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Open Access Research article

Studies of the transmissibility of the agent of bovine spongiform encephalopathy to the domestic chicken

Jo Moore13, Stephen AC Hawkins1, Anthony R Austin1, Timm Konold1, Robert B Green1, Ian W Blamire1, Ian Dexter1, Michael J Stack1, Melanie J Chaplin1, Jan PM Langeveld4, Marion M Simmons1*, Yvonne I Spencer1, Paul R Webb1, Michael Dawson2 and Gerald AH Wells1

Author affiliations

1 Department of Pathology and Host Susceptibility, Animal Health and Veterinary Laboratories Agency, Woodham Lane, New Haw, Addlestone, Surrey KT15 3NB, UK

2 Centre for Epidemiology and Risk Analysis, Animal Health and Veterinary Laboratories Agency, Woodham Lane, New Haw, Addlestone, Surrey KT15 3NB, UK

3 School of Veterinary and Biomedical Sciences, Murdoch University, South Street, Murdoch, WA 6150, Australia

4 Central Veterinary Institute of Wageningen UR (CVI), P.O. Box 65, 8200, AB Lelystad, Netherlands

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Citation and License

BMC Research Notes 2011, 4:501  doi:10.1186/1756-0500-4-501

Published: 17 November 2011

Abstract

Background

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.

Results

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.

Conclusion

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.