The History of CWD
We will start with what is CWD? CWD stands for chronic wasting disease; it comes from the Transmissible Spongiform Encephalopathies (TSE) disease family. It’s a neurological disease like mad cow, Creutzfeldt-Jakob disease that affects humans and scrapie that affects sheep. CWD is found in 23 states, 2 Canadian provinces, and in Norway (that makes 2 continents) CWD is 100% fatal. So far CWD is not proven to be transmissible to humans. (Everything that is underlined and in italics is the response I got from the Missouri Department of Conservation when I sent Conservation Agent Mark Henry this article he sent it on to the Cervid Program Supervisor in the Resource Science Division of the Missouri Department of Conservation Barbara Keller then reviewed this article and sent me her response to what I had written.)
CWD is most common in older-aged animals, In areas where CWD is established, older aged animals are more likely to be infected, especially older aged males. That does not mean that they are more susceptible to infection, just that because they are older they are more likely to have been in contact with other infected animals or environment infected with prions. The high infection rate among older aged males may be associated with the higher contact rate of males among social groups during the breeding season. Some of the symptoms are weight loss, excessive drinking and urination, decreased interaction with other animals, lowering of head, repetitive walking in set patterns, nervousness, excessive salivation, drooling and grinding of teeth.
A little more in depth on CWD, CWD is not a virus or a bacterium; it’s caused by a deformed protein called a prion. Prions are misfolded versions of a naturally occurring molecule called a cellular prion protein. Prions aren’t limited to the brain in deer, elk, and moose. They attack lymph nodes and the spleen, compared to viruses and bacterium prions are extremely resistant. In rare cases people have got prions in the brain and as of 2016 231 people have died from this worldwide the disease is called Creutzfeldt-Jakob disease in humans. So far no documented cases of people getting sick from eating meat from deer with CWD have been reported but a Dr. Zabel an immunologist at Colorado State University warns “That doesn’t mean it won’t happen.” So there is a concern about the potential threat CWD might someday pose to humans.
Dr. Zabel in his experiments has shown how easily cellular prion proteins can mis-fold; this suggests that prions may have the potential to become more harmful. With CWD and the prions that cause it being so persistent environmental factors don’t seem to stop the spread or kill the prions. Scientists have figured out that they can rid surgical instruments of prions with what’s called an ozone bath but this practice is impractical in the wild. Dr. Zabel hopes to test controlled burns in Arkansas but the fires won’t be hot enough to destroy the prions but will hopefully kill enough prion-laden plants to lower the odds of deer and elk getting sick, this is just Dr. Zabels hypothesis. The good news is that scientists have found genes that give some animal’s resistance to prions, so there is hope according to Dr. Zabels. There are several reasons we shouldn’t put all our eggs in the “genetic resistance” basket: 1) The CWD-resistance genotypes are generally very rare in free-ranging populations (<5% of the total population carry the genes) so if the population was reduced to individuals with resistance that would result in a population bottleneck, which in general is never good for wildlife, 2) There is likely a reason that genotype is so rare in the natural world, those animals probably don’t fare well in the wild. Evidence from attempts at breeding genetically resistant mule deer for pen studies seem to confirm this (researchers reported that they don’t act right). They may be more susceptible to diseases, parasites, or have behavioral adaptations that do not favor survival. 3) These deer still get CWD and still die from CWD, they are just a bit more resistant to infection (require higher doses) and take longer to die once they are infected. The latter means that once these deer become infected they still shed prions in the environment and infect other deer, they just do so for a longer time period before they die. So a genetically resistant deer infected with CWD can infect more animals through prion shedding vs. one that is not genetically resistant and dies within a shorter time period. For CWD to be so prevalent it is affecting the genetic makeup of the population that also means that the environment is also likely to be highly contaminated with prions, which means that the higher dose that might be required for the CWD resistant deer to become infected is much more present on the landscape.
