Pathogenesis and Rationale for Prophylaxis

The fundamental step in the pathogenesis of IE is the development of bacteremia, with subsequent seeding of a previously damaged endocardial surface. Experimental studies suggest that valvular endothelial damage leads to platelet and fibrin deposition and the formation of a nonbacterial thrombotic vegetation. Circulating bacteria can then adhere to these lesions and multiply within the platelet-fibrin complex, leading to an infected vegetation. Dental treatment has traditionally been considered the major cause of the bacteremia that leads to IE [3], mainly because of historical studies that demonstrated a high frequency of bacteremia after various oral invasive procedures, as well as because of previous studies documenting the viridans group streptococci (VGS, the predominant members of the oral microflora) as the leading cause of IE. The initial recognition of a relationship between viridans streptococcal IE and dental procedures is attributed to Horder in 1909 [2,3]. In 1923, Lewis and Grant proposed the hypothesis that abnormally structured heart valves may contribute to the development of IE in healthy adults by trapping and retaining organisms from the transient bacteremia [4]. In 1935, Okell and Elliott, in a series of 138 patients, demonstrated the presence of bacteremia related to tooth extraction; in 64% of the cases, the isolate was a Streptococcus spp. [5]. Another study, published in 1937 by Burket and Burn [6], confirmed the biological plausibility of the oral cavity as the source of bacteremia when they painted the gingival crevices of 90 patients with S. marcescens (which was felt to be non-pathogenic at the time) before dental extraction. Subsequent to the procedure, the organism was recovered in 20% of the blood cultures. One study demonstrated a "dose-dependent"-like effect, with a significant correlation found between the number of teeth extracted and subsequent positive blood cultures [7]. Thus, it has become well established that bacteremia may occur after dental procedures that compromise mucosal surfaces, especially dental extractions and gingival surgery [8]. This bacteremia, however, is transient, lasting typically no more than 15-30

minutes [9,10], as well as low grade (usually <100 colony-forming units/mL of blood) [9]. Transient asymptomatic bacteremia also occurs after a variety of other procedures and manipulations, particularly those associated with trauma to the mucous membranes of the respiratory, esophageal, gastrointestinal, and genito-urinary tracts. If the bacteremia following these procedures is a major cause of IE, in theory, maneuvers that decrease the magnitude and/or the duration of this bacteremia could prevent the development of IE in patients at risk for the disease.

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