Abstract
Persistent methicillin-resistant Staphylococcus aureus (MRSA) bacteremia (PB) represents an important subset of S. aureus infection and correlates with poor clinical outcomes. MRSA isolates from patients with PB differ significantly from those of resolving bacteremia (RB) with regard to several in vitro phenotypic and genotypic profiles. For instance, PB strains exhibit less susceptibility to cationic host defense peptides and vancomycin (VAN) killing under in vivo-like conditions, greater damage to endothelial cells, thicker biofilm formation, altered growth rates, early activation of many global virulence regulons (e.g., sigB, sarA, sae and agr) and higher expression of purine biosynthesis genes (e.g., purF) than RB strains. Importantly, PB strains are significantly more resistant to VAN treatment in experimental infective endocarditis as compared to RB strains, despite similar VAN minimum inhibitory concentrations (MICs) in vitro. Here, we review relevant phenotypic and genotypic characteristics related to the PB outcome. These and future insights may improve our understanding of the specific mechanism(s) contributing to the PB outcome, and aid in the development of novel therapeutic and preventative measures against this life-threatening infection.
Highlights
Staphylococcus aureus is a prominent Gram-positive bacteria that can cause a wide spectrum of diseases, ranging from minor skin and skin structure infections to life-threatening diseases [1]
We provide a summary overview of what is known about the specific genotypic and phenotypic characteristics of methicillin-resistant S. aureus (MRSA) isolates related to the Persistent MRSA bacteremia (PB) outcome, focusing on two distinct but interrelated facets: (1) Pathogen-drug interactions; and (2) pathogen-host interactions
Investigations have revealed differences between PB vs. resolving MRSA bacteremia isolates (RB; defined as initial bacteremia resolved within four days of therapy) in genotypic profiles, including pulsed-field gel electrophoresis (PFGE), multi-locus sequence typing (MLST), staphylococcal protein A
Summary
Staphylococcus aureus is a prominent Gram-positive bacteria that can cause a wide spectrum of diseases, ranging from minor skin and skin structure infections to life-threatening diseases (e.g., bacteremia and endocarditis) [1]. S. aureus is a predominant cause of bacteremia and has emerged as a common entity associated with significant morbidity, complications, and mortality [2]. 15–30% of MRSA bacteremia, is especially relevant to endovascular infection and associated with high rates of morbidity and mortality (15–40%) [2,7,8]. We and other investigators have demonstrated specific phenotypic and genotypic features of MRSA may play important roles in the PB outcome [7,9,11,12,13,14]. We provide a summary overview of what is known about the specific genotypic and phenotypic characteristics of MRSA isolates related to the PB outcome, focusing on two distinct but interrelated facets: (1) Pathogen-drug interactions; and (2) pathogen-host interactions. Salvage therapy and potential new targets to combat life-threatening MRSA outcomes are considered
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