Like in other parts of the country, the issue is becoming bigger in states like Pennsylvania where deer hunting is a 1.6 billion dollar industry with nearly 1 million hunters taking to the woods each fall. "It's been confirmed in 177 free-ranging deer in Pennsylvania since 2012, including 78 in 2017 and 26 through June 2018."
Transmission can be passed from deer to deer or from the deer to soil to deer. The prion has been found to be active 2 years in the soil where an infected animal died. This creates a huge challenge in terms of eradication.
Pennsylvania has set up 4 disease management areas (DMA) to enact restrictions on hunters to prevent potential movement of CWD and free testing of deer heads for the prion. Hunters are requested not to consume high-risk parts, properly bone out a carcass to remove brain and spinal cord material as well as cutting away all fatty tissue will remove remaining lymph nodes.
NBC 10
https://www.nbcphiladelphia.com/news/local/Pennsylvania-Sounding-the-Alarm-On-Deer-Disease-494419521.html
Pennsylvania Sounding the Alarm on Chronic Wasting Disease Among Deer
By Kurt Bresswein
Published at 5:08 PM EDT on Sep 26, 2018
Pennsylvania's efforts to control the spread of Chronic Wasting Disease have spread into Berks County, the closest to the Lehigh Valley since the illness was first confirmed in the state in 2012.
Experts say Pennsylvania's white-tailed deer and hunting culture aren't facing a CWD catastrophe. Yet.
But state game and agriculture officials are calling for a unified effort on the part of hunters and other outdoors enthusiasts, along with deer farmers, to avoid becoming another Wisconsin. Some parts of that state are seeing half their deer population infected, said Wayne Laroche, special assistant to the Pennsylvania Game Commission for Chronic Wasting Disease.
"They're probably not ever going to get rid of that unless we come up with some novel ways of disinfecting the landscape," Laroche told a recent meeting on CWD set up by state Rep. Marcia Hahn, R-Northampton, at the East Bath Rod and Gun Club in East Allen Township.
Hunting in Pennsylvania is a $1.6 billion industry, Hahn said.
"So we want to make sure that we keep hunters happy, for one, that we can keep the economy going," she said Wednesday. "It generates a lot of tax revenue for us and helps the state."
Chronic Wasting Disease affects members of the cervid family: black-tailed deer, elk, moose, mule deer, red deer, reindeer, sika deer and white-tailed deer, and hybrids of these species.
It was first confirmed in the United States in 1967, in northern Colorado. Now it's in almost half the states in the nation. Along with Pennsylvania, it's since been found in Arkansas, Illinois, Iowa, Kansas, Maryland, Michigan, Minnesota, Mississippi, Missouri, Montana, Nebraska, New Mexico, New York, North Dakota, Ohio, Oklahoma, South Dakota, Texas, Utah, Virginia, West Virginia, Wisconsin, Wyoming and Alberta and Saskatchewan in Canada.
Regionally, the disease turned up in eastern West Virginia in 2005, northern Virginia in 2009 and western Maryland in 2010 — all near the Pennsylvania border.
It's been confirmed in 177 free-ranging deer in Pennsylvania since 2012, including 78 in 2017 and 26 through June 2018.
"This disease doesn't respect bounds, OK, this is not a PA problem," Dr. Kevin Brightbill, a veterinarian leading the fight against CWD for the Pennsylvania Department of Agriculture, told the gun club meeting. "This is kind of an East Coast-Maryland-West Virginia-PA problem. ...
"I'm here to say I don't care where it came from. If we care about this, if we care about our hunting future, we need to think about strategies that wildlife enthusiasts, captive cervid facilities, hunters, how we can all come together and mitigate this."
Similar to mad cow disease in cattle and scrapie in sheep, CWD is part of the family of diseases known as transmissable spongiform encephalopathies. It's caused by an abnormal protein, called a prion, rather than a living organism like a virus that an animal's immune system could fight.
There is no treatment, no cure and no vaccine.
"And so animals start wandering around, ears drooping, salivating, falling down and end up dying 18 to 24 months usually after they're infected," Laroche said. "It's only in those last stages that you see signs. ... And any animal getting the infection always dies. ...
"They all die in the end."
CWD is not known to affect humans. The U.S. Centers for Disease Control and Prevention has been surveilling for increased incidences of Creutzfeld-Jakob Disease, linked to mad cow, to look for spikes possibly associated with Chronic Wasting Disease, according to Laroche. There's been no evidence of human infections.
It spreads between cervids through feces, urine and saliva. The prion can remain infectious outside an animal for up to 15 years, Laroche said. That could lead to deer picking up the infection from the environment if enough prions accumulate -- at a deer farm's watering station, for example.
On the first day of the 2012 firearms deer season, hunters bring deer taken within the Disease Management Area in Adams and York counties to a Pennsylvania Game Commission testing station for Chronic Wasting Disease at State Game Lands 249.
With an incubation period of up to two years, a CWD infection generally is not evident in deer. If an animal does appear ill, the experts at the gun club told the audience of about 40 people to avoid eating any of its meat. CWD is just one animal disease to be concerned about, in addition to avian flu, tuberculosis and brucellosis, to name a few.
"However, animal studies suggest CWD poses a risk to some types of non-human primates, like monkeys, that eat meat from CWD-infected animals or come in contact with brain or body fluids from infected deer or elk," the CDC says. "These studies raise concerns that there may also be a risk to people."
As a precaution, the CDC recommends against eating meat from deer and elk that test positive for CWD. State officials advise wearing protective gloves when field-dressing a deer, and say hunters should ask their butcher to process only their kill instead of mixing it with the meat of other deer.
The state asks hunters or other wildlife enthusiasts who see a deer they suspect might have CWD to call their regional Pennsylvania Game Commission office. A hunter who shoots a suspected ill deer can get another tag for another deer from a game warden, according to Laroche.
To stem the spread of CWD, Pennsylvania has established four Disease Management Areas in south-central Pennsylvania. DMA 1 was dissolved following control measures put in place at the Adams County captive deer farm where the disease surfaced in 2012.
DMA 4 is the furthest east, extending to Reading in Berks County. This area was set up in 2018, following the discovery of CWD in a captive deer at a farm in neighboring Lancaster County.
More than 5,895 square miles of Pennsylvania lie within DMAs.
Prohibited within DMAs are the rehabilitation of cervids; use or possession of cervid urine-based attractants in an outdoor setting; removal of high-risk cervid parts like the spinal cord/backbone and head; and the feeding of wild, free-ranging cervids.
