Post by ridge on Oct 11, 2017 16:19:45 GMT -5
Here are some of the take aways from my perspective: CWD Genetic resistance. This topic was covered by several of the research scientists who spoke. To date there is no evidence of any natural immunity to CWD in Cervids and due to the agent involved in the disease (Prion), it's unlikely that natural immunity to CWD in cervids will develop. There is, however, evidence that deer with a certain genetic makeup have some resistance to the disease. What does this mean? It means that deer with a particular genetic makeup tend to be older before first contracting the disease and after being infected tend to last longer before clinical symptoms appear. The particular genetic allele in question occurs at Codon 96 of the deers RNA. There are several variations of the chemical pairing that occurs at that Codon. Deer can be either 96GG, 96GS or 96SS. Deer with the 96GG pairing tend to be more susceptible to becoming infected and have the shortest time between infection and the emergence of clinical symptoms and death. Conversely, 96SS deer tend to have higher natural resistance to infection and tend to live longer after contracting the disease. They are not immune, if a 96SS deer becomes infected, they will die of it, it just takes longer for that to occur.
Why is this natural resistance important? At this point we don't know for sure but it has been demonstrated that that when CWD prevalence rates reach a certain level (more on this later), it could trigger population declines. If that is the case, then a herd that is composed primarily of deer with the 96SS genetics may be at less risk for population decline and may be better equipped to continue to provide a huntable population. There are some other points, though, that further complicate this hypothesis. 96SS deer make up a small minority of the deer in the herd. It varies somewhat from state to state but generally these deer make up less than 20% of the herd. It was pointed out that from a genetic standpoint, that indicates that these deer are less genetically fit than 96GG deer, which make up the vast majority of the herd. There is very likely a reason, unrelated to CWD resistance, that natural selection has resulted in 96SS deer making up such a small portion of the herd and it's very possible that other less desirable traits that also result from that particular genetic variation could prevent 96SS deer from being the potential solution to the growing impact that CWD could have on the herd in the future.
At this point, there is still a ton of research that needs to be done, further investigating the different genetic variables which may have an impact on resistance to CWD. Assay Technology Some of the most interesting information provided had to do with advances that have been made in the testing methodology and techniques used to identify whether deer are CWD positive. For some time, the "gold standard" test has been Immunohistochemistry or IHC test. Recent advances have developed two new types of test that use amplified samples to allow for identifying the positive presence of CWD in tissue at much more sensitive levels. One of these tests, referred to as RT-quic may have as much as a 30% higher rate of sensitivity than the standard IHC test. While this means that testing may be much more accurate in the future, which will allow us to identify the presence of the disease at much younger ages and in lower concentrations, it also raises the specter that it's very possible that many animals that had previously tested negative with the standard IHC test, were in fact possible for CWD and that it simply went undetected due to the sensitivity of the IHC test. The new assay methods are still largely used in research settings and it will take awhile before they become the standardized test used by State Game Agencies to test hunter killed deer, which certainly provides some food for thought.
CWD Transmission Blood, saliva, feces and urine all have been demonstrated to have prions in them and are thought to be involved in the direct transmission of CWD. Of those, urine tends to be the least likely to concentrate prions. There was some discussion of urine based scent products and the potential that they may have for causing the long distance transmission of the disease, particularly across state lines. While nobody suggested definitively that there was not any risk involved, the general consensus among the presenters was that the risk is probably pretty low and that there are lot of other potential transmission sources that have much higher levels of risk associated with them. There is some evidence that mothers milk from lactating does contains prions and may be a source of transmission from mothers to offspring. The question was asked as to whether semen may be another method of transmission but none of the presenters were aware of any research that has documented that one way or the other. There was a lot of discussion about indirect or environmental transmission. Environmental transmission probably plays more of a role after CWD has become established for some time in a particular location. When prevalence rates are low and the disease is in the early stages of introduction to an area, most of the transmission probably occurs through direct sharing of bodily fluids. As more deer become infected and the load of Prions being shed increases, environmental transmission becomes a greater avenue for passing the disease to naive animals. It is hypothesized that at some point in an outbreak, environmental transmission will eclipse direct transmission, particularly when populations start to decrease as a result of the disease.
