Chronic Wasting Disease (CWD), a transmissible spongiform encephalopathy affecting North American deer and elk, has recently emerged as an internationally important wildlife management issue. Interest and concern over the spread of this disease and its potential impact on free-ranging cervid populations has increased with discovery of the disease in numerous states and provinces. Current studies suggest that CWD may have long-term adverse population effects on these highly visible, socially desirable, and economically valuable keystone species. Scientific understanding of the ecology and transmission of CWD in free-ranging wildlife is limited, but this information is critical to providing knowledge for making management decisions and helping to better understand the ecology of CWD in free-ranging populations. Current research is being conducted on CWD in Wisconsin white-tailed deer in collaboration with the Wisconsin Department of Natural Resources and USGS National Wildlife Health Research Center.

The guiding principles of CWD research activities being conducted by the USGS-Wisconsin Cooperative Wildlife Research Unit are to:
                1) improve our scientific knowledge of CWD in free-ranging deer, and
                2) develop research to facilitate and refine CWD management actions.

Our primary research objectives are aimed at providing reliable scientific information to inform chronic wasting disease management through an integrated approach to understanding:

  • the epidemiology and transmission of CWD in white-tailed deer,
  • the role of genetic variation in disease dynamics and impacts,
  • the landscape patterns associated with CWD distribution and spread,
  • potential for accumulation of CWD prions in the environment,
  • possible prion exposure to other wildlife species, and
  • evaluation of CWD surveillance and management actions.

 CWD Basics

Chronic wasting disease (CWD) is a fatal neurodegenerative disease of mule deer (Odocoileus hemionus), white-tailed deer (O. virginianus), and elk (Cervus elaphus) associated with the presence of transmissible protease resistant prion proteins (or prions). CWD infection can occur through ingestion of prions and it may be transmitted among deer and elk by direct contact or indirectly through the environment. Maternal transmission does not appear to be an important component of CWD epidemiology. Appearance of clinical signs is usually delayed, but symptoms typically appear within 18-24 months after experimental infections, and include weight loss, anorexia, repetitive behaviors, hyperesthesia and intractability with progression to severe emaciation, severe behavioral changes, excessive salivation, tremors, and mild ataxia. Pre-clinical disease can be detected in animal lymph node and brain tissues using a variety of diagnostic methods.

Prior to 2000, CWD was believed to occur only in the western United States, but it has recently been discovered in the Midwest and eastern U.S. and in central Canada. The current international distribution covers many states and provinces.  An extensive bibliography on CWD is available.  The University of Wisconsin-Madison has a website devoted to CWD, including a list of CWD experts on campus and their research programs. The CWD Alliance maintains an extensive website on CWD news, scientific information, directory of experts, and many other resources related to CWD.

CWD was discovered in south-central Wisconsin in February 2002. Three adult male deer harvested within 5-km during the fall of 2001 were diagnosed with CWD.  Additional testing has detected a growing number of CWD cases.  The disease is primarily concentrated in two focal areas: south-central Wisconsin and south-eastern Wisconsin continuing into northern Illinois.  Though the 2011 harvest season yielded the first CWD-positive deer in northern Wisconsin (Washburn County), and the 2012 season saw the first positive deer in Racine and Adams Counties.  The current distribution of CWD in Wisconsin can be seen in pdf format or interactive maps.

Almost immediately following the discovery of CWD, an Interagency Health and Science team was convened to provide scientific and management advice on CWD in Wisconsin. Various agencies were represented, including the Wisconsin Departments of Natural Resources, Health and Family Services, Agriculture Trade and Consumer Protection, the US Department of Agriculture and the US Geological Survey.  Staff of the USGS-National Wildlife Health Center (USGS-NWHC), the University of Wisconsin-Madison Department of Wildlife Ecology, and the USGS-Wisconsin Cooperative Wildlife Research Unit  (USGS-WCWRU) were asked to provide quantitative, epidemiological, and scientific support to assist in surveillance and management of CWD in Wisconsin.  An integrated research and management program has developed from this collaboration including the USGS and the Wisconsin Department of Natural Resources.