For deer killed within a DMA, the Game Commission offers free testing of heads dropped into any of the CWD Collection Containers set up around these areas. The only reliable testing for CWD is done on the brain stem and lymph nodes of a deer carcass.
The meat, hide and antlers attached to a clean skull plate may be removed from a DMA.
"Don't consume high-risk parts," the Game Commission says on its website. "Normal field-dressing, coupled with boning out a carcass, will remove most, if not all, high-risk parts. Cutting away all fatty tissue will remove remaining lymph nodes."
Pennsylvania tested 7,910 free-ranging deer and 128 elk for CWD in 2017, up from 5,707 deer and 110 elk in 2016. Since 2002, the Game Commission has tested over 69,000 deer for CWD.
According to Laroche, the Game Commission biologist, deer have been shown to demonstrate a range of resistance to CWD. For that reason, experts do not recommend eradicating a wild herd where CWD is found, in the hopes that generations pass on the resistance.
"But the truth of the matter is if we don't solve this problem the way it rose as we see in Wisconsin, Wyoming, West Virginia, Colorado, the future of deer hunting for your kids and your grandchildren will definitely be in jeopardy," Laroche said last week in Northampton County. "So we have to be serious about this and we have to be committed to do what we have to do and maybe sacrificing a little bit in order to get the job done."
https://www.pennlive.com/opinion/2018/10/chronic_wasting_disease_pennli.html
Here's what Pa. is doing to fight chronic wasting disease | PennLive Letters
Updated 7:30 AM; Posted 7:30 AM
By Letters to the Editor
Individuals planning to hunt in the state of Pennsylvania should double-check the regulations that pertain to their hunting spot. Since this time last year, Disease Management Areas 2 and 3 have been expanded and the new DMA 4 was established due to the detection of new chronic wasting disease (CWD) positives.
Disease Management Area (DMA) 2 now includes parts of Juniata, Mifflin, anad Perry counties, in addition to all or parts of Adams, Bedford, Blair, Cambria, Clearfield, Cumberland, Franklin, Fulton, Huntingdon and Somerset counties. Meanwhile, DMA 3 now includes parts of Armstrong, Cambria and Clarion counties, as well as parts of Clearfield, Indiana, and Jefferson counties.
DMA 4, which was established earlier this year when a CWD-positive deer was found in a captive deer farm in Lancaster County, covers parts of Berks, Lancaster, and Lebanon counties. Hunters should verify whether they are hunting in a DMA prior to hunting.
Within DMAs, specific regulations apply to help reduce the risk of spreading CWD, a fatal neurodegenerative disease that affects deer and elk. Individuals hunting within DMAs should note that the use or field possession of urine-based attractants is prohibited. In addition, it is unlawful to export high-risk deer parts from a DMA or to import high-risk parts from a CWD-positive state. High-risk parts include brain, spinal cord, eyes, tonsils, lymph nodes, and spleen.
Emerging Infectious Diseases
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3309570/
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
Samuel E. Saunders,1 Shannon L. Bartelt-Hunt, and Jason C. Bartz
University of Nebraska-Lincoln, Omaha, Nebraska, USA (S.E. Saunders, S.L. Bartelt-Hunt);
Creighton University, Omaha (J.C. Bartz)
Corresponding author.
Address for correspondence: Jason C. Bartz, Department of Medical Microbiology and Immunology, Creighton University, 2500 California Plaza, Omaha, NE 68178, USA; email: ude.nothgierc@ztrabj
Author information ► Copyright and License information ► Disclaimer
Abstract
Chronic wasting disease (CWD) is a fatal, transmissible prion disease that affects captive and free-ranging deer, elk, and moose. Although the zoonotic potential of CWD is considered low, identification of multiple CWD strains and the potential for agent evolution upon serial passage hinders a definitive conclusion. Surveillance for CWD in free-ranging populations has documented a continual geographic spread of the disease throughout North America. CWD prions are shed from clinically and preclinically affected hosts, and CWD transmission is mediated at least in part by the environment, perhaps by soil. Much remains unknown, including the sites and mechanisms of prion uptake in the naive host. There are no therapeutics or effective eradication measures for CWD-endemic populations. Continued surveillance and research of CWD and its effects on cervid ecosystems is vital for controlling the long-term consequences of this emerging disease.
Keywords: Chronic wasting disease, prions and related diseases, bovine spongiform encephalopathy, BSE, transmissible spongiform encephalopathy, TSE, interspecies transmission, environmental persistence, zoonotic potential, cervids, United States, Canada, zoonoses
Chronic wasting disease (CWD) is an inevitably fatal, infectious neurodegenerative prion disease naturally affecting North American mule deer (Odocoileus hemionus), white-tailed deer (Odocoileus virginianus), elk (wapiti, Cervus canadensis), and moose (Alces alces) (1,2). Other prion diseases, or transmissible spongiform encephalopathies, include bovine spongiform encephalopathy (BSE), scrapie in sheep and goats, and Creutzfeldt-Jakob disease (CJD) in humans (3). CWD was identified in the late 1960s and recognized as a spongiform encephalopathy by Williams in 1980 (1).
Clinical signs of CWD include weight loss and behavioral changes such as altered stance, pacing, excessive salivation, and hyperexcitability that progress over weeks or months (1). The infectious agent of CWD is the abnormally folded prion protein (the prion) designated PrPSc, which is distinguished from the normal cellular prion protein (PrPc) by its resistance to proteolysis, propensity for aggregation, and insolubility in detergents (4). Misfolded prion (PrPSc) can initiate conversion of PrPc to PrPSc and replicate through a yet unknown mechanism. The exact role that PrPSc plays in prion disease remains unclear, but PrPSc is known to accumulate in the central nervous system (CNS) (1).
CWD continues to emerge and spread in free-ranging and captive cervids throughout the United States and Canada. Effective therapeutics or and management practices for animal populations in areas to which CWD is endemic do not currently exist. Long-term effects of CWD on cervid ecosystems remain unclear, but the potential for economic consequences is serious because of the role cervids play in the hunting, tourism, and agricultural industries. Moreover, the zoonotic potential of CWD is uncertain, and exposure to CWD-contaminated meat and material will only increase as the disease continues to spread and the incidence increases in areas to which CWD is endemic. We discuss current CWD prevalence and distribution and broadly review surveillance efforts to date. We also present a detailed conceptual model for transmission of the CWD agent and provide an update on CWD interspecies transmission, strains, and zoonotic potential. In addition, we suggest key research needs that may offer hope of slowing or halting the continued emergence of CWD.