In 1755 the British parliament started discussing a spreading fatal disease in sheep and the economic effects it was having and the need for the government to get involved. This was the beginning of the recorded history of scrapie.
In the early 1920’s Creutzfeldt-Jakob’s disease was described by two German neurologists. Then in 1959 an American veterinarian discovered that endemic disease of sheep was similar to a newly described disease in humans called kuru. Kuru is a neurological disorder found only in the Eastern highlands of Papua New Guinea. A neuropathological study of kuru suggested a resemblance to Creutzfeldt-Jakob disease.
In 1967 nearly 50 years ago CWD was a rarity and only affected a handful of deer. First discovered and documented by researchers from Colorado State University and the Colorado Division of Wildlife at a cervid research facility near Fort Collins. By the end of the decade CWD was found in captive mule deer, blacktail deer, and elk in Colorado and Wyoming.
Then in 1981 the first case of CWD was found in wild elk in Colorado.
In 1986 Britain identified the first case of Bovine spongiform encephalopathy or mad cow disease. In 1996 mad cow disease was linked to a variant form of Creutzfeldt-Jakob disease. On August 19th 1996 a British coroner ruled that a 20 year old male died from variant Creutzfeldt-Jakob disease caught from eating beef burgers as a child. This was the first verdict to legally link a human’s death to mad cow disease.
By 2000 CWD was found in captive herds in Nebraska and Oklahoma along with wild populations in Saskatchewan and Mississippi
.
By 2002 free ranging whitetails in Wisconsin had tested positive for CWD. Wisconsin’s response to was the state created an eradication zone of roughly 287 square miles and they killed every deer they possibly could within that zone. This response turned out to be a failure. Numerous studies have demonstrated the culling (removing infected deer) is the best option for management of the disease.
March 15 2016 a young reindeer was found in the mountains of Nordfjella Norway with CWD. Then in May two moose were documented with CWD, both moose were older mature moose. Then in the fall 2016 hunting season two more cases of infected reindeer happened.
In Norway since finding two more reindeer with CWD, in April the Norway minister of agriculture and food approved the culling of 2,000 reindeer nearly 6% of the countries wild population in attempt to stop the spread. They will also quarantine the habitat for 5 years. The culling was set to begin in August. Wisconsin tried a similar method and it didn’t work so hopefully it will in Norway, the population is going to be cut down by 2,000 and no matter how you look at it that can’t be good for the reindeer population but it will rebuild and with the hope that the CWD doesn’t get out of hand.
In the beginning of 2017 it is known to be in 23 states and on 2 continents. We still don’t know exactly where it came from or how to stop the spread of it. It could be a mutated version of scrapie that crossed species since sheep where at the facility it was first found at and scrapie has been around for 100’s of years. It could have spontaneously occurred and it could have been here for a very long time and we just started looking for it. Everything we know about this disease does not support the hypothesis that it has historically been on the landscape for a long time period. It grows in prevalence in a very predictable manner. We are seeing population-level effects on deer and elk herds in Wyoming and Colorado. Wisconsin may also be experiencing this, they have just started a research study to find out. We have not yet discovered the disease at say 5% prevalence, done nothing, and come back 5 years later to find it at the same prevalence or lower. It is a highly contagious disease, if it has been around for a very long time we would find it at a very high prevalence throughout the country. Nothing fact based in science has been able to prove how it started or when.
We know that it can be spread from deer to deer and from infected environments to deer. Prions can be shed in saliva, feces, and urine, and are concentrated in the central nervous system tissue. The incubation period between infection and development of the clinical disease is approximately 16 months and is extremely resistant to the environment so transmission of CWD may be both direct and indirect.
CWD is most common in older-aged animals, In areas where CWD is established, older aged animals are more likely to be infected, especially older aged males. That does not mean that they are more susceptible to infection, just that because they are older they are more likely to have been in contact with other infected animals or environment infected with prions. The high infection rate among older aged males may be associated with the higher contact rate of males among social groups during the breeding season. Some of the symptoms are weight loss, excessive drinking and urination, decreased interaction with other animals, lowering of head, repetitive walking in set patterns, nervousness, excessive salivation, drooling and grinding of teeth.
