Skip to main content

Thank you for visiting You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

Asymptomatic deer excrete infectious prions in faeces

A Corrigendum to this article was published on 29 July 2010


Infectious prion diseases1—scrapie of sheep2 and chronic wasting disease (CWD) of several species in the deer family3,4—are transmitted naturally within affected host populations. Although several possible sources of contagion have been identified in excretions and secretions from symptomatic animals5,6,7,8, the biological importance of these sources in sustaining epidemics remains unclear. Here we show that asymptomatic CWD-infected mule deer (Odocoileus hemionus) excrete CWD prions in their faeces long before they develop clinical signs of prion disease. Intracerebral inoculation of irradiated deer faeces into transgenic mice overexpressing cervid prion protein (PrP) revealed infectivity in 14 of 15 faecal samples collected from five deer at 7–11 months before the onset of neurological disease. Although prion concentrations in deer faeces were considerably lower than in brain tissue from the same deer collected at the end of the disease, the estimated total infectious dose excreted in faeces by an infected deer over the disease course may approximate the total contained in a brain. Prolonged faecal prion excretion by infected deer provides a plausible natural mechanism that might explain the high incidence and efficient horizontal transmission of CWD within deer herds3,4,9, as well as prion transmission among other susceptible cervids.

This is a preview of subscription content, access via your institution

Relevant articles

Open Access articles citing this article.

Access options

Buy article

Get time limited or full article access on ReadCube.


All prices are NET prices.

Figure 1
Figure 2: Bioassays using irradiated faecal homogenates collected from infected mule deer by intracerebral inoculation into Tg(ElkPrP) mice.
Figure 3: Western blots of brain homogenates of Tg(ElkPrP) mice.
Figure 4: Neuropathology of brain sections from Tg(ElkPrP) mice.


  1. Prusiner, S. B. in Fields Virology (eds Knipe, D. M. et al.) 3059—3092 (Lippincott Williams & Wilkins, 2007)

    Google Scholar 

  2. Detwiler, L. A. & Baylis, M. The epidemiology of scrapie. Rev. Sci. Tech. 22, 121—143 (2003)

    CAS  Article  Google Scholar 

  3. Williams, E. S. & Young, S. Chronic wasting disease of captive mule deer: a spongiform encephalopathy. J. Wildl. Dis. 16, 89—98 (1980)

    CAS  Article  Google Scholar 

  4. Williams, E. S. Chronic wasting disease. Vet. Pathol. 42, 530—549 (2005)

    CAS  Article  Google Scholar 

  5. Mathiason, C. K. et al. Infectious prions in the saliva and blood of deer with chronic wasting disease. Science 314, 133—136 (2006)

    ADS  CAS  Article  Google Scholar 

  6. Angers, R. C. et al. Chronic wasting disease prions in elk antler velvet. Emerg. Infect. Dis. 15, 696—703 (2009)

    CAS  Article  Google Scholar 

  7. Haley, N. J., Seelig, D. M., Zabel, M. D., Telling, G. C. & Hoover, E. A. Detection of CWD prions in urine and saliva of deer by transgenic mouse bioassay. PLoS ONE 4, e4848 (2009)

    ADS  Article  Google Scholar 

  8. Konold, T., Moore, S. J., Bellworthy, S. J. & Simmons, H. A. Evidence of scrapie transmission via milk. BMC Vet. Res. 4, 14 (2008)

    Article  Google Scholar 

  9. Miller, M. W. & Williams, E. S. Prion disease: horizontal prion transmission in mule deer. Nature 425, 35—36 (2003)

    ADS  CAS  Article  Google Scholar 

  10. Baeten, L. A., Powers, B. E., Jewell, J. E., Spraker, T. R. & Miller, M. W. A natural case of chronic wasting disease in a free-ranging moose (Alces alces shirasi). J. Wildl. Dis. 43, 309—314 (2007)

    Article  Google Scholar 

  11. Miller, M. W. et al. Lions and prions and deer demise. PLoS ONE 3, e4019 (2008)

    ADS  Article  Google Scholar 

  12. Miller, M. W., Hobbs, N. T. & Tavener, S. J. Dynamics of prion disease transmission in mule deer. Ecol. Appl. 16, 2208—2214 (2006)

