Chicken model of Enterococcus faecalis native-valve endocarditis
Abstract number: P1935
Larsen J., Chadfield M.S., Schønheyder H.C., Bojesen A.M., Christensen J.P., Bisgaard M.
Objectives: Enterococci represent the third most common cause of infective endocarditis (IE) and are responsible for 5% to 20% of all cases, of which Enterococcus faecalis accounts for >80%. In parallel, antimicrobial resistance continues to evolve and presents serious challenges in the therapy of invasive enterococcal infections. In one recent series, native-valve IE accounted for 61.3% of 44 patients with enterococcal endocarditis. However, most small-animal models of IE more closely mimic the pathophysiology of prosthetic-valve IE. These models rely on the production of sterile aortic vegetations by the insertion of a polyethylene catheter via the right carotid artery, prior to bacterial challenge, which increases the ability of the bacteria to adhere to and colonise the endocardium and, at the same time, decreases the efficacy of the antimicrobial therapy. Therefore, new in vivo technologies for screening novel candidate agents to prevent and treat native-valve IE are urgently needed. The objective of the present study was to develop a small-animal (chicken) model of E. faecalis native-valve endocarditis.
Methods:E. faecalis isolates 20326H2 and HEF5 from native-valve IE in chickens and humans, respectively, were tested. Single-age groups of chickens (5 weeks and 50 weeks of age) were injected intravenously (jugular vein) with 109 CFU stationary-phase bacteria or sterile phosphate-buffered saline (control groups). Definite IE was identified pathologically according to the modified Duke criteria by 21 days postinfection (at autopsy).
Results: Both groups were highly susceptible to infection with 20326H2 (90% definite IE cases in each group). By contrast, only the adult group exhibited high susceptibility to infection with HEF5 (80% versus 40% in the juvenile group), although the observed difference only reached borderline significance (one-tailed p value = 0.08, Fisher's exact test).
Conclusion: Overall, our data suggest that the chicken model closely mimics the pathophysiology of enterococcal native-valve IE. This conclusion is supported by the observation that the susceptibility to infection with HEF5 increased with age (i.e., due to degenerative valve disease). The present chicken model is readily adaptable to evaluating antimicrobial efficacy and should prove to be a useful tool in identifying bacterial virulence-related factors involved in adhesion to and colonisation of native valves.
|Session name:||18th European Congress of Clinical Microbiology and Infectious Diseases|
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