A little more in depth on CWD, CWD is not a virus or a bacterium; it’s caused by a deformed protein called a prion. Prions are misfolded versions of a naturally occurring molecule called a cellular prion protein. Prions aren’t limited to the brain in deer, elk, and moose. They attack lymph nodes and the spleen, compared to viruses and bacterium prions are extremely resistant. In rare cases people have got prions in the brain and as of 2016 231 people have died from this worldwide the disease is called Creutzfeldt-Jakob disease in humans. So far no documented cases of people getting sick from eating meat from deer with CWD have been reported but a Dr. Zabel an immunologist at Colorado State University warns “That doesn’t mean it won’t happen.” So there is a concern about the potential threat CWD might someday pose to humans.
Dr. Zabel in his experiments has shown how easily cellular prion proteins can mis-fold; this suggests that prions may have the potential to become more harmful. With CWD and the prions that cause it being so persistent environmental factors don’t seem to stop the spread or kill the prions. Scientists have figured out that they can rid surgical instruments of prions with what’s called an ozone bath but this practice is impractical in the wild. Dr. Zabel hopes to test controlled burns in Arkansas but the fires won’t be hot enough to destroy the prions but will hopefully kill enough prion-laden plants to lower the odds of deer and elk getting sick, this is just Dr. Zabels hypothesis. The good news is that scientists have found genes that give some animal’s resistance to prions, so there is hope according to Dr. Zabels. There are several reasons we shouldn’t put all our eggs in the “genetic resistance” basket: 1) The CWD-resistance genotypes are generally very rare in free-ranging populations (<5% of the total population carry the genes) so if the population was reduced to individuals with resistance that would result in a population bottleneck, which in general is never good for wildlife, 2) There is likely a reason that genotype is so rare in the natural world, those animals probably don’t fare well in the wild. Evidence from attempts at breeding genetically resistant mule deer for pen studies seem to confirm this (researchers reported that they don’t act right). They may be more susceptible to diseases, parasites, or have behavioral adaptations that do not favor survival. 3) These deer still get CWD and still die from CWD, they are just a bit more resistant to infection (require higher doses) and take longer to die once they are infected. The latter means that once these deer become infected they still shed prions in the environment and infect other deer, they just do so for a longer time period before they die. So a genetically resistant deer infected with CWD can infect more animals through prion shedding vs. one that is not genetically resistant and dies within a shorter time period. For CWD to be so prevalent it is affecting the genetic makeup of the population that also means that the environment is also likely to be highly contaminated with prions, which means that the higher dose that might be required for the CWD resistant deer to become infected is much more present on the landscape.
In 1755 the British parliament started discussing a spreading fatal disease in sheep and the economic effects it was having and the need for the government to get involved. This was the beginning of the recorded history of scrapie.
In the early 1920’s Creutzfeldt-Jakob’s disease was described by two German neurologists. Then in 1959 an American veterinarian discovered that endemic disease of sheep was similar to a newly described disease in humans called kuru. Kuru is a neurological disorder found only in the Eastern highlands of Papua New Guinea. A neuropathological study of kuru suggested a resemblance to Creutzfeldt-Jakob disease.
In 1967 nearly 50 years ago CWD was a rarity and only affected a handful of deer. First discovered and documented by researchers from Colorado State University and the Colorado Division of Wildlife at a cervid research facility near Fort Collins. By the end of the decade CWD was found in captive mule deer, blacktail deer, and elk in Colorado and Wyoming.
Then in 1981 the first case of CWD was found in wild elk in Colorado.
