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      Antimicrobial resistance patterns and virulence factors of enterococci isolates in hospitalized burn patients

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          Abstract

          Objective

          The objective of this study was to determine the frequency of the antimicrobial resistance and genes encoding virulence factors of enterococci isolated in hospitalized burn patients in a major burn center in Ahvaz, southwest of Iran. A total of 340 bacterial isolates were collected from the burn center from February 2014 to February 2015. The antimicrobial susceptibility and MIC of vancomycin were determined using the disk diffusion and micro-agar dilution techniques. The genus and species-specific genes, potential virulence genes, and vanA and vanB genes were detected by polymerase chain reaction.

          Results

          According to our results, out of the 340 bacterial isolates, 16.4% (n = 56) were identified as enterococci. Out of the 56 enterococcal isolates, 35 (62.5%) were Enterococcus faecalis and 21 (37.5%) were Enterococcus faecium. More than 20% (n = 5) of E. faecium demonstrated resistance to vancomycin. The gelE and asa genes were the most prevalent virulence genes in E. faecalis (48.5%) and E. faecium (43%) isolates. The emergence of vancomycin resistant E. faecium strains which have several virulence factors should be considered as a major cause of concern for burn centers. Control and management of infections induced by enterococci should be regarded as highly important in burn patients.

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          Molecular screening of Enterococcus virulence determinants and potential for genetic exchange between food and medical isolates.

          T J Eaton, M. J. Gasson (2001)
          Enterococci are used as starter and probiotic cultures in foods, and they occur as natural food contaminants. The genus Enterococcus is of increased significance as a cause of nosocomial infections, and this trend is exacerbated by the development of antibiotic resistance. In this study, we investigated the incidence of known virulence determinants in starter, food, and medical strains of Enterococcus faecalis, E. faecium, and E. durans. PCR and gene probe strategies were used to screen enterococcal isolates from both food and medical sources. Different and distinct patterns of incidence of virulence determinants were found for the E. faecalis and E. faecium strains. Medical E. faecalis strains had more virulence determinants than did food strains, which, in turn, had more than did starter strains. All of the E. faecalis strains tested possessed multiple determinants (between 6 and 11). E. faecium strains were generally free of virulence determinants, with notable exceptions. Significantly, esp and gelE determinants were identified in E. faecium medical strains. These virulence determinants have not previously been identified in E. faecium strains and may result from regional differences or the evolution of pathogenic E. faecium. Phenotypic testing revealed the existence of apparently silent gelE and cyl genes. In E. faecalis, the trend in these silent genes mirrors that of the expressed determinants. The potential for starter strains to acquire virulence determinants by natural conjugation mechanisms was investigated. Transconjugation in which starter strains acquired additional virulence determinants from medical strains was demonstrated. In addition, multiple pheromone-encoding genes were identified in both food and starter strains, indicating their potential to acquire other sex pheromone plasmids. These results suggest that the use of Enterococcus spp. in foods requires careful safety evaluation.
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            Development of a multiplex PCR for the detection of asa1, gelE, cylA, esp, and hyl genes in enterococci and survey for virulence determinants among European hospital isolates of Enterococcus faecium.

            Vanessa Vankerckhoven, Tim Van Autgaerden, Carl Vael … (2004)
            A multiplex PCR for the simultaneous detection of five virulence genes (asa1, gelE, cylA, esp, and hyl) in enterococci was developed. The presence of these genes was investigated in 153 clinical and 118 fecal Enterococcus faecium isolates from inpatients at an increased risk of developing infections (such as patients in intensive care units and hematology wards) from 13 hospitals in eight European countries. Of the 271 E. faecium isolates, 135 were vancomycin resistant E. faecium (VREF) isolates and 136 were vancomycin susceptible E. faecium (VSEF) isolates. Susceptibilities to ampicillin, gentamicin, streptomycin, vancomycin, teicoplanin, ramoplanin, quinupristin-dalfopristin, and linezolid were tested by the microdilution method. Overall, the prevalence of esp was significantly higher (P = 0.03) in clinical VREF isolates (92%) than in fecal VREF isolates (73%). In Italy, the prevalence of esp was significantly higher (P = 0.02) in VREF isolates (91%) than in VSEF isolates (68%), whereas in the United Kingdom, hyl was significantly more prevalent (P = 0.01) in VREF isolates (71%) than in VSEF isolates (29%). No significant differences were found for the other countries. Pulsed-field gel electrophoresis was used to check the clonality among the strains tested and showed the spread of two center-specific (esp-positive) VREF clones in Italy and one center-specific (hyl-positive) clone in the United Kingdom. These clones were resistant to ampicillin, gentamicin, and streptomycin. The multiplex PCR reported in this study is a convenient and rapid method for the simultaneous detection of the virulence genes asa1, gelE, cylA, esp, and hyl in enterococci. Molecular analysis showed the intrahospital spread of esp-positive VREF clones (in Italy) and hyl-positive VREF clones (in the United Kingdom); the role of hyl remains to be elucidated.
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              Relationships between enterococcal virulence and antimicrobial resistance.

