Iguchi Aiko, Soma Takehisa, Suzuki Hiroshi, Xuan Xuenan
National Research Center for Protozoan Diseases, Obihiro University of Agriculture and Veterinary Medicine, Inada-cho, Obihiro, Hokkaido 080-8555, Japan.
J Vet Med Sci. 2016 Mar;78(3):489-91. doi: 10.1292/jvms.15-0480. Epub 2015 Nov 9.
In 73 gDNA samples from Babesia gibsoni-infected dogs, the M121I variant population was measured by using allele-specific real-time PCR. Although the mechanism of atovaquone against B. gibsoni has not been clearly identified, it is reported that the mitochondria cytochrome b gene of the atovaquone-resistant B. gibsoni had a single-nucleotide substitution at nt363 (G to T), which resulted in the substitution of methionine with isoleucine (M121I). In this study, 3/73 samples showed over 5% M121I variant population. Although the M121I variant population is a low percentage, it runs the risk of spreading drug-resistant parasites. It is important to prevent the spread of drug-resistance, so we need to gather information about this at regular intervals.
在73份感染吉氏巴贝斯虫的犬类基因组DNA样本中,通过等位基因特异性实时PCR检测M121I变异种群。尽管阿托伐醌抗吉氏巴贝斯虫的机制尚未明确,但据报道,对阿托伐醌耐药的吉氏巴贝斯虫线粒体细胞色素b基因在nt363处有单核苷酸替换(G到T),导致甲硫氨酸被异亮氨酸取代(M121I)。在本研究中,73份样本中有3份显示M121I变异种群超过5%。尽管M121I变异种群比例较低,但存在耐药寄生虫传播的风险。防止耐药性传播很重要,因此我们需要定期收集有关此方面的信息。