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Antimicrobial Agents and Chemotherapy, February 2006, p. 649-653, Vol. 50, No. 2
0066-4804/06/$08.00+0 doi:10.1128/AAC.50.2.649-653.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
Servei de Microbiología, Centre de Diagnostic Biomèdic, Hospital Clinic, IDIBAPS, Facultat de Medicina, Universitat de Barcelona, Barcelona, Spain
Received 18 April 2005/ Returned for modification 29 June 2005/ Accepted 23 November 2005
Escherichia coli is the most common microorganism causing urinary tract infections. Quinolone-resistant E. coli strains have fewer virulence factors than quinolone-susceptible strains. Several urovirulence genes are located in pathogenicity islands (PAIs). We investigated the capacity of quinolones to induce loss of virulence factors such as hemolysin, cytotoxic necrotizing factor 1, P fimbriae, and autotransporter Sat included in PAIs in three uropathogenic E. coli strains. In a multistep selection, all strains lost hemolytic capacity at between 1 and 4 passages when they were incubated with subinhibitory concentrations of ciprofloxacin, showing a partial or total loss of the PAI containing the hly (hemolysin) and cnf-1 (cytotoxic necrotizing factor 1) genes. RecA mutants were obtained from the two E. coli strains with partial or total loss of the PAI. The inactivation of the RecA protein affected only the partial loss of the PAI induced by quinolones. No spontaneous loss of PAIs was observed on incubation in the absence of quinolones in either the wild-type or mutant E. coli strains. Quinolones induce partial or total loss of PAIs in vitro in uropathogenic E. coli by SOS-dependent or -independent pathways, respectively.
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