Prevalence and Surveillance
Originally recognized only in southeastern Wyoming and northeastern Colorado, USA, CWD was reported in Canada in 1996 and Wisconsin in 2001 and continues to be identified in new geographic locations (Figure 1, panel A). CWD has been identified in free-ranging cervids in 15 US states and 2 Canadian provinces and in ≈100 captive herds in 15 states and provinces and in South Korea (Figure 1, panel B). Except in South Korea, CWD has not been detected outside North America. In most locations reporting CWD cases in free-ranging animals, the disease continues to emerge in wider geographic areas, and prevalence appears to be increasing in many disease-endemic areas. Areas of Wyoming now have an apparent CWD prevalence of near 50% in mule deer, and prevalence in areas of Colorado and Wisconsin is <15% in deer. However, prevalence in many areas remains between 0% and 5% according to reports and data obtained from state and provincial wildlife agencies. Prevalence in elk is lower than in deer but reaches 10% in parts of Wyoming. Known risk factors for CWD include sex and age, and adult male deer show the highest prevalence (5). Polymorphisms in the PrP (PRNP) gene appear to influence susceptibility in deer and elk (2,6,7), but remain less understood than the strong genetic influences for scrapie.
CWD surveillance programs are now in place in almost all US states and Canadian provinces (Figure 2, panel A). More than 1,060,000 free-ranging cervids have reportedly been tested for CWD (Figure 2, panel B) and ≈6,000 cases have been identified (Figure 2, panel C) according to data from state and provincial wildlife agencies. Following years of limited surveillance in select states and provinces, a nationwide surveillance effort was initiated for the 2002–2003 season, which greatly increased the number of states and provinces performing testing, animals tested, and cases identified (Figure 2). Initial surveillance in most states was generally designed to detect >1 positive animal at a 95% confidence level if the population disease prevalence was >1%, although this goal has not always been achieved.
Many states have now shifted to more targeted surveillance of known disease-endemic areas, areas bordering states reporting cases, or areas surrounding facilities for captive cervids. Samples tested are typically from animals killed by hunters, animals clinically suspected of having CWD, animals killed by vehicles, and targeted sharpshooter kills. Testing of captive cervids is routine in most states and provinces, but varies considerably in scope from mandatory testing of all dead animals to voluntary herd certification programs or mandatory testing of only animals suspected of dying of CWD. A detailed analysis of state and provincial CWD surveillance regimens and disease prevalence is beyond the scope of this report. However, such an analysis would be valuable, not only to evaluate and improve surveillance strategies across the continent (and world) but also to provide insights into spatial and temporal disease dynamics.
Long-term effects of CWD on cervid populations and ecosystems remain unclear as the disease continues to spread and prevalence increases. In captive herds, CWD might persist at high levels and lead to complete herd destruction in the absence of human culling. Epidemiologic modeling suggests the disease could have severe effects on free-ranging deer populations, depending on hunting policies and environmental persistence (8,9). CWD has been associated with large decreases in free-ranging mule deer populations in an area of high CWD prevalence (Boulder, Colorado, USA) (5). In addition, CWD-infected deer are selectively preyed upon by mountain lions (5), and may also be more vulnerable to vehicle collisions (10). Long-term effects of the disease may vary considerably geographically, not only because of local hunting policies, predator populations, and human density (e.g., vehicular collisions) but also because of local environmental factors such as soil type (11) and local cervid population factors, such as genetics and movement patterns (S.E. Saunders, unpub. data).
Transmission and Role of the Environment
Horizontal Transmission and Agent Shedding
Horizontal transmission of the agent causing CWD is a major mechanism of natural transmission (Figure 3), and maternal transmission is not necessary for disease transmission (1). Oral inoculation is an effective route of CWD agent transmission (1). Oral lesions facilitate CWD agent transmission in transgenic mice expressing cervid PrPc (12). Nasal inoculation is also an effective route of transmission in transgenic mice expressing cervid PrPc (13). However, nasal infection and the effect of oral lesions on infection have not yet been evaluated for cervids. Overall, the natural routes and mechanisms of CWD prion uptake are incompletely described.
https://dailyjournalonline.com/sports/outdoors/overview-cwd-in-the-midwest/article_709b80c6-8f8f-551b-ad16-155a46a08de3.html
Overview: CWD in the Midwest
Sep 29, 2018
Chronic Wasting Disease, or CWD, was first discovered in the United States in 1967 in captive mule deer in Colorado.
Since then CWD has been found in Missouri, Illinois and 20 other states and several Canadian provinces. These include Colorado, Illinois, Iowa, Kansas, Maryland, Michigan, Minnesota, Montana Nebraska, New Mexico, Missouri, New York, North Dakota, Oklahoma, Pennsylvania, South Dakota, Texas, Utah, Virginia, West Virginia, Wisconsin, Wyoming, and Alberta and Saskatchewan.
Missouri
CWD was first discovered in Missouri in 2010 in captive deer on private hunting preserves in Linn and Macon counties. But the Missouri Department of Conservation had begun statewide CWD surveillance of free-ranging deer in 2001 when the deadly disease began spreading through nearby states.
Since that time the MDC has tested more than 100,000 free-ranging deer. Deer are sampled during the opening weekend of fall firearms deer hunting season in targeted counties based on the findings from the previous year.
During the 2017-2018 deer seasons period the MDC tested nearly 24,500 deer for CWD and found 33 new cases for a total of 75 cases in Missouri.
The CWD Management Zone includes counties within approximately 25 miles of CWD detections.
The zone includes these counties within or that touch a radius of approximately 25 miles from where the disease has been found: Adair, Barry, Benton, Bollinger, Boone, Callaway, Cape Girardeau, Carroll, Cedar, Chariton, Cole, Cooper, Crawford, Dade, Franklin, Gasconade, Grundy, Hickory, Jefferson, Knox, Linn, Livingston, Macon, Madison, Mercer, McDonald, Miller, Moniteau, Morgan, Osage, Ozark, Perry, Polk, Putnam, Randolph, Schuyler, Scotland, Shelby, St. Charles, St. Clair, St. Francois, Ste. Genevieve, St. Louis, Stone, Sullivan, Taney, Warren, and Washington.
Hunters who harvest deer in certain CWD Management Zone counties on Nov. 10-11 of this year, the opening weekend of fall firearms deer season, must present their deer, or the head with at least six inches of the neck in place, to an MDC CWD sampling location on the day of harvest. The testing is free and hunters can also get free results.
A complete list, with interactive map, of sampling stations can be found at: https://huntfish.mdc.mo.gov/hunting-trapping/wildlife-diseases/chronic-wasting-disease-cwd/mandatory-cwd-sampling-2018.
