Dean-Nystrom Evelyn A, Melton-Celsa Angela R, Pohlenz Joachim F L, Moon Harley W, O'Brien Alison D
Pre-Harvest Food Safety and Enteric Research Unit, National Animal Disease Center, USDA Agricultural Research Service, Ames, Iowa 50010-0070, USA.
Infect Immun. 2003 Nov;71(11):6526-33. doi: 10.1128/IAI.71.11.6526-6533.2003.
We compared the pathogenicity of intimin-negative non-O157:H7 Shiga toxin (Stx)-producing Escherichia coli (STEC) O91:H21 and O104:H21 strains with the pathogenicity of intimin-positive O157:H7 and O157:H(-) strains in neonatal pigs. We also examined the role of Stx2d-activatable genes and the large hemolysin-encoding plasmid of O91:H21 strain B2F1 in the pathogenesis of STEC disease in pigs. We found that all E. coli strains that made wild-type levels of Stx caused systemic illness and histological lesions in the brain and intestinal crypts, whereas none of the control Stx-negative E. coli strains evoked comparable central nervous system signs or intestinal lesions. By contrast, the absence of intimin, hemolysin, or motility had little impact on the overall pathogenesis of systemic disease during STEC infection. The most striking differences between pigs inoculated with non-O157 STEC strains and pigs inoculated with O157 STEC strains were the absence of attaching and effacing intestinal lesions in pigs inoculated with non-O157:H7 strains and the apparent association between the level of Stx2d-activatable toxin produced by an STEC strain and the severity of lesions.
我们比较了产志贺毒素(Stx)的无紧密素的非O157:H7大肠杆菌(STEC)O91:H21和O104:H21菌株与产志贺毒素的有紧密素的O157:H7和O157:H(-)菌株对新生仔猪的致病性。我们还研究了Stx2d可激活基因和O91:H21菌株B2F1的大溶血素编码质粒在猪STEC病发病机制中的作用。我们发现,所有产生野生型水平Stx的大肠杆菌菌株都会引发全身疾病以及大脑和肠道隐窝的组织学损伤,而对照的Stx阴性大肠杆菌菌株均未引发类似的中枢神经系统症状或肠道损伤。相比之下,紧密素、溶血素或运动性的缺失对STEC感染期间全身疾病的总体发病机制影响不大。接种非O157 STEC菌株的猪与接种O157 STEC菌株的猪之间最显著的差异在于,接种非O157:H7菌株的猪没有肠道黏附与脱落性损伤,以及STEC菌株产生的Stx2d可激活毒素水平与损伤严重程度之间存在明显关联。