CWD Disease Information

Chronic wasting disease (CWD) is a chronic, fatal disease of the central nervous system of mule deer,white-tailed deer, Rocky Mountain elk, and (rarely) moose. Chronic wasting disease belongs to the group of diseases called transmissible spongiform encephalopathies (TSEs). These disorders are thought to be caused by abnormal proteins called “prion proteins.” Prion proteins are neither bacteria nor viruses. They are proteins devoid of nucleic acid, thus they are not living organisms.

How do Prion Proteins Cause CWD?

Prion proteins have similar amino acid sequences as normal cellular proteins but in a different conformation. The functional role of the normal cellular proteins is unknown. Prion proteins cause a conformational change in the normal cellular protein and disease is induced when the normal cellular protein is converted into the prion protein, which apparently can no longer serve its normal role. This eventually causes brain cells to die. As more and more cells die, the disease can be observed to progress, ultimately ending in death.

What Does CWD Look Like?

CWD Positive Deer

The only animals known to get CWD are members of the Cervidae family (deer, elk, moose). Affected animals will have one or more of the below signs:

1. Emaciation, poor body condition, rough hair coat.
2. Behavioral changes (hyperactive when constrained; reluctance to move; ears droop).
3. Excessive salivation (sometimes).
4. Excessive drinking (or staying close to water source).
5. Lethargy (but will react when approached closely).
6. Death.

How is CWD Transmitted?

The mode of transmission of CWD has not been identified. Evidence suggests that CWD can be transmitted from animal to animal or from animal to the environment (soil, water, plants) back to another animal. The prion proteins can probably be shed in saliva, urine, or feces where they can contaminate the environment. The most likely rout of exposure is through ingestion.

Are There Other Diseases Like CWD?

There are other transmissible spongiform encephalopathies that tend to be species specific and most are not naturally transmissible between species due to a "species barrier.” Examples include:

1. Scrapie of domestic sheep
2. Bovine spongiform encephalopathy (a.k.a. BSE or "mad cow disease) of cattle and a few domestic cats and zoo ruminants in Great Britain and Europe
3. Transmissible mink encephalopathy of ranched mink.

Humans can also suffer from transmissible spongiform encephalopathies, the most notable include:

1. Creutzfeldt-Jakobdisease (CJD), a sporadic disease found worldwide at about 1 in one millionpopulation
2. New variant CJD, probably caused by the prion protein of BSE or "madcow disease.”
3. Kuru, a nearly extinct disease of the Foretribe of Papau, NewGuinea.

None known public health significance at this time. Research on non-human surrogates (primates, transgenic mice) has indicated that humans are not likely to contract CWD from contacting or eating an infected animal. However, CWD is one of a group of diseases termed transmissible spongiform encephalopathies (TSEs). Bovine spongiform encephalopahty (aka "mad cow disease") is a TSE that has been implicated in causing human deaths. Thus, human health agencies caution that known CWD-infected animals not be consumed by humans.

Can Humans Get CWD?

Chronic wasting disease is not known to be a disease of humans. Because some humans in Europe contracted variant Creutzfeldt-Jakob disease after presumably eating beef contaminated with BSE (mad cow disease) prion proteins, some feared that humans could also develop a transmissible spongiform encephalopathy after eating CWD-infected venison. Thus far, there is no evidence that this is likely. This is due to several lines of evidence, to wit:

1. The case rate for Creutzfeldt-Jakob disease in Wyoming and Colorado is less than the national average of 1 in one million, yet CWD has been in these states for > 40 years.

2. In laboratory studies, prion protein-induced conversions of the normal human protein is low (< 3%), demonstrating a barrier at the molecular level that limits human susceptibility to CWD.

3. Laboratory mice genetically modified to express the normal human protein do not get CWD, even when the prion protein is inoculated directly into the brain.

4. After several years, primates given the CWD prion protein have not developed any disease.

Nonetheless to avoid any risk of contracting any disease, parts or products from any animal that looks sick, or tests positive for CWD, should not be eaten.

Although CWD has existed for at least 40 years, we still do not know how the disease will ultimately impact deer and elk populations. Early mathematical modeling suggested that CWD could eliminate entire populations of deer or elk. Few scientists today believe that is likely. Rather, more recent models suggest that CWD will eventually decrease the population, sometimes substantially, but over time the population will rebound and stabilize, albeit at levels less than those prior to the disease’s arrival.

Can the Spread of CWD be Stopped or Controlled?

Despite herculean efforts by some state and provincial wildlife management agencies to stop CWD, these efforts have not stopped or controlled the spread of CWD. Today, there are many commonly accepted management practices (i.e. targeted/individual animal removal, annual statewide surveillance, carcass transportation regulations) adopted by most states and provinces, including Wyoming, to help slow the spread of CWD. Few wildlife professionals today think that CWD can be eradicated once it becomes established.

Can Livestock get CWD?

Studies conducted by the Wyoming Game and Fish Department, the Colorado Division of Wildlife, and the University of Wyoming concluded that it is highly unlikely that domestic cattle can contract CWD. These conclusions were based on the following findings:

1. After 10 years, 10 cattle given a single oral inoculum of CWD showed no signs of disease.
2. After 10 years, 20 cattle living amongst CWD-infected deer and elk showed no signs of disease.
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