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      Characterization of Plasmid-Mediated Quinolone Resistance and Serogroup Distributions of Uropathogenic Escherichia coli among Iranian Kidney Transplant Patients

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      BioMed Research International
      Hindawi

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          Abstract

          Introduction

          Urinary tract infection (UTI) is one of the most frequent infections in kidney transplant patients (KTPs). This infection is mainly caused by uropathogenic Escherichia coli (UPEC). Plasmid-mediated quinolone resistance (PMQR) was also increasingly identified in UPEC. This study proposed to investigate the frequency of quinolone-resistance plasmid genes and the O-antigen serogroup among UPEC isolated from KTPs and non-KTP with UTI.

          Methods

          Totally, 114 UPEC isolates from 49 KTPs and 65 non-KTPs patients diagnosed with an UPEC-associated UTI were obtained from June 2019 to December 2019 at three laboratory centers in Isfahan, Iran. The isolates were confirmed through phenotypic and genotypic methods. Moreover, the antimicrobial susceptibility test to nalidixic acid, ciprofloxacin, norfloxacin, and ofloxacin was performed using a disk diffusion method. The presence of the qnr gene as well as the serogroup distribution was identified using the PCR method.

          Result

          According to data, the distribution of O1, O2, O4, O16, and O25 serogroups were 3.5%, 2.6, 3.5, 3.5, and 20.2%, respectively. Antibiotic susceptibility pattern revealed that the highest and lowest resistance rates were to nalidixic acid (69.3%) and norfloxacin (43.9%), respectively. Also, the frequency of qnrS and qnrB genes were 33.3% and 15.8%, respectively, while none of the isolates was found to be positive for the qnrA gene. There was no significant association between the presence of qnr genes and higher antibiotic resistance.

          Conclusion

          This study recognized that the qnrS gene, O25 serotype, and resistance to nalidixic acid had the highest frequencies in UPEC strains isolated from UTI patients.

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          Most cited references37

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          Diarrheagenic Escherichia coli

          Escherichia coli is the predominant nonpathogenic facultative flora of the human intestine. Some E. coli strains, however, have developed the ability to cause disease of the gastrointestinal, urinary, or central nervous system in even the most robust human hosts. Diarrheagenic strains of E. coli can be divided into at least six different categories with corresponding distinct pathogenic schemes. Taken together, these organisms probably represent the most common cause of pediatric diarrhea worldwide. Several distinct clinical syndromes accompany infection with diarrheagenic E. coli categories, including traveler’s diarrhea (enterotoxigenic E. coli), hemorrhagic colitis and hemolytic-uremic syndrome (enterohemorrhagic E. coli), persistent diarrhea (enteroaggregative E. coli), and watery diarrhea of infants (enteropathogenic E. coli). This review discusses the current level of understanding of the pathogenesis of the diarrheagenic E. coli strains and describes how their pathogenic schemes underlie the clinical manifestations, diagnostic approach, and epidemiologic investigation of these important pathogens.
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            Mechanisms of drug resistance: quinolone resistance.

            Quinolone antimicrobials are synthetic and widely used in clinical medicine. Resistance emerged with clinical use and became common in some bacterial pathogens. Mechanisms of resistance include two categories of mutation and acquisition of resistance-conferring genes. Resistance mutations in one or both of the two drug target enzymes, DNA gyrase and DNA topoisomerase IV, are commonly in a localized domain of the GyrA and ParE subunits of the respective enzymes and reduce drug binding to the enzyme-DNA complex. Other resistance mutations occur in regulatory genes that control the expression of native efflux pumps localized in the bacterial membrane(s). These pumps have broad substrate profiles that include quinolones as well as other antimicrobials, disinfectants, and dyes. Mutations of both types can accumulate with selection pressure and produce highly resistant strains. Resistance genes acquired on plasmids can confer low-level resistance that promotes the selection of mutational high-level resistance. Plasmid-encoded resistance is due to Qnr proteins that protect the target enzymes from quinolone action, one mutant aminoglycoside-modifying enzyme that also modifies certain quinolones, and mobile efflux pumps. Plasmids with these mechanisms often encode additional antimicrobial resistances and can transfer multidrug resistance that includes quinolones. Thus, the bacterial quinolone resistance armamentarium is large.
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              A simple and rapid method for the preparation of gram-negative bacterial genomic DNA.

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                Author and article information

                Contributors
                Journal
                Biomed Res Int
                Biomed Res Int
                BMRI
                BioMed Research International
                Hindawi
                2314-6133
                2314-6141
                2020
                27 October 2020
                : 2020
                : 2850183
                Affiliations
                Department of Microbiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
                Author notes

                Academic Editor: Yun Peng Chao

                Author information
                https://orcid.org/0000-0002-5629-8817
                https://orcid.org/0000-0002-4576-8203
                https://orcid.org/0000-0002-0383-6722
                https://orcid.org/0000-0002-3353-336X
                Article
                10.1155/2020/2850183
                7641683
                33195692
                daf30ca4-b849-4e73-b5e0-1bd876a25919
                Copyright © 2020 Amin Sadeghi et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 26 June 2020
                : 12 August 2020
                : 22 October 2020
                Funding
                Funded by: Isfahan University of Medical Science
                Award ID: 398312
                Categories
                Research Article

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