产毒性大肠杆菌对豚鼠致病性的实验研究

EXPERIMENT STUDY ON THE PATHOGENICITY OF ENTROTOXIGENIC ESCHERICHIA COLI IN GUINEA PIG

目的 试图通过产毒性大肠杆菌 (ETEC)对豚鼠致病性的实验研究 ,进一步探讨该菌的致病机理。方法 利用人源性ETEC菌株E44 813、E44 815、E44 82 2和E44 82 3攻击豚鼠 ,造成豚鼠ETEC感染模型 ,观察豚鼠ETEC感染的病变特点。结果 4株ETEC菌株均能造成豚鼠发病 ,以E44 813致病性最大。ETEC能定植于豚鼠肠道至少达 14天。发病豚鼠肠道明显充血、肿胀 ,以回肠为最严重。感染组无发病症状的豚鼠也有 5 /12出现空肠和回肠轻度肿胀。光镜下发病动物肠粘膜组织结构大致完整 ,但有较明显的病理改变 ,特别是空肠和回肠 ,主要表现为水肿、淋巴细胞浸润和充血 ,病变部位可见于空肠和回肠肠组织各层。病变程度与症状严重程度相关 ,感染组 9/12无症状豚鼠也有显微病理改变 ,但较轻。超微结构观察显示发病动物空肠和回肠上皮细胞部分变性 ,细胞内未见细菌入侵。结论 ETEC不仅影响小肠上皮细胞的分泌和吸收功能 。

Aim\ To study the mechanisms of pathogenicity of diarrheal disease due to enterotoxigenic Escherichia coli(ETEC),guinea pig model was used for this purpose. Method\ Experimental strains of ETEC were E44813(LT\++STh\++STp\++CFAI\++)、E44814(LT\++STh\++ CFAII\++)、E44822(LT\++)and E44823(STh\++),originally isolated from stools of patients with diarrhea. After oral inoculating with the bacteria ,the morbidity, clinical symptoms, bacterial colonization and pathogenic changes of experimental animals were examined. Result\ Four strains of ETEC could caused diarrheal disease of guinea pigs. Bacteria became colonized with challenge organisms within 24h of inoculation and continuing at least for 14 days. The small intestines of infected guinea pigs were hydrops and hyperemia. Histological changes were mainly seen in jejunum and ileum. The changes mainly were edema, lymphocytes infiltration and hyperemia. Histological changes correlated with clinical symptoms, the animals with asymptoms infection lesions were less . The positions of histological changes were seen in mucous membrane, mucosal muscularis, submucosa, lamina muscularis and fibrosa. Observing by TEM, ileal epithelium cells showed denaturation partly. No obvious invasion of the bacteria was found. Conclusion\ The study suggests that ETEC not only disturbs the functions of absorption and secretion of intestinal epithelial cells, but induces extensive and obvious inflammation with frequent edemas and denaturation of cells in the small intestine.