Evidence map›Paper›PMID 22905192›Full record

ArticlePloS one2012

Differentiation in quinolone resistance by virulence genotype in Pseudomonas aeruginosa.

Melissa Agnello, Annie Wong-Beringer

Abstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing 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

39 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Differences in antimicrobial resistance between exoU and exoS isolates of Pseudomonas aeruginosa.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2025
    Article
  5. Article
  6. Article
  7. The fitness connection of antibiotic resistance.Frontiers in microbiology · 2025
    Article
  8. Article
  9. Review
  10. High prevalence of multidrug-resistantHealth science reports · 2024
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Virulence Factors ofFrontiers in cellular and infection microbiology · 2022
    Review
  17. Article
  18. Article
  19. Review
  20. 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

2 authors.

Melissa AgnelloSchool of Pharmacy, University of Southern California, Los Angeles, California, United States of America.
Annie Wong-Beringer

Funding

Impact of Fluoroquinolone resistance on Pseudomonas virulence and patient outcomeR21AI073467 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI WONG-BERINGER, ANNIE · 2008 to 2009
$407k
NIAID NIH HHS R21 AI073467NIAID NIH HHS R21AI073467
6 · The paper itself

Abstract

Pseudomonas aeruginosa is a leading pathogen that has become increasingly resistant to the fluoroquinolone antibiotics due to widespread prescribing. Adverse outcomes have been shown for patients infected with fluoroquinolone-resistant strains. The type III secretion system (TTSS) is a major virulence determinant during acute infections through the injection of effector toxins into host cells. Most strains exhibit a unique TTSS virulence genotype defined by the presence of either exoS or exoU gene encoding two of the effector toxins, ExoS and ExoU, respectively. Specific TTSS effector genotype has been shown previously to differentially impact virulence in pneumonia. In this study, we examined the relationship between TTSS effector genotype and fluoroquinolone resistance mechanisms in a collection of 270 respiratory isolates. We found that a higher proportion of exoU+ strains were fluoroquinolone-resistant compared to exoS+ strains (63% vs 49%, p = 0.03) despite its lower overall prevalence (38% exoU+ vs 56% exoS+). Results from sequencing the quinolone resistance determining regions (QRDRs) of the 4 target genes (gyrA, gyrB, parC, parE) indicated that strains containing the exoU gene were more likely to acquire ≥ 2 mutations than exoS+ strains at MICs ≤ 8 µg/ml (13% vs none) and twice as likely to have mutations in both gyrA and parC than exoS+ strains (48% vs 24% p = 0.0439). Our findings indicate that P. aeruginosa strains differentially develop resistance-conferring mutations that correlate with TTSS effector genotype and the more virulent exoU+ subpopulation. Differences in mutational processes by virulence genotype that were observed suggest co-evolution of resistance and virulence traits favoring a more virulent genotype in the quinolone-rich clinical environment.

Indexed as

ADP Ribose TransferasesBacterial ProteinsBacterial ToxinsDrug Resistance, BacterialFluoroquinolonesGenotypeHumansMicrobial Sensitivity TestsMutationPhenotypePneumoniaPseudomonas aeruginosaPseudomonas InfectionsVirulenceADP Ribose TransferasesBacterial ProteinsBacterial Toxinsexoenzyme SFluoroquinolonespseudomonas exoprotein A protein, Pseudomonas aeruginosa

Identifiers

PMID22905192
PMCPMC3414457

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Registered trials

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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.