March 01, 2017Currently, there is no treatment for CWD, and no sure way of diagnosing it based on appearance or observable behavior in live animals during early stages of infection. And, there seems to be little agreement among the experts as how to control the disease. Or, for that matter, if it can be controlled at all.
As noted by University of Wyoming researchers, led by David Edmunds, most CWD studies to date have dealt with recently infected deer populations. Few have investigated the long-term effects of the disease where the problem has persisted for lengthy periods of time.
Available evidence suggests that CWD can cause population declines, and possibly even localized extinction, in some species. However, this has not been definitely proven.
Therefore, although CWD may have relatively minor effects on deer population dynamics early in a disease epidemic, there is concern that it might have serious negative effects on deer population trends years or even decades later once the disease becomes well-established.
CWD is like no other deer disease. It is relatively new, poorly understood, and always fatal in white-tailed deer, mule deer, elk, and moose. To date, it has been found in 21 U.S. states and two Canadian provinces.
Technically, CWD is classified as a transmissible spongiform encephalopathy (TSE); a slow degenerative disease of the central nervous system that literally eats holes in the victims' brains. In time, animals that contract the disease become emaciated, behave abnormally and salivate profusely. Once these symptoms appear, most animals die within a couple of months.
Prions, which are mutant, self-propagating versions of proteins that occur normally in the body, are the disease-causing agent. They are essentially indestructible and can lie dormant in the environment for years and still be infective.
Available evidence suggests the disease is most often spread between adult animal and adult animal through contamination of feed and water sources with infectious saliva, urine or feces. Typically, bucks have been found to have higher infection rates than does and CWD-infection rate increases in both sexes with deer age.
Given the dearth of well-studied population-level effects of CWD, the Wyoming investigators view the entire issue as being "worrisome."
"Confounding the issue," they say, "is the temptation of, and pressure on, managers to react to newly discovered diseases (such as CWD) in ways that may not he optimal."
Since CWD has potential to cause population declines, or even localized extinctions at high prevalence rates, Edmunds and his coworkers conducted a lengthy study (2003-2010) to determine if such is actually the case with white-tailed deer.
Their objective was to monitor CWD-positive and CWD-negatives whitetails in a high-prevalence CWD area throughout their lifespan using telemetry and global positioning system (GPS) collars.
Specifically, their goal was to evaluate differences in such things as behavior, reproduction, survival, mortality factors, etc., and ultimately determine if CWD had a negative impact on deer population performance. They theorized that deer population dynamics might be altered by CWD to the extent that the population growth rate would decline.
The study was conducted primarily on one ranch and surrounding areas near Glenrock, Wyoming. Based on examination of hunter-killed deer, about 33 percent of the deer in the general area had CWD.
Using live traps and helicopter net-gunning, the investigators captured 112 deer as fawns and 63 deer as adults. All deer were fitted with tracking collars and recaptured annually (which in itself must have been a daunting task).
All animals handled during the study period (January 2003-February 2010) were examined for CWD using a tonsil biopsy technique and general body condition. Blood samples were used for pregnancy testing in does and observational data were used to determine fawn-rearing success. A complete examination of all dead deer was made to determine cause of death and all were subjected to a thorough CWD examination.
While this investigation confirmed certain findings from previous CWD studies, other findings concerning aspects of behavior and resultant effects on deer population dynamics differ. Findings from the Wyoming study also indicate that changes in management are probably necessary in order stabilize CWD-infected deer populations at socially acceptable levels.
Overall CWD prevalence during the study was 35.4 percent, being higher in does (42 percent) than bucks (28.8 percent). Of the 118 deer mortalities documented during the study, hunter harvest was the most common cause of death (46 deer) and, as expected, bucks were more heavily harvested than does. Mortality due to predation was rare.
This study left little doubt, however, that CWD can account for declining deer population trends. The CWD-positive deer were 4.5 times more likely to die annually than CWD-negative deer. According to the Wyoming researchers, "It is likely that CWD and hunter harvest, the main causes of mortality, have produced young age structure observed in this population."
In their view, provided there is no immigration or genetic selection for less CWD susceptible genotypes, "this population is not sustainable with possible extinction in 48 years at current levels of mortality and fecundity."
The researchers note that their findings are particularly concerning, in that the study species was white-tailed deer, which have a higher lifetime reproductive potential than other species that are susceptible to the disease.
More bucks than does (76 percent versus 24 percent) occurred in the annual hunter-harvest, which probably explains why more females than males (71 percent versus 24 percent) died from CWD. That is, females just simply lived longer (137.2 days), compared to males (107.4 days), after testing positive for CWD.
