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      Plasmid-mediated fluoroquinolone resistance associated with extra-intestinal Escherichia coli isolates from hospital samples

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          Abstract

          Background & objectives:

          Infection from fluoroquinolone-resistant extra-intestinal Escherichia coli is a global concern. In this study, isolation and characterization of fluoroquinolone-resistant extra-intestinal E. coli isolates obtained from hospital samples were undertaken to detect plasmid-mediated quinolone resistance ( PMQR) genes.

          Methods:

          Forty three isolates of E. coli obtained from patients with extra-intestinal infections were subjected to antibiogram to detect fluoroquinolone resistance. The mechanism of fluoroquinolone resistance was determined by the detection of PMQR genes and mutations in quinolone resistance determining region (QRDR).

          Results:

          Of the 43 isolates, 36 were resistant to nalidixic acid (83.72%) and 28 to ciprofloxacin (65.11%). Eight E. coli isolates showed total resistance to both the antimicrobials without any minimum inhibitory concentration. The detection of PMQR genes with qnr primers showed the presence of qnrA in two, qnrB in six and qnrS in 21 isolates. The gene coding for quinolone efflux pump ( qepA) was not detected in any of the isolates tested. The presence of some unexpressed PMQR genes in fluoroquinolone sensitive isolates was also observed.

          Interpretation & conclusions:

          The detection of silent PMQR genes as observed in the present study presents a risk of the transfer of the silent resistance genes to other microorganisms if present in conjugative plasmids, thus posing a therapeutic challenge to the physicians. Hence, frequent monitoring is to be done for all resistance determinants.

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          Most cited references32

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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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            Food Reservoir for Escherichia coli Causing Urinary Tract Infections

            Closely related strains of Escherichia coli have been shown to cause extraintestinal infections in unrelated persons. This study tests whether a food reservoir may exist for these E. coli. Isolates from 3 sources over the same time period (2005–2007) and geographic area were compared. The sources comprised prospectively collected E. coli isolates from women with urinary tract infection (UTI) (n = 353); retail meat (n = 417); and restaurant/ready-to-eat foods (n = 74). E. coli were evaluated for antimicrobial drug susceptibility and O:H serotype and compared by using 4 different genotyping methods. We identified 17 clonal groups that contained E. coli isolates (n = 72) from >1 source. E. coli from retail chicken (O25:H4-ST131 and O114:H4-ST117) and honeydew melon (O2:H7-ST95) were indistinguishable from or closely related to E. coli from human UTIs. This study provides strong support for the role of food reservoirs or foodborne transmission in the dissemination of E. coli causing common community-acquired UTIs.
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              Emergence of plasmid-mediated resistance to quinolones in Enterobacteriaceae.

              Although quinolone resistance results mostly from chromosomal mutations in Enterobacteriaceae, it may also be mediated by plasmid-encoded Qnr determinants. Qnr proteins protect DNA from quinolone binding and compromise the efficacy of quinolones such as nalidixic acid. Qnr proteins (QnrA-like, QnrB and QnrS) have been identified worldwide with a quite high prevalence among Asian isolates with a frequent association with clavulanic acid inhibited expanded-spectrum beta-lactamases and plasmid-mediated cephalosporinases. The qnrA genes are embedded in complex sul1-type integrons. A very recent identification of the origin of QnrA determinants in the water-borne species Shewanella algae underlines the role of the environment as a reservoir for this emerging threat. It may help to determine the location of in vivo transfer of qnrA genes. Further analysis of the role (if any) of quinolones for enhancing this gene transfer may be conducted. This could prevent the spread, if still possible, of this novel antibiotic resistance mechanism.
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                Author and article information

                Journal
                Indian J Med Res
                Indian J. Med. Res
                IJMR
                The Indian Journal of Medical Research
                Wolters Kluwer - Medknow (India )
                0971-5916
                February 2019
                : 149
                : 2
                : 192-198
                Affiliations
                [1 ] Division of Infectious Diseases, Mangaluru, India
                [2 ] Department of Microbiology, Madras Medical Mission, Chennai, India
                [] Nitte University Centre for Science Education & Research, Mangaluru, India
                Author notes
                For correspondence: Dr Indrani Karunasagar, Nitte Centre for Science Education and Research, Kotekar-Beeri Road, Paneer Campus, Derelakatte, Mangalore 575 018, Karnataka, India e-mail: indrani.karunasagar@ 123456nitte.edu.in
                Article
                IJMR-149-192
                10.4103/ijmr.IJMR_2092_17
                6563729
                31219083
                985968b6-af44-40b8-9ea3-469c944af44a
                Copyright: © 2019 Indian Journal of Medical Research

                This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

                History
                : 30 December 2017
                Categories
                Original Article

                Medicine
                antibiotic resistance,plasmid-mediated quinolone resistances,quinolone resistance determining regions

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