In addition, the MDC is offering free CWD sampling and testing of deer harvested anywhere in the state throughout the entire deer hunting season – Sept. 15 through Jan. 15, 2019 – with several sampling locations including MDC offices. The sampling is voluntary and hunters can also get free test results for their deer.
Hunters can have their deer sampled at 11 select MDC offices around the state. Hunters can also take their deer to 64 participating taxidermists and meat processors located in the 48 counties of MDC’s CWD Management Zone.
MDC asks hunters to Telecheck their deer before taking them to a CWD sampling location. Hunters can bring the entire deer – preferably field dressed – or the head with at least 6 inches of the neck in place. Heads that have the cape removed for taxidermy can also be sampled.
CWD test results can take up to four weeks from the time of sample submission. Hunters can get test results for their CWD-sampled deer online at mdc.mo.gov/CWDTestResults.
Of the 33 new cases identified in the past year, 16 were from hunter-harvested deer, 1 was from a road-killed deer, and 16 were found through post-season targeted culling.
Also, more than 200 cases of CWD have been found in deer and elk in northwest Arkansas since early 2016. This has prompted MDC to increase CWD surveillance efforts in southwest Missouri. The good news is, to date no deer from counties bordering Arkansas have tested positive for the disease.
So what is Missouri doing to combat the spread of CWD?
The agency works with hunters, landowners, taxidermists, and others through mandatory and voluntary sampling to collect tissue samples for CWD testing in areas where CWD has been found.
The state agency has removed the antler-point restriction for counties in the CWD Management Zone because young bucks can spread the disease to new areas as they search for territory and mates.
MDC allows the use of two firearms antlerless permits in counties in the CWD Management Zone to help prevent undesired population increases in local deer numbers.
Furthermore, the conservation agency has restricted feeding deer and placing minerals for deer in counties of the CWD Management Zone. Experts also strongly discourage the removal of deer carcasses from counties in the CWD Management Zone, and encourages people to report sick deer to local staff.
Illinois
According to the Illinois Department of Natural Resources, CWD was first found in northwest Boone County in northern Illinois in the fall of 2002. Since that time more than 100,000 deer have been tested in order to accurately identify where the disease occurs and how severe it is.
CWD has been found in 17 Illinois counties (Boone, Carroll, DeKalb, DuPage, Grundy, JoDaviess, Kane, Kankakee, Kendall, Lake, LaSalle, Livingston, McHenry, Ogle, Stephenson, Will, Winnebago).
Illinois conservation officials have utilized trained agency sharpshooters to help reduce deer populations in known CWD areas in an effort to slow the spread of the disease. Additionally, they’ve managed hunter harvest pressure through season and limits to help control numbers.
According to IDNR, as of June 30, 2017 the department has sampled at least 105,836 deer, with 685 confirmed CWD cases. “While overall prevalence remains low in JoDaviess and Stephenson counties, disease is firmly established and appears to be worsening, accounting for 21 out of 75 (28%) of all positives identified this year. Prevalence is somewhat higher in some eastern counties of the range, but deer populations in those areas are smaller and habitat much more fragmented.”
Most recently CWD testing has been done at the University of Illinois’ Veterinary Diagnostic Laboratory in Urbana, Illinois.
A report from IDNR states, “In order to manage deer densities at the county level, IDNR has liberalized hunting regulations in the northern Illinois CWD area, using virtually unlimited gun permit quotas, a special CWD management hunting season with reduced-price permits, and more days of hunting.
“These changes have not resulted in increased levels of deer harvest. Illinois DNR supplements hunter harvest with agency sharpshooting after the hunting seasons to allow a focused removal of deer from areas in which CWD is known to occur. Sharpshooting occurs on both private and public property through a network of cooperating landowners with a concern for natural resource management.
“Addressing disease control in this fashion at the local level actually allows us to more effectively fight CWD without drastically reducing deer populations throughout the entire county, as would be the case if we were forced to use hunting as the only tool for disease control. Our goal is to suppress CWD prevalence rates so that they remain very low, and to slow the spread of the disease to the remainder of the state.
“Our approach to CWD management impacts CWD dynamics by increasing removal of CWD-positive deer from the population, by reducing contact rates between sick and susceptible individuals, and by reducing the rate of environmental contamination.
Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease
Samuel E. Saunders,1 Shannon L. Bartelt-Hunt, and Jason C. Bartz
University of Nebraska-Lincoln, Omaha, Nebraska, USA (S.E. Saunders, S.L. Bartelt-Hunt);
Creighton University, Omaha (J.C. Bartz)
Corresponding author.Address for correspondence: Jason C. Bartz, Department of Medical Microbiology and Immunology, Creighton University, 2500 California Plaza, Omaha, NE 68178, USA; email: ude.nothgierc@ztrabj
Author information ► Copyright and License information ► Disclaimer
Abstract
Chronic wasting disease (CWD) is a fatal, transmissible prion disease that affects captive and free-ranging deer, elk, and moose. Although the zoonotic potential of CWD is considered low, identification of multiple CWD strains and the potential for agent evolution upon serial passage hinders a definitive conclusion. Surveillance for CWD in free-ranging populations has documented a continual geographic spread of the disease throughout North America. CWD prions are shed from clinically and preclinically affected hosts, and CWD transmission is mediated at least in part by the environment, perhaps by soil. Much remains unknown, including the sites and mechanisms of prion uptake in the naive host. There are no therapeutics or effective eradication measures for CWD-endemic populations. Continued surveillance and research of CWD and its effects on cervid ecosystems is vital for controlling the long-term consequences of this emerging disease.
Keywords: Chronic wasting disease, prions and related diseases, bovine spongiform encephalopathy, BSE, transmissible spongiform encephalopathy, TSE, interspecies transmission, environmental persistence, zoonotic potential, cervids, United States, Canada, zoonoses
Chronic wasting disease (CWD) is an inevitably fatal, infectious neurodegenerative prion disease naturally affecting North American mule deer (Odocoileus hemionus), white-tailed deer (Odocoileus virginianus), elk (wapiti, Cervus canadensis), and moose (Alces alces) (1,2). Other prion diseases, or transmissible spongiform encephalopathies, include bovine spongiform encephalopathy (BSE), scrapie in sheep and goats, and Creutzfeldt-Jakob disease (CJD) in humans (3). CWD was identified in the late 1960s and recognized as a spongiform encephalopathy by Williams in 1980 (1).
