Staphylococcus aureus strains sustain their high-virulent phenotype during native endocarditis

Staphylococcus aureus endocarditis is a severe infection associated with valve destruction and cardiac tissue damage. The aim of this study was to analyse the virulence characteristics of S. aureus endocarditis isolates and to assess their potential adaptation to the host environment.

Paired S. aureus isolates were collected from valve tissue and corresponding blood cultures of ten patients undergoing valve surgery for infective endocarditis. The strain pairs were characterized using molecular and phenotypic analyses to detect potential early bacterial adaptation during the course of endocarditis. Furthermore, we conducted a quantitative analysis of wild-type phenotypes and small-colony variants of S. aureus isolates directly plated from native heart tissue compared with isolates obtained from bacteraemia and deep-seated infections, including soft tissue infections and osteomyelitis.

Whole-genome analysis confirmed a high degree of genetic identity between paired blood and valve isolates from the same patient. Genes commonly associated with S. aureus endocarditis, such as those encoding adhesins and toxins, were highly prevalent. In vitro assays assessing endothelial cell invasion, cytotoxicity, and biofilm formation revealed no significant differences between blood and valve isolate groups. Yet, within one strain pair isolated from a cardiac device-associated endocarditis case, the valve isolate showed reduced metabolic activity, endothelial cell invasion capacity, and cytotoxicity. Furthermore, isolates directly recovered from native heart tissue predominantly exhibited fully virulent wild-type phenotypes, whereas higher rates of adapted small-colony variants were detected in samples derived from soft tissue infections and osteomyelitis.

Our in vitro analysis of endocarditis isolates indicates that S. aureus largely maintains a highly virulent phenotype during native valve endocarditis, potentially contributing to the marked tissue destruction characteristic of this infection. Continuous exposure to the intravascular environment and its immune pressures may constrain phenotypic adaptation, thereby sustaining bacterial metabolic activity and virulence.