Clostridium perfringens strains of various origin can cause hemorrhagic enteritis in a calf intestinal loop model

产气荚膜梭菌 肠炎 微生物学 发病机制 生物 毒素 固有层 细菌 免疫学 上皮 遗传学
作者
Bonnie Valgaeren,Evy Goossens,Stefanie Verherstraeten,Bart Pardon,Leen Timbermont,Stijn Schauvlieghe,Richard Ducatelle,Filip Van Immerseel,Piet Deprez
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摘要

Hemorrhagic enteritis is one of numerous pathologies caused by Clostridium perfringens in cattle. It is an acute syndrome with a case fatality rate close to 100%, that affects mainly suckling and veal calves in good to excellent body condition up to four months of age. In Belgian Blue cattle, losses due to hemorrhagic enteritis may be responsible for up to 20% of total mortality. The pathogenesis and the toxins involved in bovine hemorrhagic enteritis remain to be elucidated. Therefore an intestinal loop model was developed to test a collection of Clostridium perfringens strains for their ability to reproduce the pathology. Loops were injected with logarithmic C. perfringens cultures in combination or not with commercial milk replacer for veal calves. The tested set of strains consisted of bovine strains isolated from both hemorrhagic enteritis cases and healthy animals, as well as human, NetB positive and negative chicken and Beta toxin positive porcine isolates. Also a VirR, α and θ mutant were tested. All tested strains were capable of eliciting hemorrhagic enteritis in this experimental setup when inoculated together with commercial milk replacer. A time course experiment showed that the pathogenesis is characterized by early capillary congestion, followed by hemorrhages and necrosis of the lamina propria, originating from the tips of the villi. No edema was present. C. perfringens bacteria were often attached to cellular debris in the lumen. These observations indicate that any Clostridium perfringens strain, independent of the isolation source, may be capable of eliciting hemorrhagic enteritis, and that this syndrome is not caused by host-specific strains or toxins. In addition, the pathological process seems to be independent of α- or θ-toxin or VirR-regulated mechanisms.

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