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Campylobacter has become increasingly resistant to erythromycin, a macrolide antibiotic and the most commonly used drug to treat human Campylobacter infections. Although macrolide usage in agriculture is considered a major driving force for the increasing resistance rate, its actual contribution to the emergence and prevalence of macrolide-resistant Campylobacter in food producing animals remain to be elucidated. In this study the effect of macrolide treatment on the emergence of erythromycin resistance in C. jejuni and C. coli and the genetic mechanisms associated with the resistance are investigated using both in vitro and in vivo studies. In vitro plating of C. jejuni or C. coli cultures on MH agar plates with erythromycin revealed that both Campylobacter species had similar, but low mutation rates (approximately 10-10) to erythromycin. Chickens infected with C. jejuni or C. coli were subject to single or multiple treatments with tylosin using the dose and regime recommended for poultry production. The treatments transiently reduced the level of Campylobacter colonization in chickens, but did not select or enrich erythromycin-resistant mutants in the treated chickens. This finding is in contrast to the rapid emergence of fluoroquinolone-resistant Campylobacter in chickens treated with enrofloxacin (29). Interestingly, the in vitro selected erythromycin-resistant mutants did not have the known resistance-associated mutations in the 23S RNA gene; however, inactivation of CmeABC, a

Emergence frequencies and mechanisms of Fluoroquinolone and Macrolide resistance in Campylobacter