Michael D. Samuel, PhD
(Lab Leader)


Ian H. Plummer
(M.S. program)


Stacie J. Robinson, PhD (Former PhD Student & Postdoc)


Daniel J. Storm, PhD
(Former PhD Student & Postdoc)


Christopher S. Jennelle, PhD
(Former Postdoc)


Eric E. Osnas, PhD
(Former Postdoc)


 Gideon E. Wasserberg, PhD
(Former Postdoc)


Andrew ???
(Former Postdoc)


Julie A. Blanchong, PhD
(Former Postdoc)


Damien O. Joly, PhD
(Former Postdoc)


Daniel A. Grear, PhD
(Former MS Student)


Abbey K. Thompson
(Former MS Student)


Cherie A. Nolden
(Former MS Student)




Storm D. J., M. D. Samuel, R. E. Rolley, P. Shelton, N. S. Keuler, B. J. Richards, and T. R. Van Deelen.  Deer density and disease prevalence influence transmission of chronic wasting disease in white-tailed deer.  Ecosphere.  In Press.

 Blanchong, J. A., D. A. Grear, B. V. Weckworth, D. P. Keane, K. T. Scribner, and M. D. Samuel.  2012.  Effect of chronic wasting disease on reporduction and fwan harvest vulnerability in Wisconsin white-tailed deer.  Journal of Wildlife Diseases 48:361-370.

 Johnson, C. J., J. M. Aiken, D. McKenzie, M. D. SAMUEL, and J. A. Pedersen.  2012.  Highly efficient amplification of chronic wasting disease agent by protein misfolding cyclic amplification wit beads (PMCAb).  PLos ONE  e35383.

 Matsumoto, T., M. D. SAMUEL, T. Bolinger, M. Pybus, and D. W. Coltman.  2012.  Association mapping of genetic risk factors for chronic wasting disease in wild deer.  Evolutionary Applications.  doi:10.1111/eva.12003

Robinson, SJ, MD Samuel, D Lopez, P Shelton.  2012.  The walk is never random: landscape genetics detect subtle effects of landscape barriers to white-tailed deer gene flow.  Molecular Ecology 21: 4190-4205.

Robinson, SJ, MD Samuel, KI O’Rourke, CJ Johnson.  2012.  The role of PRNP genetics in chronic wasting disease of wild cervids.  A commissioned review in PRION 6: e1-e10.

Robinson, SJ, MD Samuel, CJ Johnson, J Aitken, M Adams.  2012.  Emerging prion disease drives host selection in a wildlife population. Ecological Applications 22: 1050–1059.

Walsh, D. P., and M. D. Samuel.  2012.  Factors affecting chronic wasting disease: a deer is not a deer is not a deer.  Pages 1-9 in D. P. Walsh, ed.  Enhanced surveillance strategies for detecting and monitoring chronic wasting disease in free-ranging cervids: U.S. Geological Survey Open-File Report 2012–1036. 

Rogers, K. G., S. J. Robinson, and M. D. Samuel.  2011.  Diversity and distribution of white-tailed deer mtDNA lineages in CWD outbreak areas in southern Wisconsin, USA.  Journal of Toxicology and Environmental Health 74:1521-1535.

Storm, D. J., M. D. Samuel, T. R. Van Deelen, K. D. Malcolm, R. E. Rolley, N. A. Frost, D. P. Bates, and B. J. Richards.  2011.  Comparison of Visual-based Helicopter and Fixed-wing Forward-looking Infrared Surveys for Counting White-tailed Deer.  Wildlife Biology 17:431-440. 

Grear, D.A., M.D. Samuel, K.T. Scribner, B.V. Weckworth, and J.A. Langenberg. 2010. Influence of genetic relatedness and spatial proximity on chronic wasting disease infection among female white-tailed deer. Journal of Applied Ecology 74:532-540

Blanchong, J. A., D. M., Heisey, K. T. S. Libants, Scribner, C. Johnson, J. M. Aiken, J. A. Langenberg, and M. D. Samuel.  2009.  Genetic susceptibility to chronic wasting disease in free-ranging white-tailed deer: Complement component C1q and Prnp polymorphisms.  Infection, Genetics, and Evolution 9:1329-1335.

