Elsevier

The Lancet

Volume 363, Issue 9403, 10 January 2004, Pages 139-149
The Lancet

Seminar
Infective endocarditis

https://doi.org/10.1016/S0140-6736(03)15266-XGet rights and content

Summary

Despite improvements in health care, the incidence of infective endocarditis has not decreased over the past decades. This apparent paradox is explained by a progressive evolution in risk factors; while classic predisposing conditions such as rheumatic heart disease have been all but eradicated, new risk factors for infective endocarditis have emerged. These include intravenous drug use, sclerotic valve disease in elderly patients, use of prosthetic valves, and nosocomial disease. Newly identified pathogens, which are difficult to cultivate—eg, Bartonella spp and Tropheryma whipplei—are present in selected individuals, and resistant organisms are challenging conventional antimicrobial therapy. Keeping up with these changes depends on a comprehensive approach, allying understanding of the pathogenesis of disease with the development of new drugs for infective endocarditis. Infection by staphylococci and streptococci is being dissected at the molecular level. New ideas for antimicrobial agents are being developed. These novel insights should help redefine preventive and therapeutic strategies against infective 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

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

References (145)

  • PattiJM et al.

    Microbial adhesins recognizing extracellular matrix macromolecules

    Curr Opin Cell Biol

    (1994)
  • JT Van der Meer et al.

    Efficacy of antibiotic prophylaxis for prevention of native-valve endocarditis

    Lancet

    (1992)
  • BayerAS et al.

    Evaluation of new clinical criteria for the diagnosis of infective endocarditis

    Am J Med

    (1994)
  • DoddsGA et al.

    Negative predictive value of the Duke criteria for infective endocarditis

    Am J Cardiol

    (1996)
  • HabibG et al.

    Value and limitations of the Duke criteria for the diagnosis of infective endocarditis

    J Am Coll Cardiol

    (1999)
  • HoupikianP et al.

    Diagnostic methods current best practices and guidelines for identification of difficult-to-culture pathogens in infective endocarditis

    Infect Dis Clin North Am

    (2002)
  • HeldmanAW et al.

    Oral antibiotic treatment of right-sided staphylococcal endocarditis in injection drug users: prospective randomized comparison with parenteral therapy

    Am J Med

    (1996)
  • RehmSJ

    Outpatient intravenous antibiotic therapy for endocarditis

    Infect Dis Clin North Am

    (1998)
  • HiramatsuK et al.

    Dissemination in Japanese hospitals of strains of Staphylococcus aureus heterogeneously resistant to vancomycin

    Lancet

    (1997)
  • HiramatsuK

    Vancomycin-resistant Staphylococcus aureus: a new model of antibiotic resistance

    Lancet Infect Dis

    (2001)
  • NobleWC et al.

    Co-transfer of vancomycin and other resistance genes from Enterococcus faecalis NCTC 12201 to Staphylococcus aureus

    FEMS Microbiol Lett

    (1992)
  • CF Von Reyn et al.

    Infective endocarditis: an analysis based on strict case definitions

    Ann Intern Med

    (1981)
  • LiJS et al.

    Proposed modifications to the Duke criteria for the diagnosis of infective endocarditis

    Clin Infect Dis

    (2000)
  • WatanakunakornC et al.

    Infective endocarditis at a large community teaching hospital, 1980–1990: a review of 210 episodes

    Medicine (Baltimore)

    (1993)
  • SandreRM et al.

    Infective endocarditis: review of 135 cases over 9 years

    Clin Infect Dis

    (1996)
  • MathewJ et al.

    Clinical features, site of involvement, bacteriologic findings, and outcome of infective endocarditis in intravenous drug users

    Arch Intern Med

    (1995)
  • HoenB et al.

    Changing profile of infective endocarditis: results of a 1-year survey in France

    JAMA

    (2002)
  • DH Johnson et al.

    A forty-year review of bacterial endocarditis in infancy and childhood

    Circulation

    (1975)
  • NormandJ et al.

    Changing patterns and prognosis of infective endocarditis in childhood

    Eur Heart J

    (1995)
  • BouzaE et al.

    Infective endocarditis: a prospective study at the end of the twentieth century—new predisposing conditions, new etiologic agents, and still a high mortality

    Medicine (Baltimore)

    (2001)
  • HoenB et al.

    Changing profile of infective endocarditis, results of a 1-year survey in France

    JAMA

    (2002)
  • AbbottKC et al.

    Hospitalizations for bacterial endocarditis after initiation of chronic dialysis in the United States

    Nephron

    (2002)
  • BrouquiP et al.

    Endocarditis due to rare and fastidious bacteria

    Clin Microbiol Rev

    (2001)
  • RoderBL et al.

    Clinical features of Staphylococcus aureus endocarditis: a 10-year experience in Denmark

    Arch Intern Med

    (1999)
  • MylonakisE et al.

    Infective endocarditis in adults

    N Engl J Med

    (2001)
  • MorrisCD et al.

    Thirty-year incidence of infective endocarditis after surgery for congenital heart defect

    JAMA

    (1998)
  • VarstelaE

    Personal follow-up of 100 aortic valve replacement patients for 1081 patient years

    Ann Chir Gynaecol

    (1998)
  • TornosP et al.

    Clinical outcome and long-term prognosis of late prosthetic valve endocarditis: a 20-year experience

    Clin Infect Dis

    (1997)
  • ShekarR et al.

    Outbreak of endocarditis caused by Pseudomonas aeruginosa serotype O11 among pentazocine and tripelennamine abusers in Chicago

    J Infect Dis

    (1985)
  • WilsonLE et al.

    Prospective study of infective endocarditis among injection drug users

    J Infect Dis

    (2002)
  • GouelloJP et al.

    Nosocomial endocarditis in the intensive care unit: an analysis of 22 cases

    Crit Care Med

    (2000)
  • VG Fowler et al.

    Infective endocarditis due to Staphylococcus aureus: 59 prospectively identified cases with follow-up

    Clin Infect Dis

    (1999)
  • MartinoP et al.

    Catheter-related right-sided endocarditis in bone marrow transplant recipients

    Rev Infect Dis

    (1990)
  • CabellCH et al.

    Changing patient characteristics and the effect on mortality in endocarditis

    Arch Intern Med

    (2002)
  • VeltropMH et al.

    Role of monocytes in experimental Staphylococcus aureus endocarditis

    Infect Immun

    (2000)
  • BancsiMJ et al.

    Role of phagocytosis in activation of the coagulation system in Streptococcus sanguis endocarditis

    Infect Immun

    (1996)
  • CrawfordJ et al.

    Comparative adhesion of seven species of streptococci isolated from the blood of patients with sub-acutebacterial endocarditis to fibrin-platelet clots in vitro

    J Appl Bacteriol

    (1986)
  • HemlerME et al.

    Structure of the integrin VLA-4 and its cell-cell and cell-matrix adhesion functions

    Immunol Rev

    (1990)
  • SinhaB et al.

    Heterologously expressed Staphylococcus aureus fibronectin-binding proteins are sufficient for invasion of host cells

    Infect Immun

    (2000)
  • NovickRP et al.

    Synthesis of staphylococcal virulence factors is controlled by a regulatory RNA molecule

    EMBO J

    (1993)
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