Pathogenesis:

Endocarditis arise from implantation of bacteria onto endocardium from bloodstream or by bacterial embolism of valve capillaries. Endocarditis is predisposed by trauma to the endothelial surface exposing collagen and leading to binding of platelets, activation of the extrinsic coagulation cascade with deposition of fibrin and the formation of sterile platelet-fibrin deposits.

Following infection, bacteria from other system gets dislodged, enters the blood and circulates in bloodstream.

Bacteria then settles in healthy valves and inner lining and starts to produce pathological changes.

Vegetation are formed on endo-cardial surface of valves. They are formed by platelets, fibrin, bacteria and inflammatory cells.

These infections then extend to myocardium causing infarction in smaller areas to occlusion of small branches.

Infection further extends to pericardium and finally cardiac rhythm disrupts due to toxaemia and septicaemia.