In 1986 Britain identified the first case of Bovine spongiform encephalopathy or mad cow disease. In 1996 mad cow disease was linked to a variant form of Creutzfeldt-Jakob disease. On August 19th 1996 a British coroner ruled that a 20 year old male died from variant Creutzfeldt-Jakob disease caught from eating beef burgers as a child. This was the first verdict to legally link a human’s death to mad cow disease.
By 2000 CWD was found in captive herds in Nebraska and Oklahoma along with wild populations in Saskatchewan and Mississippi
.
By 2002 free ranging whitetails in Wisconsin had tested positive for CWD. Wisconsin’s response to was the state created an eradication zone of roughly 287 square miles and they killed every deer they possibly could within that zone. This response turned out to be a failure. Numerous studies have demonstrated the culling (removing infected deer) is the best option for management of the disease.
March 15 2016 a young reindeer was found in the mountains of Nordfjella Norway with CWD. Then in May two moose were documented with CWD, both moose were older mature moose. Then in the fall 2016 hunting season two more cases of infected reindeer happened.
In Norway since finding two more reindeer with CWD, in April the Norway minister of agriculture and food approved the culling of 2,000 reindeer nearly 6% of the countries wild population in attempt to stop the spread. They will also quarantine the habitat for 5 years. The culling was set to begin in August. Wisconsin tried a similar method and it didn’t work so hopefully it will in Norway, the population is going to be cut down by 2,000 and no matter how you look at it that can’t be good for the reindeer population but it will rebuild and with the hope that the CWD doesn’t get out of hand.
In the beginning of 2017 it is known to be in 23 states and on 2 continents. We still don’t know exactly where it came from or how to stop the spread of it. It could be a mutated version of scrapie that crossed species since sheep where at the facility it was first found at and scrapie has been around for 100’s of years. It could have spontaneously occurred and it could have been here for a very long time and we just started looking for it. Everything we know about this disease does not support the hypothesis that it has historically been on the landscape for a long time period. It grows in prevalence in a very predictable manner. We are seeing population-level effects on deer and elk herds in Wyoming and Colorado. Wisconsin may also be experiencing this, they have just started a research study to find out. We have not yet discovered the disease at say 5% prevalence, done nothing, and come back 5 years later to find it at the same prevalence or lower. It is a highly contagious disease, if it has been around for a very long time we would find it at a very high prevalence throughout the country. Nothing fact based in science has been able to prove how it started or when.
We know that it can be spread from deer to deer and from infected environments to deer. Prions can be shed in saliva, feces, and urine, and are concentrated in the central nervous system tissue. The incubation period between infection and development of the clinical disease is approximately 16 months and is extremely resistant to the environment so transmission of CWD may be both direct and indirect.
CWD in Missouri
Since I’m here in Missouri I wanted to talk about CWD for the state, it was found in 2010 and 11 in captive deer on two private deer farms. We actually started surveillance in 2001-2002. This is when Wisconsin detected the disease so a lot of Midwest states that thought this was a predominately a western disease started looking for it in their state. We have sampled for the disease throughout the state since that time. Prior to the detection of the disease in the free-ranging population we had tested roughly 38,000 deer for CWD statewide with no positive detections. This is another reason we are confident the disease did not persist in the state for a long time period prior to our detection of it. During the 2016 deer season in Missouri 19,200 tissue samples from 29 counties in northeast, central, and east central Missouri resulted in 4 adult bucks and 1 yearling testing positive for CWD. This was just the samples from mandatory sampling. We also have our statewide surveillance efforts, targeted sampling within known CWD core areas, and the SW surveillance you mentioned below. For the 2016-2017 sampling year we tested a total of 25,644 samples including the 19,200 from mandatory sampling (the 29 counties) and 983 from the SW counties on the border with Arkansas. We collected 3,203 samples as part of our statewide surveillance – we work with taxidermists to collect samples throughout the state.
