The synergistic activity of triclosan and ciprofloxacin on biofilms of Salmonella Typhimurium.

Triclosan is a biocide whose wide use has raised a debate about the potential benefits vs. hazards of the incorporation of antimicrobials in consumer products. The purpose of the present study was to determine whether exposure of biofilms of Salmonella enterica serovar Typhimurium to triclosan influences the tolerance of the bacteria towards antibiotics such as ciprofloxacin and vice versa. A synergistic antibiofilm activity was observed when the biofilms were treated with triclosan before or together with ciprofloxacin, and an additive activity was observed with planktonic cells. For example 500 microg mL(-1) triclosan and 500 microg mL(-1) ciprofloxacin reduced the number of viable cells in the biofilm by 1.6 and 0.5 log, respectively. However, the sequential treatment of 500 microg mL(-1) triclosan followed by ciprofloxacin resulted in 4.8 log reduction. Combination indexes (CI) for biofilms treated with triclosan followed by ciprofloxacin were 0.7, 0.32 and 0.25 for reduction of 90%, 99% and 99.9%, respectively, indicating a synergism. For planktonic cells, CIs were 1+/-0.1, indicating an additive effect. Therefore, it was suggested that triclosan weakens the ability of biofilm-associated cells to survive exposure to ciprofloxacin in the biofilm, probably by improving the permeability or the activity of ciprofloxacin.

Quinolone resistance of Salmonella enterica serovar Virchow isolates from humans and poultry in Israel: evidence for clonal expansion.

Salmonella enterica serovar Virchow is highly prevalent in humans and farm animals in Israel. In addition to high rates of resistance to multiple antibiotics, this serovar exhibits a high incidence of resistance to nalidixic acid. More than 90% of Salmonella serovar Virchow isolates of human and poultry origin obtained from 1997 to 2004 were resistant to nalidixic acid (MIC > or = 128 microg/ml), with reduced susceptibility to ciprofloxacin (MIC between 0.125 and 0.250 microg/ml). Most isolates belonged to two predominant, closely related pulsed-field gel electrophoresis image types. Investigation of the mechanisms of quinolone resistance revealed that this pathogen probably emerged from a parental clone that overproduced the AcrAB efflux pump and had a single point mutation in gyrA leading to the Asp87Tyr substitution. The close resemblance between human and poultry isolates points to poultry as a likely source of Salmonella serovar Virchow in the food chain.

Effect of triclosan on Salmonella typhimurium at different growth stages and in biofilms.

Triclosan is a potent biocide that is included in a diverse range of products. This research was aimed to investigate the susceptibility of planktonic and biofilm-associated Salmonella enterica serovar Typhimurium to triclosan, and to identify potential mechanisms of adaptation. The effect of triclosan was studied on planktonic Salmonella (log and stationary phases), on biofilm-associated cells, on bacteria derived from disrupted biofilms and on a biofilm-deficient mutant. An eight-log reduction of exponentially growing cells was observed with 1000 micro g mL(-1) triclosan within 10 min, a 3.6-log reduction in stationary cells and a 6.3-log reduction in stationary cells of a biofilm-deficient mutant (P<0.05). Biofilm-associated cells were tolerant (1-log reduction). However, biofilm-derived cells showed sensitivity to triclosan similar to stationary-phase cells. Triclosan induced the transcription of fabI and micF. Within biofilms, triclosan also up-regulated the transcription of acrAB, encoding for an efflux pump, marA, and the cellulose-synthesis-coding genes bcsA and bcsE. Thus, Salmonella within biofilms could experience reduced influx, increased efflux and enhanced exopolysaccharides production. Our results demonstrated that the tolerance of Salmonella towards triclosan in the biofilm was attributed to low diffusion through the extracellular matrix, while changes of gene expression might provide further resistance to triclosan and to other antimicrobials.

Inhibition of Helicobacter pylori adhesion to human gastric mucus by a high-molecular-weight constituent of cranberry juice.

A high-molecular-weight constituent of cranberry juice has been found to inhibit the sialyllactose specific adhesion of Helicobacter pylori strains to immobilized human mucus, erythrocytes, and cultured gastric epithelial cells. Different isolates of H. pylori differ in their affinity to the cranberry juice constituent. Cranberry juice may also inhibit adhesion of bacteria to the stomach in vivo, and may prove useful for the prevention of stomach ulcer that is caused by H. pylori.

Effect of Ascorbic Acid and Its Hydrophobic Derivative Palmitoyl Ascorbate on the Redox State of Primary Human Fibroblasts.

Ascorbic acid (AA) and its derivatives participate in vitro in oxidative-reductive reactions both as antioxidants and as prooxidants. The physiological relevance of these prooxidant effects of AA and its derivatives remains unclear. There is little evidence that AA can initiate formation of reactive oxygen species (ROS) or lipid peroxidation in cells or tissue. In order to examine the effect of AA and its derivative palmitoyl ascorbate on in situ intracellular ROS production and lipid peroxidation, 2('),7(')-dichlorofluorescin diacetate (DCFH-DA) and cis-parinaric acid were used as fluorescent probes in cultural neonatal foreskin fibroblasts. The results demonstrated that the effect of AA depended on the in vitro growth conditions. AA induced augmentation of the intracellular ROS concentration in newly plated (24 hours) cells. However, in cells cultured for 72 hours, AA had a different effect: it moderately reduced intracellular ROS concentration but stimulated lipid peroxidation in the cytoplasmic membrane. Palmitoyl ascorbate demonstrated significant inhibition of intracellular DCFH-DA oxidation presumably caused by inhibition of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase.