Captive Cervid and the Economic Burden of Chronic Wasting Disease CWD TSE Prion?
Captive Cervid and the Economic Burden of Chronic Wasting Disease CWD TSE Prion?
The economic burden of ignoring CWD would be far greater, imo, with time, if no cervid were left, or just a select few, if the environment/property was so exposed and saturated with CWD, that you couldn’t sell it, you couldn’t grow crops because of the soil saturation of the CWD, water tables saturated with CWD, saturation of hay, grains, from crops uptake on said property, cervid meat saturated from Cervid CWD, remember, You cannot cook the TSE prion disease out of meat, In fact new data now shows that exposure to high temperatures used to cook the meat increased the availability of prions for in vitro amplification. So, what Do we do, how many humans and animals do we continue to expose, continue to saturate with the CWD TSE Prion, how many will become infected, what about friendly fire, ie iatrogenic exposure to the CWD TSE Prion, do we just ignore all science, all transmission studies that confirm all this is very possible, is this what we want to leave our children and grandchildren? Just because no documentation of human TSE Prion disease from CWD has not been documented, does not mean it cannot happen, or has not already happened. It’s kinda hard to state categorically that CWD has transmitted to humans, or not, when no diagnostic diagnosis criteria is set up for any such event, especially for iatrogenic, that I am aware of…terry
The economic costs of chronic wasting disease in the United States
Scott J. Chiavacci
Published: December 8, 2022
https://doi.org/10.1371/journal.pone.0278366
Appendix F
Data on Cervid Farms and Captive Cervids by State and Costs
This appendix provides an expanded visualization of the cervid data reported in Chiavacci (2022). It also provides descriptions on cervid numbers, number of paid hunting licenses, and years since first detection in wild cervid populations. The committee developed several sets of figures presenting relationships of these data, separated into two frames—states with mule deer and states without mule deer. The appendix concludes with a discussion of public agency costs.
DATA ON CERVID FARMS AND CAPTIVE CERVIDS
Chiavacci (2022) documents the number of cervid farms and captive cervids by state in 2020. Figure F.1 groups those in states with mule deer habitat (Figure F.1a) and those without (Figure F.1b). Most states have less than 150 cervid farms and less than 10,000 captive cervids. The number of cervid farms and captive cervids in Texas exceeds that of others states by over an order of magnitude. Most of the Great Plains and western states with mule deer have less than 50 farms and 3,000 captive cervids. There are, on average, more cervid farms and captive cervids in states with only white-tailed deer habitat (i.e., the central and eastern states).
Some states such as Texas have both breeding and breeding and hunting operations. Little data exist on the scale of those operations apart from the facilities surveyed by Outlaw and others (2017). They determined that the average breeding farm size was found to be 21 acres for breeding and 30 acres for breeding and hunting. The sizes of these facilities are much smaller than those in Alberta documented by Arnot and others (2009), which are in the hundreds of acres.
Figure F.2 plots the years since first detection of chronic wasting disease (CWD) in wild cervids in each state against captive cervids in each state in 2020 in Figure F.2a and Figure F.2b, and against the number of cervid farms in 2020 in Figure F.2c and Figure F.2d.
While CWD was first detected relatively recently in Texas, there is a relatively high number of locales with endemic CWD. The remaining states all have less than 4,000 captive cervids and fewer than 100 farms (Chiavacci, 2022). Both Idaho and Oklahoma have seen a few cases.
For the more eastern states without mule deer, there are regular groupings based on the years since first detection and number of endemic locales, each across the full range of number of cervids and farms. Exceptions to the pattern include Arkansas and Tennessee, which both have only recently detected CWD yet have several endemic locations. New York is also different in that CWD was detected 18 years ago, but few other cases have been found. This is fortuitus for New York as the state has almost 7,500 captive cervids and over 100 farms (Chiavacci, 2022).
National Academies of Sciences, Engineering, and Medicine. 2025. State of Knowledge Regarding Transmission, Spread, and Management of Chronic Wasting Disease in U.S. Captive and Free-Ranging Cervid Populations. Washington, DC: The National Academies Press. https://doi.org/10.17226/27449.
FIGURE F.1 Relationships between the number of cervid farms and number of captive cervids by state. *Texas had significantly more cervid farms and captive cervids than any other state with 1,498 cervid farms and 117,120 farmed cervids in 2020. Texas is excluded from panel (a) to keep the two panels comparable. SOURCE: Data from Chiavacci (2022, Table 1).
Data were obtained by the committee from a variety of digital sources on the state-by-state number of hunting licenses issued annually and populations of wild cervids. (The committee realizes these population estimates are rough and does not employ them in a formal analysis but rather as an indication of the magnitude of those populations at risk.) Considering deer as the most widespread species at risk, for the same states as employed in Chiavacci (2022) and grouped by states with and without mule deer habitat, Figure F.3 plots the number of hunters in 2022 and wild deer populations in 2022. Figure F.3 illustrates that those states with more deer have more hunters, but the general pattern in the states with mule deer habitat is quite different than that of states with just white-tail deer. It is important to note that there may be significant differences in the benefits and costs of hunting across cervid species and states, and the relative proportions of cervids in states vary significantly—for example, many states with mule deer also include significant populations of elk and moose. Also important to note is there is great variation in access to hunting across states and public lands and in resident and non-resident demand for hunting.
Figure F.4 plots the years since first detection and wild deer populations in 2022 in Figure F.4a and Figure F.4b, and the number of hunters in 2022 in Figure F.4c and Figure F.4d.
The plots illustrate again the differences in the pattern of the data between the western/Great Plains states and those further east. For the states with mule deer (Figure F.4a and Figure F.4c), both risk factors (long period of time since first detection and number of endemic locales) increase together apart from Montana (with lower numbers of deer and hunters) and Texas (with higher numbers of deer and hunters), where they have several endemic locales given a relatively recent first detection. The same general risk factor pattern persists for states without mule deer (Figure F.4b and Figure F.4d), although the groupings of each risk factor combination are maintained across broad ranges of deer populations and number of hunters. Again, outliers are Arkansas and Tennessee (having relatively recent detection and high numbers of endemic locales) and New York, which has only had a few cases of CWD since its initial detection many years ago.
CWD-RELATED COSTS
To help understand drivers in public agency costs, the cost data from Table 1 of Chiavacci (2022) were grouped by mule deer habitat and plotted against the number of years since CWD was first detected (Figure F.5a and Figure F.5b); against the population of wild deer (Figure F.5c and Figure F.5d); and against the number of hunting license holders (Figure F.5e and Figure F.5f). As one might expect, on average, states that have experienced more years since the first detection have high numbers of hunters and high numbers of deer, and tend to have the
National Academies of Sciences, Engineering, and Medicine. 2025. State of Knowledge Regarding Transmission, Spread, and Management of Chronic Wasting Disease in U.S. Captive and Free-Ranging Cervid Populations. Washington, DC: The National Academies Press. https://doi.org/10.17226/27449.
highest public agency costs from CWD. But the effects depend on whether the states have mule deer habitat or not, and within each grouping there are further differentiations.
For both states with mule deer and without, costs (on average) are higher with years since first detection and more endemic locales (Figure F.5a and Figure F.5b). For the most part, costs are highest in states without mule deer for those which have higher numbers of endemic locales. However, states can have detected CWD relatively recently and have several endemic locales with relatively low costs (Montana, Figure F.5a; Arkansas, Figure F.5b) or high costs (Texas, Figure F.5a; Missouri and Michigan, Figure F.5b). In addition, there are states that first detected CWD many years ago and have several endemic locales yet have low costs (Kansas, South Dakota, and Nebraska, Figure F.5a; West Virginia and Maryland, Figure F.5b).
The pattern of costs and deer populations or hunters clearly depends on whether, or not, mule deer habitat is in the state. For states with mule deer, costs are higher with higher deer populations or more hunters and more endemic locales. The pattern is less clear in states without mule deer. While costs can be higher for states with more deer or hunters and with more endemic locales, there are wide ranges of deer populations and hunters with the same number of endemic locales and wide ranges of costs. For example, Maryland and West Virginia have lower deer populations and lower numbers of hunters yet moderate to high numbers of endemic locales and low costs.
National Academies of Sciences, Engineering, and Medicine. 2025. State of Knowledge Regarding Transmission, Spread, and Management of Chronic Wasting Disease in U.S. Captive and Free-Ranging Cervid Populations. Washington, DC: The National Academies Press. https://doi.org/10.17226/27449.
https://nap.nationalacademies.org/read/27449/chapter/17#185
Please note, the following chart is several years old, more States have documented CWD since then…terry
The economic costs of chronic wasting disease in the United States
Scott J. Chiavacci
State, CWD Detected(a), Natural Resources Agency Costs, Agriculture/Animal Health Agency, Farmed Cervid Industry Costs(b), Cervid Farms/Farmed Cervids(c)
Alabama No $42,500(d) Unknown 97/5,013
Alaska No $9,000(f) $40,000 Unknown 6/260
Arizona No $83,500 Unknown Unknown(g) 5/208
Arkansas Yes $592,218 Not applicable(e) Unknown 13/446
California No $500,000 Not applicable(e)Unknown(g) 8/256
Colorado Yes $600,000 Unknown Unknown 46/1,336
Connecticut No $95,000 Not applicable(e) Unknown(g) 15/168
Delaware No $32,500 Unknown Unknown(g) unknown 1/Unknown
Florida No $200,000(d) Unknown(h) $500 86/7,494
Georgia No $127,500 Unknown(j) Unknown(g) 12/361
Idaho No $95,000 $15,000 $20,000 18/2,427
Illinois Yes $1,100,000(d) Unknown Unknown 83/1,543
Indiana No $127,856(j) 113,863(d,j) Unknown 143/3,888
lowa Yes $505,000(d) Unknown Unknown 66/3,583
Kansas Yes $142,000 Unknown(h) Unknown 35/2,957
Kentucky No $237,812(d, j) $345,300(j) Unknown 22/429
Louisiana No $404,425 $200,000 $1,200 82/3,733
Maine No $50,000 $42,448(k) Unknown 50/7,837
Maryland Yes $20,000 …(i) …(i) 0/0
Massachusetts No $500 Not applicable(e) Unknown(g) 4/11
Michigan Yes $2,045,702(j) Unknown Unknown 178/16,842
Minnesota Yes $2,800,000 Unknown Unknown 227/8,044
Mississippi Yes $425,000 Not applicable(e) Unknown 44/1,611
Missouri Yes $2,752,403 Unknown Unknown 70/4,163
Montana Yes $350,000 Unknown 16/372
Nebraska Yes $149,336(j) Unknown 17/409
Nevada No $40,000 …(j) …(j) 0/0
New Hampshire No $25,000 Unknown(h) Unknown(g) 8/654
New Jersey No $51,142(k) Not Applicable (e) Unknown(g) 9/172
New Mexico Yes $150,100 Not Applicable(e) Unknown 9/2,836
New York Yes $369,249(j) $240,534 Unknown 107/7,437
North Carolina No $245,730 Unknown Unknown 5/0
North Dakota Yes $300,000 $12,500 Unknown 26/2,256
Ohio Yes $246,000 Unknown Unknown 215/6,223
Oklahoma Yes $2,500(d) $85,000 Unknown 86/3,740
Oregon No $75,000 Not Applicable(e) Unknown(g) 11/283
Pennsylvania Yes $2,900,000 $1,300,00 Unknown 346/11,456
Rhode Island No $37,000 …(i) …(i) 0/0
South Carolina No $0 ...(i) …(i) 10/387
South Dakota Yes $255,712(j) $58,700(k) Unknown 16/978
Tennessee Yes $1,179,776 Unknown(h) Unknown 46/2,465
Texas Yes $1,495,718(j) Not applicable(e) Unknown 1,498/117,120
Utah Yes $31,300(d, k) $123,320(d, k) Unknown 21/733
Vermont No $1,000 Unknown unknown 4/unknown
Virginia Yes $368,226(j) …i …i 2/unknown
Washington No $1,100 $500 Unknown 12/523
West Virginia Yes $280,000(d) $900(d) $4,000 16/284
Wisconsin Yes $2,900,000 $318,852(j) $246,608(j) 137/9,397
Wyoming Yes $800,000(d) …(i) …(i) 1/unknown
A "Denotes if CWD was detected in farmed or wild cervids as of the year for which CWD-related expenditures are reported. Note, four states (Alabama, Idaho, Louisiana, and North Carolina detected Wafter data were collected
B All costs listed are for only sample extraction and testing costs paid by cervid farmers, as reported by state agencies that regulate farmed cervids
C Data are from the 2017 Census of Agriculture [37) and include deer and elk combined. These data may not correspond with the number of farms and animals in a state at the time of CWD cost data collection. 'Unknown' conveys that data on the number of cervid farms or cervids are not reported in the 2017 Census of Agriculture.
D Cost data provided by agency do not include all expenditures related to CWD work
E Farmed cervids are regulated by the state natural resources agency
F Cost was estimated at "less than $10,000 annually" so $9,000 was assumed to be costs for CWD-related work
G Costs to farmed cervid industry presumed small, if any, because of relatively small scale of industry, few animals, and regulations restricting animal importation and exportation
H did not provide specific costs for farmed cervid oversight, but noted costs were minimal
I No farmed cervid industry cost data were collected
J Original values provided applied to fiscal year 2019 costs. These were converted to 2020 dollars using the U.S. Bureau of Labor Statistics CPI Inflation Calculator
K Original values provided applied to fiscal year 2021 costs. These were converted to 2020 dollars using the U.S. Bureau of Labor Statistics CPI Inflation Calculator
https://doi.org/10.1371/journal.pone.0278366.t001
https://journals.plos.org/plosone/article/figure?id=10.1371/journal.pone.0278366.t001
+ Reset zoom Table 1. Direct costs related to chronic wasting disease paid by state agencies and cervid farmers in the continental United States in 2020 dollars. Show
The economic costs of chronic wasting disease in the United States
Scott J. Chiavacci PLOS.svg Published: December 8, 2022
https://doi.org/10.1371/journal.pone.02783
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0278366
CWD, who’s getting paid?
USDA EXPLANATORY NOTES ANIMAL AND PLANT HEALTH INSPECTION SERVICE 2025-2014 CHRONIC WASTING DISEASE CWD TSE CERVID
2025 USDA EXPLANATORY NOTES – ANIMAL AND PLANT HEALTH INSPECTION SERVICE
In 2023, eight percent of the farmed cervids in the HCP were tested for CWD at APHIS and State laboratories.
Of the 303,242 farmed cervids tested in 2023, APHIS confirmed 22 new CWD positive farmed cervid herds.
APHIS provided Federal indemnity to depopulate one of the newly identified positive herds and approved an indemnity payment for a second positive herd which will be provided in 2024 once depopulation occurs. The remaining infected herds are under State quarantines.
https://www.usda.gov/sites/default/files/documents/22-APHIS-2025-ExNotes.pdf
2024 USDA EXPLANATORY NOTES – ANIMAL AND PLANT HEALTH INSPECTION SERVICE
Cervids
In 2022, 7 percent of the 285,589 farmed cervids in the HCP participating states were tested for CWD at State and APHIS laboratories.
APHIS confirmed 23 new CWD positive farmed cervid herds.
APHIS provided Federal indemnity to depopulate nine of the newly identified positive herds in 2022. The remaining infected herds are under State quarantines. APHIS determines the use of Federal indemnity payments within the CWD program on a case-by-case basis.
https://www.usda.gov/sites/default/files/documents/23-2024-APHIS.pdf
2023 USDA EXPLANATORY NOTES – ANIMAL AND PLANT HEALTH INSPECTION SERVICE
Cervids
APHIS coordinates with State agencies to encourage cervid owners to certify their herds and comply with the CWD Herd Certification Program (HCP) Standards…
APHIS’ voluntary national CWD HCP helps States, Tribes, and the cervid industry control CWD in farmed cervids by allowing the interstate movement only from certified herds.
Currently, 28 States participate in the national CWD HCP. In FY 2021, more than 20,502 farmed cervids were tested for CWD at State and APHIS laboratories.
As a result, APHIS identified 35 new CWD positive farmed cervid herds.
APHIS provided Federal indemnity to depopulate nine of the newly identified deer herds in FY 2021. The remaining infected herds are under State quarantines. APHIS determines the use of Federal indemnity payments within the CWD program on a case-by-case basis.
https://www.usda.gov/sites/default/files/documents/23-2023-APHIS.pdf
2022 USDA EXPLANATORY NOTES – ANIMAL AND PLANT HEALTH INSPECTION SERVICE
Cervids
APHIS coordinates with State agencies to encourage cervid owners to certify their herds and comply with the CWD Herd Certification Program Standards…
APHIS’ voluntary national CWD Herd Certification Plan (HCP) helps States, Tribes, and the cervid industry control CWD in farmed cervids by allowing the interstate movement only from certified herds.
Currently, 28 States participate in the national CWD HCP. In FY 2020, more than 11,182 farmed cervids were tested for CWD at State and APHIS laboratories.
As a result, APHIS identified 22 new CWD positive farmed cervid herds.
APHIS provided Federal indemnity to depopulate 15 of the 22 newly identified deer herds in FY 2020.
Four additional farmed cervid herds that were identified as CWD positive herds in FY 2019, were indemnified in FY 2020.
The remaining infected herds are under State quarantines.
https://www.usda.gov/sites/default/files/documents/22APHIS2022Notes.pdf
2021 USDA EXPLANATORY NOTES – ANIMAL AND PLANT HEALTH INSPECTION SERVICE
In FY 2019 APHIS tested more than 11,000 farmed cervids for CWD.
As a result, APHIS identified 17 new CWD positive farmed cervid herds.
APHIS provided Federal indemnity to depopulate 7 of the 17 newly identified deer herds in FY 2019. The remaining infected herds found in FY 2019 are under State quarantines.
https://www.usda.gov/sites/default/files/documents/20aphis2021notes.pdf
2020 USDA EXPLANATORY NOTES – ANIMAL AND PLANT HEALTH INSPECTION SERVICE
Cervids
APHIS’ voluntary national CWD Herd Certification Plan (HCP) helps States, Tribes, and the cervid industry control CWD in farmed cervids by allowing the interstate movement only from certified herds.
Currently, 28 States participate in the national CWD HCP and the program used an immunohistochemistry test method to test 21,584 farmed cervids for CWD.
In FY 2018, APHIS identified 15 new CWD positive farmed cervid herds (14 deer herds and 1 reindeer herd).
The reindeer herd in Illinois was the first confirmed case of CWD in a reindeer in North America.
APHIS provided Federal indemnity to depopulate seven of the 15 newly identified deer herds in FY 2018.
The Agency also provided funding for the test and removal of 161 high risk animals that were in close proximity to reactors.
The remaining herds in FY 2018 are under State quarantines.
The Agency determines the use of Federal indemnities within the CWD program on a case-by-case basis. 20-59
https://www.usda.gov/sites/default/files/documents/20aphis2020notes.pdf
2019 President’s Budget Animal and Plant Health Inspection Service
Cervids
APHIS’ voluntary national CWD Herd Certification Plan (HCP) helps States, Tribes, and the cervid industry control CWD in farmed cervids by allowing the interstate movement only from certified herds.
Currently, 28 States participate in the national CWD HCP and the program tested 23,053 farmed cervids for CWD.
In FY 2017, eight new CWD positive farmed corvid herds were identified– one white-tail deer in Iowa, one white-tail deer herd in Minnesota, one white-tail and mule deer herd in Minnesota, one white-tail and sika deer herd in Michigan, three white-tail deer herds in Pennsylvania, and one white-tail deer herd in Texas.
APHIS provided Federal indemnity to depopulate the Iowa herd, the white-tail deer herd in Minnesota, one herd in Pennsylvania and the Texas herd. The State depopulated the Michigan herd. The remaining herds are under State quarantines. One Texas herd used Federal indemnity to remove and test select, high-risk animals to inform the epidemiological investigation and to evaluate the performance of ante-mortem tests.
The Agency determines the use of Federal indemnities within the CWD program on a case-by-case basis.
https://www.usda.gov/sites/default/files/documents/20aphis2019notes.pdf
2018 President’s Budget Animal and Plant Health Inspection Service
Cervids
APHIS’ voluntary national CWD Herd Certification Plan (HCP) helps States, Tribes, and the cervid industry control CWD in farmed cervids by allowing the interstate movement only from certified herds considered to be low risk.
Currently, 29 States participate in the national CWD HCP.
In FY 2016, the program tested 14,503 farmed cervids for CWD and identified seven new CWD positive farmed cervid herds – two white-tail deer herds in Texas, three white-tail deer herds in Wisconsin, one elk herd in Colorado and one elk herd in Iowa. The elk herd in Colorado was depopulated without Federal indemnity and the rest of the herds are under State quarantines. One Texas herd used Federal indemnity to remove and test select animals to inform the epidemiological investigation and to evaluate 20-72 the performance of ante-mortem tests.
The use of Federal indemnities within the CWD program is determined on a case-by-case basis. APHIS is also conducting several pilot projects related to new technologies. In FY 2016, the Agency
https://www.usda.gov/sites/default/files/documents/20aphisexnotes2018.pdf
2017 Explanatory Notes Animal and Plant Health Inspection Service
Cervids
APHIS’ voluntary national CWD Herd Certification Plan (HCP) helps States, Tribes, and the cervid industry control CWD in farmed cervids by allowing the interstate movement only from certified herds considered to be low risk.
Currently, 30 States participate in the national CWD HCP: 29 have Approved Status and 1 has Provisional Approved Status. States that meet the CWD HCP requirements have Approved Status and States that do not meet CWD HCP program requirements but have developed a work plan and time frame with APHIS to complete those requirements have Provisional Approved Status.
In FY 2015, the program tested approximately 20,000 farmed cervids for CWD and identified eight new CWD positive farmed white-tailed deer herds – one in Utah, one in Pennsylvania, two in Ohio, two in Wisconsin, and two in Texas.
APHIS depopulated five of these herds (Pennsylvania, Utah, and one each in Wisconsin, Texas, and Ohio). Six elk herds in Colorado, four elk herds in Nebraska, one white-tailed deer herd in Wisconsin and one white-tailed deer herd in Texas remained in quarantine at the end of FY 2015.
APHIS also provided indemnity for and was the lead agency for the depopulation and disposal of four large CWD infected farmed cervid herds in Pennsylvania, Ohio, Utah, and Texas. In cooperation with the National Agricultural Statistics Service, APHIS conducted the first national study of the U.S. farmed-cervid industry in FY 2015. The study provides baseline industry statistics, a description of production practices and challenges, producer-reported disease occurrences, and an overview of health management and biosecurity practices.
https://www.usda.gov/sites/default/files/documents/20aphis2017notes.pdf
2016 Explanatory Notes Animal and Plant Health Inspection Service
https://www.usda.gov/sites/default/files/documents/20aphis2016notes.pdf
2015 Explanatory Notes Animal and Plant Health Inspection Service
https://www.usda.gov/sites/default/files/documents/20aphis2015notes.pdf
2014 Explanatory Notes Animal and Plant Health Inspection Service
https://www.usda.gov/sites/default/files/documents/18aphis2014notes.pdf
Louisiana House of Representative Aug 27, 9:30 AM, HCR-6 CWD
Louisiana House of Representative
Chronic Wasting Disease CWD
(A letter written from a Mississippi farmer who’s farm has been in his family for more than 100 years, and submitted it in this video presentation, 28 minute mark, another wake up call for sure, of what some have been warning for years, about CWD, but sadly will go by the wayside by the conspiracy theorists spreading fake news…terry)
Alston Ross
Marshall County, Mississippi
My family owns a 2,000 acre farm in Marshall County, which is in North Mississippi. CWD has plagued my farm since 2018 and has become progressively worse over time. We no longer have mature deer over the age of 3 years old on our property. Every buck harvested on our land has tested positive this year. The owners of our neighboring properties have continued to feed deer and ignore MDWFP regulations, which has exacerbated the spread of the disease throughout our area. This farm has been in my family for over 100 years, and due to the rapid spread of CWD, we are concerned about the future of our deer herd and the value of our hunting land…end
Snip…
Arkansas
Snip…
40:35 “…and conversely, I was co-Principle Investigator in NW Arkansas, where prevalence is approaching 50 percent.”
Snip…
41:00 “Specific to the work in Arkansas, in 2020, the state agency was showing the Prevalence at 30 percent in the Northwest part of the State, so flip a coin, so, 1 out of every 3 deer had the disease. We started that research in 2020, and now, the prevalence rate is now exceeding 40% in both sexes, and 50% in males.”
43:00 “what we’re seeing Arkansas now is, that population is declining about 11% a year.”
Snip…see full video presentation;
https://house.louisiana.gov/H_Video/VideoArchivePlayer?v=house/2025/Aug/0827_25_NR_Joint
CWD IS RAVAGING MY FAMILY’S LAND, BUT IT’S NOT TOO LATE FOR YOU
September 9, 2025 By: Paul Annear
My first season deer hunting in Wisconsin was 2001, the same season that produced Wisconsin’s first deer to test positive for chronic wasting disease. CWD has always been at the forefront of deer hunting discussions in my time as a hunter, and I’ve watched the disease slowly spread and worsen. Since 2019, eight of 11 deer I’ve taken on my family’s property in Richland County in Southwest Wisconsin have tested positive for CWD – including the buck in the photo above.
Aside from harvesting otherwise perfectly healthy-looking deer that test positive for CWD, we are now seeing live deer walking around in the awful final stages of this disease. Research has now confirmed what I’ve seen occurring on our hunting land in the last five to six years: CWD is beginning to reduce deer populations in high-prevalence areas like mine.
It didn’t have to reach this point. Hunters in areas with low CWD prevalence can keep infection rates low and deer populations healthy overall by accepting and implementing certain strategies. Some of the strategies I will lay out will challenge you as a hunter to play the “long game,” but there are ways to slow the spread of CWD in areas where it is newly discovered and infection rates are still low.
If you’re rolling your eyes at another guy talking about CWD, I get it, but I urge you to keep reading. Hear my personal story, how it has affected my hunting experiences, and what can happen if hunters ignore CWD.
“Where Are the Deer?”
Up until about seven years ago, I was still trying to figure out this CWD thing and what I thought of it all. I hadn’t yet seen or felt the effects. I was trying to improve my hunting in a variety of different ways like everyone else.
In Iowa County, hunters killed only 916 bucks during the 2024 nine-day firearms season. The last time Iowa County recorded less than 1,000 bucks killed during the nine-day firearms season was in 1971.
We began testing every deer taken on our farm in 2019, and with 72% of them testing positive, it’s safe to say we’re in the thick of it. I’m not alone. I speak to countless hunters in Southwest Wisconsin at trade shows and other events, and many of them are saying the same thing: “What is happening? Where are the deer?”
Since 2019, eight of 11 deer taken on Paul’s family land in southwest Wisconsin tested positive for CWD. This wall of bucks includes deer taken since 2006, and six of the more recent bucks added to this wall were CWD-positive.
In Iowa County, hunters killed only 916 bucks during the 2024 nine-day firearms season. The last time Iowa County recorded less than 1,000 bucks killed during the nine-day firearms season was in 1971. Iowa County tested 694 deer during the 2024 deer season, and 25% of deer tested were positive. Richland and Sauk counties both had a 33% positive CWD rate and together tested 2,193 deer. In 2004, a few years after the initial surge of testing occurred in Wisconsin, Richland County tested 1,691 deer and no deer tested positive for CWD. So, we haven’t been finding CWD just because we’re testing more. It arrived and has spread significantly.
The first time I saw what I believed to be CWD up close and personal was in spring 2023 when my dad and I were marching up a steep ridge for an afternoon turkey hunt. Just a short distance into the walk, I spotted a buck with velvet sprouts. “Dad,” I said. “Deer.”
We both thought it was unusual this deer wasn’t bounding off since we were within 40 yards. Springtime bucks are certainly not the paranoid creatures they become in fall, though. So, we closed the distance since we were headed that way and wanted a closer look.
The buck was very clearly sick. The hair on the back of my neck stood up instantly. A better view revealed his shaking, emaciated body and drool spilling from his mouth (see the photo below). His spine, shoulder blades, and scars up and down his legs told me this deer was in the final stage of CWD but had just enough energy to escape a few predators in the days prior. I had begun to wonder why so many of my 3½-year-old bucks never returned, and this moment convinced me CWD is playing a role in bucks constantly disappearing. This buck was days away from dying of holes eaten in his brain. We were able to put him out of his misery with permission from the Wisconsin DNR.
Though CWD has been in his area for more than 20 years, it wasn’t until 2023 that Paul Annear encountered a visibly sick deer. By the time hunters are seeing sick deer in the woods, the infection rate is usually too high to do anything about it.
I travel 200 miles one way to hunt this property in Southwest Wisconsin. The disease has in a way disrupted my motivation to keep traveling here, knowing full well there is a high likelihood of any deer we kill testing positive, resulting in us throwing out the meat. If you don’t hunt in a CWD zone, your routine following a successful hunt is probably simple and relatively careless. The presence of CWD changes that real quick. Shooting a deer means we could be in for a few frustrating weeks to follow as we wait for CWD test results. I’ve wasted countless hours butchering deer only to throw out the venison.
My friend and fellow Wisconsin deer hunter Bradie Ewing follows the same recommended protocols I do regarding CWD-positive venison.
“We have made the decision that we will not eat or feed a CWD positive deer to our kids or family, so this has caused some logistical headaches,” said Bradie. “The investment of time up front in butchering a deer is significant only to later throw it away if its positive.”
In 2020, I had nearly 30 bucks on trail-camera I estimated to be 3½ years old or older. In 2024, I felt confident we had only seven or eight deer in that age class. A stark decrease. I also ran about 20 more trail cameras on this 115-acre property in 2024 than I did in 2020, so fewer photos are not playing a role in my estimation of fewer mature deer. There are simply fewer mature deer, and DNR harvest data shows it’s not because hunters killed more older bucks in recent seasons. It’s because of CWD.
