Knoop F C
Infect Immun. 1979 Dec;26(3):1196-201. doi: 10.1128/iai.26.3.1196-1201.1979.
An in vivo animal model was used to assess the enteropathogenicity of the etiological agent (Treponema hyodysenteriae) of swine dysentery. Multiple ligated ileal loops, prepared in New Zealand white rabbits, were challenged with either pathogenic (B78 and B204) or nonpathogenic (Pu) isolates of the organism. The pathogenic isolates induced the onset of intestinal fluid accumulation as early as 4 h, with maximal fluid induction at 18 h postchallenge. Gross lesions of the intestinal mucosa, observed in ileal loops of rabbits sacrificed 24 h postchallenge, were characteristic of swine dysentery. Both pathogenic isolates colonized the epithelial surface and eroded the mucosal barrier, as determined by histological and scanning electron microscopic observations. Intestinal fluid accumulation and erosion of the mucosal barrier were not observed in ileal loops exposed to the nonpathogenic isolate (Pu) or to either of the nonviable pathogenic (B78 and B204) isolates. The ability of pathogenic isolates to initiate and produce infection in rabbit ligated ileal loops, which closely resembles the disease in swine, provides a system with which to study experimental swine dysentery.
采用体内动物模型评估猪痢疾病原体（猪痢疾短螺旋体）的肠道致病性。在新西兰白兔中制备多个结扎回肠袢，用该生物体的致病菌株（B78和B204）或非致病菌株（Pu）进行攻击。致病菌株早在4小时就引发肠液积聚，攻击后18小时肠液诱导量最大。在攻击后24小时处死的兔子回肠袢中观察到的肠黏膜大体病变是猪痢疾的特征。组织学和扫描电子显微镜观察表明，两种致病菌株均定殖于上皮表面并侵蚀黏膜屏障。在暴露于非致病菌株（Pu）或任何一种无活力致病菌株（B78和B204）的回肠袢中未观察到肠液积聚和黏膜屏障侵蚀。致病菌株在兔结扎回肠袢中引发并产生感染的能力与猪的疾病非常相似，提供了一个研究实验性猪痢疾的系统。
