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Widmer E, Que YA, Entenza JM, et al. New concepts in the pathophysiology of infective endocarditis. Curr Infect Dis Rep. 2006;8(4):271-9doi: 10.1007/s11908-006-0071-z.
Widmer, E., Que, Y. A., Entenza, J. M., & Moreillon, P. (2006). New concepts in the pathophysiology of infective endocarditis. Current infectious disease reports, 8(4), 271-9. https://doi.org/10.1007/s11908-006-0071-z
Widmer, Eleonora, et al. "New concepts in the pathophysiology of infective endocarditis." Current infectious disease reports vol. 8,4 (2006): 271-9. doi: https://doi.org/10.1007/s11908-006-0071-z
Widmer E, Que YA, Entenza JM, Moreillon P. New concepts in the pathophysiology of infective endocarditis. Curr Infect Dis Rep. 2006 Jun;8(4):271-9. doi: 10.1007/s11908-006-0071-z. PMID: 16822370.
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Curr Infect Dis Rep. 2006 Jun;8(4):271-9. doi: 10.1007/s11908-006-0071-z.

New concepts in the pathophysiology of infective endocarditis.

Current infectious disease reports

Eleonora Widmer, Yok-Ai Que, José M Entenza, Philippe Moreillon

Affiliations

  1. Department of Fundamental Microbiology, University of Lausanne, Biophore building, CH-1015 Lausanne, Switzerland.

PMID: 16822370 DOI: 10.1007/s11908-006-0071-z

Abstract

Endocarditis pathogens colonize valves with pre-existing sterile vegetations or valves with minimal endothelial lesions. Inflamed endothelia produce cytokines, integrins, and tissue factor, which in turn attract fibronectin, monocytes, and platelets. Bacteria attaching to such structures further activate the cascade, becoming embedded and protected from host defenses. Staphylococcus aureus also actively invade the endothelium, causing apoptosis and endothelial damage. Knowledge of this interplay identifies host factors as potential therapeutic targets. Blocking infection by modulating host factors might be opportune because host factors are conserved. In contrast, interfering with bacterial virulence factors might be more complicated because they vary among different bacteria.

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