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Virulence of non-type 1-fimbriated and nonfimbriated nonflagellated Salmonella typhimurium mutants in murine typhoid fever.

机译:鼠伤寒中非类型1纤毛和非纤毛无鞭毛鼠伤寒沙门氏菌突变体的毒力。

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The virulence of Salmonella typhimurium mutants that were unable to synthesize type 1 fimbriae was tested in a murine typhoid fever model. Nonfimbriated mutants (fim) exhibited a lower 50% lethal dose than a wild-type (fim+) strain and produced significantly higher mortality (fim, 55%; fim+, 37% [P less than 0.002]) in mice that were challenged orally. There was no difference in virulence when the wild-type and mutant strains were injected intraperitoneally into mice. The progress of a short-term lethal infection was monitored after oral inoculation of mice with a mixture containing equivalent numbers of fim+ wild-type and fim mutant bacteria. The results indicated that while both strains colonized the intestinal tract equally well and invaded internal organs, the S. typhimurium fim mutant proliferated in the blood of the mice faster than the fim+ strain. The results of the mixed oral challenge suggested that bacteremia caused by fim+ S. typhimurium was reduced or delayed by the sequestration of the fimbriated bacteria in the spleen, liver, and kidneys. Thus, type 1 fimbriae were not virulence factors for S. typhimurium in this model, and the fimbriae may be an impediment to the pathogen in this setting. An S. typhimurium double mutant lacking type 1 fimbriae and flagella (fla) also was tested in mice. The virulence of the fim fla mutant was greatly reduced compared with that of the wild-type strain (mortality from fim fla challenge, 11% [P less than 0.0005]). The significance of this latter result is discussed in relation to host adaptation by pathogenic salmonellae.
机译:在鼠伤寒模型中测试了不能合成1型菌毛的鼠伤寒沙门氏菌突变体的毒力。非纤毛突变体(fim)的致死剂量低于野生型(fim +)菌株,并且在口服攻击的小鼠中产生了更高的死亡率(fim,55%; fim +,37%[P小于0.002])。当将野生型和突变株腹膜内注射到小鼠中时,毒力没有差异。在小鼠口服含有相等数量的fim +野生型细菌和fim突变细菌的混合物后,对短期致命感染的进程进行了监测。结果表明,尽管两种菌株均能很好地在肠道中定植并侵袭内部器官,但鼠伤寒沙门氏菌fim突变体在小鼠血液中的增殖速度要快于fim +菌株。混合口服攻击的结果表明,通过将fim +鼠伤寒沙门氏菌引起的菌血症减少或延缓了脾脏,肝脏和肾脏中细菌的螯合。因此,在该模型中,1型菌毛不是鼠伤寒沙门氏菌的致病因子,在这种情况下,菌丝可能是病原体的障碍。还在小鼠中测试了缺乏1型菌毛和鞭毛(fla)的鼠伤寒沙门氏菌双突变体。与野生型菌株相比,fim fla突变体的毒力大大降低(fim fla攻击的死亡率为11%[P小于0.0005])。关于病原性沙门氏菌对宿主的适应性,讨论了后者的意义。

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