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Rapid adaptation drives invasion of airway donor microbiota by Pseudomonas after lung transplantation.

Type of publication Peer-reviewed
Publikationsform Original article (peer-reviewed)
Author Beaume M, Köhler T, Greub G, Manuel O, Aubert J-D, Baerlocher L, Farinelli L, Buckling A, van Delden C, van Delden C,
Project Pseudomonas aeruginosa in lung transplant recipients: adaptation and competition in the new host environment
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Original article (peer-reviewed)

Journal Scientific reports
Volume (Issue) 7
Page(s) 40309 - 40309
Title of proceedings Scientific reports
DOI 10.1038/srep40309


In cystic fibrosis (CF) patients, chronic airway infection by Pseudomonas leads to progressive lung destruction ultimately requiring lung transplantation (LT). Following LT, CF-adapted Pseudomonas strains, potentially originating from the sinuses, may seed the allograft leading to infections and reduced allograft survival. We investigated whether CF-adapted Pseudomonas populations invade the donor microbiota and adapt to the non-CF allograft. We collected sequential Pseudomonas isolates and airway samples from a CF-lung transplant recipient during two years, and followed the dynamics of the microbiota and Pseudomonas populations. We show that Pseudomonas invaded the host microbiota within three days post-LT, in association with a reduction in richness and diversity. A dominant mucoid and hypermutator mutL lineage was replaced after 11 days by non-mucoid strains. Despite antibiotic therapy, Pseudomonas dominated the allograft microbiota until day 95. We observed positive selection of pre-LT variants and the appearance of novel mutations. Phenotypic adaptation resulted in increased biofilm formation and swimming motility capacities. Pseudomonas was replaced after 95 days by a microbiota dominated by Actinobacillus. In conclusion, mucoid Pseudomonas adapted to the CF-lung remained able to invade the allograft. Selection of both pre-existing non-mucoid subpopulations and of novel phenotypic traits suggests rapid adaptation of Pseudomonas to the non-CF allograft.