Investigating the in vivo mechanism behind fibronectin binding protein-mediated hypervirulence of Staphylococcus aureus
Abstract
Staphylococcus aureus is a resourceful Gram-positive pathogen that is a leading cause of disease worldwide. To cause infections, S. aureus uses a range of virulence factors including fibronectin binding protein A (FnbA). FnbA aids in invasion of host cells and S. aureus overexpressing FnbA was previously shown to be hypervirulent in a murine model of systemic infection. Indeed, FnbA overexpression increased the bacterial burden in visceral organs, as compared to WT-infected mice, as early as 1 hour post-infection. Moreover, heterologous non-pathogenic Staphylococci overexpressing FnbA better colonize murine organs during early infection. I have shown that FnbA overexpression permits an increased number of bacterial foci throughout infected organs, however, this alone is not sufficient for the hypervirulent phenotype due to FnbA overexpression. These findings shed further light on the mechanisms for FnbA-mediated hypervirulence and display the need for coordination between multiple S. aureus virulence factors to cause disease.