Why do I keep making the drive back to Richland County? My parents have lived on this land since 1987. This is the land where I was born and raised, where I grew up exploring the woods and learning to hunt squirrels and deer. It’s where I feel I belong, and I know that strong emotional attachment will keep me coming back to hunt deer with my family every fall.
Common Sense
Chronic Wasting Disease prions can be shed via saliva at mineral sites. CWD prions can exist in the soil below licking branches in a scrape. We’re never going to eliminate deer-to-deer contact in the wild. But if you’re in a low CWD prevalence area, there are some common-sense practices you should follow. You can learn from a few of my mistakes.
In the last few years, I’ve wondered if we can truly do anything to curb the spread of CWD in extremely high prevalence areas. One day I would feel the CWD battle is worth fighting, then just days later I’d harvest a CWD positive deer and be discouraged to the point of thinking “this is a bridge too far.”
With 33% of deer in Paul’s county now testing positive for CWD, he has begun to see visibly sick deer in the last two years. Paul’s trail-camera captured the photos above and below in fall 2024. Paul found the remains of the buck above three months after this photo was taken. Note: Deer with EHD die within 5 to 10 days of infection, which isn’t enough time for this kind of drastic weight loss.
I told myself I just wanted to get back to hunting. In the midst of these internal battles, I set out a tank-style waterhole on a Southwest Wisconsin property I hunt. While baiting or feeding is illegal in every Southwest Wisconsin county to help slow the spread of disease, the Wisconsin DNR has not banned the creation of artificial water sources. There are limited water resources on this property, and I thought a waterhole would be a unique way to attract deer near a stand site.
I had an abundance of deer visiting the water tank in the few months it was set up. Despite all the trail-camera photos, a famous Aldo Leopold quote would occasionally run through my mind: “A thing is right when it tends to preserve the integrity, stability, and the beauty of the biotic community – it is wrong if it tends otherwise.”
During the short time I had the waterhole out, I emptied and re-filled it many times since I still wanted to be cognizant of disease transmission. But I have to be honest with myself and admit that if I care about wild deer and the places they live, setting out a small, non-flowing waterhole in a CWD zone was a mistake. Not long after killing a visibly sick, CWD-positive doe that came to drink from the waterhole, we removed it.
In certain regions of the U.S., baiting is just a way of life and how it’s always been done. So, I get the enjoyment and desire to feed or provide artificial water sources for deer. I know hunters in states like Texas and Kansas who would hardly have a deer pass through their land if they didn’t run a feeder.
Are we going to stop the spread of CWD by banning waterholes or baiting? No. But common sense would say those things don’t help an infected herd. Artificially inflating your local deer population in a high CWD prevalence zone by feeding is dangerous because deer that may not otherwise come in contact with one another could share infectious prions at a bait or water site.
Does the presence of CWD mean you should never hang a mock licking branch or plant food plots to improve your hunting opportunities? I believe that’s an unreasonable way of thinking. I am still going to create food plots and mock scrapes. However, I strongly believe we need to practice common sense and realize there are matters we can take into our own hands when it comes to mitigating the spread of CWD. It begins with pulling triggers and landowners making strong, individual decisions regarding their deer herd and holding to them.
Sound Management and Testing
“Earn-A-Buck” was a tool some states used intermittently to effectively manage high deer herds. Wisconsin had implemented EAB off and on beginning in 1996, until it was signed out of law by Wisconsin Governor Scott Walker. I believe EAB is an effective tool for managing deer herds in some places, and I believe it’s no coincidence CWD rates have steadily increased in Wisconsin since Gov. Walker got rid of the law with pressure from other politicians and interest groups. There are few better incentives to take a doe than requiring it before you can take a buck. The only incentive that worked is now gone.
Earn-A-Buck cannot be signed back into law without the Wisconsin legislature doing so. Wisconsin hunters are left with a distinct choice that Wisconsin hunter Doug Duren is often heard saying. “Where CWD is established or taking hold, we have one of two choices,” Doug says. “We are going to manage the herd and the disease, or CWD is going to do it for us.” Wisconsin has had no effective deer management plan since the elimination of EAB in 2011.
In talking with countless hunters in my region, it appears CWD can be somewhat pocketed even within high prevalence counties like mine. The variability of CWD prevalence within a county could be due to availability of better habitat, people not illegally baiting in certain areas, or for unknown reasons. But we do know that high deer density helps CWD spread faster, so simply continuing to harvest deer – especially does – works. Doe harvest helps keep deer density in balance with the habitat and reduces deer-to-deer spread of CWD, which means healthier deer in all respects. But it’s not just about doe harvest.
Bucks test positive at a higher rate than does because of behaviors like traveling farther during the rut. I would encourage you to be less picky about harvesting bucks if CWD has just been discovered and you’re trying to keep prevalence rates low. NDA’s advice for hunters in CWD zones is to continue managing for older bucks if you wish but apply increased harvest pressure on all bucks 2½ years of age or older.
Do I wish we could go back to those days of low prevalence and undergo targeted removal missions on my family’s land to see if it would prevent or delay the problem we have today? Yes. Sustained harvest on all deer, bucks and does, means a better chance of removing infected deer from the landscape sooner. If hunters back off deer harvest because of CWD, infected deer enjoy greater protection, and they can spread more CWD prions into the environment and to other deer. In fact, every time you harvest a deer that tests positive for CWD, you should look at this as a win in the fight against this disease.
Jason Sumners is the Director of the Missouri Department of Conservation and has guided Missouri through a proactive approach to CWD.
“If all you are doing is testing to show you are doing something, it’s a complete waste of critical agency resources,” said Jason. “Short of documenting the demise of deer and giving some hunters a little more comfort when consuming deer harvested in CWD areas, it’s not doing anything to help the herd.”
What is Missouri doing? A lot of testing but also Targeted harvesting in select zones with landowner approval. In 2025, they’ve killed 4,793 deer with 68 (1.4%) of those being positive. While the CWD positive rate of these targeted removals is still low, that’s the point. This is a relatively small number of deer removed statewide, but because they are removed with precision from sites where deer previously tested positive, sick deer are removed sooner. Missouri is keeping CWD prevalence rates in check throughout these surveillance zones.
Would I have been hesitant to allow targeted deer removal or “sharpshooting”’on my property back when CWD had just been discovered? Yes. Do I wish we could go back to those days of low prevalence and undergo targeted removal missions on my family’s land to see if it would prevent or delay the problem we have today? Yes.
The early stage of CWD is the only stage when intervention and management can hope to hold infection rates low. If you wait until you are seeing sick deer in the woods, which is a sign you are in “late-stage” CWD, it’s too late to do anything about it.
If CWD isn’t in your woods yet, you should still make it a point to submit deer for testing anytime an opportunity is presented. Early detection of a new outbreak is critical. Early detection gives hunters and the state wildlife agency the opportunity to respond. CWD testing isn’t a proclamation of any political views or ideologies. However, it is absolutely a pledge that you care about deer and their future.
Paul Annear grew up hunting with his dad on family land in southwest Wisconsin and is now teaching his son Hudson how to hunt. We Are Not Doomed
I believe there will always be white-tailed deer in my area of Wisconsin. However, within 20 to 25 years, I believe fewer bucks will reach maturity than today, and a lot fewer than when I began hunting over 20 years ago.
This is despite more people than ever before passing younger deer and managing for older deer. I think in some areas like mine with high CWD prevalence, the average age of bucks has already dropped significantly from where it was just a few years ago – at a time when NDA’s Deer Report shows more bucks aged 3½ years old or older being harvested nationally than ever before.
If CWD has been found in your woods, ignoring it will take your hunting down the wrong path. Private landowners especially will play a critical role in properly managing whitetails in America in the next 30 years. I’m reminded of this Aldo Leopold quote: “Conservation will ultimately boil down to rewarding the private landowner who conserves the public interest.”
In this case, public interest is healthy deer. In most of whitetail country, unlike Southwest Wisconsin, it’s not too late to do something. Common-sense practices might seem like a burden to you now, but it’s nothing compared to what I’m experiencing. Ignoring those practices might help your short-term hunting opportunities, but remember you are in the position I wish I could go back to. Ask yourself if the choices you are making now will help conserve a better future for all.
Categories: Hunting
Tags: Chronic Wasting Disease, Cwd
About Paul Annear:
Paul Annear is an avid deer hunter, freelance writer and NDA member from the Driftless Region of southwest Wisconsin.
https://deerassociation.com/cwd-is-ravaging-my-familys-land-but-its-not-too-late-for-you/
Wisconsin DNR says CWD sinking deer herds in disease-endemic areas
PATRICK DURKIN Outdoors Columnist
CWD culprits
Snip…
“We can now say it’s not EHD (epizootic hemorrhagic disease), it’s not coyotes, it’s not bobcats, and it’s not earn-a-buck regulations from 15 years ago that are causing the herd declines we’re seeing,” said Dan Storm, the study’s chief researcher. “CWD is the cause, and we have solid evidence to back it up.
This is what’s going on, and so let’s proceed with what to do about it.” “We already did that and look how it went,” Storm said. “Before we lost earn-a-buck (in 2011), hunters dropped Iowa County’s deer herd below 20,000. After earn-a-buck, the herd took 7%, 10% and 12% annual increases until 2020.
That herd should have kept growing, but it didn’t. CWD is pulling it down and boxing it in.” The DNR’s annual post-hunt population estimates show Iowa County’s herd rose 51.3% from 16,900 in 2011 to 25,566, the 2018-2020 three-year average.
The herd has since fallen 15.25% to 21,666, the 2021-2023 three-year average.
Bryan Richards, CWD project leader at the USDA’s National Wildlife Health Center in Madison, said backing off would backfire. “You won’t recover a population by letting CWD run its course,” Richards said. “When you try to stockpile deer by not shooting, you protect sick deer, too. Contamination worsens and the healthy proportion of the herd declines.
Shooting removes sick deer from the herd sooner than CWD will. They’ll spread fewer prions over time, and you’ll probably shoot them before CWD reaches its worst stages for shedding prions.”
Storm put it this way: “The more CWD you have in your area, the more the herd will decline.”
Which areas already exceed 29% infection rates for adult does?
The latest DNR data from a year ago shows southeastern Richland County on the edge at 27%, northwestern Iowa County at 35%, and the Devil’s Lake area in eastern Sauk County at 34%. Further, CWD testing of hunter-killed deer in autumn 2024 shows overall (bucks and does) detection rates at or above 29% in six townships (6-mile by 6-mile areas) in Columbia County, three townships in Dane County, eight townships in Iowa County, 11 townships in Richland County, and 15 townships in Sauk County.
How low will deer populations drop where CWD is endemic?
Storm said CWD won’t exterminate deer, but no one can predict how it will affect specific valleys, woodlands or watersheds. CWD has spread at varying rates in different Wisconsin habitats, and appears to have leveled off at high infection rates in some areas while still rising and spreading in others.
The disease has so far been verified in wild deer in 48 of Wisconsin’s 72 counties, even though testing has been totally voluntary for years.
During the 2024 hunting season, 1,755 more deer tested positive for CWD across the state, a record 10.4% detection rate despite the least amount of samples (16,939) volunteered since 2017. Richland County hunters provided the most samples, 1,335, in 2024, and 444 (33.4%) had CWD.
https://www.antigojournal.com/sports/outdoors/durkin-wisconsin-dnr-says-cwd-sinking-deer-herds-in-disease-endemic-areas/article_cb73b5ca-dd9e-11ef-853c-d3fb206ddf8c.html
18% of mule deer in northeastern Montana have deadly chronic wasting disease “In the 2024-25 hunting FWP submitted 9,066 samples for chronic wasting disease testing – the largest number of CWD samples ever collected in a single year. More than 1,100 of these samples were collected by hunters. Of those samples, 335 tested positive for the disease, including 202 white-tailed deer, 127 mule deer and six elk.”
https://billingsgazette.com/outdoors/article_de5278b8-f2e1-11ef-b479-cf42652717a4.html
Southwest Wisconsin CWD, Deer and Predator Study
key takeaways ;
CWD substantially reduces deer survival rates and suppresses population growth.
Where CWD prevalence is high, deer populations are likely declining.
If CWD continues to spread, it will eventually impact deer populations elsewhere.
https://dnr.wisconsin.gov/topic/research/projects/dpp/StudyResults
MONDAY, APRIL 28, 2025
Wisconsin DNR 2024 CWD 1,786 samples testing positive
https://chronic-wasting-disease.blogspot.com/2025/04/wisconsin-dnr-2024-cwd-1786-samples.html
This CWD Study Could Change Deer Hunting FOREVER | The Check Station October 8, 2025 NW Arkansas
NW Arkansas CWD 11:25 minutes;
50% of all deer positive for CWD.
35% of Does are Positive for CWD.
68% Bucks are Positive for CWD.
Most Bucks NW Arkansas that where Tested, are Positive for CWD.
https://m.youtube.com/watch?v=kTicUE-xsQU&t=695s&pp=2AG3BZACAQ%3D%3D
MEMORANDUM
To: Members of the Colorado Parks and Wildlife Commission
From: Dan Prenzlow, Director
Date: April 22, 2022
Subject: Chronic Wasting Disease Update for Parks and Wildlife Commission Chronic wasting disease, a fatal neurological disease found in deer, elk, and moose, is well established in herds throughout much of Colorado. We have detected CWD in 40 of our 54 deer herds, 17 of 42 elk herds, and 2 of 9 moose herds. Disease prevalence (percent infected) is highest in deer and lowest in moose. This disease is always fatal and animals die from the disease within about 2-2.5 years of infection. CWD infection shortens the lifespan of infected animals. If infection rates become too high, CWD can affect a herd’s ability to sustain itself.
Snip…
http://web.archive.org/web/20220609004350/https://cpw.state.co.us/Documents/Commission/2022/May/Item.11-PWC_Memo_CWD_Update_EckertMillerWood_April2022-Matthew_Eckert-DNR.pdf
18% of mule deer in northeastern Montana have deadly chronic wasting disease “In the 2024-25 hunting FWP submitted 9,066 samples for chronic wasting disease testing – the largest number of CWD samples ever collected in a single year. More than 1,100 of these samples were collected by hunters. Of those samples, 335 tested positive for the disease, including 202 white-tailed deer, 127 mule deer and six elk.”
https://billingsgazette.com/outdoors/article_de5278b8-f2e1-11ef-b479-cf42652717a4.html
Southwest Wisconsin CWD, Deer and Predator Study
key takeaways ;
CWD substantially reduces deer survival rates and suppresses population growth.
Where CWD prevalence is high, deer populations are likely declining.
If CWD continues to spread, it will eventually impact deer populations elsewhere.
https://dnr.wisconsin.gov/topic/research/projects/dpp/StudyResults
The effectiveness of harvest for limiting wildlife disease: Insights from 20 years of chronic wasting disease in Wyoming
First published: 21 January 2025
https://doi.org/10.1002/eap.3089
https://esajournals.onlinelibrary.wiley.com/doi/10.1002/eap.3089
https://www.usgs.gov/news/national-news-release/new-study-finds-deer-hunting-can-help-keep-chronic-wasting-disease-check
Since identifying its first cases of CWD in captive deer in the 70s and finding the first wild infected deer in 1985, Wyoming has seen the disease slowly spread throughout the state. CWD has now been documented in members of the deer family in most of Wyoming’s deer hunting areas, with 20% to 40% percent of mule deer affected in some herds. A 2017 study estimated a 21% annual population decline as a result of the fatal disease.
https://freerangeamerican.us/chronic-wasting-disease-wyoming/#:~:text=CWD%20has%20now%20been%20documented,result%20of%20the%20fatal%20disease.
How does CWD impact deer, elk, and moose populations? Recent research in Wyoming has demonstrated declines in both mule and white-tailed deer populations in deer hunt area 65 due to CWD (see below for citations). These declines are in the core endemic area where prevalence is highest. In areas with lower prevalence, effects of CWD are poorly understood but are considered additive along with other factors that can negatively affect deer populations in Wyoming (i.e. habitat loss, predation, other diseases). The distribution and prevalence of CWD in Wyoming elk is less than that of deer. Currently there are no documented direct population impacts in Wyoming elk from CWD; however, research from Rocky Mountain National Park suggests that CWD could impact elk populations at higher prevalence (13%). While CWD has been found in free ranging moose, there have been few detections, and there is no evidence that CWD is currently having an impact on moose populations.
https://wgfd.wyo.gov/Wildlife-in-Wyoming/More-Wildlife/Wildlife-Disease/Chronic-Wasting-Disease
TUESDAY, SEPTEMBER 30, 2025
USDA EXPLANATORY NOTES ANIMAL AND PLANT HEALTH INSPECTION SERVICE 2025-2014 CHRONIC WASTING DISEASE CWD TSE CERVID
https://chronic-wasting-disease.blogspot.com/2025/09/usda-explanatory-notes-animal-and-plant.html
one of the old studies that has always stuck out in my mind, one that the late great Dr. Gibbs, Gajdusek, et al did way back, and to this day is still amazes me...friendly fire, iatrogenic transmission, including field dressing a deer, includes risks for exposure to the Cwd tse prion…take precautions!
*** Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery ***
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract
Chronic wasting disease (CWD) prion detection in environmental and biological samples from a taxidermy site and nursing facility, and instruments used in surveillance activities
Author links open overlay panel Paulina Soto a b , Nancy Ho a , Mitch Lockwood c , Austin Stolte c , J. Hunter Reed c , Rodrigo Morales a b
https://doi.org/10.1016/j.scitotenv.2025.179318
• CWD prions were identified in a taxidermy and deer nursing facility.
• Contaminated samples included waters, soils, dermestid beetles, domestic flies and a dumpster.
• Surgical instruments used to collect deer samples can get contaminated with CWD prions.
• Some of the infectious particles are readily released from surgical instruments when washed.
• Our results suggest that taxidermy practices actively contribute in the spreading of CWD.
Abstract
Chronic wasting disease (CWD) is a transmissible prionopathy affecting free-ranging and captive cervids. CWD is thought to spread through both direct and indirect transmission mechanisms. Along this line, human activities have not been thoroughly explored for their potential to spread this disease. One area of concern involves taxidermy procedures and surveillance activities as handled animals or carcasses are of unknown CWD statuses. Worrisomely, taxidermy facilities can act as foci of prion infectivity if appropriate biosecurity practices are not implemented. In this study, we evaluated the presence of infectious prions in a taxidermy facility that was possibly exposed to CWD prions. To determine this, we collected biological and environmental specimens from this site and screened them using the protein misfolding cyclic amplification (PMCA) technique. Additionally, we swabbed different surfaces possibly exposed to CWD-infected animals or carcasses. We report the presence of prions in i) waters used to digest tissues from deer carcasses, ii) soils that were in contact with the previously mentioned waters, iii) dermestid beetles used to clean skulls, iv) other insects found in the beetle shed, and iv) dumpsters where animal carcasses were disposed. Additionally, we report that surgical materials used in surveillance practices may also hold CWD prions, even after being washed with aqueous solutions. All these results suggest that CWD prions may be disseminated due to human practices and that protocols should be established to decontaminate potentially contaminated materials.
https://www.sciencedirect.com/science/article/abs/pii/S0048969725009544?via%3Dihub
CWD, Oh Deer, August 2021
https://trerc.tamu.edu/article/oh-deer-2314/
Published: 05 August 2025
Vertical transmission of chronic wasting disease in free-ranging white-tailed deer populations
Snip…
Our detection of CWD-positive fawns ≤ 10-month-old by ELISA testing provides indirect evidence of gestational infection, although direct or indirect CWD transmission after birth cannot be ruled out in these fawns (Table 5). The detection of CWD infection in ≤ 6-month-old fawns in the Arkansas and Tennessee study sites by ELISA test, which is not as sensitive as amplification assays37, was particularly suggestive of vertical transmission. Fawns less than 6 months of age are not routinely incorporated into statewide CWD surveillance programs because of the low likelihood of detectable infection using traditional assays (i.e., ELISA, IHC), yet have been previously identified17. Future studies should investigate the potential role of in utero transmission in local CWD transmission cycles. Considering the strong relationship between CWD infection probability and female white-tailed deer relatedness, in utero CWD transmission may serve as a small yet important route of transmission in addition to social interactions and indirect exposures53.
Overall, this study describes the dissemination of CWD prions throughout tissues and birthing fluids of the pregnancy microenvironment demonstrating that offspring are routinely exposed to the infectious prion in-utero prior to parturition. We report infectious prions in the reproductive and fetal tissue of naturally exposed free-ranging white-tailed deer suggesting that in utero maternal transmission is likely an underappreciated mode of CWD transmission. Our study shows that vertical transmission is indeed a viable route of infection within the southeastern U.S. and is another potential factor contributing to the relentless spread of chronic wasting disease.
https://www.nature.com/articles/s41598-025-12727-8
Just remember;
Chronic Wasting Disease CWD TSE Prion
THE CWD TSE Prion aka mad cow type disease is not your normal pathogen.
The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.
It’s not your ordinary pathogen you can just cook it out and be done.
You cannot cook the TSE prion disease out of meat. In fact new data now shows that exposure to high temperatures used to cook the meat increased the availability of prions for in vitro amplification.
You can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.
The TSE prion agent also survives Simulated Wastewater Treatment Processes.
The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.
IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades. 15 to 21 years.
You can bury it and it will not go away.
Prions in Waterways
https://vimeo.com/898941380?fbclid=IwAR3Di7tLuU-iagCetdt4-CVPrOPQQrv037QS1Uxz0tX3z7BuvPeYlwIp7IY
Prion. 2009 Jul-Sep;3(3):171–183. doi: 10.4161/pri.3.3.9819
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
TA Nichols 1,2, Bruce Pulford 1, A Christy Wyckoff 1,2, Crystal Meyerett 1, Brady Michel 1, Kevin Gertig 3, Edward A Hoover 1, Jean E Jewell 4, Glenn C Telling 5, Mark D Zabel 1,
Abstract
Chronic wasting disease (CWD) is the only known transmissible spongiform encephalopathy affecting free-ranging wildlife. Although the exact mode of natural transmission remains unknown, substantial evidence suggests that prions can persist in the environment, implicating components thereof as potential prion reservoirs and transmission vehicles.1–4 CWD-positive animals may contribute to environmental prion load via decomposing carcasses and biological materials including saliva, blood, urine and feces.5–7 Sensitivity limitations of conventional assays hamper evaluation of environmental prion loads in soil and water. Here we show the ability of serial protein misfolding cyclic amplification (sPMCA) to amplify a 1.3 × 10−7 dilution of CWD-infected brain homogenate spiked into water samples, equivalent to approximately 5 × 107 protease resistant cervid prion protein (PrPCWD) monomers. We also detected PrPCWD in one of two environmental water samples from a CWD endemic area collected at a time of increased water runoff from melting winter snow pack, as well as in water samples obtained concurrently from the flocculation stage of water processing by the municipal water treatment facility. Bioassays indicated that the PrPCWD detected was below infectious levels. These data demonstrate detection of very low levels of PrPCWD in the environment by sPMCA and suggest persistence and accumulation of prions in the environment that may promote CWD transmission.
Snip…
The data presented here demonstrate that sPMCA can detect low levels of PrPCWD in the environment, corroborate previous biological and experimental data suggesting long term persistence of prions in the environment2,3 and imply that PrPCWD accumulation over time may contribute to transmission of CWD in areas where it has been endemic for decades. This work demonstrates the utility of sPMCA to evaluate other environmental water sources for PrPCWD, including smaller bodies of water such as vernal pools and wallows, where large numbers of cervids congregate and into which prions from infected animals may be shed and concentrated to infectious levels.
Key words: prions, chronic wasting disease, water, environment, serial protein misfolding cyclic amplification
https://pmc.ncbi.nlm.nih.gov/articles/PMC2802782/
Detection of chronic wasting disease prions in soil at an illegal white-tailed deer carcass disposal site
Published online: 06 Jun 2025
Abstract
Chronic wasting disease (CWD) is a contagious prion disorder affecting cervids such as deer, elk, caribou, and moose, causing progressive and severe neurological degeneration followed by eventual death. As CWD prions (PrPSc) accumulate in the body, they are shed through excreta and secreta, as well as through decomposing carcasses. Prions can persist in the environment for years, posing significant concerns for ongoing transmission to susceptible cervids and pose an unknown risk to sympatric species. We used a validated protocol for real-time quaking-induced conversion (RT-QuIC) in vitro prion amplification assay to detect prions in soil collected within and around an illegal white-tailed deer (Odocoileus virginianus, WTD) carcass disposal site and associated captive WTD farm in Beltrami County, Minnesota. We detected PrPSc in 26 of 201 soil samples across 15 locations within the illegal disposal site and one on the farm that housed the cervids. Importantly, a subset of RT-QuIC positive soil samples was collected from soils where carcasses were recovered, providing direct evidence that environmental contamination resulted from this illegal activity. These findings reveal that improper cervid carcass disposal practices may have important implications for ongoing CWD transmission through the environment.
Snip…
Conclusions
Using RT-QuIC, we detected PrPSc in 26 of 201 soil samples collected across 16 locations on public land where WTD carcasses had been disposed and the captive facility from where they originated. Within the disposal site, 25 out of 124 soil samples (20%) tested positive for PrPSc. Among those positive detections, 17, or 68%, were collected from locations where CWD-positive WTD remains had been previously recovered. This environmental investigation demonstrates how improper cervid carcass disposal practices can result in persistent environmental contamination, posing a potential risk to wildlife health. Given that disposal of livestock on the landscape is a common practice among producers [Citation54–56], these findings underscore the need for improved disposal practices and further investigation of environmental impacts. Expanding on this area of environmental research is crucial as the geographic range of CWD continues to expand [Citation57]. The use of RT-QuIC for prion detection in environmental samples offers an exciting advancement to environmental surveillance for prions, though as we demonstrate here and in Grunklee et al. [Citation41], assay optimization and validation for use with different environmental samples, including new soil types, is still necessary. Further enhancements to RT-QuIC and other methodologies for prion detection will facilitate more opportunities to explore the persistence, degradation, transport, and remediation of environmental prions.
https://www.tandfonline.com/doi/full/10.1080/19336896.2025.2514947
While the disease control measures effectively eliminated prion seeding activity in CWD-affected farms, CWD recurred at two of the 18 remediated farms 4 to 5 years after restocking animals. It remains unclear whether the recurrence of CWD at the two farms was due to residual prions in the environment after the control measures, or the introduction of the infected animals from other farms. This uncertainty is heightened by the annual occurrence of CWD at multiple farms and the absence of a traceability system for farmed cervids.
Keywords: Chronic wasting disease (CWD); NaOH; Protein-misfolding cyclic amplification (PMCA); Republic of Korea; farm; prions; remediation; topsoil.
https://www.tandfonline.com/doi/full/10.1080/19336896.2025.2527588
“While the disease control measures effectively eliminated prion seeding activity in CWD-affected farms, CWD recurred at two of the 18 remediated farms 4 to 5 years after restocking animals.”
I remember what “deep throat” told me about Scrapie back around 2001, during early days of my BSE investigation, after my Mom died from hvCJD, I never forgot, and it seems it’s come to pass;
***> Confidential!!!!
***> As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!
---end personal email---end...tss
and so it seems…
so, this is what we leave our children and grandchildren?
Rapid recontamination of a farm building occurs after attempted prion removal
First published: 19 January 2019 https://doi.org/10.1136/vr.105054
The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease.
snip...
This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapie positive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.
https://bvajournals.onlinelibrary.wiley.com/doi/abs/10.1136/vr.105054
***>This is very likely to have parallels with control efforts for CWD in cervids.
https://pubmed.ncbi.nlm.nih.gov/30602491/
Front. Vet. Sci., 14 September 2015 | https://doi.org/10.3389/fvets.2015.00032
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination.
http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full
"Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation."
15 YEARS!
Detection of prions in soils contaminated by multiple routes
Results: We are able to detect prion seeding activity at multiple types of environmental hotspots, including carcass sites, contaminated captive facilities, and scrapes (i.e. urine and saliva). Differences in relative prion concentration vary depending on the nature and source of the contamination. Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation.
Conclusions: Detection of prions in the environment is of the utmost importance for controlling chronic wasting disease spread. Here, we have demonstrated a viable method for detection of prions in complex environmental matrices. However, it is quite likely that this method underestimates the total infectious prion load in a contaminated sample, due to incomplete recovery of infectious prions. Further refinements are necessary for accurate quantification of prions in such samples, and to account for the intrinsic heterogeneities found in the broader environment.
Funded by: Wisconsin Department of Natural Resources
Prion 2023 Abstracts
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
SUNDAY, APRIL 06, 2025
Failure to prevent classical scrapie after repeated decontamination of a barn
https://scrapie-usa.blogspot.com/2025/04/failure-to-prevent-classical-scrapie.html
https://prpsc.proboards.com/thread/165/failure-prevent-scrapie-repeated-decontamination
CWD, So, this is what we leave our children and grandchildren?
Detection of chronic wasting disease prions in the farm soil of the Republic of Korea
Here, we show that prion seeding activity was detected in extracts from farm soil following 4 years of incubation with CWD-infected brain homogenate.
https://journals.asm.org/doi/10.1128/msphere.00866-24
Artificial mineral sites that pre-date endemic chronic wasting disease become prion hotspots
The detection of PrPCWD in soils at attractant sites within an endemic CWD zone significantly advances our understanding of environmental PrPCWD accumulation dynamics, providing valuable information for advancing adaptive CWD management approaches.
https://int-cwd-sympo.org/wp-content/uploads/2023/06/final-agenda-with-abstracts.pdf
Chronic wasting disease detection in environmental and biological samples from a taxidermy site
Results: The PMCA analysis demonstrated CWD seeding activity in some of the components of this facility, including insects involved in head processing, soils, and a trash dumpster.
