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Evolution of the Pseudomonas aeruginosa mutational resistome in an international Cystic Fibrosis clone

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López-Causapé, C, Sommer, LM, Cabot, G, Rubio, R, Ocampo-Sosa, AA, Johansen, HK, Figuerola, J, Cantón, R, Kidd, TJ, Molin, S & Oliver, A 2017, 'Evolution of the Pseudomonas aeruginosa mutational resistome in an international Cystic Fibrosis clone' Scientific Reports, bind 7, nr. 1, s. 5555. https://doi.org/10.1038/s41598-017-05621-5

APA

CBE

López-Causapé C, Sommer LM, Cabot G, Rubio R, Ocampo-Sosa AA, Johansen HK, Figuerola J, Cantón R, Kidd TJ, Molin S, Oliver A. 2017. Evolution of the Pseudomonas aeruginosa mutational resistome in an international Cystic Fibrosis clone. Scientific Reports. 7(1):5555. https://doi.org/10.1038/s41598-017-05621-5

MLA

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Author

López-Causapé, Carla ; Sommer, Lea Mette ; Cabot, Gabriel ; Rubio, Rosa ; Ocampo-Sosa, Alain A ; Johansen, Helle Krogh ; Figuerola, Joan ; Cantón, Rafael ; Kidd, Timothy J ; Molin, Soeren ; Oliver, Antonio. / Evolution of the Pseudomonas aeruginosa mutational resistome in an international Cystic Fibrosis clone. I: Scientific Reports. 2017 ; Bind 7, Nr. 1. s. 5555.

Bibtex

@article{a52f3182765442129eefb57dcc7246e7,
title = "Evolution of the Pseudomonas aeruginosa mutational resistome in an international Cystic Fibrosis clone",
abstract = "Emergence of epidemic clones and antibiotic resistance development compromises the management of Pseudomonas aeruginosa cystic fibrosis (CF) chronic respiratory infections. Whole genome sequencing (WGS) was used to decipher the phylogeny, interpatient dissemination, WGS mutator genotypes (mutome) and resistome of a widespread clone (CC274), in isolates from two highly-distant countries, Australia and Spain, covering an 18-year period. The coexistence of two divergent CC274 clonal lineages was revealed, but without evident geographical barrier; phylogenetic reconstructions and mutational resistome demonstrated the interpatient transmission of mutators. The extraordinary capacity of P. aeruginosa to develop resistance was evidenced by the emergence of mutations in >100 genes related to antibiotic resistance during the evolution of CC274, catalyzed by mutator phenotypes. While the presence of classical mutational resistance mechanisms was confirmed and correlated with resistance phenotypes, results also showed a major role of unexpected mutations. Among them, PBP3 mutations, shaping up β-lactam resistance, were noteworthy. A high selective pressure for mexZ mutations was evidenced, but we showed for the first time that high-level aminoglycoside resistance in CF is likely driven by mutations in fusA1/fusA2, coding for elongation factor G. Altogether, our results provide valuable information for understanding the evolution of the mutational resistome of CF P. aeruginosa.",
keywords = "Journal Article",
author = "Carla L{\'o}pez-Causap{\'e} and Sommer, {Lea Mette} and Gabriel Cabot and Rosa Rubio and Ocampo-Sosa, {Alain A} and Johansen, {Helle Krogh} and Joan Figuerola and Rafael Cant{\'o}n and Kidd, {Timothy J} and Soeren Molin and Antonio Oliver",
year = "2017",
month = "7",
day = "17",
doi = "10.1038/s41598-017-05621-5",
language = "English",
volume = "7",
pages = "5555",
journal = "Scientific Reports",
issn = "2045-2322",
publisher = "Nature Publishing Group",
number = "1",

}

RIS

TY - JOUR

T1 - Evolution of the Pseudomonas aeruginosa mutational resistome in an international Cystic Fibrosis clone

AU - López-Causapé, Carla

AU - Sommer, Lea Mette

AU - Cabot, Gabriel

AU - Rubio, Rosa

AU - Ocampo-Sosa, Alain A

AU - Johansen, Helle Krogh

AU - Figuerola, Joan

AU - Cantón, Rafael

AU - Kidd, Timothy J

AU - Molin, Soeren

AU - Oliver, Antonio

PY - 2017/7/17

Y1 - 2017/7/17

N2 - Emergence of epidemic clones and antibiotic resistance development compromises the management of Pseudomonas aeruginosa cystic fibrosis (CF) chronic respiratory infections. Whole genome sequencing (WGS) was used to decipher the phylogeny, interpatient dissemination, WGS mutator genotypes (mutome) and resistome of a widespread clone (CC274), in isolates from two highly-distant countries, Australia and Spain, covering an 18-year period. The coexistence of two divergent CC274 clonal lineages was revealed, but without evident geographical barrier; phylogenetic reconstructions and mutational resistome demonstrated the interpatient transmission of mutators. The extraordinary capacity of P. aeruginosa to develop resistance was evidenced by the emergence of mutations in >100 genes related to antibiotic resistance during the evolution of CC274, catalyzed by mutator phenotypes. While the presence of classical mutational resistance mechanisms was confirmed and correlated with resistance phenotypes, results also showed a major role of unexpected mutations. Among them, PBP3 mutations, shaping up β-lactam resistance, were noteworthy. A high selective pressure for mexZ mutations was evidenced, but we showed for the first time that high-level aminoglycoside resistance in CF is likely driven by mutations in fusA1/fusA2, coding for elongation factor G. Altogether, our results provide valuable information for understanding the evolution of the mutational resistome of CF P. aeruginosa.

AB - Emergence of epidemic clones and antibiotic resistance development compromises the management of Pseudomonas aeruginosa cystic fibrosis (CF) chronic respiratory infections. Whole genome sequencing (WGS) was used to decipher the phylogeny, interpatient dissemination, WGS mutator genotypes (mutome) and resistome of a widespread clone (CC274), in isolates from two highly-distant countries, Australia and Spain, covering an 18-year period. The coexistence of two divergent CC274 clonal lineages was revealed, but without evident geographical barrier; phylogenetic reconstructions and mutational resistome demonstrated the interpatient transmission of mutators. The extraordinary capacity of P. aeruginosa to develop resistance was evidenced by the emergence of mutations in >100 genes related to antibiotic resistance during the evolution of CC274, catalyzed by mutator phenotypes. While the presence of classical mutational resistance mechanisms was confirmed and correlated with resistance phenotypes, results also showed a major role of unexpected mutations. Among them, PBP3 mutations, shaping up β-lactam resistance, were noteworthy. A high selective pressure for mexZ mutations was evidenced, but we showed for the first time that high-level aminoglycoside resistance in CF is likely driven by mutations in fusA1/fusA2, coding for elongation factor G. Altogether, our results provide valuable information for understanding the evolution of the mutational resistome of CF P. aeruginosa.

KW - Journal Article

U2 - 10.1038/s41598-017-05621-5

DO - 10.1038/s41598-017-05621-5

M3 - Journal article

VL - 7

SP - 5555

JO - Scientific Reports

JF - Scientific Reports

SN - 2045-2322

IS - 1

ER -

ID: 52702222