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      Control of Fluoroquinolone Resistance through Successful Regulation, Australia

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          Abstract

          Restricted Fluoroquinolone use in humans and food animals has result in low rates of resistance in human pathogens

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          Most cited references30

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          The worldwide emergence of plasmid-mediated quinolone resistance.

          Fluoroquinolone resistance is emerging in gram-negative pathogens worldwide. The traditional understanding that quinolone resistance is acquired only through mutation and transmitted only vertically does not entirely account for the relative ease with which resistance develops in exquisitely susceptible organisms, or for the very strong association between resistance to quinolones and to other agents. The recent discovery of plasmid-mediated horizontally transferable genes encoding quinolone resistance might shed light on these phenomena. The Qnr proteins, capable of protecting DNA gyrase from quinolones, have homologues in water-dwelling bacteria, and seem to have been in circulation for some time, having achieved global distribution in a variety of plasmid environments and bacterial genera. AAC(6')-Ib-cr, a variant aminoglycoside acetyltransferase capable of modifying ciprofloxacin and reducing its activity, seems to have emerged more recently, but might be even more prevalent than the Qnr proteins. Both mechanisms provide low-level quinolone resistance that facilitates the emergence of higher-level resistance in the presence of quinolones at therapeutic levels. Much remains to be understood about these genes, but their insidious promotion of substantial resistance, their horizontal spread, and their co-selection with other resistance elements indicate that a more cautious approach to quinolone use and a reconsideration of clinical breakpoints are needed.
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            Mechanisms of resistance to quinolones: target alterations, decreased accumulation and DNA gyrase protection.

            Quinolones are broad-spectrum antibacterial agents, commonly used in both clinical and veterinary medicine. Their extensive use has resulted in bacteria rapidly developing resistance to these agents. Two mechanisms of quinolone resistance have been established to date: alterations in the targets of quinolones, and decreased accumulation due to impermeability of the membrane and/or an overexpression of efflux pump systems. Recently, mobile elements have also been described, carrying the qnr gene, which confers resistance to quinolones.
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              In vitro antimicrobial resistance of urinary Escherichia coli isolates among U.S. outpatients from 2000 to 2010.

              This study examines in vitro antimicrobial resistance data from Escherichia coli isolates obtained from urine samples of U.S. outpatients between 2000 and 2010 using The Surveillance Network (TSN). Antimicrobial susceptibility results (n = 12,253,679) showed the greatest increases in E. coli resistance from 2000 to 2010 for ciprofloxacin (3% to 17.1%) and trimethoprim-sulfamethoxazole (TMP-SMX) (17.9% to 24.2%), whereas nitrofurantoin (0.8% to 1.6%) and ceftriaxone (0.2% to 2.3%) showed minimal change. From 2000 to 2010, the antimicrobial resistance of urinary E. coli isolates to ciprofloxacin and TMP-SMX among outpatients increased substantially.

                Author and article information

                Journal
                Emerg Infect Dis
                Emerging Infect. Dis
                EID
                Emerging Infectious Diseases
                Centers for Disease Control and Prevention
                1080-6040
                1080-6059
                September 2012
                : 18
                : 9
                : 1453-1460
                Affiliations
                [-1-1]Monash University, Melbourne, Victoria, Australia (A.C. Cheng);
                [-1-2]Alfred Hospital, Melbourne (A.C. Cheng);
                [-1-3]Women’s and Children’s Hospital, Adelaide, South Australia, Australia (J. Turnidge);
                [-1-4]University of Adelaide, Adelaide (J. Turnidge);
                [-1-5]The Canberra Hospital, Garran, Canberra, Australia (P. Collignon);
                [-1-6]Australian National University, Canberra (P. Collignon);
                [-1-7]Princess Alexandra Hospital, Brisbane, Queensland, Australia (D. Looke);
                [-1-8]University of Queensland, Brisbane (D. Looke);
                [-1-9]University of South Australia, Adelaide (M. Barton);
                [-1-10]Concord Hospital, Sydney, New South Wales, Australia (T. Gottlieb);
                [-1-11]and University of Sydney, Sydney (T. Gottlieb)
                [-2-1]Monash University, Melbourne, Victoria, Australia (A.C. Cheng);
                [-2-2]Alfred Hospital, Melbourne (A.C. Cheng);
                [-2-3]Women’s and Children’s Hospital, Adelaide, South Australia, Australia (J. Turnidge);
                [-2-4]University of Adelaide, Adelaide (J. Turnidge);
                [-2-5]The Canberra Hospital, Garran, Canberra, Australia (P. Collignon);
                [-2-6]Australian National University, Canberra (P. Collignon);
                [-2-7]Princess Alexandra Hospital, Brisbane, Queensland, Australia (D. Looke);
                [-2-8]University of Queensland, Brisbane (D. Looke);
                [-2-9]University of South Australia, Adelaide (M. Barton);
                [-2-10]Concord Hospital, Sydney, New South Wales, Australia (T. Gottlieb);
                [-2-11]and University of Sydney, Sydney (T. Gottlieb)
                [-3-1]Monash University, Melbourne, Victoria, Australia (A.C. Cheng);
                [-3-2]Alfred Hospital, Melbourne (A.C. Cheng);
                [-3-3]Women’s and Children’s Hospital, Adelaide, South Australia, Australia (J. Turnidge);
                [-3-4]University of Adelaide, Adelaide (J. Turnidge);
                [-3-5]The Canberra Hospital, Garran, Canberra, Australia (P. Collignon);
                [-3-6]Australian National University, Canberra (P. Collignon);
                [-3-7]Princess Alexandra Hospital, Brisbane, Queensland, Australia (D. Looke);
                [-3-8]University of Queensland, Brisbane (D. Looke);
                [-3-9]University of South Australia, Adelaide (M. Barton);
                [-3-10]Concord Hospital, Sydney, New South Wales, Australia (T. Gottlieb);
                [-3-11]and University of Sydney, Sydney (T. Gottlieb)
                Author notes
                Address for correspondence: Thomas Gottlieb, Department of Infectious Diseases and Microbiology, Concord Hospital, Hospital Road, Concord, NSW, 2139, Australia; email: thomas.gottlieb@ 123456sswahs.nsw.gov.au
                Address for correspondence: Thomas Gottlieb, Department of Infectious Diseases and Microbiology, Concord Hospital, Hospital Road, Concord, NSW, 2139, Australia; email: thomas.gottlieb@ 123456sswahs.nsw.gov.au
                Article
                11-1515
                10.3201/eid1809.111515
                3437704
                22932272
                334d67bd-ac1f-4521-9618-7c65da56c523
                History
                Categories
                CME
                Policy Review
                Policy Review

                Infectious disease & Microbiology
                bacterial drug resistance,antimicrobial drug resistance,fluoroquinolones,health policy,human,animal,bacteria,australia

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