The Effect of Shear Stress on the Von Willebrand Factor and its Implications in Infective Endocarditis Caused by Staphylococcus

Abstract

Endocarditis is caused by destruction of heart valve tissue. Infective endocarditis (IE) results from damage caused by microorganisms. IE is a serious disease with a mortality rate of 40%. Even though first described in 1885, IE incidence and mortality rate remains unchanged. In fact, the incidence of IE caused by staphylococci infections has increased over the few past decades. Part of the increase is associated with advancement in healthcare technology like hemodialysis, prosthetic valves, and intracardiac devices and their ability to introduce potential infective sites. Treatment of this disease also has been impacted over the years. Resistance to antibiotics by treatment of staphylococcal strains has been growing. Increasing our understanding of the epidemiology of the bacteria that cause IE is vital. This paper will link our knowledge about the binding tendencies abilities of two IE causing staphylococcal strains, S. aureus and S. lugdunensis, and to what is known about immune cells using that same binding factor under shear stress. This correlation will be used to establish a hypothesis stating that the cleavage of the VWF under shear stress creates an opportunistic environment for S. aureus and S. lugdunensis target high shear force locations, as seen in IE, as another mechanism to evade elimination by the immune system and increase proliferation. No such link currently has been made.