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Published on: March 3, 2023
Spread of Multidrug-Resistant Rhodococcus equi, United States
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.
Insights
Mass antibiotic use in horses has led to multidrug-resistant Rhodococcus equi, a pathogen with zoonotic potential. This resistance, driven by plasmid pRERm46, is spreading in the US and may become international.
Area of Science:
- Veterinary Microbiology
- Antimicrobial Resistance
- Genomics
Background:
- Multidrug resistance (MDR) in Rhodococcus equi, an animal and zoonotic pathogen, has been identified in US equine farms.
- This emergence follows widespread macrolide/rifampin antibioprophylaxis.
Purpose of the Study:
- To investigate the emergence and genetic basis of MDR R. equi.
- To understand the role of plasmid pRERm46 and chromosomal mutations in resistance.
- To assess the potential for zoonotic transmission and international spread.
Main Methods:
- Phylogenomic analyses of R. equi isolates.
- Plasmid characterization (pRERm46) and resistance profiling.
- Identification of specific mutations in chromosomal genes (e.g., rpoB).
Main Results:
- MDR R. equi emerged due to acquisition of the conjugative plasmid pRERm46, conferring resistance to macrolides, lincosamides, streptogramins, and tetracycline.
- Phylogenomic data revealed a dominant MDR clone (R. equi 2287) linked to coselection of pRERm46 and an rpoBS531F mutation.
- A novel MDR clone (G2016) arose from pRERm46 transfer to other R. equi genotypes, associated with an rpoBS531Y mutation.
Conclusions:
- Overuse of antimicrobial prophylaxis in animal agriculture can generate MDR pathogens with zoonotic potential.
- MDR R. equi and pRERm46-mediated resistance are actively disseminating within the US.
- International spread is probable due to global horse movements, necessitating surveillance and control measures.
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