#Microbiota-derived #lantibiotic restores resistance against #vancomycin-resistant #Enterococcus (Nature, abstract)

[Source: Nature, full page: (LINK). Abstract, edited.]

Microbiota-derived lantibiotic restores resistance against vancomycin-resistant Enterococcus

Sohn G. Kim, Simone Becattini, […] Eric G. Pamer

Nature (2019)

 

Abstract

Intestinal commensal bacteria can inhibit dense colonization of the gut by vancomycin-resistant Enterococcus faecium (VRE), a leading cause of hospital-acquired infections1,2. A four-strained consortium of commensal bacteria that contains Blautia producta BPSCSK can reverse antibiotic-induced susceptibility to VRE infection3. Here we show that BPSCSK reduces growth of VRE by secreting a lantibiotic that is similar to the nisin-A produced by Lactococcus lactis. Although the growth of VRE is inhibited by BPSCSK and L. lactis in vitro, only BPSCSK colonizes the colon and reduces VRE density in vivo. In comparison to nisin-A, the BPSCSK lantibiotic has reduced activity against intestinal commensal bacteria. In patients at high risk of VRE infection, high abundance of the lantibiotic gene is associated with reduced density of E. faecium. In germ-free mice transplanted with patient-derived faeces, resistance to VRE colonization correlates with abundance of the lantibiotic gene. Lantibiotic-producing commensal strains of the gastrointestinal tract reduce colonization by VRE and represent potential probiotic agents to re-establish resistance to VRE.

Keywords: Antibiotics; Drugs Resistance; Vancomycin; Enterococcus faecium; Lantibiotics; Microbiota.

——

Emergence of #plasmid-mediated #oxazolidinone #resistance #gene poxtA from CC17 #Enterococcus faecium of #pig origin (J Antimicrob Chemother., abstract)

[Source: Journal of Antimicrobial Chemotherapy, full page: (LINK). Abstract, edited.]

Emergence of plasmid-mediated oxazolidinone resistance gene poxtA from CC17 Enterococcus faecium of pig origin

Jinhu Huang, Mengli Wang, Yi Gao, Li Chen, Liping Wang

Journal of Antimicrobial Chemotherapy, dkz250, https://doi.org/10.1093/jac/dkz250

Published: 24 June 2019

 

Abstract

Objectives

To characterize the oxazolidinone resistance gene poxtA on broad-host-range Inc18 plasmids from CC17 Enterococcus faecium of pig origin.

Methods

Oxazolidinone-resistant E. faecium isolates were screened for the presence of poxtA. The poxtA-carrying isolates were characterized by antimicrobial susceptibility testing, conjugation, S1-PFGE and hybridization. The poxtA-carrying plasmids were completely sequenced and their instability was verified.

Results

Two individual CC17 E. faecium strains were positive for poxtA. S1-PFGE and hybridization revealed the presence of a poxtA-carrying plasmid of ∼62 kb in both WZ27-2 and the transconjugant, while poxtA-carrying plasmids of different sizes were observed in QF25-1 and the transconjugant. The two poxtA-carrying plasmids, pC25-1 and pC27-2, belonged to the broad-host-range plasmids of the Inc18 family and carried dfrG, aadE, Δsat4, aph(3′)-III, erm(B), tet(M), tet(L) and fexB. Plasmid pC27-2 was virtually identical to pC25-1, with minor differences. The calculated transfer frequency was ∼0.87 × 10−8 and ∼1.03 × 10−7 per recipient to plasmids pC25-1 and pC27-2, respectively. Instability assays of the region with four adjacent IS1216Es, which forms three IS1216E translocatable units, revealed the formation of a series of mosaic circular intermediates.

Conclusions

We report the emergence of the plasmid-mediated oxazolidinone resistance gene poxtA in E. faecium from different farms in China. Comparison of the poxtAgenetic context suggests that IS1216E elements play an important role in the dissemination of poxtA. The co-occurrence of poxtA with other antimicrobial and heavy metal resistance genes on the broad-host-range plasmids of the Inc18 family may lead to the co-selection of poxtA, contributing to its persistence and accelerating its dissemination.

Topic: plasmids – electrophoresis, gel, pulsed-field – enterococcus faecium – genetics – antimicrobials – antimicrobial susceptibility test – transfer technique – resistance genes

Issue Section: ORIGINAL RESEARCH

© The Author(s) 2019. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For permissions, please email: journals.permissions@oup.com.

