| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||

Christina M. J. E. Vandenbroucke-Grauls,1,4
Jan J. Weening,3 and
Sebastian A. J. Zaat1*
Department of Medical Microbiology, CINIMA (Center for Infection and Immunity Amsterdam), Academic Medical Center, University of Amsterdam, Meibergdreef 15, 1105 AZ Amsterdam, The Netherlands,1 Emergent Europe, 540-545 Eskdale Road, Winnersh Triangle, Wokingham, RG41 5TU, Berkshire, United Kingdom,2 Department of Pathology, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands,3 Department of Medical Microbiology and Infectious Diseases, VU Medical Center, Amsterdam, The Netherlands4
Received 7 August 2006/ Returned for modification 11 September 2006/ Accepted 28 November 2006
Biomaterial-associated infections (BAI), which are predominantly caused by Staphylococcus epidermidis, are a significant problem in modern medicine. Biofilm formation is considered the pivotal element in the pathogenesis, but in previous mouse studies we retrieved S. epidermidis from peri-implant tissue. To assess the kinetics and generality of tissue colonization, we investigated BAI using two S. epidermidis strains, two biomaterials, and two mouse strains. With small inocula all implants were culture negative, whereas surrounding tissues were positive. When higher doses were used, tissues were culture positive more often than implants, with higher numbers of CFU. This was true for the different biomaterials tested, for both S. epidermidis strains, at different times, and for both mouse strains. S. epidermidis colocalized with host cells at a distance that was >10 cell layers from the biomaterial-tissue interface. We concluded that in mouse experimental BAI S. epidermidis peri-implant tissue colonization is more important than biofilm formation.
Published ahead of print on 11 December 2006.
| J. Bacteriol. | J. Virol. | Eukaryot. Cell |
|---|
| Microbiol. Mol. Biol. Rev. | Clin. Vaccine Immunol. | All ASM Journals |
|---|