    Article  Google Scholar 

  13. Sigurdson, C. J. et al. Oral transmission and early lymphoid tropism of chronic wasting disease PrPres in mule deer fawns (Odocoileus hemionus). J. Gen. Virol. 80, 2757—2764 (1999)

    CAS  Article  Google Scholar 

  14. Fox, K. A., Jewell, J. E., Williams, E. S. & Miller, M. W. Patterns of PrPCWD accumulation during the course of chronic wasting disease infection in orally inoculated mule deer (Odocoileus hemionus). J. Gen. Virol. 87, 3451—3461 (2006)

    CAS  Article  Google Scholar 

  15. Miller, M. W., Williams, E. S., Hobbs, N. T. & Wolfe, L. L. Environmental sources of prion transmission in mule deer. Emerg. Infect. Dis. 10, 1003—1006 (2004)

    Article  Google Scholar 

  16. Angers, R. C. et al. Prions in skeletal muscles of deer with chronic wasting disease. Science 311, 1117 (2006)

    CAS  Article  Google Scholar 

  17. Tamgüney, G. et al. Transmission of elk and deer prions to transgenic mice. J. Virol. 80, 9104—9114 (2006)

    Article  Google Scholar 

  18. Dougherty, R. in Techniques in Experimental Virology (ed. Harris, R. J. C.) 169—224 (Academic, 1964)

    Google Scholar 

  19. Cox, D. R. Regression models and life-tables. J. R. Stat. Soc. A 34, 187—220 (1972)

    MathSciNet  MATH  Google Scholar 

  20. Prusiner, S. B. et al. Measurement of the scrapie agent using an incubation time interval assay. Ann. Neurol. 11, 353—358 (1982)

    CAS  Article  Google Scholar 

  21. Wolfe, L. L. et al. PrPCWD in rectal lymphoid tissue of deer (Odocoileus spp.). J. Gen. Virol. 88, 2078—2082 (2007)

    CAS  Article  Google Scholar 

  22. Tamgüney, G. et al. Transmission of scrapie and sheep-passaged bovine spongiform encephalopathy prions to transgenic mice expressing elk prion protein. J. Gen. Virol. 90, 1035—1047 (2009)

    Article  Google Scholar 

  23. Miekka, S. I. et al. Inactivation of viral and prion pathogens by gamma-irradiation under conditions that maintain the integrity of human albumin. Vox Sang. 84, 36—44 (2003)

    CAS  Article  Google Scholar 

  24. Judge, J., Greig, A., Kyriazakis, I. & Hutchings, M. R. Ingestion of faeces by grazing herbivores—risk of inter-species disease transmission. Agric. Ecosyst. Environ. 107, 267—274 (2005)

    Article  Google Scholar 

  25. Arthur, W. J. & Alldredge, A. W. Seasonal estimates of masses of mule deer fecal pellets and pellet groups. J. Wildl. Mgmt 44, 750—752 (1980)

    Article  Google Scholar 

  26. Diringer, H., Roehmel, J. & Beekes, M. Effect of repeated oral infection of hamsters with scrapie. J. Gen. Virol. 79, 609—612 (1998)

    CAS  Article  Google Scholar 

  27. Johnson, C. J., Pedersen, J. A., Chappell, R. J., McKenzie, D. & Aiken, J. M. Oral transmissibility of prion disease is enhanced by binding to soil particles. PLoS Pathog. 3, e93 (2007)

    Article  Google Scholar 

  28. Arthur, W. J. & Alldredge, A. W. Soil ingestion by mule deer in northcentral Colorado. J. Range Mgmt 32, 67—71 (1979)

    CAS  Article  Google Scholar 

  29. Hadlow, W. J., Kennedy, R. C. & Race, R. E. Natural infection of Suffolk sheep with scrapie virus. J. Infect. Dis. 146, 657—664 (1982)

    CAS  Article  Google Scholar 

  30. Raymond, G. J. et al. Evidence of a molecular barrier limiting susceptibility of humans, cattle and sheep to chronic wasting disease. EMBO J. 19, 4425—4430 (2000)

