Early ReportQuinolone resistance from a transferable plasmid
Introduction
Quinolone resistance is increasing in clinical isolates and has reached a minimum inhibitory concentration (MIC) in Escherichia coli of 256 μg/mL for ciprofloxacin.1, 2, 3 The mechanisms for this resistance involve chromosomal mutations that modify DNA gyrase or DNA topoisomerase IV, the targets of quinolone action, or result in decreased quinolone accumulation.4, 5 Plasmid-mediated resistance to nalidixic acid in Shigella dysenteriae was reported in 1987,6 but has never been confirmed.7 We investigated the ability of a multiresistance plasmid in hospital isolates of Klebsiella pneumoniae and E coli from southern USA, to encode transferable resistance to nalidixic acid, ciprofloxacin, and other fluoroquinolones.
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Methods
β-lactam-resistant clinical isolates of K pneumoniae and E coli were provided by Dr Ken B Waites, University of Alabama, USA, as part of a study on the prevalence of extended-spectrum β-lactamases. Whether resistance was transferable was investigated by mating to E coli J53 (requiring methionine and proline and resistant to sodium azide) with selection on trypticase soy agar, containing 100 μg/mL of sodium azide and 10 μg/mL ceftazidime.8 We measured antimicrobial susceptibility of
Results
Quinolone resistance was discovered inadvertently during a study of the properties of a plasmid, pMG252, that gives broad resistance to β-lactam antibiotics. The plasmid came from a ciprofloxacin-resistant strain of K pneumoniae (strain UAB1) isolated in July, 1994, from the urine of a patient at the University of Alabama. On transfer to E coli J53, plasmid pMG252 conferred resistance to aztreonam, ceftazidime, cefotaxime, cefoxitin, cefotetan, chloramphenicol, kanamycin, gentamicin,
Discussion
Surveys in the 1970s failed to detect transferable resistance to nalidixic acid,16 but in 1987, Munshi and colleagues6 reported transfer of resistance and a 30 kb plasmid to E coli from a nalidixic-acid-resistant strain of S dysenteriae. In retrospect, the presumed transconjugants were probably resistant mutants,7 because they were selected with nalidixic acid and had no other plasmid-mediated resistances. Serial transfer of the plasmid was not attempted, and its elimination with acridine
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