Clinical signs of CWD include weight loss and behavioral changes such as altered stance, pacing, excessive salivation, and hyperexcitability that progress over weeks or months (1). The infectious agent of CWD is the abnormally folded prion protein (the prion) designated PrPSc, which is distinguished from the normal cellular prion protein (PrPc) by its resistance to proteolysis, propensity for aggregation, and insolubility in detergents (4). Misfolded prion (PrPSc) can initiate conversion of PrPc to PrPSc and replicate through a yet unknown mechanism. The exact role that PrPSc plays in prion disease remains unclear, but PrPSc is known to accumulate in the central nervous system (CNS) (1).
CWD continues to emerge and spread in free-ranging and captive cervids throughout the United States and Canada. Effective therapeutics or and management practices for animal populations in areas to which CWD is endemic do not currently exist. Long-term effects of CWD on cervid ecosystems remain unclear, but the potential for economic consequences is serious because of the role cervids play in the hunting, tourism, and agricultural industries. Moreover, the zoonotic potential of CWD is uncertain, and exposure to CWD-contaminated meat and material will only increase as the disease continues to spread and the incidence increases in areas to which CWD is endemic. We discuss current CWD prevalence and distribution and broadly review surveillance efforts to date. We also present a detailed conceptual model for transmission of the CWD agent and provide an update on CWD interspecies transmission, strains, and zoonotic potential. In addition, we suggest key research needs that may offer hope of slowing or halting the continued emergence of CWD.
Prevalence and Surveillance
Originally recognized only in southeastern Wyoming and northeastern Colorado, USA, CWD was reported in Canada in 1996 and Wisconsin in 2001 and continues to be identified in new geographic locations (Figure 1, panel A). CWD has been identified in free-ranging cervids in 15 US states and 2 Canadian provinces and in ≈100 captive herds in 15 states and provinces and in South Korea (Figure 1, panel B). Except in South Korea, CWD has not been detected outside North America. In most locations reporting CWD cases in free-ranging animals, the disease continues to emerge in wider geographic areas, and prevalence appears to be increasing in many disease-endemic areas. Areas of Wyoming now have an apparent CWD prevalence of near 50% in mule deer, and prevalence in areas of Colorado and Wisconsin is <15% in deer. However, prevalence in many areas remains between 0% and 5% according to reports and data obtained from state and provincial wildlife agencies. Prevalence in elk is lower than in deer but reaches 10% in parts of Wyoming. Known risk factors for CWD include sex and age, and adult male deer show the highest prevalence (5). Polymorphisms in the PrP (PRNP) gene appear to influence susceptibility in deer and elk (2,6,7), but remain less understood than the strong genetic influences for scrapie.
Many states have now shifted to more targeted surveillance of known disease-endemic areas, areas bordering states reporting cases, or areas surrounding facilities for captive cervids. Samples tested are typically from animals killed by hunters, animals clinically suspected of having CWD, animals killed by vehicles, and targeted sharpshooter kills. Testing of captive cervids is routine in most states and provinces, but varies considerably in scope from mandatory testing of all dead animals to voluntary herd certification programs or mandatory testing of only animals suspected of dying of CWD. A detailed analysis of state and provincial CWD surveillance regimens and disease prevalence is beyond the scope of this report. However, such an analysis would be valuable, not only to evaluate and improve surveillance strategies across the continent (and world) but also to provide insights into spatial and temporal disease dynamics.
Long-term effects of CWD on cervid populations and ecosystems remain unclear as the disease continues to spread and prevalence increases. In captive herds, CWD might persist at high levels and lead to complete herd destruction in the absence of human culling. Epidemiologic modeling suggests the disease could have severe effects on free-ranging deer populations, depending on hunting policies and environmental persistence (8,9). CWD has been associated with large decreases in free-ranging mule deer populations in an area of high CWD prevalence (Boulder, Colorado, USA) (5). In addition, CWD-infected deer are selectively preyed upon by mountain lions (5), and may also be more vulnerable to vehicle collisions (10). Long-term effects of the disease may vary considerably geographically, not only because of local hunting policies, predator populations, and human density (e.g., vehicular collisions) but also because of local environmental factors such as soil type (11) and local cervid population factors, such as genetics and movement patterns (S.E. Saunders, unpub. data).
Transmission and Role of the Environment
Horizontal Transmission and Agent Shedding
Horizontal transmission of the agent causing CWD is a major mechanism of natural transmission (Figure 3), and maternal transmission is not necessary for disease transmission (1). Oral inoculation is an effective route of CWD agent transmission (1). Oral lesions facilitate CWD agent transmission in transgenic mice expressing cervid PrPc (12). Nasal inoculation is also an effective route of transmission in transgenic mice expressing cervid PrPc (13). However, nasal infection and the effect of oral lesions on infection have not yet been evaluated for cervids. Overall, the natural routes and mechanisms of CWD prion uptake are incompletely described.
The CWD agent is shed from infected hosts in urine, feces, saliva, blood, and antler velvet (Figure 3) and can occur in preclinical and clinically affected animals (14). CWD prions are also present nearly ubiquitously throughout a diseased host, including skeletal muscle; cardiac muscle; fat; a wide range of glands, organs, and peripheral nervous tissue; and in the highest concentrations in the CNS (2,15). Thus, CWD prions will enter the environment through shedding from diseased and deaths animals (carcasses). Although quantification of infectious CWD titers in excreta and tissue is challenging, the total titer shed from an infected animal during its lifespan may be approximately equal to the total titer contained in an infected carcass (16).
Indirect Environmental Transmission
Environmental transmission of the CWD agent was reported in studies demonstrating that an infected deer carcass left in a pasture for 2 years could transmit the agent to immunologically naive deer (17). Exposure of naive deer to pasture previously inhabited by an infected deer also led to CWD transmission, as did cohabitation of naive and infected deer (17). Naive deer exposed to water, feed buckets, and bedding used by CWD-infected deer contracted the disease (18).
Epidemiologic modeling suggests that indirect environmental routes of CWD transmission also play a major role in transmission (8). Environmental transmission of scrapie is well documented, and scrapie prions may remain infectious after years in the environment (19,20; S.E. Saunders, unpub. data). Nevertheless, environmental transmission of scrapie may be less efficient than transmission by direct contact (19). Conversely, the relative efficiency of CWD transmission by direct contact versus indirect, environmental routes remains unclear, but evidence suggests environmental transmission may be a major mechanism (8). The proportion of transmission by direct versus indirect routes may vary not only between captive and free-ranging cervid populations, but also among cervid species and free-ranging habitats and ecosystems. Transmission dynamics may also vary over time as CWD prevalence and ecosystem residence times continue to increase (8).
