The inclusion of abnormal 18F-FDG cardiac uptake as a major criterion at admission enabled a re-categorization of 76% (47/62) of PVE/AAPI cases initially classified as "possible" to "definite" IE.
Guidelines and/or recommendations of clinical societies have incorporated nuclear medicine tests (using both labeled leucocytes and FDG) in their suggested work-up for evaluation of infective endocarditis and in certain patients with suspected vascular graft infections.
<sup>18</sup>F-FDG PET proved to be a sensitive technique with a high diagnostic value in patients with prosthetic valves and intracardiac devices and suspected IE.
In the NVE group, <sup>18</sup>F-FDG PET/CT was not associated with occurrence of the primary endpoint CONCLUSIONS: In addition to its good diagnostic performance, <sup>18</sup>F-FDG PET/CT is predictive of major cardiac events in PVE and new embolic events within the first year following IE.
Pooled sensitivity of <sup>18</sup>F-FDG studies with adequate cardiac preparation for the diagnosis of IE was 81% (95% CI, 73%-86%) and pooled specificity was 85% (95% CI, 78%-91%).
Besides echocardiography, contrast-enhanced CT (ce-CT), radiolabelled leucocyte (white blood cell, WBC) SPECT/CT and [<sup>18</sup>F]FDG PET/CT are included as diagnostic tools in the diagnostic flow chart for IE.
Clinical utility of <sup>18</sup>F-FDG positron emission tomography/computed tomography scan vs. <sup>99m</sup>Tc-HMPAO white blood cell single-photon emission computed tomography in extra-cardiac work-up of infective endocarditis.
<sup>18</sup>F-FDG-PET/CT angiography in the diagnosis of infective endocarditis and cardiac device infection in adult patients with congenital heart disease and prosthetic material.
In the past 5 years, several groups confirmed the incremental value of FDG-PET imaging and radiolabeled leukocyte scintigraphy over echocardiography for the diagnosis of IE.
The proportion of methicillin-resistant <i>S. aureus</i> (MRSA; 83.8%) infection accounting for <i>S. aureus</i> IE in the HD group was higher than that (28.6%) in the non-HD group.
In the IE animal model for all CC types, treatment with telavancin produced significantly greater reductions in MRSA counts as compared with daptomycin-treated animals in all target tissues.
We previously showed that MRSA isolates from soft tissue infection (SSTI) produced significantly higher levels of PSM than MRSA isolates from hospital-acquired pneumonia (HAP) or infective endocarditis (IE).
Infective endocarditis (IE) due to CA-MRSA with heterogeneous vancomycin-intermediate susceptibility-(h-VISA) has been recently reported, associated to an epidemic USA 300 CA-MRSA clone.
Our findings suggest that agr dysfunction does not correlate with vancomycin treatment failures in this experimental IE model in two distinct MRSA genetic backgrounds.
The fibronectin-binding protein A gene (<i>fnbpA</i>) was sequenced.Of 2,365 cases of SAB, 92 had IE.After matching, 37 pairs of <i>S. aureus</i> isolates from the IE cases and non-IE controls were compared; <i>fnbpA</i> was detected in 91.9% of the IE isolates and 100% of the non-IE isolates (<i>p</i> = 0.24).
Streptococcus mutans autolysin AtlA is a fibronectin-binding protein and contributes to bacterial survival in the bloodstream and virulence for infective endocarditis.
We thus conclude that (sub)domains of the staphylococcal FnBPA molecule that express Fn-binding modules, alone or in combination, are sufficient to evoke an endothelial proinflammatory as well as a procoagulant response and thus account for IE severity.
The results are consistent with the conclusion that the 63-kDa SmFnB protein of S. mutans is a fibronectin-binding protein that may contribute to the interaction of S. mutans with damaged heart tissue during pathogenesis of infective endocarditis.
The adherence characteristics in vivo and virulence of two isogenic strains of Staphylococcus aureus differing in fibronectin binding were compared in a rat model of catheter-induced infective endocarditis.