Slime production by most strains of Staphylococcus epidermidis was enhanced by conditions of iron limitation produced by the addition of ethylenediamine-di-o-hydroxyphenol acetic acid to the growth medium. The density of the biofilm which formed on the base of microtiter plates was dependent on the degree of iron limitation, the stage of the growth cycle, and the nutritional state of the initial inoculum. One repeatedly * Corresponding author.
SUMMARYThe ability to produce large quantities of biofilm on solid surfaces in vitro is believed to distinguish potentially pathogenic strains of Staphylococcus epidermidis from commensals. Biofilm 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.
Two colonial variants of Staphylococcus epidernidis were isolated from the valvular tissue of a patient with native valve endocarditis. In addition to differing in colonial morphology, the two variants differed in hemolysis on blood-containing media, in adherence capacity, and in the expression of certain enzymes. Under suitable conditions, both variants were themselves capable of phenotypic variation, although they differed in the rate at which variants were generated. The variants yielded identical profiles on restriction endonuclease analysis of plasmid DNA and pulsed-field gel electrophoresis of whole-cell DNA. This report suggests a possible role for phenotypic variation in coagulase-negative staphylococcal virulence. Congo red agar would be an excellent medium for studying the contribution of variation to the virulence of these organisms.
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