I took out the highlights of the 19 pages. For you that don't have time to read it all.
"Highlights" of Dr. Kroll's "white paper"
Grear, et al. (2006) examined demographic patterns and harvest vulnerability of CWD infected deer in Wisconsin. They concluded: “We found no difference in harvest rates between CWD infected and non- infected deer. Our results show that the probability of infection increased with age and that adult
males were more likely to be infected than adult females.
These studies tend to support my opinion there is no evidence CWD has an impact on the population dynamics of whitetails or mule deer.
CWD infection rates for U.S. testing to date (USDA/APHIS) total 164,500 captive deer and elk and 775,000 free-ranging deer and elk, with only 171 captive (1/1000) and 3,130 (4/1,000) free-ranging animals testing positive.
In spite of the heavy harvest and presence of the disease, the deer herd actually grew during eradication efforts, significantly exceeding population goals for the zone.
In a white paper by Dr. Don Davis, Wildlife Disease Scientist at Texas A&M University College of Veterinary Medicine, noted although CWD has been found in 20 (40%) of the 50 states (USDA/APHIS records), “This is somewhat misleading because there are about 3,500 counties in the US and CWD has been found in about 175 of them or in 5%. Five % is a closer figure to the actual occurrence and distribution of CWD.” I concur with Dr. Davis’ finding.
Although it may be possible to artificially induce limited SE response, I must conclude there is no evidence to date of likely CWD transmission from deer to livestock.
Anderson et al. (2007) found no convincing cases of CWD transmission to humans.
“Surveillance continues to show an annual CJD incidence rate of about 1 case per 1,000,000 persons
Therefore, it is my opinion CWD does not pose a threat to human health.
Purdey (2000), which suggests a nutritional deficiency involving copper and manganese may be one factor, supporting the “spontaneous” appearance in some areas such as New Mexico.
Hence, as with sheep it appears to be possible to identify resistant and susceptible deer through genetic analysis.
showed that rectal biopsy sample testing was an effective method in detecting subclinical CWD infection.” Most critical of these findings and report was the recommendation that, “...rectal biopsy sample testing was an effective method in detecting subclinical CWD infection.”
My finding is that the rectal mucosa biopsy, when done in conjunction with genetic testing is a viable alternative to postmortem brain stem, retropharyngeal lymph node and palatine tonsil IHC testing, and could be used to reduce the spread of the disease.
Yet, it is my opinion finding a positive animal in these translocation projects is tantamount to the “horse out of the barn.” The question arises: Should not the regulations for translocation be applied equally for public and private movement of animals? The Missouri state web site claimed in 2010: “Since 2000, there has been significant progress made in our understanding of chronic wasting disease (CWD), including a live-animal test for elk. Our extensive animal health protocols include testing all elk for chronic wasting disease.”
It is my opinion, results from rectal mucosa biopsy tests, plus the acceptance by a state agency (Missouri) of this test prior to relocating Rocky Mountain elk, validates the use of these procedures for private deer/elk breeding operations; especially when combined with genetic testing.
It generally is considered that CWD prions are difficult to remove from a site where infected deer have existed. Although this is considered as fact, methodologies for detecting CWD contamination has not be developed (Saunders et al. 2008). At this time, it is possible CWD prions can remain infective for at least two years.
Urine-feces in daily oral doses for 90 days, recipient deer remained PrPCWD – negative throughout 19 month period.
Hence, it is my professional opinion, an 8 feet tall, netwire fence, with a 3-wire outrigger on each side would reduce nose to nose contact between deer at a reliable level.
