Infectious Deployment of Staphylococcus aureus on the Endothelium of Blood Vessels and on Blood Components

Infective endocarditis continues to represent a challenge for healthcare systems, requiring careful management and resources. It appears that there may have been something of a shift, in recent years, from Streptococcus sp a to Staphylococcus sp and Enterococcus sp as the primary pathogens of concern. This shift is of concern as it is associated with Staphylococcus Aureus which has a high virulence rate and a tendency to form a biofilm, meaning that non-surgical therapy may not be effective. It is imperative to deliberate on the likelihood of platelet blood clot formation, which may be accompanied by bacterial infestation and the development of a biofilm. An endocarditis lesion is believed to comprise primarily a fibrin and platelet blood clot infested with bacteria, which adheres to the cardiac valves. Consequently, infective endocarditis serves as a paradigm of immunothrombosis that has developed in an unfavorable manner. The concept of immunothrombosis involves a multifacetered interaction among the coagulation system, innate immunity, and the function of coagulation in isolating and eliminating invasive pathogens. However, in the context of infective endocarditis, immunothrombosis unintentionally establishes an optimal environment that is conducive to bacteria proliferation. The process of immunothrombosis functions to impede the host immune system, thus enabling bacterial proliferation in a manner that is largely uninhibited. The coagulation system plays a pivotal role in the progression of this condition at each stage. It has been demonstrated that the coagulation system plays a pivotal role in the initial adhesion of bacteria to the leaflets, the subsequent proliferation and maturation of vegetations, and the development of complications such as embolization and valve dysfunction. Furthermore, the primary etiological agent of infective endocarditis, Staphylococcus aureus, has been demonstrated to manipulate immunothrombosis, thriving within the fibrin-rich milieu of an endocarditis vegetation. Given its central role in infective endocarditis, the coagulation system emerges as an attractive therapeutic target for this deadly disease. However, it is crucial to exercise caution, as the use of antithrombotic agents in patients with endocarditis frequently accompanies an elevated bleeding risk.