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. Author manuscript; available in PMC: 2012 Mar 1.
Published in final edited form as: Nat Med. 2011 Aug 21;17(9):1142–1146. doi: 10.1038/nm.2423

Figure 1. Identification of coagulase-positive endocarditis in a mouse model using a fluorescent prothrombin analog.

Figure 1

(a-d) Representative S. aureus vegetation induced in a murine model of endocarditis. Hematoxylin and Eosin (H&E; a,b) and Gram staining (c,d) are shown with 400× total magnification in panels (b) and (d). (e) A schematic representation of vegetation formation in S. aureus endocarditis including a hypothetical mechanism for probe localization (AF680-ProT, yellow) after endothelial trauma and induction of bacteremia. Staphylocoagulase (SC) is shown tethering AF680-ProT to fibrinogen/fibrin via D domain interactions. Fibrinogen (inset) has a central E domain flanked by two D domains (dark blue). Schematics of AF680-ProT and SC are also shown. (f-h) Ex vivo fluorescence reflectance imaging (FRI) showed that localization of AF680-ProT is limited to pathogenic S. aureus. White light (f) and fluorescence images show excised aortas with vegetations (g; arrow heads) as well as the location of the suture (arrow). Quantitation of FRI data is given in panel (h) for the controls (either no bacteria or coagulase-negative S. epidermidis) and for three S. aureus strains. TBR: target to background ratio. * indicates P < 0.01. (i-l) Microscopic localization of AF680-ProT correlates with SC-positive immunostaining. Gram stain (i), SC immunohistochemistry (j), in situ hybridization against digoxigenin-SC RNA (DIG-SC) (k) and fluorescence microscopy (l) demonstrate that SC is differentially expressed in growing vegetations and limited to the growing edge. Distance bar equals 50 μm.