Abstract
Multidrug resistance has been detected in the animal and zoonotic human pathogen Rhodococcus equi after mass macrolide/rifampin antibioprophylaxis in endemically affected equine farms in the United States. Multidrug-resistant (MDR) R. equi emerged upon acquisition of pRERm46, a conjugative plasmid conferring resistance to macrolides, lincosamides, streptogramins, and, as we describe, tetracycline. Phylogenomic analyses indicate that the increasing prevalence of MDR R. equi since it was first documented in 2002 is caused by a clone, R. equi 2287, attributable to coselection of pRErm46 with a chromosomal rpoBS531F mutation driven by macrolide/rifampin therapy. pRErm46 spillover to other R. equi genotypes has given rise to a novel MDR clone, G2016, associated with a distinct rpoBS531Y mutation. Our findings illustrate that overuse of antimicrobial prophylaxis in animals can generate MDR pathogens with zoonotic potential. MDR R. equi and pRErm46-mediated resistance are currently disseminating in the United States and are likely to spread internationally through horse movements.
Highlights
Multidrug resistance has been detected in the animal and zoonotic human pathogen Rhodococcus equi after mass macrolide/rifampin antibioprophylaxis in endemically affected equine farms in the United States
Analysis of the virulence plasmids carried by the isolates and comparison of genomic profiles indicate that human R. equi infections originate from animals [4,5,6]
We recently determined that the emerging MRR phenotype among R. equi equine isolates was linked to a novel methyltransferase gene, erm[46], which confers cross-resistance to macrolides, lincosamides, and streptogramins (MLSR phenotype) [13]. erm[46] is part of a 6.9-kb transposable element, TnRErm46, which is carried by the conjugative resistance plasmid pRErm46 [15]
Summary
Multidrug resistance has been detected in the animal and zoonotic human pathogen Rhodococcus equi after mass macrolide/rifampin antibioprophylaxis in endemically affected equine farms in the United States. Multidrug-resistant (MDR) R. equi emerged upon acquisition of pRErm, a conjugative plasmid conferring resistance to macrolides, lincosamides, streptogramins, and, as we describe, tetracycline. We recently determined that the emerging MRR phenotype among R. equi equine isolates was linked to a novel methyltransferase gene, erm[46], which confers cross-resistance to macrolides, lincosamides, and streptogramins (MLSR phenotype) [13]. Upon pRErm acquisition, TnRErm stabilizes itself in R. equi by transposing to the host genome, including the conjugative virulence plasmid pVAPA. Despite its high potential for horizontal spread, we found that pRErm46/TnRErm was restricted to a specific R. equi clone, designated 2287, likely because of co-selection with a chromosomal rifampin-resistance rpoBS531F mutation in response to macrolide/rifampin therapy [15]. We investigate the spread of the erm[46] determinant in a contemporary sample
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