Jennelle, C. S., M. D. Samuel, C. A. Nolden, and E. A. Berkley.  2009.  White-tailed deer carcass decomposition and potential exposure of scavengers to chronic wasting disease.  Journal of Wildlife Management 73:655-662.

Jennelle, C. S., M. D. Samuel, C. A. Nolden, D. P. Keane, D. J. Barr, C. Johnson, J. P. Vanderloo, and J. M. Aiken.  2009.  Surveillance for transmissible spongiform encephalopathy in scavengers of white-tailed deer carcasses in the chronic wasting disease area of Wisconsin.  Journal of Toxicology and Environmental Health 72:1018-1024

Joly, D. O., M. D. Samuel, J. A. Langenberg, R. E. Rolley, and D. P. Keane. 2009.  Surveillance to detect chronic wasting disease in Wisconsin white-tailed deer. Journal of Wildlife Diseases 45:989-997

Osnas, E.E, D.M. Heisey, R.E. Rolley, and M.D. Samuel. 2009. Spatial and temporal patterns of an emerging epidemic: fine scale mapping of a wildlife epidemic in Wisconsin. Ecological Applications 19:1311-1322.

Wasserberg, G., E. E. Osnas, R.E. Rolley, and M.D. Samuel. 2009. Host culling as an adaptive management tool for chronic wasting disease – a modeling study. Journal of Applied Ecology 46:457-466.

Keane, D. P., D. J. Barr, P. N. Bochsler, S. M. Hall, T. Gidlewski, K. I. O’Rourke, T. R. Spraker, and M. D. Samuel.  2008.  Chronic wasting disease in a Wisconsin white-tailed deer farm. Journal of Veterinary Diagnostic Investigation 20:698-703.

Thompson, A. K, M. D. Samuel, and T. R. Van Deelen.  2008.  Alternative feeding strategies and potential disease transmission in Wisconsin white-tailed deer. Journal of Wildlife Management 72: 416-421.

Thompson, A. K., and M. D. Samuel. 2007. Alternative bait marker systems for white-tailed deer. Pages 223-231 in Proceedings of the 12th Wildlife Damage Management Conference.

Blanchong, J. A., M. D. Samuel, K. T. Scribner, B. V. Weckworth, J. A. Langenberg, and K. Filcek. 2007. Landscape genetics and the spatial distribution of chronic wasting disease. Biology Letters. doi:10.1098/rsbl.2007.0523

Conner M. M. et al. 2007. Scale-dependent approaches to modeling spatial epidemiology of chronic wasting disease.

Samuel, M. D. and B. J. Richards. 2007. Chronic Wasting Disease in Free-Ranging North American Cervids. Proc. 22nd Vertebr. Pest Conf.

Blanchong, J.A., D.O. Joly, M.D. Samuel, J.A. Langenberg, R.E. Rolley, and J.F. Sausen. 2006. White-tailed deer harvest from the chronic wasting disease zone in south-central Wisconsin. Wildlife Society Bulletin 34:725-731.

Joly D.O., M.D. Samuel, J.A. Langenberg, J.A. Blanchong, C.A. Batha, R.E. Rolley, D.P. Keane, and C.A. Ribic. 2006. Spatial epidemiology of chronic wasting disease in Wisconsin white-tailed deer. Journal of Wildlife Diseases 42:578-588.

Grear, D.A., M.D. Samuel, J.A. Langenberg, and D. Keane. 2006. Demographic patterns and harvest vulnerability of CWD infected white-tailed deer in Wisconsin. Journal of Wildlife Management 70:546-545.

Joly, D.O., C.A. Ribic, J.A. Langenberg, K. Beheler, C.A. Batha, B.J. Dhuey, R.E. Rolley, G. Bartelt, T. Van Deelen, and M.D. Samuel. 2003. Chronic wasting disease in wild Wisconsin white-tailed deer. Emerging Infectious Diseases 9: 599-601. (pdf reprints)

Samuel, M.D., D.O. Joly, M.A. Wild, S.D. Wright, D. Otis, R. Werge, and M. Miller. 2003. Surveillance strategies for detecting chronic wasting disease in free-ranging deer and elk: results of a CWD surveillance workshop, December 10-12, 2002. USGS-National Wildlife Health Center. (pdf version)