Almost a year ago, January 25, 2018, in Issaquena County, Mississippi, a 4.5 year old male, white-tailed deer tested positive for chronic wasting disease (CWD). This is the first time an animal in Mississippi has tested positive for the disease, which is fatal to white-tailed deer. The disease has since been found in Pontotoc and Marshall counties. This article, the first in a four-part series, will give you a closer look at CWD. It will touch on the various challenges posed by this disease and begin to update you about the status of CWD and what we know about it.
CWD is an infectious prion disease that occurs in at least five cervid species. Cervids are hoofed mammals in the deer family. The native North American cervid species in which CWD has been found are the white-tailed deer, mule deer, Rocky Mountain elk, moose, and caribou. CWD belongs to a group of diseases known as transmissible spongiform encephalopathies (TSEs). Mad cow disease, although distinctly different from CWD, is also a TSE. CWD causes a characteristic spongy degeneration of the brain resulting in loss of appetite, loss of weight, an insatiable thirst, abnormal behavior, loss of body functions, and death. Deer infected with CWD tend to stay away from herds, walk in patterns, carry their head low, salivate, and grind their teeth. Despite its likely occurrence in multiple locations since the 1960s or earlier, many wildlife and animal health professionals, as well as the public, perceive CWD as having emerged and spread rapidly only since the early 2000s. This perception has fostered the broader notion that the disease is a recent occurrence. To the contrary, given imperfect surveillance approaches, incomplete or inaccurate knowledge about local exposure risks, and the progression of an outbreak in its early stages, the first case detected in a locale is rarely the first case that has occurred.
CWD history remains incompletely documented; it was first recognized in captive mule deer held for research in Colorado in the 1960s. CWD has been reported in captive and/or free-ranging deer in 26 U.S. states, 3 Canadian provinces, South Korea, and Norway. Natural and human controlled factors have contributed to the geographic spread and persistence of CWD. Natural factors include CWD prions’ environmental persistence and the movement of wild deer. Human factors include movement of infected live animals (and perhaps infectious tissues and other materials), concentration of normally dispersed wild deer, and other artificial management practices.
Many facets of CWD biology and ecology are now well understood, but effective management and control strategies remain incomplete. Eradicating CWD will not be easily done. Regardless, flexible and responsive approaches for containing it and reducing infection and transmission rates have shown some promise. Such pursuits undoubtedly will be more difficult to obtain support for, particularly when disease control measures will negatively impact or conflict with commercial hunting.
Moving forward, this wildlife disease merits great attention. Collective experiences and observations made over the last 5 decades can serve—for better or worse—as a solid foundation for wildlife and animal health professionals to build upon in addressing anticipated challenges posed by CWD in the decades to come.
In the next three columns, I will present an overview of what professionals regard as the key lessons learned over the first 5 or more decades of North America’s experience with CWD.
This column, the second of a four-part series, will give readers a closer look at CWD. In this column, we will discuss “Detecting CWD.”
Detecting CWD in captive and wild settings is difficult. Most states and provinces have, at least for a time since the early 2000s, engaged in extensive, if not intensive, surveillance to identify affected wild herds. Although these efforts were well-intentioned, many were too flawed or too short-lived to reliably indicate the absence of disease. I will briefly review common shortcomings of CWD surveillance, as widely practiced, to provide a basis for improving the efficiency and effectiveness of future efforts.
There is no known, practical, “live animal test.” The only known and conclusive diagnosis involves a test or examination of the brain, lymph nodes, or tonsils after death of the animal. Preferred approaches for detecting CWD in new locations (termed “surveillance” here) differ from approaches for following epidemic trends over time in affected populations (“monitoring”). It is important that CWD surveillance of wild deer be an ongoing activity in areas where it has not been detected previously. Monitoring may be more intermittent (e.g., at multi-year intervals) when resources are limited because infection rates in wild herds tend to change slowly.
Regardless of the purpose, CWD surveillance and monitoring should be undertaken at a meaningful scale, and any conclusions should reflect the highly patchy distribution of CWD in wild cervids. CWD distribution in the wild typically is highly uneven within an affected population, and the target population itself often is distributed unevenly across the area being assessed. In our experience, statements indicating that examination of a few hundred (or even a few thousand) harvested animals has proven a state’s freedom from CWD rarely are supported by the data.
In areas where CWD is regularly found, it has been demonstrated that animals falling into certain categories are more likely to test positive. These animals may have clinical signs of CWD, such as emaciation and abnormal behavior, may have been killed by a vehicle or predator, or may be older-age, male deer. Consequently, it may be more cost-effective to concentrate testing on animals with a higher probability of infection when surveillance is conducted to detect CWD in new locations than testing large numbers of apparently healthy, hunter-harvested animals. The effectiveness of this type of surveillance assumes relatively even sampling effort over a geographic area, but it does have limitations. For example, clinical disease may not be observed in remote areas, vehicle-killed animals do not occur in roadless areas, and animals killed by predators may be consumed before sampling can occur.
For monitoring, random sampling (e.g., from harvested animals) provides relatively unbiased estimates of infection rates. Comparisons over time or between locations should be based on a common denominator (e.g., harvested males aged 2 years or older) to assure that conclusions are reliable. Even though affected areas emerge and grow slowly, infection rates may be remarkably high on first detection when jurisdictions rely on random sampling and have not tested adequate numbers of animals at a particular location.
In the next column, I will discuss how CWD spreads.
This column, the third of a four-part series, will give readers a closer look at CWD. In this column, we will discuss “How CWD Spreads.”
