Antimicrobial activity of a novel catheter lock solution

Abstract

Intravascular catheter-associated bloodstream infections significantly increase rates of morbidity and hospital costs. Microbial colonization and development of biofilms, which are known to be recalcitrant to antibiotic therapy, often lead to the loss of otherwise patent vascular access systems. We evaluated a new taurolidine- and citrate-based catheter lock solution (Neutrolin; Biolink Corporation, Norwell, Mass.) for its activity against planktonic microbes, antimicrobial activity in a catheter model, and biofilm eradication activity. In studies of planktonic microbes, after 24 h of contact, 675 mg of taurolidine-citrate solution per liter caused > 99% reductions in the initial counts of Staphylococcus aureus, Staphylococcus epidermidis, Pseudomonas aeruginosa, and Entercoccus faecalis. A solution of 13,500 mg/liter was cidal for Candida albicans. Ports and attached catheters inoculated with 50 to 600 CFU of these bloodstream isolates per ml were locked with heparin or the taurolidine-citrate solution. After 72 h, there was no growth in the taurolidine-citrate-treated devices but the heparin-treated devices exhibited growth in the range of 6 x 10(2) to 5 x 10(6) CFU/ml. Biofilms were developed on silicone disks in modified Robbins devices with broth containing 6% serum (initial counts, 10(6) to 10(8) CFU/cm(2)). The axenic biofilms were treated for 24 h with taurolidine-citrate or heparin. Taurolidine-citrate exposure resulted in a median reduction of 4.8 logs, whereas heparin treatment resulted in a median reduction of 1.7 logs (P < 0.01). No significant differences in the effects of the two treatments against P. aeruginosa and C. albicans were observed. These findings suggest that taurolidine-citrate is a promising combination agent for the prevention and treatment of intravascular catheter-related infections.

Figures

FIG. 1.

Dialock access port, catheters, and needles.

FIG. 2.

Taurolidine-citrate activity against S. aureus (A), S. epidermidis (B), E. faecalis (C), P. aeruginosa (D), and C. albicans (E) at different concentrations at 24 h. The bars labeled “initial” indicate the organism counts in broth at time zero (T = 0 h). The control bars (0 mg/liter) indicate no treatment with taurolidine-citrate. The results are expressed as means ± standard deviations (the standard deviations are indicated by error bars).

FIG. 2.

Taurolidine-citrate activity against S. aureus (A), S. epidermidis (B), E. faecalis (C), P. aeruginosa (D), and C. albicans (E) at different concentrations at 24 h. The bars labeled “initial” indicate the organism counts in broth at time zero (T = 0 h). The control bars (0 mg/liter) indicate no treatment with taurolidine-citrate. The results are expressed as means ± standard deviations (the standard deviations are indicated by error bars).

FIG. 2.

Taurolidine-citrate activity against S. aureus (A), S. epidermidis (B), E. faecalis (C), P. aeruginosa (D), and C. albicans (E) at different concentrations at 24 h. The bars labeled “initial” indicate the organism counts in broth at time zero (T = 0 h). The control bars (0 mg/liter) indicate no treatment with taurolidine-citrate. The results are expressed as means ± standard deviations (the standard deviations are indicated by error bars).

FIG. 3.

Comparison of the efficacies of taurolidine-citrate and heparin against biofilm organisms. The results are expressed as means ± standard deviations (the standard deviations are indicated by error bars). The detection limit was 100 CFU/cm2 (2 logs). Bars with light shading, initial viable counts; bars with medium shading, viable counts for heparin-treated cultures; solid bars, viable counts for taurolidine-citrate-treated cultures; ∗, significant difference (P < 0.05) between taurolidine-citrate and heparin.