Bigliardi E, Bernuzzi A M, Corona S, Gatti S, Scaglia M, Sacchi L
Department of Evolutionary Biology, University of Siena, Pavia, Italy.
Antimicrob Agents Chemother. 2000 Nov;44(11):3012-6. doi: 10.1128/AAC.44.11.3012-3016.2000.
Since 1985 microsporidia have been recognized as a cause of emerging infections in humans, mainly in immunocompromised human immunodeficiency virus-positive subjects. As chitin is a basic component of the microsporidian infective stage, the spore, we evaluated in vitro the susceptibility of a human-derived strain of Encephalitozoon hellem to nikkomycin Z, a peptide-nucleoside antibiotic known as a competitive inhibitor of chitin synthase enzymes. Transmission electron microscopy showed that this drug, at 25 microgram/ml, reduced the number of parasitic foci by about 35% +/- standard deviation after 7 days of culture (P < 0.0001) and induced cell damage of both mature and immature spores and also other sporogonic and merogonic stages. In particular, an irregular outline of the cell shape and an abnormally condensed cytoplasm in meronts and sporonts were documented. Also, the polar tubule and the polaroplast membranes appeared disarrayed in the sporoblast stage. The spore wall showed an enlarged endospore and delaminated exospore. Mature spores had a complete cytoplasmic disorganization and a swollen and delaminated cell wall. No ultrastructural cell damage was observed in uninfected control cultures treated with the drug.
自1985年以来,微孢子虫已被确认为人类新发感染的病因,主要发生在免疫功能低下的人类免疫缺陷病毒阳性个体中。由于几丁质是微孢子虫感染阶段(即孢子)的基本成分,我们在体外评估了一株源自人类的海伦脑炎微孢子虫对尼可霉素Z的敏感性,尼可霉素Z是一种肽 - 核苷抗生素,已知是几丁质合酶的竞争性抑制剂。透射电子显微镜显示,该药物在浓度为25微克/毫升时,培养7天后寄生虫灶数量减少了约35%±标准差(P < 0.0001),并导致成熟和未成熟孢子以及其他孢子生殖和裂殖生殖阶段的细胞损伤。特别是,记录到裂殖体和孢子体的细胞形状轮廓不规则以及细胞质异常浓缩。此外,在孢子母细胞阶段,极管和极膜似乎排列紊乱。孢子壁显示内膜增大和外膜分层。成熟孢子的细胞质完全紊乱,细胞壁肿胀且分层。在用该药物处理的未感染对照培养物中未观察到超微结构的细胞损伤。