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Pathogenic potential and virulence genotypes of intestinal and faecal isolates of porcine post-weaning enteropathogenic Escherichia coli

机译:猪断奶后肠致病性大肠杆菌肠道和粪便分离株的致病潜力和毒力基因型

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摘要

Enteropathogenic Escherichia coli (EPEC) are frequent causes of diarrhoea in infants and in young mammals by inducing attaching effacing (AE) lesions of the intestinal epithelium. EPEC bacteria have also been implicated in cases of porcine post-weaning diarrhoea but their pathogenicity for conventional weaned pigs remains less elucidated. This present study investigates differences in pathogenic potential and virulence genotypes of intestinal and faecal isolates of EPEC from newly-weaned pigs. For this we inoculated ligated ileal loops of four weeks old weaned pigs to assess EPEC adherence to enterocytes by histology and immunohistology. Virulence gene patterns were identified by using a PCR-microarray. Intestinal EPEC isolates of sero −/intimin types O45:H11:eae-β, O49:NM:eae-β, O84:H7:eae-γ, and O123:H11:eae-β formed adherent microcolonies of EPEC with AE lesions on ileal villi more frequently than faecal isolates of O28:H28:eae-NT, O108:H9:eae-β, O145:H28:eae-γ and O157:H2:eae-β (p ≤ 0.05). The PCR-array analysis of both groups detected all together 25 virulence genes of LEE (Locus of Enterocyte Effacement), and of non-LEE pathogenicity islands, of plasmids and phages characteristic to EPEC. Intestinal isolates carried significantly more virulence genes than faecal isolates (p ≤ 0.05). Intestinal isolates possessed efa1, lpfA, and tsh genes most likely contributing to enterocyte adhesion while faecal isolates did not carry these genes (p ≤ 0.05). Overall, the ileal loop model in weaned pigs combined with virulence genotyping PCR-array indicated a greater pathogenic potential of intestinal isolates over faecal isolates of porcine post-weaning EPEC. Differing virulence genotypes of the intestinal and faecal isolates as demonstrated here suggests dynamic evolutionary events within the population of porcine EPEC. © 2017 Elsevier Ltd
机译:肠致病性大肠杆菌(EPEC)通过诱导肠上皮的附着性表皮(AE)损伤,是婴儿和幼年哺乳动物腹泻的常见原因。 EPEC细菌也与猪断奶后腹泻有关,但对常规断奶猪的致病性尚不清楚。本研究调查了来自断奶仔猪的EPEC肠道和粪便分离株的致病潜能和毒力基因型的差异。为此,我们接种了四周龄断奶猪的回肠结扎环,以通过组织学和免疫组织学评估EPEC对肠上皮细胞的依从性。通过使用PCR-微阵列鉴定毒力基因模式。 O45:H11:eae-β,O49:NM:eae-β,O84:H7:eae-γ和O123:H11:eae-β血清/内膜蛋白类型的肠道EPEC分离株形成了带有AE病变的EPEC粘附微菌落回肠绒毛比O28:H28:eae-NT,O108:H9:eae-β,O145:H28:eae-γ和O157:H2:eae-β的粪便分离株更频繁(p≤0.05)。两组的PCR阵列分析共检测到LEE(肠上皮细胞形成部位)和非LEE致病岛的25个毒力基因,EPEC特有的质粒和噬菌体。肠道分离株比粪便分离株携带更多的毒力基因(p≤0.05)。肠道分离株具有efa1,lpfA和tsh基因,最有可能导致肠细胞粘附,而粪便分离株不携带这些基因(p≤0.05)。总体而言,断奶仔猪回肠loop回模型与毒力基因分型PCR阵列相结合表明,肠道分离株的致病潜力要高于猪断奶后EPEC的粪便分离株。如本文所示,肠道和粪便分离株的毒力基因型不同,表明在猪EPEC群体中存在动态进化事件。 ©2017爱思唯尔有限公司

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