The Genetic Relatedness and Antimicrobial Resistance Patterns of Mastitis-Causing Staphylococcus aureus Strains Isolated from New Zealand Dairy Cattle

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Date
2021-11-22
Open Access Location
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Publisher
MDPI (Basel, Switzerland)
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(c) The author/s
CC BY 4.0
Abstract
Staphylococcus aureus is one of the leading causes of bovine mastitis worldwide and is a common indication for use of antimicrobials on dairy farms. This study aims to investigate the association between on-farm antimicrobial usage and the antimicrobial resistance (AMR) profiles of mastitis-causing S. aureus. Whole-genome sequencing was performed on 57 S. aureus isolates derived from cows with either clinical or subclinical mastitis from 17 dairy herds in New Zealand. The genetic relatedness between isolates was examined using the core single nucleotide polymorphism alignment whilst AMR and virulence genes were identified in-silico. The association between gene presence-absence and sequence type (ST), antimicrobial susceptibility and dry cow therapy treatment was investigated using Scoary. Altogether, eight STs were identified with 61.4% (35/57) belonging to ST-1. Furthermore, 14 AMR-associated genes and 76 virulence-associated genes were identified, with little genetic diversity between isolates belonging to the same ST. Several genes including merR1 which is thought to play a role in ciprofloxacin-resistance were found to be significantly overrepresented in isolates sampled from herds using ampicillin/cloxacillin dry cow therapy. Overall, the presence of resistance genes remains low and current antimicrobial usage patterns do not appear to be driving AMR in S. aureus associated with bovine mastitis.
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Keywords
Staphylococcus aureus, antimicrobial resistance, cattle, mastitis, whole-genome sequencing
Citation
Greening SS, Zhang J, Midwinter AC, Wilkinson DA, McDougall S, Gates MC, French NP. (2021). The Genetic Relatedness and Antimicrobial Resistance Patterns of Mastitis-Causing Staphylococcus aureus Strains Isolated from New Zealand Dairy Cattle.. Vet Sci. 8. 11. (pp. 287-).
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