This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)

Keywords: Antibiotics; Drugs Resistance; Oxazolidinone; Enterococcus faecium; Pigs.

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#Detection in #Greece of a #clinical #Enterococcus faecium isolate carrying the novel #oxazolidinone #resistance gene poxtA (J Antimicrob Chemother., abstract)

[Source: Journal of Antimicrobial Chemotherapy, full page: (LINK). Abstract, edited.]

Detection in Greece of a clinical Enterococcus faeciumisolate carrying the novel oxazolidinone resistance gene poxtA

Costas C Papagiannitsis, Katerina Tsilipounidaki, Ergina Malli, Efi Petinaki

Journal of Antimicrobial Chemotherapy, dkz155, https://doi.org/10.1093/jac/dkz155

Published: 22 April 2019

___

Sir,

Oxazolidinones possess potent activity against Gram-positive pathogens such as VRE. Soon after their introduction into clinical practice, linezolid-resistant enterococcal isolates were reported.1 Resistance of enterococci to oxazolidines is mainly associated with mutations in 23S rRNA genes and L3 and L4 ribosomal proteins.2 Additionally, transferable resistance determinants including the cfr, optrAand poxtA genes have also emerged.3–5 Here we report, to the best of our knowledge, the first detection of a poxtA-positive Enterococcus faecium strain isolated in Greece.

…E. faecium isolate (Efa-955) was recovered, in 2018, from a urine sample of a patient treated in the University Hospital…

(…)

____

© The Author(s) 2019. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For permissions, please email: journals.permissions@oup.com.

This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)

Keywords: Antibiotics; Drugs Resistance; Linezolid; Enterococcus faecium; Greece.

——

#WGS of 1058 #Enterococcus faecium from Copenhagen, #Denmark, reveals rapid clonal expansion of #vancomycin-resistant clone ST80 combined with widespread dissemination of a vanA-containing #plasmid and acquisition of a heterogeneous accessory genome (J Antimicrob Chemother., abstract9

[Source: Journal of Antimicrobial Chemotherapy, full page: (LINK). Abstract, edited.]

WGS of 1058 Enterococcus faecium from Copenhagen, Denmark, reveals rapid clonal expansion of vancomycin-resistant clone ST80 combined with widespread dissemination of a vanA-containing plasmid and acquisition of a heterogeneous accessory genome

Mette Pinholt, Sion C Bayliss, Heidi Gumpert, Peder Worning, Veronika V S Jensen, Michael Pedersen, Edward J Feil, Henrik Westh

Journal of Antimicrobial Chemotherapy, dkz118, https://doi.org/10.1093/jac/dkz118

Published: 30 March 2019

 

Abstract

Objectives

From 2012 to 2015, a sudden significant increase in vancomycin-resistant (vanA) Enterococcus faecium (VREfm) was observed in the Capital Region of Denmark. Clonal relatedness of VREfm and vancomycin-susceptible E. faecium(VSEfm) was investigated, transmission events between hospitals were identified and the pan-genome and plasmids from the largest VREfm clonal group were characterized.

Methods

WGS of 1058 E. faecium isolates was carried out on the Illumina platform to perform SNP analysis and to identify the pan-genome. One isolate was also sequenced on the PacBio platform to close the genome. Epidemiological data were collected from laboratory information systems.

Results

Phylogeny of 892 VREfm and 166 VSEfm revealed a polyclonal structure, with a single clonal group (ST80) accounting for 40% of the VREfm isolates. VREfm and VSEfm co-occurred within many clonal groups; however, no VSEfm were related to the dominant VREfm group. A similar vanA plasmid was identified in ≥99% of isolates belonging to the dominant group and 69% of the remaining VREfm. Ten plasmids were identified in the completed genome, and ∼29% of this genome consisted of dispensable accessory genes. The size of the pan-genome among isolates in the dominant group was 5905 genes.

Conclusions

Most probably, VREfm emerged owing to importation of a successful VREfm clone which rapidly transmitted to the majority of hospitals in the region whilst simultaneously disseminating a vanA plasmid to pre-existing VSEfm. Acquisition of a heterogeneous accessory genome may account for the success of this clone by facilitating adaptation to new environmental challenges.