Conclusions: Different areas of this property were used for various taxidermy procedures. We were able to detect the presence of prions in i) soils that were in contact with the heads of dead animals, ii) insects involved in the cleaning of skulls, and iii) an empty dumpster where animal carcasses were previously placed. This is the first report demonstrating that swabbing is a helpful method to screen for prion infectivity on surfaces potentially contaminated with CWD. These findings are relevant as this swabbing and amplification strategy may be used to evaluate the disease status of other free-ranging and captive settings where there is a concern for CWD transmissions, such as at feeders and water troughs with CWD-exposed properties. This approach could have substantial implications for free-ranging cervid surveillance as well as in epidemiological investigations of CWD.
Prion 2022 Conference abstracts: pushing the boundaries
https://www.tandfonline.com/doi/full/10.1080/19336896.2022.2091286
https://intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf?force_download=true
***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years
***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded.
JOURNAL OF GENERAL VIROLOGY Volume 87, Issue 12
Infectious agent of sheep scrapie may persist in the environment for at least 16 years Free
https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.82011-0
Rapid recontamination of a farm building occurs after attempted prion removal
First published: 19 January 2019 https://doi.org/10.1136/vr.105054
The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease. snip...
This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapie positive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.
https://bvajournals.onlinelibrary.wiley.com/doi/abs/10.1136/vr.105054
***>This is very likely to have parallels with control efforts for CWD in cervids.
https://pubmed.ncbi.nlm.nih.gov/30602491/
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
http://www.pnas.org/content/97/7/3418.full
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/
Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals
https://bmcvetres.biomedcentral.com/track/pdf/10.1186/1746-6148-9-134.pdf
THURSDAY, FEBRUARY 28, 2019
BSE infectivity survives burial for five years with only limited spread
https://link.springer.com/content/pdf/10.1007%2Fs00705-019-04154-8.pdf
So, this is what we leave our children and grandchildren?
MONDAY, SEPTEMBER 15, 2025
Chronic Wasting Disease CWD TSE Prion Environmental Factors Update
https://chronic-wasting-disease.blogspot.com/2025/09/chronic-wasting-disease-cwd-tse-prion.html
https://chronic-wasting-disease.blogspot.com/
Chronic Wasting Disease CWD TSE Prion Environmental & Zoonosis Factors Update September 2025
What does CDC say?
CDC CWD TSE Prion Update 2025
KEY POINTS
Chronic wasting disease affects deer, elk and similar animals in the United States and a few other countries.
The disease hasn't been shown to infect people.
However, it might be a risk to people if they have contact with or eat meat from animals infected with CWD.
https://www.cdc.gov/chronic-wasting/about/index.html
Prions in Muscles of Cervids with Chronic Wasting Disease, Norway
Volume 31, Number 2—February 2025
Research
Prions in Muscles of Cervids with Chronic Wasting Disease, Norway
Snip…
In summary, the results of our study indicate that prions are widely distributed in peripheral and edible tissues of cervids in Norway, including muscles. This finding highlights the risk of human exposure to small amounts of prions through handling and consuming infected cervids. Nevertheless, we note that this study did not investigate the zoonotic potential of the Norway CWD prions. In North America, humans have historically consumed meat from CWD-infected animals, which has been documented to harbor prions (35,44–47). Despite the potential exposure to prions, no epidemiologic evidence indicates a correlation between the occurrence of CWD cases in animals and the prevalence of human prion diseases (48). A recent bioassay study reported no transmissions from 3 Nordic isolates into transgenic mice expressing human PrP (49). Therefore, our findings should be interpreted with caution in terms of human health implications, and further research is required to determine the zoonotic potential of these CWD strains.
The presence of prions in peripheral tissues indicates that CWD may have a systemic nature in all Norwegian cervid species, challenging the view that prions are exclusively localized in the CNS in sporadic CWD of moose and red deer. Our findings expand the notion of just how widely distributed prions can be in cervids affected with CWD and call into question the capability of emerging CWD strains in terms of infectivity to other species, including humans.
Appendix
https://wwwnc.cdc.gov/eid/article/31/2/24-0903-app1.pdf
https://wwwnc.cdc.gov/eid/article/31/2/24-0903_article
Volume 31, Number 2—February 2025
Dispatch
Detection of Chronic Wasting Disease Prions in Raw, Processed, and Cooked Elk Meat, Texas, USA
Rebeca Benavente, Fraser Brydon, Francisca Bravo-Risi, Paulina Soto, J. Hunter Reed, Mitch Lockwood, Glenn Telling, Marcelo A. Barria, and Rodrigo MoralesComments to Author
Snip…
CWD prions have been detected in the muscle of both farmed and wild deer (10), and at concentrations relevant to sustain disease transmission (11). CWD prions have also been identified across several cervid species and in multiple tissues, including lymph nodes, spleen, tongue, intestines, adrenal gland, eyes, reproductive tissues, ears, lungs, and liver, among others (12–14). Those findings raise concerns about the safety of ingesting processed meats that contain tissues other than skeletal muscle (15) (Appendix). https://wwwnc.cdc.gov/eid/article/31/2/24-0906-app1.pdf
In addition, those findings highlight the need for continued vigilance and research on the transmission risks of prion diseases and for development of new preventative and detection measures to ensure the safety of the human food supply.
Snip…
Overall, our study results confirm previous reports describing the presence of CWD prions in elk muscles (13). The data also demonstrated CWD prion persistence in food products even after processing through different procedures, including the addition of salts, spices, and other edible elements. Of note, our data show that exposure to high temperatures used to cook the meat increased the availability of prions for in vitro amplification. Considering the potential implications in food safety and public health, we believe that the findings described in this study warrant further research. Our results suggest that although the elk meat used in this study resisted different manipulations involved in subsequent consumption by humans, their zoonotic potential was limited. Nevertheless, even though no cases of CWD transmission to human have been reported, the potential for human infection is still unclear and continued monitoring for zoonotic potential is warranted.
https://wwwnc.cdc.gov/eid/article/31/2/24-0906_article
The detection and decontamination of chronic wasting disease prions during venison processing
Aims: There is a growing concern that chronic wasting disease (CWD) prions in venison pose a risk to human health. CWD prions accumulate in infected deer tissues that commonly enter the human food chain through meat processing and consumption. The United States (US) Food and Drug Administration and US Department of Agriculture now formally consider CWD-positive venison unfit for human and animal consumption. Yet, the degree to which prion contamination occurs during routine venison processing is unknown. Here, we use environmental surface swab methods to:
a) experimentally test meat processing equipment (i.e., stainless steel knives and polyethylene cutting boards) before and after processing CWD-positive venison and
b) test the efficacy of five different disinfectant types (i.e., Dawn dish soap, Virkon-S, Briotech, 10% bleach, and 40% bleach) to determine prion decontamination efficacy.
Materials and Methods: We used a real-time quaking-induced conversion (RT-QuIC) assay to determine CWD infection status of venison and to detect CWD prions in the swabs. We collected three swabs per surface and ran eight technical replicates on RT-QuIC.
Results: CWD prions were detected on all cutting boards (n= 3; replicates= 8/8, 8/8, 8/8 and knives (n= 3; replicates= 8/8, 8/8, 8/8) used in processing CWD-positive venison, but not on those used for CWD-negative venison. After processing CWD-positive venison, allowing the surfaces to dry, and washing the cutting board with Dawn dish soap, we detected CWD prions on the cutting board surface (n= 3; replicates= 8/8, 8/8, 8/8) but not on the knife (n= 3, replicates = 0/8, 0/8, 0/8). Similar patterns were observed with Briotech (cutting board: n= 3; replicates= 7/8, 1/8, 0/8; knife: n= 3; replicates = 0/8, 0/8, 0/8). We did not detect CWD prions on the knives or cutting boards after disinfecting with Virkon-S, 10% bleach, and 40% bleach.
Conclusions: These preliminary results suggest that Dawn dish soap and Briotech do not reliably decontaminate CWD prions from these surfaces. Our data suggest that Virkon-S and various bleach concentrations are more effective in reducing prion contamination of meat processing surfaces; however, surface type may also influence the ability of prions to adsorb to surfaces, preventing complete decontamination. Our results will directly inform best practices to prevent the introduction of CWD prions into the human food chain during venison processing.
Prion 2023 Abstracts
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
DETECTION OF CHRONIC WASTING DISEASE PRIONS IN PROCESSED MEATS.
The zoonotic potential of chronic wasting disease (CWD) remains unknown. Currently, there are no known natural cases of CWD transmission to humans but increasing evidence suggests that the host range of CWD is not confined only to cervid species. Alarmingly, recent experimental evidence suggests that certain CWD isolates can induce disease in non-human primates. While the CDC strongly recommends determining CWD status in animals prior to consumption, this practice is voluntary. Consequently, it is plausible that a proportion of the cervid meat entering the human food chain may be contaminated with CWD. Of additional concern is that traditional diagnostic techniques used to detect CWD have relatively low sensitivity and are only approved for use in tissues other than those typically ingested by humans. In this study, we analyzed different processed meats derived from a pre-clinical, CWD-positive free-ranging elk. Products tested included filets, sausages, boneless steaks, burgers, ham steaks, seasoned chili meats, and spiced meats. CWD-prion presence in these products were assessed by PMCA using deer and elk substrates. Our results show positive prion detection in all products. To confirm the resilience of CWD-prions to traditional cooking methods, we grilled and boiled the meat products and evaluated them for any remnant PMCA seeding activity. Results confirmed the presence of CWD-prions in these meat products suggesting that infectious particles may still be available to people even after cooking. Our results strongly suggest ongoing human exposure to CWD-prions and raise significant concerns of zoonotic transmission through ingestion of CWD contaminated meat products.
***> Products tested included filets, sausages, boneless steaks, burgers, ham steaks, seasoned chili meats, and spiced meats.
***> CWD-prion presence in these products were assessed by PMCA using deer and elk substrates.
***> Our results show positive prion detection in all products.
***> Results confirmed the presence of CWD-prions in these meat products suggesting that infectious particles may still be available to people even after cooking.
***> Our results strongly suggest ongoing human exposure to CWD-prions and raise significant concerns of zoonotic transmission through ingestion of CWD contaminated meat products.
https://intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf?force_download=true
Detection of chronic wasting disease prions in processed meats
Results: Our results show positive prion detection in all the samples analyzed using deer and elk substrates. Surprisingly, cooked meats displayed increased seeding activities. This data suggests that CWD-prions are available to people even after meats are processed and cooked.
Conclusions: These results suggest CWD prions are accessible to humans through meats, even after processing and cooking. Considering the fact that these samples were collected from already processed specimens, the availability of CWD prions to humans is probably underestimated.
"Our results show positive prion detection in all the samples analyzed using deer and elk substrates. Surprisingly, cooked meats displayed increased seeding activities."
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
Fortuitous generation of a zoonotic cervid prion strain
Aims: Whether CWD prions can infect humans remains unclear despite the very substantial scale and long history of human exposure of CWD in many states or provinces of USA and Canada. Multiple in vitro conversion experiments and in vivo animal studies indicate that the CWD-to-human transmission barrier is not unbreakable. A major long-term public health concern on CWD zoonosis is the emergence of highly zoonotic CWD strains. We aim to address the question of whether highly zoonotic CWD strains are possible.
Materials and Methods: We inoculated several sCJD brain samples into cervidized transgenic mice (Tg12), which were intended as negative controls for bioassays of brain tissues from sCJD cases who had potentially been exposed to CWD. Some of the Tg12mice became infected and their brain tissues were further examined by Western blot as well as serial passages in humanized or cervidized mice.
Results: Passage of sCJDMM1 in transgenic mice expressing elk PrP (Tg12) resulted in a “cervidized” CJD strain that we termed CJDElkPrP. We observed 100% transmission of the original CJDElkPrP in transgenic mice expressing human PrP. We passaged CJDElkPrP two more times in the Tg12mice. We found that such second and third passage CJDElkPrP prions retained 100% transmission rate in the humanized mice, despite that the natural elk CWD isolates and CJDElkPrP share the same elk PrP sequence. In contrast, we and others found zero or poor transmission of natural elk CWD isolates in humanized mice.
Conclusions: Our data indicate that highly zoonotic cervid prion strains are not only possible but also can retain zoonotic potential after serial passages in cervids, suggesting a very significant and serious long-term risk of CWD zoonosis given that the broad and continuing spread of CWD prions will provide fertile grounds for the emergence of zoonotic CWD strains over time.
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
Transmission of cervid prions to humanized mice demonstrates the zoonotic potential of CWD
Samia Hannaoui1 · Irina Zemlyankina1 · Sheng Chun Chang1 · Maria Immaculata Arifn1 · Vincent Béringue2 · Debbie McKenzie3 · Hermann M. Schatzl1 · Sabine Gilch1
Received: 24 May 2022 / Revised: 5 August 2022 / Accepted: 7 August 2022
© The Author(s) 2022
Abstract
Prions cause infectious and fatal neurodegenerative diseases in mammals. Chronic wasting disease (CWD), a prion disease of cervids, spreads efficiently among wild and farmed animals. Potential transmission to humans of CWD is a growing concern due to its increasing prevalence. Here, we provide evidence for a zoonotic potential of CWD prions, and its probable signature using mice expressing human prion protein (PrP) as an infection model. Inoculation of these mice with deer CWD isolates resulted in atypical clinical manifestation with prion seeding activity and efficient transmissible infectivity in the brain and, remarkably, in feces, but without classical neuropathological or Western blot appearances of prion diseases. Intriguingly, the protease-resistant PrP in the brain resembled that found in a familial human prion disease and was transmissible upon second passage. Our results suggest that CWD might infect humans, although the transmission barrier is likely higher compared to zoonotic transmission of cattle prions. Notably, our data suggest a different clinical presentation, prion signature, and tissue tropism, which causes challenges for detection by current diagnostic assays. Furthermore, the presence of infectious prions in feces is concerning because if this occurs in humans, it is a source for human-to-human transmission. These findings have strong implications for public health and CWD management.
Keywords Chronic wasting disease · CWD · Zoonotic potential · Prion strains · Zoonotic prions
HIGHLIGHTS OF THIS STUDY
================================
Our results suggest that CWD might infect humans, although the transmission barrier is likely higher compared to zoonotic transmission of cattle prions. Notably, our data suggest a different clinical presentation, prion signature, and tissue tropism, which causes challenges for detection by current diagnostic assays. Furthermore, the presence of infectious prions in feces is concerning because if this occurs in humans, it is a source for human-to-human transmission. These findings have strong implications for public health and CWD management.
In this study, we evaluated the zoonotic potential of CWD using a transgenic mouse model overexpressing human M129-PrPC (tg650 [12]). We inoculated tg650 mice intracerebrally with two deer CWD isolates, Wisc-1 and 116AG [22, 23, 27, 29]. We demonstrate that this transgenic line was susceptible to infection with CWD prions and displayed a distinct leading clinical sign, an atypical PrPSc signature and unusual fecal shedding of infectious prions. Importantly, these prions generated by the human PrP transgenic mice were transmissible upon passage. Our results are the first evidence of a zoonotic risk of CWD when using one of the most common CWD strains, Wisc-1/CWD1 for infection. We demonstrated in a human transgenic mouse model that the species barrier for transmission of CWD to humans is not absolute. The fact that its signature was not typical raises the questions whether CWD would manifest in humans as a subclinical infection, whether it would arise through direct or indirect transmission including an intermediate host, or a silent to uncovered human-to-human transmission, and whether current detection techniques will be suffcient to unveil its presence.
Our findings strongly suggest that CWD should be regarded as an actual public health risk. Here, we use humanized mice to show that CWD prions can cross the species barrier to humans, and remarkably, infectious prions can be excreted in feces.
Our results indicate that if CWD crosses the species-barrier to humans, it is unlikely to resemble the most common forms of human prion diseases with respect to clinical signs, tissue tropism and PrPSc signature. For instance, PrPSc in variable protease-sensitive prionopathy (VPSPr), a sporadic form of human prion disease, and in the genetic form Gerstmann-Sträussler-Scheinker syndrome (GSS) is defined by an atypical PK-resistant PrPSc fragment that is non-glycosylated and truncated at both C- and N-termini, with a molecular weight between 6 and 8 kDa [24, 44–46]. These biochemical features are unique and distinctive from PrPSc (PrP27-30) found in most other human or animal prion disease. The atypical PrPSc signature detected in brain homogenate of tg650 mice #321 (1st passage) and #3063 (2nd passage), and the 7–8 kDa fragment (Figs. 2, 4) are very similar to that of GSS, both in terms of migration profile and the N-terminal cleavage site.
CWD in humans might remain subclinical but with PrPSc deposits in the brain with an unusual morphology that does not resemble the patterns usually seen in different prion diseases (e.g., mouse #328; Fig. 3), clinical with untraceable abnormal PrP (e.g., mouse #327) but still transmissible and uncovered upon subsequent passage (e.g., mouse #3063; Fig. 4), or prions have other reservoirs than the usual ones, hence the presence of infectivity in feces (e.g., mouse #327) suggesting a potential for human-to-human transmission and a real iatrogenic risk that might be unrecognizable.
“suggesting a potential for human-to-human transmission and a real iatrogenic risk that might be unrecognizable.”
=================================
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/s00401-022-02482-9
snip...see full text;
https://link.springer.com/article/10.1007/s00401-022-02482-9
https://link.springer.com/content/pdf/10.1007/s00401-022-02482-9.pdf
Macaque tissues to rodent models demonstrates the zoonotic potential of chronic wasting disease.
Samia Hannaoui1,2, Ginny Cheng1,2, Wiebke Wemheuer3, Walter Schulz-Schaeffer3, Sabine Gilch1,2, Hermann Schatzl1,2 1University of Calgary, Calgary, Canada. 2Calgary Prion Research Unit, Calgary, Canada. 3Institute of Neuropathology, Medical Faculty, Saarland University, Homburg/Saar, Germany
Snip…
***> Further passage to cervidized mice revealed transmission with a 100% attack rate.
***> Our findings demonstrate that macaques, considered the best model for the zoonotic potential of prions, were infected upon CWD challenge, including the oral one.
****> The disease manifested as atypical in macaques and initial transgenic mouse transmissions, but with infectivity present at all times, as unveiled in the bank vole model with an unusual tissue tropism.
***> Epidemiologic surveillance of prion disease among cervid hunters and people likely to have consumed venison contaminated with chronic wasting disease
=====
https://intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf?force_download=true
Transmission of Cervid Prions to Humanized Mice Demonstrates the Zoonotic Potential of CWD
Samia Hannaouia, Irina Zemlyankinaa, Sheng Chun Changa, Maria Immaculata Arifina, Vincent Béringueb, Debbie McKenziec, Hermann M. Schatzla, and Sabine Gilcha
Results: Here, we provide the strongest evidence supporting the zoonotic potential of CWD prions, and their possible phenotype in humans. Inoculation of mice expressing human PrPCwith deer CWD isolates (strains Wisc-1 and 116AG) resulted in atypical clinical manifestations in > 75% of the mice, with myoclonus as leading clinical sign. Most of tg650brain homogenates were positive for seeding activity in RT-QuIC. Clinical disease and presentation was transmissible to tg650 mice and bank voles. Intriguingly, protease-resistant PrP in the brain of tg650 mice resembled that found in a familial human prion disease and was transmissible upon passage. Abnormal PrP aggregates upon infection with Wisc-1 were detectable in thalamus, hypothalamus, and midbrain/pons regions.
Unprecedented in human prion disease, feces of CWD-inoculated tg650 mice harbored prion seeding activity and infectious prions, as shown by inoculation of bank voles and tg650 with fecal homogenates.
Conclusions: This is the first evidence that CWD can infect humans and cause disease with a distinctive clinical presentation, signature, and tropism, which might be transmissible between humans while current diagnostic assays might fail to detect it. These findings have major implications for public health and CWD-management.
https://www.tandfonline.com/doi/full/10.1080/19336896.2022.2091286
18. Zoonotic potential of moose-derived chronic wasting disease prions after adaptation in intermediate species
Tomás Barrioa, Jean-Yves Doueta, Alvina Huora, Séverine Lugana, Naïma Arona, Hervé Cassarda, Sylvie L. Benestadb, Juan Carlos Espinosac, Juan María Torresc, Olivier Andréolettia
aUnité Mixte de Recherche de l’Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement 1225 Interactions Hôtes-Agents Pathogènes, École Nationale Vétérinaire de Toulouse, 31076 Toulouse, France; bNorwegian Veterinary Institute, P.O. Box 64, NO-1431 Ås, Norway; cCentro de Investigación en Sanidad Animal (CISA-INIA), 28130, Valdeolmos, Madrid, Spain
Aims: Chronic wasting disease (CWD) is an emerging prion disease in Europe. To date, cases have been reported in three Nordic countries and in several species, including reindeer (Rangifer tarandus), moose (Alces alces) and red deer (Cervus elaphus). Cumulating data suggest that the prion strains responsible for the European cases are distinct from those circulating in North America. The biological properties of CWD prions are still poorly documented, in particular their spillover and zoonotic capacities. In this study, we aimed at characterizing the interspecies transmission potential of Norwegian moose CWD isolates.
Materials and Methods: For that purpose, we performed experimental transmissions in a panel of transgenic models expressing the PrPC sequence of various species.
Results: On first passage, one moose isolate propagated in the ovine PrPC-expressing model (Tg338). After adaptation in this host, moose CWD prions were able to transmit in mice expressing either bovine or human PrPC with high efficacy.
Conclusions: These results suggest that CWD prions can acquire enhanced zoonotic properties following adaptation in an intermediate species.
Funding
Grant number: AAPG2020 EU-CWD, ICRAD2020 TCWDE, NRC2022 NorCWD
Acknowledgement
https://www.tandfonline.com/doi/full/10.1080/19336896.2024.2424058
“ After adaptation in this host, moose CWD prions were able to transmit in mice expressing either bovine or human PrPC with high efficacy.”
regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD
Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY
Date: Fri, 18 Oct 2002 23:12:22 +0100
From: Steve Dealler
Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member
To: BSE-L@ …
######## Bovine Spongiform Encephalopathy <BSE-L@UNI-KARLSRUHE.DE> #########
Dear Terry,
An excellent piece of review as this literature is desparately difficult to get back from Government sites.
What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported.
Well, if you dont look adequately like they are in USA currenly then you wont find any!
Steve Dealler
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
Subject: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY
From: "Terry S. Singeltary Sr." <flounder@WT.NET>
Reply To: Bovine Spongiform Encephalopathy <BSE-L@UNI-KARLSRUHE.DE>
Date: Thu, 17 Oct 2002 17:04:51 -0700
snip...
''The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).''
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss) These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
http://web.archive.org/web/20090506050043/http://www.bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf
http://web.archive.org/web/20090506050007/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
http://web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf
Stephen Dealler is a consultant medical microbiologist deal@airtime.co.uk
BSE Inquiry Steve Dealler
Management In Confidence
BSE: Private Submission of Bovine Brain Dealler
snip...end
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BSE INQUIRY
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane
BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended.. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
TSE in wild UK deer? The first case of BSE (as we now realise) was in a nyala in London zoo and the further zoo cases in ungulates were simply thought of as being interesting transmissions of scrapie initially. The big problem started to appear with animals in 1993-5 when it became clear that there was an increase in the CJD cases in people that had eaten deer although the statistics involved must have been questionable. The reason for this was that the CJD Surveillance was well funded to look into the diet of people dying of CJD. This effect is not clear with vCJD...if only because the numbers involved are much smaller and hence it is difficult to gain enough statistics. They found that many other foods did not appear to have much association at all but that deer certainly did and as years went by the association actually became clearer. The appearance of vCJD in 1996 made all this much more difficult in that it was suddenly clearer that the cases of sporadic CJD that they had been checking up until then probably had nothing to do with beef...and the study decreased. During the period there was an increasing worry that deer were involved with CJD..
see references:
DEER BRAIN SURVEY
https://web.archive.org/web/20090506025229/http://www.bseinquiry.gov.uk/files/yb/1991/11/20004001.pdf
CONFIDENTIAL AND IN CONFIDENCE TRANSMISSION TO CHIMPANZEES AND PIGS
IN CONFIDENCE
TRANSMISSION TO CHIMPANZEES
Kuru and CJD have been successfully transmitted to chimpanzees but scrapie and TME have not.
We cannot say that scrapie will not transmit to chimpanzees. There are several scrapie strains and I am not aware that all have been tried (that would have to be from mouse passaged material). Nor has a wide enough range of field isolates subsequently strain typed in mice been inoculated by the appropriate routes (i/c, i/p and i/v).
I believe the proposed experiment to determine transmissibility, if conducted, would only show the susceptibility or resistance of the chimpanzee to infection/disease by the routes used and the result could not be interpreted for the predictability of the susceptibility for man. proposals for prolonged oral exposure of chimpanzees to milk from cattle were suggested a long while ago and rejected.
In view of Dr Gibbs' probable use of chimpazees Mr Wells' comments (enclosed) are pertinent. I have yet to receive a direct communication from Dr Schellekers but before any collaboration or provision of material we should identify the Gibbs' proposals and objectives.
A positive result from a chimpanzee challenged severely would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
A negative result would take a lifetime to determine but that would be a shorter period than might be available for human exposure and it would still not answer the question regarding mans ‘susceptibility. In the meantime no doubt the negativity would be used defensively. It would however be counterproductive if the experiment finally became positive. We may learn more about public reactions following next Monday's meeting.
R Bradley
CVO (+ Mr Wells’ commenters 23 September 1990 Dr T W A Little Dr B J Shreeve
90/9.23/1.1
https://web.archive.org/web/20090506041740/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf
*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.
see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????
“Our conclusion stating that we found no strong evidence of CWD transmission to humans”
From: TSS Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam, In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091).
Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease
2018 President’s Budget Animal and Plant Health Inspection Service
Cervids
APHIS’ voluntary national CWD Herd Certification Plan (HCP) helps States, Tribes, and the cervid industry control CWD in farmed cervids by allowing the interstate movement only from certified herds considered to be low risk.
Currently, 29 States participate in the national CWD HCP.
In FY 2016, the program tested 14,503 farmed cervids for CWD and identified seven new CWD positive farmed cervid herds – two white-tail deer herds in Texas, three white-tail deer herds in Wisconsin, one elk herd in Colorado and one elk herd in Iowa. The elk herd in Colorado was depopulated without Federal indemnity and the rest of the herds are under State quarantines. One Texas herd used Federal indemnity to remove and test select animals to inform the epidemiological investigation and to evaluate 20-72 the performance of ante-mortem tests.
The use of Federal indemnities within the CWD program is determined on a case-by-case basis. APHIS is also conducting several pilot projects related to new technologies. In FY 2016, the Agency
https://www.usda.gov/sites/default/files/documents/20aphisexnotes2018.pdf
2017 Explanatory Notes Animal and Plant Health Inspection Service
Cervids
APHIS’ voluntary national CWD Herd Certification Plan (HCP) helps States, Tribes, and the cervid industry control CWD in farmed cervids by allowing the interstate movement only from certified herds considered to be low risk.
Currently, 30 States participate in the national CWD HCP: 29 have Approved Status and 1 has Provisional Approved Status. States that meet the CWD HCP requirements have Approved Status and States that do not meet CWD HCP program requirements but have developed a work plan and time frame with APHIS to complete those requirements have Provisional Approved Status.
In FY 2015, the program tested approximately 20,000 farmed cervids for CWD and identified eight new CWD positive farmed white-tailed deer herds – one in Utah, one in Pennsylvania, two in Ohio, two in Wisconsin, and two in Texas.
APHIS depopulated five of these herds (Pennsylvania, Utah, and one each in Wisconsin, Texas, and Ohio). Six elk herds in Colorado, four elk herds in Nebraska, one white-tailed deer herd in Wisconsin and one white-tailed deer herd in Texas remained in quarantine at the end of FY 2015.
APHIS also provided indemnity for and was the lead agency for the depopulation and disposal of four large CWD infected farmed cervid herds in Pennsylvania, Ohio, Utah, and Texas. In cooperation with the National Agricultural Statistics Service, APHIS conducted the first national study of the U.S. farmed-cervid industry in FY 2015. The study provides baseline industry statistics, a description of production practices and challenges, producer-reported disease occurrences, and an overview of health management and biosecurity practices.
https://www.usda.gov/sites/default/files/documents/20aphis2017notes.pdf
2016 Explanatory Notes Animal and Plant Health Inspection Service
https://www.usda.gov/sites/default/files/documents/20aphis2016notes.pdf
2015 Explanatory Notes Animal and Plant Health Inspection Service
https://www.usda.gov/sites/default/files/documents/20aphis2015notes.pdf
2014 Explanatory Notes Animal and Plant Health Inspection Service
https://www.usda.gov/sites/default/files/documents/18aphis2014notes.pdf
Louisiana House of Representative Aug 27, 9:30 AM, HCR-6 CWD
Louisiana House of Representative
Chronic Wasting Disease CWD
(A letter written from a Mississippi farmer who’s farm has been in his family for more than 100 years, and submitted it in this video presentation, 28 minute mark, another wake up call for sure, of what some have been warning for years, about CWD, but sadly will go by the wayside by the conspiracy theorists spreading fake news…terry)
Alston Ross
Marshall County, Mississippi
My family owns a 2,000 acre farm in Marshall County, which is in North Mississippi. CWD has plagued my farm since 2018 and has become progressively worse over time. We no longer have mature deer over the age of 3 years old on our property. Every buck harvested on our land has tested positive this year. The owners of our neighboring properties have continued to feed deer and ignore MDWFP regulations, which has exacerbated the spread of the disease throughout our area. This farm has been in my family for over 100 years, and due to the rapid spread of CWD, we are concerned about the future of our deer herd and the value of our hunting land…end
Snip…
Arkansas
Snip…
40:35 “…and conversely, I was co-Principle Investigator in NW Arkansas, where prevalence is approaching 50 percent.”
