Evidence map›Paper›PMID 25672496›Full record

ReviewCritical care (London, England)2014

Association between Pseudomonas aeruginosa type III secretion, antibiotic resistance, and clinical outcome: a review.

Teiji Sawa, Masaru Shimizu, Kiyoshi Moriyama, Jeanine P Wiener-Kronish

Open access · goldAbstract readReview
In one paragraph

Review in Critical care (London, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 6% of its field
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

77 citing papers in PubMed, 1 synthesis or guideline pooled it, 140 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Comparison of virulence factors genes between exoU and exoS Pseudomonas aeruginosa in microbial keratitis.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026
    Article
  9. Molecular Mechanisms Underlying the Pathogenicity ofMedicina (Kaunas, Lithuania) · 2026
    Review
  10. Article
  11. Article
  12. Anti-QS Strategies AgainstMicroorganisms · 2025
    Review
  13. 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
  14. Article
  15. Impact of Antimicrobial Resistance ofVeterinary sciences · 2025
    Review
  16. Multidrug resistance ofFrontiers in microbiology · 2025
    Article
  17. Impact ofCurrent research in microbial sciences · 2025
    Article
  18. Molecular Epidemiology ofAntibiotics (Basel, Switzerland) · 2024
    Review
  19. A Supramolecular Antibiotic Targeting Drug-ResistantACS applied materials & interfaces · 2024
    Article
  20. Review

17 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 2 countries.

Teiji Sawa
Masaru Shimizu
Kiyoshi Moriyama
Jeanine P Wiener-Kronish
Kyoto Prefectural University of Medicine · JPKyorin University · JPMassachusetts General Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pseudomonas aeruginosa uses a complex type III secretion system to inject the toxins ExoS, ExoT, ExoU, and ExoY into the cytosol of target eukaryotic cells. This system is regulated by the exoenzyme S regulon and includes the transcriptional activator ExsA. Of the four toxins, ExoU is characterized as the major virulence factor responsible for alveolar epithelial injury in patients with P. aeruginosa pneumonia. Virulent strains of P. aeruginosa possess the exoU gene, whereas non-virulent strains lack this particular gene. The mechanism of virulence for the exoU+ genotype relies on the presence of a pathogenic gene cluster (PAPI-2) encoding exoU and its chaperone, spcU. The ExoU toxin has a patatin-like phospholipase domain in its N-terminal, exhibits phospholipase A2 activity, and requires a eukaryotic cell factor for activation. The C-terminal of ExoU has a ubiquitinylation mechanism of activation. This probably induces a structural change in enzymatic active sites required for phospholipase A2 activity. In P. aeruginosa clinical isolates, the exoU+ genotype correlates with a fluoroquinolone resistance phenotype. Additionally, poor clinical outcomes have been observed in patients with pneumonia caused by exoU+-fluoroquinolone-resistant isolates. Therefore, the potential exists to improve clinical outcomes in patients with P. aeruginosa pneumonia by identifying virulent and antimicrobial drug-resistant strains through exoU genotyping or ExoU protein phenotyping or both.

Indexed as

Anti-Bacterial AgentsBacterial ProteinsBacterial ToxinsDrug Resistance, BacterialHumansPseudomonas aeruginosaPseudomonas InfectionsTreatment OutcomeAnti-Bacterial AgentsBacterial ProteinsBacterial Toxinspseudomonas exoprotein A protein, Pseudomonas aeruginosa

Identifiers

PMID25672496
PMCPMC4331484
OpenAlexW2129781699

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.