What Is Chronic Wasting Disease?
Chronic Wasting Disease (CWD) is a contagious neurological disease affecting deer, elk and moose. It causes a characteristic spongy degeneration of the brains of infected animals resulting in emaciation, abnormal behavior, loss of bodily functions and death.
CWD belongs to a group of diseases known as transmissible spongiform encephalopathies (TSEs). Within this family of diseases, there are several other variants that affect domestic animals: scrapie, which has been identified in domestic sheep and goats for more than 200 years, bovine spongiform encephalopathy (BSE) in cattle (also known as “mad cow disease”), and transmissible mink encephalopathy in farmed mink.
Several rare human diseases are also TSEs. Creutzfeldt-Jakob disease (CJD) occurs naturally in about one out of every one million people worldwide. Variant Creutzfeldt-Jakob disease (v-CJD) has been associated with the large-scale outbreak of BSE in cattle herds in Great Britain.
What Wildlife Species Are Affected By CWD?
Only four species of the deer family are known to be naturally susceptible to CWD: elk, mule deer, white-tailed deer and moose. Several subspecies of Sika deer and red deer hybrids housed in captive cervid facilities in Korea have reportedly contracted CWD from infected elk. Susceptibility of other members of the deer family (cervids) and other wildlife species is not entirely known, although ongoing research is further exploring this question.
Can Humans Get CWD?
Though many observers try to compare CWD with “mad cow disease”, the diseases are distinctly different. Currently, there is no evidence that CWD poses a risk for humans; however, public health officials recommend that human exposure to the CWD infectious agent be avoided as they continue to evaluate any potential health risk.
The World Health Organization has reviewed available scientific information and concluded that currently there is no evidence that CWD can be transmitted to humans. During the period 1997-1998, three cases of sporadic Creutzfeldt-Jakob disease (CJD) occurred in the U.S. in young adults. These individuals had consumed venison. This led to speculation about possible transmission of CWD from deer or elk to humans. However, review of the clinical records and pathological studies of all three cases by the Centers for Disease Control and Prevention in Atlanta, Georgia, did not find a causal link to CWD.
Nonetheless, health and wildlife officials advise caution. Hunters are encouraged not to consume meat from animals known to be infected. In addition, hunters should take common sense precautions when field dressing and processing deer or elk taken in areas where CWD is found.
More information on the Centers for Disease Control and Prevention website.
Can Livestock Get CWD?
Cattle and other domestic livestock appear to be resistant to natural infection. There are no reported cases of natural transmission of CWD from infected elk or deer to domestic livestock. However, the disease has been experimentally reproduced in cattle by the direct injection of the infectious agent into their brains. Several investigations are currently underway to further study this question.
What Causes CWD?
The most widely accepted theory is that the agent is a prion, an abnormal form of cellular protein that is most commonly found in the central nervous system and in lymphoid tissue. The prion “infects” the host animal by promoting conversion of normal cellular protein to the abnormal form.
The CWD infectious agent is smaller than most viral particles and does not evoke any detectable immune response or inflammatory reaction in the host animal. Based on experience with other TSE agents, the CWD infectious agent is assumed to be resistant to enzymes and chemicals that normally break down proteins, as well as resistant to heat and normal disinfecting procedures.
Where Does CWD Occur?
The CWD distribution map shows general CWD areas where the disease has been detected in the wild as well as areas that have had positives in captive farms (many have been eliminated).
Where and How Did CWD Originate?
The origin of CWD is unknown, and it may never be possible to definitively determine how or when CWD arose. It was first recognized as a syndrome in captive mule deer held in wildlife research facilities in Colorado in the late 1960s, but it was not identified as a TSE until the 1970s. Computer modeling suggests the disease may have been present in free-ranging populations of mule deer for more than 40 years.
Scrapie, a TSE of domestic sheep, has been recognized in the United States since 1947, and it is possible that CWD was derived from scrapie. It is possible, though never proven, that deer came into contact with scrapie-infected sheep either on shared pastures or in captivity somewhere along the front range of the Rocky Mountains, where high levels of sheep grazing occurred in the early 1900s.
It may be possible that CWD is a spontaneous TSE that arose in deer in the wild or in captivity and has biological features promoting transmission to other deer and elk.
How Does CWD Spread?
It is not known exactly how CWD is transmitted. The infectious agent may be passed in feces, urine or saliva. Transmission is thought to be lateral (from animal to animal). Although maternal transmission (from mother to fetus) may occur, it appears to be relatively unimportant in maintaining epidemics. The minimal incubation period between infection and development of clinical disease appears to be approximately 16 months. The maximal incubation period is unknown, as is the point at which shedding of the CWD agent begins during the prolonged course of infection.
Because CWD infectious agents are extremely resistant in the environment, transmission may be both direct and indirect. Concentrating deer and elk in captivity or by artificial feeding probably increases the likelihood of both direct and indirect transmission between individuals. Contaminated pastures appear to have served as sources of infection in some CWD epidemics. The apparent persistence of the infectious agents in contaminated environments represents a significant obstacle to eradication of CWD from either captive or free-ranging cervid populations.