The widely held belief that all CWD occurrences can be traced back to a single Colorado research facility prevents wildlife and animal health professionals from considering that some outbreaks may be arising from unrecognized exposure events that occur repeatedly over time.
In fact, natural and human-facilitated factors have contributed to the geographic spread and persistence of CWD over the last 5 decades. Regardless of the origin, much of the spread of CWD appears attributable to natural movements of wild deer. For example, Wyoming has only one private game farm, and consequently commercial enterprise is unlikely to have driven the widespread distribution there. Alternatively, the role of commercial elk operations in CWD outbreaks in captive herds in Saskatchewan and South Korea was well documented, with inadvertent spillover apparently giving rise to a large, freeranging focus spanning the Saskatchewan-Alberta border. In Colorado, a combination of natural and human-facilitated factors likely contributed in different measures to separate outbreaks.
Natural factors contributing to persistence and geographic spread include prolonged incubation of the disease, multiple routes of CWD prion disease shedding, its environmental persistence, and the movements of free-ranging deer. Infected deer likely shed prions in feces, urine, and saliva for most of the disease course, thus allowing for ample opportunities for transmission to other deer. Migration movements also have the potential for contributing to longer distance jumps in distribution. Because CWD can bind to soil and plants, it can remain in the environment for an extended time. Therefore, transmission can occur on overlapping ranges even in the absence of direct interactions between infected and uninfected animals. Indirect transmission also increases the likelihood of interspecies transmission.
The primary human-facilitated factor identified in the spread of CWD is movement of live animals, and to date, this is the only confirmed contributing activity linked to CWD’s spread between distant locations. These animal movements typically are associated with other highly artificial wildlife management activities, such as captive wildlife propagation and high-fenced shooting enclosures. Moving free-ranging deer from an infected source would also present a similar risk for spreading CWD. Local wildlife may be exposed to CWD if infected captive animals escape, or if free-ranging deer are exposed to infected captive animals or contaminated environments. Fence-line contact offers another opportunity for direct transmission. Note that these transmission opportunities are a two-way street (i.e., CWD can move in either direction between captive and wild deer). Other possible modes for human-facilitated spread of CWD include transport of infected carcasses, products manufactured or contaminated with prion-laden deer or elk urine, saliva, or feces, or possibly the movement of hay or grain crops contaminated with the CWD agent.
In addition, other human activities can substantially increase the likelihood of establishing, maintaining, and spreading CWD and other diseases in free-ranging wildlife. In particular, artificial management activities, such as wildlife baiting and feeding or other practices that congregate normally dispersed wild animals enhance transmission opportunities.
This column, the last of a four-part series, will give readers a closer look at CWD. In this column, we will discuss “How CWD Spreads.”
Eradicating CWD doesn’t seem feasible given its extensive distribution and other attributes as well as the limited number of tools. With few exceptions, CWD in free-ranging deer has persisted in affected areas in the face of widely varied control attempts.
In recent years, evidence from some control attempts suggests that combinations of intensive deer removal around case clusters, as well as more sustained reduction of the affected population, may offer some measure of disease suppression. A sustained, localized culling program underway since 2003 has stabilized occurrence in northern Illinois whitetails as compared to the increasing trends in southern Wisconsin where disease control largely was suspended in 2007. In north-central Colorado, a combination of focal culling and broader, hunter-harvest population reduction (approximately 25 percent) in the early 2000s appears likely to have contributed to reduced prevalence, whereas estimated occurrence in other Colorado mule deer herds has increased since 2002.
In addition to adopting approaches for stabilizing or suppressing CWD outbreaks, wildlife managers should consider how recent trends in deer management may be contributing to disease establishment. Harvest-based control of CWD may be most effective when focused on male deer, perhaps because infection rates among adult male deer tend to be higher than among adult females. On the other hand, harvest strategies intended to increase the percentage of male deer or the percentage of older class males, could inadvertently facilitate CWD persistence. This may explain why the dramatic increases in occurrence observed since 2002 in Colorado in several affected mule deer herds coincide with changes in harvest strategies intended to reduce buck harvest and increase buck to doe ratios over the same period. Given the potential for unintended consequences, we should be thinking through how this and other harvest management strategies (e.g., season timing, baiting, and/or feeding, “quality deer management”) may be affecting CWD dynamics.
Control efforts undoubtedly will be difficult to obtain support for, particularly when disease control measures will negatively impact or conflict with commercial deer enclosures and/or hunting by the public. The human dimensions of managing wildlife diseases present a substantial challenge for those determining the management objectives and actions. For example, surveys of hunters and landowners in Wisconsin identified several factors that contributed to hunter opposition to the state’s CWD management plan for affected areas including: opposition to deer population goals (initially zero), conflicts with traditions, uncertainty about the likelihood of success, questions about agency credibility, and no sense of urgency.
The lessons learned over the past 5 decades relate to how wildlife and animal health professionals should (and probably should not) approach the control of CWD. In contrast to advances in our understanding of CWD, the science informing effective management and control strategies remains incomplete. However, recent insights and modest strides seem to offer a path forward, and adaptive approaches for containing CWD within limited geographic areas and for reducing infection and transmission rates deserve further attention.
James L. Cummins is executive director of Wildlife Mississippi, a non profit, conservation organization founded to conserve, restore and enhance fish, wildlife and plant resources throughout Mississippi. Their website is
www.wildlifemiss.org. The Southeastern Cooperative Wildlife Disease Study contributed to this article.
