(A) Valve colonization as a consequence of mechanical injury. (1) Initially sterile platelet-fibrin nidus. (2) Bacteria bind to coagulum and colonize it during transient bacteraemia. Adhered monocytes release tissue factor and cytokines. (3) More platelets are attracted and become activated, and the vegetation grows. (4) Endothelial cells are infected and can be lysed by bacterial products or bacteria can persist inside the cells by changing phenotype into small colony variants.
(B) Valve colonization as a consequence of an inflammatory endothelial lesion. (1) Activated endothelial cells express integrins that promote the local deposition of fibronectin; bacteria such as Staphylococcus aureus adhere to this protein. (2) Bacteria are internalized, and endothelial cells release tissue factor and cytokines, causing blood clotting and promoting the extension of inflammation and vegetation formation. (3) Infected endothelial cells can be lysed by bacterial products or bacteria can persist inside the cells by changing phenotype into small colony variants.
Reprinted by permission from Macmillan Publishers Ltd: Nature Reviews Cardiology. Werdan K, Dietz S, Löffler B, et al. Mechanisms of infective endocarditis: pathogen–host interaction and risk states. Nat Rev Cardiol 2014; 11:35.
www.nature.com/nrcardio.
