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肯尼亚由热带利什曼原虫引起的人类皮肤利什曼病。

Indigenous human cutaneous leishmaniasis caused by Leishmania tropica in Kenya.

作者信息

Mebrahtu Y, Lawyer P, Githure J, Kager P, Leeuwenburg J, Perkins P, Oster C, Hendricks L D

机构信息

Biomedical Sciences Research Centre, Kenya Medical Research Institute, Nairobi.

出版信息

Am J Trop Med Hyg. 1988 Sep;39(3):267-73. doi: 10.4269/ajtmh.1988.39.267.

Abstract

Six Leishmania isolates from 3 indigenous Kenyans (2 isolates from one patient) and 2 Canadian visitors in Kenya were characterized by cellulose acetate electrophoresis. The isolates were compared among themselves and with reference strains of Leishmania donovani, L. aethiopica, L. major, L. tropica, and L. arabica using 9 enzymes: malate dehydrogenase (MDH), malic enzyme (ME), phosphogluconate dehydrogenase (6PGD), glucose-6-phosphate dehydrogenase (G6PD), aspartate aminotransferase (ASAT), adenylate kinase (AK), mannose phosphate isomerase (MPI), glucose phosphate isomerase (GPI), and phosphoglucomutase (PGM). Enzyme migration patterns of isolates from the 3 indigenous Kenyans were indistinguishable from those of 2 L. tropica reference strains. The isolates from the 2 Canadians yielded migration patterns of 7 enzymes that were indistinguishable from those of 2 L. tropica reference strains. However, migration patterns of 2 enzymes, PGM and ME, differed from all migration patterns of the 10 reference strains. Balb/c mice were inoculated with stationary phase promastigotes cultured from 3 stabilates from the lesions of 2 of the Kenyan patients. The mice developed no gross pathological lesions in 6 months time. All of the study patients developed cutaneous leishmaniasis while living in or visiting districts in Central and Rift Valley Provinces, Kenya. This is the first report of human cutaneous leishmaniasis caused by L. tropica indigenous to Africa south of the Sahara.

摘要

对来自3名肯尼亚当地人(其中1名患者分离出2株)以及2名在肯尼亚的加拿大游客的6株利什曼原虫分离株进行了醋酸纤维素电泳分析。使用9种酶:苹果酸脱氢酶(MDH)、苹果酸酶(ME)、磷酸葡萄糖酸脱氢酶(6PGD)、葡萄糖-6-磷酸脱氢酶(G6PD)、天冬氨酸转氨酶(ASAT)、腺苷酸激酶(AK)、甘露糖磷酸异构酶(MPI)、葡萄糖磷酸异构酶(GPI)和磷酸葡萄糖变位酶(PGM),将这些分离株相互之间以及与杜氏利什曼原虫、埃塞俄比亚利什曼原虫、硕大利什曼原虫、热带利什曼原虫和阿拉伯利什曼原虫的参考菌株进行比较。来自3名肯尼亚当地人的分离株的酶迁移模式与2株热带利什曼原虫参考菌株的酶迁移模式无法区分。来自2名加拿大人的分离株产生的7种酶的迁移模式与2株热带利什曼原虫参考菌株的迁移模式无法区分。然而,PGM和ME这2种酶的迁移模式与10株参考菌株的所有迁移模式都不同。用从2名肯尼亚患者病变部位的3个保种培养的稳定期前鞭毛体接种Balb/c小鼠。6个月内小鼠未出现明显病理损伤。所有研究患者在生活或访问肯尼亚中部和裂谷省的地区时均患上了皮肤利什曼病。这是撒哈拉以南非洲本土热带利什曼原虫引起人类皮肤利什曼病的首次报告。

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