We searched PubMed for articles on infective endocarditis with the key phrase infective endocarditis associated with epidemiology, pathogenesis, experimental, clinics, or therapy. The search was limited to English articles involving people. We also reviewed books written in English on the subject. To generate the epidemiological data presented in figure 1, we searched the PubMed database from 1993 to 2003, using the key phrase infective endocarditis, with English and Review as limits. Only
SeminarInfective endocarditis
Section snippets
Risk factors
Infective endocarditis is often classified in four categories: native-valve infective endocarditis, prosthetic-valve infective endocarditis, infective endocarditis in intravenous drug users, and nosocomial infective endocarditis. These categories delineate clinical conditions and distributions in microbial pathogens (figure 1 and table 1). Additionally, the increasing frequency of disease in haemodialysis patients12 suggests new categories could arise in the future.
Risk of native-valve disease
Pathogenesis
The primary event is bacterial adherence to damaged valves. This event is completed within minutes during transient bacteraemia, and involves valve tissue and bacterial factors. The second step involves persistence and growth of bacteria within the cardiac lesions, usually associated with local extension and tissue damage. Dissemination of septic emboli to distant organs—eg, kidney, spleen, and brain—then takes place.
Prophylaxis
Because of its severity, infective endocarditis should be prevented whenever possible. Determination of adequate prophylaxis implies establishing the patients at risk, the procedures that might provoke bacteraemia, the most effective prophylactic regimen, and a balance between the risks of side-effects of prophylaxis and of developing the disease. Patients at risk and procedures that induce bacteraemia have been identified by clinical studies, and recommendations for prophylaxis have been
Diagnosis: Duke criteria
Precise diagnosis is mandatory to guide therapy. In theory, infective endocarditis combines both persistent bacteraemia and anatomical lesions of the valves. However, blood cultures remain negative in about 10% of cases (figure 1 and table 1). Diagnosis is difficult in culture-negative cases, or when the valve status is unclear.2, 3
In 1994, new diagnostic criteria based on both microbiological data and echocardiographic imaging were proposed.2 These so-called Duke criteria were validated
Management
Treatment of infective endocarditis depends on a multidisciplinary approach, involving at least specialists in infectious disease, cardiologists, and cardiac surgeons. The standard therapeutic regimens proposed below are a consensus based on five articles79, 80, 81, 82, 83 selected in the 1993–2003 PubMed search described above. Regimens for resistant organisms or blood culture negative infective endocarditis are addressed in further sections. Most publications express specialist opinion or
New developments
Developments on ways to prevent and treat infective endocarditis reflect modification of both the bacterium and the host. Vaccines or artificial peptides directed against specific bacterial adhesins could interfere with valve colonisation. Some experimental successes have been achieved with a vaccination against the streptococcal FimA protein121 and the staphylococcal fibronectin-binding and collagen-binding proteins.122, 123, 124, 125 Encouraging clinical successes were reported in
Conclusion
Improvements in health care have almost eradicated classical forms of infective endocarditis. Increased life expectancy and new medical and social behaviours have, however, generated a new group of at-risk patients. Prosthetic-valve endocarditis, nosocomial endocarditis, and endocarditis in intravenous drug users and in haemodialysis patients are not due to classic pneumococci, gonococci, or streptococci, but rather to staphylococci, gram-negative bacteria, and fungi. The apparent increase in
Search strategy
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