Snip…
41:00 “Specific to the work in Arkansas, in 2020, the state agency was showing the Prevalence at 30 percent in the Northwest part of the State, so flip a coin, so, 1 out of every 3 deer had the disease. We started that research in 2020, and now, the prevalence rate is now exceeding 40% in both sexes, and 50% in males.”
43:00 “what we’re seeing Arkansas now is, that population is declining about 11% a year.”
Snip…see full video presentation;
https://house.louisiana.gov/H_Video/VideoArchivePlayer?v=house/2025/Aug/0827_25_NR_Joint
CWD IS RAVAGING MY FAMILY’S LAND, BUT IT’S NOT TOO LATE FOR YOU
September 9, 2025 By: Paul Annear
My first season deer hunting in Wisconsin was 2001, the same season that produced Wisconsin’s first deer to test positive for chronic wasting disease. CWD has always been at the forefront of deer hunting discussions in my time as a hunter, and I’ve watched the disease slowly spread and worsen. Since 2019, eight of 11 deer I’ve taken on my family’s property in Richland County in Southwest Wisconsin have tested positive for CWD – including the buck in the photo above.
Aside from harvesting otherwise perfectly healthy-looking deer that test positive for CWD, we are now seeing live deer walking around in the awful final stages of this disease. Research has now confirmed what I’ve seen occurring on our hunting land in the last five to six years: CWD is beginning to reduce deer populations in high-prevalence areas like mine.
It didn’t have to reach this point. Hunters in areas with low CWD prevalence can keep infection rates low and deer populations healthy overall by accepting and implementing certain strategies. Some of the strategies I will lay out will challenge you as a hunter to play the “long game,” but there are ways to slow the spread of CWD in areas where it is newly discovered and infection rates are still low.
If you’re rolling your eyes at another guy talking about CWD, I get it, but I urge you to keep reading. Hear my personal story, how it has affected my hunting experiences, and what can happen if hunters ignore CWD.
“Where Are the Deer?”
Up until about seven years ago, I was still trying to figure out this CWD thing and what I thought of it all. I hadn’t yet seen or felt the effects. I was trying to improve my hunting in a variety of different ways like everyone else.
In Iowa County, hunters killed only 916 bucks during the 2024 nine-day firearms season. The last time Iowa County recorded less than 1,000 bucks killed during the nine-day firearms season was in 1971.
We began testing every deer taken on our farm in 2019, and with 72% of them testing positive, it’s safe to say we’re in the thick of it. I’m not alone. I speak to countless hunters in Southwest Wisconsin at trade shows and other events, and many of them are saying the same thing: “What is happening? Where are the deer?”
Since 2019, eight of 11 deer taken on Paul’s family land in southwest Wisconsin tested positive for CWD. This wall of bucks includes deer taken since 2006, and six of the more recent bucks added to this wall were CWD-positive.
In Iowa County, hunters killed only 916 bucks during the 2024 nine-day firearms season. The last time Iowa County recorded less than 1,000 bucks killed during the nine-day firearms season was in 1971. Iowa County tested 694 deer during the 2024 deer season, and 25% of deer tested were positive. Richland and Sauk counties both had a 33% positive CWD rate and together tested 2,193 deer. In 2004, a few years after the initial surge of testing occurred in Wisconsin, Richland County tested 1,691 deer and no deer tested positive for CWD. So, we haven’t been finding CWD just because we’re testing more. It arrived and has spread significantly.
The first time I saw what I believed to be CWD up close and personal was in spring 2023 when my dad and I were marching up a steep ridge for an afternoon turkey hunt. Just a short distance into the walk, I spotted a buck with velvet sprouts. “Dad,” I said. “Deer.”
We both thought it was unusual this deer wasn’t bounding off since we were within 40 yards. Springtime bucks are certainly not the paranoid creatures they become in fall, though. So, we closed the distance since we were headed that way and wanted a closer look.
The buck was very clearly sick. The hair on the back of my neck stood up instantly. A better view revealed his shaking, emaciated body and drool spilling from his mouth (see the photo below). His spine, shoulder blades, and scars up and down his legs told me this deer was in the final stage of CWD but had just enough energy to escape a few predators in the days prior. I had begun to wonder why so many of my 3½-year-old bucks never returned, and this moment convinced me CWD is playing a role in bucks constantly disappearing. This buck was days away from dying of holes eaten in his brain. We were able to put him out of his misery with permission from the Wisconsin DNR.
Though CWD has been in his area for more than 20 years, it wasn’t until 2023 that Paul Annear encountered a visibly sick deer. By the time hunters are seeing sick deer in the woods, the infection rate is usually too high to do anything about it.
I travel 200 miles one way to hunt this property in Southwest Wisconsin. The disease has in a way disrupted my motivation to keep traveling here, knowing full well there is a high likelihood of any deer we kill testing positive, resulting in us throwing out the meat. If you don’t hunt in a CWD zone, your routine following a successful hunt is probably simple and relatively careless. The presence of CWD changes that real quick. Shooting a deer means we could be in for a few frustrating weeks to follow as we wait for CWD test results. I’ve wasted countless hours butchering deer only to throw out the venison.
My friend and fellow Wisconsin deer hunter Bradie Ewing follows the same recommended protocols I do regarding CWD-positive venison.
“We have made the decision that we will not eat or feed a CWD positive deer to our kids or family, so this has caused some logistical headaches,” said Bradie. “The investment of time up front in butchering a deer is significant only to later throw it away if its positive.”
In 2020, I had nearly 30 bucks on trail-camera I estimated to be 3½ years old or older. In 2024, I felt confident we had only seven or eight deer in that age class. A stark decrease. I also ran about 20 more trail cameras on this 115-acre property in 2024 than I did in 2020, so fewer photos are not playing a role in my estimation of fewer mature deer. There are simply fewer mature deer, and DNR harvest data shows it’s not because hunters killed more older bucks in recent seasons. It’s because of CWD.
Why do I keep making the drive back to Richland County? My parents have lived on this land since 1987. This is the land where I was born and raised, where I grew up exploring the woods and learning to hunt squirrels and deer. It’s where I feel I belong, and I know that strong emotional attachment will keep me coming back to hunt deer with my family every fall.
Common Sense
Chronic Wasting Disease prions can be shed via saliva at mineral sites. CWD prions can exist in the soil below licking branches in a scrape. We’re never going to eliminate deer-to-deer contact in the wild. But if you’re in a low CWD prevalence area, there are some common-sense practices you should follow. You can learn from a few of my mistakes.
In the last few years, I’ve wondered if we can truly do anything to curb the spread of CWD in extremely high prevalence areas. One day I would feel the CWD battle is worth fighting, then just days later I’d harvest a CWD positive deer and be discouraged to the point of thinking “this is a bridge too far.”
With 33% of deer in Paul’s county now testing positive for CWD, he has begun to see visibly sick deer in the last two years. Paul’s trail-camera captured the photos above and below in fall 2024. Paul found the remains of the buck above three months after this photo was taken. Note: Deer with EHD die within 5 to 10 days of infection, which isn’t enough time for this kind of drastic weight loss.
I told myself I just wanted to get back to hunting. In the midst of these internal battles, I set out a tank-style waterhole on a Southwest Wisconsin property I hunt. While baiting or feeding is illegal in every Southwest Wisconsin county to help slow the spread of disease, the Wisconsin DNR has not banned the creation of artificial water sources. There are limited water resources on this property, and I thought a waterhole would be a unique way to attract deer near a stand site.
I had an abundance of deer visiting the water tank in the few months it was set up. Despite all the trail-camera photos, a famous Aldo Leopold quote would occasionally run through my mind: “A thing is right when it tends to preserve the integrity, stability, and the beauty of the biotic community – it is wrong if it tends otherwise.”
During the short time I had the waterhole out, I emptied and re-filled it many times since I still wanted to be cognizant of disease transmission. But I have to be honest with myself and admit that if I care about wild deer and the places they live, setting out a small, non-flowing waterhole in a CWD zone was a mistake. Not long after killing a visibly sick, CWD-positive doe that came to drink from the waterhole, we removed it.
In certain regions of the U.S., baiting is just a way of life and how it’s always been done. So, I get the enjoyment and desire to feed or provide artificial water sources for deer. I know hunters in states like Texas and Kansas who would hardly have a deer pass through their land if they didn’t run a feeder.
Are we going to stop the spread of CWD by banning waterholes or baiting? No. But common sense would say those things don’t help an infected herd. Artificially inflating your local deer population in a high CWD prevalence zone by feeding is dangerous because deer that may not otherwise come in contact with one another could share infectious prions at a bait or water site.
Does the presence of CWD mean you should never hang a mock licking branch or plant food plots to improve your hunting opportunities? I believe that’s an unreasonable way of thinking. I am still going to create food plots and mock scrapes. However, I strongly believe we need to practice common sense and realize there are matters we can take into our own hands when it comes to mitigating the spread of CWD. It begins with pulling triggers and landowners making strong, individual decisions regarding their deer herd and holding to them.
Sound Management and Testing
“Earn-A-Buck” was a tool some states used intermittently to effectively manage high deer herds. Wisconsin had implemented EAB off and on beginning in 1996, until it was signed out of law by Wisconsin Governor Scott Walker. I believe EAB is an effective tool for managing deer herds in some places, and I believe it’s no coincidence CWD rates have steadily increased in Wisconsin since Gov. Walker got rid of the law with pressure from other politicians and interest groups. There are few better incentives to take a doe than requiring it before you can take a buck. The only incentive that worked is now gone.
Earn-A-Buck cannot be signed back into law without the Wisconsin legislature doing so. Wisconsin hunters are left with a distinct choice that Wisconsin hunter Doug Duren is often heard saying. “Where CWD is established or taking hold, we have one of two choices,” Doug says. “We are going to manage the herd and the disease, or CWD is going to do it for us.” Wisconsin has had no effective deer management plan since the elimination of EAB in 2011.
In talking with countless hunters in my region, it appears CWD can be somewhat pocketed even within high prevalence counties like mine. The variability of CWD prevalence within a county could be due to availability of better habitat, people not illegally baiting in certain areas, or for unknown reasons. But we do know that high deer density helps CWD spread faster, so simply continuing to harvest deer – especially does – works. Doe harvest helps keep deer density in balance with the habitat and reduces deer-to-deer spread of CWD, which means healthier deer in all respects. But it’s not just about doe harvest.
Bucks test positive at a higher rate than does because of behaviors like traveling farther during the rut. I would encourage you to be less picky about harvesting bucks if CWD has just been discovered and you’re trying to keep prevalence rates low. NDA’s advice for hunters in CWD zones is to continue managing for older bucks if you wish but apply increased harvest pressure on all bucks 2½ years of age or older.
Do I wish we could go back to those days of low prevalence and undergo targeted removal missions on my family’s land to see if it would prevent or delay the problem we have today? Yes. Sustained harvest on all deer, bucks and does, means a better chance of removing infected deer from the landscape sooner. If hunters back off deer harvest because of CWD, infected deer enjoy greater protection, and they can spread more CWD prions into the environment and to other deer. In fact, every time you harvest a deer that tests positive for CWD, you should look at this as a win in the fight against this disease.
Jason Sumners is the Director of the Missouri Department of Conservation and has guided Missouri through a proactive approach to CWD.
“If all you are doing is testing to show you are doing something, it’s a complete waste of critical agency resources,” said Jason. “Short of documenting the demise of deer and giving some hunters a little more comfort when consuming deer harvested in CWD areas, it’s not doing anything to help the herd.”
What is Missouri doing? A lot of testing but also Targeted harvesting in select zones with landowner approval. In 2025, they’ve killed 4,793 deer with 68 (1.4%) of those being positive. While the CWD positive rate of these targeted removals is still low, that’s the point. This is a relatively small number of deer removed statewide, but because they are removed with precision from sites where deer previously tested positive, sick deer are removed sooner. Missouri is keeping CWD prevalence rates in check throughout these surveillance zones.
Would I have been hesitant to allow targeted deer removal or “sharpshooting”’on my property back when CWD had just been discovered? Yes. Do I wish we could go back to those days of low prevalence and undergo targeted removal missions on my family’s land to see if it would prevent or delay the problem we have today? Yes.
The early stage of CWD is the only stage when intervention and management can hope to hold infection rates low. If you wait until you are seeing sick deer in the woods, which is a sign you are in “late-stage” CWD, it’s too late to do anything about it.
If CWD isn’t in your woods yet, you should still make it a point to submit deer for testing anytime an opportunity is presented. Early detection of a new outbreak is critical. Early detection gives hunters and the state wildlife agency the opportunity to respond. CWD testing isn’t a proclamation of any political views or ideologies. However, it is absolutely a pledge that you care about deer and their future.
Paul Annear grew up hunting with his dad on family land in southwest Wisconsin and is now teaching his son Hudson how to hunt. We Are Not Doomed
I believe there will always be white-tailed deer in my area of Wisconsin. However, within 20 to 25 years, I believe fewer bucks will reach maturity than today, and a lot fewer than when I began hunting over 20 years ago.
This is despite more people than ever before passing younger deer and managing for older deer. I think in some areas like mine with high CWD prevalence, the average age of bucks has already dropped significantly from where it was just a few years ago – at a time when NDA’s Deer Report shows more bucks aged 3½ years old or older being harvested nationally than ever before.
If CWD has been found in your woods, ignoring it will take your hunting down the wrong path. Private landowners especially will play a critical role in properly managing whitetails in America in the next 30 years. I’m reminded of this Aldo Leopold quote: “Conservation will ultimately boil down to rewarding the private landowner who conserves the public interest.”
In this case, public interest is healthy deer. In most of whitetail country, unlike Southwest Wisconsin, it’s not too late to do something. Common-sense practices might seem like a burden to you now, but it’s nothing compared to what I’m experiencing. Ignoring those practices might help your short-term hunting opportunities, but remember you are in the position I wish I could go back to. Ask yourself if the choices you are making now will help conserve a better future for all.
Categories: Hunting
Tags: Chronic Wasting Disease, Cwd
About Paul Annear:
Paul Annear is an avid deer hunter, freelance writer and NDA member from the Driftless Region of southwest Wisconsin.
https://deerassociation.com/cwd-is-ravaging-my-familys-land-but-its-not-too-late-for-you/
Wisconsin DNR says CWD sinking deer herds in disease-endemic areas
PATRICK DURKIN Outdoors Columnist
CWD culprits
Snip…
“We can now say it’s not EHD (epizootic hemorrhagic disease), it’s not coyotes, it’s not bobcats, and it’s not earn-a-buck regulations from 15 years ago that are causing the herd declines we’re seeing,” said Dan Storm, the study’s chief researcher. “CWD is the cause, and we have solid evidence to back it up.
This is what’s going on, and so let’s proceed with what to do about it.” “We already did that and look how it went,” Storm said. “Before we lost earn-a-buck (in 2011), hunters dropped Iowa County’s deer herd below 20,000. After earn-a-buck, the herd took 7%, 10% and 12% annual increases until 2020.
That herd should have kept growing, but it didn’t. CWD is pulling it down and boxing it in.” The DNR’s annual post-hunt population estimates show Iowa County’s herd rose 51.3% from 16,900 in 2011 to 25,566, the 2018-2020 three-year average.
The herd has since fallen 15.25% to 21,666, the 2021-2023 three-year average.
Bryan Richards, CWD project leader at the USDA’s National Wildlife Health Center in Madison, said backing off would backfire. “You won’t recover a population by letting CWD run its course,” Richards said. “When you try to stockpile deer by not shooting, you protect sick deer, too. Contamination worsens and the healthy proportion of the herd declines.
Shooting removes sick deer from the herd sooner than CWD will. They’ll spread fewer prions over time, and you’ll probably shoot them before CWD reaches its worst stages for shedding prions.”
Storm put it this way: “The more CWD you have in your area, the more the herd will decline.”
Which areas already exceed 29% infection rates for adult does?
The latest DNR data from a year ago shows southeastern Richland County on the edge at 27%, northwestern Iowa County at 35%, and the Devil’s Lake area in eastern Sauk County at 34%. Further, CWD testing of hunter-killed deer in autumn 2024 shows overall (bucks and does) detection rates at or above 29% in six townships (6-mile by 6-mile areas) in Columbia County, three townships in Dane County, eight townships in Iowa County, 11 townships in Richland County, and 15 townships in Sauk County.
How low will deer populations drop where CWD is endemic?
Storm said CWD won’t exterminate deer, but no one can predict how it will affect specific valleys, woodlands or watersheds. CWD has spread at varying rates in different Wisconsin habitats, and appears to have leveled off at high infection rates in some areas while still rising and spreading in others.
The disease has so far been verified in wild deer in 48 of Wisconsin’s 72 counties, even though testing has been totally voluntary for years.
During the 2024 hunting season, 1,755 more deer tested positive for CWD across the state, a record 10.4% detection rate despite the least amount of samples (16,939) volunteered since 2017. Richland County hunters provided the most samples, 1,335, in 2024, and 444 (33.4%) had CWD.
https://www.antigojournal.com/sports/outdoors/durkin-wisconsin-dnr-says-cwd-sinking-deer-herds-in-disease-endemic-areas/article_cb73b5ca-dd9e-11ef-853c-d3fb206ddf8c.html
18% of mule deer in northeastern Montana have deadly chronic wasting disease “In the 2024-25 hunting FWP submitted 9,066 samples for chronic wasting disease testing – the largest number of CWD samples ever collected in a single year. More than 1,100 of these samples were collected by hunters. Of those samples, 335 tested positive for the disease, including 202 white-tailed deer, 127 mule deer and six elk.”
https://billingsgazette.com/outdoors/article_de5278b8-f2e1-11ef-b479-cf42652717a4.html
Southwest Wisconsin CWD, Deer and Predator Study
key takeaways ;
CWD substantially reduces deer survival rates and suppresses population growth.
Where CWD prevalence is high, deer populations are likely declining.
If CWD continues to spread, it will eventually impact deer populations elsewhere.
https://dnr.wisconsin.gov/topic/research/projects/dpp/StudyResults
MONDAY, APRIL 28, 2025
Wisconsin DNR 2024 CWD 1,786 samples testing positive
https://chronic-wasting-disease.blogspot.com/2025/04/wisconsin-dnr-2024-cwd-1786-samples.html
This CWD Study Could Change Deer Hunting FOREVER | The Check Station October 8, 2025 NW Arkansas
NW Arkansas CWD 11:25 minutes;
50% of all deer positive for CWD.
35% of Does are Positive for CWD.
68% Bucks are Positive for CWD.
Most Bucks NW Arkansas that where Tested, are Positive for CWD.
https://m.youtube.com/watch?v=kTicUE-xsQU&t=695s&pp=2AG3BZACAQ%3D%3D
MEMORANDUM
To: Members of the Colorado Parks and Wildlife Commission
From: Dan Prenzlow, Director
Date: April 22, 2022
Subject: Chronic Wasting Disease Update for Parks and Wildlife Commission Chronic wasting disease, a fatal neurological disease found in deer, elk, and moose, is well established in herds throughout much of Colorado. We have detected CWD in 40 of our 54 deer herds, 17 of 42 elk herds, and 2 of 9 moose herds. Disease prevalence (percent infected) is highest in deer and lowest in moose. This disease is always fatal and animals die from the disease within about 2-2.5 years of infection. CWD infection shortens the lifespan of infected animals. If infection rates become too high, CWD can affect a herd’s ability to sustain itself.
Snip…
http://web.archive.org/web/20220609004350/https://cpw.state.co.us/Documents/Commission/2022/May/Item.11-PWC_Memo_CWD_Update_EckertMillerWood_April2022-Matthew_Eckert-DNR.pdf
18% of mule deer in northeastern Montana have deadly chronic wasting disease “In the 2024-25 hunting FWP submitted 9,066 samples for chronic wasting disease testing – the largest number of CWD samples ever collected in a single year. More than 1,100 of these samples were collected by hunters. Of those samples, 335 tested positive for the disease, including 202 white-tailed deer, 127 mule deer and six elk.”
https://billingsgazette.com/outdoors/article_de5278b8-f2e1-11ef-b479-cf42652717a4.html
Southwest Wisconsin CWD, Deer and Predator Study
key takeaways ;
CWD substantially reduces deer survival rates and suppresses population growth.
Where CWD prevalence is high, deer populations are likely declining.
If CWD continues to spread, it will eventually impact deer populations elsewhere.
https://dnr.wisconsin.gov/topic/research/projects/dpp/StudyResults
The effectiveness of harvest for limiting wildlife disease: Insights from 20 years of chronic wasting disease in Wyoming
First published: 21 January 2025
https://doi.org/10.1002/eap.3089
https://esajournals.onlinelibrary.wiley.com/doi/10.1002/eap.3089
https://www.usgs.gov/news/national-news-release/new-study-finds-deer-hunting-can-help-keep-chronic-wasting-disease-check
Since identifying its first cases of CWD in captive deer in the 70s and finding the first wild infected deer in 1985, Wyoming has seen the disease slowly spread throughout the state. CWD has now been documented in members of the deer family in most of Wyoming’s deer hunting areas, with 20% to 40% percent of mule deer affected in some herds. A 2017 study estimated a 21% annual population decline as a result of the fatal disease.
https://freerangeamerican.us/chronic-wasting-disease-wyoming/#:~:text=CWD%20has%20now%20been%20documented,result%20of%20the%20fatal%20disease.
How does CWD impact deer, elk, and moose populations? Recent research in Wyoming has demonstrated declines in both mule and white-tailed deer populations in deer hunt area 65 due to CWD (see below for citations). These declines are in the core endemic area where prevalence is highest. In areas with lower prevalence, effects of CWD are poorly understood but are considered additive along with other factors that can negatively affect deer populations in Wyoming (i.e. habitat loss, predation, other diseases). The distribution and prevalence of CWD in Wyoming elk is less than that of deer. Currently there are no documented direct population impacts in Wyoming elk from CWD; however, research from Rocky Mountain National Park suggests that CWD could impact elk populations at higher prevalence (13%). While CWD has been found in free ranging moose, there have been few detections, and there is no evidence that CWD is currently having an impact on moose populations.
https://wgfd.wyo.gov/Wildlife-in-Wyoming/More-Wildlife/Wildlife-Disease/Chronic-Wasting-Disease
TUESDAY, SEPTEMBER 30, 2025
USDA EXPLANATORY NOTES ANIMAL AND PLANT HEALTH INSPECTION SERVICE 2025-2014 CHRONIC WASTING DISEASE CWD TSE CERVID
https://chronic-wasting-disease.blogspot.com/2025/09/usda-explanatory-notes-animal-and-plant.html
one of the old studies that has always stuck out in my mind, one that the late great Dr. Gibbs, Gajdusek, et al did way back, and to this day is still amazes me...friendly fire, iatrogenic transmission, including field dressing a deer, includes risks for exposure to the Cwd tse prion…take precautions!
*** Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery ***
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.
Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract
Chronic wasting disease (CWD) prion detection in environmental and biological samples from a taxidermy site and nursing facility, and instruments used in surveillance activities
Author links open overlay panel Paulina Soto a b , Nancy Ho a , Mitch Lockwood c , Austin Stolte c , J. Hunter Reed c , Rodrigo Morales a b
https://doi.org/10.1016/j.scitotenv.2025.179318
• CWD prions were identified in a taxidermy and deer nursing facility.
• Contaminated samples included waters, soils, dermestid beetles, domestic flies and a dumpster.
• Surgical instruments used to collect deer samples can get contaminated with CWD prions.
• Some of the infectious particles are readily released from surgical instruments when washed.
• Our results suggest that taxidermy practices actively contribute in the spreading of CWD.
Abstract
Chronic wasting disease (CWD) is a transmissible prionopathy affecting free-ranging and captive cervids. CWD is thought to spread through both direct and indirect transmission mechanisms. Along this line, human activities have not been thoroughly explored for their potential to spread this disease. One area of concern involves taxidermy procedures and surveillance activities as handled animals or carcasses are of unknown CWD statuses. Worrisomely, taxidermy facilities can act as foci of prion infectivity if appropriate biosecurity practices are not implemented. In this study, we evaluated the presence of infectious prions in a taxidermy facility that was possibly exposed to CWD prions. To determine this, we collected biological and environmental specimens from this site and screened them using the protein misfolding cyclic amplification (PMCA) technique. Additionally, we swabbed different surfaces possibly exposed to CWD-infected animals or carcasses. We report the presence of prions in i) waters used to digest tissues from deer carcasses, ii) soils that were in contact with the previously mentioned waters, iii) dermestid beetles used to clean skulls, iv) other insects found in the beetle shed, and iv) dumpsters where animal carcasses were disposed. Additionally, we report that surgical materials used in surveillance practices may also hold CWD prions, even after being washed with aqueous solutions. All these results suggest that CWD prions may be disseminated due to human practices and that protocols should be established to decontaminate potentially contaminated materials.
https://www.sciencedirect.com/science/article/abs/pii/S0048969725009544?via%3Dihub
CWD, Oh Deer, August 2021
https://trerc.tamu.edu/article/oh-deer-2314/
Published: 05 August 2025
Vertical transmission of chronic wasting disease in free-ranging white-tailed deer populations
Snip…
Our detection of CWD-positive fawns ≤ 10-month-old by ELISA testing provides indirect evidence of gestational infection, although direct or indirect CWD transmission after birth cannot be ruled out in these fawns (Table 5). The detection of CWD infection in ≤ 6-month-old fawns in the Arkansas and Tennessee study sites by ELISA test, which is not as sensitive as amplification assays37, was particularly suggestive of vertical transmission. Fawns less than 6 months of age are not routinely incorporated into statewide CWD surveillance programs because of the low likelihood of detectable infection using traditional assays (i.e., ELISA, IHC), yet have been previously identified17. Future studies should investigate the potential role of in utero transmission in local CWD transmission cycles. Considering the strong relationship between CWD infection probability and female white-tailed deer relatedness, in utero CWD transmission may serve as a small yet important route of transmission in addition to social interactions and indirect exposures53.
Overall, this study describes the dissemination of CWD prions throughout tissues and birthing fluids of the pregnancy microenvironment demonstrating that offspring are routinely exposed to the infectious prion in-utero prior to parturition. We report infectious prions in the reproductive and fetal tissue of naturally exposed free-ranging white-tailed deer suggesting that in utero maternal transmission is likely an underappreciated mode of CWD transmission. Our study shows that vertical transmission is indeed a viable route of infection within the southeastern U.S. and is another potential factor contributing to the relentless spread of chronic wasting disease.
https://www.nature.com/articles/s41598-025-12727-8
Just remember;
Chronic Wasting Disease CWD TSE Prion
THE CWD TSE Prion aka mad cow type disease is not your normal pathogen.
The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.
It’s not your ordinary pathogen you can just cook it out and be done.
You cannot cook the TSE prion disease out of meat. In fact new data now shows that exposure to high temperatures used to cook the meat increased the availability of prions for in vitro amplification.
You can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.
The TSE prion agent also survives Simulated Wastewater Treatment Processes.
The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.
IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades. 15 to 21 years.
You can bury it and it will not go away.
Prions in Waterways
https://vimeo.com/898941380?fbclid=IwAR3Di7tLuU-iagCetdt4-CVPrOPQQrv037QS1Uxz0tX3z7BuvPeYlwIp7IY
Prion. 2009 Jul-Sep;3(3):171–183. doi: 10.4161/pri.3.3.9819
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
TA Nichols 1,2, Bruce Pulford 1, A Christy Wyckoff 1,2, Crystal Meyerett 1, Brady Michel 1, Kevin Gertig 3, Edward A Hoover 1, Jean E Jewell 4, Glenn C Telling 5, Mark D Zabel 1,
Abstract
Chronic wasting disease (CWD) is the only known transmissible spongiform encephalopathy affecting free-ranging wildlife. Although the exact mode of natural transmission remains unknown, substantial evidence suggests that prions can persist in the environment, implicating components thereof as potential prion reservoirs and transmission vehicles.1–4 CWD-positive animals may contribute to environmental prion load via decomposing carcasses and biological materials including saliva, blood, urine and feces.5–7 Sensitivity limitations of conventional assays hamper evaluation of environmental prion loads in soil and water. Here we show the ability of serial protein misfolding cyclic amplification (sPMCA) to amplify a 1.3 × 10−7 dilution of CWD-infected brain homogenate spiked into water samples, equivalent to approximately 5 × 107 protease resistant cervid prion protein (PrPCWD) monomers. We also detected PrPCWD in one of two environmental water samples from a CWD endemic area collected at a time of increased water runoff from melting winter snow pack, as well as in water samples obtained concurrently from the flocculation stage of water processing by the municipal water treatment facility. Bioassays indicated that the PrPCWD detected was below infectious levels. These data demonstrate detection of very low levels of PrPCWD in the environment by sPMCA and suggest persistence and accumulation of prions in the environment that may promote CWD transmission.
Snip…
The data presented here demonstrate that sPMCA can detect low levels of PrPCWD in the environment, corroborate previous biological and experimental data suggesting long term persistence of prions in the environment2,3 and imply that PrPCWD accumulation over time may contribute to transmission of CWD in areas where it has been endemic for decades. This work demonstrates the utility of sPMCA to evaluate other environmental water sources for PrPCWD, including smaller bodies of water such as vernal pools and wallows, where large numbers of cervids congregate and into which prions from infected animals may be shed and concentrated to infectious levels.