In addition to the 5 CWD positive deer detected as a result of the mandatory sampling effort, 4 additional CWD positive deer were detected during other sampling efforts, for a total of 9 positive deer for the sampling year. Out of 983 tissue samples tested in southwest Missouri no deer from southern Missouri tested positive even though 212 cases tested positive in northwest Arkansas. Since 2010 42 free ranging deer in Missouri have tested positive for CWD.
The Missouri department of conservation has put out new regulations to slow the spread of CWD and has expanded the CWD management zones from 29 to 41 for the 2017 deer season. In the CWD management zones grain, salt products, minerals and other consumable products that are intended to attract deer are now prohibited year-round. The antler point restriction has been removed and the increase of antlerless permits is in effect for CWD management zones. As well as mandatory CWD sampling for all deer harvested within the management zones during the opening weekend of the firearms deer season. This regulation is no longer for every county within a management zone. With the expansion of the management zone to 41 counties, we are only requiring mandatory sampling in 25 of those counties. The counties where mandatory sampling is in effect are listed in the 2017 Fall Deer and Turkey Hunting booklet.
This is the information I could come up with when I researched CWD and the reason I thought I would research it was because of the expanding zones for CWD testing here in Missouri. This is scary for the traditions so many of us love and want to continue but from everything I read it shouldn’t completely destroy the deer population. The science points to the fact that if nothing is done to manage the disease, population-level impacts are likely. That is why we have a proactive management plan here in Missouri. We do have a very localized culling program in areas where the disease is established. The Missouri department of conservation is trying everything they can to stop the spread of it throughout the state and that is why they are making and expanding regulations. We don’t know how to stop CWD but at least our state isn’t just saying they will kill all the deer and hope they comeback healthy and without CWD.
I have my own thoughts and theories on things and ways to study CWD but I’m just a Hillbilly that loves to hunt with no background in science or biology so they probably aren’t very good or have been tried. All I do know is hunting is not just a way of life for me it’s a tradition and heritage that has been passed on from one generation to the next to the next and I plan on passing it on to my daughters. I really hope that smarter people than me can figure out how to get a handle on CWD and the other Transmissible Spongiform Encephalopathies diseases that I have discussed throughout this article.
I wanted to take a few more minutes of your time and thank Conservation Agent Mark Henry and Cervid Program Supervisor from the Resource Science Division of the Missouri Department of Conservation Barbara Keller for the time they took out of there busy schedules to help me with this article to make it the most accurate and informative article it could be. Without Mark getting me in contact with Barbara this article would not have been as accurate and informative as it is. I have found through my interactions with them with questions and comments about Missouri’s wildlife that they have been nothing but helpful and willing to answer all of my questions. They truly represent what I feel any Department of Conservation should be and in my eyes they are doing everything they can to educate the public on the concerns of wildlife here in Missouri. I look forward to picking their brains again on future articles and I trust them that the information they pass on to me is accurate and I will continue to pass it on to everyone I can to help educate hunters in any way possible. I have really enjoyed doing the research for this article and learning about the deer across the country and in Missouri along with making new contacts that can help me write more informative and accurate articles to share. By doing articles like this I hope to educate and pass on information to fellow hunters and outdoorsmen not only in Missouri but across our great country. Thank you again Mark and Barbara for all that you do, have done, and will continue to do.
-The Hillbilly
Sources:
https://www.nytimes.com/2017/06/26/science/chronic-wasting-disease-deer-elk-prions.html
http://cwd-info.org/
https://mdc.mo.gov/newsroom/mdc-reports-three-new-cases-cwd-mandatory-sampling
http://www.sciencemag.org/news/2017/04/norway-plans-exterminate-large-reindeer-herd-stop-fatal-infectious-brain-disease
http://www.cjdinsight.com/history.html
http://edmontonjournal.com/news/local-news/a-brief-history-of-mad-cow-disease
http://www.cbsnews.com/news/chronology-of-mad-cow-crisis/
In addition to the 5 CWD positive deer detected as a result of the mandatory sampling effort, 4 additional CWD positive deer were detected during other sampling efforts, for a total of 9 positive deer for the sampling year. Out of 983 tissue samples tested in southwest Missouri no deer from southern Missouri tested positive even though 212 cases tested positive in northwest Arkansas. Since 2010 42 free ranging deer in Missouri have tested positive for CWD.
