Pseudomonas aeruginosa clinical blood isolates display significant phenotypic variability.

TitlePseudomonas aeruginosa clinical blood isolates display significant phenotypic variability.
Publication TypeJournal Article
Year of Publication2022
AuthorsScheffler, RJ, Bratton, BP, Gitai, Z
JournalPLoS One
Volume17
Issue7
Paginatione0270576
Date Published2022
ISSN1932-6203
KeywordsBiological Variation, Population, Humans, Pseudomonas aeruginosa, Pseudomonas Infections, Pyocyanine, Virulence Factors
Abstract

<p>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.</p>

DOI10.1371/journal.pone.0270576
Alternate JournalPLoS One
PubMed ID35793311
PubMed Central IDPMC9258867
Grant ListDP1 AI124669 / AI / NIAID NIH HHS / United States
T32 GM007388 / GM / NIGMS NIH HHS / United States