    CAS  Article  Google Scholar 

  31. Williams, E. S. et al. Epidemiology of Chronic Wasting Disease: Detection of PrPres, Shedding, and Environmental Contamination (United States Department of Defense National Prion Research Program, 2003)

    Google Scholar 

  32. Bellinger-Kawahara, C. G., Kempner, E., Groth, D. F., Gabizon, R. & Prusiner, S. B. Scrapie prion liposomes and rods exhibit target sizes of 55,000 Da. Virology 164, 537—541 (1988)

    CAS  Article  Google Scholar 

  33. Büeler, H. et al. Normal development and behaviour of mice lacking the neuronal cell-surface PrP protein. Nature 356, 577—582 (1992)

    ADS  Article  Google Scholar 

  34. Tamgüney, G. et al. Genes contributing to prion pathogenesis. J. Gen. Virol. 89, 1777—1788 (2008)

    Article  Google Scholar 

  35. Carlson, G. A. et al. Genetics and polymorphism of the mouse prion gene complex: control of scrapie incubation time. Mol. Cell. Biol. 8, 5528—5540 (1988)

    CAS  Article  Google Scholar 

  36. Scott, M. et al. Propagation of prions with artificial properties in transgenic mice expressing chimeric PrP genes. Cell 73, 979—988 (1993)

    CAS  Article  Google Scholar 

  37. Cox, D. R. & Oakes, D. Analysis of Survival Data (Chapman & Hall and CRC, 1984)

    Google Scholar 

  38. Vittinghoff, E., Glidden, D. V., Shiboski, S. C. & McCulloch, C. E. Regression Methods in Biostatistics: Linear, Logistic, Survival, and Repeated Measures Models (Springer Science+Business Media, 2005)

    MATH  Google Scholar 

  39. Laemmli, U. K. Cleavage of structural proteins during the assembly of the head of bacteriophage T4. Nature 227, 680—685 (1970)

    ADS  CAS  Article  Google Scholar 

  40. Safar, J. G. et al. Measuring prions causing bovine spongiform encephalopathy or chronic wasting disease by immunoassays and transgenic mice. Nature Biotechnol. 20, 1147—1150 (2002)

    CAS  Article  Google Scholar 

  41. Muramoto, T. et al. Heritable disorder resembling neuronal storage disease in mice expressing prion protein with deletion of an α-helix. Nature Med. 3, 750—755 (1997)

    CAS  Article  Google Scholar 

Download references


G.T. was supported by a fellowship from the Larry L. Hillblom Foundation. This work was supported by the Colorado Division of Wildlife and grants from the US Department of Defense National Prion Research Program (NP020152), the National Institutes of Health (AG02132) and the Hillblom Foundation. We thank P. Lessard and the staff of the Hunters Point animal facility for support with the transgenic animal experiments, K. Giles for screening transgenic animals, A. Serban for antibodies, K. Pomeroy for technical assistance, J. Safar for discussions, H. Nguyen for editorial assistance and B. Williams for insights on CWD transmission.

Author Contributions G.T., M.W.M. and S.B.P. designed the transgenic mouse studies; G.T., M.W.M., L.L.W., T.M.S., C.P., A.L. and S.J.D. performed various aspects of the research on mule deer or transgenic mice; G.T., M.W.M, D.V.G., S.J.D. and S.B.P. analysed the data; G.T., M.W.M., S.J.D. and S.B.P. wrote the paper. All authors discussed the results and commented on the manuscript.

Author information

Authors and Affiliations


Corresponding author

Correspondence to Stanley B. Prusiner.

Supplementary information

Supplementary Information

This file contains Supplementary Figures 1-3 with Legends, Supplementary Tables 1-3 and Supplementary Notes. (PDF 781 kb)

PowerPoint slides

Rights and permissions

Reprints and Permissions

About this article

Cite this article

Tamgüney, G., Miller, M., Wolfe, L. et al. Asymptomatic deer excrete infectious prions in faeces. Nature 461, 529–532 (2009).

Download citation

  • Received:

  • Accepted:

  • Published:

  • Issue Date:

  • DOI:

This article is cited by


By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.


Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing