Infective Endocarditis
Bloodstream bacteria seed a damaged or abnormal endocardial surface and become trapped in a platelet-fibrin vegetation that shields them from the immune system, so the disease is driven simultaneously by local valve destruction, embolisation of vegetation fragments, and immune complex deposition at distant sites.
First principles
Why bacteria can only take hold on damaged or turbulent endothelium
Healthy endothelium resists bacterial adherence. Turbulent flow or endothelial injury (an abnormal or prosthetic valve, a congenital defect, or repeated jet trauma from intravenous drug use) exposes subendothelial collagen, onto which platelets and fibrin deposit even before infection occurs. A transient bacteraemia, from dental work, skin infection, an infected line, or intravenous drug use, then seeds this ready-made nidus, and bacteria proliferate within the fibrin-platelet mesh.
Educational content pending clinical review. Not medical advice.