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Genetic Basis of Emerging Vancomycin, Linezolid, and Daptomycin Heteroresistance in a Case of Persistent Enterococcus faecium Bacteremia.

Authors
  • Chacko, Kieran I1
  • Sullivan, Mitchell J1
  • Beckford, Colleen1
  • Altman, Deena R2
  • Ciferri, Brianne1
  • Pak, Theodore R1
  • Sebra, Robert1
  • Kasarskis, Andrew1
  • Hamula, Camille L3
  • van Bakel, Harm4
  • 1 Icahn Institute for Genomics and Multiscale Biology, Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
  • 2 Division of Infectious Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
  • 3 Department of Pathology, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
  • 4 Icahn Institute for Genomics and Multiscale Biology, Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, New York, USA [email protected]
Type
Published Article
Journal
Antimicrobial Agents and Chemotherapy
Publisher
American Society for Microbiology
Publication Date
Apr 01, 2018
Volume
62
Issue
4
Identifiers
DOI: 10.1128/AAC.02007-17
PMID: 29339387
Source
Medline
Keywords
License
Unknown

Abstract

Whole-genome sequencing was used to examine a persistent Enterococcus faecium bacteremia that acquired heteroresistance to three antibiotics in response to prolonged multidrug therapy. A comparison of the complete genomes before and after each change revealed the emergence of known resistance determinants for vancomycin and linezolid and suggested that a novel mutation in fabF, encoding a fatty acid synthase, was responsible for daptomycin nonsusceptibility. Plasmid recombination contributed to the progressive loss of vancomycin resistance after withdrawal of the drug.

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