All Staphylococcus aureus bacteraemia-inducing strains can cause infective endocarditis: Results of GWAS and experimental animal studies.

Animals Rabbits Mice Genome-Wide Association Study Bacteremia / microbiology Staphylococcal Infections / microbiology Staphylococcus aureus / genetics Endocarditis, Bacterial / microbiology Endocarditis / microbiology

Bacteraemia Experimental animal model Genome-wide association study Infective endocarditis Staphylococcus aureus

Journal

The Journal of infection

ISSN: 1532-2742

Titre abrégé: J Infect

Pays: England

ID NLM: 7908424

Informations de publication

Date de publication:
02 2023

Historique:

received: 22 07 2022

revised: 21 11 2022

accepted: 24 12 2022

pubmed: 6 1 2023

medline: 2 2 2023

entrez: 5 1 2023

Statut: ppublish

Résumé

We aimed at determining whether specific S. aureus strains cause infective endocarditis (IE) in the course of Staphylococcus aureus bacteraemia (SAB). A genome-wide association study (GWAS) including 924 S. aureus genomes from IE (274) and non-IE (650) SAB patients from international cohorts was conducted, and a subset of strains was tested with two experimental animal models of IE, one investigating the early step of bacterial adhesion to inflamed mice valves, the second evaluating the local and systemic developmental process of IE on mechanically-damaged rabbit valves. The genetic profile of S. aureus IE and non-IE SAB strains did not differ when considering single nucleotide polymorphisms, coding sequences, and k-mers analysed in GWAS. In the murine inflammation-induced IE model, no difference was observed between IE and non-IE SAB strains both in terms of adhesion to the cardiac valves and in the propensity to cause IE; in the mechanical IE-induced rabbit model, there was no difference between IE and non-IE SAB strains regarding the vegetation size and CFU. All strains of S. aureus isolated from SAB patients must be considered as capable of causing this common and lethal infection once they have accessed the bloodstream.

Identifiants

DOI: 10.1016/j.jinf.2022.12.028 PMID: 36603774 PMC: PMC10399548

pubmed: 36603774

pii: S0163-4453(22)00754-X

doi: 10.1016/j.jinf.2022.12.028

pmc: PMC10399548

mid: NIHMS1917496

pii:

doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

Pagination

123-133

Subventions

Organisme : NIAID NIH HHS

ID : R01 AI134692

Pays : United States

Organisme : NIAID NIH HHS

ID : R01 AI165671

Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

Déclaration de conflit d'intérêts

Declaration of Competing Interest FV reports research funding outside the scope of the present study by bioMérieux, two patents pending in antimicrobial resistance detection and shares in Weezion. VGF reports personal fees from Novartis, Novadigm, Durata, Debiopharm, Genentech, Achaogen, Affinium, Medicines Co., Cerexa, Tetraphase, Trius, MedImmune, Bayer, Theravance, Basilea, Affinergy, Janssen, xBiotech, Contrafect, Regeneron, Basilea, Destiny, Amphliphi Biosciences. Integrated Biotherapeutics; C3J, grants from NIH, MedImmune, Cerexa/Forest/Actavis/Allergan, Pfizer, Advanced Liquid Logics, Theravance, Novartis, Cubist/Merck; Medical Biosurfaces; Locus; Affinergy; Contrafect; Karius; Genentech, Regeneron, Basilea, Janssen, from Green Cross, Cubist, Cerexa, Durata, Theravance; Debiopharm, Royalties from UpToDate; and a patent pending in sepsis diagnostics.

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