Moore Jo, Hawkins Stephen Ac, Austin Anthony R, Konold Timm, Green Robert B, Blamire Ian W, Dexter Ian, Stack Michael J, Chaplin Melanie J, Langeveld Jan Pm, Simmons Marion M, Spencer Yvonne I, Webb Paul R, Dawson Michael, Wells Gerald Ah
Department of Pathology and Host Susceptibility, Animal Health and Veterinary Laboratories Agency, Woodham Lane, New Haw, Addlestone, Surrey KT15 3NB, UK.
BMC Res Notes. 2011 Nov 17;4:501. doi: 10.1186/1756-0500-4-501.
Transmission of the prion disease bovine spongiform encephalopathy (BSE) occurred accidentally to cattle and several other mammalian species via feed supplemented with meat and bone meal contaminated with infected bovine tissue. Prior to United Kingdom controls in 1996 on the feeding of mammalian meat and bone meal to farmed animals, the domestic chicken was potentially exposed to feed contaminated with the causal agent of BSE. Although confirmed prion diseases are unrecorded in avian species a study was undertaken to transmit BSE to the domestic chicken by parenteral and oral inoculations. Transmissibility was assessed by clinical monitoring, histopathological examinations, detection of a putative disease form of an avian prion protein (PrP) in recipient tissues and by mouse bioassay of tissues. Occurrence of a progressive neurological syndrome in the primary transmission study was investigated by sub-passage experiments.
No clinical, pathological or bioassay evidence of transmission of BSE to the chicken was obtained in the primary or sub-passage experiments. Survival data showed no significant differences between control and treatment groups. Neurological signs observed, not previously described in the domestic chicken, were not associated with significant pathology. The diagnostic techniques applied failed to detect a disease associated form of PrP.
Important from a risk assessment perspective, the present study has established that the domestic chicken does not develop a prion disease after large parenteral exposures to the BSE agent or after oral exposures equivalent to previous exposures via commercial diets. Future investigations into the potential susceptibility of avian species to mammalian prion diseases require species-specific immunochemical techniques and more refined experimental models.
朊病毒疾病牛海绵状脑病(BSE)通过添加了被感染牛组织污染的肉骨粉的饲料意外传播给了牛和其他几种哺乳动物。在1996年英国对向养殖动物投喂哺乳动物肉骨粉进行管控之前,家鸡有可能接触到被BSE病原体污染的饲料。尽管在禽类中尚未记录到确诊的朊病毒疾病,但仍开展了一项研究,通过肠胃外和口服接种将BSE传播给家鸡。通过临床监测、组织病理学检查、在受体组织中检测一种假定的禽类朊病毒蛋白(PrP)疾病形式以及对组织进行小鼠生物测定来评估传播性。通过传代实验研究了初次传播研究中是否出现进行性神经综合征。
在初次或传代实验中,均未获得BSE传播到家鸡的临床、病理或生物测定证据。生存数据显示对照组和处理组之间无显著差异。所观察到的家鸡中以前未描述过的神经症状与明显的病理学无关。所应用的诊断技术未能检测到与疾病相关的PrP形式。
从风险评估的角度来看,本研究确定,家鸡在通过肠胃外大量接触BSE病原体后或在口服相当于以前通过商业饲料接触量的病原体后,不会患上朊病毒疾病。未来对禽类对哺乳动物朊病毒疾病潜在易感性的研究需要物种特异性免疫化学技术和更精细的实验模型。