Investigation of extended spectrum beta-lactamase and quinolone resistance in Serratia marcescens strains isolated from clinical samples

Objective: This study aimed to investigate the ESBL production and sensitivity to quinolone group antibiotics and to demonstrate the mechanism of plasmid-mediated resistance spread of Serratia marcescens strains isolated from clinical samples at Karadeniz Technical University Medical Microbiology Laboratory between January 2018 and December 2022. Materials and Methods: In this study S. marcescens isolates were identified by conventional methods and matrix assisted laser desorption ıonization time-of-flight (MALDI-TOF) (Bruker, Germany). In addition to these methods, S-adenosylhomocysteine nucleosidase (pfs) and S-ribosylhomocysteinase (luxS) genes were screened by the polymerase chain reaction (PCR). Antimicrobial susceptibility testing was determined using an automated system and disc diffusion method. ESBL production in isolates that were not sensitive to ceftazidime and/or cefotaxime was determined by cefepime/cefepime + clavulanate strip test and blaTEM, blaSHV, blaCTX-M and blaOXA genes were screened by PCR. Conjugation experiments were performed ESBL positive strains. Plasmid-mediated quinolone resistance genes, qnrA, qnrB, qnrS, aac-(6')-Ib and qepA were screened by PCR in strains that were not sensitive to ciprofloxacin and/or levofloxacin. Results: pfs and luxS genes were postive in all S. marcescens. In strains that were not sensitive to ceftazidime and/or cefotaxime, ESBL production was detected in one strain by gradient strip test and 9.3% (n=4) blaTEM, 4.7% (n=2) blaSHV, 2.3% (n=1) blaCTX-M. No blaOXA postive strains were found. No conjugative plasmid was detected in any ESBL producer strains. 2.3% (n=1) qnrA, 7% (n=3) qnrS and 4.7% (n=2) aac(6')-Ib genes were found in not sensivite to ciprofloxacin and/or levofloxacin strains. No qnrB and qepA postive strains were found. Conclusion: As a result, this study provides epidemiological data on ESBL production of S. marcescens in our region and quinolone resistance mechanisms, leading to both national antimicrobial resistance research and the determination of empirical treatment protocols.