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莱利斯塔德病毒在实验性诱发的神秘猪病(同义词:猪流行性流产和呼吸综合征(PEARS))感染中引起的病理、超微结构和免疫组织化学变化。

Pathological, ultrastructural, and immunohistochemical changes caused by Lelystad virus in experimentally induced infections of mystery swine disease (synonym: porcine epidemic abortion and respiratory syndrome (PEARS)).

作者信息

Pol J M, van Dijk J E, Wensvoort G, Terpstra C

机构信息

Central Veterinary Institute, Virology Department, Lelystad, The Netherlands.

出版信息

Vet Q. 1991 Jul;13(3):137-43. doi: 10.1080/01652176.1991.9694298.

DOI:10.1080/01652176.1991.9694298
PMID:1949540
Abstract

The pathogenicity and pathogenesis of Lelystad virus was studied in six 6-day-old SPF piglets. A third passage of the agent was propagated on porcine alveolar macrophages and intranasally inoculated into pigs. Pigs were killed at hours 24, 48, 60, and 72, and on days 6 and 8 after inoculation. From day 2 on pigs developed diffuse interstitial pneumonia with focal areas of catarrhal pneumonia, and from this day on splenic red pulp macrophages were enlarged and vacuolated. Lelystad virus was re-isolated from the lungs of infected pigs from day 2 after inoculation. Lelystad virus antigens were detected by immunohistochemical techniques in bronchiolar epithelium and alveolar cells, and in spleen cells of infected pigs from day 2 after inoculation. Ultrastructural examination of tissues by electron microscopy revealed degenerating alveolar macrophages and epithelial cells in lungs and nasal mucosa, with excessive vacuolation of the endoplasmic reticulum. Although the respiratory tract seems to be the target organ for this virus, macrophages in other organs, such as the spleen, can also be infected. This preference for macrophages may impair immunological defences.

摘要

在6只6日龄的无特定病原体(SPF)仔猪中研究了莱利斯塔德病毒的致病性和发病机制。该病原体的第三代培养物在猪肺泡巨噬细胞上增殖,并经鼻接种到猪体内。在接种后24小时、48小时、60小时和72小时以及第6天和第8天对猪实施安乐死。从第2天起,猪出现弥漫性间质性肺炎,并伴有局灶性卡他性肺炎区域,从这天起,脾红髓巨噬细胞肿大且出现空泡化。从接种后第2天起,可从感染猪的肺中重新分离出莱利斯塔德病毒。通过免疫组织化学技术在接种后第2天起的感染猪的细支气管上皮细胞、肺泡细胞以及脾细胞中检测到莱利斯塔德病毒抗原。通过电子显微镜对组织进行超微结构检查发现,肺和鼻黏膜中的肺泡巨噬细胞和上皮细胞发生变性,内质网出现过度空泡化。尽管呼吸道似乎是这种病毒的靶器官,但其他器官(如脾脏)中的巨噬细胞也会被感染。这种对巨噬细胞的偏好可能会损害免疫防御功能。

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