Key words: prions, chronic wasting disease, water, environment, serial protein misfolding cyclic amplification
https://pmc.ncbi.nlm.nih.gov/articles/PMC2802782/
Detection of chronic wasting disease prions in soil at an illegal white-tailed deer carcass disposal site
Published online: 06 Jun 2025
Abstract
Chronic wasting disease (CWD) is a contagious prion disorder affecting cervids such as deer, elk, caribou, and moose, causing progressive and severe neurological degeneration followed by eventual death. As CWD prions (PrPSc) accumulate in the body, they are shed through excreta and secreta, as well as through decomposing carcasses. Prions can persist in the environment for years, posing significant concerns for ongoing transmission to susceptible cervids and pose an unknown risk to sympatric species. We used a validated protocol for real-time quaking-induced conversion (RT-QuIC) in vitro prion amplification assay to detect prions in soil collected within and around an illegal white-tailed deer (Odocoileus virginianus, WTD) carcass disposal site and associated captive WTD farm in Beltrami County, Minnesota. We detected PrPSc in 26 of 201 soil samples across 15 locations within the illegal disposal site and one on the farm that housed the cervids. Importantly, a subset of RT-QuIC positive soil samples was collected from soils where carcasses were recovered, providing direct evidence that environmental contamination resulted from this illegal activity. These findings reveal that improper cervid carcass disposal practices may have important implications for ongoing CWD transmission through the environment.
Snip…
Conclusions
Using RT-QuIC, we detected PrPSc in 26 of 201 soil samples collected across 16 locations on public land where WTD carcasses had been disposed and the captive facility from where they originated. Within the disposal site, 25 out of 124 soil samples (20%) tested positive for PrPSc. Among those positive detections, 17, or 68%, were collected from locations where CWD-positive WTD remains had been previously recovered. This environmental investigation demonstrates how improper cervid carcass disposal practices can result in persistent environmental contamination, posing a potential risk to wildlife health. Given that disposal of livestock on the landscape is a common practice among producers [Citation54–56], these findings underscore the need for improved disposal practices and further investigation of environmental impacts. Expanding on this area of environmental research is crucial as the geographic range of CWD continues to expand [Citation57]. The use of RT-QuIC for prion detection in environmental samples offers an exciting advancement to environmental surveillance for prions, though as we demonstrate here and in Grunklee et al. [Citation41], assay optimization and validation for use with different environmental samples, including new soil types, is still necessary. Further enhancements to RT-QuIC and other methodologies for prion detection will facilitate more opportunities to explore the persistence, degradation, transport, and remediation of environmental prions.
https://www.tandfonline.com/doi/full/10.1080/19336896.2025.2514947
While the disease control measures effectively eliminated prion seeding activity in CWD-affected farms, CWD recurred at two of the 18 remediated farms 4 to 5 years after restocking animals. It remains unclear whether the recurrence of CWD at the two farms was due to residual prions in the environment after the control measures, or the introduction of the infected animals from other farms. This uncertainty is heightened by the annual occurrence of CWD at multiple farms and the absence of a traceability system for farmed cervids.
Keywords: Chronic wasting disease (CWD); NaOH; Protein-misfolding cyclic amplification (PMCA); Republic of Korea; farm; prions; remediation; topsoil.
https://www.tandfonline.com/doi/full/10.1080/19336896.2025.2527588
“While the disease control measures effectively eliminated prion seeding activity in CWD-affected farms, CWD recurred at two of the 18 remediated farms 4 to 5 years after restocking animals.”
I remember what “deep throat” told me about Scrapie back around 2001, during early days of my BSE investigation, after my Mom died from hvCJD, I never forgot, and it seems it’s come to pass;
***> Confidential!!!!
***> As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!
---end personal email---end...tss
and so it seems…
so, this is what we leave our children and grandchildren?
Rapid recontamination of a farm building occurs after attempted prion removal
First published: 19 January 2019 https://doi.org/10.1136/vr.105054
The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease.
snip...
This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapie positive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.
https://bvajournals.onlinelibrary.wiley.com/doi/abs/10.1136/vr.105054
***>This is very likely to have parallels with control efforts for CWD in cervids.
https://pubmed.ncbi.nlm.nih.gov/30602491/
Front. Vet. Sci., 14 September 2015 | https://doi.org/10.3389/fvets.2015.00032
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination.
http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full
"Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation."
15 YEARS!
Detection of prions in soils contaminated by multiple routes
Results: We are able to detect prion seeding activity at multiple types of environmental hotspots, including carcass sites, contaminated captive facilities, and scrapes (i.e. urine and saliva). Differences in relative prion concentration vary depending on the nature and source of the contamination. Additionally, we have determined that prion seeding activity is retained for at least fifteen years at a contaminated site following attempted remediation.
Conclusions: Detection of prions in the environment is of the utmost importance for controlling chronic wasting disease spread. Here, we have demonstrated a viable method for detection of prions in complex environmental matrices. However, it is quite likely that this method underestimates the total infectious prion load in a contaminated sample, due to incomplete recovery of infectious prions. Further refinements are necessary for accurate quantification of prions in such samples, and to account for the intrinsic heterogeneities found in the broader environment.
Funded by: Wisconsin Department of Natural Resources
Prion 2023 Abstracts
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
SUNDAY, APRIL 06, 2025
Failure to prevent classical scrapie after repeated decontamination of a barn
https://scrapie-usa.blogspot.com/2025/04/failure-to-prevent-classical-scrapie.html
https://prpsc.proboards.com/thread/165/failure-prevent-scrapie-repeated-decontamination
CWD, So, this is what we leave our children and grandchildren?
Detection of chronic wasting disease prions in the farm soil of the Republic of Korea
Here, we show that prion seeding activity was detected in extracts from farm soil following 4 years of incubation with CWD-infected brain homogenate.
https://journals.asm.org/doi/10.1128/msphere.00866-24
Artificial mineral sites that pre-date endemic chronic wasting disease become prion hotspots
The detection of PrPCWD in soils at attractant sites within an endemic CWD zone significantly advances our understanding of environmental PrPCWD accumulation dynamics, providing valuable information for advancing adaptive CWD management approaches.
https://int-cwd-sympo.org/wp-content/uploads/2023/06/final-agenda-with-abstracts.pdf
Chronic wasting disease detection in environmental and biological samples from a taxidermy site
Results: The PMCA analysis demonstrated CWD seeding activity in some of the components of this facility, including insects involved in head processing, soils, and a trash dumpster.
Conclusions: Different areas of this property were used for various taxidermy procedures. We were able to detect the presence of prions in i) soils that were in contact with the heads of dead animals, ii) insects involved in the cleaning of skulls, and iii) an empty dumpster where animal carcasses were previously placed. This is the first report demonstrating that swabbing is a helpful method to screen for prion infectivity on surfaces potentially contaminated with CWD. These findings are relevant as this swabbing and amplification strategy may be used to evaluate the disease status of other free-ranging and captive settings where there is a concern for CWD transmissions, such as at feeders and water troughs with CWD-exposed properties. This approach could have substantial implications for free-ranging cervid surveillance as well as in epidemiological investigations of CWD.
Prion 2022 Conference abstracts: pushing the boundaries
https://www.tandfonline.com/doi/full/10.1080/19336896.2022.2091286
https://intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf?force_download=true
***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years
***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded.
JOURNAL OF GENERAL VIROLOGY Volume 87, Issue 12
Infectious agent of sheep scrapie may persist in the environment for at least 16 years Free
https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.82011-0
Rapid recontamination of a farm building occurs after attempted prion removal
First published: 19 January 2019 https://doi.org/10.1136/vr.105054
The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease. snip...
This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapie positive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.
https://bvajournals.onlinelibrary.wiley.com/doi/abs/10.1136/vr.105054
***>This is very likely to have parallels with control efforts for CWD in cervids.
https://pubmed.ncbi.nlm.nih.gov/30602491/
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
http://www.pnas.org/content/97/7/3418.full
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2493038/
Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals
https://bmcvetres.biomedcentral.com/track/pdf/10.1186/1746-6148-9-134.pdf
THURSDAY, FEBRUARY 28, 2019
BSE infectivity survives burial for five years with only limited spread
https://link.springer.com/content/pdf/10.1007%2Fs00705-019-04154-8.pdf
So, this is what we leave our children and grandchildren?
MONDAY, SEPTEMBER 15, 2025
Chronic Wasting Disease CWD TSE Prion Environmental Factors Update
https://chronic-wasting-disease.blogspot.com/2025/09/chronic-wasting-disease-cwd-tse-prion.html
https://chronic-wasting-disease.blogspot.com/
Chronic Wasting Disease CWD TSE Prion Environmental & Zoonosis Factors Update September 2025
What does CDC say?
CDC CWD TSE Prion Update 2025
KEY POINTS
Chronic wasting disease affects deer, elk and similar animals in the United States and a few other countries.
The disease hasn't been shown to infect people.
However, it might be a risk to people if they have contact with or eat meat from animals infected with CWD.
https://www.cdc.gov/chronic-wasting/about/index.html
Prions in Muscles of Cervids with Chronic Wasting Disease, Norway
Volume 31, Number 2—February 2025
Research
Prions in Muscles of Cervids with Chronic Wasting Disease, Norway
Snip…
In summary, the results of our study indicate that prions are widely distributed in peripheral and edible tissues of cervids in Norway, including muscles. This finding highlights the risk of human exposure to small amounts of prions through handling and consuming infected cervids. Nevertheless, we note that this study did not investigate the zoonotic potential of the Norway CWD prions. In North America, humans have historically consumed meat from CWD-infected animals, which has been documented to harbor prions (35,44–47). Despite the potential exposure to prions, no epidemiologic evidence indicates a correlation between the occurrence of CWD cases in animals and the prevalence of human prion diseases (48). A recent bioassay study reported no transmissions from 3 Nordic isolates into transgenic mice expressing human PrP (49). Therefore, our findings should be interpreted with caution in terms of human health implications, and further research is required to determine the zoonotic potential of these CWD strains.
The presence of prions in peripheral tissues indicates that CWD may have a systemic nature in all Norwegian cervid species, challenging the view that prions are exclusively localized in the CNS in sporadic CWD of moose and red deer. Our findings expand the notion of just how widely distributed prions can be in cervids affected with CWD and call into question the capability of emerging CWD strains in terms of infectivity to other species, including humans.
Appendix
https://wwwnc.cdc.gov/eid/article/31/2/24-0903-app1.pdf
https://wwwnc.cdc.gov/eid/article/31/2/24-0903_article
Volume 31, Number 2—February 2025
Dispatch
Detection of Chronic Wasting Disease Prions in Raw, Processed, and Cooked Elk Meat, Texas, USA
Rebeca Benavente, Fraser Brydon, Francisca Bravo-Risi, Paulina Soto, J. Hunter Reed, Mitch Lockwood, Glenn Telling, Marcelo A. Barria, and Rodrigo MoralesComments to Author
Snip…
CWD prions have been detected in the muscle of both farmed and wild deer (10), and at concentrations relevant to sustain disease transmission (11). CWD prions have also been identified across several cervid species and in multiple tissues, including lymph nodes, spleen, tongue, intestines, adrenal gland, eyes, reproductive tissues, ears, lungs, and liver, among others (12–14). Those findings raise concerns about the safety of ingesting processed meats that contain tissues other than skeletal muscle (15) (Appendix). https://wwwnc.cdc.gov/eid/article/31/2/24-0906-app1.pdf
In addition, those findings highlight the need for continued vigilance and research on the transmission risks of prion diseases and for development of new preventative and detection measures to ensure the safety of the human food supply.
Snip…
Overall, our study results confirm previous reports describing the presence of CWD prions in elk muscles (13). The data also demonstrated CWD prion persistence in food products even after processing through different procedures, including the addition of salts, spices, and other edible elements. Of note, our data show that exposure to high temperatures used to cook the meat increased the availability of prions for in vitro amplification. Considering the potential implications in food safety and public health, we believe that the findings described in this study warrant further research. Our results suggest that although the elk meat used in this study resisted different manipulations involved in subsequent consumption by humans, their zoonotic potential was limited. Nevertheless, even though no cases of CWD transmission to human have been reported, the potential for human infection is still unclear and continued monitoring for zoonotic potential is warranted.
https://wwwnc.cdc.gov/eid/article/31/2/24-0906_article
The detection and decontamination of chronic wasting disease prions during venison processing
Aims: There is a growing concern that chronic wasting disease (CWD) prions in venison pose a risk to human health. CWD prions accumulate in infected deer tissues that commonly enter the human food chain through meat processing and consumption. The United States (US) Food and Drug Administration and US Department of Agriculture now formally consider CWD-positive venison unfit for human and animal consumption. Yet, the degree to which prion contamination occurs during routine venison processing is unknown. Here, we use environmental surface swab methods to:
a) experimentally test meat processing equipment (i.e., stainless steel knives and polyethylene cutting boards) before and after processing CWD-positive venison and
b) test the efficacy of five different disinfectant types (i.e., Dawn dish soap, Virkon-S, Briotech, 10% bleach, and 40% bleach) to determine prion decontamination efficacy.
Materials and Methods: We used a real-time quaking-induced conversion (RT-QuIC) assay to determine CWD infection status of venison and to detect CWD prions in the swabs. We collected three swabs per surface and ran eight technical replicates on RT-QuIC.
Results: CWD prions were detected on all cutting boards (n= 3; replicates= 8/8, 8/8, 8/8 and knives (n= 3; replicates= 8/8, 8/8, 8/8) used in processing CWD-positive venison, but not on those used for CWD-negative venison. After processing CWD-positive venison, allowing the surfaces to dry, and washing the cutting board with Dawn dish soap, we detected CWD prions on the cutting board surface (n= 3; replicates= 8/8, 8/8, 8/8) but not on the knife (n= 3, replicates = 0/8, 0/8, 0/8). Similar patterns were observed with Briotech (cutting board: n= 3; replicates= 7/8, 1/8, 0/8; knife: n= 3; replicates = 0/8, 0/8, 0/8). We did not detect CWD prions on the knives or cutting boards after disinfecting with Virkon-S, 10% bleach, and 40% bleach.
Conclusions: These preliminary results suggest that Dawn dish soap and Briotech do not reliably decontaminate CWD prions from these surfaces. Our data suggest that Virkon-S and various bleach concentrations are more effective in reducing prion contamination of meat processing surfaces; however, surface type may also influence the ability of prions to adsorb to surfaces, preventing complete decontamination. Our results will directly inform best practices to prevent the introduction of CWD prions into the human food chain during venison processing.
Prion 2023 Abstracts
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
DETECTION OF CHRONIC WASTING DISEASE PRIONS IN PROCESSED MEATS.
The zoonotic potential of chronic wasting disease (CWD) remains unknown. Currently, there are no known natural cases of CWD transmission to humans but increasing evidence suggests that the host range of CWD is not confined only to cervid species. Alarmingly, recent experimental evidence suggests that certain CWD isolates can induce disease in non-human primates. While the CDC strongly recommends determining CWD status in animals prior to consumption, this practice is voluntary. Consequently, it is plausible that a proportion of the cervid meat entering the human food chain may be contaminated with CWD. Of additional concern is that traditional diagnostic techniques used to detect CWD have relatively low sensitivity and are only approved for use in tissues other than those typically ingested by humans. In this study, we analyzed different processed meats derived from a pre-clinical, CWD-positive free-ranging elk. Products tested included filets, sausages, boneless steaks, burgers, ham steaks, seasoned chili meats, and spiced meats. CWD-prion presence in these products were assessed by PMCA using deer and elk substrates. Our results show positive prion detection in all products. To confirm the resilience of CWD-prions to traditional cooking methods, we grilled and boiled the meat products and evaluated them for any remnant PMCA seeding activity. Results confirmed the presence of CWD-prions in these meat products suggesting that infectious particles may still be available to people even after cooking. Our results strongly suggest ongoing human exposure to CWD-prions and raise significant concerns of zoonotic transmission through ingestion of CWD contaminated meat products.
***> Products tested included filets, sausages, boneless steaks, burgers, ham steaks, seasoned chili meats, and spiced meats.
***> CWD-prion presence in these products were assessed by PMCA using deer and elk substrates.
***> Our results show positive prion detection in all products.
***> Results confirmed the presence of CWD-prions in these meat products suggesting that infectious particles may still be available to people even after cooking.
***> Our results strongly suggest ongoing human exposure to CWD-prions and raise significant concerns of zoonotic transmission through ingestion of CWD contaminated meat products.
https://intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf?force_download=true
Detection of chronic wasting disease prions in processed meats
Results: Our results show positive prion detection in all the samples analyzed using deer and elk substrates. Surprisingly, cooked meats displayed increased seeding activities. This data suggests that CWD-prions are available to people even after meats are processed and cooked.
Conclusions: These results suggest CWD prions are accessible to humans through meats, even after processing and cooking. Considering the fact that these samples were collected from already processed specimens, the availability of CWD prions to humans is probably underestimated.
"Our results show positive prion detection in all the samples analyzed using deer and elk substrates. Surprisingly, cooked meats displayed increased seeding activities."
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
Fortuitous generation of a zoonotic cervid prion strain
Aims: Whether CWD prions can infect humans remains unclear despite the very substantial scale and long history of human exposure of CWD in many states or provinces of USA and Canada. Multiple in vitro conversion experiments and in vivo animal studies indicate that the CWD-to-human transmission barrier is not unbreakable. A major long-term public health concern on CWD zoonosis is the emergence of highly zoonotic CWD strains. We aim to address the question of whether highly zoonotic CWD strains are possible.
Materials and Methods: We inoculated several sCJD brain samples into cervidized transgenic mice (Tg12), which were intended as negative controls for bioassays of brain tissues from sCJD cases who had potentially been exposed to CWD. Some of the Tg12mice became infected and their brain tissues were further examined by Western blot as well as serial passages in humanized or cervidized mice.
Results: Passage of sCJDMM1 in transgenic mice expressing elk PrP (Tg12) resulted in a “cervidized” CJD strain that we termed CJDElkPrP. We observed 100% transmission of the original CJDElkPrP in transgenic mice expressing human PrP. We passaged CJDElkPrP two more times in the Tg12mice. We found that such second and third passage CJDElkPrP prions retained 100% transmission rate in the humanized mice, despite that the natural elk CWD isolates and CJDElkPrP share the same elk PrP sequence. In contrast, we and others found zero or poor transmission of natural elk CWD isolates in humanized mice.
Conclusions: Our data indicate that highly zoonotic cervid prion strains are not only possible but also can retain zoonotic potential after serial passages in cervids, suggesting a very significant and serious long-term risk of CWD zoonosis given that the broad and continuing spread of CWD prions will provide fertile grounds for the emergence of zoonotic CWD strains over time.
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
Transmission of cervid prions to humanized mice demonstrates the zoonotic potential of CWD
Samia Hannaoui1 · Irina Zemlyankina1 · Sheng Chun Chang1 · Maria Immaculata Arifn1 · Vincent Béringue2 · Debbie McKenzie3 · Hermann M. Schatzl1 · Sabine Gilch1
Received: 24 May 2022 / Revised: 5 August 2022 / Accepted: 7 August 2022
© The Author(s) 2022
Abstract
Prions cause infectious and fatal neurodegenerative diseases in mammals. Chronic wasting disease (CWD), a prion disease of cervids, spreads efficiently among wild and farmed animals. Potential transmission to humans of CWD is a growing concern due to its increasing prevalence. Here, we provide evidence for a zoonotic potential of CWD prions, and its probable signature using mice expressing human prion protein (PrP) as an infection model. Inoculation of these mice with deer CWD isolates resulted in atypical clinical manifestation with prion seeding activity and efficient transmissible infectivity in the brain and, remarkably, in feces, but without classical neuropathological or Western blot appearances of prion diseases. Intriguingly, the protease-resistant PrP in the brain resembled that found in a familial human prion disease and was transmissible upon second passage. Our results suggest that CWD might infect humans, although the transmission barrier is likely higher compared to zoonotic transmission of cattle prions. Notably, our data suggest a different clinical presentation, prion signature, and tissue tropism, which causes challenges for detection by current diagnostic assays. Furthermore, the presence of infectious prions in feces is concerning because if this occurs in humans, it is a source for human-to-human transmission. These findings have strong implications for public health and CWD management.
Keywords Chronic wasting disease · CWD · Zoonotic potential · Prion strains · Zoonotic prions
HIGHLIGHTS OF THIS STUDY
================================
Our results suggest that CWD might infect humans, although the transmission barrier is likely higher compared to zoonotic transmission of cattle prions. Notably, our data suggest a different clinical presentation, prion signature, and tissue tropism, which causes challenges for detection by current diagnostic assays. Furthermore, the presence of infectious prions in feces is concerning because if this occurs in humans, it is a source for human-to-human transmission. These findings have strong implications for public health and CWD management.
In this study, we evaluated the zoonotic potential of CWD using a transgenic mouse model overexpressing human M129-PrPC (tg650 [12]). We inoculated tg650 mice intracerebrally with two deer CWD isolates, Wisc-1 and 116AG [22, 23, 27, 29]. We demonstrate that this transgenic line was susceptible to infection with CWD prions and displayed a distinct leading clinical sign, an atypical PrPSc signature and unusual fecal shedding of infectious prions. Importantly, these prions generated by the human PrP transgenic mice were transmissible upon passage. Our results are the first evidence of a zoonotic risk of CWD when using one of the most common CWD strains, Wisc-1/CWD1 for infection. We demonstrated in a human transgenic mouse model that the species barrier for transmission of CWD to humans is not absolute. The fact that its signature was not typical raises the questions whether CWD would manifest in humans as a subclinical infection, whether it would arise through direct or indirect transmission including an intermediate host, or a silent to uncovered human-to-human transmission, and whether current detection techniques will be suffcient to unveil its presence.
Our findings strongly suggest that CWD should be regarded as an actual public health risk. Here, we use humanized mice to show that CWD prions can cross the species barrier to humans, and remarkably, infectious prions can be excreted in feces.
Our results indicate that if CWD crosses the species-barrier to humans, it is unlikely to resemble the most common forms of human prion diseases with respect to clinical signs, tissue tropism and PrPSc signature. For instance, PrPSc in variable protease-sensitive prionopathy (VPSPr), a sporadic form of human prion disease, and in the genetic form Gerstmann-Sträussler-Scheinker syndrome (GSS) is defined by an atypical PK-resistant PrPSc fragment that is non-glycosylated and truncated at both C- and N-termini, with a molecular weight between 6 and 8 kDa [24, 44–46]. These biochemical features are unique and distinctive from PrPSc (PrP27-30) found in most other human or animal prion disease. The atypical PrPSc signature detected in brain homogenate of tg650 mice #321 (1st passage) and #3063 (2nd passage), and the 7–8 kDa fragment (Figs. 2, 4) are very similar to that of GSS, both in terms of migration profile and the N-terminal cleavage site.
CWD in humans might remain subclinical but with PrPSc deposits in the brain with an unusual morphology that does not resemble the patterns usually seen in different prion diseases (e.g., mouse #328; Fig. 3), clinical with untraceable abnormal PrP (e.g., mouse #327) but still transmissible and uncovered upon subsequent passage (e.g., mouse #3063; Fig. 4), or prions have other reservoirs than the usual ones, hence the presence of infectivity in feces (e.g., mouse #327) suggesting a potential for human-to-human transmission and a real iatrogenic risk that might be unrecognizable.
“suggesting a potential for human-to-human transmission and a real iatrogenic risk that might be unrecognizable.”
=================================
Supplementary Information The online version contains supplementary material available at
https://doi.org/10.1007/s00401-022-02482-9
snip...see full text;
https://link.springer.com/article/10.1007/s00401-022-02482-9
https://link.springer.com/content/pdf/10.1007/s00401-022-02482-9.pdf
Macaque tissues to rodent models demonstrates the zoonotic potential of chronic wasting disease.
Samia Hannaoui1,2, Ginny Cheng1,2, Wiebke Wemheuer3, Walter Schulz-Schaeffer3, Sabine Gilch1,2, Hermann Schatzl1,2 1University of Calgary, Calgary, Canada. 2Calgary Prion Research Unit, Calgary, Canada. 3Institute of Neuropathology, Medical Faculty, Saarland University, Homburg/Saar, Germany
Snip…
***> Further passage to cervidized mice revealed transmission with a 100% attack rate.
***> Our findings demonstrate that macaques, considered the best model for the zoonotic potential of prions, were infected upon CWD challenge, including the oral one.
****> The disease manifested as atypical in macaques and initial transgenic mouse transmissions, but with infectivity present at all times, as unveiled in the bank vole model with an unusual tissue tropism.
***> Epidemiologic surveillance of prion disease among cervid hunters and people likely to have consumed venison contaminated with chronic wasting disease
=====
https://intcwdsympo.files.wordpress.com/2023/06/final-agenda-with-abstracts.pdf?force_download=true
Transmission of Cervid Prions to Humanized Mice Demonstrates the Zoonotic Potential of CWD
Samia Hannaouia, Irina Zemlyankinaa, Sheng Chun Changa, Maria Immaculata Arifina, Vincent Béringueb, Debbie McKenziec, Hermann M. Schatzla, and Sabine Gilcha
Results: Here, we provide the strongest evidence supporting the zoonotic potential of CWD prions, and their possible phenotype in humans. Inoculation of mice expressing human PrPCwith deer CWD isolates (strains Wisc-1 and 116AG) resulted in atypical clinical manifestations in > 75% of the mice, with myoclonus as leading clinical sign. Most of tg650brain homogenates were positive for seeding activity in RT-QuIC. Clinical disease and presentation was transmissible to tg650 mice and bank voles. Intriguingly, protease-resistant PrP in the brain of tg650 mice resembled that found in a familial human prion disease and was transmissible upon passage. Abnormal PrP aggregates upon infection with Wisc-1 were detectable in thalamus, hypothalamus, and midbrain/pons regions.
Unprecedented in human prion disease, feces of CWD-inoculated tg650 mice harbored prion seeding activity and infectious prions, as shown by inoculation of bank voles and tg650 with fecal homogenates.
Conclusions: This is the first evidence that CWD can infect humans and cause disease with a distinctive clinical presentation, signature, and tropism, which might be transmissible between humans while current diagnostic assays might fail to detect it. These findings have major implications for public health and CWD-management.
https://www.tandfonline.com/doi/full/10.1080/19336896.2022.2091286
18. Zoonotic potential of moose-derived chronic wasting disease prions after adaptation in intermediate species
Tomás Barrioa, Jean-Yves Doueta, Alvina Huora, Séverine Lugana, Naïma Arona, Hervé Cassarda, Sylvie L. Benestadb, Juan Carlos Espinosac, Juan María Torresc, Olivier Andréolettia
aUnité Mixte de Recherche de l’Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement 1225 Interactions Hôtes-Agents Pathogènes, École Nationale Vétérinaire de Toulouse, 31076 Toulouse, France; bNorwegian Veterinary Institute, P.O. Box 64, NO-1431 Ås, Norway; cCentro de Investigación en Sanidad Animal (CISA-INIA), 28130, Valdeolmos, Madrid, Spain
Aims: Chronic wasting disease (CWD) is an emerging prion disease in Europe. To date, cases have been reported in three Nordic countries and in several species, including reindeer (Rangifer tarandus), moose (Alces alces) and red deer (Cervus elaphus). Cumulating data suggest that the prion strains responsible for the European cases are distinct from those circulating in North America. The biological properties of CWD prions are still poorly documented, in particular their spillover and zoonotic capacities. In this study, we aimed at characterizing the interspecies transmission potential of Norwegian moose CWD isolates.
Materials and Methods: For that purpose, we performed experimental transmissions in a panel of transgenic models expressing the PrPC sequence of various species.
Results: On first passage, one moose isolate propagated in the ovine PrPC-expressing model (Tg338). After adaptation in this host, moose CWD prions were able to transmit in mice expressing either bovine or human PrPC with high efficacy.
Conclusions: These results suggest that CWD prions can acquire enhanced zoonotic properties following adaptation in an intermediate species.
Funding
Grant number: AAPG2020 EU-CWD, ICRAD2020 TCWDE, NRC2022 NorCWD
Acknowledgement
https://www.tandfonline.com/doi/full/10.1080/19336896.2024.2424058
“ After adaptation in this host, moose CWD prions were able to transmit in mice expressing either bovine or human PrPC with high efficacy.”
regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD
Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY
Date: Fri, 18 Oct 2002 23:12:22 +0100
From: Steve Dealler
Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member
To: BSE-L@ …
######## Bovine Spongiform Encephalopathy <BSE-L@UNI-KARLSRUHE.DE> #########
Dear Terry,
An excellent piece of review as this literature is desparately difficult to get back from Government sites.
What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported.
Well, if you dont look adequately like they are in USA currenly then you wont find any!
Steve Dealler
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
Subject: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY
From: "Terry S. Singeltary Sr." <flounder@WT.NET>
Reply To: Bovine Spongiform Encephalopathy <BSE-L@UNI-KARLSRUHE.DE>
Date: Thu, 17 Oct 2002 17:04:51 -0700
snip...
''The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).''
CREUTZFELDT JAKOB DISEASE SURVEILLANCE IN THE UNITED KINGDOM THIRD ANNUAL REPORT AUGUST 1994
Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. (not nvCJD, but sporadic CJD...tss) These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...
Table 9 presents the results of an analysis of these data.
There is STRONG evidence of an association between ‘’regular’’ veal eating and risk of CJD (p = .0.01).
Individuals reported to eat veal on average at least once a year appear to be at 13 TIMES THE RISK of individuals who have never eaten veal.
There is, however, a very wide confidence interval around this estimate. There is no strong evidence that eating veal less than once per year is associated with increased risk of CJD (p = 0.51).
The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04).