Topic: vancomycin – plasmids – heterogeneity – clone cells – denmark – enterococcus  faecium – genes – genome – whole genome sequencing

Issue Section: ORIGINAL RESEARCH

© The Author(s) 2019. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For permissions, please email: journals.permissions@oup.com.

This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)

Keywords: Antibiotics; Drugs Resistance; Vancomycin; Denmark.

——

Expansion of #Vancomycin-resistant #Enterococcus faecium in an academic tertiary #hospital in Southwest #Germany: a large-scale whole genome-based #outbreak investigation (Antimicrob Agents Chemother., abstract)

[Source: Antimicrobial Agents and Chemotherapy, full page: (LINK). Abstract, edited.]

Expansion of Vancomycin-resistant Enterococcus faecium in an academic tertiary hospital in Southwest Germany: a large-scale whole genome-based outbreak investigation

Jan Liese, Leonard Schüle, Philipp Oberhettinger, Leonie Tschörner, Tran Nguyen, Daniela Dörfel, Wichard Vogel, Matthias Marschal, Ingo Autenrieth, Matthias Willmann, Silke Peter

DOI: 10.1128/AAC.01978-18

 

ABSTRACT

Background:

Vancomycin-resistant Enterococcus faecium (VREfm) is a frequent cause of nosocomial outbreaks. In the second half of 2015 a sharp increase in the incidence of VREfmwas observed at our university medical center. Next-generation sequencing (NGS) was used to analyze the first isolates of VREfm recovered from patients between 2010 and 2016 (n=773) in order to decipher epidemiological change, outbreak dynamics, and possible transmission routes.

Materials and methods:

VREfm isolates were analyzed using whole genome sequencing followed by sequence type extraction, and phylogenetic analysis. We examined epidemiological data, room occupancy data, and patient transferals and calculated an intensity score for patient-to-patient contact.

Results:

Phylogenetic analysis revealed the presence of 38 NGS clusters and 110 single clones. The increase of VREfm was mainly caused by the expansion of two newly introduced NGS clusters, comprising VanB-type strains of the MLST sequence type (ST)80 and ST117. Combining phylogenetic information with epidemiological data, intra-hospital transmission could be demonstrated, however to a lesser extent than initially expected based solely on epidemiological data. The outbreak clones were continuously imported from other hospitals, suggesting a change of the epidemiological situation at a regional scale. Tracking intra-hospital patient transferals, two major axes could be identified that contributed to the spread of VREfmwithin the hospital.

Conclusions:

NGS-based outbreak analysis revealed a dramatic change in the local and regional epidemiology of VREfm, emphasizing the role of healthcare networks in the spread of VREfm.

Copyright © 2019 American Society for Microbiology. All Rights Reserved.

Keywords: Antibiotics; Drugs resistance; Enterococcus faecium; Nosocomial outbreaks; Germany.

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Characterization of a new transferable #MDR #plasmid carrying the pbp5 gene from a clade B commensal #Enterococcus faecium (J Antimicrob Chemother., abstract)

[Source: Journal of Antimicrobial Chemotherapy, full page: (LINK). Abstract, edited.]

Characterization of a new transferable MDR plasmid carrying the pbp5 gene from a clade B commensal Enterococcus faecium

Gianluca Morroni, Andrea Brenciani, Alice Litta-Mulondo, Carla Vignaroli, Gianmarco Mangiaterra, Simona Fioriti, Barbara Citterio, Oscar Cirioni, Eleonora Giovanetti, Francesca Biavasco

Journal of Antimicrobial Chemotherapy, dky549, https://doi.org/10.1093/jac/dky549

Published: 10 January 2019

 

Abstract

Objectives

To evaluate the transferability of antibiotic resistance from an MDR clade B Enterococcus faecium and to characterize the genetic elements involved.

Methods

The erm(B)-positive strain E. faecium 37BA (donor) and strains E. faecium 64/3 and Listeria welshimeri 11857RF (recipients) were used in mating experiments. Donors and transconjugants were characterized using MIC assays, PFGE, Southern blotting and hybridization, quantitative RT–PCR (RT–qPCR), next-generation sequencing and PCR mapping.

