Triclosan

Triclosan at 1% is mostly bactericidal (3 min) and yeasticidal (1 min). Mycobactericidal activity is unknown. The antimicrobial effect of triclosan is explained by blocking the enoyl acyl carrier protein reductase and by affecting several cellular processes. Efflux pumps, membrane and gene expression changes, and the use of triclosan as the sole carbon source are cellular defence mechanisms. Biofilm formation was reduced in S. aureus, S. enteritidis, S. mutans, and A. fumigatus, but not in P. aeruginosa and mixed biofilms. No relevant biofilm reduction was reported with 1–30 mg/l triclosan in A. naeslundii, S. oralis, and S. gordonii (1 h exposure), but a significant reduction with 1000–3000 mg/l triclosan in L. innocua, L. monocytogenes, L. welshimeri, and P. acnes (18–24 h exposure). Elevated MICs have been reported in many species, but their relevance is uncertain. Low-level exposure results in no MIC change in 33 species, a weak MIC change in 27 species, and a strong MIC change in 33 species (13 of which are stable), resulting in MIC values as high as 8000 mg/l (E. coli) or 3000 mg/l (Salmonella spp.). Cross-tolerance to chlorhexidine, benzalkonium chloride, hexachlorophene, and selected antibiotics may occur in many species. Horizontal gene transfer can be induced in E. coli. P. aeruginosa and S. marcescens isolates have been isolated in liquid soaps causing infections. K. oxytoca, S. liquefaciens, S. sonnei, E. gergoviae, S. odorifera, and E. cloacae have been detected in liquid soaps (0.15%–0.65% triclosan). The overall probability of resistance to triclosan of practical relevance is low to moderate in the absence of biofilm.