If the environment serves as a reservoir of CWD infectivity, hot spots of concentrated prion infectivity could be formed at areas of communal activity where shedding occurs (Figure 3) (12). Animal mortality sites, where highly infectious CNS matter would enter the environment, could also be hot spots (21). In a study of deer carcass decomposition in Wisconsin, carcasses persisted for 18–101 days depending on the season, and were visited by deer (22). In addition, cervid carcasses are visited by numerous scavenger species, such as raccoons, opossums, coyotes, vultures, and crows, which could consume and transport CWD-infected tissue and increase CWD spread (21,22). Thus, there is the potential for CWD to spread from sites of animal deaths. Predators may also contribute to spread of the CWD agent and transmission (5), as could transport by surface water (23) or insect vectors. Natural migration and dispersion of cervids is also a likely mechanism of geographic spread of CWD (24).
Given that cervids habitually ingest considerable amounts of soil, soil has been hypothesized to play a key role in CWD transmission (Figure 3) (11,20; S.E. Saunders et al., unpub. data). Inhalation of dust-bound CWD prions may also represent a route of transmission. It is known that CWD prions can bind to a range of soils and soil minerals (25,26) and retain the ability to replicate (27). In addition, rodent prions retain or gain infectivity when bound to soil and soil minerals (20,27; S.E. Saunders et al., unpub. data). Prion fate and transmission in soil has been recently reviewed (20). Although the potential for CWD transmission by soil and soil reservoirs is considerable, this transmission remains to be directly evaluated with cervids.
CWD Zoonotic Potential, Species Barriers, and Strains
Current Understanding of the CWD Species Barrier
Strong evidence of zoonotic transmission of BSE to humans has led to concerns about zoonotic transmission of CWD (2,3). As noted above, CWD prions are present nearly ubiquitously throughout diseased hosts, including in muscle, fat, various glands and organs, antler velvet, and peripheral and CNS tissue (2,14,15). Thus, the potential for human exposure to CWD by handling and consumption of infectious cervid material is substantial and increases with increased disease prevalence.
Interspecies transmission of prion diseases often yields a species-barrier effect, in which transmission is less efficient compared with intraspecies transmission, as shown by lower attack rates and extended incubation periods (3,28). The species barrier effect is associated with minor differences in PrPc sequence and structure between the host and target species (3). Prion strain (discussed below) and route of inoculation also affect the species barrier (3,28). For instance, interspecies transmission by intracerebral inoculation is often possible but oral challenge is completely ineffective (29).
Most epidemiologic studies and experimental work have suggested that the potential for CWD transmission to humans is low, and such transmission has not been documented through ongoing surveillance (2,3). In vitro prion replication assays report a relatively low efficiency of CWD PrPSc-directed conversion of human PrPc to PrPSc (30), and transgenic mice overexpressing human PrPc are resistant to CWD infection (31); these findings indicate low zoonotic potential. However, squirrel monkeys are susceptible to CWD by intracerebral and oral inoculation (32). Cynomolgus macaques, which are evolutionarily closer to humans than squirrel monkeys, are resistant to CWD infection (32). Regardless, the finding that a primate is orally susceptible to CWD is of concern.
Interspecies transmission of CWD to noncervids has not been observed under natural conditions. CWD infection of carcass scavengers such as raccoons, opossums, and coyotes was not observed in a recent study in Wisconsin (22). In addition, natural transmission of CWD to cattle has not been observed in experimentally controlled natural exposure studies or targeted surveillance (2). However, CWD has been experimentally transmitted to cattle, sheep, goats, mink, ferrets, voles, and mice by intracerebral inoculation (2,29,33).
CWD is likely transmitted among mule, white-tailed deer, and elk without a major species barrier (1), and other members of the cervid family, including reindeer, caribou, and other species of deer worldwide, may be vulnerable to CWD infection. Black-tailed deer (a subspecies of mule deer) and European red deer (Cervus elaphus) are susceptible to CWD by natural routes of infection (1,34). Fallow deer (Dama dama) are susceptible to CWD by intracerebral inoculation (35). Continued study of CWD susceptibility in other cervids is of considerable interest.
Reasons for Caution
There are several reasons for caution with respect to zoonotic and interspecies CWD transmission. First, there is strong evidence that distinct CWD strains exist (36). Prion strains are distinguished by varied incubation periods, clinical symptoms, PrPSc conformations, and CNS PrPSc depositions (3,32). Strains have been identified in other natural prion diseases, including scrapie, BSE, and CJD (3). Intraspecies and interspecies transmission of prions from CWD-positive deer and elk isolates resulted in identification of >2 strains of CWD in rodent models (36), indicating that CWD strains likely exist in cervids. However, nothing is currently known about natural distribution and prevalence of CWD strains. Currently, host range and pathogenicity vary with prion strain (28,37). Therefore, zoonotic potential of CWD may also vary with CWD strain. In addition, diversity in host (cervid) and target (e.g., human) genotypes further complicates definitive findings of zoonotic and interspecies transmission potentials of CWD.
Intraspecies and interspecies passage of the CWD agent may also increase the risk for zoonotic CWD transmission. The CWD prion agent is undergoing serial passage naturally as the disease continues to emerge. In vitro and in vivo intraspecies transmission of the CWD agent yields PrPSc with an increased capacity to convert human PrPc to PrPSc (30). Interspecies prion transmission can alter CWD host range (38) and yield multiple novel prion strains (3,28). The potential for interspecies CWD transmission (by cohabitating mammals) will only increase as the disease spreads and CWD prions continue to be shed into the environment. This environmental passage itself may alter CWD prions or exert selective pressures on CWD strain mixtures by interactions with soil, which are known to vary with prion strain (25), or exposure to environmental or gut degradation.
Given that prion disease in humans can be difficult to diagnose and the asymptomatic incubation period can last decades, continued research, epidemiologic surveillance, and caution in handling risky material remain prudent as CWD continues to spread and the opportunity for interspecies transmission increases. Otherwise, similar to what occurred in the United Kingdom after detection of variant CJD and its subsequent link to BSE, years of prevention could be lost if zoonotic transmission of CWD is subsequently identified,
Management Policies
CWD will likely continue to emerge in North America. Given the current extent of CWD and the lack of an effective therapeutic, complete eradication is currently not feasible. As more is learned about disease transmission, it may be possible to manage the prevalence in CWD-endemic areas through hunting policies (9). However, long exposures of the environment to CWD prions may create strong environmental reservoirs of CWD capable of efficient transmission, which could sustain or heighten disease incidence (Figure 3) (8; S.E. Saunders et al., unpub. data).
