在胚胎早期进行低温曝晒以提高雏鸡对传染病的抵抗力

E. Fedorova, O. Stanishevskaya
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引用次数: 0

摘要

文章主要探讨了通过技术方法提高雏鸡从孵化到 3 周龄对传染病的抵抗力问题。在胚胎早期形成的敏感期,提出了对胚胎进行定量低温暴露的影响因素;使用流感疫苗病毒作为试验病毒,对胚胎进行实验性感染。结果发现,与对照组相比,冷却后胚胎中的病毒滴度明显降低了 1.5-12.0 倍(p<0.001)。这表明病毒株在该组胚胎中的复制活性下降。俄罗斯雪白鸡种的鸡胚冷却后,甲型流感病毒的感染活性降低了 11.5%,传染性支气管炎病毒的感染活性降低了 3.6-6.9%,具体取决于鸡胚的品种。实验组雏鸡对细菌性疾病的抵抗力也更强,3 周龄雏鸡的安全性更高(比对照组高 0.8-1.1%),12 日龄雏鸡的法氏囊指数更高(比对照组高 8.5-9.0%)。实验组鸡蛋的孵化率也比对照组高 4.5%。在胚胎发育的这一敏感时期,低温暴露所产生的影响可解释为诱导胚胎产生热休克蛋白和冷休克蛋白,进而激活由主要组织相容性复合体引起的先天性抗病毒反应。不过,这个问题还需要通过分子遗传学方法进行进一步研究,因为导致胚胎早期低温暴露时抵抗力增强的假定机制还有待证实。
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Low-temperature exposure in early embryogenesis as a way of increasing the resistance of chicks to infectious diseases
The article is devoted to the problem of increasing the resistance of chicks from hatching to the age of 3 weeks to infectious diseases by technological methods. Dosed low-temperature exposure to the embryo during the sensitive period of early embryogenesis was proposed as an impact factor; influenza vaccine virus was used as a test virus for experimental infection of embryos. It was found that in the embryos after cooling, the titer of the virus was significantly lower by 1.5-12.0 times (p<0.001) compared with the control. This fact indicates a decrease in the replicative activity of viral strains in embryos of this group. In chicken embryos of Russian Snow-White breed after cooling, there was a decrease in the infectious activity of the influenza A virus by 11.5 %, as well as a decrease in the infectious activity of the infectious bronchitis virus by 3.6-6.9 %, depending on the breed of the embryos. The level of chick resistance in the experimental group to diseases of bacterial etiology was also higher, as evidenced by the higher safety of 3-week-old chicks (0.8-1.1 % higher than in the control) and a higher bursa index in 12-day-old chicks (8.5-9.0 % higher than in the control). The hatchability of eggs of the experimental group was also 4.5 % higher than in the control. The effects obtained as a result of hypothermic exposure during this sensitive period of embryogenesis can be explained by inducing the production of heat and cold shock proteins by the embryo, which, in turn, activate innate antiviral reactions caused by major histocompatibility complex. However, this issue requires additional study with the involvement of molecular genetics methods, since the supposed mechanisms that cause an increase in resistance in response to low-temperature exposure in early ontogenesis need to be confirmed.
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