In-host evolution of Yersinia enterocolitica during a chronic human infection

Cyril Savin (), Pierre Lê-Bury, Julien Guglielmini, Thibaut Douché, Guillem Mas Fiol, Rodolphe Buzelé, Cécile Brun, Frédéric Bastides, Maud François, Béatrice Birmelé, Laura Guichard, Julien Madej, Rémi Beau, Nicolas Cabanel, Laurent Dortet, Mariette Matondo, Olivier Dussurget, Elisabeth Carniel, Philippe Lanotte and Javier Pizarro-Cerdá ()
Additional contact information
Cyril Savin: Yersinia Research Unit
Pierre Lê-Bury: Yersinia Research Unit
Julien Guglielmini: Biostatistics and Bioinformatics Hub
Thibaut Douché: Mass Spectrometry for Biology Unit
Guillem Mas Fiol: Yersinia Research Unit
Rodolphe Buzelé: CHRU de Tours
Cécile Brun: CHRU de Tours
Frédéric Bastides: CHRU de Tours
Maud François: CHRU de Tours
Béatrice Birmelé: CHRU de Tours
Laura Guichard: Yersinia Research Unit
Julien Madej: Yersinia Research Unit
Rémi Beau: Yersinia Research Unit
Nicolas Cabanel: Yersinia Research Unit
Laurent Dortet: Center for Immunology of Viral, Auto-immune, Hematological and Bacterial diseases (IMVA-HB/IDMIT/UMRS1184)
Mariette Matondo: Mass Spectrometry for Biology Unit
Olivier Dussurget: Yersinia Research Unit
Elisabeth Carniel: Yersinia Research Unit
Philippe Lanotte: CHRU de Tours
Javier Pizarro-Cerdá: Yersinia Research Unit

Nature Communications, 2025, vol. 16, issue 1, 1-17

Abstract: Abstract Bacteria exhibit remarkable adaptability in response to selective pressures encountered during infection and antibiotic treatment. We characterize four Yersinia enterocolitica clonal isolates from successive bacteremia episodes that evolved within an elderly patient over 14 years. Their common evolution is characterized by a genome size reduction resulting in the loss of about a hundred genes and a so far undescribed deletion in the DNA gyrase gene gyrA conferring quinolone resistance. Third-generation cephalosporin resistance of the last isolate correlates with a truncation of OmpF in synergy with an increased production of BlaA and AmpC β-lactamases. A strong proteome remodeling of the isolates reveals a perturbed stringent response, as well as impaired metabolism which substantiate their severe growth defects in vitro, accounting for antibiotics tolerance and possibly therapeutic failure. This study documents previously unreported genetic and phenotypic changes associated with in-host adaptation of a pathogenic Yersinia species under antibiotic pressure.

Date: 2025
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DOI: 10.1038/s41467-025-60782-6

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