A COMPARISON OF ENDOGENOUS DEVELOPMENT OF 3 ISOLATES OF CRYPTOSPORIDIUM IN SUCKLING MICE
A COMPARISON OF ENDOGENOUS DEVELOPMENT OF 3 ISOLATES OF CRYPTOSPORIDIUM IN SUCKLING MICE
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DOI：
10.1111/j.1550-7408.1986.tb05567.x
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发表时间：
1986-02-01
期刊：
影响因子：
--
通讯作者：
REESE, NC
中科院分区：
文献类型：
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作者：
CURRENT, WL;REESE, NC
乳鼠被用作模型宿主，以比较三种不同隐孢子虫分离株的内源性发育：一种来自自然感染的小牛，一种来自具有免疫活性的短期腹泻病患者，一种来自患有获得性免疫缺陷综合征（AIDS）和持续性、危及生命的胃肠道隐孢子虫病的患者。经口接种小鼠卵囊后，没有发现三个分离株的感染部位，出现时间，持续时间，形态和精细结构的发展阶段之间的差异。子孢子在十二指肠和回肠腔中出囊，进入绒毛肠上皮细胞的微绒毛区，并发育成具有6或8个裂殖子的I型裂殖体。I型裂殖子穿透肠上皮细胞并经历作为I型裂殖子的周期性发育，或者它们成为具有四个裂殖子的II型裂殖子。II型裂殖子没有表现出周期性发育，而是直接发育成有性形式。小配子体产生。16个小的子弹形小配子，观察到它们附着并穿透大配子。在肠上皮细胞中观察到的约80%的卵囊具有厚的双层壁。在寄生虫空泡内形成孢子后，这些厚壁卵囊通过肠道，不发生变化，并以抗性形式将感染传播给新宿主。肠上皮细胞中约20%的卵囊由四个子孢子和一个残留物组成，所述残留物仅被一个卵囊膜包围，所述卵囊膜在寄生虫从宿主细胞释放后不久破裂。薄壁，自身感染的卵囊和回收的I型meront的存在下，可以解释为什么一个小的口服接种物可以产生压倒性的感染在一个合适的主机，为什么免疫缺陷的人可以有持续的，危及生命的隐孢子虫病在没有反复的口腔接触厚壁卵囊。
Suckling mice were used as a model host to compare the endogenous development of three different isolates of Cryptosporidium: one from a naturally infected calf, one from an immunocompetent human with a short-term diarrheal illness, and one from a patient with acquired immune deficiency syndrome (AIDS) and persistent, life-threatening, gastrointestinal cryptosporidiosis. After oral inoculation of mice with oocysts, no differences were noted among developmental stages of the three isolates in their sites of infection, times of appearance, and duration, morphology, and fine structure. Sporozoites excysted within the lumen of the duodenum and ileum, penetrated into the microvillous region of villous enterocytes, and developed into type I meronts with six or eight merozoites. Type I merozoites penetrated enterocytes and underwent cyclic development as type I meronts or they became type II meronts with four merozoites. Type II merozoites did not exhibit cyclic development but developed directly into sexual forms. Microgamonts produced .apprx. 16 small, bullet-shaped microgametes, which were observed attaching to and penetrating macrogametes. Approximately 80% of the oocysts observed in enterocytes had a thick, two-layered wall. After sporulating within the parasitophorous vacuole, these thick-walled oocysts passed through the gut unaltered and were the resistant forms that transmitted the infection to a new host. Approximately 20% of the oocysts in enterocytes consisted of four sporozoites and a residuum surrounded only by a single oocyst membrane that ruptured soon after the parasite was released from the host cell. The presence of thin-walled, autoinfective oocysts and recycling of type I meronts may explain why a small oral inoculum can produce an overwhelming infection in a suitable host and why immune deficient persons can have persistent, life-threatening cryptosporidiosis in the absence of repeated oral exposure to thick-walled oocysts.