Ostensible elimination of CWD in free-ranging cervids has been achieved in only 1 state (New York). After an intensive depopulation and surveillance effort, only 2 free-ranging deer tested were positive for CWD in New York. A similar depopulation and surveillance effort was recently conducted in Minnesota, where only 1 free-ranging deer tested was positive for CWD. Success of the effort in Minnesota and the experience in New York offer hope that new isolated CWD outbreaks can be contained and eliminated by immediate depopulation efforts. However, environmental reservoirs or unknown disease foci may hinder such efforts, and attempts to eliminate CWD in other states in addition to New York have failed. Most notably, an extensive culling effort in Wisconsin that was initiated after CWD detection in 3 free-ranging deer was most likely unsuccessful because the disease was long established in the deer population and environment (8,9).
Controlling the spread of CWD, especially by human action, is a more attainable goal than eradication. Human movement of cervids has likely led to spread of CWD in facilities for captive animals, which has most likely contributed to establishment of new disease foci in free-ranging populations (Figure 1, panel A). Thus, restrictions on human movement of cervids from disease-endemic areas or herds continue to be warranted. Anthropogenic factors that increase cervid congregation such as baiting and feeding should also be restricted to reduce CWD transmission. Appropriate disposal of carcasses of animals with suspected CWD is necessary to limit environmental contamination (20), and attractive onsite disposal options such as composting and burial require further investigation to determine contamination risks. The best options for lowering the risk for recurrence in facilities for captive animals with outbreaks are complete depopulation, stringent exclusion of free-ranging cervids, and disinfection of all exposed surfaces. However, even the most extensive decontamination measures may not be sufficient to eliminate the risk for disease recurrence (20; S.E. Saunders et al. unpub. data)
Research Needs
The influence of environmental factors, such as local climate and habitat characteristics (e.g., vegetation and soil type), on CWD incidence has not been assessed in detail (S.E. Saunders et al., unpub. data). Epidemiologic comparisons of well-established CWD-endemic populations/habitats and newly exposed populations/habitats could yield insights on transmission dynamics. Detection and quantification of environmental CWD prions would be a key step in defining the role of indirect, environmental exposure routes in CWD transmission. Although CWD PrPSc was detected in a river water sample from an area in Colorado with endemic CWD by using protein misfolding cyclic amplification, the amount detected was below the limit of transgenic mouse bioassay detection, which complicated interpretation of data (23).
If environmental reservoirs were implicated in CWD transmission, it may be possible to target these reservoirs for disinfection with a topical enzymatic solution (26) or another yet untested treatment and thereby greatly reduce disease incidence. However, cervid density, behavior, and movement may be more significant factors in CWD transmission regardless of the environment. However, such factors also require more investigation. In either case, additional research is needed to determine the natural routes of exposure and agent uptake (Figure 3). CWD prion shedding from cervid birthing matter, milk, nasal secretions, and nonantler skin also warrants investigation because such shedding has been observed with other noncervid prion-infected animals (Figure 3) (14).
CWD research tools have been used to make major advances in the past 5 years. Transgenic mouse models of CWD are now invaluable tools for studying CWD infectivity and strains (2,12,13,15,16,23,30,36), and protein misfolding cyclic amplification has been used effectively for CWD detection, replication, and interspecies studies (14,23,27,30). A CWD-susceptible cell culture line is now available (39). Continued use of captive cervids in CWD research remains critical to understanding the disease in its natural hosts. Recent advances in premortem detection techniques, including excreta testing (14) and rectal biopsy (40), may lead to more reliable and noninvasive surveillance programs and enhance experimental capabilities.
Future CWD Surveillance
The origin of CWD is unknown but may have been either a spontaneous occurrence or caused by interspecies transmission of scrapie or another prion agent. However, because scrapie cases have been reported globally in sheep-farming countries, the potential exits for CWD to occur globally. To our knowledge, CWD surveillance outside the United States and Canada has been largely or completely confined to the industrialized countries of Europe and Asia and has not approached the extensiveness of US and Canadian efforts (Figure 2). Even within North America, surveillance of some cervids, such as caribou, has been limited, and continued enthusiasm for funding and conducting current surveillance programs is uncertain. Given that surveillance efforts are still limited compared with total cervid populations, CWD could be present at low levels in many areas considered free of CWD. At a minimum, targeted surveillance of all cervids within and outside North America should be conducted to understand the true extent of the disease geographically and its host range. This surveillance might be facilitated by more convenient premortem testing methods (14,40).
Conclusions
Much remains unknown about prion diseases and CWD in particular, especially about CWD strains (which may have varied zoonotic potentials) and the long-term effects of CWD on cervid ecosystems. CWD prevalence and geographic range appear likely to continue to increase. Moreover, the disease is inevitably fatal, and no effective therapeutic measures are presently available. As such, it would seem wise to continue research and surveillance of CWD to elucidate the details of its transmission, pathogenesis, and continued emergence in cervid populations in hopes that strategies for mitigating its negative effects on humans and cervid ecosystems can be identified.
Chemosphere
https://www.sciencedirect.com/science/article/pii/S0045653512000057
Soil-mediated prion transmission: Is local soil-type a key determinant of prion disease incidence?
Author links open overlay panel Samuel E. Saunders a, Jason C. Bartz b, Shannon L. Bartelt-Hunt a
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https://doi.org/10.1016/j.chemosphere.2011.12.076Get rights and content
Abstract
Prion diseases, including chronic wasting disease (CWD) and scrapie, can be transmitted via indirect environmental routes. Animals habitually ingest soil, and results from laboratory experiments demonstrate prions can bind to a wide range of soils and soil minerals, retain the ability to replicate, and remain infectious, indicating soil could serve as a reservoir for natural prion transmission and a potential prion exposure route for humans. Preliminary epidemiological modeling suggests soil texture may influence the incidence of prion disease. These results are supported by experimental work demonstrating variance in prion interactions with soil, including variance in prion soil adsorption and soil-bound prion replication with respect to soil type. Thus, local soil type may be a key determinant of prion incidence. Further experimental and epidemiological work is required to fully elucidate the dynamics of soil-mediated prion transmission, an effort that should lead to effective disease management and mitigation strategies.
https://dailyjournalonline.com/sports/outdoors/overview-cwd-in-the-midwest/article_709b80c6-8f8f-551b-ad16-155a46a08de3.html
Overview: CWD in the Midwest
Sep 29, 2018
Chronic Wasting Disease, or CWD, was first discovered in the United States in 1967 in captive mule deer in Colorado.
