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Antimicrobial Resistance in Pseudomonas aeruginosa

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A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Antimicrobial Agents and Resistance".

Deadline for manuscript submissions: closed (15 September 2021) | Viewed by 14016

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Special Issue Editors

Prof. José Luis Martínez

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Guest Editor

Centro Nacional de Biotecnología, CSIC, Darwin 3, 28043 Madrid, Spain
Interests: bacterial evolution; antibiotic resistance; cross resistance; co-resistance; fitness costs; collateral sensitivity

Dr. Sara Hernando Amado

E-Mail Website
Co-Guest Editor

Centro Nacional de Biotecnología, CSIC, Darwin 3, 28043 Madrid, Spain
Interests: antibiotic resistance; epistasis; trade-offs of bacterial evolution; pseudomonas aeruginosa

Special Issue Information

Dear Colleagues,

Pseudomonas aeruginosa is currently one of the most important nosocomial pathogens and the most relevant agent causing chronic infections in cystic fibrosis patients. Part of the success of this opportunistic pathogen in producing infections, even in patients under antibiotic therapy, relies on its intrinsically low susceptibility to antibiotics and on its capacity to increase such resistance by mutations and also through the acquisition of resistance genes. The reduced intrinsic susceptibility to antibiotics of this microorganism is due mainly to the low permeability of its cellular envelope and the presence in its core genome of several genes encoding antibiotic resistance genes, such as multidrug efflux pumps and antibiotic-inactivating enzymes.

The aim of this Special Issue is to present new information on the mechanisms of the intrinsic and acquired resistance of P. aeruginosa, on the routes of evolution and the effect of the acquisition of such resistance in bacterial physiology, including virulence, and on the cross-resistance and collateral sensitivity networks regarding antibiotics of this bacterial species. Since P. aeruginosa is an environmental microorganism, one-health-based studies are welcome.

Prof. José Luis Martínez
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Microorganisms is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

Pseudomonas aeruginosa
Intrinsic resistance
Multidrug efflux pumps
Beta-lactamases
Evolution of antibiotic resistance
Role of antibiotic resistance beyond clinics
Consequences of acquiring antibiotic resistance
Cross resistance
Collateral sensitivity

Published Papers (5 papers)

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Editorial

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4 pages, 233 KiB

Open AccessEditorial

Special Issue: “Antimicrobial Resistance in Pseudomonas aeruginosa”

by Sara Hernando-Amado and José Luis Martínez

Microorganisms 2023, 11(3), 744; https://doi.org/10.3390/microorganisms11030744 - 14 Mar 2023

Cited by 2 | Viewed by 1824

Abstract

Pseudomonas aeruginosa is one of the most prevalent pathogens causing nosocomial infections, mainly in patients presenting with basal pathologies or those who are immunocompromised [...] Full article

(This article belongs to the Special Issue Antimicrobial Resistance in Pseudomonas aeruginosa)

Research

Jump to: Editorial

12 pages, 1857 KiB

Open AccessArticle

Reversal of Polymicrobial Biofilm Tolerance to Ciprofloxacin by Blue Light plus Carvacrol

by Yongli Li and Mei X. Wu

Microorganisms 2021, 9(10), 2074; https://doi.org/10.3390/microorganisms9102074 - 1 Oct 2021

