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细胞毒素坏死性因子2(CNF2)和细胞致死性膨胀毒素III(CDTIII)毒素在2型产坏死毒素大肠杆菌(NTEC2)菌株对犊牛的实验性感染中的假定作用。

Putative roles of the CNF2 and CDTIII toxins in experimental infections with necrotoxigenic Escherichia coli type 2 (NTEC2) strains in calves.

作者信息

Van Bost Sigrid, Roels Stefan, Oswald Eric, Mainil Jacques

机构信息

Laboratory of Bacteriology, Faculty of Veterinary Medicine, University of Liège, Sart-Tilman, B43a, 20, bd de Colonster, B-4000 Liege, Belgium.

出版信息

Microbes Infect. 2003 Nov;5(13):1189-93. doi: 10.1016/j.micinf.2003.08.005.

Abstract

Newborn colostrum-restricted calves were orally inoculated with an Escherichia coli strain, identified originally as non-pathogenic, and into which the plasmid pVir was conjugally transferred. This resulted in diarrhea, intestinal lesions and extra-intestinal invasion, suggesting that factors affecting these pathogenic properties are located on pVir. In order to analyze the respective roles of the toxins CNF2 and CDTIII in the pathogenesis, colostrum-restricted calves were inoculated with isogenic mutants in the cnf2 and the cdt-III genes. The loss of cnf2 is associated with a reduction in the pathogenicity, since diarrhea does not occur in calves challenged, in spite of successful colonization of the intestine. Nevertheless, the mutant strain remains able to invade the bloodstream and to localize in the internal organs. Conversely, the calves inoculated with mutant in the cdt-III gene evolved in the same way as wild-type strain-inoculated calves with regard to clinical signs and macroscopic or microscopic lesions.

摘要

新生期限制初乳摄入的犊牛经口接种了一株最初鉴定为非致病性的大肠杆菌菌株,该菌株通过接合转移获得了质粒pVir。这导致了腹泻、肠道病变和肠外侵袭,表明影响这些致病特性的因子位于pVir上。为了分析毒素CNF2和CDTIII在发病机制中的各自作用,给新生期限制初乳摄入的犊牛接种了cnf2和cdt-III基因的同基因突变体。cnf2缺失与致病性降低相关,因为尽管肠道成功定殖,但接种的犊牛并未出现腹泻。然而,突变菌株仍能够侵入血液并定位于内脏器官。相反,接种cdt-III基因突变体的犊牛在临床症状以及大体或显微镜下病变方面的发展与接种野生型菌株的犊牛相同。

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