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© Research
Publication : Proceedings of the National Academy of Sciences of the United States of America

Enhanced in vivo fitness of carbapenem-resistant oprD mutants of Pseudomonas aeruginosa revealed through high-throughput sequencing

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Proceedings of the National Academy of Sciences of the United States of America - 18 Nov 2013

Skurnik D, Roux D, Cattoir V, Danilchanka O, Lu X, Yoder-Himes DR, Han K, Guillard T, Jiang D, Gaultier C, Guerin F, Aschard H, Leclercq R, Mekalanos JJ, Lory S, Pier GB

Link to Pubmed [PMID] – 24248354

Proc. Natl. Acad. Sci. U.S.A. 2013 Dec;110(51):20747-52

An important question regarding the biologic implications of antibiotic-resistant microbes is how resistance impacts the organism’s overall fitness and virulence. Currently it is generally thought that antibiotic resistance carries a fitness cost and reduces virulence. For the human pathogen Pseudomonas aeruginosa, treatment with carbapenem antibiotics is a mainstay of therapy that can lead to the emergence of resistance, often through the loss of the carbapenem entry channel OprD. Transposon insertion-site sequencing was used to analyze the fitness of 300,000 mutants of P. aeruginosa strain PA14 in a mouse model for gut colonization and systemic dissemination after induction of neutropenia. Transposon insertions in the oprD gene led not only to carbapenem resistance but also to a dramatic increase in mucosal colonization and dissemination to the spleen. These findings were confirmed in vivo with different oprD mutants of PA14 as well as with related pairs of carbapenem-susceptible and -resistant clinical isolates. Compared with OprD(+) strains, those lacking OprD were more resistant to killing by acidic pH or normal human serum and had increased cytotoxicity against murine macrophages. RNA-sequencing analysis revealed that an oprD mutant showed dramatic changes in the transcription of genes that may contribute to the various phenotypic changes observed. The association between carbapenem resistance and enhanced survival of P. aeruginosa in infected murine hosts suggests that either drug resistance or host colonization can cause the emergence of more pathogenic, drug-resistant P. aeruginosa clones in a single genetic event.

https://www.ncbi.nlm.nih.gov/pubmed/24248354