6%) of the E. coli and K. pneumonia isolates, respectively. Within the ESBL group, a class 1 genetic element was associated with the blaCTX-M-3 genotype in E. coli (36.58%) and K. pneumoniae (51.11%). Overall, almost half of the ESBL producers, irrespective of genus, were simultaneously resistant to quinolones. The simultaneous presence of class 1 and 2 integrons in quinolone-resistant isolates was the most frequent observation. Conclusions: The high prevalence of multidrug and ESBL-mediated resistance is a therapeutic concern. The co-emergence of ESBLs and quinolone resistance in E. coli and K. pneumoniae suggests the preservation of the power of antibiotics in the face of the antibiotic-resistance crisis. é 2016, Pediartric Infections Research Center. | |
