Official reprint from UpToDate®
www.uptodate.com ©2017 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

Pathogenesis of vegetation formation in infective endocarditis

Vivian H Chu, MD, MHS
Daniel J Sexton, MD
Section Editor
Stephen B Calderwood, MD
Deputy Editor
Elinor L Baron, MD, DTMH


Infective endocarditis arises when an adherent platelet-fibrin nidus becomes secondarily infected and produces vegetations, which in turn may directly damage the endocardial tissue and/or valves. The pathogenesis of infective endocarditis will be reviewed here.

Other aspects of infective endocarditis, including clinical consequences of vegetation formation, are discussed separately. (See "Epidemiology, risk factors, and microbiology of infective endocarditis" and "Epidemiology, clinical manifestations, and diagnosis of prosthetic valve endocarditis" and "Infective endocarditis in injection drug users" and "Infective endocarditis in children" and "Clinical manifestations and evaluation of adults with suspected native valve endocarditis" and "Antimicrobial therapy of native valve endocarditis" and "Antimicrobial therapy of prosthetic valve endocarditis" and "Surgery for left-sided native valve infective endocarditis" and "Complications and outcome of infective endocarditis".)


Vegetation formation — The endothelial lining of the heart and its valves is normally resistant to infection with bacteria and fungi. Experiments in animal models have demonstrated that a sequence of interrelated events must occur before microbes can establish an infective nidus or vegetation on the endocardium:

The initial step in the establishment of a vegetation is endocardial injury, followed by focal adherence of platelets and fibrin. Some organisms with high virulence are capable of infecting normal human heart valves, such as Staphylococcus aureus.

The initially sterile platelet-fibrin nidus becomes secondarily infected by microorganisms circulating in the blood, either from a distant source of focal infection or as a result of transient bacteremia from a mucosal or skin source [1,2].

To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:

Subscribers log in here

Literature review current through: Nov 2017. | This topic last updated: Jul 21, 2017.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2017 UpToDate, Inc.
  1. Garrison PK, Freedman LR. Experimental endocarditis I. Staphylococcal endocarditis in rabbits resulting from placement of a polyethylene catheter in the right side of the heart. Yale J Biol Med 1970; 42:394.
  2. Durack DT, Beeson PB. Experimental bacterial endocarditis. I. Colonization of a sterile vegetation. Br J Exp Pathol 1972; 53:44.
  3. Werdan K, Dietz S, Löffler B, et al. Mechanisms of infective endocarditis: pathogen-host interaction and risk states. Nat Rev Cardiol 2014; 11:35.
  4. Jung CJ, Yeh CY, Hsu RB, et al. Endocarditis pathogen promotes vegetation formation by inducing intravascular neutrophil extracellular traps through activated platelets. Circulation 2015; 131:571.
  5. Jung CJ, Yeh CY, Shun CT, et al. Platelets enhance biofilm formation and resistance of endocarditis-inducing streptococci on the injured heart valve. J Infect Dis 2012; 205:1066.
  6. Lepidi H, Casalta JP, Fournier PE, et al. Quantitative histological examination of bioprosthetic heart valves. Clin Infect Dis 2006; 42:590.
  7. Morris AJ, Drinkovic D, Pottumarthy S, et al. Gram stain, culture, and histopathological examination findings for heart valves removed because of infective endocarditis. Clin Infect Dis 2003; 36:697.
  8. Lang S, Watkin RW, Lambert PA, et al. Detection of bacterial DNA in cardiac vegetations by PCR after the completion of antimicrobial treatment for endocarditis. Clin Microbiol Infect 2004; 10:579.
  9. RODBARD S. Blood velocity and endocarditis. Circulation 1963; 27:18.
  10. Freedman LR, Valone J Jr. Experimental infective endocarditis. Prog Cardiovasc Dis 1979; 22:169.
  11. Bansal RC. Infective endocarditis. Med Clin North Am 1995; 79:1205.
  12. Pressman GS, Rodriguez-Ziccardi M, Gartman CH, et al. Mitral Annular Calcification as a Possible Nidus for Endocarditis: A Descriptive Series with Bacteriological Differences Noted. J Am Soc Echocardiogr 2017; 30:572.
  13. Gould K, Ramirez-Ronda CH, Holmes RK, Sanford JP. Adherence of bacteria to heart valves in vitro. J Clin Invest 1975; 56:1364.
  14. Scheld WM, Valone JA, Sande MA. Bacterial adherence in the pathogenesis of endocarditis. Interaction of bacterial dextran, platelets, and fibrin. J Clin Invest 1978; 61:1394.
  15. Kuypers JM, Proctor RA. Reduced adherence to traumatized rat heart valves by a low-fibronectin-binding mutant of Staphylococcus aureus. Infect Immun 1989; 57:2306.
  16. Yeh CY, Chen JY, Chia JS. Glucosyltransferases of viridans group streptococci modulate interleukin-6 and adhesion molecule expression in endothelial cells and augment monocytic cell adherence. Infect Immun 2006; 74:1273.
  17. Nomura R, Otsugu M, Naka S, et al. Contribution of the interaction of Streptococcus mutans serotype k strains with fibrinogen to the pathogenicity of infective endocarditis. Infect Immun 2014; 82:5223.