No abstract

The progressive stages in Bdellovibrio bacteriovorus penetration into two strains of Escherichia coli were examined by use of electron microscopic techniques. The initial change observed in the ultrastructure of the host following parasitic attack was the swelling of the cell envelope at the site of attachment. The Bdellovibrio then appeared to pierce the center of this swelling, forming a pore in the outer wall layers of the host. The edges of this entry pore constricted the Bdellovibrio throughout its penetration into the host cell. Although partial disruption of the cytoplasmic membrane was always apparent, the parasite did not appear to actively penetrate through this barrier. An attempt is made to correlate the fine structural changes involved in penetration with the physiological data that have accumulated to date.

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A controlled-environment membrane model for use in vitro was developed and employed in an attempt to mimic the environment of the vagina in order to study yeast-vaginal cell adhesion. Adhesion in vitro of four strains of Candida albicans (NIH 3181A, NIH 526B, ATCC 18804, and MCO 2400) to vaginal epithelial cells (VEC) appeared to be affected by the pH and the level of carbon dioxide that have been found to be present in the vagina in vivQ. Strain 3181A had a greater adhesion ability than 526B when the concentration of yeast cells was increased and when the yeast cells were incubated with VEC at pH 5 in sodium phosphate buffer in ambient air supplemented with 10%, CO2. Of the four strains of C. albicans used, 3181A had the greatest adhesion ability, with strains 2400, 18804, and 526B ranked in order of decreasing adhesion ability. Also, an enhanced, electron-dense, matted outer region of the cell walls of the yeasts was observed frequently when they were incubated in ambient air supplemented with 10% CO2. In addition, of the vaginal cells that had yeast cells attached to them, an average of 94.4% of the total yeast cells were attached to the microridge side of the VEC, whereas an average of only 5.6% of the total were found on the nonmicroridge side of the VEC. The results from this study indicate that adhesion of C. atbicans to the VEC surface was affected by the strain of yeast used, by the side of the vaginal cell exposed, and by the pH and CO2 levels present in the adhesion assay.

The postantibiotic effect (PAE) has been classically defined as the suppression of bacterial growth that persists after limited exposure of organisms to antimicrobial agents. Morphology and haemolysin activity during the PAE of three quinolones on Escherichia coli were examined in this study. A one hour exposure to the quinolones, CI-960, enoxacin and ciprofloxacin, produced a PAE of 0.5-2.0 h. When determinated by Coulter counter, at 0.5 x MIC of enoxacin or CI-960 after 1 h exposure, 58% or 42% cells, respectively, of the treated cells were filamentous (cell length greater than 12 microns). After drug removal, the population of the filamentous cells decreased, however, after even 4 h, 12% and 2% of the cells were still filamentous after exposure to enoxacin or CI-960. Further morphological studies during the PAE showed that the first division of the filamentous cell was asymmetrical, and both bacterial cell division and septation were delayed after exposure to 0.5 MIC of CI-960. Following quinolone removal, the treated E. coli did not exhibit normal activity of haemolysin for at least 2 h. Internal haemolysin activity was adversely affected for 1 h. The results of this study suggest that any consideration of postantibiotic effects should include the residual antibiotic effects on bacterial morphology and virulence factors, in addition to the defined suppression of bacterial regrowth.