Cited by 12 | Viewed by 2133

Abstract

Chronic wound infections are often caused by multi-species biofilms and these biofilm-embedded bacteria exhibit remarkable tolerance to existing antibiotics, which presents huge challenges to control such infections in the wounds. In this investigation, we established a polymicrobial biofilm composed of P. aeruginosa, S. aureus, K. pneumoniae, and A. baumannii. We tested a cocktail therapy comprising 405-nm blue light (BL), carvacrol (Ca), and antibiotics on the multispecies biofilm. Despite the fact that all strains used to form the biofilm were susceptible to ciprofloxacin (CIP) in planktonic cultures, the biofilm was found to withstand ciprofloxacin as well as BL-Ca dual treatment, mainly because K. pneumoniae outgrew and became dominant in the biofilm after each treatment. Strikingly, when ciprofloxacin was combined with BL-Ca, the multispecies biofilms succumbed substantially and were eradicated at an efficacy of 99.9%. Mechanistically, BL-Ca treatment increased membrane permeability and potentiated the anti-biofilm activity of ciprofloxacin, probably by facilitating ciprofloxacin’s entrance of the bacteria, which is particularly significant for K. pneumoniae, a species that is refractory to either ciprofloxacin or BL-Ca dual treatment. The results suggest that bacterial membrane damage can be one of the pivotal strategies to subvert biofilm tolerance and combat the recalcitrant multispecies biofilms. Full article

(This article belongs to the Special Issue Antimicrobial Resistance in Pseudomonas aeruginosa)

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17 pages, 1666 KiB

Open AccessArticle

Molecular Detection of Drug-Resistance Genes of bla_OXA-23-bla_OXA-51 and mcr-1 in Clinical Isolates of Pseudomonas aeruginosa

by Fabiana Nitz, Bruna Oliveira de Melo, Luís Cláudio Nascimento da Silva, Andrea de Souza Monteiro, Sirlei Garcia Marques, Valério Monteiro-Neto, Rosimary de Jesus Gomes Turri, Antonio Dantas Silva Junior, Patrícia Cristina Ribeiro Conceição, Hilário José Cardoso Magalhães, Adrielle Zagmignan, Thiago Azevedo Feitosa Ferro and Maria Rosa Quaresma Bomfim

Microorganisms 2021, 9(4), 786; https://doi.org/10.3390/microorganisms9040786 - 9 Apr 2021

Cited by 11 | Viewed by 3227

Abstract

Pseudomonas aeruginosa has caused high rates of mortality due to the appearance of strains with multidrug resistance (MDR) profiles. This study aimed to characterize the molecular profile of virulence and resistance genes in 99 isolates of P. aeruginosa recovered from different clinical specimens. The isolates were identified by the automated method Vitek2, and the antibiotic susceptibility profile was determined using different classes of antimicrobials. The genomic DNA was extracted and amplified by multiplex polymerase chain reaction (mPCR) to detect different virulence and antimicrobial resistance genes. Molecular typing was performed using the enterobacterial repetitive intergenic consensus (ERIC-PCR) technique to determine the clonal relationship among P. aeruginosa isolates. The drug susceptibility profiles of P. aeruginosa for all strains showed high levels of drug resistance, particularly, 27 (27.3%) isolates that exhibited extensively drug-resistant (XDR) profiles, and the other isolates showed MDR profiles. We detected the polymyxin E (mcr-1) gene in one strain that showed resistance against colistin. The genes that confer resistance to oxacillin (bla_OXA-23 and bla_OXA-51) were present in three isolates. One of these isolates carried both genes. As far as we know from the literature, this is the first report of the presence of bla_OXA-23 and bla_OXA-51 genes in P. aeruginosa. Full article

(This article belongs to the Special Issue Antimicrobial Resistance in Pseudomonas aeruginosa)

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13 pages, 2720 KiB

Open AccessArticle

Presence of Chromosomal crpP-like Genes Is Not Always Associated with Ciprofloxacin Resistance in Pseudomonas aeruginosa Clinical Isolates Recovered in ICU Patients from Portugal and Spain

by Marta Hernández-García, María García-Castillo, Sergio García-Fernández, Diego López-Mendoza, Jazmín Díaz-Regañón, João Romano, Leonor Pássaro, Laura Paixão and Rafael Cantón

Microorganisms 2021, 9(2), 388; https://doi.org/10.3390/microorganisms9020388 - 14 Feb 2021

