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Dietary trehalose enhances virulence of epidemic Clostridium difficile.

Authors
  • Collins, J1
  • Robinson, C2
  • Danhof, H1
  • Knetsch, C W3
  • van Leeuwen, H C3
  • Lawley, T D4
  • Auchtung, J M1
  • Britton, R A1
  • 1 Baylor College of Medicine, Department of Molecular Virology and Microbiology, One Baylor Plaza, Houston, Texas 77030, USA.
  • 2 University of Oregon, Institute for Molecular Biology, 1318 Franklin Boulevard, Eugene, Oregon 97403, USA.
  • 3 Leiden University Medical Centre, Department of Medical Microbiology, Albinusdreef 2, 2333 ZA Leiden, The Netherlands. , (Netherlands)
  • 4 Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire CB10 1SA, UK.
Type
Published Article
Journal
Nature
Publisher
Springer Nature
Publication Date
Jan 18, 2018
Volume
553
Issue
7688
Pages
291–294
Identifiers
DOI: 10.1038/nature25178
PMID: 29310122
Source
Medline
License
Unknown

Abstract

Clostridium difficile disease has recently increased to become a dominant nosocomial pathogen in North America and Europe, although little is known about what has driven this emergence. Here we show that two epidemic ribotypes (RT027 and RT078) have acquired unique mechanisms to metabolize low concentrations of the disaccharide trehalose. RT027 strains contain a single point mutation in the trehalose repressor that increases the sensitivity of this ribotype to trehalose by more than 500-fold. Furthermore, dietary trehalose increases the virulence of a RT027 strain in a mouse model of infection. RT078 strains acquired a cluster of four genes involved in trehalose metabolism, including a PTS permease that is both necessary and sufficient for growth on low concentrations of trehalose. We propose that the implementation of trehalose as a food additive into the human diet, shortly before the emergence of these two epidemic lineages, helped select for their emergence and contributed to hypervirulence.

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