Plasmid-Mediated Quinolone Resistance in Clinical Isolates of Escherichia coli from Shanghai, China

Abstract

Although quinolone resistance usually results from chromosomal mutations, recent studies indicate that quinolone resistance can also be plasmid mediated. The gene responsible, qnr, is distinct from the known quinolone resistance genes and in previous studies seemed to be restricted to Klebsiella pneumoniae and Escherichia coli isolates from the University of Alabama in Birmingham, where this resistance was discovered. In Shanghai, the frequency of ciprofloxacin resistance in E. coli has exceeded 50% since 1993. Seventy-eight unique ciprofloxacin-resistant clinical isolates of E. coli from Shanghai hospitals were screened for the qnr gene by colony blotting and Southern hybridization of plasmid DNA. Conjugation experiments were done with azide-resistant E. coli J53 as a recipient with selection for plasmid-encoded antimicrobial resistance (chloramphenicol, gentamicin, or tetracycline) and azide counterselection. qnr genes were sequenced, and the structure of the plasmid DNA adjacent to qnr was analyzed by primer walking with a sequential series of outward-facing sequencing primers with plasmid DNA templates purified from transconjugants. Six (7.7%) of 78 strains gave a reproducible hybridization signal with a qnr gene probe on colony blots and yielded strong signals on plasmid DNA preparations. Quinolone resistance was transferred from all six probe-positive strains. Transconjugants had 16-to 250-fold increases in the MICs of ciprofloxacin relative to that of the recipient. All six strains contained qnr with a nucleotide sequence identical to that originally reported, except for a single nucleotide change (CTA3CTG at position 537) encoding the same amino acid. qnr was located in complex In4 family class 1 integrons. Two completely sequenced integrons were designated In36 and In37. Transferable plasmid-mediated quinolone resistance associated with qnr is thus prevalent in quinoloneresistant clinical strains of E. coli from Shanghai and may contribute to the rapid increase in bacterial resistance to quinolones in China.

PMQR determinants among clinical isolates of ESBL and Amp C producing Serratia marcescens in Mansoura University Hospitals: A six year study

“…Moreover, this gene was the most common among ESBL producers signifying the relation between this gene and other resistance genes as observed by other researchers [22][23][24][25]. In contrast to the current results, the data reported by Yang et al [3], found that the aac(6′)-Ib-cr gene was the most prevalent among S. marcescens ESBL producers.…”

Carriage of Class 1 and 2 Integrons in Quinolone, Extended-Spectrum-β-Lactamase-Producing and Multi Drug Resistant E.coli and K.pneumoniae: High Burden of Antibiotic Resistance

“…Several reports are available on the mechanism of quinolone resistance in either E.coli or K.pneumoniae or even both or quinolone resistance in ESBL producing bacteria; however, no report is available on the actual resistance of nalidixic acid and ciprofloxacin in these two isolates [29][30][31][32][33][34][35] , except few published studies on urinary isolates, [36][37][38][39][40] whereby low prevalence has been reported as compared to our study. Study performed in our neighboring country reported 17% and 38% of E. coli isolates obtained from uncomplicated and complicated UTI respectively, were found resistant to ciprofloxacin.…”

Prevalence of IncI1-Iγ and IncFIA-FIB type plasmids in extended-spectrum β-lactamase-producing Klebsiella pneumoniae strains isolated from the NICU of a North Indian hospital

“…Transconjugants were screened by double selection method on a Luria-Bertani agar plate containing sodium azide (100 mg l 21 ) and cefotaxime (4 mg l 21 ) or ceftazidime (4 mg l 21 ). Furthermore, aminoglycoside markers were also screened in the presence of sodium azide (100 mg l 21 ) and amikacin (30 mg l 21 ) (Wang et al, 2003). Moreover, susceptibility testing of transconjugants was carried out by disc diffusion and micro-dilution methods.…”