Results

One E. faecium and one L. welshimeri transconjugant were selected for in-depth investigation. Both acquired an ∼40 kb plasmid carrying erm(B). An additional plasmid of ∼200 kb, encoding the full conjugation machinery, was detected in the donor and in the E. faecium transconjugant. Next-generation sequencing revealed a new 40 396 bp plasmid that was designated pEf37BA; it contained 10 antibiotic resistance genes, tet(M), tet(L), erm(B), aadE, sat4, aphA, spw, lsa(E), lnu(B) and pbp5, resulting from the recombination of pM7M2 of E. faecium with an MDR chromosomal region of Erysipelothrix rhusiopathiae. A pbp5-carrying circular form was also detected. The PBP5 amino acid sequence differed from the C46 variant by two mutations (S39T and D644N). Its expression was documented in both transconjugants. pEf37BA persisted in the absence of selective pressure.

Conclusions

The MDR clade B E. faecium plasmid, deriving from the recombination of two different resistance regions, carried a pbp5 element and was transferable to different bacterial species. This finding further documents the dissemination of ampicillin resistance among community-associated E. faecium and the key role of commensal strains in the spread of antibiotic resistance.

Issue Section: ORIGINAL RESEARCH

© The Author(s) 2019. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For permissions, please email: journals.permissions@oup.com.

This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)

Keywords: Antibiotics; Drugs Resistance; Ampicillin; Enterococcus faecium.

——

#Outbreak of #vancomycin-resistant #Enterococcus faecium clone ST796, #Switzerland, December 2017 to April 2018 (Euro Surveill., abstract)

[Source: Eurosurveillance, full page: (LINK). Abstract, edited.]

Outbreak of vancomycin-resistant Enterococcus faecium clone ST796, Switzerland, December 2017 to April 2018

Nasstasja Wassilew1, Helena MB Seth-Smith2,3, Eveline Rolli1, Yvonne Fietze1, Carlo Casanova4, Urs Führer5,Adrian Egli2,3, Jonas Marschall1, Niccolò Buetti1

Affiliations: 1 Department of Infectious Diseases, University Hospital Bern, Bern, Switzerland; 2 Division of Clinical Microbiology, University Hospital Basel, Basel, Switzerland; 3 Applied Microbiology Research, Department of Biomedicine, University of Basel, Basel, Switzerland; 4 Institute for Infectious Diseases, University of Bern, Bern, Switzerland; 5 Infectious Diseases Department, Biel Hospital, Biel, Switzerland

Correspondence:  Niccolò Buetti

Citation style for this article: Wassilew Nasstasja, Seth-Smith Helena MB, Rolli Eveline, Fietze Yvonne, Casanova Carlo, Führer Urs, Egli Adrian, Marschall Jonas,Buetti Niccolò. Outbreak of vancomycin-resistant Enterococcus faecium clone ST796, Switzerland, December 2017 to April 2018. Euro Surveill. 2018;23(29):pii=1800351. https://doi.org/10.2807/1560-7917.ES.2018.23.29.1800351

Received: 02 Jul 2018;   Accepted: 19 Jul 2018

 

Abstract

A large outbreak of vancomycin-resistant enterococci (VRE) is affecting four hospitals in the Canton of Bern, Switzerland, since December 2017. Of 89 cases identified as carriers, 77 (86.5%) VRE isolates were virtually indistinguishable using whole genome sequencing, and identified as multilocus sequence type (MLST) ST796. This clone, previously only described in Australia and New Zealand, is characterised by rapid spread and the ability to cause bloodstream infections. It requires a multifaceted infection prevention effort.

©  This work is licensed under a Creative Commons Attribution 4.0 International License.

Keywords: Antibiotics; Drugs Resistance; Vancomycin; Enterococcus faecium; Nosocomial Outbreaks.; Switzerland.

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Relentless #spread and #adaptation of non-typeable vanA #vancomycin-resistant #Enterococcus faecium: a genome-wide investigation (J Antimicrob Chemother., abstract)

[Source: Journal of Antimicrobial Chemotherapy, full page: (LINK). Abstract, edited.]

Relentless spread and adaptation of non-typeable vanA vancomycin-resistant Enterococcus faecium: a genome-wide investigation

Sebastiaan J van Hal, Alicia G Beukers, Verlaine J Timms, Justin A Ellem, Peter Taylor, Michael W Maley, Peter J Newton, John K Ferguson, Andie Lee, Sharon C -A Chen, Vitali Sintchenko

Journal of Antimicrobial Chemotherapy, dky074, https://doi.org/10.1093/jac/dky074

Published: 16 March 2018

 

Abstract

Background

VRE are prevalent among patients in ICUs. Non-typeable vanA VRE, due to loss of one of the genes used for MLST (pstS), have increased in Australia, suggestive of a new, hospital-acquired lineage.

