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Babesia gibsoni cytochrome b mutations in canine blood samples submitted to a US veterinary diagnostic laboratory
- Birkenheuer, Adam J., Marr, Henry S., Wilson, James M., Breitschwerdt, Edward B., Qurollo, Barbara A.
- Journal of veterinary internal medicine 2018 v.32 no.6 pp. 1965-1969
- American Staffordshire Terrier, Babesia gibsoni, Bull Terrier, babesiosis, blood sampling, cytochrome b, dog diseases, dogs, genes, genotyping, mitochondrial genome, mutants, mutation, polymerase chain reaction, United States
- Background: Babesiosis caused by Babesia gibsoni is recognized throughout the world and can be difficult to treat. Resistance to atovaquone is associated with mutations in the B. gibsoni mitochondrial genome, specifically the M128 position of cytochrome b (cytb). The prevalence of cytb mutations in North America has not been reported. Hypothesis/Objectives: The objective of our study was to describe the prevalence of cytb M128 mutations in B. gibsoni in canine blood samples submitted to a US veterinary diagnostic laboratory. A secondary objective was to determine whether or not some dogs had wild‐type cytb in our initial samples then had M128 mutations detected in follow‐up samples. Animals: One‐Hundred seventy‐four dogs that tested positive for the presence of B. gibsoni between 2012 and 2017. Methods: Case series of consecutive samples submitted to a veterinary diagnostic laboratory. Partial B. gibsoni cytb genes were amplified by polymerase chain reaction and screened for the presence of mutations at the M128 position. Results: The overall prevalence of M128 mutants was 3.5% (6/173 dogs) in the initial samples. The incidence of new cytb mutants in dogs that tested positive for B. gibsoni, which then had follow‐up testing, was 12.1% (5/41). Conclusions and Clinic Importance: Our study reaffirms that B. gibsoni infection is widespread and most commonly detected in American Staffordshire Terrier/American Pit Bull Terrier dogs (128/174, 74% of the infected dogs in our study). The prevalence of cytb mutations does not warrant pretreatment genotyping.