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
http://web.archive.org/web/20090506050043/http://www.bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf
http://web.archive.org/web/20090506050007/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
http://web.archive.org/web/20090506050244/http://www.bseinquiry.gov.uk/files/yb/1994/07/00001001.pdf
Stephen Dealler is a consultant medical microbiologist deal@airtime.co.uk
BSE Inquiry Steve Dealler
Management In Confidence
BSE: Private Submission of Bovine Brain Dealler
snip...end
########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
BSE INQUIRY
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane
BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended.. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
TSE in wild UK deer? The first case of BSE (as we now realise) was in a nyala in London zoo and the further zoo cases in ungulates were simply thought of as being interesting transmissions of scrapie initially. The big problem started to appear with animals in 1993-5 when it became clear that there was an increase in the CJD cases in people that had eaten deer although the statistics involved must have been questionable. The reason for this was that the CJD Surveillance was well funded to look into the diet of people dying of CJD. This effect is not clear with vCJD...if only because the numbers involved are much smaller and hence it is difficult to gain enough statistics. They found that many other foods did not appear to have much association at all but that deer certainly did and as years went by the association actually became clearer. The appearance of vCJD in 1996 made all this much more difficult in that it was suddenly clearer that the cases of sporadic CJD that they had been checking up until then probably had nothing to do with beef...and the study decreased. During the period there was an increasing worry that deer were involved with CJD..
see references:
DEER BRAIN SURVEY
https://web.archive.org/web/20090506025229/http://www.bseinquiry.gov.uk/files/yb/1991/11/20004001.pdf
CONFIDENTIAL AND IN CONFIDENCE TRANSMISSION TO CHIMPANZEES AND PIGS
IN CONFIDENCE
TRANSMISSION TO CHIMPANZEES
Kuru and CJD have been successfully transmitted to chimpanzees but scrapie and TME have not.
We cannot say that scrapie will not transmit to chimpanzees. There are several scrapie strains and I am not aware that all have been tried (that would have to be from mouse passaged material). Nor has a wide enough range of field isolates subsequently strain typed in mice been inoculated by the appropriate routes (i/c, i/p and i/v).
I believe the proposed experiment to determine transmissibility, if conducted, would only show the susceptibility or resistance of the chimpanzee to infection/disease by the routes used and the result could not be interpreted for the predictability of the susceptibility for man. proposals for prolonged oral exposure of chimpanzees to milk from cattle were suggested a long while ago and rejected.
In view of Dr Gibbs' probable use of chimpazees Mr Wells' comments (enclosed) are pertinent. I have yet to receive a direct communication from Dr Schellekers but before any collaboration or provision of material we should identify the Gibbs' proposals and objectives.
A positive result from a chimpanzee challenged severely would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.
A negative result would take a lifetime to determine but that would be a shorter period than might be available for human exposure and it would still not answer the question regarding mans ‘susceptibility. In the meantime no doubt the negativity would be used defensively. It would however be counterproductive if the experiment finally became positive. We may learn more about public reactions following next Monday's meeting.
R Bradley
CVO (+ Mr Wells’ commenters 23 September 1990 Dr T W A Little Dr B J Shreeve
90/9.23/1.1
https://web.archive.org/web/20090506041740/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf
*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.
see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????
“Our conclusion stating that we found no strong evidence of CWD transmission to humans”
From: TSS Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam, In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091).
Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease
2008 1: Vet Res. 2008 Apr 3;39(4):41
snip...
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
snip... full text ;
http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html
However, to date, no CWD infections have been reported in people.
sporadic, spontaneous CJD, 85%+ of all human TSE, did not just happen. never in scientific literature has this been proven. if one looks up the word sporadic or spontaneous at pubmed, you will get a laundry list of disease that are classified in such a way;
sporadic = 54,983 hits
https://www.ncbi.nlm.nih.gov/pubmed/?term=sporadic
spontaneous = 325,650 hits
https://www.ncbi.nlm.nih.gov/pubmed/?term=spontaneous
key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD.
SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
However, to date, no CWD infections have been reported in people. key word here is ‘reported’. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can’t, and it’s as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it’s being misdiagnosed as sporadic CJD. …terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys
http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true
https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article
So, this is what we leave our children and grandchildren?
Human iatrogenic TSE Prion Disease
France issues moratorium on prion research after fatal brain disease strikes two lab workers
By Barbara CasassusJul. 28, 2021 , 4:35 AM
PARIS—Five public research institutions in France have imposed a 3-month moratorium on the study of prions—a class of misfolding, infectious proteins that cause fatal brain diseases—after a retired lab worker who handled prions in the past was diagnosed with Creutzfeldt-Jakob disease (CJD), the most common prion disease in humans. An investigation is underway to find out whether the patient, who worked at a lab run by the National Research Institute for Agriculture, Food and Environment (INRAE), contracted the disease on the job.
If so, it would be the second such case in France in the past few years. In June 2019, an INRAE lab worker named Émilie Jaumain died at age 33, 10 years after pricking her thumb during an experiment with prion-infected mice. Her family is now suing INRAE for manslaughter and endangering life; her illness had already led to tightened safety measures at French prion labs.
Posted in: EuropeHealthScientific Community
doi:10.1126/science.abl6587
https://www.sciencemag.org/news/2021/07/france-issues-moratorium-prion-research-after-fatal-brain-disease-strikes-two-lab
Variant Creutzfeldt–Jakob Disease Diagnosed 7.5 Years after Occupational Exposure
Variant Creutzfeldt–Jakob disease was identified in a technician who had cut her thumb while handling brain sections of mice infected with adapted BSE 7.5 years earlier. The long incubation period was similar to that of the transfusion-transmitted form of the disease.
Variant Creutzfeldt–Jakob Disease Diagnosed 7.5 Years after Occupational Exposure
TO THE EDITOR:
We report a case of variant Creutzfeldt–Jakob disease (CJD) that was plausibly related to accidental occupational exposure in a technician who had handled murine samples contaminated with the agent that causes bovine spongiform encephalopathy (BSE) 7.5 years earlier.
In May 2010, when the patient was 24 years of age, she worked in a prion research laboratory, where she handled frozen sections of brain of transgenic mice that overexpressed the human prion protein with methionine at codon 129. The mice had been infected with a sheep-adapted form of BSE. During this process, she stabbed her thumb through a double pair of latex gloves with the sharp ends of a curved forceps used to handle the samples. Bleeding was noted at the puncture site.
Metrics
https://www.nejm.org/doi/full/10.1056/NEJMc2000687
WEDNESDAY, OCTOBER 15, 2025
US NATIONAL PRION DISEASE PATHOLOGY SURVEILLANCE CENTER CJD TSE REPORT 2025
https://prionunitusaupdate.blogspot.com/2025/10/us-national-prion-disease-pathology.html
Cattle, sheep, pigs, raccoons, CWD, Oh, My!
Volume 31, Number 1—January 2025
Dispatch
Detection of Prions in Wild Pigs (Sus scrofa) from Areas with Reported Chronic Wasting Disease Cases, United States
Abstract
Using a prion amplification assay, we identified prions in tissues from wild pigs (Sus scrofa) living in areas of the United States with variable chronic wasting disease (CWD) epidemiology. Our findings indicate that scavenging swine could play a role in disseminating CWD and could therefore influence its epidemiology, geographic distribution, and interspecies spread.
Snip…
Conclusions In summary, results from this study showed that wild pigs are exposed to cervid prions, although the pigs seem to display some resistance to infection via natural exposure. Future studies should address the susceptibility of this invasive animal species to the multiple prion strains circulating in the environment. Nonetheless, identification of CWD prions in wild pig tissues indicated the potential for pigs to move prions across the landscape, which may, in turn, influence the epidemiology and geographic spread of CWD.
https://wwwnc.cdc.gov/eid/article/%2031/1/24-0401_article
Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
2. Determined that pigs naturally exposed to chronic wasting disease (CWD) may act as a reservoir of CWD infectivity. Chronic wasting disease is a naturally occurring, fatal, neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of CWD disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Pigs were assigned to 1 of 3 groups: intracranially inoculated; orally inoculated; or non-inoculated. At market weight age, half of the pigs in each group were tested ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by multiple diagnostic methods. Brain samples from selected pigs were bioassayed in mice expressing porcine prion protein. Some pigs from each inoculated group were positive by one or more tests. Bioassay was positive in 4 out of 5 pigs assayed. Although only small amounts of PrPSc were detected using sensitive methods, this study demonstrates that pigs can serve as hosts for CWD. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP
https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091
Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017
Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105
This study demonstrates that pigs can serve as potential hosts for CWD, although with low attack rates and scant PrPcwd accumulation. Detection of infectivity in orally challenged pigs using mouse bioassay raises the possibility that naturally exposed pigs act as a reservoir of CWD infectivity, even though affected pigs do not develop overt clinical signs or readily detectable PrPcwd.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166
CONFIDENTIAL
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
LINE TO TAKE
3. If questions on pharmaceuticals are raised at the Press conference, the suggested line to take is as follows:-
"There are no medicinal products licensed for use on the market which make use of UK-derived porcine tissues with which any hypothetical “high risk" ‘might be associated. The results of the recent experimental work at the CSM will be carefully examined by the CSM‘s Working Group on spongiform encephalopathy at its next meeting.
DO Hagger RM 1533 MT Ext 3201
http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf
While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...
http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf
we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.
http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf
May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...
http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf
3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...
http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf
But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...
http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....
http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf
Monday, November 13, 2023
Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) Singeltary Another Request for Update 2023 Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) Singeltary Another Request for Update 2023
The infamous 1997 mad cow feed ban i.e. Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.
***>However, this recommendation is guidance and not a requirement by law.
WITH GREAT URGENCY, THE Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) MUST BE ENHANCED AND UPDATED TO INCLUDE CERVID, PIGS, AND SHEEP, SINCE RECENT SCIENCE AND TRANSMISSION STUDIES ALL, INCLUDING CATTLE, HAVE SHOWN ORAL TSE PrP TRANSMISSIONS BETWEEN THE SPECIES, AND THIS SHOULD BE DONE WITH THE UTMOST URGENCY, REASONS AS FOLLOW.
First off I will start with a single BSE feed breach 10 years after 1997 partial ban. If you got to the archived link, all the way down to bottom…THE NEXT YEAR I RECALL ONE WITH 10,000,000+ banned products recall…see this records at the bottom…terry
2016
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed
PUBLIC SUBMISSION
Comment from Terry Singeltary Sr.
Posted by the Food and Drug Administration on May 17, 2016 Comment
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed Singeltary Submission
https://www.regulations.gov/comment/FDA-2003-D-0432-0011
https://www.regulations.gov/docket/FDA-2003-D-0432
How in the hell do you make a complete recall of 27,694,240 lbs of feed that was manufactured from materials that may have been contaminated with mammalian protein, in one state, 2006? Wonder how much was fed out?
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated,
net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated,
Recall # V-103-6;
e) "Big Jim’s" BBB Deer Ration, Big Buck Blend,
Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted,
Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020,
Carbadox -- 0.0055%, Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete
Feed for Chickens from Hatch to 20 Weeks, Medicated,
Bacitracin Methylene Disalicylate, 25 and 50 Lbs,
Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying
Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED,
net wt 50 Lbs, Recall # V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs,
Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs,
Recall # V-112-6
CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER
Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006.
FDA initiated recall is complete.
REASON
Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE
125 tons
DISTRIBUTION
AL and FL
______________________________
PRODUCT
Bulk custom dairy feds manufactured from concentrates, Recall # V-113-6
CODE
All dairy feeds produced between 2/1/05 and 6/16/06 and containing H. J. Baker recalled feed products.
RECALLING FIRM/MANUFACTURER
Vita Plus Corp., Gagetown, MI, by visit beginning on June 21, 2006.
Firm initiated recall is complete.
REASON
The feed was manufactured from materials that may have been contaminated with mammalian protein.
VOLUME OF PRODUCT IN COMMERCE
27,694,240 lbs
DISTRIBUTION
MI
______________________________
PRODUCT
Bulk custom made dairy feed, Recall # V-114-6
CODE
None
RECALLING FIRM/MANUFACTURER
Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006. Firm initiated recall is ongoing.
REASON
Custom made feeds contain ingredient called Pro-Lak, which may contain ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE
???
DISTRIBUTION
KY
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
https://web.archive.org/web/20100120023832/http://www.fda.gov/Safety/Recalls/EnforcementReports/2006/ucm120413.htm
***>However, this recommendation is guidance and not a requirement by law.
THIS MUST CHANGE ASAP!
“For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.”
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012
snip.....
In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law. Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and
2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.
snip.....
https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf
PLoS One. 2020 Aug 20;15(8):e0237410. doi: 10.1371/journal.pone.0237410. eCollection 2020.
Very low oral exposure to prions of brain or saliva origin can transmit chronic wasting disease
Nathaniel D Denkers 1 , Clare E Hoover 2 , Kristen A Davenport 3 , Davin M Henderson 1 , Erin E McNulty 1 , Amy V Nalls 1 , Candace K Mathiason 1 , Edward A Hoover 1
PMID: 32817706 PMCID: PMC7446902 DOI: 10.1371/journal.pone.0237410
Abstract
The minimum infectious dose required to induce CWD infection in cervids remains unknown, as does whether peripherally shed prions and/or multiple low dose exposures are important factors in CWD transmission. With the goal of better understand CWD infection in nature, we studied oral exposures of deer to very low doses of CWD prions and also examined whether the frequency of exposure or prion source may influence infection and pathogenesis. We orally inoculated white-tailed deer with either single or multiple divided doses of prions of brain or saliva origin and monitored infection by serial longitudinal tissue biopsies spanning over two years. We report that oral exposure to as little as 300 nanograms (ng) of CWD-positive brain or to saliva containing seeding activity equivalent to 300 ng of CWD-positive brain, were sufficient to transmit CWD disease. This was true whether the inoculum was administered as a single bolus or divided as three weekly 100 ng exposures. However, when the 300 ng total dose was apportioned as 10, 30 ng doses delivered over 12 weeks, no infection occurred. While low-dose exposures to prions of brain or saliva origin prolonged the time from inoculation to first detection of infection, once infection was established, we observed no differences in disease pathogenesis. These studies suggest that the CWD minimum infectious dose approximates 100 to 300 ng CWD-positive brain (or saliva equivalent), and that CWD infection appears to conform more with a threshold than a cumulative dose dynamic.
Snip…
Discussion
As CWD expands across North America and Scandinavia, how this disease is transmitted so efficiently remains unclear, given the low concentrations of prions shed in secretions and excretions [13, 14]. The present studies demonstrated that a single oral exposure to as little as 300nmg of CWD-positive brain or equivalent saliva can initiate infection in 100% of exposed white-tailed deer. However, distributing this dose as 10, 30 ng exposures failed to induce infection. Overall, these results suggest that the minimum oral infectious exposure approaches 100 to 300 ng of CWD-positive brain equivalent. These dynamics also invite speculation as to whether potential infection co-factors, such as particle binding [46, 47] or compromises in mucosal integrity may influence infection susceptibility, as suggested from two studies in rodent models [48, 49].
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0237410
PRION 2023 CONTINUED;
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
Prion 2023 Experimental Oronasal Inoculation of the Chronic Wasting Disease Agent into White Tailed Deer
Author list: Sarah Zurbuchena,b , S. Jo Moorea,b , Jifeng Biana , Eric D. Cassmanna , and Justin J. Greenleea . a. Virus and Prion Research Unit, National Animal Disease Center, ARS, United States Department of Agriculture, Ames, IA, US b. Oak Ridge Institute for Science and Education (ORISE), U.S. Department of Energy, Oak Ridge, TN, United States
Aims: The purpose of this experiment was to determine whether white-tailed deer (WTD) are susceptible to inoculation of chronic wasting disease (CWD) via oronasal exposure.
Materials and methods: Six male, neutered WTD were oronasally inoculated with brainstem material (10% w/v) from a CWD-positive wild-type WTD. The genotypes of five inoculated deer were Q95/G96 (wild-type). One inoculated deer was homozygous S at codon 96 (96SS). Cervidized (Tg12; M132 elk PrP) mice were inoculated with 1% w/v brainstem homogenate from either a 96GG WTD (n=10) or the 96SS WTD (n=10).
Results: All deer developed characteristic clinical signs of CWD including weight loss, regurgitation, and ataxia. The 96SS individual had a prolonged disease course and incubation period compared to the other deer. Western blots of the brainstem on all deer yielded similar molecular profiles. All deer had widespread lymphoid distribution of PrPCWD and neuropathologic lesions associated with transmissible spongiform encephalopathies. Both groups of mice had a 100% attack rate and developed clinical signs, including loss of body condition, ataxia, and loss of righting reflex. Mice inoculated with material from the 96SS deer had a significantly shorter incubation period than mice inoculated with material from 96GG deer (Welch two sample T-test, P<0.05). Serial dilutions of each inocula suggests that differences in incubation period were not due to a greater concentration of PrPCWD in the 96SS inoculum. Molecular profiles from western blot of brain homogenates from mice appeared similar regardless of inoculum and appear similar to those of deer used for inoculum.
Conclusions: This study characterizes the lesions and clinical course of CWD in WTD inoculated in a similar manner to natural conditions. It supports previous findings that 96SS deer have a prolonged disease course. Further, it describes a first pass of inoculum from a 96SS deer in cervidized mice which shortened the incubation period.
Funded by: This research was funded in its entirety by congressionally appropriated funds to the United States Department of Agriculture, Agricultural Research Service. The funders of the work did not influence study design, data collection, analysis, decision to publish, or preparation of the manuscript.
Acknowledgement: We thank Ami Frank and Kevin Hassall for their technical contributions to this project.
=====end
PRION 2023 CONTINUED;
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
***> Price of TSE Prion Poker goes up substantially, all you cattle ranchers and such, better pay close attention here...terry <***
Transmission of the chronic wasting disease agent from elk to cattle after oronasal exposure
Justin Greenlee, Jifeng Bian, Zoe Lambert, Alexis Frese, and Eric Cassmann Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS, Ames, IA, USA
Aims: The purpose of this study was to determine the susceptibility of cattle to chronic wasting disease agent from elk.
Materials and Methods: Initial studies were conducted in bovinized mice using inoculum derived from elk with various genotypes at codon 132 (MM, LM, LL). Based upon attack rates, inoculum (10% w/v brain homogenate) from an LM132 elk was selected for transmission studies in cattle. At approximately 2 weeks of age, one wild type steer (EE211) and one steer with the E211K polymorphism (EK211) were fed 1 mL of brain homogenate in a quart of milk replacer while another 1 mL was instilled intranasally. The cattle were examined daily for clinical signs for the duration of the experiment. One steer is still under observation at 71 months post-inoculation (mpi).
Results: Inoculum derived from MM132 elk resulted in similar attack rates and incubation periods in mice expressing wild type or K211 bovine PRNP, 35% at 531 days post inoculation (dpi) and 27% at 448 dpi, respectively. Inoculum from LM132 elk had a slightly higher attack rates in mice: 45% (693 dpi) in wild type cattle PRNP and 33% (468) in K211 mice. Inoculum from LL132 elk resulted in the highest attack rate in wild type bovinized mice (53% at 625 dpi), but no K211 mice were affected at >700 days. At approximately 70 mpi, the EK211 genotype steer developed clinical signs suggestive of prion disease, depression, low head carriage, hypersalivation, and ataxia, and was necropsied. Enzyme immunoassay (IDEXX) was positive in brainstem (OD=4.00, but non-detect in retropharyngeal lymph nodes and palatine tonsil. Immunoreactivity was largely limited to the brainstem, midbrain, and cervical spinal cord with a pattern that was primarily glia-associated.
Conclusions: Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material.
Funded by: This research was funded in its entirety by congressionally appropriated funds to the United States Department of Agriculture, Agricultural Research Service. The funders of the work did not influence study design, data collection and analysis, decision to publish, or preparation of the manuscript.
*****>>> "Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material." <<<*****
=====end
Strain characterization of chronic wasting disease in bovine-PrP transgenic mice
Nuria Jerez-Garrido1, Sara Canoyra1, Natalia Fernández-Borges1, Alba Marín Moreno1, Sylvie L. Benestad2, Olivier Andreoletti3, Gordon Mitchell4, Aru Balachandran4, Juan María Torres1 and Juan Carlos Espinosa1. 1 Centro de Investigación en Sanidad Animal, CISA-INIA-CSIC, Madrid, Spain. 2 Norwegian Veterinary Institute, Ås, Norway. 3 UMR Institut National de la Recherche Agronomique (INRA)/École Nationale Vétérinaire de Toulouse (ENVT), Interactions Hôtes Agents Pathogènes, Toulouse, France. 4 Canadian Food Inspection Agency, Ottawa, Canada.
Aims: Chronic wasting disease (CWD) is an infectious prion disease that affects cervids. Various CWD prion strains have been identified in different cervid species from North America and Europe. The properties of the infectious prion strains are influenced by amino acid changes and polymorphisms in the PrP sequences of different cervid species. This study, aimed to assess the ability of a panel of CWD prion isolates from diverse cervid species from North America and Europe to infect bovine species, as well as to investigate the properties of the prion strains following the adaptation to the bovine-PrP context.
Materials and Methods: BoPrP-Tg110 mice overexpressing the bovine-PrP sequence were inoculated by intracranial route with a panel of CWD prion isolates from both North America (two white-tailed deer and two elk) and Europe (one reindeer, one moose and one red deer).
Results: Our results show distinct behaviours in the transmission of the CWD isolates to the BoPrP-Tg110 mouse model. Some of these isolates did not transmit even after the second passage. Those able to transmit displayed differences in terms of attack rate, survival times, biochemical properties of brain PrPres, and histopathology.
Conclusions: Altogether, these results exhibit the diversity of CWD strains present in the panel of CWD isolates and the ability of at least some CWD isolates to infect bovine species. Cattle being one of the most important farming species, this ability represents a potential threat to both animal and human health, and consequently deserves further study.
Funded by: MCIN/AEI /10.13039/501100011033 and by European Union NextGeneration EU/PRTR
Grant number: PCI2020-120680-2 ICRAD
"Altogether, these results exhibit the diversity of CWD strains present in the panel of CWD isolates and the ability of at least some CWD isolates to infect bovine species. Cattle being one of the most important farming species, this ability represents a potential threat to both animal and human health, and consequently deserves further study."
=====end
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
The chronic wasting disease agent from white-tailed deer is highly infectious to humanized mice after passage through raccoons
https://www.ars.usda.gov/research/publications/publication/?seqNo115=400777
so, this is what we leave our children and grandchildren?
Captive CHRONIC WASTING DISEASE CASES Update August 2025
https://www.aphis.usda.gov/sites/default/files/status-of-captive-herds.pdf
Captive CHRONIC WASTING DISEASE CASES Update August 2025, Pennsylvania, Wisconsin, Utah, and Texas
https://www.aphis.usda.gov/sites/default/files/status-of-captive-herds.pdf
https://chronic-wasting-disease.blogspot.com/2025/08/texas-game-wardens-near-conclusion-of.html
“APHIS’ voluntary national CWD Herd Certification Plan (HCP) helps States, Tribes, and the cervid industry control CWD in farmed cervids by allowing the interstate movement only from certified herds.”
Trucking CWD TSE Prion
Chronic Wasting Disease CWD TSE Prion of Cervid
“CWD spreads among wild populations at a relatively slow rate, limited by the natural home range and dispersed nature of wild animals.”
NOW HOLD YOUR HORSES, Chronic Wasting Disease CWD of Cervid can spread rather swiftly, traveling around 50 MPH, from the back of truck and trailer, and Here in Texas, we call it ‘Trucking CWD’…
Preventive Veterinary Medicine Volume 234, January 2025, 106385
Use of biosecurity practices to prevent chronic wasting disease in Minnesota cervid herds
Vehicles or trailers that entered the farm were used to transport other live cervids, cervid carcasses, or cervid body parts in past 3 years in 64.3 % (95 % CI 46.3–82.3) of larger elk/reindeer herds compared to 13.6 % (95 % CI 4.7–22.4) of smaller deer herds.
Snip…
Identifying the exact pathway of initial CWD transmission to cervid herds is often not possible, in part due to many potential pathways of transmission for the infection, including both direct and indirect contact with infected farmed or wild cervids (Kincheloe et al., 2021). That study identified that transmissions from infected farmed cervids may occur from direct contact with the movement of cervids from one herd to another and from indirect contact with the sharing of equipment, vehicles, clothing, reproductive equipment, and potentially through semen or embryos.
https://www.sciencedirect.com/science/article/abs/pii/S016758772400271X
“Chronic Wasting Disease (CWD) is a fatal neurological disease and can devastate deer populations by silently spreading through direct animal contact and contaminated environments. Without close monitoring, illegal movement of captive deer increases the risk of introducing CWD to areas it is not known to exist, potentially leading to widespread outbreaks which will impact more than just the health of Texas deer.”
https://tpwd.texas.gov/newsmedia/releases/?req=20250227b
Texas Chronic Wasting Disease CWD TSE Prion Dashboard Update August 2025
SEE NEW DASHBOARD FOR CWD POSITIVES!
https://experience.arcgis.com/experience/8f6c27330c444a19b4b57beb7ffabb8b/page/Dashboard#data_s=id%3AdataSource_3-1966d773e34-layer-10%3A29
Texas CWD total by calendar years
https://chronic-wasting-disease.blogspot.com/2024/12/texas-cwd-tse-prion-positive-samples-by.html
https://tpwd.texas.gov/huntwild/wild/diseases/cwd/positive-cases/listing-cwd-cases-texas.phtml#texasCWD
Counties where CWD Exposed Deer were Released
https://tpwd.texas.gov/documents/257/CWD-Trace-OutReleaseSites.pdf
Number of CWD Exposed Deer Released by County
https://tpwd.texas.gov/documents/258/CWD-Trace-OutReleaseSites-NbrDeer.pdf
CWD Status Captive Herds
https://www.aphis.usda.gov/sites/default/files/status-of-captive-herds.pdf
THURSDAY, OCTOBER 30, 2025
TEXAS PARKS & WILDLIFE: 50 CWD CASES AT SITE OF INITIAL POSITIVE IN WASHINGTON CO., BUT NO NEW CASES IN WILD
Eichler said the 50 positive cases represented roughly a third of the facility’s adult herd – the fawns, none older than 5 months of age, were not tested – and were spread across all age groups and both sexes. He said at the time of the depopulation, 72 deer were missing from the reported herd inventory and were presumed dead.
https://chronic-wasting-disease.blogspot.com/2025/10/texas-parks-wildlife-50-cwd-cases-at.html
https://prpsc.proboards.com/thread/182/cases-site-initial-positive-washington
“He said at the time of the depopulation, 72 deer were missing from the reported herd inventory and were presumed dead.”
In Canada, BSE days, they call that the SSS policy, shoot, shovel, and shut the hell up…terry
Texas Game Wardens Near Conclusion of ‘Ghost Deer’ Case with 24 Suspects, 1,400 Charges Filed Statewide
Aug. 14, 2025
Media Contact: TPWD News, Business Hours, 512-389-8030
AUSTIN – The Texas Game Warden investigation known as "Ghost Deer" has reached a possible conclusion after two additional suspects turned themselves in on felony charges. This brings the total number of individuals implicated in the case to 24, with approximately 1,400 charges filed across 11 Texas counties.
Ken Schlaudt, 64, of San Antonio, the owner of four deer breeding facilities and one release site, along with facility manager Bill Bowers, 55, of San Angelo, surrendered to the Travis County District Attorney’s Office on charges of felony tampering with a governmental record. Both men allegedly entered false information into the Texas Wildlife Information Management System (TWIMS) to facilitate illegal smuggling of white-tailed breeder deer. They also face more than 100 misdemeanor charges related to unlawful breeder deer activities in Tom Green County.
The "Ghost Deer" investigation has uncovered widespread, coordinated deer breeding violations including, but not limited to: smuggling captive breeder deer and free-range whitetail deer between breeder facilities and ranches, Chronic Wasting Disease (CWD) testing violations, license violations and misdemeanor and felony drug charges relating to the possession and mishandling of prescribed sedation drugs classified as controlled substances.
The suspects charged in the case include:
Evan Bircher, 59, San Antonio Vernon Carr, 55, Corpus Christi Jarrod Croaker, 47, Corpus Christi Terry Edwards, 54, Angleton Joshua Jurecek, 41, Alice Justin Leinneweber, 36, Orange Grove James Mann, 53, Odem Gage McKinzie, 28, Normanna Herbert “Tim” McKinzie, 47, Normanna Eric Olivares, 47, Corpus Christi Bruce Pipkin, 57, Beaumont Dustin Reynolds, 38, Robstown Kevin Soto, 55, Hockley Jared Utter, 52, Pipe Creek Reed Vollmering, 32, Orange Grove Clint West, 56, Beaumont James Whaley, 49, Sevierville, Tenn. Ryder Whitstine, 19, Rockport Ryker Whitstine, 21, Rockport Claude Wilhelm, 52, Orange Cases are pending adjudication in Bandera, Bee, Brazoria, Duval, Edwards, Jim Wells, Live Oak, Montgomery, Tom Green, Travis and Webb counties.
The investigation began in March 2024 when game wardens discovered the first violations during a traffic stop.
https://tpwd.texas.gov/newsmedia/releases/?req=20250206a
That incident led wardens to the much larger network of violations,
https://tpwd.texas.gov/newsmedia/releases/?req=20250227b
resulting in one of the largest deer smuggling operations in Texas history.
About Texas Game Wardens
Texas Game Wardens, within the Law Enforcement Division of Texas Parks and Wildlife Department, are responsible for enforcing laws related to the conservation and management of natural resources and public safety through community-based law enforcement. Their mission is to provide hunting, fishing and outdoor recreation opportunities for the use and enjoyment of present and future generations. Additionally, they play a crucial role in search and rescue operations during natural disasters, exemplifying their commitment to protecting both the environment and the people of Texas.