There was discussion about the use of baiting and minerals and the negative impact that their use can have on attempts to limit the spread. It should be made clear that the presenters who talked about that issue did not exempt food plots or agricultural fields as potentially being problematic. They clearly stated that any practice that creates aggregation is potentially a problem. That includes water holes, food plots, gardens, bait piles, orchards, etc. All of them can result in increased levels of both direct contact and environmental contamination, causing increased transmission of the disease to healthy deer. The silly idea that food plots or mineral licks or man made water holes are somehow prophylactic-ally beneficial in attempts to limit the spread of CWD needs to be put to bed, once and for all. Aggregation is a bad thing when it comes to limiting the spread of disease. Period. Anybody that wants to argue that some forms of aggregation are ok, while claiming that others are bad, is making a political statement, which is not supported by any available science and it should be soundly dismissed as such.
Frequency vs. Density dependence: It is becoming increasingly obvious that CWD is primarily a frequency dependent disease. Why is this important? It's important because the management of frequency dependant diseases is substantially different than the management of density dependent diseases. Management efforts that may be effective in limiting the prevalence of a density dependent disease may have little to no beneficial impact in thwarting a frequency dependent disease. So if we are attempting to formulate the most effective management response it's vital that it is appropriate for the specific type of disease that we are dealing with. In the past, much of the management effort employed in trying to limit CWD has been simple population reduction. Reducing the population may have relatively little impact on reducing the transmission of CWD and may in fact cause an increase in localized prevalence rates, due to the dilutive effect of removing a higher proportion of healthy deer from the herd. That is not to say that population reduction is necessarily a bad thing but if there is a finite limit to the level of harvest pressure that can be employed, from a management standpoint it will be more effective to direct that harvest pressure in a manner that reduces the frequency of contact between infected and healthy deer. This type of strategy is one of the reasons that Illinois has been more effective in keeping the disease at a low prevalence, compared to states which simply focused on herd reduction. It is also reflected in the fact that in Michigan and other states, USDA sharpshooters are much more likely to kill infected deer than the random kills made by hunters, due to the fact that sharpshooters are specifically targeting deer identified as being high risk for the disease. This may become even more important if and when the disease reaches the point where population decline starts to occur, then it will become even more imperative to try and remove infected deer, not healthy ones, from the herd. Impact on population There is increasing evidence based on what is occurring in several western states, that there is a tipping point that is reached once female prevalence rates reach a certain point, which will result in increasing population decline. Dr. Michael Samuel suggested that he thinks that some areas of Wisconsin may be reaching that tipping point, as adult female prevalence rates reach 25% and that we may start to see the population in those areas start to decline in the near future. In some areas of Wyoming, which have been endemic for decades, mule deer populations have declined by 2/3rds. While there are other factors contributing to those mule deer population declines, CWD likely is playing a primary role. In those areas prevalence rates in both sexes have passed 40%. Those population declines will continue to accelerate, as prevalence rates increase, causing a waterfall effect, which ultimately may result in localized population eradication. Prion uptake in plants None of the researchers who spoke is directly involved in studies looking at the process that has been identified that showed that some plants may be capable of transferring Prions present in the soil, through uptake, and move them to the leafy portions of the plant. Several of the presenters mentioned current research regarding this process, though, and highlighted the serious potential consequence that this may have on increasing environmental transmission of the disease, particularly in situations where agricultural commodities are transported from inside a current CWD zone to areas where the disease is not present. One presenter offered an example where farmers from the core of the Wisconsin CWD zone sent trailers of hay harvested from within that zone to try and help farmers in Kansas, which was suffering from a severe drought at the time. A well meaning humanitarian act that could have severe, unintended consequences. Both Prion uptake and the potential surface contamination that occurs when deer are defecating and urinating, while feeding on crops, as well as the fact that deer consume a lot of soil when feeding, highlight the potential for environmental transmission, as well as debunk the idea that crops grown in food plots are somehow immune from being a source of environmental transmission for this disease.
