首页> 美国卫生研究院文献>Toxins >Aflatoxin Fumonisin and Shiga Toxin-Producing Escherichia coli Infections in Calves and the Effectiveness of Celmanax®/Dairyman’s Choice™ Applications to Eliminate Morbidity and Mortality Losses
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Aflatoxin Fumonisin and Shiga Toxin-Producing Escherichia coli Infections in Calves and the Effectiveness of Celmanax®/Dairyman’s Choice™ Applications to Eliminate Morbidity and Mortality Losses

机译:小牛中产生黄曲霉毒素伏马菌素和志贺毒素的大肠杆菌感染以及Celmanax®/ Dairymans Choice™应用消除病死率和死亡率损失的有效性

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摘要

Mycotoxin mixtures are associated with Shiga toxin-producing Escherichia coli (STEC) infections in mature cattle. STEC are considered commensal bacteria in mature cattle suggesting that mycotoxins provide a mechanism that converts this bacterium to an opportunistic pathogen. In this study, we assessed the mycotoxin content of hemorrhaged mucosa in dairy calves during natural disease outbreaks, compared the virulence genes of the STECs, evaluated the effect of the mucosal mycotoxins on STEC toxin expression and evaluated a Celmanax®/Dairyman’s Choice™ application to alleviate disease. As for human infections, the OI-122 encoded nleB gene was common to STEC genotypes eliciting serious disease. Low levels of aflatoxin (1–3 ppb) and fumonisin (50–350 ppb) were detected in the hemorrhaged mucosa. Growth of the STECs with the mycotoxins altered the secreted protein concentration with a corresponding increase in cytotoxicity. Changes in intracellular calcium indicated that the mycotoxins increased enterotoxin and pore-forming toxin activity. A prebiotic/probiotic application eliminated the morbidity and mortality losses associated with the STEC infections. Our study demonstrates: the same STEC disease complex exists for immature and mature cattle; the significance of the OI-122 pathogenicity island to virulence; the significance of mycotoxins to STEC toxin activity; and, finally, provides further evidence that prebiotic/probiotic applications alleviate STEC shedding and mycotoxin/STEC interactions that lead to disease.
机译:霉菌毒素混合物与成熟牛中产生志贺毒素的大肠杆菌(STEC)感染有关。 STEC被认为是成熟牛的共生细菌,这表明霉菌毒素提供了将这种细菌转化为机会病原体的机制。在这项研究中,我们评估了自然疾病暴发期间奶牛犊中出血黏膜的霉菌毒素含量,比较了STEC的毒力基因,评估了黏膜真菌毒素对STEC毒素表达的影响,并评估了Celmanax ® / Dairyman's Choice™应用减轻疾病。至于人类感染,OI-122编码的nleB基因在引起严重疾病的STEC基因型中很常见。在出血的粘膜中检测到低水平的黄曲霉毒素(1-3 ppb)和伏马毒素(50-350 ppb)。带有霉菌毒素的STEC的生长改变了分泌蛋白的浓度,并相应地增加了细胞毒性。细胞内钙的变化表明真菌毒素增加了肠毒素和成孔毒素的活性。益生元/益生菌的应用消除了与STEC感染相关的发病率和死亡率损失。我们的研究表明:未成熟和成熟的牛存在相同的STEC疾病复合体; OI-122致病岛对毒力的重要性;霉菌毒素对STEC毒素活性的意义;最后,它提供了进一步的证据,表明益生元/益生菌的应用减轻了STEC脱落以及导致疾病的真菌毒素/ STEC相互作用。

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