Objectives

To understand the significance of this lineage and its transmission using WGS of strains isolated from patients in ICUs across New South Wales, Australia.

Methods

A total of 240 Enterococcus faecium isolates collected between February and May 2016, and identified by conventional PCR as vanA positive, were sequenced. Isolates originated from 12 ICUs in New South Wales, grouped according to six local health districts, and represented both rectal screening swab (n = 229) and clinical (n = 11) isolates.

Results

ST analysis revealed the absence of the pstS gene in 84.2% (202 of 240) of vanAisolates. Two different non-typeable STs were present based on different allelic backbone patterns. Loss of the pstS gene appeared to be the result of multiple recombination events across this region. Evidence for pstS-negative lineage spread across all six local health districts was observed suggestive of inter-hospital transmission. In addition, multiple outbreaks were detected, some of which were protracted and lasted for the duration of the study.

Conclusions

These findings confirmed the evolution, emergence and dissemination of non-typeable vanA E. faecium. This study has highlighted the utility of WGS when attempting to describe accurately the hospital-based pathogen epidemiology, which in turn will continue to inform optimal infection control measures necessary to halt the spread of this important nosocomial organism.

Issue Section: ORIGINAL RESEARCH

© The Author(s) 2018. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please email: journals.permissions@oup.com.

This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices)

Keywords: Antibiotics; Drugs Resistance; Nosocomial Outbreaks; Enterococcus Fecium.

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Identification of a #Botulinum #Neurotoxin-like Toxin in a Commensal Strain of #Enterococcus faecium (Cell Host Microbe, abstract)

[Source: Cell Host & Microbe, full page: (LINK). Abstract, edited.]

Identification of a Botulinum Neurotoxin-like Toxin in a Commensal Strain of Enterococcus faecium

Sicai Zhang7, Francois Lebreton7, Michael J. Mansfield7, Shin-Ichiro Miyashita, Jie Zhang, Julia A. Schwartzman, Liang Tao, Geoffrey Masuyer, Markel Martínez-Carranza, Pål Stenmark, Michael S. Gilmore, Andrew C. Doxey, Min Dong8

7These authors contributed equally

8Lead Contact

Publication stage: In Press Corrected Proof / DOI: https://doi.org/10.1016/j.chom.2017.12.018

Publication History: Published: January 25, 2018 – Accepted: December 14, 2017 – Received in revised form: November 20, 2017 – Received:October 18, 2017

 

Highlights

  • A botulinum neurotoxin-like toxin (BoNT/En) identified in a commensal E. faecium strain
  • The gene cluster encoding BoNT/En is located on a conjugative plasmid
  • BoNT/En cleaves both VAMP2 and SNAP-25 required for synaptic transmission in neurons
  • The cleavage sites on VAMP2 and SNAP25 are distinct from the sites for other known BoNTs

 

Summary

Botulinum neurotoxins (BoNTs), produced by various Clostridium strains, are a family of potent bacterial toxins and potential bioterrorism agents. Here we report that an Enterococcus faecium strain isolated from cow feces carries a BoNT-like toxin, designated BoNT/En. It cleaves both VAMP2 and SNAP-25, proteins that mediate synaptic vesicle exocytosis in neurons, at sites distinct from known BoNT cleavage sites on these two proteins. Comparative genomic analysis determines that the E. faecium strain carrying BoNT/En is a commensal type and that the BoNT/En gene is located within a typical BoNT gene cluster on a 206 kb putatively conjugative plasmid. Although the host species targeted by BoNT/En remains to be determined, these findings establish an extended member of BoNTs and demonstrate the capability of E. faecium, a commensal organism ubiquitous in humans and animals and a leading cause of hospital-acquired multi-drug-resistant (MDR) infections, to horizontally acquire, and possibly disseminate, a unique BoNT gene cluster.

Keywords: botulinum neurotoxin, botulinum toxin, toxin, botulism, VAMP, SNAP-25, SNARE, enterococcus, enterococcus faecium, E. faecium

© 2017 Elsevier Inc.

Keywords: Botulinum Neurotoxins; Enterococcus faecium.

