Dietary trehalose enhances virulence of epidemic Clostridium difficile

J. Collins, C. Robinson, H. Danhof, C. W. Knetsch, H. C. van Leeuwen, T. D. Lawley, J. M. Auchtung and R. A. Britton ()
Additional contact information
J. Collins: Baylor College of Medicine, One Baylor Plaza
C. Robinson: University of Oregon, Institute for Molecular Biology
H. Danhof: Baylor College of Medicine, One Baylor Plaza
C. W. Knetsch: Leiden University Medical Centre
H. C. van Leeuwen: Leiden University Medical Centre
T. D. Lawley: Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus
J. M. Auchtung: Baylor College of Medicine, One Baylor Plaza
R. A. Britton: Baylor College of Medicine, One Baylor Plaza

Nature, 2018, vol. 553, issue 7688, 291-294

Abstract: 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.

Date: 2018
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DOI: 10.1038/nature25178

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