The Science of CWD: A Chronology of Conclusions on Chronic Wasting Disease
Anthony C. Grabski, Ph.D

1980, Journal of Wildlife Diseases
Presented is a clinical characterization of CWD and pathological evidence supporting the conclusion that the disease is a specific spontaneously occurring form of spongiform encephalopathy. Currently, studies are underway to characterize fully the clinical and pathological features of CWD, and to determine its epitzootiology and transmissibility.

1997, Journal of Wildlife Diseases
The source of spongiform encephalopathy in free ranging cervids is undetermined. The mode of transmission of spongiform encephalopathy also is unknown. Equally little is known about other aspects of the epizootiology of spongiform encephalopathy in wild cervids. The number of case submissions has increased since the first case was diagnosed in 1981. We believe this increased detection rate is mostly due to greater efforts to locate affected animals. Although the occurrence of spongiform encephalopathy in wild cervids could be on the rise in this area, preliminary analysis of deer and elk harvest data from 1990 to 1994 do not reflect such a trend. .

1998, Journal of Wildlife Diseases
In 1985, all cervids residing in the FWRF and its satellite facilities were killed in an attempt to eradicate CWD. Paddocks where affected cervids had resided were treated with 1,000 ppm calcium hypochlorite solution via mobile sprayer and helicopter, plowed to a depth of 0.3 m, and treated a second time; shelters, feed bunkers and automatic waterers were either replaced or hand cleaned twice with 1,000 ppm calcium hypochlorite solution. An outbreak of CWD occurred between 1986 and 1997 with an incidence rate of 17%. Our observations provide compelling circumstantial evidence for lateral transmission of CWD among elk. We also acknowledge the possibility that an unidentified point source of infection could have independently given rise to the outbreak. Alternatively, environmental contamination could have been a factor infecting elk with CWD. If an environmental source was involved, then it apparently survived our extensive disinfection procedures in 1985 and would likely hamper elimination of CWD from the FWRF and other infected facilities in the future :

2000, Journal of Wildlife Diseases
Within species, CWD prevalence varied widely among biologically or geographically-segregated subpopulations within the 38,137 km2 endemic area but appeared stable over a 3-year period. The duration of CWD occurrence in free-ranging cervids remains as enigmatic as its geographic origin. CWD may have been present in free-ranging deer in both Colorado and Wyoming since the early 1960s, if not earlier.

Effective strategies for controlling or eliminating CWD in wild deer and elk have not been identified. It follows that random culling via harvest or other means may be relatively ineffective in reducing CWD prevalence.

2001, Journal of Wildlife Management
Once introduced and established, most infectious diseases are extremely difficult to eliminate from free-ranging populations. It follows that a new or emerging wildlife disease should be carefully evaluated early on to assess both its potential importance and prospects for effective management. The biological mechanisms underlying CWD transmission are poorly understood, and as a result model mechanisms are at best a collection of educated guesses.

Selective culling may offer the greatest promise of reducing CWD prevalence, particularly when infected populations are detected early in the course of an epidemic and tested aggressively for several decades.

2002, Journal of Wildlife Management
Although most captive deer residing in endemic research facilities eventually contract CWD, individuals occasionally survive a lifetime. Genetic resistance associated with the PNRP genotype has been demonstrated in free-ranging and farmed elk and is being investigated in deer.

The apparent persistence of PrPCWD in contaminated environments may represent a significant obstacle to eradication of CWD from either farmed or free- ranging cervid populations. Perhaps most important, impacts of CWD on population dynamics of deer and elk are presently unknown.

A quote from a 1990 issue of Ecology seems an appropriate capstone to this review of the state of knowledge on CWD:

"Not only is the science incomplete, the system itself is a moving target, evolving because of the impacts of management and the progressive expansion of the scale of human influences on the planet. Hence, the actions needed by management must be ones that achieve ever-changing understanding as well as the social goals desired. That is the heart of active experimentation at the scales appropriate to the question. Otherwise the pathologies of management are inevitable-increasingly fragile systems, myopic management, and social dependencies leading to crises."

- - - Anthony Grabski, Ph.D.

References

1. Williams, E.S. and Young, S., (1980) Chronic wasting disease of captive mule deer: A spongiform encephalopathy. J. Wildlife Diseases, 16: 89-98.
2. Spraker, T. R., Miller, M. W., Williams, E. S., Getzy, D. M., Adrian, W. J., Schoonveld, G. G., Spowart, R. A., O'Rourke, K. I., Miller, J. M., and Mertz, P. A., (1997) Spongiform encephalopathy in free-ranging mule deer, white-tailed deer, and rocky mountain elk in North Central Colorado, J. Wildlife Diseases, 33: 1-6.
3. Miller, M. W., Wild, M. A., and Williams, E.S., (1998) Epidemiology of chronic wasting disease in captive rocky mountain elk. J. Wildlife Diseases, 34: 532-538.
4. O'Rourke, K. I., Besser, T. E., Miller, M. W., Cline, T. F., Spraker, T. R., Jenny, A. L., Wild, M. A., Zebarth, G. L., and Williams, E.S., (1999) PrP genotypes of captive and free-ranging Rocky Mountain elk with chronic wasting disease. J. General Virology, 80: 2765-2769.
5. Miller, M. W., Williams, E.S., McCarty, C. W., Spraker, T. R., Kreeger, T. J., Larsen, C. T., and Thorne, E. T., (2000) Epizootiology of chronic wasting disease in free-ranging cervids in Colorado and Wyoming. J. Wildlife Diseases, 36: 676-690.
6. Gross, J. E. and Miller, M. W., (2001) CWD in mule deer: a model of disease dynamics, control options, and population consequences. J. Wildlife Management, 65: 205-215.
7. Williams, E. S., Miller, M. W., Kreeger, T. J., Kahn, R. H., and Thorne, E. T., (2002) Chronic wasting disease in mule deer and elk: A review with recommendations for management. J. Wildlife Management, 66: 551-563.
8. Walters, C.J. and Holling, C.S. (1990) Large-scale management experiments and learning by doing. Ecology 71: 2060-2068.

PostScript: An e-mail I received recently from Rob Harstad highlights the dangers of intervening in nature with an inadequate understanding of the phenomena in question. He began with a quote from Lewis Thomas writing about DNA in The Medusa and the Snail:

"The capacity to blunder slightly is the real marvel of DNA. Without this special attribute, we would still be anaerobic bacteria and there would be no music...If we had been doing it, we would have found some way to correct this, and evolution would have been stopped in its tracks."

Rob then comments:

"When I read this it occurred to me that the WDNR is trying to stop evolution in its tracks. . . .Even if they were successful in eliminating the disease from Wisconsin, or the continent for that matter, by killing all the deer, both resistant and susceptible individuals, the species is left wide open to future, and inevitable it seems to me, outbreaks of this disease. And are not deer, like mankind, afflicted with any number of potentially fatal diseases, communicable and not? How was it decided that this particular disease would be the last for all the deer? . . . ."