If you witness a fishing, wildlife or boating violation in progress, please call 1-800-792-GAME(4263) immediately and report it to Operation Game Thief (OGT), Texas’ Wildlife Crime-Stoppers Program. You can also text your tip by sending the keyword TXOGT plus your tip to 847411 or through the Texas OGT App, available for iOS and Android devices. Dispatchers are available 24/7.
https://tpwd.texas.gov/newsmedia/releases/?req=20250814c
THURSDAY, AUGUST 14, 2025
Texas Game Wardens Near Conclusion of ‘Ghost Deer’ Case with 24 Suspects, 1,400 Charges Filed Statewide
https://chronic-wasting-disease.blogspot.com/2025/08/texas-game-wardens-near-conclusion-of.html
https://prpsc.proboards.com/thread/178/texas-game-wardens-conclusion-ghost
WEDNESDAY, MAY 14, 2025
Texas CWD TSE Prion Cases Rises to 1099 Confirmed Cases To Date
https://chronic-wasting-disease.blogspot.com/2025/05/texas-cwd-tse-prion-cases-rises-to-1099.html
TAHC 425th Commission Meeting CWD 1:45:00
* See CWD speakers expressing their concerns with changed regulations…
2:00 hr mark
https://m.youtube.com/watch?v=bWawHpdn_7I
TEXAS ANIMAL HEALTH COMMISSION 423rd Commission Meeting CWD Update February 25, 2025
https://chronic-wasting-disease.blogspot.com/2025/02/texas-animal-health-commission-423rd.html
SATURDAY, OCTOBER 25, 2025
Texas Parks and Wildlife Commission Meeting November 5-6, 2025 Agenda CWD TSE Prion
https://tpwd.texas.gov/business/feedback/meetings/2026/1106/agenda/work_session/
https://chronic-wasting-disease.blogspot.com/2025/10/texas-parks-and-wildlife-commission.html
https://prpsc.proboards.com/thread/181/tpwc-november-2025-agenda-prion
***> Department records indicate that within the last five years (since January 1, 2020), 30 deer breeding facilities where CWD has been confirmed transferred a total of 8,799 deer to 249 additional deer breeding facilities and 487 release sites located in a total of 144 counties in Texas. <***
https://www.sos.state.tx.us/texreg/pdf/backview/0411/0411adop.pdf
Texas Kimble County Farm Chronic Wasting Disease CWD TSE Prion Approximate Herd Prevalence 12%
SUMMARY MINUTES OF THE 407th COMMISSION MEETING Texas Animal Health Commission
September 22, 2020
Chronic Wasting Disease (CWD):
A new CWD positive breeding herd was disclosed in February 2020 in Kimble County. This herd depopulation was completed in July 2020. Including the two index positive deer, an additional eight more positive deer were disclosed (approximate herd prevalence 12%). Since July 2015 and prior to this discovery, five positive captive breeder herds have been disclosed and four of those are in Medina County. One herd in Lavaca and three herds in Medina County were depopulated leaving one large herd in Medina County that is managed on a herd plan. A new zone was established in Val Verde County in December 2019 as a result of a positive free-ranging White-tailed Deer (WTD). A second positive WTD was also disclosed in February 2020 in the same area.
SUMMARY MINUTES OF THE 407th COMMISSION MEETING – 9/22/2020
Scrapie: The flock identified in April 2016 remains under quarantine in Hartley County.
https://www.tahc.texas.gov/agency/meetings/minutes/SummaryMinutes_CommMtg_2020-09-22
http://web.archive.org/web/20201017124040/https://www.tahc.texas.gov/agency/meetings/minutes/SummaryMinutes_CommMtg_2020-09-22.pdf
Chronic Wasting Disease in Texas A Real Disease with Proven Impacts
Produced by a coalition of concerned hunters, landowners, & conservationists (last update 1/2025)
https://storymaps.arcgis.com/stories/b93f528938ac48e9b56dcc79953cbec0
Aug 18, 2021
Oh, Deer
Heading Off a Wildlife Epidemic
CWD poses a significant threat to the future of hunting in Texas. Deer population declines of 45 and 50 percent have been documented in Colorado and Wyoming. A broad infection of Texas deer populations resulting in similar population impacts would inflict severe economic damage to rural communities and could negatively impact land markets. Specifically, those landowners seeking to establish a thriving herd of deer could avoid buying in areas with confirmed CWD infections. As they do with anthrax-susceptible properties, land brokers may find it advisable to inquire about the status of CWD infections on properties that they present for sale. Prospective buyers should also investigate the status of the wildlife on prospective properties. In addition, existing landowners should monitor developments as TPWD crafts management strategies to identify and contain this deadly disease.
Dr. Gilliland (c-gilliland@tamu.edu) is a research economist with the Texas Real Estate Research Center at Texas A&M University.
https://www.recenter.tamu.edu/articles/tierra-grande/oh-d
TEXAS BREEDER DEER ESCAPEE WITH CWD IN THE WILD, or so the genetics would show?
OH NO, please tell me i heard this wrong, a potential Texas captive escapee with cwd in the wild, in an area with positive captive cwd herd?
apparently, no ID though. tell me it ain't so please...
23:00 minute mark
''Free Ranging Deer, Dr. Deyoung looked at Genetics of this free ranging deer and what he found was, that the genetics on this deer were more similar to captive deer, than the free ranging population, but he did not see a significant connection to any one captive facility that he analyzed, so we believe, Ahhhhhh, this animal had some captive ahhh, whatnot.''
https://youtu.be/aoPDeGL6mpQ?t=1384
Commission Agenda Item No. 5 Exhibit B
DISEASE DETECTION AND RESPONSE RULES
PROPOSAL PREAMBLE
1. Introduction.
snip...
A third issue is the accuracy of mortality reporting. Department records indicate that for each of the last five years an average of 26 deer breeders have reported a shared total of 159 escapes. Department records for the same time period indicate an average of 31 breeding facilities reported a shared total of 825 missing deer (deer that department records indicate should be present in the facility, but cannot be located or verified).
https://tpwd.texas.gov/business/feedback/meetings/2022/1104/agenda/item.phtml?item=5
On January 21, 2017 a tornado took down thousands of feet of fence for a 420-acre illegal deer enclosure in Lamar County that had been subject to federal and state investigation for illegally importing white-tailed deer into Mississippi from Texas (a CWD positive state). Native deer were free to move on and off the property before all of the deer were able to be tested for CWD. Testing will be made available for a period of three years for CWD on the property and will be available for deer killed within a 5-mile radius of the property on a voluntary basis.
https://www.mdwfp.com/media/254796/2016-17-deer-report.pdf
“It is interesting to note that, in 2001, the State of Texas shifted its deer management strategies toward the same leanings that Kroll has suggested for Wisconsin. In Texas, the change was brought about via heavy lobbying from the high-fence deer ranching industry. This pressure helped convince the Texas Parks and Wildlife to change their regulations and allow private landowners to select the own deer biologists.”
http://www.texasmonthly.com/story/which-side-fence-are-you
Chronic Wasting Disease in Texas
A Real Disease with Proven Impacts
Produced by a coalition of concerned hunters, landowners, & conservationists (last update 08/2023)
Snip…
Since 2012, CWD has been detected in wild deer in just 7 counties in Texas and is only established in the western panhandle and far west Texas.
In that same period of time, captive deer breeders have exposed almost half of Texas counties to CWD.
Deer held in captive breeding facilities are confined to much tighter spaces, and have intimate contact with many more animals on a daily basis. By far the greatest factor in amplifying the spread of CWD is the artificial movement of these animals, shipped in livestock trailers hundreds of miles, far outside of their natural home range, and ultimately released to co-mingle with wild deer.
Each year, Texas captive deer breeders liberate 20,000-30,000 deer from their pens to the wild.
For every deer breeding facility where a CWD positive deer is discovered, an epidemiological investigation is conducted by the Texas Parks & Wildlife Department and the Texas Animal Health Commission to determine how many other deer may have been exposed to the disease and where they have been shipped. Because of the prolific artificial movement of captive deer, one deer with CWD can impact hundreds of other facilities and ranches across the state.
Unfortunately, released deer in Texas are not required to retain any kind of visible identification (an ear tag), and for this reason, the vast majority of released deer cannot be relocated for testing.
As of August 2023, 116 Texas counties have received possibly infected breeder deer that cannot be located, putting more than 140,000 landowners at risk of the disease.
Snip
The state of Texas has been testing for CWD since 2002. Since that time, more than 302,360 captive and free range deer have been tested.
From 2015-2022, more than 127,000 samples were collected from hunter-harvested and roadkill deer. This sampling rate and risk-based distribution provides scientists confidence that they would have detected the disease if it existed at a very low prevalence (<1%) in any given region at the time sampling began.
Snip…
We have learned from other states where CWD has been present the longest, that a constant increase in the prevalence of the disease may lead to a significant decline in the deer population. When disease prevalence exceeds 20%, deer populations have declined by up to 50%. In some areas of Colorado, where CWD has been present since 1985, mule deer abundance has declined by 45% since that time, despite adequate habitat and no hunting ( Miller et al. 2008 ). Similarly, the South Converse Game Unit in Wyoming has documented CWD prevalence exceeding 50% and has seen an approximate 50% decline in mule deer populations.
Snip…
Rural Economies
Deer hunting is the lifeblood of rural Texas. White-tailed deer hunting is by far the most impactful segment of the hunting economy, representing $4.3 billion, according to a recent Texas A&M Study. And while deer breeders represent a very small segment of that economy (less than 5%), they represent one of the greatest risks. ( Full Texas A&M Report )
Real Estate
Rural land prices are largely driven by recreational buyers with hunting as a top land amenity. Without deer hunting, many of these properties will be worth much less.
Conservation Funding
Deer hunters are the largest funders of wildlife conservation in Texas through excise taxes on firearms, ammunition, and gear along with active membership supporting and funding conservation organizations. If deer hunting suffers due to CWD, all wildlife in Texas lose.
Culture & Health
Texas’ native deer herd has iconic value for all Texans. Deer hunting brings families together, creates camaraderie in communities, and serves to connect Texans to nature. There is no better protein than wild, locally harvested, non-GMO and totally organic venison. A healthy deer herd leads to healthy Texans and a healthy and prosperous Texas.
Snip…
This isn't a disease for our lifetime. It's a disease for our grandchildren's lifetime.
- Dr. Bob Dittmar, Former Texas State Wildlife Veterinarian
Snip…
See the full text with maps, graphs, much more, excellent data…
https://bit.ly/3xL16Gm
Since 2012, CWD has been detected in wild deer in just 7 counties in Texas and is only established in the western panhandle and far west Texas.
In that same period of time, captive deer breeders have exposed almost half of Texas counties to CWD.
https://bit.ly/3xL16Gm
As of August 2023, 116 Texas counties have received possibly infected breeder deer that cannot be located, putting more than 140,000 landowners at risk of the disease.
https://bit.ly/3xL16Gm
ECONOMIC VALUES OF WHITE-TAILED DEER IN TEXAS
2022 SURVEY: PART I
http://web.archive.org/web/20230809171452/https://nri.tamu.edu/media/3702/economic-values-of-white-tailed-deer-in-texas-2022-survey-part-i.pdf
Don't mess Texas, or with Mother Nature in Texas, but, seems things went terribly wrong down here in Texas with CWD, be careful what you ask for;
TEXAS CWD STRAIN
“Wow,” he said. “Unlike anything we've seen before.”
The disease devastating deer herds may also threaten human health
Scientists are exploring the origins of chronic wasting disease before it becomes truly catastrophic.
Rae Ellen Bichell
Image credit: David Parsons/Istock
April 8, 2019
This story was published in collaboration with the Mountain West News Bureau, a collaboration between Wyoming Public Media, Boise State Public Radio in Idaho, KUER in Salt Lake City and KRCC and KUNC in Colorado.
SNIP...
One day in late February, in their laboratory in Fort Collins, Colorado, Wagner and Zabel compared the prions from the brains of CWD-infected deer in Texas with those of elk in Colorado. They want to know if the proteins were all mangled in the same way, or not. “If they are different, this would suggest that we have different strain properties, which is evidence as we're building our case that we might have multiple strains of CWD circulating in the U.S.,” says Wagner.
Step one is to see if they’re equally easy to destroy using a chemical called guanidine. The shape of a prion dictates everything, including the way it interacts with an animal’s cells and the ease with which chemicals can unfold it.
“Moment of truth,” said Wagner, as she and Zabel huddled around a computer, waiting for results to come through. When they did, Zabel was surprised.
“Wow,” he said. “Unlike anything we've seen before.”
The prions from the Texas deer were a lot harder to destroy than the ones from the Colorado elk. In fact, the guanidine barely damaged them at all. “We’ve never seen that before in any prion strain, which means that it has a completely different structure than we've ever seen before,” says Zabel. And that suggests that it might be a very different kind of chronic wasting disease. The researchers ran the same test on another Texas deer, with the same results.
Now, these are only the preliminary results from a few animals. Wagner and Zabel have a lot more experiments to do. But if future tests come to the same conclusion, it would support their hypothesis that there are multiple strains of chronic wasting disease out there, all with different origins. That, in turn, could mean that this disease will become even trickier to manage than it already is.
And, Zabel adds, there’s something else. “If it's still evolving, it may still evolve into a form that could potentially, eventually affect humans,” he says.
Zabel is not the only one worried about that possibility.
OSTERHOLM, THE EPIDEMIOLOGIST from Minnesota, is also concerned. He directs the Center for Infectious Disease Research and Policy at the University of Minnesota, and is serving a one-year stint as a “Science Envoy for Health Security” with the U.S. State Department. In February, he told Minnesota lawmakers that when it comes to chronic wasting disease, we are playing with fire. “You are going to hear from people that this is not going to be a problem other than a game farm issue. You're going to hear from people that it's not going to transmit to people, and I hope they're right, but I wouldn't bet on it,” he said. “And if we lose this one and haven’t done all we can do, we will pay a price.”
If that wasn’t warning enough, he added: “Just remember what happened in England.”
He was talking about mad cow disease. Decades ago, Osterholm got involved in studying the potential for the newly emerging condition — bovine spongiform encephalopathy, or BSE for short — to be transmitted to humans.
At that point, researchers had yet to document a prion disease in animals that could infect people. They did, however, have a few pieces of the puzzle. For one, work in Papua New Guinea had shown that people could transmit prion diseases to each other if they practiced cannibalism, especially of the brain-eating variety. They also knew that BSE was spreading quickly between cattle. Osterholm says he and others worried that the more widespread it became, the more chances it might have to change into something that could sicken people.
“A lot of people thought that it was an overreaction,” says Osterholm. “Then, of course, in 1996, 10 years later, we recognized that in fact transmission had occurred.” Variant Creutzfeldt-Jakob disease, as the illness is called when it appears in human beings, has infected about 230 people worldwide. Osterholm says he feels like he’s having déjà vu, except that instead of mad cow, now it’s chronic wasting disease that’s spreading in animals, with the potential to cross the species barrier to infect humans.
SNIP...SEE FULL TEXT;
https://www.hcn.org/articles/wildlife-the-disease-devastating-deer-herds-may-also-threaten-human-health-science
TEXAS CWD STRAIN
77. Assessing chronic wasting disease strain differences in free-ranging cervids across the United States
Kaitlyn M. Wagnera, Caitlin Ott-Connb, Kelly Strakab, Bob Dittmarc, Jasmine Battend, Robyn Piercea, Mercedes Hennessya, Elizabeth Gordona, Brett Israela, Jenn Ballarde and Mark D Zabela
aPrion Research Center at Colorado State University; bMichigan Department of Natural Resources; cTexas Parks and Wildlife Department; dMissouri Department of Conservation, 5. Arkansas Game and Fish Commission CONTACT Kaitlyn M. Wagner miedkait@rams.colostate.edu
ABSTRACT
Background/Introduction: Chronic wasting disease (CWD) is an invariably fatal prion disease affecting captive and free-ranging cervids, including white-tailed deer, mule deer, moose, elk, and reindeer. Since the initial description of the disease in the 1960’s, CWD has spread to 23 states, 3 Canadian Provinces, South Korea, Norway and, most recently, Finland. While some outbreaks of CWD were caused by transport of infected animals from endemic regions, the origin of CWD in other epizootics is unclear and has not been characterized. Previous studies have shown that there are two distinct strains of CWD. However, the continuous spread and the unclear origin of several outbreaks warrant continued surveillance and further characterization of strain diversity.
Materials and Methods: To address these knowledge gaps, we used biochemical tests to assess strain differences between CWD outbreaks in Michigan, Texas, Missouri, and Colorado, USA. Brain or lymph node samples were homogenized and digested in 50 µg/mL proteinase K (PK). These samples were then run on a Western blot to assess glycoform ratio and electrophoretic mobility. Texas samples were digested in 100 µg/mL PK. To assess conformational stability, brain or lymph node homogenates were incubated in increasing concentrations of guanidine hydrochloride from 0 M to 4 M in 0.5 M increments. Samples were then precipitated in methanol overnight, washed and PK digested in 50 µg/mL PK before slot blotting.
Results: Our results have found significant differences in glycoform ratio between CWD from Michigan and Colorado, but no differences were observed in conformational stability assays. Interestingly, when testing our CWD isolates from Texas to analyse electrophoretic mobility and glycoform ratio, we found that these samples did not exhibit the characteristic band shift when treated with PK, but PK resistant material remained. Additionally, results from our conformational stability assay demonstrate a unique profile of these Texas isolates. Testing of samples from Missouri is currently underway.
Conclusions: Thus far, our data indicate that there are strain differences between CWD circulating in Michigan and CWD in Colorado and provide important insight into CWD strain differences between two non-contiguous outbreaks. We have also identified a unique strain of CWD in Texas with biochemical strain properties not seen in any of our other CWD isolates. These results highlight the importance of continued surveillance to better understand this devastating disease. These results have important implications for CWD emergence, evolution and our understanding of prion strain heterogeneity on the landscape.
http://www.tandfonline.com/doi/full/10.1080/19336896.2019.1615197
Texas Game Wardens Bust Illegal Deer Operations Across the State Feb. 27, 2025
Media Contact: TPWD News, Business Hours, 512-389-8030
AUSTIN – A recent investigation by Texas Game Wardens resulted in approximately 1,200 pending charges and 22 suspects from across the state involved in the deer breeding industry and black-market wildlife trade.
The suspects and charges are associated with three deer breeding facilities, ten release sites, one deer management pen and three illegal facilities not registered in the Texas Wildlife Information Management Services (TWIMS) database, meaning they were operating or receiving deer in violation of registration requirements and disease monitoring protocols.
https://tpwd.texas.gov/newsmedia/releases/?req=20250227b
Texas Game Wardens Bust Illegal Deer Operations Across the State Feb. 27, 2025
https://chronic-wasting-disease.blogspot.com/2025/02/texas-game-wardens-bust-illegal-deer.html
TUESDAY, FEBRUARY 25, 2025
TEXAS ANIMAL HEALTH COMMISSION 423rd Commission Meeting CWD Update February 25, 2025
https://chronic-wasting-disease.blogspot.com/2025/02/texas-animal-health-commission-423rd.html
SUNDAY, MAY 04, 2025
Texas Senate Bill 2649 creation of a statewide Chronic Wasting Disease plan
https://chronic-wasting-disease.blogspot.com/2025/05/texas-senate-bill-2649-creation-of.html
SUNDAY, MAY 04, 2025
Texas Senate Bill 2651 establishment of a pilot program to breed deer resistant to CWD TSE Prion, what could go wrong?
https://chronic-wasting-disease.blogspot.com/2025/05/texas-senate-bill-2651-establishment-of_4.html
Texas S.B. 2843 Directs TPWD to conduct a comprehensive study of current measures to control chronic wasting disease (CWD) in deer
Trying to legislate CWD is what got Texas in this CWD mess to begin with, how did that work out$$$ Legislators and Politicians need to stay away and let TPWD and TAHC et try and contain this mess that Legislators and Politicians got us in, called CWD TSE Prion…terry
https://chronic-wasting-disease.blogspot.com/2025/04/texas-sb-2843-directs-tpwd-to-conduct.html
THURSDAY, APRIL 10, 2025
CWD TSE Prion, Politics, Friendly Fire, Unforeseen Consequences, What If?
https://chronic-wasting-disease.blogspot.com/2025/04/cwd-tse-prion-politics-friendly-fire.html
Friday, February 21, 2025
Deer don’t die from CWD, it’s the insurance companies, or it's a Government conspiracy?
https://chronic-wasting-disease.blogspot.com/2025/02/deer-dont-die-from-cwd-its-insurance.html
THURSDAY, APRIL 24, 2025
***> US Captive CWD Positive Herds Update April 2025
https://chronic-wasting-disease.blogspot.com/2025/04/us-captive-cwd-positive-herds-update.html
Captive CHRONIC WASTING DISEASE CASES Update August 2025
https://www.aphis.usda.gov/sites/default/files/status-of-captive-herds.pdf
I can’t imagine trying to regulate CWD, and any human zoonosis there from, as they tried to do with BSE TSE Prion aka mad cow disease, especially with CWD TSE being more virulent and more infectious…a terrible worst case scenario, are we there yet?
SUNDAY, MARCH 19, 2023
Abandoned factory ‘undoubtedly’ contains dormant Mad Cow Disease that could threaten humans, Thruxted Mill, Queniborough CJD
https://bseinquiry.blogspot.com/2023/03/abandoned-factory-undoubtedly-contains.html
DFA Draft Factual Accounts
DFA 11 "The Touch Test"
DFA 14
Consideration of the Risk from Mechanically Recovered Meat (MRM) in 1989-1990 Draft Factual Accounts 9 July 1999
http://web.archive.org/web/20001219041200/http://www.bse.org.uk/dfa/dfa14.htm
DFA 15
Monitoring and Enforcement of the SBO Regulations Draft Factual Accounts 9 July 1999
http://web.archive.org/web/20001219080500/http://www.bse.org.uk/dfa/dfa15.htm
DFA 16: MID 1995 TO THE FINAL DAYS
http://web.archive.org/web/20001121091600/http://www.bse.org.uk/dfa/dfa16.htm
DFA 17
http://web.archive.org/web/20001219215500/http://www.bse.org.uk/dfa/dfa17.htm
DFA 26 Public Pronouncements by the CMO, May 1990 29 November 1999
https://web.archive.org/web/20001209084800/http://www.bse.org.uk/dfa/dfa26.pdf
DFA 25 Notification of the Ruminant Feed Ban to non-EC countries 4 November 1999
https://web.archive.org/web/20001209084800/http://www.bse.org.uk/dfa/dfa25.pdf
DFA 24 Public Pronouncements by the CMO on the human heath implications of BSE, March 1993 and June 1993. 6 December 1999
https://web.archive.org/web/20001209084800/http://www.bse.org.uk/dfa/dfa24.pdf
DFA 23 Maff statements in 1990 about a cat with a spongiform encephalopathy16 November 1999
https://web.archive.org/web/20001209084800/http://www.bse.org.uk/dfa/dfa23.pdf
DFA 22 MIADFA 21 Cattle Tracking 23 November 1999
https://web.archive.org/web/20001209084800/http://www.bse.org.uk/dfa/dfa21.pdf
DFA 20 Introduction of the ruminant feed ban and compulsory notification of BSE in Northern Ireland3 December 1999
https://web.archive.org/web/20001209084800/http://www.bse.org.uk/dfa/dfa20.pdf
DFA 19 Dissection of Bovine Eye balls 8 November 1999
https://web.archive.org/web/20001209084800/http://www.bse.org.uk/dfa/dfa19.pdf
DFA 18 Cosmetics 29 October 1999
https://web.archive.org/web/20001209084800/http://www.bse.org.uk/dfa/dfa18.pdf
DFA 17 Medicines and medical devices 7 October 1999
https://web.archive.org/web/20001209084800/http://www.bse.org.uk/dfa/dfa17.pdf
DFA 17
http://web.archive.org/web/20001219215500/http://www.bse.org.uk/dfa/dfa17.htm
DFA 16 Mid 1995 to the final days 7 July 1999
https://web.archive.org/web/20001209084800/http://www.bse.org.uk/dfa/dfa16.pdf
DFA 16: MID 1995 TO THE FINAL DAYS
http://web.archive.org/web/20001121091600/http://www.bse.org.uk/dfa/dfa16.htm
DFA 15 Monitoring and Enforcements of the SBO Regulations 9 July 1999
https://web.archive.org/web/20001209084800/http://www.bse.org.uk/dfa/dfa15.pdf
DFA 15
Monitoring and Enforcement of the SBO Regulations Draft Factual Accounts 9 July 1999
http://web.archive.org/web/20001219080500/http://www.bse.org.uk/dfa/dfa15.htm
DFA 14 Consideration of the Risk from Mechanically Recovered Meat (MRM) in 1989 9 July 1999
https://web.archive.org/web/20001209084800/http://www.bse.org.uk/dfa/dfa14.pdf
DFA 14
Consideration of the Risk from Mechanically Recovered Meat (MRM) in 1989-1990 Draft Factual Accounts 9 July 1999
http://web.archive.org/web/20001219041200/http://www.bse.org.uk/dfa/dfa14.htm
BSE Inquiry Issues Factual Accounts.
https://webarchive.nationalarchives.gov.uk/ukgwa/20090505205439mp_/http://www.bseinquiry.gov.uk/files/ia/ia2/tab11.pdf
BSE Inquiry Issues more Factual Accounts, 22nd January 1999.
https://webarchive.nationalarchives.gov.uk/ukgwa/20090505205439mp_/http://www.bseinquiry.gov.uk/files/ia/ia2/tab12.pdf
BSE Inquiry Issues more Factual Accounts, 26th January 1999.
https://webarchive.nationalarchives.gov.uk/ukgwa/20090505205439mp_/http://www.bseinquiry.gov.uk/files/ia/ia2/tab13.pdf
07 February 1997 A4-0020/97
(To obtain the full text of this report in DA, EL, ES, IT, NL, PT, FI or SV , please consult " Plenary sessions" in the language of your choice, select option "Reports - by A4 number" and search for "A4-0020/97")
REPORT
on alleged contraventions or maladministration in the implementation of Community law in relation to BSE, without prejudice to the jurisdiction of the Community and national courts
https://www.europarl.europa.eu/conferences/19981130/bse/a4002097_en.htm#:~:text=At%20its%20meetings%20of%2013,submitted%20on%207%20February%201997.
BSE Inquiry Draft Factual Accounts DFAs
https://bseinquiry.blogspot.com/2022/08/bse-inquiry-draft-factual-accounts-dfas.html
Terry S. Singeltary Sr.
snip... full text ;
http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html
However, to date, no CWD infections have been reported in people.
sporadic, spontaneous CJD, 85%+ of all human TSE, did not just happen. never in scientific literature has this been proven. if one looks up the word sporadic or spontaneous at pubmed, you will get a laundry list of disease that are classified in such a way;
sporadic = 54,983 hits
https://www.ncbi.nlm.nih.gov/pubmed/?term=sporadic
spontaneous = 325,650 hits
https://www.ncbi.nlm.nih.gov/pubmed/?term=spontaneous
key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD.
SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
However, to date, no CWD infections have been reported in people. key word here is ‘reported’. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can’t, and it’s as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it’s being misdiagnosed as sporadic CJD. …terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys
http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true
https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article
So, this is what we leave our children and grandchildren?
Human iatrogenic TSE Prion Disease
France issues moratorium on prion research after fatal brain disease strikes two lab workers
By Barbara CasassusJul. 28, 2021 , 4:35 AM
PARIS—Five public research institutions in France have imposed a 3-month moratorium on the study of prions—a class of misfolding, infectious proteins that cause fatal brain diseases—after a retired lab worker who handled prions in the past was diagnosed with Creutzfeldt-Jakob disease (CJD), the most common prion disease in humans. An investigation is underway to find out whether the patient, who worked at a lab run by the National Research Institute for Agriculture, Food and Environment (INRAE), contracted the disease on the job.
If so, it would be the second such case in France in the past few years. In June 2019, an INRAE lab worker named Émilie Jaumain died at age 33, 10 years after pricking her thumb during an experiment with prion-infected mice. Her family is now suing INRAE for manslaughter and endangering life; her illness had already led to tightened safety measures at French prion labs.
Posted in: EuropeHealthScientific Community
doi:10.1126/science.abl6587
https://www.sciencemag.org/news/2021/07/france-issues-moratorium-prion-research-after-fatal-brain-disease-strikes-two-lab
Variant Creutzfeldt–Jakob Disease Diagnosed 7.5 Years after Occupational Exposure
Variant Creutzfeldt–Jakob disease was identified in a technician who had cut her thumb while handling brain sections of mice infected with adapted BSE 7.5 years earlier. The long incubation period was similar to that of the transfusion-transmitted form of the disease.
Variant Creutzfeldt–Jakob Disease Diagnosed 7.5 Years after Occupational Exposure
TO THE EDITOR:
We report a case of variant Creutzfeldt–Jakob disease (CJD) that was plausibly related to accidental occupational exposure in a technician who had handled murine samples contaminated with the agent that causes bovine spongiform encephalopathy (BSE) 7.5 years earlier.
In May 2010, when the patient was 24 years of age, she worked in a prion research laboratory, where she handled frozen sections of brain of transgenic mice that overexpressed the human prion protein with methionine at codon 129. The mice had been infected with a sheep-adapted form of BSE. During this process, she stabbed her thumb through a double pair of latex gloves with the sharp ends of a curved forceps used to handle the samples. Bleeding was noted at the puncture site.
Metrics
https://www.nejm.org/doi/full/10.1056/NEJMc2000687
WEDNESDAY, OCTOBER 15, 2025
US NATIONAL PRION DISEASE PATHOLOGY SURVEILLANCE CENTER CJD TSE REPORT 2025
https://prionunitusaupdate.blogspot.com/2025/10/us-national-prion-disease-pathology.html
Cattle, sheep, pigs, raccoons, CWD, Oh, My!
