Pathogenesis and pathophysiology

O For IE to develop, the occurrence of several factors is required. Typically, there must be an alteration of the endothelial surfaces of the heart valves to allow for organism attachment and colonization. These alterations may be produced by an inflammatory process such as rheumatic heart disease or by injury from turbulent blood flow. Platelets and fibrin now deposit on the damaged valves, forming a nonbacterial thrombotic endocarditis (NBTE). At this point, bacteria through hematogenous spread (i.e., bacteremia) adhere to and colonize the nidus, forming a vegetation.8 Further deposits of platelets and fibrin cover the bacteria, providing a protective coating that allows for the development of a suitable environment for continued organism and vegetation progression, often producing an organism density of 109 to 1010 colony-forming units (CFU) per gram. This sequence of events is summarized in Figure 74-1.

Acquisition of PVE differs in early stages, where direct inoculation may occur during surgery instead of through hematogenous seeding. The prosthetic valve also has a greater propensity for organism colonization than native valves. However, in late PVE, the process of colonization and vegetation formation is similar to native-valve IE, as described earlier.9

FIGURE 74-1. Pathogenesis of infective endocarditis. (From Ref. 1, Copyright 2005, with permission from Elsevier.)

Classically, vegetations are located on the line along valve closure on the atrial surface of the atrioventricular valves (tricuspid and mitral) or on the ventricular surface of the semilunar valves (pulmonary and aortic) (Fig. 74-2). The vegetations can vary significantly in size ranging from millimeters to several centimeters and may be single or multiple masses. Often, destruction of underlying tissue occurs and may cause perforation of the valve leaflet or rupture of the chordae tendinae, interventricular septum, or papillary muscle. Valve ring abscesses may occur, resulting in fistulas penetrating into the myocardium or pericardial sac, particularly with staphylococcal endocarditis.

Embolic events are also common. Embolization occurs as portions of the friable vegetation break lose and enter the bloodstream. These infected pieces are called septic emboli. Pulmonary abscesses are commonly formed as a result of septic emboli from right-sided IE (tricuspid and pulmonary valves). However, left-sided IE (mitral and aortic valves) is more likely to have an embolus travel to any organ system, especially the kidneys, spleen, and brain. Along with emboli, immune complex deposition may occur in organ systems, causing extracardiac manifestations of the disease. This commonly occurs in the kidneys, producing abscesses, infarction, or glomerulonephritis. Immune complexes or emboli also may produce skin manifestations of the disease, as seen with petechiae, Osler's nodes, and Janeway's lesions, or within the eye (e.g., Roth's spots).

FIGURE 74—2. Diagram of the heart indicating common sites of infection.

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