Native-valve infective endocarditis is uncommon, with an incidence of approximately 2-10 cases per hundred thousand person years.
The initiating event is injury to the valvular endothelium or endocardium.
The injury exposes subendothelial collagen and other matrix molecules to which platelets and fibrin adhere and form a microthrombotic sterile vegetation.
Subsequently circulating bacteria can bind to and colonize this lesion.
Bacteria will replicate and stimulate firther platelet and fiber and deposition to form an infected vegetation that is the
hallmark of infective endocarditis.
Vegetations have a protective microenvironment that makes neutrophils and host defense molecules only poorly accessible.
Vegetations have high density bacteria and they promote high-grade bacteremia and further the growth of the vegetation.
When the vegetation becomes friable fragments readily enter the circulation.
There are four conditions that drive, and are responsible for most of the clinical features of infective endocarditis and its complications: high bacterial densities, growing vegetation, friability, and fragmentation of the vegetation.
These four processes are the mechanisms responsible for the clinical features of infective endocarditis including: valvular destruction, paravalvular extension of infection, heart failure, and microvascular and large vessel embolization. metastatic infection of target organs including the brain, kidneys, spleen, and lungs, and immuno logic processes such as hypocomplementemic glomerulonephritis and false positive serologic findings of rheumatoid factor, anti-neutrophil antibodies, and syphilis.