Cited by 11 | Viewed by 2180

Abstract

CrpP enzymes have been recently described as a novel ciprofloxacin-resistance mechanism. We investigated by whole genome sequencing the presence of crpP-genes and other mechanisms involved in quinolone resistance in MDR/XDR-Pseudomonas aeruginosa isolates (n = 55) with both ceftolozane-tazobactam susceptible or resistant profiles recovered from intensive care unit patients during the STEP (Portugal) and SUPERIOR (Spain) surveillance studies. Ciprofloxacin resistance was associated with mutations in the gyrA and parC genes. Additionally, plasmid-mediated genes (qnrS2 and aac(6′)-Ib-cr) were eventually detected. Ten chromosomal crpP-like genes contained in related pathogenicity genomic islands and 6 different CrpP (CrpP1-CrpP6) proteins were found in 65% (36/55) of the isolates. Dissemination of CrpP variants was observed among non-related clones of both countries, including the CC175 (Spain) high-risk clone and CC348 (Portugal) clone. Interestingly, 5 of 6 variants (CrpP1-CrpP5) carried missense mutations in an amino acid position (Gly7) previously defined as essential conferring ciprofloxacin resistance, and decreased ciprofloxacin susceptibility was only associated with the novel CrpP6 protein. In our collection, ciprofloxacin resistance was mainly due to chromosomal mutations in the gyrA and parC genes. However, crpP genes carrying mutations essential for protein function (G7, I26) and associated with a restored ciprofloxacin susceptibility were predominant. Despite the presence of crpP genes is not always associated with ciprofloxacin resistance, the risk of emergence of novel CrpP variants with a higher ability to affect quinolones is increasing. Furthermore, the spread of crpP genes in highly mobilizable genomic islands among related and non-related P. aeruginosa clones alert the dispersion of MDR pathogens in hospital settings. Full article

(This article belongs to the Special Issue Antimicrobial Resistance in Pseudomonas aeruginosa)

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22 pages, 13548 KiB

Open AccessArticle

Identification of Novel phoP-phoQ Regulated Genes that Contribute to Polymyxin B Tolerance in Pseudomonas aeruginosa

by Baopeng Yang, Chang Liu, Xiaolei Pan, Weixin Fu, Zheng Fan, Yongxin Jin, Fang Bai, Zhihui Cheng and Weihui Wu

Microorganisms 2021, 9(2), 344; https://doi.org/10.3390/microorganisms9020344 - 9 Feb 2021

Cited by 22 | Viewed by 3728

Abstract

Polymyxin B and E (colistin) are the last resorts to treat multidrug-resistant Gram-negative pathogens. Pseudomonas aeruginosa is intrinsically resistant to a variety of antibiotics. The PhoP-PhoQ two-component regulatory system contributes to the resistance to polymyxins by regulating an arnBCADTEF-pmrE operon that encodes lipopolysaccharide modification enzymes. To identify additional PhoP-regulated genes that contribute to the tolerance to polymyxin B, we performed a chromatin immunoprecipitation sequencing (ChIP-Seq) assay and found novel PhoP binding sites on the chromosome. We further verified that PhoP directly controls the expression of PA14_46900, PA14_50740 and PA14_52340, and the operons of PA14_11970-PA14_11960 and PA14_52350-PA14_52370. Our results demonstrated that mutation of PA14_46900 increased the bacterial binding and susceptibility to polymyxin B. Meanwhile, mutation of PA14_11960 (papP), PA14_11970 (mpl), PA14_50740 (slyB), PA14_52350 (ppgS), and PA14_52370 (ppgH) reduced the bacterial survival rates and increased ethidium bromide influx under polymyxin B or Sodium dodecyl sulfate (SDS) treatment, indicating roles of these genes in maintaining membrane integrity in response to the stresses. By 1-N-phenylnaphthylamine (NPN) and propidium iodide (PI) staining assay, we found that papP and slyB are involved in maintaining outer membrane integrity, and mpl and ppgS-ppgH are involved in maintaining inner membrane integrity. Overall, our results reveal novel PhoP-PhoQ regulated genes that contribute to polymyxin B tolerance. Full article

(This article belongs to the Special Issue Antimicrobial Resistance in Pseudomonas aeruginosa)

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