Evidence map›Paper›PMID 36258071›Full record

ArticleAdvances in experimental medicine and biology2022

Antibiotic Resistance in Pseudomonas.

Pablo Laborda, Sara Hernando-Amado, José Luis Martínez, Fernando Sanz-García

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Article in Advances in experimental medicine and biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed.

  1. Article
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  8. Genomic characterization ofMicrobial genomics · 2025
    Article
  9. Antibiotic-ResistantMicroorganisms · 2025
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Activity of zinc oxide and zinc borate nanoparticles against resistant bacteria in an experimental lung cancer model.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2024
    Article
  18. Article
  19. Effect ofFrontiers in microbiology · 2024
    Article
  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

4 authors.

Pablo LabordaCentro Nacional de Biotecnología, Consejo Superior de Investigaciones Científicas, Madrid, Spain.
Sara Hernando-AmadoCentro Nacional de Biotecnología, Consejo Superior de Investigaciones Científicas, Madrid, Spain.
José Luis MartínezCentro Nacional de Biotecnología, Consejo Superior de Investigaciones Científicas, Madrid, Spain. jlmtnez@cnb.csic.es.
Fernando Sanz-GarcíaCentro Nacional de Biotecnología, Consejo Superior de Investigaciones Científicas, Madrid, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pseudomonas is a bacterial genus, with a bona fide environmental habitat that comprises different species, some of them causing diseases in humans and plants, as well as some strains with biotechnological potential. Amongst them, Pseudomonas aeruginosa is currently one of the most important nosocomial pathogens. In addition, this microorganism is a prevalent cause of chronic infections in cystic fibrosis patients and in people suffering from chronic obstructive pulmonary disease. The success of P. aeruginosa in colonising different habitats largely relies on its metabolic versatility and robustness. Besides, this bacterial pathogen harbours in its core genome a large set of virulence determinants that allows it to colonise/infect a variety of hosts, from unicellular organisms to humans. Nevertheless, these are not just the only conditions needed for infecting patients at hospitals. Taking into consideration that infected patients are regularly under antibiotic treatment, the ability to avoid antibiotics' action is also needed. In this sense, P. aeruginosa displays a characteristic low susceptibility to several antibiotics currently used in therapy. This is due to the reduced permeability of its cellular envelopes and the presence in its genome of an arrangement of genes encoding multidrug efflux pumps and antibiotic-inactivating enzymes that contribute to its resilience to antibiotics. Besides intrinsic resistance, P. aeruginosa is able to evolve towards antibiotic resistance through mutations (particularly relevant in the case of chronic infections) and via acquisition of antibiotic resistance genes. It is worth mentioning that acquired resistance is not the only venue that P. aeruginosa has for avoiding the action of antibiotics. Transient resistance can also confer this phenotype. Indeed, the induction of the expression of intrinsic resistance genes by conditions or compounds that P. aeruginosa could face during infection can compromise the effectiveness of antibiotics for treating such infections. In addition, tolerant cells able to survive during the exposure to bactericidal antibiotics without an increase in their antibiotic resistance phenotype are found as well in these patients, and they are the prelude of the evolution towards antibiotic resistance. Finally, P. aeruginosa biofilms, frequently encountered in the lungs of cystic fibrosis patients, in prostheses, or in catheters, present low antibiotic susceptibility and are associated with recalcitrance and disease worsening.

Indexed as

Cystic FibrosisPseudomonas InfectionsAnti-Bacterial AgentsDrug Resistance, MicrobialHumansMicrobial Sensitivity TestsPseudomonasPseudomonas aeruginosaAnti-Bacterial AgentsAntibiotic resistanceBactericidal antibioticsBiofilmsChronic infectionsESKAPEMultidrug efflux pumps

Identifiers

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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.