dc.contributor.author | Wagner, Theresa Maria | |
dc.contributor.author | Pöntinen, Anna Kaarina | |
dc.contributor.author | Fenzel, Carolin Kornelia | |
dc.contributor.author | Engi, Daniel | |
dc.contributor.author | Janice, Jessin | |
dc.contributor.author | Almeida-Santos, Ana C. | |
dc.contributor.author | Tedim, Ana P. | |
dc.contributor.author | Freitas, Ana R. | |
dc.contributor.author | Peixe, Luísa | |
dc.contributor.author | van Schaik, Willem | |
dc.contributor.author | Johannessen, Mona Susan | |
dc.contributor.author | Hegstad, Kristin | |
dc.date.accessioned | 2024-09-10T07:43:10Z | |
dc.date.available | 2024-09-10T07:43:10Z | |
dc.date.issued | 2024-03-09 | |
dc.description.abstract | Enterococcus faecium (Efm) is a versatile pathogen, responsible for multidrug-resistant infections, especially in hospitalized immuno compromised patients. Its population structure has been characterized by diverse clades (A1, A2, and B (reclassified as E. lactis (Ela)),
adapted to different environments, and distinguished by their resistomes and virulomes. These features only partially explain the
predominance of clade A1 strains in nosocomial infections. We investigated in vitro interaction of 50 clinical isolates (clade A1 Efm)
against 75 commensal faecal isolates from healthy humans (25 clade A2 Efm and 50 Ela). Only 36% of the commensal isolates inhibited
clinical isolates, while 76% of the clinical isolates inhibited commensal isolates. The most apparent overall differences in inhibition
patterns were presented between clades. The inhibitory activity was mainly mediated by secreted, proteinaceous, heat-stable compounds, likely indicating an involvement of bacteriocins. A custom-made database targeting 76 Bacillota bacteriocins was used to
reveal bacteriocins in the genomes. Our systematic screening of the interactions between nosocomial and commensal Efm and Ela on
a large scale suggests that, in a clinical setting, nosocomial strains not only have an advantage over commensal strains due to their
possession of AMR genes, virulence factors, and resilience but also inhibit the growth of commensal strains. | en_US |
dc.identifier.citation | Wagner, Pöntinen, Fenzel, Engi, Janice, Almeida-Santos, Tedim, Freitas, Peixe, van Schaik, Johannessen, Hegstad. Interactions between commensal Enterococcus faecium and Enterococcus lactis and clinical isolates of Enterococcus faecium. FEMS microbes. 2024;5 | en_US |
dc.identifier.cristinID | FRIDAID 2267001 | |
dc.identifier.doi | 10.1093/femsmc/xtae009 | |
dc.identifier.issn | 2633-6685 | |
dc.identifier.uri | https://hdl.handle.net/10037/34640 | |
dc.language.iso | eng | en_US |
dc.publisher | Oxford University Press | en_US |
dc.relation.journal | FEMS microbes | |
dc.rights.accessRights | openAccess | en_US |
dc.rights.holder | Copyright 2024 The Author(s) | en_US |
dc.rights.uri | https://creativecommons.org/licenses/by/4.0 | en_US |
dc.rights | Attribution 4.0 International (CC BY 4.0) | en_US |
dc.title | Interactions between commensal Enterococcus faecium and Enterococcus lactis and clinical isolates of Enterococcus faecium | en_US |
dc.type.version | publishedVersion | en_US |
dc.type | Journal article | en_US |
dc.type | Tidsskriftartikkel | en_US |
dc.type | Peer reviewed | en_US |