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Novel #multiresistance cfr #plasmids in #linezolid-resistant methicillin-resistant #Staphylococcus epidermidis and #vancomycin-resistant #Enterococcus faecium (VRE) from a hospital outbreak: co-location of cfr and optrA in VRE (J Antimicrob Chemother., abstract)

[Source: Journal of Antimicrobial Chemotherapy, full page: (LINK). Abstract, edited.]

Novel multiresistance cfr plasmids in linezolid-resistant methicillin-resistant Staphylococcus epidermidis and vancomycin-resistant Enterococcus faecium (VRE) from a hospital outbreak: co-location of cfr and optrA in VRE

Alexandros Lazaris, David C. Coleman, Angela M. Kearns, Bruno Pichon, Peter M. Kinnevey, Megan R. Earls, Breida Boyle, Brian O’Connell, Gráinne I. Brennan, Anna C. Shore Anna

Journal of Antimicrobial Chemotherapy, dkx292, https://doi.org/10.1093/jac/dkx292

Published: 28 August 2017 – Received: 09 June 2017 – Revision Requested: 30 June 2017 – Revision Received: 19 July 2017 – Accepted: 19 July 2017

Citation: Alexandros Lazaris, David C. Coleman, Angela M. Kearns, Bruno Pichon, Peter M. Kinnevey, Megan R. Earls, Breida Boyle, Brian O’Connell, Gráinne I. Brennan, Anna C. Shore; Novel multiresistance cfr plasmids in linezolid-resistant methicillin-resistant Staphylococcus epidermidis and vancomycin-resistant Enterococcus faecium (VRE) from a hospital outbreak: co-location of cfr and optrA in VRE, Journal of Antimicrobial Chemotherapy, , dkx292, https://doi.org/10.1093/jac/dkx292

© 2017 Oxford University Press

 

Abstract

Background:

Linezolid is often the drug of last resort to treat infections caused by Gram-positive cocci. Linezolid resistance can be mutational (23S rRNA or L-protein) or, less commonly, acquired [predominantly cfr, conferring resistance to phenicols, lincosamides, oxazolidinones, pleuromutilins and streptogramin A compounds (PhLOPSA) or optrA, encoding oxazolidinone and phenicol resistance].

Objectives:

To investigate the clonality and genetic basis of linezolid resistance in 13 linezolid-resistant (LZDR) methicillin-resistant Staphylococcus epidermidis (MRSE) isolates recovered during a 2013/14 outbreak in an ICU in an Irish hospital and an LZDR vancomycin-resistant Enterococcus faecium (VRE) isolate from an LZDR-MRSE-positive patient.

Methods:

All isolates underwent PhLOPSA susceptibility testing, 23S rRNA sequencing, DNA microarray profiling and WGS.

Results:

All isolates exhibited the PhLOPSA phenotype. The VRE harboured cfr and optrA on a novel 73 kb plasmid (pEF12-0805) also encoding erm(A), erm(B), lnu(B), lnu(E), aphA3 and aadE. One MRSE (M13/0451, from the same patient as the VRE) harboured cfr on a novel 8.5 kb plasmid (pSEM13-0451). The remaining 12 MRSE lacked cfr but exhibited linezolid resistance-associated mutations and were closely related to (1–52 SNPs) but distinct from M13/0451 (202–223 SNPs).

Conclusions:

Using WGS, novel and distinct cfr and cfr/optrA plasmids were identified in an MRSE and VRE isolate, respectively, as well as a cfr-negative LZDR-MRSE ICU outbreak and a distinct cfr-positive LZDR-MRSE from the same ICU. To our knowledge, this is the first report of cfr and optrA on a single VRE plasmid. Ongoing surveillance of linezolid resistance is essential to maintain its therapeutic efficacy.

Topic: phenotype – mutation – plasmids – disease outbreaks – gram-positive cocci – intensive care unit – methicillin – oxazolidinones – single nucleotide polymorphism – rna, ribosomal, 23s – staphylococcus epidermidis – streptogramin a – infection – genetics – linezolid – dna microarrays – lincosamide – surveillance, medical – enterococcus, vancomycin-resistant – clonality (genetic analysis) – pleuromutilins

Issue Section: ORIGINAL RESEARCH

© The Author 2017. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please email: journals.permissions@oup.com.

Keywords: Antibiotics; Drugs Resistance; Enterococcus faecium; Staphylococcus Epidermidis; Vancomycin; Nosocomial Outbreaks.

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