In fact, it is my opinion (and that of most deer biologists) whitetail populations have exceeded carrying capacity in most of the areas where they reside, and may be declining in some areas. We already are seeing significant habitat degradation, disease and economic and human health impacts (accidents, Lyme disease, agricultural damage, landscape damage, etc.) from this species. At the same time, deer are the most popular and economically important game species in the US, if not the world; fostering concerns both by sportsmen and game agencies when populations appear to be threatened. Deer not only generate significant incomes and value-added products to the private sector, but deer hunting licenses, fines and fees provide a great deal of financial support to game agencies. At the same time, the deer farming industry has grown exponentially over the last two decades, and now ranks high in agricultural commodities. In Texas, deer farming and ranching now ranks as a top 10 agricultural commodity. So, it is understandable when a disease such as CWD seems to appear from “no where,” alarms are sounded!
although millions of dollars have been spent on research and “control” of CWD, scientists only recently have considered the potential for genetic resistance within the genome of deer and elk. Yet, genetic resistance has been used to advantage by the sheep industry to produce scrapie resistant herds. Scientists at the University of Wisconsin-Madison and Stevens Point have suggested in the long-term deer may make genetic shifts to deal with the disease, and I am in agreement.
After 10 years of dealing with CWD issues, my experiences in Wisconsin, and after my review of knowledge relating to this white paper, I feel concerns for devastating impacts of CWD on the nation’s deer herds needs to be revisited! Understanding the biology of white-tailed deer as I do, and combining this knowledge with that discussed in this report, I must conclude the long-term impact of CWD will not be significant declines in deer populations. I must question the rationale behind CWD as a serious reportable disease. As noted in this report, studies support:
CWD has not been demonstrated to have significant impacts on deer population dynamics.
CWD has not been demonstrated to have a significant human health concern.
CWD has not be demonstrated to affect other species, particularly livestock.
I did not come to these opinions lightly. These are strong statements and I make them after a great deal of thought. However, I am not alone in my skepticism. The white-paper (“What we know about CWD that isn’t so?” 2013) by my respected colleague, Dr. Don Davis (Texas A&M University Veterinary College) clearly states:
“It is often stated that CWD is a threat to the natural resource, and ‘is a devastating disease to wild populations’. This belief again is not supported either by scientific data or empirical observations through time. The USDA/APHIS data based on a huge sample collected over 10 years indicates that CWD occurs at a very low prevalence. The loss of 10-40 animals per one million animals due to CWD is not significant in wild populations when those populations number in the 100,000s or in the 1,000,000s. Therefore clearly CWD is neither an epidemic nor is it population limiting. Losses at that a level of 1-4 per 1000 are hardly ‘devastating’. Populations of game animal species such as deer and elk are routinely harvested by hunters at a level of 10% to 25% without deleterious effects on those populations. A disease such as CWD with a prevalence rate of 0.1 to 0.4% will not have a significant effect on those populations. These levels of morality loses, even if the losses are additive instead of compensatory, will be insignificant. Despite some reports of population losses due to CWD in isolated or local instances, there is no supporting scientific data to either support these speculative hypotheses or rule out other possible causes for the population decrease such as drought, other diseases, or loss of suitable habitat.
Another popular misconception about CWD is that it is highly contagious.
CWD is a chronic disease (hence the name) and not an acute disease. CWD can have an incubation period of many years, it can be transmitted from one individual to another but not often or easily. If indeed, CWD is a contagious disease then why does it exist with a very low prevalence rate and rare occurrence? If CWD is a contagious disease then why with a history of more than 45 years in North Eastern Colorado has CWD not completely eliminated populations of elk and deer in that area? If CWD is easily and often transmitted, why is the disease only found in 1-4 animals per 1000? The answer is obvious. Many of the widespread and accepted ‘facts’ about the prevalence of CWD and the host distribution of CWD are erroneous, illogical, and untrue.
It is notable that Dr. Beth Williams stated that CWD ‘is more correctly perceived and classified as a special type of toxicity’ than as an infectious disease.”
I stand firmly in support of Dr. Davis’ conclusions, and have arrived at the exact same positions independently. In a 2001 TV program (Journal of the Texas Trophy Hunters) on the Outdoor Channel I correctly predicted the outcome of the ill-conceived, yet well-meaning, “eradication” program in Wisconsin. Ten years later, my predictions were mostly validated.
These are my professional opinions, given with a great deal of thought and review of current information. Knowledge never is perfect or complete, but decisions have to be made based on the best available science.