The Missouri department of conservation has put out new regulations to slow the spread of CWD and has expanded the CWD management zones from 29 to 41 for the 2017 deer season. In the CWD management zones grain, salt products, minerals and other consumable products that are intended to attract deer are now prohibited year-round. The antler point restriction has been removed and the increase of antlerless permits is in effect for CWD management zones. As well as mandatory CWD sampling for all deer harvested within the management zones during the opening weekend of the firearms deer season. This regulation is no longer for every county within a management zone. With the expansion of the management zone to 41 counties, we are only requiring mandatory sampling in 25 of those counties. The counties where mandatory sampling is in effect are listed in the 2017 Fall Deer and Turkey Hunting booklet.
This is the information I could come up with when I researched CWD and the reason I thought I would research it was because of the expanding zones for CWD testing here in Missouri. This is scary for the traditions so many of us love and want to continue but from everything I read it shouldn’t completely destroy the deer population. The science points to the fact that if nothing is done to manage the disease, population-level impacts are likely. That is why we have a proactive management plan here in Missouri. We do have a very localized culling program in areas where the disease is established. The Missouri department of conservation is trying everything they can to stop the spread of it throughout the state and that is why they are making and expanding regulations. We don’t know how to stop CWD but at least our state isn’t just saying they will kill all the deer and hope they comeback healthy and without CWD.
I have my own thoughts and theories on things and ways to study CWD but I’m just a Hillbilly that loves to hunt with no background in science or biology so they probably aren’t very good or have been tried. All I do know is hunting is not just a way of life for me it’s a tradition and heritage that has been passed on from one generation to the next to the next and I plan on passing it on to my daughters. I really hope that smarter people than me can figure out how to get a handle on CWD and the other Transmissible Spongiform Encephalopathies diseases that I have discussed throughout this article.
I wanted to take a few more minutes of your time and thank Conservation Agent Mark Henry and Cervid Program Supervisor from the Resource Science Division of the Missouri Department of Conservation Barbara Keller for the time they took out of there busy schedules to help me with this article to make it the most accurate and informative article it could be. Without Mark getting me in contact with Barbara this article would not have been as accurate and informative as it is. I have found through my interactions with them with questions and comments about Missouri’s wildlife that they have been nothing but helpful and willing to answer all of my questions. They truly represent what I feel any Department of Conservation should be and in my eyes they are doing everything they can to educate the public on the concerns of wildlife here in Missouri. I look forward to picking their brains again on future articles and I trust them that the information they pass on to me is accurate and I will continue to pass it on to everyone I can to help educate hunters in any way possible. I have really enjoyed doing the research for this article and learning about the deer across the country and in Missouri along with making new contacts that can help me write more informative and accurate articles to share. By doing articles like this I hope to educate and pass on information to fellow hunters and outdoorsmen not only in Missouri but across our great country. Thank you again Mark and Barbara for all that you do, have done, and will continue to do.
-The Hillbilly
Sources:
https://www.nytimes.com/2017/06/26/science/chronic-wasting-disease-deer-elk-prions.html
http://cwd-info.org/
https://mdc.mo.gov/newsroom/mdc-reports-three-new-cases-cwd-mandatory-sampling
http://www.sciencemag.org/news/2017/04/norway-plans-exterminate-large-reindeer-herd-stop-fatal-infectious-brain-disease
http://www.cjdinsight.com/history.html
http://edmontonjournal.com/news/local-news/a-brief-history-of-mad-cow-disease
http://www.cbsnews.com/news/chronology-of-mad-cow-crisis/