Mainil J
Faculté de médecine vétérinaire, université de Liège, Belgium.
Vet Res. 1999 Mar-Jun;30(2-3):235-57.
Vero/Shiga toxins (VT/Stx) have an A-B structure: the A subunit carries the enzymatic activity and the B subunit binds the toxin to the membrane receptor (Gb3 or Gb4). The VT/Stx inhibit protein synthesis in the target eucaryotic cells, mainly the endothelial cells of blood vessels. The VT/Stx are subdivided into two families. VT1/Stx1 is a homogeneous family of toxins identical to the Stx of Shigella dysenteriae. VT2/Stx2 is a more heterogeneous family of toxins more distantly related to this Stx toxin. The VT2/Stx2 variants can be distinguished by the polymerase chain reaction (PCR) and/or the reaction with monoclonal antibodies. The VT/Stx-producing Escherichia coli are also subdivided into two main groups on the basis of the presence or absence of additional properties: the enterohaemorrhagic E. coli (EHEC) induce the formation of attaching/effacing lesions and carry a 60 MD plasmid encoding a specific haemolysin (the enterohaemolysin); the vero/shiga-toxigenic E. coli (VTEC/STEC) do not show these properties. The EHEC are isolated from humans and ruminants, especially young calves. They are associated with haemorrhagic enterocolitis and its sequelae in humans, the haemolytic-uraemic syndrome (HUS). The VT/Stx play a role in the occurrence of blood in the faeces and in the HUS by their action on the endothelial cells of blood vessels in the intestinal submucosa and in the renal glomeruli, after resorption through the intestinal walls. The VTEC/STEC are isolated from piglets, calves and humans. In recently weaned piglets, they cause the oedema disease, an enterotoxaemia characterized by subcutaneous, mesenteric and cerebral oedemas, with nervous disorders as main clinical signs. The oedema disease is the consequence of the action of the VT/Stx on the endothelial cells of blood vessels in various organs. In calves and humans, the role in disease of VTEC/STEC is controversial, but they could be associated with some cases of diarrhoea and HUS. The case of the O157:H7 EHEC which are present in healthy cattle of various ages, but are highly virulent for humans is of special interest. The potential zoonotic aspect of VT/Stx-producing E. coli infections in animals is detailed chapter by chapter. Prophylaxis of these infections by vaccination is the subject of the discussion on the future of the research studies on these pathogenic bacteria.
志贺毒素(VT/Stx)具有A-B结构:A亚基具有酶活性,B亚基将毒素与膜受体(Gb3或Gb4)结合。VT/Stx抑制靶真核细胞中的蛋白质合成,主要是血管内皮细胞。VT/Stx分为两个家族。VT1/Stx1是与痢疾志贺菌的Stx相同的同质毒素家族。VT2/Stx2是与这种Stx毒素关系更远的异质毒素家族。VT2/Stx2变体可通过聚合酶链反应(PCR)和/或与单克隆抗体的反应来区分。产VT/Stx的大肠杆菌也根据是否存在其他特性分为两个主要组:肠出血性大肠杆菌(EHEC)诱导形成紧密黏附/抹平损伤,并携带一个编码特定溶血素(肠溶血素)的60 MD质粒;志贺毒素/产志贺毒素大肠杆菌(VTEC/STEC)不表现出这些特性。EHEC从人和反刍动物特别是小牛中分离得到。它们与人类的出血性小肠结肠炎及其后遗症溶血尿毒综合征(HUS)有关。VT/Stx通过作用于肠黏膜下层和肾小球血管的内皮细胞,在粪便带血和HUS的发生中起作用,这些毒素是通过肠壁吸收的。VTEC/STEC从仔猪、小牛和人中分离得到。在刚断奶的仔猪中,它们引起水肿病,这是一种以皮下、肠系膜和脑水肿为特征的肠毒素血症,主要临床症状为神经紊乱。水肿病是VT/Stx作用于各器官血管内皮细胞的结果。在小牛和人中,VTEC/STEC在疾病中的作用存在争议,但它们可能与一些腹泻和HUS病例有关。O157:H7 EHEC存在于不同年龄的健康牛中,但对人类具有高毒力,这一情况特别值得关注。动物中产VT/Stx大肠杆菌感染的潜在人畜共患病方面将逐章详细阐述。通过疫苗接种预防这些感染是关于这些病原菌研究未来的讨论主题。