Inhibition of Streptococcus mutans NS adhesion to glass with and without a salivary conditioning film by biosurfactant- releasing Streptococcus mitis strains.

The release of biosurfactants by adhering microorganisms as a defense mechanism against other colonizing strains on the same substratum surface has been described previously for probiotic bacteria in the urogenital tract, the intestines, and the oropharynx but not for microorganisms in the oral cavity. Two Streptococcus mitis strains (BA and BMS) released maximal amounts of biosurfactants when they were grown in the presence of sucrose and were harvested in the early stationary phase. The S. mitis biosurfactants reduced the surface tensions of aqueous solutions to about 30 to 40 mJ m(-2). Biochemical and physicochemical analyses revealed that the biosurfactants released were glycolipids. An acid-precipitated fraction was extremely surfactive and was identified as a rhamnolipidlike compound. In a parallel-plate flow chamber, the number of Streptococcus mutans NS cells adhering to glass with and without a salivary conditioning film in the presence of biosurfactant-releasing S. mitis BA and BMS (surface coverage, 1 to 4%) was significantly reduced compared with the number of S. mutans NS cells adhering to glass in the absence of S. mitis. S. mutans NS adhesion in the presence of non-biosurfactant-releasing S. mitis BA and BMS was not reduced at all. In addition, preadsorption of isolated S. mitis biosurfactants to glass drastically reduced the adhesion of S. mutans NS cells and the strength of their bonds to glass, as shown by the increased percentage of S. mutans NS cells detached by the passage of air bubbles through the flow chamber. Preadsorption of the acid-precipitated fraction inhibited S. mutans adhesion up to 80% in a dose-responsive manner. These observations indicate that S. mitis plays a protective role in the oral cavity and protects against colonization of saliva-coated surfaces by cariogenic S. mutans.

Streptococcus thermophilus and its biosurfactants inhibit adhesion by Candida spp. on silicone rubber.

The adhesion of yeasts, two Candida albicans and two Candida tropicalis strains isolated from naturally colonized voice prostheses, to silicone rubber with and without a salivary conditioning film in the absence and presence of adhering Streptococcus thermophilus B, a biosurfactant-releasing dairy isolate, was studied. Coverage of 1 to 4% of the surface of silicone rubber substrata with adhering S. thermophilus B gave significant reductions in the initial yeast adhesion regardless of the presence of a conditioning film. Mechanistically, this interference in yeast adhesion by S. thermophilus B was not due to direct physical effects but to biosurfactant release by the adhering bacteria, because experiments with S. thermophilus B cells that had released their biosurfactants prior to adhesion to silicone rubber and competition with yeasts did not show interference with initial yeast adhesion. The amounts of biosurfactants released were highest for mid-exponential- and early-stationary-phase bacteria (37 mg.g of cells-1 [dry weight]), but biosurfactants released by stationary-phase bacteria (14 mg.g of cells-1 [dry weight]) were the most surface active. The crude biosurfactants released were mixtures of various components, with a glycolipid-like component being the most surface active. A lipid-enriched biosurfactant fraction reduced the surface tension of an aqueous solution to about 35 mJ.m-2 at a concentration of only 0.5 mg.ml-1. The amount of biosurfactant released per S. thermophilus B cell was estimated to be sufficient to cover approximately 12 times the area of the cross section of the bacterium, making biosurfactant release a powerful defense weapon in the postadhesion competition of the bacterium with microorganisms such as yeasts. Preadsorption of biosurfactants to the silicone rubber prior to allowing yeasts to adhere was as effective against C. albicans GB 1/2 adhesion as covering 1 to 2% of the silicone rubber surface with adhering S. thermophilus B, but a preadsorbed biosurfactant layer was less effective against C. tropicalis GB 9/9.

Effects of ciprofloxacin and vancomycin on physicochemical surface properties of Staphylococcus epidermidis, Escherichia coli, Lactobacillus casei and Lactobacillus acidophilus.

Under clinical conditions, during antibiotic treatment, micro-organisms often grow at sub-inhibitory concentrations. This may lead to altered adhesive cell surface properties and to a disruption of the indigenous microflora, in addition to the creation of a more pathogenic biofilm. The effects of growing Staphylococcus epidermidis, Escherichia coli and lactobacilli in the presence of sub-inhibitory concentrations of ciprofloxacin and vancomycin were determined. Growing the cells under antibiotic burden sometimes led to altered cell surface hydrophobicity (by adhesion to hexadecane), changes in the pH-dependence of zeta potentials, and elemental surface compositions or in different SDS-PAGE protein profiles. For several isolates only one of the surface properties was altered by the presence of an antibiotic in the growth medium and no systematic effects were observed for all isolates representing a certain species or even strain. The important conclusion to be drawn from the results of this study is that the effects of growing cells under antibiotic burden on their adhesive cell surface properties can only be established when using a variety of techniques.