The researchers also suggest that the matriarchal social structure of females may explain the higher incidence of CWD in females. They theorize the following:
"Males were removed earlier in disease progression and had less time to spread disease directly to susceptible bucks in their bachelor herds throughout most of the year. Meanwhile females progressed to clinical CWD, presumably shedding infectious prions into the environment and transmitting prions directly to susceptible females in their familial groups early in infection and throughout most of the year…prolonged prion shedding by CWD-positive does within their home range, including favored bedding locations, accompanied by communal grooming and shared home ranges with females provided opportunity for disease transmission through time."
Clearly, these findings of higher CWD incidence in does than bucks contradict other studies that found just the opposite sex differences. The authors of this report also suggest, "This discrepancy may be a function of the riparian habitat concentrating white-tailed deer and thus environmental contamination and allowing the proposed role of does in the transmission of CWD in our study system."
Most importantly, they raise the following question: What will happen when CWD becomes more established in northern areas where deer commonly migrate long distances and concentrate at high densities in preferred conifer wintering areas?
"In other words," they say, "perhaps our study population is an indicator of things to come, where initially bucks experience higher incidence until a threshold is met when does experience higher CWD incidence."
Nonetheless, they acknowledge bucks may always experience higher incidence than females where deer range widely and populations are well dispersed.
From the hunter's standpoint, I find this study particularly interesting because the findings suggest that CWD-positive deer behave differently than CWD-negative deer, even in the early stages of disease development when other physical differences are indiscernible. For example, CWD-positive whitetails were over-represented in the annual hunter harvest, logically because they were behaviorally more vulnerable to hunting.
Other investigators found that CWD-positive mule deer were also more vulnerable to hunter harvest, as compared to disease-free individuals. They suggested that behavioral shifts, including movement patterns, changes in breeding behavior during harvest, decreased reaction time to stimuli and changes in habitat type used by diseased animals may have made them more vulnerable to hunters.
There certainly is no evidence that hunters purposely harvest emaciated or sick animals. So, one must wonder if these same diseased deer also then become easier prey for natural predators, even during the very early stages of disease development.
Conversely, studies conducted in Wisconsin, found no such difference in harvest susceptibility, possibly because CWD prevalence was much lower (6.3 percent) as compared to that in the Wyoming study (33 percent).
Edmunds' group emphasizes the following:
"Rather than thinking of CWD as a strictly pre-clinical disease followed by a short, obvious clinical stage of disease, we believe CWD infection should be envisioned as a slow, progressive decline in health and alteration of normal behavior, which ends with the clinically recognizable disease. Given the relatively short clinical stage of CWD and the limited hunting season, it is hard to believe CWD-positive deer would be more susceptible to harvest if this slow alteration in health and behavior - does not occur."
As with previous studies, the Wyoming study found no significant negative impact of CWD on doe pregnancy rates or resultant annual recruitment. This strongly suggests that does participate in the rut regardless of CWD infection-status. Also, observations indicate that does in the early stages of CWD development give birth to fawns an can successfully raise them to weaning age.
Nonetheless, given that CWD infection tends to alter deer behavior to the extent that infected deer become abnormally vulnerable to hunter-harvest, one must wonder if diseased does exhibit certain maternal care weaknesses that jeopardize newborn fawn survival.
For example, there is good evidence that malnourished does are more likely to abandon their fawns or do not protect them from predators. In fact, the Wyoming researchers propose that future research concerning the impact of CWD upon doe fawn-rearing success is "warranted."
Few areas have attained whitetail CWD prevalence as high as noted here, due to the relatively short time the disease has been present in most areas. However, this study shows what can, and likely will, happen in the future when CWD becomes well-established; deer populations with high CWD prevalence and high deer hunting mortality will likely be driven to extinction in relatively few decades.
Also, one of the statistical models employed in this study suggests removing additive hunting mortality in female deer will sustain the population. Therefore, if the management objective is to maintain deer population numbers in the face of high CWD prevalence, then it seems rather obvious that hunting of does must be limited or stopped altogether.
As noted by Edmunds and his group, "this study highlights and stresses the importance of preventing CWD from becoming endemic in a population, rather than attempting to manage it after the fact."
Therefore, as determined from previous research, the best strategy remains minimizing dispersal of CWD infected deer to new areas --
a real challenge for managers, given our current understanding (or lack thereof) of what motivates long-distance deer movements.