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小鼠艾美耳球虫(Eimeria krijgsmanni)第二代裂殖体残余子孢子诱导长期感染的潜在发育能力

Potential Development Ability of Residual Zoites, a Second-Generation Meront, Inducing Long-Term Infection by the Mouse Eimerian Parasite, Eimeria krijgsmanni.

作者信息

Mizuno Masanobu, Kiyotake Satoru, Matsubayashi Makoto, Kaneko Takane, Hatai Hitoshi, Fujimoto Yoshikazu, Ijiri Moe, Kawaguchi Hiroaki, Matsui Toshihiro, Matsuo Tomohide

机构信息

Laboratory of Parasitology, Joint Faculty of Veterinary Medicine, Kagoshima University, Kagoshima, 890-0065, Japan.

Laboratory of Veterinary Immunology, Graduate School of Veterinary Science, Osaka Metropolitan University, Izumisano, 598-5831, Osaka, Japan.

出版信息

Acta Parasitol. 2024 Dec;69(4):1860-1865. doi: 10.1007/s11686-024-00910-2. Epub 2024 Aug 29.

Abstract

PURPOSE

Coccidiosis caused by eimerian parasites results in lethal watery or bloody diarrhea in hosts, and markedly impairs the growth of and feed utilization by host animals. We previously investigated detailed the life cycle of Eimeria krijgsmanni as a mouse eimerian parasite. Only second-generation meronts, as an asexual stage, were morphologically detected in the epithelium of the host cecum for at least 8 weeks after infection, even though oocyst shedding finished approximately 3 weeks after infection. The presence of zoites was of interest because infection by eimerian parasites is considered to be self-limited after their patent period.

METHODS

To clarify the significance of residual second-generation meronts in E. krijgsmanni infection, we performed infection experiments using immunocompetent mice under artificial immunosuppression and congenital immunodeficient mice.

RESULTS

The number of oocysts discharged and the duration of oocyst discharge both increased in immunosuppressed mice. In immunodeficient mice, numerous oocysts were shed over a markedly longer period, and oocyst discharge did not finish until 56 days after inoculation.

CONCLUSIONS

The present results suggest that the second-generation meronts survived in the epithelial cells of the cecum after the patent period, thereby contributing to extended infection as an asexual stage. The results obtained on E. krijgsmanni indicate that infections by Eimeria spp. are not self-limited and potentially continue for a long period of time.

摘要

目的

艾美耳属寄生虫引起的球虫病可导致宿主出现致死性水样或血性腹泻,并显著损害宿主动物的生长和饲料利用率。我们之前详细研究了小鼠艾美耳球虫(Eimeria krijgsmanni)的生命周期。尽管感染后约3周卵囊排出结束,但在感染后至少8周内,仅在宿主盲肠上皮中形态学检测到作为无性阶段的第二代裂殖体。由于艾美耳属寄生虫感染在其显性期后被认为是自限性的,因此子孢子的存在令人感兴趣。

方法

为阐明E. krijgsmanni感染中残留第二代裂殖体的意义,我们在人工免疫抑制下对免疫活性小鼠和先天性免疫缺陷小鼠进行了感染实验。

结果

免疫抑制小鼠排出的卵囊数量和卵囊排出持续时间均增加。在免疫缺陷小鼠中,大量卵囊在明显更长的时间内排出,并且直到接种后56天卵囊排出才结束。

结论

目前的结果表明,第二代裂殖体在显性期后在盲肠上皮细胞中存活,从而作为无性阶段导致感染延长。关于E. krijgsmanni的结果表明,艾美耳属物种的感染不是自限性的,并且可能持续很长时间。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ffaf/11649722/aa5a6f37c524/11686_2024_910_Fig1_HTML.jpg

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