Parallel Evolution of Pseudomonas aeruginosa during a Prolonged ICU-Infection Outbreak

Cameron, David R.; Pitton, Melissa; Oberhaensli, Simone; Schlegel, Katja; Prod’hom, Guy; Blanc, Dominique; Jakob, Stephan M.; Que, Yok-Ai

doi:10.1128/spectrum.02743-22

Cited by 5 publications

(3 citation statements)

References 58 publications

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“…The evolution of AMR may be followed in vivo by comparing the isolates obtained from patients treated with antimicrobial drugs. This method was successfully used to study the phenotypic and genetic features of P. aeruginosa resistance in different infections, including bloodstream, lung, wound, etc., [3][4][5][6][7]. However, in such in vivo evolution studies, only a limited number of successful mutants, with the likely loss of intermediate forms, are usually available for analysis.…”

Section: Introductionmentioning

confidence: 99%

Genetic Alternatives for Experimental Adaptation to Colistin in Three Pseudomonas aeruginosa Lineages

Chebotar,

Savinova,

Bocharova

et al. 2024

Antibiotics

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Pseudomonas aeruginosa is characterized by a high adaptive potential, developing resistance in response to antimicrobial pressure. We employed a spatiotemporal evolution model to disclose the pathways of adaptation to colistin, a last-resort polymyxin antimicrobial, among three unrelated P. aeruginosa lineages. The P. aeruginosa ATCC-27833 reference strain (Pa_ATCC), an environmental P. aeruginosa isolate (Pa_Environment), and a clinical isolate with multiple drug resistance (Pa_MDR) were grown over an increasing 5-step colistin concentration gradient from 0 to 400 mg/L. Pa_Environment demonstrated the highest growth pace, achieving the 400 mg/L band in 15 days, whereas it took 37 and 60 days for Pa_MDR and Pa_ATCC, respectively. To identify the genome changes that occurred during adaptation to colistin, the isolates selected during the growth of the bacteria (n = 185) were subjected to whole genome sequencing. In total, 17 mutation variants in eight lipopolysaccharide-synthesis-associated genes were detected. phoQ and lpxL/PA0011 were affected in all three lineages, whereas changes in pmrB were found in Pa_Environment and Pa_MDR but not in Pa_ATCC. In addition, mutations were detected in 34 general metabolism genes, and each lineage developed mutations in a unique set of such genes. Thus, the three examined distinct P. aeruginosa strains demonstrated different capabilities and genetic pathways of colistin adaptation.

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Section: Introductionmentioning

confidence: 99%

Genetic Alternatives for Experimental Adaptation to Colistin in Three Pseudomonas aeruginosa Lineages

Chebotar,

Savinova,

Bocharova

et al. 2024

Antibiotics

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“…Biofilms adopt a specific architecture with a complex matrix trapping and protecting bacteria that merges with human tissues and secretions [ 3 ]. Bacteria in a biofilm display high tolerance to antimicrobials and host immune defense, enabling pathogens to survive in hostile environments and to disperse and colonize new tissues [ 4 , 5 ]. In addition, a small percentage of cells in biofilms adopt the persister phenotype.…”

Section: Introductionmentioning

confidence: 99%

The natriuretic peptide receptor agonist osteocrin disperses Pseudomonas aeruginosa biofilm

Louis¹,

Tahrioui²,

Lendon

et al. 2023

Biofilm

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“…β-lactams with or without β-lactamase inhibitors are often the first-line therapy for severe infections caused by P. aeruginosa, but this bacterium may render β-lactams useless through a range of complex resistance mechanisms [9][10][11][12][13]. Several β-lactamases can be carried by P. aeruginosa, but the metallo-β-lactamases (MBLs) have, in recent years, become more frequent.…”

Section: Introductionmentioning

confidence: 99%

The First Swedish Outbreak with VIM-2-Producing Pseudomonas aeruginosa, Occurring between 2006 and 2007, Was Probably Due to Contaminated Hospital Sinks

et al. 2023

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Multidrug-resistant Pseudomonas aeruginosa is an increasing clinical problem worldwide. The aim of this study was to describe the first outbreak of a Verona integron-borne metallo-ß-lactamase (VIM)-2-producing P. aeruginosa strain in Sweden and its expansion in the region. A cluster of multidrug-resistant P. aeruginosa appeared at two neighbouring hospitals in 2006. The isolates were characterized by PCR, pulsed-field gel electrophoresis (PFGE), and whole-genome sequencing. Patient charts, laboratory records, and hygiene routines were reviewed, and patients, staff, and the environment were screened. The investigation revealed a clonal outbreak of a VIM-2-producing P. aeruginosa strain belonging to the high-risk clonal complex 111, susceptible only to gentamicin and colistin. No direct contact between patients could be established, but most of them had stayed in certain rooms/wards weeks to months apart. Cultures from two sinks yielded growth of the same strain. The outbreak ended when control measures against the sinks were taken, but new cases occurred in a tertiary care hospital in the region. In conclusion, when facing prolonged outbreaks with this bacterium, sinks and other water sources in the hospital environment should be considered. By implementing proactive control measures to limit the bacterial load in sinks, the waterborne transmission of P. aeruginosa may be reduced.

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Parallel Evolution of Pseudomonas aeruginosa during a Prolonged ICU-Infection Outbreak

Abstract: Pseudomonas aeruginosa is a Gram-negative pathogen causing infections in acutely burned patients. The precise mechanisms required for the establishment of infection in the burn setting, and adaptive traits underpinning prolonged outbreaks are not known.

Cited by 5 publications

References 58 publications

Genetic Alternatives for Experimental Adaptation to Colistin in Three Pseudomonas aeruginosa Lineages

Genetic Alternatives for Experimental Adaptation to Colistin in Three Pseudomonas aeruginosa Lineages

The natriuretic peptide receptor agonist osteocrin disperses Pseudomonas aeruginosa biofilm

The First Swedish Outbreak with VIM-2-Producing Pseudomonas aeruginosa, Occurring between 2006 and 2007, Was Probably Due to Contaminated Hospital Sinks

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