Outbreak of vancomycin-susceptible Enterococcus faecium containing the wild-type vanA gene - PubMed (original) (raw)

Outbreak of vancomycin-susceptible Enterococcus faecium containing the wild-type vanA gene

Tom A Szakacs et al. J Clin Microbiol. 2014 May.

Abstract

Accurate detection of vancomycin-resistant enterococci (VRE) is essential in preventing transmission in health care settings. Chromogenic media are widely used for screening VRE because of fast turnaround times (TAT) and high sensitivity. We report an outbreak of Enterococcus faecium bearing vanA yet susceptible to vancomycin (vancomycin-variable Enterococcus [VVE]). Between October 2009 to March 2011, clinical and screening specimens (n=14,747) were screened for VRE using VRE-selective medium and/or PCR. VVE isolates were genotyped to determine relatedness. Plasmids from these isolates were characterized by sequencing. Overall, 52 VVE isolates were identified, comprising 15% of all VRE isolates identified. Isolates demonstrated growth on Brilliance VRE agar (Oxoid) at 24 h of incubation but did not grow on brain heart infusion agar with 6 μg/ml vancomycin (Oxoid) or bile esculin azide agar with 6 μg/ml vancomycin (Oxoid) and were susceptible to vancomycin. Genotyping of 20 randomly selected VVE isolates revealed that 15/20 were identical, while 5 were highly related. PCR of the VVE transposon confirmed the presence of vanHAXY gene cluster; however, vanS (sensor) and vanR (regulator) genes were absent. The outbreak was controlled through routine infection control measures. We report an emergence of a fit strain of E. faecium containing vanA yet susceptible to vancomycin. Whether this new strain represents VRE has yet to be determined; however, unique testing procedures are required for reliable identification of VVE.

PubMed Disclaimer

Figures

FIG 1

FIG 1

Genetic map and PCR amplification position of Tn_1546_. A schematic diagram of overlapping primers used to amplify and detect the transposon is shown.

FIG 2

FIG 2

Genetic map of the full-length 31,136-bp plasmid, pF856. Coding regions are represented by arrows indicating the direction of transcription. Insertion sequence elements and type 1 RM-S are shown in gray, and Tn_1546_ transposon elements are in white. Putative ORFs are labeled according to the most significant homologue (pS177) in the public databases.

FIG 3

FIG 3

Pulse-field gel electrophoresis (PFGE) patterns of VVE strains. Chromosomal DNA was digested with SmaI.

Similar articles

Cited by

References

    1. Woodford N. 2001. Epidemiology of the genetic elements responsible for acquired glycopeptide resistance in enterococci. Microb. Drug Resist. 7:229–236. 10.1089/10766290152652774 - DOI - PubMed
    1. Leclercq R, Derlot E, Duval J, Courvalin P. 1988. Plasmid-mediated resistance to vancomycin and teicoplanin in Enterococcus faecium. N. Engl. J. Med. 319:157–161. 10.1056/NEJM198807213190307 - DOI - PubMed
    1. Ofner-Agostini M, Johnston BL, Simor AE, Embil J, Matlow A, Mulvey M, Ormiston D, Conly J, Canadian Nosocomial Infection Surveillance Program 2008. Vancomycin-resistant enterococci in Canada: results from the Canadian nosocomial infection surveillance program, 1999–2005. Infect. Control Hosp. Epidemiol. 29:271–274. 10.1086/528812 - DOI - PubMed
    1. Arthur M, Courvalin P. 1993. Genetics and mechanisms of glycopeptide resistance in enterococci. Antimicrob. Agents Chemother. 37:1563–1571. 10.1128/AAC.37.8.1563 - DOI - PMC - PubMed
    1. Carmeli Y, Eliopoulos G, Mozaffari E, Samore M. 2002. Health and economic outcomes of vancomycin-resistant enterococci. Arch. Intern. Med. 162:2223–2228. 10.1001/archinte.162.19.2223 - DOI - PubMed

Publication types

MeSH terms

Substances

LinkOut - more resources