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微小隐孢子虫作为感染猿猴免疫缺陷病毒的免疫缺陷猕猴(恒河猴)增生性浆膜炎的病因。

Enterocytozoon bieneusi as a cause of proliferative serositis in simian immunodeficiency virus-infected immunodeficient macaques (Macaca mulatta).

作者信息

Chalifoux L V, Carville A, Pauley D, Thompson B, Lackner A A, Mansfield K G

机构信息

New England Regional Primate Research Center, Harvard Medical School, One Pine Hill Dr, Southborough, MA 01772-9012, USA.

出版信息

Arch Pathol Lab Med. 2000 Oct;124(10):1480-4. doi: 10.5858/2000-124-1480-EBAACO.

Abstract

CONTEXT

Enterocytozoon bieneusi is the most frequent microsporidian parasite of human patients with acquired immunodeficiency syndrome and is a significant cause of diarrhea and wasting. Recently, this organism has also been recognized as a spontaneous infection of several species of captive macaques. As in humans, E bieneusi frequently causes enteropathy and cholangiohepatitis in immunodeficient simian immunodeficiency virus (SIV)-infected macaques.

OBJECTIVE

To examine E bieneusi as an etiologic agent of nonsuppurative proliferative serositis in immunodeficient rhesus macaques (Macaca mulatta).

DESIGN

Retrospective analysis of necropsy material obtained from immunodeficient SIV-infected rhesus macaques.

RESULTS

Examination of SIV-infected rhesus macaques (n = 225) revealed E bieneusi proliferative serositis in 7 of 16 cases of peritonitis of unknown origin. The organism could be identified by in situ hybridization and polymerase chain reaction in sections of pleura and peritoneum obtained at necropsy. Serositis was always accompanied by moderate-to-severe infection of the alimentary tract, and morphologic evidence suggested dissemination through efferent lymphatics. Colabeling experiments revealed most infected cells to be cytokeratin positive and less frequently positive for the macrophage marker CD68. Sequencing of a 607-base pair segment of the small subunit ribosomal gene revealed 100% identity to sequences obtained from rhesus macaques (Genbank accession AF023245) and human patients (Genbank accession AF024657 and L16868).

CONCLUSIONS

These findings indicate that E bieneusi disseminates in immunodeficient macaques and may be a cause of peritonitis in the immunocompromised host.

摘要

背景

比氏肠胞微孢子虫是获得性免疫缺陷综合征患者中最常见的微孢子虫寄生虫,是腹泻和消瘦的重要病因。最近,该生物体也被认为是几种圈养猕猴的自发性感染源。与人类一样,比氏肠胞微孢子虫在免疫缺陷的感染猿猴免疫缺陷病毒(SIV)的猕猴中经常引起肠病和胆管肝炎。

目的

研究比氏肠胞微孢子虫作为免疫缺陷恒河猴非化脓性增殖性浆膜炎的病原体。

设计

对从免疫缺陷的感染SIV的恒河猴获得的尸检材料进行回顾性分析。

结果

对感染SIV的恒河猴(n = 225)进行检查发现,在16例不明原因的腹膜炎病例中有7例出现比氏肠胞微孢子虫增殖性浆膜炎。在尸检时获得的胸膜和腹膜切片中,可通过原位杂交和聚合酶链反应鉴定该生物体。浆膜炎总是伴有中度至重度的消化道感染,形态学证据表明其通过输出淋巴管扩散。共标记实验显示,大多数感染细胞细胞角蛋白呈阳性,而巨噬细胞标志物CD68呈阳性的频率较低。对小亚基核糖体基因607个碱基对片段进行测序,结果显示与从恒河猴(Genbank登录号AF023245)和人类患者(Genbank登录号AF024657和L16868)获得的序列100%相同。

结论

这些发现表明,比氏肠胞微孢子虫在免疫缺陷的猕猴中扩散,可能是免疫受损宿主腹膜炎的病因。

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