The Truth About Chronic Wasting Disease
Jerry Nelson, Deer and Elk Section Manager

If you’ve read an outdoor magazine recently or watched the news on TV, you’ve probably been inundated with sensationalized reports of diseases in both domestic livestock and wild animals. One of the maladies that may have been discussed is a disease of the central nervous system found in deer and elk called chronic wasting disease.

Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy (TSE). Other TSE’s currently known to science include scrapie in domestic sheep, bovine spongiform encephalopathy (BSE) in cattle, kuru in humans, and Creutzfeldt-Jacob disease in humans.

CWD was first observed in captive mule deer at a research facility in Ft. Collins Colorado in the late 1960s. Scientists in Wyoming determined the disease was a TSE in 1978. Currently, CWD is found in wild herds of deer and elk in north-central Colorado and southeastern Wyoming. It’s also been found in captive elk on a few game farms in the west. Most recently, two cases of CWD have been confirmed in wild mule deer in Saskatchewan. Animals affected by the disease will exhibit excessive weight loss, appear lethargic with their heads down and ears drooping, salivate excessively, drink water more than usual, spend less time with other animals in the herd or pen, and eventually die. There are a variety of other diseases that may cause one or more of these symptoms. Observing a sick deer doesn’t provide conclusive evidence of CWD, or any other disease for that matter. Laboratory tests are necessary to determine the type of disease a deer might have.

The agent that causes CWD is not fully understood, however scientists are confident that the cause is not a virus or bacterium. The mode of transmission is another mystery that hasn’t been completely unraveled. It is suspected that animal-to-animal contact is one form of transmission. Doe-to-fawn transmission may be possible as well, but is less likely. The origin of the disease is also unknown. One theory suggests that the disease developed spontaneously on it’s own, similar to a genetic mutation. Another theory is that a disease like scrapie in domestic sheep was able to cross the species barrier and infect deer.

Clues to the disease are in the proteins that occur in mammal nerve cells. Normal proteins are found on the membranes of nerve cells and they seem to play a role in the transfer of impulses between nerve cells. If the shape of the protein is altered in a certain way, it becomes a proteinaceous infectious particle or prion (PREE-ON). Scientists don’t fully understand why proteins reconfigure into prions. One characteristic for all TSE’s is that the brain of the afflicted animal contains irregular prions, and these abnormal prions have the ability to make other proteins change shape simply by coming in contact with them. Although they are made up of approximately 250 amino acids, prions contain no nucleic acid such as DNA or RNA. Prions cause neighbor proteins to “mutate”, despite the fact that they lack the genetic material that we normally associate with a mutation. The result is a slow, degenerative, chain reaction in adjacent proteins changing to prions and ultimately causing sponge-like holes in the brain tissue. As the lesions spread, brain function deteriorates, and the animal dies. CWD is always fatal.

There is no scientific evidence at this time that CWD can be transmitted from deer or elk to humans. Scrapie is a TSE that has been recognized in domestic sheep since the 1700s. Scrapie has never had an impact on the humans that worked with or ate domestic sheep. There is evidence to suggest that a variant Creutzfeldt-Jacob disease that is affecting people in Great Britain may have come from cattle infected with BSE. This is quite an unusual development, because TSE’s were believed to be species specific. Because proteins are similar in similar types of animals, it makes sense that two closely related species would be more likely to trade prions that cause disease. In experiments, a small percentage of healthy elk have come down with the disease when they were held in the same pen with mule deer that had CWD. Less closely related animals like pronghorn, bighorn sheep and mouflon sheep exposed to the same conditions did not contract the disease. Research by the National Institute of Health is being conducted to determine if prions from one species can alter proteins from another species in a test tube. There is still a lot we don’t know about inter-species transfer of these types of diseases.

Although CWD has never been documented in Washington, hunters should still exercise caution when hunting deer and elk. Don’t harvest an animal that appears sick or is behaving strangely. Wear rubber gloves while field dressing the animal. Don’t eat the brain, spinal cord, eyes, or spleen.

Washington Department of Fish and Wildlife (WDFW) has been conducting targeted surveillance sampling for CWD since 1995. When deer and elk show symptoms similar to CWD, samples are collected by Department staff and sent to a laboratory in Wyoming to be tested. Last year WDFW expanded CWD testing to include locker checks of some meat processors that handled wild game. To date, all of the samples tested from Washington deer and elk have been negative for CWD. One of the difficulties in testing for CWD is that no test currently exists that can be conducted on live animals. Only brain stem samples from dead animals can be tested. Therefore the two best sources for test subjects come from hunter-harvested deer and elk and road-kills. WDFW will substantially increase sampling efforts this hunting season in an attempt to achieve statewide coverage. At this time we have no reason to believe that CWD occurs in Washington. With the cooperation of hunters, the expanded testing effort will provide an increased level of confidence that Washington deer and elk are CWD free. Biologists will be collecting samples from hunters during the season. If you are contacted please cooperate in this important effort.