The Biocide and Antibiotic Resistance in Campylobacter jejuni and Campylobacter coli

Abstract

The use of antibiotics and biocides has recently provoked the development and spread of resistant and multidrug-resistant microorganisms. We examined the resistance of Campylobacter jejuni and C. coli from food, animal, human and environmental water sources to biocides triclosan, benzalkonium chloride, cetylpyridinium chloride, chlorhexidine diacetate and trisodium phosphate, to sodium dodecyl sulphate and to antibiotics, erythromycin and ciprofloxacin. The involvement of efflux mechanism was confirmed as an important mechanism for biocide and antibiotic resistance on the basis of the effect of efflux pump inhibitors and putative efflux pump inducers. The contribution of the CmeABC and CmeDEF efflux pumps was confirmed by the study of resistance in cmeB, cmeF and cmeR mutants. This study has not provided evidence to confirm that tolerance to biocides is directly linked to antibiotic resistance of the strains. However, when the stepwise exposure to increasing sub-inhibitory concentrations of five biocides as triclosan, benzalkonium chloride, cetylpyridinium chloride, chlorhexidine diacetate and trisodium phosphate was investigated to identify the mechanisms underlying resistance, this resulted in increased tolerances to biocides itself, to other biocides and antibiotics. More than one type of active efflux was identified in adapted strains. Beside active efflux, alterations in the outer membrane protein profiles and morphological cell changes were involved in adaptation to biocides, which was unique to each strain of Campylobacter and has not result from a single species-specific mechanism.