Multiple point mutations in cytochrome b gene of Babesia gibsoni - A possible cause for buparvaquone resistance.

Abstract

The development and rise in drug-resistant Babesia gibsoni strain is a serious concern among veterinary practitioners. Of several therapeutic strategies followed, buparvaquone-azithromycin combination therapy is widely used to treat small Babesia infections in Asia. The present study focused on buparvaquone-induced mutations in B. gibsoni by analyzing its cytochrome b gene sequence. Among the 12 dogs that were administered with buparvaquone-azithromycin combination therapy, 8 of them were unresponsive to drug-resistant B. gibsoni infection. Hematological parameters were recorded before and after 10 day treatment plan and an improvement in these values was observed. Eight samples with persistent parasitemia after 10 day treatment plan was subjected to cytochrome b gene amplification and analyzed for mutations. On analysis, out of the 25 mutations only 9 were non-synonymous in nature; T15N, S48T, P152L, V167I, A217T, F258Y, M311I, S336G, A337S. Mutation P152L was seen near to Q01 (130-148) binding region and F258Y within the drug binding region Q02 (244-266).