Mineral blocks, grain piles, watering holes and other features which concentrate wild deer and increase their risk of contacting saliva and other secretions, and ingesting soil containing prions, may be very important in transmitting CWD.
 
It has been over ten years since chronic wasting disease (CWD) was first detected in wild deer in Saskatchewan and over twenty years
since it was introduced into Saskatchewan game farms by infected elk from the United States. Initial attempts to eradicate or control the disease in the wild through herd reduction failed and the reasons for this failure are numerous: lack of knowledge of the true geographic extent of the disease, poor understanding of how CWD is transmitted and spread, lack of longterm support for programs, and lack of a coordinated response between agriculture and wildlife interests, to name a few. Attempts to manage CWD in the United States have, for the most part, met a similar fate and the disease is now found in 15 states and two provinces in North America. CWD has also been introduced to South Korea by exportation of infected elk from Saskatchewan. Although CWD management programs have been curtailed, most wildlife agencies have maintained surveillance programs to track the change in prevalence (number infected/ population size) over time and to monitor spread of the disease across North America. As expected, the disease has spread into Alberta and continues to spread unimpeded across large tracts of North America. These CWD surveillance programs rely on hunters voluntarily submitting elk, deer and moose heads for testing but, based on steadily declining participation in these programs, interest or concern about this disease is on the decline. Maintaining interest in these long term programs is difficult especially when there is no obvious reduction in deer numbers, the risk to humans is not known with certainty but appears to be very low, and the risk to domestic animals and impact on the economy is also unknown. A common public sentiment is that this disease has been around forever and scientists are making a large fuss over nothing; evidence and logic suggest otherwise. In the following article I will discuss research findings which show CWD will likely have longterm implications for deer populations, and for the ecosystems they support.


What are the long-term implications of
chronic wasting disease for wild deer
populations and their ecosystems?

Following the “mad cow disease” or BSE crisis and the detection of CWD in Canada there was a large investment in research on prion diseases through agencies such as PrioNet Canada (www.prionetcanada.ca) and the Alberta Prion Research Institute (www.prioninstitute.ca). Similar investments have occurred in the United States, Europe and elsewhere and this has revealed much about these enigmatic diseases. Research continues to show these diseases are caused by an infectious protein called a Sc prion or PrP for short. We know that BSE is transmitted to other animals by feeding tissues from infected animals to other susceptible animals, which include: cattle, sheep, cats, humans and several other species. CWD and another prion disease called scrapie are different, however. Chronic wasting disease, which infects mule deer, whitetailed deer, elk and moose, and scrapie, its counterpart in sheep and goats, are readily transmitted from animal-to-animal and from soils or environments contaminated with prions shed by infected animals. In other words, CWD and scrapie are contagious diseases. Prions are shed in urine, saliva, feces and blood of infected deer andare shed months before animals begin to show signs of disease. This means deer can transmit CWD for long periods prior to their death. The reason we don't see a rapid increase in deaths is because it is a slowly developing disease with infected deer taking a year and half or more to die, but once infected, none recover. The genetic make-up of the deer can determine how readily they become infected, and how long it takes for them to die, but no individual appears to be resistant.

Research has also revealed the importance of the environment and in particular soil in transmission of CWD. Prions shed from infected live animals and from decomposing carcasses can persist in soils for years and in some cases over a decade. Prions bound to certain clays are held close to the surface of the soil making them available to other deer and these bound prions are actually more infectious than unbound forms. For example, prions bound to montmorillonite clay are reportedly 680 times more infectious than unbound prions. In Colorado mule deer which inhabited regions of high clay content soils were more likely to be infected with CWD. A 1% increase in clay-sized particles increased the odds of infection by ~ 9%. Soil type may help explain the current distribution and prevalence of CWD and will be important in attempts to manage the disease.

It is likely we will never know the origin of CWD with certainty. First detected in Colorado and Wyoming in the late 1960s, it is thought to be either the result of scrapie transmission from sheep to deer, transmission of a yet to be recognized prion disease in an unknown host to deer, or spontaneous conversion of normal deer prions to the disease form and then subsequent transmission. The observation that scrapie, when inoculated into white-tailed deer, produces a disease similar to CWD lends support to the first hypothesis. Natural transmission of CWD to sheep, or alternatively scrapie to deer, has yet to be demonstrated, but if shown to occur, this will further complicate strategies to manage these diseases.


