Evidence map›Paper›PMID 21747788›Full record

ArticleFrontiers in microbiology2011

Pseudomonas aeruginosa: resistance to the max.

Keith Poole

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Frontiers in microbiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06811727 (CONTinuous Infusion Versus Intermittent Dosing of ceftaZidime/AVIbactam in Critically Ill Patients With Klebsiella Pneumoniae OXA-48 or Pseudomonas Aeruginosa Infections), which is not on this map. Cited by 443 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
443citing papers in PubMed, 1 pooled it
13.7field-weighted citation impact, top 1% 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.

NCT06811727 phase4not yet recruitingnot on this mapstarted 2025, after this paper: background citation

CONTinuous Infusion Versus Intermittent Dosing of ceftaZidime/AVIbactam in Critically Ill Patients With Klebsiella Pneumoniae OXA-48 or Pseudomonas Aeruginosa Infections: A Single-centre Randomized Open-label Trial (ZAVICONT)

TypeinterventionalSponsorIvan Šitum, MDRan2025 to 2027Enrolled140ConditionsSevere InfectionArmsContinuos ceftazidime/avibactam infusion, Intermitent dosing as per SMPC
3 · Its place in the literature

Who cites it

443 citing papers in PubMed, 1 synthesis or guideline pooled it, 926 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
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  6. Prevalence and Antimicrobial Resistance ofInfectious disease reports · 2026
    Article
  7. Article
  8. Article
  9. Calcium regulation ofApplied and environmental microbiology · 2026
    Article
  10. Antibiotic resistance mechanisms and global resistance patterns of Pseudomonas aeruginosa in microbial keratitis.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026
    Review
  11. Article
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  17. Clearance of hypermutator XDRASM case reports · 2026
    Article
  18. Article
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  20. Article

383 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

1 author at 1 institution in 1 country.

Keith PooleDepartment of Microbiology and Immunology, Queen's University Kingston, ON, Canada.
Queen's University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pseudomonas aeruginosa is intrinsically resistant to a variety of antimicrobials and can develop resistance during anti-pseudomonal chemotherapy both of which compromise treatment of infections caused by this organism. Resistance to multiple classes of antimicrobials (multidrug resistance) in particular is increasingly common in P. aeruginosa, with a number of reports of pan-resistant isolates treatable with a single agent, colistin. Acquired resistance in this organism is multifactorial and attributable to chromosomal mutations and the acquisition of resistance genes via horizontal gene transfer. Mutational changes impacting resistance include upregulation of multidrug efflux systems to promote antimicrobial expulsion, derepression of ampC, AmpC alterations that expand the enzyme's substrate specificity (i.e., extended-spectrum AmpC), alterations to outer membrane permeability to limit antimicrobial entry and alterations to antimicrobial targets. Acquired mechanisms contributing to resistance in P. aeruginosa include β-lactamases, notably the extended-spectrum β-lactamases and the carbapenemases that hydrolyze most β-lactams, aminoglycoside-modifying enzymes, and 16S rRNA methylases that provide high-level pan-aminoglycoside resistance. The organism's propensity to grow in vivo as antimicrobial-tolerant biofilms and the occurrence of hypermutator strains that yield antimicrobial resistant mutants at higher frequency also compromise anti-pseudomonal chemotherapy. With limited therapeutic options and increasing resistance will the untreatable P. aeruginosa infection soon be upon us?

Indexed as

antimicrobialbiofilmeffluxhypermutabilityPseudomonas aeruginosaresistanceβ-lactamase

Identifiers

PMID21747788
PMCPMC3128976
OpenAlexW2057418340

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.