The movement of live animals is one of the greatest risk factors in spreading the disease into new areas. Natural movements of wild deer and elk contribute to the spread of the disease, and human-aided transportation of both captive and wild animals greatly exacerbates this risk factor. The apparent spread of CWD between captive and wild cervids is a matter of hot debate. Although strong circumstantial evidence suggests that CWD has spread from positive captive elk to wild cervids in some instances, it may never be proven which group of animals represents the source of infection. It is likely that the disease has been passed in both directions (from captive to wild animals, and from wild to captive animals).
What Are the Symptoms of CWD?
While yearlings and even fawns can contract CWD (often getting the disease in utero from their mother), late-stage CWD symptoms are usually only visible in adult animals because of CWD’s long incubation period (usually around 18 months but may be as long as two years). In most cases, animals with CWD show no visible, outward symptoms of the disease for all but the last few months of the disease’s cycle. Thus, the majority of infected animals are virtually impossible to distinguish from healthy, non-infected animals. Because CWD affects the neurological system of an infected animal first, other causes of mortality (predators, vehicle collisions, other diseases) usually remove the animals from the population far before outward signs of the disease become apparent.
However, if an infected animal survives to the final stage of this always-fatal disease, the most obvious and consistent clinical sign is emaciation. CWD affected animals continue to eat but amounts of feed consumed are reduced, leading to gradual loss of body condition. Excessive drinking and urination are also common in the terminal stages.
Behavioral changes also occur in the majority of cases of late-stage CWD, including decreased interactions with other animals, listlessness, lowering of the head, blank facial expression and repetitive walking in set patterns. In elk, behavioral changes may also include hyper-excitability and nervousness. Excessive salivation, drooling and grinding of the teeth also are observed.
It is important to note that the above-mentioned clinical signs alone are not sufficient to definitively diagnose CWD. There are other maladies that have symptoms that mimic those of CWD such as brain abscesses, trauma-related injuries, or other diseases such as epizootic hemorrhagic disease. Currently, the only conclusive diagnosis for CWD involves an examination of the brain, tonsils or lymph nodes performed after death to detect the presence of CWD prions.
How Is CWD Detected?
Clinical signs of CWD alone are not conclusive, and there is currently no practical live animal test. Currently, the only conclusive diagnosis involves an examination of the brain, tonsils or lymph nodes performed after death.
A definitive diagnosis is based on examination of the brain for the characteristic microscopic spongiform lesions and/or accumulation of the CWD associated prion protein in brain and lymphoid tissues using a technique called immunohistochemistry. Gross lesions seen at necropsy reflect the clinical signs of CWD, primarily emaciation. Aspiration pneumonia, which may be the actual cause of death, also is a common finding in animals affected with CWD.
Research is being conducted to develop live-animal diagnostic tests for CWD. Early results indicate that a new live-test utilizing tissues from an animal’s tonsils may be viable in deer, but so far has been ineffective in elk.
Why Are We Concerned About CWD?
CWD poses serious problems for wildlife managers, and the implications for free-ranging deer and elk are significant:
- Ongoing surveillance programs are expensive and draw resources from other wildlife management needs.
- Impacts of CWD on population dynamics of deer and elk are presently unknown. Computer modeling suggests that CWD could substantially reduce infected cervid populations by lowering adult survival rates and destabilizing long-term population dynamics.
- Where it occurs, CWD may alter the management of wild deer and elk populations, and it has already begun to do so.
- Ultimately, public and agency concerns and perceptions about human health risks associated with all TSE’s may erode hunters confidence and their willingness to hunt in areas where CWD occurs.
What Preventive Measures Should Hunters Take?
Do not shoot, handle or consume an elk or deer that is acting abnormally or appears to be sick. When field-dressing game, wear rubber gloves and minimize the use of a bone saw to cut through the brain or spinal cord (backbone). Bone out the meat. Minimize contact with and do not consume brain or spinal cord tissues, eyes, spleen, or lymph nodes. Always wash hands thoroughly after dressing and processing game meat. (More)
Practical CWD Video for hunters who want to learn and see more is available online.
Is the Meat Safe to Eat?
Hunters are recommended to not eat meat from animals known to be infected with CWD. Hunters in CWD areas are also advised to bone out their meat and to not consume those parts where prions likely accumulate.
In the absence of complete information on risk, and in light of similarities of animal and human TSEs, public health officials and wildlife management professionals recommend that hunters harvesting deer and elk in the endemic area, as well as meat processors and taxidermists handling cervid carcasses, should take some common sense measures to avoid exposure to the CWD agent and to other known zoonotic pathogens.
Where Can I Learn More About CWD?
Additional information is available on this website, including a number of links to other websites providing credible information about CWD. The links to state wildlife agencies provide considerable in-depth information regarding the status of CWD in those states.