Experimental transmission of chronic wasting disease (CWD) of elk (Cervus elaphus nelsoni), white-tailed deer (Odocoileus virginianus), and mule deer (Odocoileus hemionus hemionus) to white-tailed deer by intracerebral route
Experimental transmission of chronic wasting disease (CWD) of elk (Cervus elaphus nelsoni), white-tailed deer (Odocoileus virginianus), and mule deer (Odocoileus hemionus hemionus) to white-tailed deer by intracerebral route
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DOI：
10.1354/vp.45-3-297
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发表时间：
2008-05-01
影响因子：
2.4
通讯作者：
Williams, E. S.
中科院分区：
文献类型：
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作者：
Hamir, A. N.;Richt, J. A.;Williams, E. S.
为了比较慢性消耗病（CWD）在自然宿主中的临床和病理学发现，3组（n = 5）白尾鹿（WTD）幼仔脑内接种WTD，骡鹿，或麋鹿来源的CWD朊病毒。另外三只未接种的幼仔作为对照。接种后约10个月（MPI），对3个接种组中的各1只鹿进行尸检，并通过免疫组织化学（IHC）和蛋白质印迹（WB）检查其组织中是否存在海绵状脑病（SE）病变和异常朊病毒蛋白（Prp（d））。其余的鹿被允许存活，直到它们出现大约18 MPI开始的疾病临床体征。到26 MPI，所有鹿都被人道地安乐死。3组动物的临床症状和潜伏期无明显差异。在10 MPI处以安乐死的1/3只非临床鹿中，在中枢神经系统（CNS）组织中观察到极轻微的SE显微镜病变，并通过IHC在所有3只鹿的组织中观察到Prpd。在临床鹿中，SE和Prpd蓄积的CNS病变更严重和广泛。可以得出结论，慢性消耗病朊病毒的3个来源并没有引起临床疾病的时间或WTD的体征或病变的定性差异的显着差异。然而，这一观察结果并不意味着这些CWD代理人一定会表现出类似的其他受体物种。
To compare clinical and pathologic findings of chronic wasting disease (CWD) in a natural host, 3 groups (n = 5) of white-tailed deer (WTD) fawns were intracerebrally inoculated with a CWD prion of WTD, mule deer, or elk origin. Three other uninoculated fawns served as controls. Approximately 10 months postinoculation (MPI), 1 deer from each of the 3 inoculated groups was necropsied and their tissues were examined for lesions of spongiform encephalopathy (SE) and for the presence of abnormal prion protein (Prp(d)) by immunohistochemistry (IHC) and Western blot (WB). The remaining deer were allowed to live until they developed clinical signs of the disease which began approximately 18 MPI. By 26 MPI, all deer were euthanatized on humane grounds. Obvious differences in clinical signs or the incubation periods were not observed between the 3 groups of deer given CWD. In 1 of 3 nonclinical deer euthanatized at 10 MPI, minimal microscopic lesions of SE were seen in the central nervous system (CNS) tissues, and Prpd was observed by IHC in tissues of all 3 deer. In the clinical deer, CNS lesions of SE and Prpd accumulations were more severe and extensive. It is concluded that the 3 sources of CWD prion did not induce significant differences in time to clinical disease or qualitative differences in signs or lesions in WTD. However, this observation does not imply that these CWD agents would necessarily behave similarly in other recipient species.