7 - colonized mucous membranes are traumatized, as in...

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7. Pathogenesis of Infective Endocarditis: How did it get there? For in depth review of pathophysiology and molecular basis of fingronectin-mediated adherence see Moreillon P, Que Y-A. Infective Endocarditis. The Lancet 2004;363:139-149 and Schwarz- Linek U, Hook M, Potts JR. The molecular basis of fibronectin-mediated bacterial adherence to host cells. Molec Microbiol 2004;52:631-641 Damage to the endocardial surface (usually the heart valve) and subsequent direct contact with blood triggers coagulation and platelet and fibrinogen-fibrin deposition at the site. This collection is called non-bacterial thrombotic endocarditis (NBTE). Damaged endothelial cells express transmembrane proteins called integrins which can bind fibronectin to the cell surface. Some bacteria, especially Stapholococcus aureus, express fibronectin-binding proteins on their surface and avidly bind to the integrin bound fibronectin on the endothelial cell surface. If heavily
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Unformatted text preview: colonized mucous membranes are traumatized, as in dental cleaning, for example, transient bacteremia can occur and bacteria adhere to the NBTE lesion(s) mediated by their surface adhesins called MSCRAMMs or Microbial Surface Component Reacting with Adhesive Matrix Molecules. Once adhered, bacterial virulence mechanisms, such as induction of tissue factor production by monocytes or platelet-activating factors enhance adherence. The cardiac vegetation is the hallmark of IE resulting from the collection of fibrin, platelet aggregates and microorganisms. The host responds to the invasion by release of proinflammatory cytokines (IL-6, IL-8) and thromboplastin which increases fibrin deposition and promotes growth of the vegetation. Ultimately circulating immune complexes develop....
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