Singh A, McFeters G A
Department of Microbiology, Montana State University, Bozeman 59717.
Appl Environ Microbiol. 1987 Aug;53(8):1768-74. doi: 10.1128/aem.53.8.1768-1774.1987.
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.
在小鼠体内测定了胃内pH值对肠炎耶尔森菌O:8在接触亚致死浓度的铜和氯后活力及毒力的影响。用非选择性TLY琼脂（含乳糖、酵母提取物和琼脂的胰蛋白胨大豆肉汤）以及两种选择性培养基TLYD琼脂（TLY琼脂加脱氧胆酸钠）和CIN琼脂（头孢磺啶-伊红-新生霉素琼脂）评估活力和损伤情况。铜和氯均造成损伤，表现为细胞无法在选择性培养基上生长。CIN琼脂比TLYD琼脂对受损细胞的生长限制更大。在小鼠胃环境中，暴露细胞的损伤进一步加剧。除损伤外，低胃内pH值导致铜暴露细胞活力大量丧失。氯暴露细胞的致死率较低，接种后5分钟有一部分接种物（接种的1×10⁷个细胞中的5.2×10⁵个）到达小肠。在小肠中未观察到对受损细胞有明显不利影响，腔内接种后3至4小时损伤有显著恢复（约70%）。口服接种小鼠后，氯胁迫的肠炎耶尔森菌毒力与对照培养物相似，但铜胁迫的细胞毒力降低。在接种铜暴露细胞前口服碳酸氢钠可部分恢复毒力。中和胃酸对对照或氯胁迫细胞的毒力无影响。本研究结果表明，低胃内pH值造成的广泛损伤不影响氯暴露细胞的毒力潜能。然而，小鼠胃内大量细胞死亡导致铜胁迫细菌毒力降低。
