Carbapenemase-producing Pseudomonas aeruginosa in Spain: interregional dissemination of the high-risk clones ST175 and ST244 carrying blaVIM-2, blaVIM-1, blaIMP-8, blaVIM-20 and blaKPC-2

Pérez-Vázquez, Marı́a; Sola‐Campoy, Pedro J.; Zurita, Ángela María; Ávila, Alicia; Gómez‐Bertomeu, Frederic; Solís, Sonia; López-Urrutia, Luis; González-Barberá, Eva M.; Cercenado, Emilia; Bautista, Verónica; Lara, Noelia; Aracil, Belén; Oliver, Antonio; Campos, José; Oteo, Jesús

doi:10.1016/j.ijantimicag.2020.106026

Cited by 32 publications

(11 citation statements)

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“…These results show the importance of using a cgMLST scheme to evaluate the effect of recombination on the genetic similarity between isolates. Such schemes have been proposed, but none of the studies addressed a comparison with a SNP calling approach or the effect of recombination (Mellmann et al, 2016;de Sales et al, 2020;Perez-Vazquez et al, 2020;Royer et al, 2020;Stanton et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

Comparison of Whole Genome (wg-) and Core Genome (cg-) MLST (BioNumericsTM) Versus SNP Variant Calling for Epidemiological Investigation of Pseudomonas aeruginosa

et al. 2020

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Section: Discussionmentioning

confidence: 99%

Comparison of Whole Genome (wg-) and Core Genome (cg-) MLST (BioNumericsTM) Versus SNP Variant Calling for Epidemiological Investigation of Pseudomonas aeruginosa

et al. 2020

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“…Kinetics assays with these inhibitors were also performed using the metallo-β-lactamase VIM-1, a class B β-lactamase frequently produced by P. aeruginosa . The K i app parameter was calculated for avibactam and compounds 1–3 against the VIM-1 enzyme.…”

Section: Methodsmentioning

confidence: 99%

6-Halopyridylmethylidene Penicillin-Based Sulfones Efficiently Inactivate the Natural Resistance of Pseudomonas aeruginosa to β-Lactam Antibiotics

et al. 2021

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Pseudomonas aeruginosa, a major cause of nosocomial infections, is considered a paradigm of antimicrobial resistance, largely due to hyperproduction of chromosomal cephalosporinase AmpC. Here, we explore the ability of 6pyridylmethylidene penicillin-based sulfones 1−3 to inactivate the AmpC β-lactamase and thus rescue the activity of the antipseudomonal ceftazidime. These compounds increased the susceptibility to ceftazidime in a collection of clinical isolates and PAO1 mutant strains with different ampC expression levels and also improved the inhibition kinetics relative to avibactam, displaying a slow deacylation rate and involving the formation of an indolizine adduct. Bromide 2 was the inhibitor with the lowest K I (15.6 nM) and the highest inhibitory efficiency (k inact /K I ). Computational studies using diverse AmpC enzymes revealed that the aromatic moiety in 1−3 targets a tunnel-like site adjacent to the catalytic serine and induces the folding of the H10 helix, indicating the potential value of this not-always-evident pocket in drug design.

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“…The acquisition of carbapenemases by P. aeruginosa has contributed towards a significant proportion of overall carbapenemase resistance [264]. In a study of 232 carbapenemresistant P. aeruginosa isolates, 71 isolates had carbapenemases that had likely been acquired through HGT [265]. In P. aeruginosa acquisition of β-lactamase genes by horizontal transfer occurs via plasmids or through integrative and conjugative elements (ICEs) that integrate into the chromosome of recipient cells following transfer.…”

Section: β-Lactamases Acquired By Horizontal Gene Transfermentioning

confidence: 99%

β-lactam Resistance in Pseudomonas aeruginosa: Current Status, Future Prospects

Glen

Lamont

2021

Pathogens

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Pseudomonas aeruginosa is a major opportunistic pathogen, causing a wide range of acute and chronic infections. β-lactam antibiotics including penicillins, carbapenems, monobactams, and cephalosporins play a key role in the treatment of P. aeruginosa infections. However, a significant number of isolates of these bacteria are resistant to β-lactams, complicating treatment of infections and leading to worse outcomes for patients. In this review, we summarize studies demonstrating the health and economic impacts associated with β-lactam-resistant P. aeruginosa. We then describe how β-lactams bind to and inhibit P. aeruginosa penicillin-binding proteins that are required for synthesis and remodelling of peptidoglycan. Resistance to β-lactams is multifactorial and can involve changes to a key target protein, penicillin-binding protein 3, that is essential for cell division; reduced uptake or increased efflux of β-lactams; degradation of β-lactam antibiotics by increased expression or altered substrate specificity of an AmpC β-lactamase, or by the acquisition of β-lactamases through horizontal gene transfer; and changes to biofilm formation and metabolism. The current understanding of these mechanisms is discussed. Lastly, important knowledge gaps are identified, and possible strategies for enhancing the effectiveness of β-lactam antibiotics in treating P. aeruginosa infections are considered.

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Carbapenemase-producing Pseudomonas aeruginosa in Spain: interregional dissemination of the high-risk clones ST175 and ST244 carrying blaVIM-2, blaVIM-1, blaIMP-8, blaVIM-20 and blaKPC-2

Cited by 32 publications

References 38 publications

Comparison of Whole Genome (wg-) and Core Genome (cg-) MLST (BioNumericsTM) Versus SNP Variant Calling for Epidemiological Investigation of Pseudomonas aeruginosa

Comparison of Whole Genome (wg-) and Core Genome (cg-) MLST (BioNumericsTM) Versus SNP Variant Calling for Epidemiological Investigation of Pseudomonas aeruginosa

6-Halopyridylmethylidene Penicillin-Based Sulfones Efficiently Inactivate the Natural Resistance of Pseudomonas aeruginosa to β-Lactam Antibiotics

β-lactam Resistance in Pseudomonas aeruginosa: Current Status, Future Prospects

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