Infective endocarditis is an uncommon but serious and often life-threatening condition. While developments in cardiac imaging, therapeutics and surgical techniques have led to improved outcomes in individual patients, the overall incidence of infective endocarditis has remained relatively stable from 1950 through 2000, i.e., about 3.6 to 7.0 cases per 100,000 patient-years.1 The predisposing risk factors have changed over time with the emergence of intravenous drug abuse, intravascular prostheses, nosocomial exposure, hemodialysis, and age-related valvular sclerosis as more prevalent than rheumatic heart disease, especially in the developed countries.2 In addition to the risk factors, studies show that the causative flora implicated in infective endocarditis have also evolved, with Staphylococcus aureus emerging as the predominant pathogen, while a recent population-based study disputes this.3 Infective endocarditis is characterized by the presence of vegetations composed of platelets, fibrin, microorganisms, and inflammatory cells. The pathogenesis of infective endocarditis involves a complex sequence or confluence of events.4 Endothelial damage caused by turbulent blood flow seen in congenital or acquired heart disease causes platelets and fibrin deposition leading to formation of non-bacterial thrombotic endocarditis (NBTE). In this setting an episode of bacteremia could result in bacterial adherence to NBTE, bacterial proliferation within the NBTE, and formation of vegetations, the typical lesions of infective endocarditis (figure 1 ▶). Figure 1. Pathogenesis of infectious endocarditis and rationale for antibiotic prophylaxis.