Since then CWD has been found in Missouri, Illinois and 20 other states and several Canadian provinces. These include Colorado, Illinois, Iowa, Kansas, Maryland, Michigan, Minnesota, Montana Nebraska, New Mexico, Missouri, New York, North Dakota, Oklahoma, Pennsylvania, South Dakota, Texas, Utah, Virginia, West Virginia, Wisconsin, Wyoming, and Alberta and Saskatchewan.
Missouri
CWD was first discovered in Missouri in 2010 in captive deer on private hunting preserves in Linn and Macon counties. But the Missouri Department of Conservation had begun statewide CWD surveillance of free-ranging deer in 2001 when the deadly disease began spreading through nearby states.
Since that time the MDC has tested more than 100,000 free-ranging deer. Deer are sampled during the opening weekend of fall firearms deer hunting season in targeted counties based on the findings from the previous year.
During the 2017-2018 deer seasons period the MDC tested nearly 24,500 deer for CWD and found 33 new cases for a total of 75 cases in Missouri.
The CWD Management Zone includes counties within approximately 25 miles of CWD detections.
The zone includes these counties within or that touch a radius of approximately 25 miles from where the disease has been found: Adair, Barry, Benton, Bollinger, Boone, Callaway, Cape Girardeau, Carroll, Cedar, Chariton, Cole, Cooper, Crawford, Dade, Franklin, Gasconade, Grundy, Hickory, Jefferson, Knox, Linn, Livingston, Macon, Madison, Mercer, McDonald, Miller, Moniteau, Morgan, Osage, Ozark, Perry, Polk, Putnam, Randolph, Schuyler, Scotland, Shelby, St. Charles, St. Clair, St. Francois, Ste. Genevieve, St. Louis, Stone, Sullivan, Taney, Warren, and Washington.
Hunters who harvest deer in certain CWD Management Zone counties on Nov. 10-11 of this year, the opening weekend of fall firearms deer season, must present their deer, or the head with at least six inches of the neck in place, to an MDC CWD sampling location on the day of harvest. The testing is free and hunters can also get free results.
A complete list, with interactive map, of sampling stations can be found at: https://huntfish.mdc.mo.gov/hunting-trapping/wildlife-diseases/chronic-wasting-disease-cwd/mandatory-cwd-sampling-2018.
In addition, the MDC is offering free CWD sampling and testing of deer harvested anywhere in the state throughout the entire deer hunting season – Sept. 15 through Jan. 15, 2019 – with several sampling locations including MDC offices. The sampling is voluntary and hunters can also get free test results for their deer.
Hunters can have their deer sampled at 11 select MDC offices around the state. Hunters can also take their deer to 64 participating taxidermists and meat processors located in the 48 counties of MDC’s CWD Management Zone.
MDC asks hunters to Telecheck their deer before taking them to a CWD sampling location. Hunters can bring the entire deer – preferably field dressed – or the head with at least 6 inches of the neck in place. Heads that have the cape removed for taxidermy can also be sampled.
CWD test results can take up to four weeks from the time of sample submission. Hunters can get test results for their CWD-sampled deer online at mdc.mo.gov/CWDTestResults.
Of the 33 new cases identified in the past year, 16 were from hunter-harvested deer, 1 was from a road-killed deer, and 16 were found through post-season targeted culling.
Also, more than 200 cases of CWD have been found in deer and elk in northwest Arkansas since early 2016. This has prompted MDC to increase CWD surveillance efforts in southwest Missouri. The good news is, to date no deer from counties bordering Arkansas have tested positive for the disease.
So what is Missouri doing to combat the spread of CWD?
The agency works with hunters, landowners, taxidermists, and others through mandatory and voluntary sampling to collect tissue samples for CWD testing in areas where CWD has been found.
The state agency has removed the antler-point restriction for counties in the CWD Management Zone because young bucks can spread the disease to new areas as they search for territory and mates.
MDC allows the use of two firearms antlerless permits in counties in the CWD Management Zone to help prevent undesired population increases in local deer numbers.
Furthermore, the conservation agency has restricted feeding deer and placing minerals for deer in counties of the CWD Management Zone. Experts also strongly discourage the removal of deer carcasses from counties in the CWD Management Zone, and encourages people to report sick deer to local staff.
Illinois
According to the Illinois Department of Natural Resources, CWD was first found in northwest Boone County in northern Illinois in the fall of 2002. Since that time more than 100,000 deer have been tested in order to accurately identify where the disease occurs and how severe it is.
CWD has been found in 17 Illinois counties (Boone, Carroll, DeKalb, DuPage, Grundy, JoDaviess, Kane, Kankakee, Kendall, Lake, LaSalle, Livingston, McHenry, Ogle, Stephenson, Will, Winnebago).
Illinois conservation officials have utilized trained agency sharpshooters to help reduce deer populations in known CWD areas in an effort to slow the spread of the disease. Additionally, they’ve managed hunter harvest pressure through season and limits to help control numbers.
According to IDNR, as of June 30, 2017 the department has sampled at least 105,836 deer, with 685 confirmed CWD cases. “While overall prevalence remains low in JoDaviess and Stephenson counties, disease is firmly established and appears to be worsening, accounting for 21 out of 75 (28%) of all positives identified this year. Prevalence is somewhat higher in some eastern counties of the range, but deer populations in those areas are smaller and habitat much more fragmented.”
Most recently CWD testing has been done at the University of Illinois’ Veterinary Diagnostic Laboratory in Urbana, Illinois.
A report from IDNR states, “In order to manage deer densities at the county level, IDNR has liberalized hunting regulations in the northern Illinois CWD area, using virtually unlimited gun permit quotas, a special CWD management hunting season with reduced-price permits, and more days of hunting.
“These changes have not resulted in increased levels of deer harvest. Illinois DNR supplements hunter harvest with agency sharpshooting after the hunting seasons to allow a focused removal of deer from areas in which CWD is known to occur. Sharpshooting occurs on both private and public property through a network of cooperating landowners with a concern for natural resource management.
“Addressing disease control in this fashion at the local level actually allows us to more effectively fight CWD without drastically reducing deer populations throughout the entire county, as would be the case if we were forced to use hunting as the only tool for disease control. Our goal is to suppress CWD prevalence rates so that they remain very low, and to slow the spread of the disease to the remainder of the state.
“Our approach to CWD management impacts CWD dynamics by increasing removal of CWD-positive deer from the population, by reducing contact rates between sick and susceptible individuals, and by reducing the rate of environmental contamination.
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