Movement Concerns: The movement of the disease across state lines by man is both the likely explanation for how it has spread from the West to a number of Eastern states, as well as one of the most likely avenues for the future expansion of the disease, both inter and intra-state, in the future. Forms of movement that were mentioned as concerns are; Carcass movement Movement of captive Cervids Movement of deer parts & urine Movement of agricultural commodities Translocation of living cervids by wildlife agencies for re-stocking purposes These factors were all discussed as possible means of moving the disease across the landscape. There was a lot of discussion about captive Cervids, including a lot of information about attempts at both the State and Federal level to enroll captive Cervid herds in Certified Herd programs, that require extensive live testing and quarantine periods, before allowing deer to be moved off of the facility, which is hoped to limit the likelihood of an infected deer being moved, potentially spreading the disease. While live testing is not 100% accurate, it was pointed out that these programs require whole herd testing, so even if a live test misses a single positive deer within the herd, the fact that all of the animals are tested makes it likely that CWD will be detected if present in the herd. There is clearly a love/hate relationship between the captive Cervid industry and the hunting community. Some of the researchers who spoke made a compelling point, however, that I had not really given much thought to; as much as we may hate the potential that CC facilities may have for spreading CWD into the wild herd, the fact remains that from a research standpoint, CC facilities provide a highly valuable resource for experimentation, for testing assay procedures, vaccine development, knowledge about transmission and how the disease works, genetic research and maybe ultimately providing the genetic stock for wild deer restocking, should the predicted population declines ultimately occur in the future. I used to be of the mindset that CC facilities should be phased out and shut down but I have changed that opinion. I think that stopping the interstate transfer of captive deer would be a good
idea and that there should be rigorous regulation and enforcement (which is largely not occurring), as well as increased security measures such as mandatory double fencing, electric fences & monitoring, etc. but simply shutting down the industry no longer seems like the best solution to me.
Other movement issues, such as banning the importation of carcasses from other states, banning the use of deer urine, etc. are all worthy of being looked at and have already been adopted by some states. I suspect Michigan will get to that point in the future but that it will take awhile. The current prohibition that Michigan has about only allowing de-boned meat is essentially useless, as multiple researchers pointed out that Prions are present in muscle tissue, so that prohibition is not really accomplishing much, in terms of stopping the importation of CWD.
What other states are doing or have done: The second day of the symposium was a compilation of speakers from a number of state game agencies, as well as speakers from the captive deer farming association and Kip Adams from QDMA. Without going into detail about what each state has or has not done, it became clear what some of the mistakes that had been made in the approach that some states have taken were and also what some of the more successful approaches taken by other states have been. There are two different focal points in the management of CWD, spread and prevalence. These are distinctly different aspects and some management techniques may be effective at limiting one but not both of these factors. The consensus is that Illinois and Missouri have been effective in limiting prevalence rates to single digits, primarily through the use of targeted culling
by sharpshooters. At the other end of the spectrum, Wisconsin and Wyoming are seeing increasing prevalence rates and are at the point now where those rates are unlikely to ever come down in the future, due to environmental contamination playing an increasing role in exposing uninfected deer to the disease. Wisconsin has tried a variety of things since 2002, when the disease was first discovered and none of them have worked very well. In fairness, the disease had probably been in place in Wisconsin for 20+ years before being identified and was so endemic at that point that there was no chance that the early methods used to try and eradicate the disease could have been successful.
