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Didecyldimethylammonium Chloride

  • Günter Kampf

摘要

Didecyldimethylammonium chloride (DDAC) is mostly bactericidal at 1% (1 min) and yeasticidal at 0.0525% (15 min), but not mycobactericidal. Its antimicrobial activity is explained by membrane damage. Cellular defence mechanisms include metabolisation of DDAC in P. fluorescens and efflux pumps in S. epidermidis and Serratia spp. The effect of DDAC on biofilm development, removal and fixation is unknown. High MIC values indicating tolerance to DDAC have been reported for isolates of Serratia spp. (2873 mg/l), P. aeruginosa (>1000 mg/l), E. cloacae and Salmonella spp. (512 mg/l), but their relevance is uncertain. Low-level exposure results in no MIC change in 24 species, a weak MIC change in 19 species and a strong MIC change in seven species (two of which are stable), resulting in MIC values as high as >1000 mg/l (P. aeruginosa) or 125 mg/l (A. proteolyticus, Ralstonia spp.). A significant increase of intrageneric and intergeneric conjugation frequency has been reported with E. coli and P. putida. Cross-tolerance to benzalkonium chloride and other biocides may occur in E. coli and P. fluorescens. Occasional cross-resistance to selected antibiotics has been reported in C. coli, E. coli, L. monocytogenes and S. enterica. DDAC-resistant isolates have been described in outbreaks and pseudo-outbreaks (A. xylosoxidans, P. fluorescens, B. cepacia complex, ESBL E. cloacae) and with contaminated disinfectants (B. cepacia, Serratia spp.). The overall probability of resistance to DDAC of practical relevance is low to moderate in the absence of biofilm.