Abstract
Genetic context of extended spectrum β-Lactamase (ESBL) producing Enterobacterales and its association with plasmid mediated quinolone resistance (PMQR), aminoglycoside modifying enzymes (AME) and Trimethoprim/Sulfamethoxazole (TMP-SMX) resistance is little known from North India. Therefore, the current study was aimed to investigate the frequency of Non-β-Lactam antibiotic resistance associated genes in extended spectrum β-Lactamase producing Enterobacterales. For this study, Non-Duplicate phenotypically confirmed ESBL producing Enterobacterales isolates (N = 186) were analyzed for ESBLs, PMQRs, AMEs and TMP-SMX resistance genes using polymerase chain reaction (PCR). PCR detected presence of PMQR genes in 81.29% (N = 139) of ESBL isolates (N = 171), AME genes in 60.82% and TMP-SMX resistance genes in 63.74% of the isolates. Molecular characterization of ESBL producing Enterobacterales showed 84.79% blaTEM followed by 73.68% blaCTX-M, 43.86% blaSHV, 19.88% blaPER and 9.94% blaVEB, respectively. Analysis of PMQR genes revealed 77.7% aac(6′)-lb-cr the most commonly detected gene followed by 67.63% oqxB, 62.59% oqxA, 43.17% qnrB, 19.42% qnrD, 18.7% qnrS, 9.35% qnrA, 3.6% qepA and 2.88% qnrC, respectively. Analysis of AMEs gene profile demonstrated 81.73% aac(6′)-Ib, the most frequently encountered gene followed by 46.15% aph(3′)-Ia, 44.23% ant(3”)-Ia, respectively. A 100% prevalence of sul1, followed by dfrA (54.63%) and sul2 (15.74%) was observed. In summary, prevalence of ESBL-Producing genes (particularly blaTEM and blaCTX-M) along with PMQR, AMEs, and TMP-SMX resistant genes may potentially aid in the transfer of antimicrobial resistance among these strains.
Highlights
Introduction βLactam antibiotics are used for treating most of the human infections that are caused byGram-negative bacteria belonging to the family Enterobacterales [1]
Genes coding for ESBLs production are often located on plasmids that carry genes coding for resistance to fluoroquinolones, aminoglycosides, trimethoprimsulfamethoxazole (TMP-SMX) [1]
The current study demonstrated widespread occurrence of plasmid mediated quinolone resistance (PMQR), aminoglycoside modifying enzymes (AME), and TMP-SMX drug resistant genetic determinants in the ESBL producing Enterobacterales strains
Summary
Introduction βLactam antibiotics are used for treating most of the human infections that are caused byGram-negative bacteria belonging to the family Enterobacterales [1]. Lactam antibiotics are used for treating most of the human infections that are caused by. Genes coding for ESBLs production are often located on plasmids that carry genes coding for resistance to fluoroquinolones, aminoglycosides, trimethoprimsulfamethoxazole (TMP-SMX) [1]. A high level of fluoroquinolone resistance was reported among ESBLs producing Enterobacterales [2,3]. Chromosomal mutations and plasmid-mediated quinolone resistance (PMQR) are considered the most relevant mechanisms of fluoroquinolone resistance among Enterobacterales [4,5]. PMQR determinants produce low-level of quinolone resistance, reports reveal that the presence of PMQR determinants may enhance the degree of chromosomal mediated quinolone resistance if present in the same strain [3,6,7,8]. PMQRs are mainly categorized into three groups; (i) quinolone resistance (qnr) gene mediated (ii) quinolones modifying aminoglycoside acetyltransferase encoding genes (aac(60 )-Ib-c), (iii) plasmid-mediated quinolone efflux pumps qepA, oqxA, and oqxB [6]
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