              L M Mundy, D Sahm, M. Gilmore (2000)
              Enterococci have become a vexing problem in clinical medicine because of their ability to infect patients who are typically receiving antibiotic therapy for unrelated underlying illness. Moreover, the infections have become extremely difficult to manage because of the accumulation of antibiotic resistances among enterococci. The ability of enterococci to cause disease is an intrinsic property of the organism or possibly subpopulations within enterococcal species. The probability of an infection's becoming established, however, is almost certainly in part a function of the enterococcal burden. By altering endogenous bacterial flora, antibiotic therapy promotes increased colonization by antibiotic-resistant organisms. Therefore, antibiotic resistance and intrinsic virulence both contribute to disease, but in separate and complementary ways. We review the virulence of enterococci, as distinct from the acquisition of antimicrobial resistance genes, and identify current gaps in our understanding of enterococcal virulence and the basis for disease.
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                Author and article information

                Contributors
                Leili Shokoohizadeh: shokoohizadeh@yahoo.com
                Alireza Ekrami: + 98983373825 , +989166064072 , aekrami@yahoo.com , ekrami@ajums.ac.ir
                Maryam Labibzadeh: labibzadeh4@yahoo.com
                Liaqat Ali: liaqatbiotech@gmail.com
                Seyed Mohammad Alavi: alavi1329dr@yahoo.com
                Journal
                Journal ID (nlm-ta): BMC Res Notes
                Journal ID (iso-abbrev): BMC Res Notes
                Title: BMC Research Notes
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1756-0500
                Publication date (Electronic): 2 January 2018
                Publication date PMC-release: 2 January 2018
                Publication date Collection: 2018
                Volume: 11
                Electronic Location Identifier: 1
                Affiliations
                [1 ]ISNI 0000 0000 9296 6873, GRID grid.411230.5, Infectious and Tropical Diseases Research Center, Health Research Institute, , Ahvaz Jundishapur University of Medical Sciences, ; P.O. Box: 61357-15794, Ahvaz, Iran
                [2 ]ISNI 0000 0000 9296 6873, GRID grid.411230.5, Department of Medical Laboratory Sciences, Faculty of Para Medicine, , Ahvaz Jundishapur University of Medical Sciences, ; P.O. Box: 61357-15794, Ahvaz, Iran
                [3 ]Infertility Research and Treatment Center of Jahad Daneshgahi, Khuzestan, Ahvaz, Iran
                [4 ]ISNI 0000 0000 9428 7911, GRID grid.7708.8, Department of Internal Medicine II, , University Hospital Freiburg, ; Freiburg, Germany
                [5 ]Department of Molecular Medicine, National University of Medical Sciences, Rawalpindi/Islamabad, Pakistan
                Article
                Publisher ID: 3088
                DOI: 10.1186/s13104-017-3088-5
                PMC ID: 5749016
                PubMed ID: 29291749
                SO-VID: b186673e-c209-4e8c-a557-eb5235b878db
                Copyright © © The Author(s) 2017
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 22 August 2017
                Date accepted : 13 December 2017
                Categories
                Subject: Research Note
                Custom metadata
                issue-copyright-statement © The Author(s) 2018

                ScienceOpen disciplines: Medicine
                Keywords: enterococci,vancomycin resistant,virulence genes,burn
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: enterococci, vancomycin resistant, virulence genes, burn

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