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致病性耐格里属阿米巴的发病机制。

Pathogenesis of pathogenic Naegleria amoeba.

作者信息

Chang S L

出版信息

Folia Parasitol (Praha). 1979;26(3):195-200.

PMID:120297
Abstract

In brain sections of the Naegleria-caused cases of primary amoebic meningoencephalitis, extensive demyelinization was found in the white matter, besides the severe histopathological changes and large clusters of trophozoites in the grey matter. The myelinoclasis appeared to be a result of a specific phospholipolytic effect, unlike that in post-viral encephalomyelitis, which has been attributed to vascular blockade or hemorrhages. In monkey kidney cell cultures a very early cytopathic effect was observed and traced to the cytolytic property of the seeding culture fluid. Rat brain slices inoculated with Naegleria culture exhibited amoebic growth and demyelinization in 28-52 hours incubation at 35 degrees C. In a chemically defined medium containing sphingomyelin, casein and glucose, the Naegleria produced a limited growth parallelling the clearance of the lipid turbidity during a 72 hour incubation at 35 degrees C. Chromatographic analysis of the turbidity-cleared cultures revealed decomposition of sphingomyeline with liberation of choline, sphingosine and fatty acids. It is, hence, concluded that the pathogenicity of cytopathic effect of pathogenic Naegleria can be attributed to the latter's capacity to liberate a phospholipolytic enzyme or factor during active growth, which "makes holes" in the lipid-rich cytoplasmic membrane of cells as well as demyelinizes nerve tissue.

摘要

在由耐格里属原虫引起的原发性阿米巴脑膜脑炎病例的脑切片中,除了灰质中有严重的组织病理学变化和大量滋养体聚集外,白质中还发现了广泛的脱髓鞘现象。与病毒性脑脊髓炎中脱髓鞘现象归因于血管阻塞或出血不同,耐格里属原虫引起的脱髓鞘似乎是一种特定的磷脂分解作用的结果。在猴肾细胞培养物中观察到了非常早期的细胞病变效应,并追溯到接种培养液的细胞溶解特性。接种耐格里属原虫培养物的大鼠脑切片在35℃孵育28 - 52小时后出现阿米巴生长和脱髓鞘现象。在含有鞘磷脂、酪蛋白和葡萄糖的化学限定培养基中,耐格里属原虫在35℃孵育72小时期间生长有限,同时脂质浊度也逐渐清除。对浊度清除后的培养物进行色谱分析,发现鞘磷脂分解,释放出胆碱、鞘氨醇和脂肪酸。因此,可以得出结论,致病性耐格里属原虫的细胞病变效应的致病性可归因于其在活跃生长过程中释放磷脂分解酶或因子的能力,这种酶或因子会在富含脂质的细胞质膜上“打孔”,并使神经组织脱髓鞘。

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