Evidence map›Paper›PMID 30165811›Full record

ArticleBMC genomics2018

Whole genome sequencing reveals the emergence of a Pseudomonas aeruginosa shared strain sub-lineage among patients treated within a single cystic fibrosis centre.

Bryan A Wee, Anna S Tai, Laura J Sherrard, Nouri L Ben Zakour, Kirt R Hanks, Timothy J Kidd, Kay A Ramsay, Iain Lamont, David M Whiley, Scott C Bell and 1 more

Abstract read
In one paragraph

Article in BMC genomics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. The role of theFrontiers in cellular and infection microbiology · 2022
    Review
  9. Review
  10. Antibiotics (Basel, Switzerland) · 2021
    Review
  11. Article
  12. Article
  13. Genotypic characterization ofInfection and drug resistance · 2019
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Bryan A WeeSchool of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, QLD, Australia.
Anna S TaiFaculty of Medicine, The University of Queensland, Brisbane, QLD, Australia.
Laura J SherrardLung Bacteria Group, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
Nouri L Ben ZakourSchool of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, QLD, Australia.
Kirt R HanksSchool of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, QLD, Australia.
Timothy J KiddSchool of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, QLD, Australia.
Kay A RamsayFaculty of Medicine, The University of Queensland, Brisbane, QLD, Australia.
Iain LamontDepartment of Biochemistry, University of Otago, Dunedin, New Zealand.
David M WhileyFaculty of Medicine, UQ Centre for Clinical Research, The University of Queensland, Brisbane, QLD, Australia.
Scott C BellFaculty of Medicine, The University of Queensland, Brisbane, QLD, Australia.
Scott A BeatsonSchool of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, QLD, Australia. s.beatson@uq.edu.au.ORCID http://orcid.org/0000-0002-1806-3283

Funding

National Health and Medical Research Council 1088448National Health and Medical Research Council 1090456National Health and Medical Research Council 45919
6 · The paper itself

Abstract

backgroundChronic lung infections caused by Pseudomonas aeruginosa are a significant cause of morbidity and mortality in people with cystic fibrosis (CF). Shared P. aeruginosa strains, that can be transmitted between patients, are of concern and in Australia the AUST-02 shared strain is predominant in individuals attending CF centres in Queensland and Western Australia. M3L7 is a multidrug resistant sub-type of AUST-02 that was recently identified in a Queensland CF centre and was shown to be associated with poorer clinical outcomes. The main aim of this study was to resolve the relationship of the emergent M3L7 sub-type within the AUST-02 group of strains using whole genome sequencing.

resultsA whole genome core phylogeny of 63 isolates indicated that M3L7 is a monophyletic sub-lineage within the context of the broader AUST-02 group. Relatively short branch lengths connected all of the M3L7 isolates. A phylogeny based on nucleotide polymorphisms present across the genome showed that the chronological estimation of the most recent common ancestor was around 2001 (± 3 years). SNP differences between sequential non-hypermutator M3L7 isolates collected 3-4 years apart from five patients suggested both continuous infection of the same strain and cross-infection of some M3L7 variants between patients. The majority of polymorphisms that were characteristic of M3L7 (i.e. acquired after divergence from all other AUST-02 isolates sequenced) were found to produce non-synonymous mutations in virulence and antibiotic resistance genes.

conclusionsM3L7 has recently diverged from a common ancestor, indicating descent from a single carrier at a CF treatment centre in Australia. Both adaptation to the lung and transmission of M3L7 between adults attending this centre may have contributed to its rapid dissemination. Further genomic investigations are required on multiple intra-sample isolates of this sub-type to decipher potential mechanisms which facilitates its epidemiological success.

Indexed as

AdultCystic FibrosisGenetic VariationGenotypeHumansPhylogenyPseudomonas aeruginosaPseudomonas InfectionsWhole Genome SequencingAUST-02Chronic lung infectionsCystic fibrosisEvolutionPseudomonas aeruginosaWhole genome sequencing

Identifiers

PMID30165811
PMCPMC6117919

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.