In vitro resistance to thrombin-induced platelet microbicidal protein among clinical bacteremic isolates of Staphylococcus aureus correlates with an endovascular infectious source

Platelet microbicidal proteins (PMPs), small cationic peptides released at sites of endovascular damage, kill common bloodstream pathogens in vitro. O ur group previously showed that in vitro resistance of clinical staphylococ cal and viridans group streptococcal bacteremic strains to PMPs correlated with the diagnosis of infective endocarditis (IE) (Wu et al., Antimicrob. A gents Chemother. 38:729-732, 1994). However, that study was limited by (i) the small number of Staphylococcus aureus isolates from IE patients, (ii) t he retrospective nature of the case definitions, and (iii) the diverse geog raphic sources of strains. The present study evaluated the in vitro PMP sus ceptibility phenotype of a large number of staphylococcemic isolates (n = 6 0), collected at a single medical center and categorized by defined and val idated clinical criteria. A significantly higher proportion of staphylococc emic strains from patients with IE was PMP resistant in vitro than the prop ortion of strains from patients with soft tissue sepsis (83% and 33%, respe ctively; P < 0.01). Moreover, the levels of PMP resistance (mean percent su rvival of strains after 2-h exposure to PMP in vitro) were significantly hi gher for isolates from patients with IE and,vith vascular catheter sepsis t han for strains from patients with abscess sepsis (P < 0.005 and P < 0.01, respectively), These data further support the concept that bloodstream path ogens that exhibit innate or acquired PMP resistance have a survival advant age with respect to either the induction or progression of endovascular inf ections.