One lesson learned from the Wisconsin experience, though, is that it highlighted the ineffective nature of using density dependent measures, in this case general herd reduction, in combating a frequency dependent disease. It's become abundantly clear that hunters will only participate in herd reduction efforts to a certain point and when they start to believe that the lowered number of deer starts to negatively impact the quality of their hunting experience, they will simply stop killing antlerless deer, thus thwarting attempts to further lower the population. This is known as hunter harvest overload and is one of the fundamental flaws in the suggestion of using hunters to drastically reduce game populations for disease control purposes. Instead, targeted removal, either by sharpshooters or by hunters, based on regulatory measures that focus harvest on specific cohorts of the herd, which are most likely to be infected, looks like a much more effective means of combating frequency dependent diseases like CWD. The other factor of CWD is the spread of the disease. Once CWD becomes established it is going to spread, that seems to be a given. While a number of different methods have been used to try and limit the spread of the disease, none of them stand out as being particularly effective. What needs to be kept in mind, however, is that it is impossible to measure whether the disease would have spread more rapidly had no action had been taken. For example, Wyoming has historically taken a passive approach to CWD, essentially no attempts at managing it were done. Over the past several decades it has spread over almost the entire state. Illinois has taken measures to try and limit the spread. Over the last decade and a half the disease has spread to about 17 counties but more than 3/4 of the State appears to remain CWD free. Was it a waste of time for Illinois to take action to try and prevent the spread, even thought they have not been completely successful in doing so? If I was hunting in one of the downstate counties in Illinois, where CWD has not yet been detected, I'd say very vocally that those efforts have been worth it. So the lesson to be learned is that just because the odds are that CWD will continue to spread in states where it has become established is not sufficient justification to decide that continued efforts to contain the spread are waste of time and should be abandoned. Consensus Goals of CWD management
The following are some goals which most of the presenters were in agreement are ones which will result in the best chance of limiting both the spread and prevalence of CWD, once established. Young herd age structure, for both sexes but particularly males. Frequent turnover within the herd. Reduce Deer densities below carrying capacity. limit amplification factors such as aggregation. Keep hunters engaged and prevent trends, such as hunter harvest overload, from removing sport hunting as a management tool. Utilize targeted culling to remove high risk animals from the herd.
Better educate hunters, both about the seriousness of the disease and about what they can do to help fight the disease. State Game agencies need to take a proactive, not reactive approach, in dealing with diseases like CWD. If your states CWD response plan is not incorporating these goals, then it is probably not going to be effective as it could be in limiting the impact of CWD.
One final note: As I mentioned earlier, I was very impressed with almost all of the speakers who participated in this symposium. The two exceptions were the speakers who were representing the captive cervid industry and QDMA. In contrast to all of the other participants, these two came off as hired guns pushing a political agenda that was frequently contradicted by the science that was being presented by some of the best CWD researchers and biologists in the country. It's kind of unfortunate that these two shills were included in the symposium, although it did serve as a reminder of the political divisions that exist within the deer hunting world and provided almost embarrassing examples of how some of those with an agenda are perfectly willing to turn a blind eye towards science and instead embrace dogma, in the pursuit of those agendas.
So where do we go from here? This symposium was particularly timely given the recent confirmation of the tenth CWD positive free ranging deer in Michigan, which was harvested in Montcalm County during the youth hunt. While speaking to the NRC last year, I predicted that it was likely that the CWD outbreak in Michigan would follow the same pattern as has been seen in several other states, where there are relatively few positive deer found during the first several years of an outbreak and then during years 3 & 4, both the number of positive deer identified and
the geographic scope of the outbreak take a major jump. I hope that Michigan does not follow that pattern but I suspect that the Montcalm deer is just the first of several dozen new positives that will be identified over the next 12 - 18 months and that the geographic scope of the current outbreak will continue to expand. The DNR has appointed a CWD workgroup that is tasked with coming up with a list of recommendations for the NRC, for modifications to the existing CWD response plan. In looking at the makeup of that Workgroup, I have some serious concerns that the recommendations made will be more political than scientific but hopefully I will be proved wrong. Hopefully that body will act quickly. Time is of the essence and the more time it takes to enact policy changes, the less likely that those changes can have a positive impact in slowing the spread of CWD in Michigan.
Jim Sweeney The Concerned Sportsmen of Michigan