Institute of Parasitology, Biology Centre, Czech Academy of Science, České Budějovice, Czech Republic.
Faculty of Science, University of South Bohemia in České Budějovice, České Budějovice, Czech Republic.
Exp Parasitol. 2021 May;224:108101. doi: 10.1016/j.exppara.2021.108101. Epub 2021 Mar 25.
Out of three genotypes of Encephalitozoon cuniculi (I-III) available for experimental studies, E. cuniculi genotype I remains the less characterized. This study describes for the first time individual phases of microsporidiosis caused by E. cuniculi genotype I and efficacy of albendazole treatment in immunocompetent BALB/c and C57Bl/6 mice and immunodeficient SCID, CD4 and CD8 mice using molecular detection and quantification methods. We demonstrate asymptomatic infection despite an intense dissemination of microsporidia into most organs within the first weeks post infection, followed by a chronic infection characterized by significant microsporidia persistence in immunocompetent, CD4 and CD8 mice and a lethal outcome for SCID mice. Albendazole application led to loss E. cuniculi genotype I infection in immunocompetent mouse strains, decreased spore burden by half in CD4 and CD8 mice, and prolongation of survival of SCID mice. These results showed Encephalitozoon cuniculi genotype I infection extend and albendazole sensitivity was comparable to E. cuniculi genotype II, but the infection onset speed and mortality rate was similar to E. cuniculi genotype III. These imply that differences in the course of infection and the response to treatment depend not only on immunological status of the host, but also on the genotype causing the infection.
在可用于实验研究的三种肠微孢子虫基因型(I-III)中,肠微孢子虫基因型 I 的特征仍然最少。本研究首次描述了由肠微孢子虫基因型 I 引起的微孢子虫病的各个阶段,以及在免疫功能正常的 BALB/c 和 C57Bl/6 小鼠以及免疫缺陷的 SCID、CD4 和 CD8 小鼠中,使用分子检测和定量方法,评价阿苯达唑治疗的效果。我们发现,尽管在感染后最初几周内,微孢子虫强烈扩散到大多数器官,但仍存在无症状感染,随后是慢性感染,其特征是在免疫功能正常、CD4 和 CD8 小鼠中微孢子虫持续存在,而 SCID 小鼠则出现致命后果。阿苯达唑的应用导致免疫功能正常的小鼠品系中肠微孢子虫基因型 I 的感染丧失,CD4 和 CD8 小鼠中的孢子负担减少一半,并延长了 SCID 小鼠的存活时间。这些结果表明,肠微孢子虫基因型 I 的感染持续时间延长,并且阿苯达唑的敏感性与肠微孢子虫基因型 II 相当,但感染的起始速度和死亡率与肠微孢子虫基因型 III 相似。这意味着感染过程和对治疗的反应的差异不仅取决于宿主的免疫状态,还取决于引起感染的基因型。