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首页> 外文期刊>Infection and immunity >Epsilon Toxin Is Essential for the Virulence of Clostridium perfringens Type D Infection in Sheep, Goats, and Mice
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Epsilon Toxin Is Essential for the Virulence of Clostridium perfringens Type D Infection in Sheep, Goats, and Mice

机译：Epsilon毒素对于绵羊，山羊和小鼠的产气荚膜梭状芽孢杆菌D型感染的毒力至关重要

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Clostridium perfringens type D causes disease in sheep, goats, and other ruminants. Type D isolates produce, at minimum, alpha and epsilon (ETX) toxins, but some express up to five different toxins, raising questions about which toxins are necessary for the virulence of these bacteria. We evaluated the contribution of ETX to C. perfringens type D pathogenicity in an intraduodenal challenge model in sheep, goats, and mice using a virulent C. perfringens type D wild-type strain (WT), an isogenic ETX null mutant (etx mutant), and a strain where the etx mutation has been reversed (etx complemented). All sheep and goats, and most mice, challenged with the WT isolate developed acute clinical disease followed by death in most cases. Sheep developed various gross and/or histological changes that included edema of brain, lungs, and heart as well as hydropericardium. Goats developed various effects, including necrotizing colitis, pulmonary edema, and hydropericardium. No significant gross or histological abnormalities were observed in any mice infected with the WT strain. All sheep, goats, and mice challenged with the isogenic etx mutant remained clinically healthy for ≥24 h, and no gross or histological abnormalities were observed in those animals. Complementation of etx knockout restored virulence; most goats, sheep, and mice receiving this complemented mutant developed clinical and pathological changes similar to those observed in WT-infected animals. These results indicate that ETX is necessary for type D isolates to induce disease, supporting a key role for this toxin in type D disease pathogenesis.
机译：D型产气荚膜梭菌会在绵羊，山羊和其他反刍动物中引起疾病​​。 D型分离株至少产生α和ε（ETX）毒素，但有些分离株最多表达五种不同的毒素，这引发了关于哪些毒素对于这些细菌的毒性必需的问题。我们在绵羊，山羊和小鼠的十二指肠内挑战模型中评估了ETX对产气荚膜梭菌D型致病性的贡献，使用了强毒的产气荚膜梭菌D型野生型菌株（WT），等基因的ETX无效突变体（etx突变体） ，以及etx突变已被逆转（etx互补）的菌株。用WT分离物攻击的所有绵羊和山羊，以及大多数小鼠都发展为急性临床疾病，随后在大多数情况下死亡。绵羊发生了各种总体和/​​或组织学变化，包括脑，肺和心脏以及水囊心包的水肿。山羊表现出各种作用，包括坏死性结肠炎，肺水肿和心包积水。在感染WT株的任何小鼠中均未观察到明显的总体或组织学异常。用等基因etx突变体攻击的所有绵羊，山羊和小鼠在临床上均保持健康≥24 h，并且在这些动物中未观察到总体或组织学异常。补充基因敲除恢复毒力;接受这种互补突变体的大多数山羊，绵羊和小鼠的临床和病理变化与在WT感染的动物中观察到的相似。这些结果表明，ETX对于D型分离物诱导疾病是必需的，支持该毒素在D型疾病发病机理中的关键作用。

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