Abstract
Chlorhexidine digluconate (CHG) is bactericidal at 2–4% (5 min) except Enterococcus spp., S. epidermidis and MRSA, and yeasticidal at 2% (30 min). A general mycobactericidal activity cannot be expected. Epidemiological cut-off values to determine acquired resistance have been proposed for E. coli, E. faecalis and K. pneumoniae (64 mg/l); Salmonella spp. and E. faecium (32 mg/l); C. albicans and Enterobacter spp. (16 mg/l); and S. aureus (8 mg/l). Elevated MIC values suggestive of CHG resistance have been reported among numerous species including B. subtilis, E. faecalis, K. pneumoniae and Proteus spp. (≤10,000 mg/l); P. aeruginosa (≤5,000 mg/l); L. monocytogenes, E. faecium and S. aureus (≤2,500 mg/l). Specific resistance mechanisms are sometimes known, e.g. resistance genes, efflux pumps, membrane changes or plasmids. Cross-tolerance to triclosan, benzalkonium chloride, hydrogen peroxide and selected antibiotics can occur. Low-level exposure leads to no MIC change in 33 species, a weak MIC change in 25 species and a strong MIC change in 16 species (8 of them being stable) resulting in MIC values as high as 2,048 mg/l (S. marcescens) or 1,024 mg/l (P. aeruginosa). Bacterial biofilm formation is rather inhibited than enhanced by CHG. CHG removes biofilm only poorly.
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Kampf, G. (2018). Chlorhexidine Digluconate. In: Antiseptic Stewardship. Springer, Cham. https://doi.org/10.1007/978-3-319-98785-9_13
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