Chousalkar K K, Roberts J R
Animal Science, School of Rural Science and Agriculture, University of New England, Armidale, New South Wales, Australia.
Vet Microbiol. 2007 Jun 21;122(3-4):223-36. doi: 10.1016/j.vetmic.2007.01.021. Epub 2007 Feb 2.
The infundibulum and magnum of the oviduct were examined in hens in full lay which were infected with two Australian strains of infectious bronchitis virus (IBV). The ultramicroscopic changes in the infundibulum and magnum were compared with control hens which had eggs at different positions in the oviduct. The ciliated and granular cells of the surface epithelia and secretory epithelial cells of the tubular glands were the target cells of IBV. No pathological changes were recorded during 2-8 days post-infection (p.i.). Patchy loss of cilia occurred at 10-14 days p.i. Between 16 and 24 days p.i., there was no cilia loss and lymphoid nodules were observed in the muscularis layer of the infundibulum and magnum of some hens from both infected groups. Virus particles were detected mostly in the rough endoplasmic reticulum (RER) and Golgi complex between 10 and 12 days p.i. Cytopathology was noticed in various cell organelles between the 10th and 14th days p.i. There was an increase in RER deposits in infected cells, irrespective of egg position in the oviduct. The magnum was more affected than the infundibulum. Cellular changes were more severe in the infundibulum and magnum of T-infected hens as compared to N1/88-infected hens. Eggs with watery whites which were laid by infected hens could be attributed to cytopathological changes in the granular epithelial cells and tubular gland epithelial cells of the magnum resulting in reduced synthesis of albumen proteins. IBV can cause pathology in parts of the fully functional oviduct which may persist up to the 30th day p.i. However, both the challenge strains of IBV can cause a small number of hens to cease production. Loss of cilia in both the infundibulum and magnum pose a potential threat of secondary bacterial infection and also may affect fertility in breeder hens.
对处于产蛋高峰期、感染了两种澳大利亚传染性支气管炎病毒(IBV)毒株的母鸡的输卵管漏斗部和膨大部进行了检查。将漏斗部和膨大部的超微结构变化与输卵管中处于不同位置有蛋的对照母鸡进行了比较。表面上皮的纤毛细胞和颗粒细胞以及管状腺的分泌上皮细胞是IBV的靶细胞。感染后2至8天未记录到病理变化。感染后10至14天出现纤毛局部脱落。感染后16至24天,两个感染组的一些母鸡的漏斗部和膨大部肌层未出现纤毛脱落,但观察到淋巴小结。感染后10至12天,病毒颗粒大多在粗面内质网(RER)和高尔基体中被检测到。感染后第10至14天,各种细胞器出现细胞病理学变化。无论输卵管中蛋的位置如何,感染细胞中的RER沉积物均增加。膨大部比漏斗部受影响更大。与N1/88感染的母鸡相比,T感染的母鸡的漏斗部和膨大部的细胞变化更严重。感染母鸡所产蛋白稀薄的蛋可归因于膨大部颗粒上皮细胞和管状腺上皮细胞的细胞病理学变化,导致蛋清蛋白合成减少。IBV可在功能完全正常的输卵管部分引起病变,这种病变可能持续到感染后第30天。然而,两种IBV攻击毒株均可导致少数母鸡停止产蛋。漏斗部和膨大部的纤毛脱落对继发细菌感染构成潜在威胁,也可能影响种母鸡的繁殖力。