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Benzalkonium Chloride

  • Günter Kampf

摘要

Benzalkonium chloride (BAC) is mostly bactericidal at 1% and yeasticidal at 0.2% (5 min) but not mycobactericidal. Its antimicrobial activity is explained by membrane damage and protein aggregation. Cellular defence mechanisms include various resistance genes such as qacA/B and smr (qacC) in S. aureus, cell membrane alterations and efflux pumps, mainly in Gram-negative species. BAC reduces the formation of a developing biofilm in the majority of species. Biofilm removal by BAC is low in isolates from eight species and higher in isolates from five species (exposure ≤1 h). High MIC values indicating tolerance to BAC have been reported for isolates of A. hydrophila (31,300 mg/l), B. cereus and E. meningoseptica (7800 mg/l) and P. aeruginosa (5000 mg/l), but their relevance is uncertain. Low-level exposure results in no MIC change in 24 species, a weak MIC change in 34 species and a strong MIC change in 38 species (14 of which are stable), resulting in MIC values as high as 3000 mg/l (S. enterica) or 2500 mg/l (P. aeruginosa). In B. cepacia complex, E. coli and L. monocytogenes, low BAC concentrations caused an upregulation of transporter and efflux pump genes. Cross-tolerance to chlorhexidine, triclosan, hexachlorophene and selected antibiotics can occur in many species. BAC-resistant isolates have been described with insufficient efficacy in suspension tests (Achromobacter spp. 3, M. rhodesianum, S. marcescens) and with a contamination of disinfectants (17 species). The overall probability of resistance to BAC of practical relevance is low to moderate in the absence of biofilm.