How endocarditis takes place ? (PATHOGENESIS)

The pathogenesis of endocarditis starts with an area of endocardial injury leading to platelet-firin deposition. The next step requires a microorganism to enter the bloodstream and adhere to the area of injury. Injury and infection most commonly occur on the valve leaflts but can also occur on or near congenital defects, chordae, chamber walls, prosthetic valve attachments, pacemaker leads, or any other endocardial location where conditions are met. Subacute bacterial endocarditis most commonly occurs on the downstream side of a signifiant pressure gradient related to the rheumatic heart lesions, bicuspid aortic valve, or a variety of congenital heart lesions such as ventricular septal defect. Predisposing factors select organisms to enter the blood stream, and once present, adherence factors determine the like lihood of a particular organism causing endocarditis. Adherence facilitates the initial colonization of the valve surface. Certain species of bacteria—for example, Staphylococcus and Streptococcus species—produce the majority of the human cases of endocarditis because of their ability to adhere to damaged tissues of the heart. Conversely, Escherichia coli can be a common cause of bacteremia from urinary or gastrointestinal sources but is a rare cause of endocarditis because it lacks these adherence factors.


In 1978 Drs. Sheld, Valone, and Sande described the role of dextran, platelets, and fibrin in the adherence of streptococci to damaged endocardial tissue. Staphylococci use a variety of surface-bound adhesion components to bind to firinogen for colonization and fironectin for invasion. Certain enzyme possess clumping factor binding firinogen and fironectin as a virulence factor. Once attached to the platelet-firin nidus, bacteria begin to multiply, increasing coagulation activation, attraction of leukocytes, and growth of inflmmation-promoting vegetation This in effect buries bacteria deep within the mature vegetation, contributing to the treatment challenge of IE.