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首页> 外文期刊>Applied and Environmental Microbiology >Survival and virulence of copper- and chlorine-stressed Yersinia enterocolitica in experimentally infected mice.
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Survival and virulence of copper- and chlorine-stressed Yersinia enterocolitica in experimentally infected mice.

机译:铜和氯胁迫的小肠结肠炎耶尔森氏菌在实验感染小鼠中的存活和毒力。

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The effect of gastric pH on the viability and virulence of Yersinia enterocolitica O:8 after exposure to sublethal concentrations of copper and chlorine was determined in mice. Viability and injury were assessed with a nonselective TLY agar (tryptic soy broth containing lactose, yeast extract, and agar) and two selective media, TLYD agar (TLY agar plus sodium deoxycholate) and CIN agar (cefsulodin-Irgasan-novobiocin agar). Both copper and chlorine caused injury which was manifested by the inability of the cells to grow on selective media. CIN agar was more restrictive to the growth of injured cells than TLYD agar. Injury of the exposed cells was further enhanced in the gastric environment of mice. Besides injury, the low gastric pH caused extensive loss of viability in copper-exposed cells. Lethality in the chlorine-exposed cells was less extensive, and a portion of the inoculum (5.2 X 10(5) of 1 X 10(7) inoculated cells) reached the small intestine 5 min postinoculation. No adverse effect on the injured cells was apparent in the small intestine, and a substantial revival (approximately 70%) of the injury occurred in 3 to 4 h after intraluminal inoculation. The virulence of chlorine-stressed Y. enterocolitica in orally inoculated mice was similar to that of the control culture, but copper-stressed cells showed reduced virulence. Virulence was partly restored by oral administration of sodium bicarbonate before the inoculation of copper-exposed cells. Neutralization of gastric acidity had no effect on the virulence of the control or chlorine-stressed cells. The results of this study indicate that the extensive injury caused by the low gastric pH does not affect the virulence potential of chlorine-exposed cells. However, extensive cell death in the mouse stomach is responsible for the reduced virulence of the copper-stressed bacteria.
机译:在小鼠中,测定了暴露于亚致死浓度的铜和氯后,胃pH对小肠结肠炎耶尔森菌O:8活力和毒力的影响。用非选择性TLY琼脂(含有乳糖,酵母提取物和琼脂的胰蛋白酶大豆肉汤)和两种选择性培养基TLYD琼脂(TLY琼脂加脱氧胆酸钠)和CIN琼脂(头孢磺啶-Irgasan-novobiocin琼脂)评估生存力和损伤。铜和氯均引起损伤,这表现为细胞无法在选择性培养基上生长。与TLYD琼脂相比,CIN琼脂对受损细胞的生长更具限制性。在小鼠的胃环境中,暴露细胞的损伤进一步增强。除损伤外,低的胃液pH导致暴露于铜的细胞大量丧失活力。暴露于氯的细胞中的致死性较差,接种后5分钟,一部分接种物(5.2 X 10(5)的1 X 10(7)接种的细胞)到达小肠。在小肠中对损伤的细胞没有明显的不良影响,并且在腔内接种后3到4小时内,损伤的恢复了实质性的恢复(大约70%)。在口服接种的小鼠中,氯胁迫的小肠结肠炎耶尔森氏菌的毒力与对照培养物相似,但铜胁迫的细胞显示出降低的毒力。在接种铜暴露的细胞之前,通过口服碳酸氢钠可部分恢复毒力。胃酸的中和对对照或氯胁迫细胞的毒性没有影响。这项研究的结果表明,低胃pH引起的广泛损伤并不影响暴露于氯的细胞的潜在毒性。但是,小鼠胃中大量的细胞死亡是造成铜胁迫细菌毒力降低的原因。

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