Chronic wasting disease infected mule deer on the left and similar aged uninfected
deer on the right. Infected deer gradually become emaciated and die, if
not removed by predators. This infected deer died of CWD several months later.
The radio-collar and ear tag allow us to monitor its movement and its contact
with other deer over time.

Fortunately there is little evidence to suggest CWD is transmissible to humans, but since there is still uncertainty, research is continuing in this area. Since prions can change once they infect a new host species, infection of humans and other domestic animals could potentially take a circuitous route. Humankind's centuries old relationship with sheep scrapie, without evidence of transmission to humans, suggests these risks are small, if they exist at all.

So why should we be concerned about chronic wasting disease? Research predicts the most significant effect of CWD will be on deer populations and on ecosystems in which deer, and other CWD susceptible cervids, play a critical role. These effects are projected to take decades to become apparent and, because this is a relatively new disease, projections are primarily based on mathematical models. Only recently, in localized areas, are we beginning to see glimpses of what the future may hold. In Colorado there are populations of mule deer where the prevalence is over 25% and is thought to be a contributing factor in observed population decline. In one of our study areas in southern Saskatchewan we are beginning to reach similar levels of infection and CWD is currently the leading cause of mortality in adult deer. Most models predict population declines and, in some cases, local extinction. However, in reality the outcome is likely to be highly variable and dependent on soil types, predation rates and the behaviour and social structure of deer in a particular area. An important factor in these models is increasing levels of prions in the environment as infection rates increase in the population which results in higher infection pressure, shorter incubation periods and younger animals dying of CWD. Human alteration of habitat causing localized increases in deer numbers and focal points of deer concentration are also likely important.Understanding the relative importance of these various factors influencing the transmission of CWD in order to improve these models is an active area of research in Saskatchewan and elsewhere.

As most people know deer are highly mobile. Researchers have quantified these movements by estimating home range sizes, migration rates and rates of dispersal for various species of deer in various habitats. Our research has shown that mule deer in southern Saskatchewan have high rates of migration and dispersal, and dispersal tends to be oriented along river valleys. These findings help to explain the observed geographic spread of CWD and why initial herd reduction programs with boundaries of up to ten kilometers from CWD positive deer would have been ineffective in controlling disease spread, as would even Wildlife Management Zones in some cases. Some would argue high rates of dispersal means areas depleted of deer due to CWD will be rapidly repopulated by healthy deer; however, persistence of high levels of CWD prions in the environment means newly arriving deer are at risk of becoming infected.

Map showing migratory movements of radio-collared mule deer in southern Saskatchewan.
The dashed horizontal line, with the hump, running across the centre of the map
is the Wildlife Management Zone boundary which was used at one point to mark the
perimeter of a CWD herd reduction zone to the south. Clearly a significant number of
deer move across this boundary.



Map showing dispersal movements of radio-collared mule deer. Note how
many of the dispersal movements follow river valleys.


The proportion of different age and sex classes of deer are likely to change in CWD infected populations. Because of longincubation periods, animals die while in their prime of reproduction and mature males are typically over twice as likely to become infected and die of disease than are females. High rates of disease will have effects on predator and scavenger species. Our studies in southern Saskatchewan have shown coyote predation is a significant cause of fawn deaths. If coyote numbers increase due to the increased availability of carcasses from deer dying of CWD (deaths due to CWD typically occur in the winter when food for coyotes is scarce), predation of fawns by coyotes may also increase. However, on the positive side, predators may play a role in reducing levels of CWD. Studies in Colorado have shown cougars and wolves preferentially killed CWD infected deer and elk and the removal of sick deer and elk may help in limiting disease in areas where sufficient numbers of these predators exist. The role coyotes may play in the control of CWD is unknown.

In regards to the question of crisis or hysteria, the answer is likely somewhere in between. Clearly, predicting the implications of CWD on deer populations and ecosystems is complex. The fact that CWD is an emerging disease with potential long-term deleterious effects strongly argues for continued research to estimate its impact and for development of management programs to minimize its effect. Failure to do so will result in reactive, rather than proactive, responses. Naturalists and hunters that value this resource are critical to this effort. They must speak out in support of these programs and demonstrate their support through actions by making the effort to submit heads for CWD surveillance and, when possible, supporting ongoing CWD research programs.



Author: Dr. Trent Bollinger. Trent is an Associate
Professor and Director of the Canadian
Cooperative Wildlife Health Centre specializing
in Veterinary Pathology. We at the WCGW
are happy to have Dr. Bollinger as a regular
contributor to our staff.


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