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Virulence of Staphylococcus epidermidis in a mouse model: significance of extracellular slime

Published online by Cambridge University Press:  15 May 2009

M. A. Deighton ,
R. Borland  and
J. A. Capstick
M. A. Deighton
Affiliation:
Department of Applied Biology and Biotechnology
R. Borland
Affiliation:
Faculty of Biomedical and Health Sciences, Royal Melbourne Institute of Technology, 124 LaTrobe St, Melbourne 3000, Australia
J. A. Capstick
Affiliation:
Department of Applied Biology and Biotechnology
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The ability to produce large quantities of bioflim on solid surfaces in vitro is believed to distinguish potentially pathogenic strains of Staphylococcus epidermidis from commensals. Bioflim consists of staphylococcal cells encased in a matrix of extracellular polysaccharide (also referred to as slime), firmly adherent to each other and to the underlying surface structure. The association of slime with colonization of catheter surfaces in vivo has been examined extensively. Less attention has been paid to the contribution of slime to infections that occur in the absence of an inserted device. In a mouse model of subcutaneous infection without an implanted device 10 S. epidermidis strains (5 slime-positive, 5 slime-negative) produced abscesses; thus a foreign body is not essential for the expression of virulence by S. epidermidis. Biofilm-positive strains produced significantly more abscesses, that persisted longer than biofilm-negative strains. In these chronic infections, large numbers of staphylococci were associated with macrophages and viable staphylococci were cultured from specimens of pus collected at autopsy. Thus slime or components of slime appear to delay the clearance of S. epidermidis from host tissues, possibly by interfering with intracellular killing mechanisms. However, differences in the capacity to produce abscesses, within both the slime-positive and slime-negative groups, indicate that other factors also contribute to the virulence of S. epidermidis.

Type
Research Article
Information
Epidemiology & Infection , Volume 117 , Issue 2 , October 1996 , pp. 267 - 280
Copyright
Copyright © Cambridge University Press 1996

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