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      Virulence factors and antimicrobial resistance in uropathogenic Escherichia coli strains isolated from cystitis and pyelonephritis

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          Abstract

          Background/aim

          The aim of this study was to investigate the prevalence of virulence genes as well as patterns of antibiotic resistance in cystitis and pyelonephritis uropathogenic Escherichia coli (UPEC) isolates.

          Materials and methods

          Two hundred UPEC isolates were collected from hospitalized patients with pyelonephritis (n = 50) and cystitis (n = 150) in Shafa Hospital in Iran. Antimicrobial susceptibility and ESBL production were determined with confirmatory tests. Polymerase chain reaction assay was performed to determine the prevalence of virulence genes in UPEC strains.

          Results

          Of a total 200 UPEC isolates, the highest and lowest resistance rates to antibiotics were for cephalexin (74%) and nitrofurantoin (9%), respectively. Of these isolates, 72 (36%) and 128 (64%) strains were ESBL-positive and ESBL-negative, respectively. The frequency of fimH, papC, and hly was 64%, 38%, and 12%, respectively. The most commonly identified virulence gene in ESBL-positive and ESBL-negative strains was fimH 46 (23%) and 86 (43%), respectively. The hlyA gene was more prevalent among patients with pyelonephritis than cystitis.

          Conclusion

          The frequency of virulence genes was not significantly different between pyelonephritis and cystitis UPEC strains in the studied patients, but the prevalence rates of hlyA and papC genes were higher among UPEC strains isolated from inpatients compared to outpatients; hence, they could be considered as useful targets for prophylactic interventions.

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          Most cited references28

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          Extended-spectrum β-lactamases in Gram Negative Bacteria

          Extended-spectrum β-lactamases (ESBLs) are a group of plasmid-mediated, diverse, complex and rapidly evolving enzymes that are posing a major therapeutic challenge today in the treatment of hospitalized and community-based patients. Infections due to ESBL producers range from uncomplicated urinary tract infections to life-threatening sepsis. Derived from the older TEM is derived from Temoniera, a patient from whom the strain was first isolated in Greece. β-lactamases, these enzymes share the ability to hydrolyze third-generation cephalosporins and aztreonam and yet are inhibited by clavulanic acid. In addition, ESBL-producing organisms exhibit co-resistance to many other classes of antibiotics, resulting in limitation of therapeutic option. Because of inoculum effect and substrate specificity, their detection is also a major challenge. At present, however, organizations such as the Clinical and Laboratory Standards Institute (formerly the National Committee for Clinical Laboratory Standards) provide guidelines for the detection of ESBLs in Klebsiella pneumoniae, K. oxytoca, Escherichia coli and Proteus mirabilis. In common to all ESBL-detection methods is the general principle that the activity of extended-spectrum cephalosporins against ESBL-producing organisms will be enhanced by the presence of clavulanic acid. Carbapenems are the treatment of choice for serious infections due to ESBL-producing organisms, yet carbapenem-resistant isolates have recently been reported. ESBLs represent an impressive example of the ability of gram-negative bacteria to develop new antibiotic-resistance mechanisms in the face of the introduction of new antimicrobial agents. Thus there is need for efficient infection-control practices for containment of outbreaks; and intervention strategies, e.g., antibiotic rotation to reduce further selection and spread of these increasingly resistant pathogens.
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            Origins and virulence mechanisms of uropathogenic Escherichia coli.

            Strains of uropathogenic E. coli (UPEC) are the primary cause of urinary tract infections, including both cystitis and pyelonephritis. These bacteria have evolved a multitude of virulence factors and strategies that facilitate bacterial growth and persistence within the adverse settings of the host urinary tract. Expression of adhesive organelles like type 1 and P pili allow UPEC to bind and invade host cells and tissues within the urinary tract while expression of iron-chelating factors (siderophores) enable UPEC to pilfer host iron stores. Deployment of an array of toxins, including hemolysin and cytotoxic necrotizing factor 1, provide UPEC with the means to inflict extensive tissue damage, facilitating bacterial dissemination as well as releasing host nutrients and disabling immune effector cells. These toxins also have the capacity to modulate, in more subtle ways, host signaling pathways affecting myriad processes, including inflammatory responses, host cell survival, and cytoskeletal dynamics. Here, we discuss the mechanisms by which these and other virulence factors promote UPEC survival and growth within the urinary tract. Comparisons are also made between UPEC and other strains of extraintestinal pathogenic E. coli that, although closely related to UPEC, are distinct in their abilities to colonize the host and cause disease.
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              Distribution of uropathogenic virulence genes in Escherichia coli isolated from patients with urinary tract infection.

              Escherichia coli is the predominant pathogen causing urinary tract infection (UTI), the most common bacterial infectious disease encountered in clinical practice, accounting for significant morbidity and high medical costs. The severity of UTI produced by E. coli is due to the expression of a wide spectrum of virulence factors. In this study we evaluated the role of E. coli virulence determinants in the pathogenesis of UTI. A total of 90 uropathogenic E. coli strains were screened by PCR for the prevalence of seven virulence genes encoding type 1 fimbriae (fimH), pili associated with pyelonephritis (pap), S and F1C fimbriae (sfa and foc), afimbrial adhesins (afa), cytotoxic necrotizing factor (cnf), hemolysin (hly), and aerobactin (aer). The prevalence of genes coding for fimbrial adhesive systems was 68% for fimH, 41% for pap, and 34% for sfa/foc. The operons coding for afa afimbrial adhesins were identified in 20% of strains. The hly and cnf genes coding for toxins were amplified in 19% and 3% of strains, respectively. A prevalence of 52% was found for the aer gene. The various combinations of detected genes were designated as virulence patterns. The strains isolated from hospitalized patients displayed a great diversity of gene associations compared to those isolated from ambulatory patients. Our study showed that investigation of the bacterial pathogenicity associated with UTI may contribute to a better medical intervention. Copyright © 2013 International Society for Infectious Diseases. Published by Elsevier Ltd. All rights reserved.
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                Author and article information

                Journal
                Turk J Med Sci
                Turk J Med Sci
                Turkish Journal of Medical Sciences
                The Scientific and Technological Research Council of Turkey
                1300-0144
                1303-6165
                2019
                11 February 2019
                : 49
                : 1
                : 361-367
                Affiliations
                [1 ] Department of Biology, Damghan Branch, Islamic Azad University, Damghan Iran
                [2 ] Department of Microbiology, Kerman Branch, Islamic Azad University, Kerman Iran
                [3 ] Department of Microbiology, Faculty of Medicine, Iran University of Medical Sciences, Tehran Iran
                [4 ] Azarbaijan-Gharbi Regional Blood Transfusion Center, Urmia Iran
                [5 ] Institute of Immunology and Infectious Disease, Iran University of Medical Sciences, Tehran Iran
                Author notes
                * To whom correspondence should be addressed. E-mail: mirkalantari.sh@ 123456iums.ac.ir

                CONFLICT OF INTEREST:

                none declared

                Author information
                https://orcid.org/0000-0002-8440-3928
                https://orcid.org/0000-0002-5341-7382
                https://orcid.org/0000-0002-5730-3964
                https://orcid.org/0000-0002-8361-2904
                https://orcid.org/0000-0003-2158-8598
                Article
                10.3906/sag-1805-100
                7350878
                30761847
                1c6ab380-66d7-4ee8-b02b-d5a73b88cbda
                Copyright © 2019 The Author(s)

                This article is distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use and redistribution provided that the original author and source are credited.

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                Categories
                Article

                urinary tract infections,escherichia coli,antimicrobial resistance, virulence genes, cystitis, pyelonephritis

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