Abstract:Exposure of ADP1 to sublethal concentrations of chlorhexidine confers inducible resistance to lethal concentrations of chlorhexidine itself and to oxidants. An important link was demonstrated between exposure to a biocide and the gaining of resistance to both the biocide and oxidative stress.
“…Since several biocides have multiple, nonspecific mechanisms of action, similarly to tea tree oil, this same concern could apply to the oil. Although decreased antibiotic susceptibility following biocide exposure has been demonstrated in vitro (4,16), there is still debate as to what impact, if any, this has in clinical practice (17). The current study has demonstrated that tea tree oil has little impact on the development of antibiotic resistance, and that exposure to the major component terpinen-4-ol does not significantly alter antimicrobial susceptibility.…”
This study examined the effect of subinhibitory Melaleuca alternifolia (tea tree) essential oil on the development of antibiotic resistance in Staphylococcus aureus and Escherichia coli. Frequencies of single-step antibiotic-resistant mutants were determined by inoculating bacteria cultured with or without subinhibitory tea tree oil onto agar containing 2 to 8 times the MIC of each antibiotic and with or without tea tree oil. Whereas most differences in resistance frequencies were relatively minor, the combination of kanamycin and tea tree oil yielded approximately 10-fold fewer resistant E. coli mutants than kanamycin alone. The development of multistep antibiotic resistance in the presence of tea tree oil or terpinen-4-ol was examined by culturing S. aureus and E. coli isolates daily with antibiotic alone, antibiotic with tea tree oil, and antibiotic with terpinen-4-ol for 6 days. Median MICs for each antibiotic alone increased 4-to 16-fold by day 6. Subinhibitory tea tree oil or terpinen-4-ol did not greatly alter results, with day 6 median MICs being either the same as or one concentration different from those for antibiotic alone. For tea tree oil and terpinen-4-ol alone, day 6 median MICs had increased 4-fold for S. aureus (n ؍ 18) and 2-fold for E. coli (n ؍ 18) from baseline values. Lastly, few significant changes in antimicrobial susceptibility were seen for S. aureus and S. epidermidis isolates that had been serially subcultured 14 to 22 times with subinhibitory terpinen-4-ol. Overall, these data indicate that tea tree oil and terpinen-4-ol have little impact on the development of antimicrobial resistance and susceptibility.
“…Since several biocides have multiple, nonspecific mechanisms of action, similarly to tea tree oil, this same concern could apply to the oil. Although decreased antibiotic susceptibility following biocide exposure has been demonstrated in vitro (4,16), there is still debate as to what impact, if any, this has in clinical practice (17). The current study has demonstrated that tea tree oil has little impact on the development of antibiotic resistance, and that exposure to the major component terpinen-4-ol does not significantly alter antimicrobial susceptibility.…”
This study examined the effect of subinhibitory Melaleuca alternifolia (tea tree) essential oil on the development of antibiotic resistance in Staphylococcus aureus and Escherichia coli. Frequencies of single-step antibiotic-resistant mutants were determined by inoculating bacteria cultured with or without subinhibitory tea tree oil onto agar containing 2 to 8 times the MIC of each antibiotic and with or without tea tree oil. Whereas most differences in resistance frequencies were relatively minor, the combination of kanamycin and tea tree oil yielded approximately 10-fold fewer resistant E. coli mutants than kanamycin alone. The development of multistep antibiotic resistance in the presence of tea tree oil or terpinen-4-ol was examined by culturing S. aureus and E. coli isolates daily with antibiotic alone, antibiotic with tea tree oil, and antibiotic with terpinen-4-ol for 6 days. Median MICs for each antibiotic alone increased 4-to 16-fold by day 6. Subinhibitory tea tree oil or terpinen-4-ol did not greatly alter results, with day 6 median MICs being either the same as or one concentration different from those for antibiotic alone. For tea tree oil and terpinen-4-ol alone, day 6 median MICs had increased 4-fold for S. aureus (n ؍ 18) and 2-fold for E. coli (n ؍ 18) from baseline values. Lastly, few significant changes in antimicrobial susceptibility were seen for S. aureus and S. epidermidis isolates that had been serially subcultured 14 to 22 times with subinhibitory terpinen-4-ol. Overall, these data indicate that tea tree oil and terpinen-4-ol have little impact on the development of antimicrobial resistance and susceptibility.
“…The mechanism of chlorhexidine resistance in A. baumannii is purportedly associated with bacterial efflux pumps. 10 In this study, although the magnitude of chlorhexidine exposure resulting in the increase in A. baumannii chlorhexidine MICs 50/90 during the 12-month advanced source control period, it did not achieve the threshold for the emergence of chlorhexidine-resistant XDR A. baumannii detection, yet our data suggest that ongoing active surveillance for chlorhexidineresistant A. baumannii as well as its MIC 50/90 is needed to evaluate the emergence of chlorhexidine-resistant A. baumannii.…”
Section: Increase In Chlorhexidine Minimal Inhibitory Concentration Omentioning
Molecular analysis of the pathogenicity locus and polymorphism in the putative negative regulator of toxin production (TcdC) among Clostridium difficile clinical isolates. / Clin Microbiol 2002;40:3470-3475. 10. Spigaglia P, Mastrantonio P. Comparative analysis oi Clostridium difficile clinical isolates belonging to different genetic lineages and time periods. / Med Microbiol 2004;53:1129-1136.
“…AceI belongs to the bacterial transmembrane pair family and is grouped as a prototype member of the proteobacterial chlorhexidine efflux family (563). Similarly, the exposure of Acinetobacter baylyi to chlorhexidine also induced resistance to chlorhexidine and oxidants (564), which could potentially be attributed to efflux pumps.…”
SUMMARY
The global emergence of multidrug-resistant Gram-negative bacteria is a growing threat to antibiotic therapy. The chromosomally encoded drug efflux mechanisms that are ubiquitous in these bacteria greatly contribute to antibiotic resistance and present a major challenge for antibiotic development. Multidrug pumps, particularly those represented by the clinically relevant AcrAB-TolC and Mex pumps of the resistance-nodulation-division (RND) superfamily, not only mediate intrinsic and acquired multidrug resistance (MDR) but also are involved in other functions, including the bacterial stress response and pathogenicity. Additionally, efflux pumps interact synergistically with other resistance mechanisms (e.g., with the outer membrane permeability barrier) to increase resistance levels. Since the discovery of RND pumps in the early 1990s, remarkable scientific and technological advances have allowed for an in-depth understanding of the structural and biochemical basis, substrate profiles, molecular regulation, and inhibition of MDR pumps. However, the development of clinically useful efflux pump inhibitors and/or new antibiotics that can bypass pump effects continues to be a challenge. Plasmid-borne efflux pump genes (including those for RND pumps) have increasingly been identified. This article highlights the recent progress obtained for organisms of clinical significance, together with methodological considerations for the characterization of MDR pumps.
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