Abstract
Ace is an adhesin to collagen from Enterococcus faecalis expressed conditionally after growth in serum or in the presence of collagen. Here, we generated an ace deletion mutant and showed that it was significantly attenuated versus wild-type OG1RF in a mixed infection rat endocarditis model (P<0.0001), while no differences were observed in a peritonitis model. Complemented OG1RFΔace (pAT392::ace) enhanced early (4 h) heart valve colonization versus OG1RFΔace (pAT392) (P = 0.0418), suggesting that Ace expression is important for early attachment. By flow cytometry using specific anti-recombinant Ace (rAce) immunoglobulins (Igs), we showed in vivo expression of Ace by OG1RF cells obtained directly from infected vegetations, consistent with our previous finding of anti-Ace antibodies in E. faecalis endocarditis patient sera. Finally, rats actively immunized against rAce were less susceptible to infection by OG1RF than non-immunized (P = 0.0004) or sham-immunized (P = 0.0475) by CFU counts. Similarly, animals given specific anti-rAce Igs were less likely to develop E. faecalis endocarditis (P = 0.0001) and showed fewer CFU in vegetations (P = 0.0146). In conclusion, we have shown for the first time that Ace is involved in pathogenesis of, and is useful for protection against, E. faecalis experimental endocarditis.
Highlights
Enterococci are gram-positive cocci of intestinal origin first reported as a cause of infective endocarditis (IE) in 1899 [1]
Enterococcus faecalis was recognized as a common cause of infective endocarditis (IE) by the early 1900s
We show that ace contributes to E. faecalis IE pathogenesis and demonstrate that Ace is expressed at high levels during IE even though produced at low levels under laboratory conditions; both active and passive immunization based on the collagen-binding domain of Ace conferred significant protection against IE
Summary
Enterococci are gram-positive cocci of intestinal origin first reported as a cause of infective endocarditis (IE) in 1899 [1]. They were recognized as the 3rd most common cause of IE as early as the 1920’s, and have remained the 3rd most common cause of community onset IE since with Enterococcus faecalis accounting for .90% of isolates from enterococcal IE when identified to the species level [1,2,3,4,5]. Over the past 20 years, enterococci have become the 2nd–3rd most common organisms isolated from nosocomial (healthcare-associated) infections including UTIs, bacteremia, intraabdominal and wound infections, endocarditis, sepsis in neonates, among others [1,3]. The attributable mortality of enterococcal bacteremia was 31% [8], emphasizing the clinical, not just the financial, seriousness of these infections
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