Wells G A, Hawkins S A, Green R B, Austin A R, Dexter I, Spencer Y I, Chaplin M J, Stack M J, Dawson M
Veterinary Laboratories Agency, Central Veterinary Laboratory, New Haw, Addlestone, Surrey.
Vet Rec. 1998 Jan 31;142(5):103-6. doi: 10.1136/vr.142.5.103.
Further preliminary observations are reported of an experiment to examine the spread of infectivity and the occurrence of pathological changes in cattle exposed orally to infection with bovine spongiform encephalopathy. Calves were dosed at four months of age and clinically monitored groups were killed sequentially from two to 40 months after inoculation. Tissues were collected for bioassay, for histopathological examinations and for the detection of PrP. Previous reported observations have included the presence of infectivity in the distal ileum of cattle killed after six to 18 months, the earliest onset of clinical signs in an exposed animal after 35 months, and diagnostic histopathological changes in the brain, in association with clinical disease, after 36, 38 and 40 months. In spite of the relative inefficiency of the bioassay of scrapie-like agents across a species barrier the new observations confirm that the onset of clinical signs and pathological changes in the central nervous system (CNS) occur at approximately the same time. The earliest pathological change, the presence of abnormal PrP 32 months after inoculation, coincided with the earliest detected infectivity in the CNS and occurred shortly before there was evidence of typical spongiform changes in the brain 36 months after inoculation. Infectivity has now been demonstrated in the peripheral nervous system, in the cervical and thoracic dorsal root ganglia 32 to 40 months after inoculation and in the trigeminal ganglion 36 and 38 months after inoculation. At the time of writing evidence of infectivity in other tissues is confined to the distal ileum, not only after six to 18 months but also after 38 and 40 months, but these findings may be supplemented by the results of further mouse assays. Nevertheless, they are in general agreement with current knowledge of the pathogenesis of scrapie.
本文报告了一项进一步的初步观察结果，该实验旨在研究经口感染牛海绵状脑病的牛的传染性传播情况以及病理变化的发生情况。犊牛在4月龄时接种病毒，接种后2至40个月，对临床监测组的犊牛依次进行宰杀。收集组织用于生物测定、组织病理学检查以及检测朊蛋白（PrP）。先前报告的观察结果包括：接种后6至18个月宰杀的牛的回肠末端存在传染性；暴露动物在35个月后最早出现临床症状；接种后36、38和40个月，与临床疾病相关的脑部出现诊断性组织病理学变化。尽管跨物种屏障对类瘙痒病病原体进行生物测定的效率相对较低，但新的观察结果证实，中枢神经系统（CNS）临床症状和病理变化的出现时间大致相同。最早的病理变化是接种后32个月出现异常PrP，这与CNS中最早检测到的传染性同时出现，且在接种后36个月大脑出现典型海绵状变化的证据之前不久发生。现已证明，接种后32至40个月，在外周神经系统的颈和胸背根神经节以及接种后36和38个月的三叉神经节中存在传染性。在撰写本文时，其他组织中存在传染性的证据仅限于回肠末端，不仅在接种后6至18个月，而且在接种后38和40个月也有发现，但这些发现可能会因进一步的小鼠试验结果而得到补充。尽管如此，它们总体上与目前关于瘙痒病发病机制的认识一致。
