ArticlePloS one2022
Pseudomonas aeruginosa clinical blood isolates display significant phenotypic variability.
Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Molecular Insight into the Inhibition ofACS omega · 2026Article
- Comparison ofInfection and immunity · 2026Article
- Establishment and application of a vesicle extraction method for clinical strains ofMicrobiology spectrum · 2026Article
- Article
- The genomic configurations driving antimicrobial resistance and virulence in colistin resistant Pseudomonas aeruginosa from an Egyptian Tertiary Oncology Hospital.PLOS global public health · 2025Article
- Bacteriophage as an anti-biofilm agent against Pseudomonas aeruginosa from wound infection.PloS one · 2025Article
- Article
- Analysis of the utility of a rapid vesicle isolation method for clinical strains ofMicrobiology spectrum · 2024Article
- Phenotypic diversity of type III secretion system activity in enteropathogenicJournal of medical microbiology · 2024Article
- A folate inhibitor exploits metabolic differences in Pseudomonas aeruginosa for narrow-spectrum targeting.Nature microbiology · 2024Article
- Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Pseudomonas aeruginosa is a significant threat in healthcare settings where it deploys a wide host of virulence factors to cause disease. Many virulence-related phenotypes such as pyocyanin production, biofilm formation, and twitching motility have been implicated in causing disease in a number of hosts. In this study, we investigate these three virulence factors in a collection of 22 clinical strains isolated from blood stream infections. Despite the fact that all 22 strains caused disease and came from the same body site of different patients, they show significant variability in assays for each of the three specific phenotypes examined. There was no significant correlation between the strength of the three phenotypes across our collection, suggesting that they can be independently modulated. Furthermore, strains deficient in each of the virulence-associated phenotypes examined could be identified. To understand the genetic basis of this variability we sequenced the genomes of the 22 strains. We found that the majority of genes responsible for pyocyanin production, biofilm formation, and twitching motility were highly conserved among the strains despite their phenotypic variability, suggesting that the phenotypic variability is likely due to regulatory changes. Our findings thus demonstrate that no one lab-assayed phenotype of pyocyanin production, biofilm production, and twitching motility is necessary for a P. aeruginosa strain to cause blood stream infection and that additional factors may be needed to fully predict what strains will lead to specific human diseases.
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