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Infective endocarditis (IE) is a disease caused by a microbial infection involving the endothelial lining of intracardiac structures such as the heart valves. The infection is invariably fatal if untreated. Infection commonly resides on one or more of the heart valve leaflets, but may involve mural endocardium, chordal structures, deeper layers of the myocardium, and/or the pericardium. The presence of an intracardiac or endovascular device provides a nidus for infection, as well as a barrier to eradication. Despite significant advances in the diagnosis and treatment of IE, 6-month mortality still approaches 25%.1,2 Changes in both patient demographics and microbial biology involving an increased incidence of antibiotic-resistant organisms create challenges for contemporary physicians. Prompt recognition and diagnosis, triggered by a high index of clinical suspicion in susceptible patients, trigger aggressive treatment and represent the critical components of a successful management strategy. Combined medical and surgical intervention leads to improved outcomes for selected patients. However, recent years have not seen improved clinical outcomes, despite medical and surgical advances.3 Patient education, attention to general oral-mucosal hygiene, and the appropriate limited use of prophylactic antibiotics are the mainstays of a preventive strategy. IE is often a complex disease with abnormal function in a number of organ systems. Management by a team of physicians and allied healthcare providers is usually required.3,4
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Our current understanding of IE began with the observations of Sir William Osler, who made several important advances in the understanding of this illness, as summarized in his famed Gulstonian lectures of 1885.5,6 Osler defined IE as a primary “mycotic” process and provided the first formal description of two clinical variants of the disease—the acute and fulminating form versus the chronic and insidious form. Despite his extensive knowledge of the disease, Osler acknowledged the reality of diagnostic uncertainty in many cases.
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In the first half of the 20th century, IE was predominantly a complication of rheumatic heart disease and poor dentition. In developing countries, rheumatic heart disease remains the most frequent predisposing cardiac condition.7 However, the epidemiologic features of IE in developed countries have changed considerably in recent decades. The aging of the population has been paralleled by increases in the prevalence of degenerative heart valve disease and in the use of prosthetic heart valves and other intracardiac devices. The numbers of patients with chronic, predisposing medical comorbidities, such as diabetes, human immunodeficiency virus (HIV) infection, end-stage renal disease, and immunosuppressive therapy, have markedly increased, as has the commensurate risk of exposure to nosocomial bacteremia, often with antibiotic resistance.8,9,10 A recent prospective study of 2781 adults with IE found that 25% of cases were associated with recent healthcare exposure.2 These changing demographics are reflected in two observations. First, the median age of patients with IE has gradually increased from 30 to 40 years ...