Evidence map›Paper›PMID 35323912›Full record

ArticleThe Journal of antimicrobial chemotherapy2022

Resistance mechanisms and molecular epidemiology of Pseudomonas aeruginosa strains from patients with bronchiectasis.

Roberto Cabrera, Laia Fernández-Barat, Nil Vázquez, Victoria Alcaraz-Serrano, Leticia Bueno-Freire, Rosanel Amaro, Rubén López-Aladid, Patricia Oscanoa, Laura Muñoz, Jordi Vila and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of antimicrobial chemotherapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 28 citations in OpenAlex.

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  18. Isolation ofMolecules (Basel, Switzerland) · 2023
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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

11 authors at 4 institutions in 1 country.

Roberto CabreraHospital Clínic, Cellex Laboratory, CIBERES (Center for net Biomedical Research Respiratory diseases, 06/06/0028) - Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), School of Medicine, University of Barcelona, Spain.
Laia Fernández-BaratHospital Clínic, Cellex Laboratory, CIBERES (Center for net Biomedical Research Respiratory diseases, 06/06/0028) - Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), School of Medicine, University of Barcelona, Spain.
Nil VázquezHospital Clínic, Cellex Laboratory, CIBERES (Center for net Biomedical Research Respiratory diseases, 06/06/0028) - Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), School of Medicine, University of Barcelona, Spain.
Victoria Alcaraz-SerranoHospital Clínic, Cellex Laboratory, CIBERES (Center for net Biomedical Research Respiratory diseases, 06/06/0028) - Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), School of Medicine, University of Barcelona, Spain.
Leticia Bueno-FreireHospital Clínic, Cellex Laboratory, CIBERES (Center for net Biomedical Research Respiratory diseases, 06/06/0028) - Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), School of Medicine, University of Barcelona, Spain.
Rosanel AmaroHospital Clínic, Cellex Laboratory, CIBERES (Center for net Biomedical Research Respiratory diseases, 06/06/0028) - Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), School of Medicine, University of Barcelona, Spain.
Rubén López-AladidHospital Clínic, Cellex Laboratory, CIBERES (Center for net Biomedical Research Respiratory diseases, 06/06/0028) - Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), School of Medicine, University of Barcelona, Spain.
Patricia OscanoaHospital Clínic, Cellex Laboratory, CIBERES (Center for net Biomedical Research Respiratory diseases, 06/06/0028) - Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), School of Medicine, University of Barcelona, Spain.
Laura MuñozBarcelona Global Health Institute, Department of Clinical Microbiology, Hospital Clínic, University of Barcelona, Barcelona, Spain.
Jordi VilaBarcelona Global Health Institute, Department of Clinical Microbiology, Hospital Clínic, University of Barcelona, Barcelona, Spain.
Antoni TorresHospital Clínic, Cellex Laboratory, CIBERES (Center for net Biomedical Research Respiratory diseases, 06/06/0028) - Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), School of Medicine, University of Barcelona, Spain.
Universitat de Barcelona · ESCentro de Investigación Biomédica en Red de Enfermedades Respiratorias · ESConsorci Institut D'Investigacions Biomediques August Pi I Sunyer · ESHospital Clínic de Barcelona · ES

Funding

CIBERES ES18PI01FIS PI1800145SEPAR 208
6 · The paper itself

Abstract

backgroundNon-cystic fibrosis bronchiectasis (BE) is a chronic structural lung condition that facilitates chronic colonization by different microorganisms and courses with recurrent respiratory infections and frequent exacerbations. One of the main pathogens involved in BE is Pseudomonas aeruginosa.

objectivesTo determine the molecular mechanisms of resistance and the molecular epidemiology of P. aeruginosa strains isolated from patients with BE.

methodsA total of 43 strains of P. aeruginosa were isolated from the sputum of BE patients. Susceptibility to the following antimicrobials was analysed: ciprofloxacin, meropenem, imipenem, amikacin, tobramycin, aztreonam, piperacillin/tazobactam, ceftazidime, ceftazidime/avibactam, ceftolozane/tazobactam, cefepime and colistin. The resistance mechanisms present in each strain were assessed by PCR, sequencing and quantitative RT-PCR. Molecular epidemiology was determined by MLST. Phylogenetic analysis was carried out using the eBURST algorithm.

resultsHigh levels of resistance to ciprofloxacin (44.19%) were found. Mutations in the gyrA, gyrB, parC and parE genes were detected in ciprofloxacin-resistant P. aeruginosa strains. The number of mutated QRDR genes was related to increased MIC. Different β-lactamases were detected: blaOXA50, blaGES-2, blaIMI-2 and blaGIM-1. The aac(3)-Ia, aac(3)-Ic, aac(6″)-Ib and ant(2″)-Ia genes were associated with aminoglycoside-resistant strains. The gene expression analysis showed overproduction of the MexAB-OprM efflux system (46.5%) over the other efflux system. The most frequently detected clones were ST619, ST676, ST532 and ST109.

conclusionsResistance to first-line antimicrobials recommended in BE guidelines could threaten the treatment of BE and the eradication of P. aeruginosa, contributing to chronic infection.

Indexed as

BronchiectasisPseudomonas InfectionsAnti-Bacterial Agentsbeta-LactamasesCeftazidimeCiprofloxacinHumansMicrobial Sensitivity TestsMolecular EpidemiologyMultilocus Sequence TypingPhylogenyPseudomonas aeruginosaTazobactamAnti-Bacterial Agentsbeta-LactamasesCeftazidimeCiprofloxacinTazobactam

Identifiers

PMID35323912
PMCPMC9155640
OpenAlexW4220772140

What OpenQuestion holds

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LicenceCC BY-NC
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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.