Evidence map›Paper›PMID 23045355›Full record

ArticleAntimicrobial agents and chemotherapy2012

Genetic markers of widespread extensively drug-resistant Pseudomonas aeruginosa high-risk clones.

Gabriel Cabot, Alain A Ocampo-Sosa, M Angeles Domínguez, Juan F Gago, Carlos Juan, Fe Tubau, Cristina Rodríguez, Bartolomé Moyà, Carmen Peña, Luis Martínez-Martínez and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Antimicrobial agents and chemotherapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed
6.6field-weighted citation impact, top 2% 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

127 citing papers in PubMed, 222 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Antimicrobial agents and chemotherapy · 2026
    Article
  4. Review
  5. Correlation of type 3 secretion system genes with antimicrobial resistance inJournal of Taibah University Medical Sciences · 2026
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  8. Virulence and Resistance ofMicroorganisms · 2025
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  10. Detection of the ST111 Global High-RiskCurrent issues in molecular biology · 2025
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  11. Article
  12. Article
  13. Article
  14. Article
  15. Carbapenem-ResistantAntibiotics (Basel, Switzerland) · 2025
    Review
  16. Genomic Epidemiology of Pseudomonas aeruginosa Sequence Type 111.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2025
    Article
  17. High-riskHeliyon · 2025
    Article
  18. The Role ofInfection and drug resistance · 2025
    Article
  19. The fitness connection of antibiotic resistance.Frontiers in microbiology · 2025
    Article
  20. Article

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

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

12 authors at 3 institutions in 1 country.

Gabriel CabotServicio de Microbiología y Unidad de Investigación, Hospital Universitario Son Espases, Palma de Mallorca, Spain.
Alain A Ocampo-Sosa
M Angeles Domínguez
Juan F Gago
Carlos Juan
Fe Tubau
Cristina Rodríguez
Bartolomé Moyà
Carmen Peña
Luis Martínez-Martínez
Antonio Oliver
Spanish Network for Research in Infectious Diseases (REIPI)
Hospital Universitario Son Espases · ESBellvitge University Hospital · ESFundación Marques de Valdecilla · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent reports have revealed the existence of widespread extensively drug-resistant (XDR) P. aeruginosa high-risk clones in health care settings, but there is still scarce information on their specific chromosomal (mutational) and acquired resistance mechanisms. Up to 20 (10.5%) of 190 bloodstream isolates collected from 10 Spanish hospitals met the XDR criteria. A representative number (15 per group) of isolates classified as multidrug-resistant (MDR) (22.6%), resistant to 1 to 2 classes (moderately resistant [modR]) (23.7%), or susceptible to all antibiotics (multiS) (43.2%) were investigated in parallel. Multilocus sequence typing (MLST) analysis revealed that all XDR isolates belonged to sequence type 175 (ST175) (n = 19) or ST111 (n = 1), both recognized as international high-risk clones. Clonal diversity was higher among the 15 MDR isolates (4 ST175, 2 ST111, and 8 additional STs) and especially high among the 15 modR (13 different STs) and multiS (14 STs) isolates. The XDR/MDR pattern in ST111 isolates correlated with the production of VIM-2, but none of the ST175 isolates produced acquired β-lactamases. In contrast, the analysis of resistance markers in 12 representative isolates (from 7 hospitals) of ST175 revealed that the XDR pattern was driven by the combination of AmpC hyperproduction, OprD inactivation (Q142X), 3 mutations conferring high-level fluoroquinolone resistance (GyrA T83I and D87N and ParC S87W), a G195E mutation in MexZ (involved in MexXY-OprM overexpression), and the production of a class 1 integron harboring the aadB gene (gentamicin and tobramycin resistance). Of particular interest, in nearly all the ST175 isolates, AmpC hyperproduction was driven by a novel AmpR-activating mutation (G154R), as demonstrated by complementation studies using an ampR mutant of PAO1. This work is the first to describe the specific resistance markers of widespread P. aeruginosa XDR high-risk clones producing invasive infections.

Indexed as

Clone CellsCross InfectionDrug Resistance, BacterialDrug Resistance, Multiple, BacterialElectrophoresis, Gel, Pulsed-FieldGenetic Complementation TestGenetic MarkersMicrobial Sensitivity TestsMutationPolymerase Chain ReactionPseudomonas aeruginosaPseudomonas InfectionsSpainGenetic Markers

Identifiers

PMID23045355
PMCPMC3497190
OpenAlexW2132109557

What OpenQuestion holds

Textmetadata
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.