Volume 31, Number 1—January 2025
Dispatch
Detection of Prions in Wild Pigs (Sus scrofa) from Areas with Reported Chronic Wasting Disease Cases, United States
Abstract
Using a prion amplification assay, we identified prions in tissues from wild pigs (Sus scrofa) living in areas of the United States with variable chronic wasting disease (CWD) epidemiology. Our findings indicate that scavenging swine could play a role in disseminating CWD and could therefore influence its epidemiology, geographic distribution, and interspecies spread.
Snip…
Conclusions In summary, results from this study showed that wild pigs are exposed to cervid prions, although the pigs seem to display some resistance to infection via natural exposure. Future studies should address the susceptibility of this invasive animal species to the multiple prion strains circulating in the environment. Nonetheless, identification of CWD prions in wild pig tissues indicated the potential for pigs to move prions across the landscape, which may, in turn, influence the epidemiology and geographic spread of CWD.
https://wwwnc.cdc.gov/eid/article/%2031/1/24-0401_article
Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
2. Determined that pigs naturally exposed to chronic wasting disease (CWD) may act as a reservoir of CWD infectivity. Chronic wasting disease is a naturally occurring, fatal, neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of CWD disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Pigs were assigned to 1 of 3 groups: intracranially inoculated; orally inoculated; or non-inoculated. At market weight age, half of the pigs in each group were tested ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by multiple diagnostic methods. Brain samples from selected pigs were bioassayed in mice expressing porcine prion protein. Some pigs from each inoculated group were positive by one or more tests. Bioassay was positive in 4 out of 5 pigs assayed. Although only small amounts of PrPSc were detected using sensitive methods, this study demonstrates that pigs can serve as hosts for CWD. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
The agent of chronic wasting disease from pigs is infectious in transgenic mice expressing human PRNP
https://www.ars.usda.gov/research/publications/publication/?seqNo115=353091
Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
https://www.ars.usda.gov/research/project/?accnNo=432011&fy=2017
Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=337105
This study demonstrates that pigs can serve as potential hosts for CWD, although with low attack rates and scant PrPcwd accumulation. Detection of infectivity in orally challenged pigs using mouse bioassay raises the possibility that naturally exposed pigs act as a reservoir of CWD infectivity, even though affected pigs do not develop overt clinical signs or readily detectable PrPcwd.
https://www.ars.usda.gov/research/publications/publication/?seqNo115=326166
CONFIDENTIAL
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
LINE TO TAKE
3. If questions on pharmaceuticals are raised at the Press conference, the suggested line to take is as follows:-
"There are no medicinal products licensed for use on the market which make use of UK-derived porcine tissues with which any hypothetical “high risk" ‘might be associated. The results of the recent experimental work at the CSM will be carefully examined by the CSM‘s Working Group on spongiform encephalopathy at its next meeting.
DO Hagger RM 1533 MT Ext 3201
http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf
While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...
http://web.archive.org/web/20031026000118/www.bseinquiry.gov.uk/files/yb/1990/08/23004001.pdf
we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.
http://web.archive.org/web/20030822031154/www.bseinquiry.gov.uk/files/yb/1990/09/10007001.pdf
May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...
http://web.archive.org/web/20030822052332/www.bseinquiry.gov.uk/files/yb/1990/09/11005001.pdf
3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...
http://web.archive.org/web/20030822052438/www.bseinquiry.gov.uk/files/yb/1990/09/12002001.pdf
But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...
http://web.archive.org/web/20030518170213/www.bseinquiry.gov.uk/files/yb/1990/09/13004001.pdf
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....
http://web.archive.org/web/20030822054419/www.bseinquiry.gov.uk/files/yb/1990/09/21009001.pdf
Monday, November 13, 2023
Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) Singeltary Another Request for Update 2023 Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) Singeltary Another Request for Update 2023
The infamous 1997 mad cow feed ban i.e. Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.
***>However, this recommendation is guidance and not a requirement by law.
WITH GREAT URGENCY, THE Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) MUST BE ENHANCED AND UPDATED TO INCLUDE CERVID, PIGS, AND SHEEP, SINCE RECENT SCIENCE AND TRANSMISSION STUDIES ALL, INCLUDING CATTLE, HAVE SHOWN ORAL TSE PrP TRANSMISSIONS BETWEEN THE SPECIES, AND THIS SHOULD BE DONE WITH THE UTMOST URGENCY, REASONS AS FOLLOW.
First off I will start with a single BSE feed breach 10 years after 1997 partial ban. If you got to the archived link, all the way down to bottom…THE NEXT YEAR I RECALL ONE WITH 10,000,000+ banned products recall…see this records at the bottom…terry
2016
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed
PUBLIC SUBMISSION
Comment from Terry Singeltary Sr.
Posted by the Food and Drug Administration on May 17, 2016 Comment
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed Singeltary Submission
https://www.regulations.gov/comment/FDA-2003-D-0432-0011
https://www.regulations.gov/docket/FDA-2003-D-0432
How in the hell do you make a complete recall of 27,694,240 lbs of feed that was manufactured from materials that may have been contaminated with mammalian protein, in one state, 2006? Wonder how much was fed out?
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated,
net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated,
Recall # V-103-6;
e) "Big Jim’s" BBB Deer Ration, Big Buck Blend,
Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted,
Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020,
Carbadox -- 0.0055%, Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete
Feed for Chickens from Hatch to 20 Weeks, Medicated,
Bacitracin Methylene Disalicylate, 25 and 50 Lbs,
Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying
Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED,
net wt 50 Lbs, Recall # V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs,
Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs,
Recall # V-112-6
CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER
Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006.
FDA initiated recall is complete.
REASON
Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE
125 tons
DISTRIBUTION
AL and FL
______________________________
PRODUCT
Bulk custom dairy feds manufactured from concentrates, Recall # V-113-6
CODE
All dairy feeds produced between 2/1/05 and 6/16/06 and containing H. J. Baker recalled feed products.
RECALLING FIRM/MANUFACTURER
Vita Plus Corp., Gagetown, MI, by visit beginning on June 21, 2006.
Firm initiated recall is complete.
REASON
The feed was manufactured from materials that may have been contaminated with mammalian protein.
VOLUME OF PRODUCT IN COMMERCE
27,694,240 lbs
DISTRIBUTION
MI
______________________________
PRODUCT
Bulk custom made dairy feed, Recall # V-114-6
CODE
None
RECALLING FIRM/MANUFACTURER
Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006. Firm initiated recall is ongoing.
REASON
Custom made feeds contain ingredient called Pro-Lak, which may contain ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE
???
DISTRIBUTION
KY
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
https://web.archive.org/web/20100120023832/http://www.fda.gov/Safety/Recalls/EnforcementReports/2006/ucm120413.htm
***>However, this recommendation is guidance and not a requirement by law.
THIS MUST CHANGE ASAP!
“For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.”
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012
snip.....
In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law. Animals considered at high risk for CWD include:
1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and
2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.
Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.
The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES.
It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.
Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.
There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.
snip.....
https://web.archive.org/web/20170404125557/http://webarchive.nationalarchives.gov.uk/20130822084033/http://www.defra.gov.uk/animal-diseases/files/qra_chronic-wasting-disease-121029.pdf
PLoS One. 2020 Aug 20;15(8):e0237410. doi: 10.1371/journal.pone.0237410. eCollection 2020.
Very low oral exposure to prions of brain or saliva origin can transmit chronic wasting disease
Nathaniel D Denkers 1 , Clare E Hoover 2 , Kristen A Davenport 3 , Davin M Henderson 1 , Erin E McNulty 1 , Amy V Nalls 1 , Candace K Mathiason 1 , Edward A Hoover 1
PMID: 32817706 PMCID: PMC7446902 DOI: 10.1371/journal.pone.0237410
Abstract
The minimum infectious dose required to induce CWD infection in cervids remains unknown, as does whether peripherally shed prions and/or multiple low dose exposures are important factors in CWD transmission. With the goal of better understand CWD infection in nature, we studied oral exposures of deer to very low doses of CWD prions and also examined whether the frequency of exposure or prion source may influence infection and pathogenesis. We orally inoculated white-tailed deer with either single or multiple divided doses of prions of brain or saliva origin and monitored infection by serial longitudinal tissue biopsies spanning over two years. We report that oral exposure to as little as 300 nanograms (ng) of CWD-positive brain or to saliva containing seeding activity equivalent to 300 ng of CWD-positive brain, were sufficient to transmit CWD disease. This was true whether the inoculum was administered as a single bolus or divided as three weekly 100 ng exposures. However, when the 300 ng total dose was apportioned as 10, 30 ng doses delivered over 12 weeks, no infection occurred. While low-dose exposures to prions of brain or saliva origin prolonged the time from inoculation to first detection of infection, once infection was established, we observed no differences in disease pathogenesis. These studies suggest that the CWD minimum infectious dose approximates 100 to 300 ng CWD-positive brain (or saliva equivalent), and that CWD infection appears to conform more with a threshold than a cumulative dose dynamic.
Snip…
Discussion
As CWD expands across North America and Scandinavia, how this disease is transmitted so efficiently remains unclear, given the low concentrations of prions shed in secretions and excretions [13, 14]. The present studies demonstrated that a single oral exposure to as little as 300nmg of CWD-positive brain or equivalent saliva can initiate infection in 100% of exposed white-tailed deer. However, distributing this dose as 10, 30 ng exposures failed to induce infection. Overall, these results suggest that the minimum oral infectious exposure approaches 100 to 300 ng of CWD-positive brain equivalent. These dynamics also invite speculation as to whether potential infection co-factors, such as particle binding [46, 47] or compromises in mucosal integrity may influence infection susceptibility, as suggested from two studies in rodent models [48, 49].
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0237410
PRION 2023 CONTINUED;
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
Prion 2023 Experimental Oronasal Inoculation of the Chronic Wasting Disease Agent into White Tailed Deer
Author list: Sarah Zurbuchena,b , S. Jo Moorea,b , Jifeng Biana , Eric D. Cassmanna , and Justin J. Greenleea . a. Virus and Prion Research Unit, National Animal Disease Center, ARS, United States Department of Agriculture, Ames, IA, US b. Oak Ridge Institute for Science and Education (ORISE), U.S. Department of Energy, Oak Ridge, TN, United States
Aims: The purpose of this experiment was to determine whether white-tailed deer (WTD) are susceptible to inoculation of chronic wasting disease (CWD) via oronasal exposure.
Materials and methods: Six male, neutered WTD were oronasally inoculated with brainstem material (10% w/v) from a CWD-positive wild-type WTD. The genotypes of five inoculated deer were Q95/G96 (wild-type). One inoculated deer was homozygous S at codon 96 (96SS). Cervidized (Tg12; M132 elk PrP) mice were inoculated with 1% w/v brainstem homogenate from either a 96GG WTD (n=10) or the 96SS WTD (n=10).
Results: All deer developed characteristic clinical signs of CWD including weight loss, regurgitation, and ataxia. The 96SS individual had a prolonged disease course and incubation period compared to the other deer. Western blots of the brainstem on all deer yielded similar molecular profiles. All deer had widespread lymphoid distribution of PrPCWD and neuropathologic lesions associated with transmissible spongiform encephalopathies. Both groups of mice had a 100% attack rate and developed clinical signs, including loss of body condition, ataxia, and loss of righting reflex. Mice inoculated with material from the 96SS deer had a significantly shorter incubation period than mice inoculated with material from 96GG deer (Welch two sample T-test, P<0.05). Serial dilutions of each inocula suggests that differences in incubation period were not due to a greater concentration of PrPCWD in the 96SS inoculum. Molecular profiles from western blot of brain homogenates from mice appeared similar regardless of inoculum and appear similar to those of deer used for inoculum.
Conclusions: This study characterizes the lesions and clinical course of CWD in WTD inoculated in a similar manner to natural conditions. It supports previous findings that 96SS deer have a prolonged disease course. Further, it describes a first pass of inoculum from a 96SS deer in cervidized mice which shortened the incubation period.
Funded by: This research was funded in its entirety by congressionally appropriated funds to the United States Department of Agriculture, Agricultural Research Service. The funders of the work did not influence study design, data collection, analysis, decision to publish, or preparation of the manuscript.
Acknowledgement: We thank Ami Frank and Kevin Hassall for their technical contributions to this project.
=====end
PRION 2023 CONTINUED;
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
***> Price of TSE Prion Poker goes up substantially, all you cattle ranchers and such, better pay close attention here...terry <***
Transmission of the chronic wasting disease agent from elk to cattle after oronasal exposure
Justin Greenlee, Jifeng Bian, Zoe Lambert, Alexis Frese, and Eric Cassmann Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS, Ames, IA, USA
Aims: The purpose of this study was to determine the susceptibility of cattle to chronic wasting disease agent from elk.
Materials and Methods: Initial studies were conducted in bovinized mice using inoculum derived from elk with various genotypes at codon 132 (MM, LM, LL). Based upon attack rates, inoculum (10% w/v brain homogenate) from an LM132 elk was selected for transmission studies in cattle. At approximately 2 weeks of age, one wild type steer (EE211) and one steer with the E211K polymorphism (EK211) were fed 1 mL of brain homogenate in a quart of milk replacer while another 1 mL was instilled intranasally. The cattle were examined daily for clinical signs for the duration of the experiment. One steer is still under observation at 71 months post-inoculation (mpi).
Results: Inoculum derived from MM132 elk resulted in similar attack rates and incubation periods in mice expressing wild type or K211 bovine PRNP, 35% at 531 days post inoculation (dpi) and 27% at 448 dpi, respectively. Inoculum from LM132 elk had a slightly higher attack rates in mice: 45% (693 dpi) in wild type cattle PRNP and 33% (468) in K211 mice. Inoculum from LL132 elk resulted in the highest attack rate in wild type bovinized mice (53% at 625 dpi), but no K211 mice were affected at >700 days. At approximately 70 mpi, the EK211 genotype steer developed clinical signs suggestive of prion disease, depression, low head carriage, hypersalivation, and ataxia, and was necropsied. Enzyme immunoassay (IDEXX) was positive in brainstem (OD=4.00, but non-detect in retropharyngeal lymph nodes and palatine tonsil. Immunoreactivity was largely limited to the brainstem, midbrain, and cervical spinal cord with a pattern that was primarily glia-associated.
Conclusions: Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material.
Funded by: This research was funded in its entirety by congressionally appropriated funds to the United States Department of Agriculture, Agricultural Research Service. The funders of the work did not influence study design, data collection and analysis, decision to publish, or preparation of the manuscript.
*****>>> "Cattle with the E211K polymorphism are susceptible to the CWD agent after oronasal exposure of 0.2 g of infectious material." <<<*****
=====end
Strain characterization of chronic wasting disease in bovine-PrP transgenic mice
Nuria Jerez-Garrido1, Sara Canoyra1, Natalia Fernández-Borges1, Alba Marín Moreno1, Sylvie L. Benestad2, Olivier Andreoletti3, Gordon Mitchell4, Aru Balachandran4, Juan María Torres1 and Juan Carlos Espinosa1. 1 Centro de Investigación en Sanidad Animal, CISA-INIA-CSIC, Madrid, Spain. 2 Norwegian Veterinary Institute, Ås, Norway. 3 UMR Institut National de la Recherche Agronomique (INRA)/École Nationale Vétérinaire de Toulouse (ENVT), Interactions Hôtes Agents Pathogènes, Toulouse, France. 4 Canadian Food Inspection Agency, Ottawa, Canada.
Aims: Chronic wasting disease (CWD) is an infectious prion disease that affects cervids. Various CWD prion strains have been identified in different cervid species from North America and Europe. The properties of the infectious prion strains are influenced by amino acid changes and polymorphisms in the PrP sequences of different cervid species. This study, aimed to assess the ability of a panel of CWD prion isolates from diverse cervid species from North America and Europe to infect bovine species, as well as to investigate the properties of the prion strains following the adaptation to the bovine-PrP context.
Materials and Methods: BoPrP-Tg110 mice overexpressing the bovine-PrP sequence were inoculated by intracranial route with a panel of CWD prion isolates from both North America (two white-tailed deer and two elk) and Europe (one reindeer, one moose and one red deer).
Results: Our results show distinct behaviours in the transmission of the CWD isolates to the BoPrP-Tg110 mouse model. Some of these isolates did not transmit even after the second passage. Those able to transmit displayed differences in terms of attack rate, survival times, biochemical properties of brain PrPres, and histopathology.
Conclusions: Altogether, these results exhibit the diversity of CWD strains present in the panel of CWD isolates and the ability of at least some CWD isolates to infect bovine species. Cattle being one of the most important farming species, this ability represents a potential threat to both animal and human health, and consequently deserves further study.
Funded by: MCIN/AEI /10.13039/501100011033 and by European Union NextGeneration EU/PRTR
Grant number: PCI2020-120680-2 ICRAD
"Altogether, these results exhibit the diversity of CWD strains present in the panel of CWD isolates and the ability of at least some CWD isolates to infect bovine species. Cattle being one of the most important farming species, this ability represents a potential threat to both animal and human health, and consequently deserves further study."
=====end
https://prion2023.org/wp-content/uploads/2023/10/Meeting-book-final-version2.pdf
The chronic wasting disease agent from white-tailed deer is highly infectious to humanized mice after passage through raccoons
https://www.ars.usda.gov/research/publications/publication/?seqNo115=400777
so, this is what we leave our children and grandchildren?
Captive CHRONIC WASTING DISEASE CASES Update August 2025
https://www.aphis.usda.gov/sites/default/files/status-of-captive-herds.pdf
Captive CHRONIC WASTING DISEASE CASES Update August 2025, Pennsylvania, Wisconsin, Utah, and Texas
https://www.aphis.usda.gov/sites/default/files/status-of-captive-herds.pdf
https://chronic-wasting-disease.blogspot.com/2025/08/texas-game-wardens-near-conclusion-of.html
“APHIS’ voluntary national CWD Herd Certification Plan (HCP) helps States, Tribes, and the cervid industry control CWD in farmed cervids by allowing the interstate movement only from certified herds.”
Trucking CWD TSE Prion
Chronic Wasting Disease CWD TSE Prion of Cervid
“CWD spreads among wild populations at a relatively slow rate, limited by the natural home range and dispersed nature of wild animals.”
NOW HOLD YOUR HORSES, Chronic Wasting Disease CWD of Cervid can spread rather swiftly, traveling around 50 MPH, from the back of truck and trailer, and Here in Texas, we call it ‘Trucking CWD’…
Preventive Veterinary Medicine Volume 234, January 2025, 106385
Use of biosecurity practices to prevent chronic wasting disease in Minnesota cervid herds
Vehicles or trailers that entered the farm were used to transport other live cervids, cervid carcasses, or cervid body parts in past 3 years in 64.3 % (95 % CI 46.3–82.3) of larger elk/reindeer herds compared to 13.6 % (95 % CI 4.7–22.4) of smaller deer herds.
Snip…
Identifying the exact pathway of initial CWD transmission to cervid herds is often not possible, in part due to many potential pathways of transmission for the infection, including both direct and indirect contact with infected farmed or wild cervids (Kincheloe et al., 2021). That study identified that transmissions from infected farmed cervids may occur from direct contact with the movement of cervids from one herd to another and from indirect contact with the sharing of equipment, vehicles, clothing, reproductive equipment, and potentially through semen or embryos.
https://www.sciencedirect.com/science/article/abs/pii/S016758772400271X
“Chronic Wasting Disease (CWD) is a fatal neurological disease and can devastate deer populations by silently spreading through direct animal contact and contaminated environments. Without close monitoring, illegal movement of captive deer increases the risk of introducing CWD to areas it is not known to exist, potentially leading to widespread outbreaks which will impact more than just the health of Texas deer.”
https://tpwd.texas.gov/newsmedia/releases/?req=20250227b
Texas Chronic Wasting Disease CWD TSE Prion Dashboard Update August 2025
SEE NEW DASHBOARD FOR CWD POSITIVES!
https://experience.arcgis.com/experience/8f6c27330c444a19b4b57beb7ffabb8b/page/Dashboard#data_s=id%3AdataSource_3-1966d773e34-layer-10%3A29
Texas CWD total by calendar years
https://chronic-wasting-disease.blogspot.com/2024/12/texas-cwd-tse-prion-positive-samples-by.html
https://tpwd.texas.gov/huntwild/wild/diseases/cwd/positive-cases/listing-cwd-cases-texas.phtml#texasCWD
Counties where CWD Exposed Deer were Released
https://tpwd.texas.gov/documents/257/CWD-Trace-OutReleaseSites.pdf
Number of CWD Exposed Deer Released by County
https://tpwd.texas.gov/documents/258/CWD-Trace-OutReleaseSites-NbrDeer.pdf
CWD Status Captive Herds
https://www.aphis.usda.gov/sites/default/files/status-of-captive-herds.pdf
THURSDAY, OCTOBER 30, 2025
TEXAS PARKS & WILDLIFE: 50 CWD CASES AT SITE OF INITIAL POSITIVE IN WASHINGTON CO., BUT NO NEW CASES IN WILD
Eichler said the 50 positive cases represented roughly a third of the facility’s adult herd – the fawns, none older than 5 months of age, were not tested – and were spread across all age groups and both sexes. He said at the time of the depopulation, 72 deer were missing from the reported herd inventory and were presumed dead.
https://chronic-wasting-disease.blogspot.com/2025/10/texas-parks-wildlife-50-cwd-cases-at.html
https://prpsc.proboards.com/thread/182/cases-site-initial-positive-washington
“He said at the time of the depopulation, 72 deer were missing from the reported herd inventory and were presumed dead.”
In Canada, BSE days, they call that the SSS policy, shoot, shovel, and shut the hell up…terry
Texas Game Wardens Near Conclusion of ‘Ghost Deer’ Case with 24 Suspects, 1,400 Charges Filed Statewide
Aug. 14, 2025
Media Contact: TPWD News, Business Hours, 512-389-8030
AUSTIN – The Texas Game Warden investigation known as "Ghost Deer" has reached a possible conclusion after two additional suspects turned themselves in on felony charges. This brings the total number of individuals implicated in the case to 24, with approximately 1,400 charges filed across 11 Texas counties.
Ken Schlaudt, 64, of San Antonio, the owner of four deer breeding facilities and one release site, along with facility manager Bill Bowers, 55, of San Angelo, surrendered to the Travis County District Attorney’s Office on charges of felony tampering with a governmental record. Both men allegedly entered false information into the Texas Wildlife Information Management System (TWIMS) to facilitate illegal smuggling of white-tailed breeder deer. They also face more than 100 misdemeanor charges related to unlawful breeder deer activities in Tom Green County.
The "Ghost Deer" investigation has uncovered widespread, coordinated deer breeding violations including, but not limited to: smuggling captive breeder deer and free-range whitetail deer between breeder facilities and ranches, Chronic Wasting Disease (CWD) testing violations, license violations and misdemeanor and felony drug charges relating to the possession and mishandling of prescribed sedation drugs classified as controlled substances.
The suspects charged in the case include:
Evan Bircher, 59, San Antonio Vernon Carr, 55, Corpus Christi Jarrod Croaker, 47, Corpus Christi Terry Edwards, 54, Angleton Joshua Jurecek, 41, Alice Justin Leinneweber, 36, Orange Grove James Mann, 53, Odem Gage McKinzie, 28, Normanna Herbert “Tim” McKinzie, 47, Normanna Eric Olivares, 47, Corpus Christi Bruce Pipkin, 57, Beaumont Dustin Reynolds, 38, Robstown Kevin Soto, 55, Hockley Jared Utter, 52, Pipe Creek Reed Vollmering, 32, Orange Grove Clint West, 56, Beaumont James Whaley, 49, Sevierville, Tenn. Ryder Whitstine, 19, Rockport Ryker Whitstine, 21, Rockport Claude Wilhelm, 52, Orange Cases are pending adjudication in Bandera, Bee, Brazoria, Duval, Edwards, Jim Wells, Live Oak, Montgomery, Tom Green, Travis and Webb counties.
The investigation began in March 2024 when game wardens discovered the first violations during a traffic stop.
https://tpwd.texas.gov/newsmedia/releases/?req=20250206a
That incident led wardens to the much larger network of violations,
https://tpwd.texas.gov/newsmedia/releases/?req=20250227b
resulting in one of the largest deer smuggling operations in Texas history.
About Texas Game Wardens
Texas Game Wardens, within the Law Enforcement Division of Texas Parks and Wildlife Department, are responsible for enforcing laws related to the conservation and management of natural resources and public safety through community-based law enforcement. Their mission is to provide hunting, fishing and outdoor recreation opportunities for the use and enjoyment of present and future generations. Additionally, they play a crucial role in search and rescue operations during natural disasters, exemplifying their commitment to protecting both the environment and the people of Texas.
If you witness a fishing, wildlife or boating violation in progress, please call 1-800-792-GAME(4263) immediately and report it to Operation Game Thief (OGT), Texas’ Wildlife Crime-Stoppers Program. You can also text your tip by sending the keyword TXOGT plus your tip to 847411 or through the Texas OGT App, available for iOS and Android devices. Dispatchers are available 24/7.
https://tpwd.texas.gov/newsmedia/releases/?req=20250814c
THURSDAY, AUGUST 14, 2025
Texas Game Wardens Near Conclusion of ‘Ghost Deer’ Case with 24 Suspects, 1,400 Charges Filed Statewide
https://chronic-wasting-disease.blogspot.com/2025/08/texas-game-wardens-near-conclusion-of.html
https://prpsc.proboards.com/thread/178/texas-game-wardens-conclusion-ghost
WEDNESDAY, MAY 14, 2025
Texas CWD TSE Prion Cases Rises to 1099 Confirmed Cases To Date
https://chronic-wasting-disease.blogspot.com/2025/05/texas-cwd-tse-prion-cases-rises-to-1099.html
TAHC 425th Commission Meeting CWD 1:45:00
* See CWD speakers expressing their concerns with changed regulations…
2:00 hr mark
https://m.youtube.com/watch?v=bWawHpdn_7I
TEXAS ANIMAL HEALTH COMMISSION 423rd Commission Meeting CWD Update February 25, 2025
https://chronic-wasting-disease.blogspot.com/2025/02/texas-animal-health-commission-423rd.html
SATURDAY, OCTOBER 25, 2025
Texas Parks and Wildlife Commission Meeting November 5-6, 2025 Agenda CWD TSE Prion
https://tpwd.texas.gov/business/feedback/meetings/2026/1106/agenda/work_session/
https://chronic-wasting-disease.blogspot.com/2025/10/texas-parks-and-wildlife-commission.html
https://prpsc.proboards.com/thread/181/tpwc-november-2025-agenda-prion
***> Department records indicate that within the last five years (since January 1, 2020), 30 deer breeding facilities where CWD has been confirmed transferred a total of 8,799 deer to 249 additional deer breeding facilities and 487 release sites located in a total of 144 counties in Texas. <***
https://www.sos.state.tx.us/texreg/pdf/backview/0411/0411adop.pdf
Texas Kimble County Farm Chronic Wasting Disease CWD TSE Prion Approximate Herd Prevalence 12%
SUMMARY MINUTES OF THE 407th COMMISSION MEETING Texas Animal Health Commission
September 22, 2020
Chronic Wasting Disease (CWD):
A new CWD positive breeding herd was disclosed in February 2020 in Kimble County. This herd depopulation was completed in July 2020. Including the two index positive deer, an additional eight more positive deer were disclosed (approximate herd prevalence 12%). Since July 2015 and prior to this discovery, five positive captive breeder herds have been disclosed and four of those are in Medina County. One herd in Lavaca and three herds in Medina County were depopulated leaving one large herd in Medina County that is managed on a herd plan. A new zone was established in Val Verde County in December 2019 as a result of a positive free-ranging White-tailed Deer (WTD). A second positive WTD was also disclosed in February 2020 in the same area.
SUMMARY MINUTES OF THE 407th COMMISSION MEETING – 9/22/2020
Scrapie: The flock identified in April 2016 remains under quarantine in Hartley County.
https://www.tahc.texas.gov/agency/meetings/minutes/SummaryMinutes_CommMtg_2020-09-22
http://web.archive.org/web/20201017124040/https://www.tahc.texas.gov/agency/meetings/minutes/SummaryMinutes_CommMtg_2020-09-22.pdf
Chronic Wasting Disease in Texas A Real Disease with Proven Impacts
Produced by a coalition of concerned hunters, landowners, & conservationists (last update 1/2025)
https://storymaps.arcgis.com/stories/b93f528938ac48e9b56dcc79953cbec0
Aug 18, 2021
Oh, Deer
Heading Off a Wildlife Epidemic
CWD poses a significant threat to the future of hunting in Texas. Deer population declines of 45 and 50 percent have been documented in Colorado and Wyoming. A broad infection of Texas deer populations resulting in similar population impacts would inflict severe economic damage to rural communities and could negatively impact land markets. Specifically, those landowners seeking to establish a thriving herd of deer could avoid buying in areas with confirmed CWD infections. As they do with anthrax-susceptible properties, land brokers may find it advisable to inquire about the status of CWD infections on properties that they present for sale. Prospective buyers should also investigate the status of the wildlife on prospective properties. In addition, existing landowners should monitor developments as TPWD crafts management strategies to identify and contain this deadly disease.
Dr. Gilliland (c-gilliland@tamu.edu) is a research economist with the Texas Real Estate Research Center at Texas A&M University.
https://www.recenter.tamu.edu/articles/tierra-grande/oh-d
TEXAS BREEDER DEER ESCAPEE WITH CWD IN THE WILD, or so the genetics would show?
OH NO, please tell me i heard this wrong, a potential Texas captive escapee with cwd in the wild, in an area with positive captive cwd herd?
apparently, no ID though. tell me it ain't so please...
23:00 minute mark
''Free Ranging Deer, Dr. Deyoung looked at Genetics of this free ranging deer and what he found was, that the genetics on this deer were more similar to captive deer, than the free ranging population, but he did not see a significant connection to any one captive facility that he analyzed, so we believe, Ahhhhhh, this animal had some captive ahhh, whatnot.''
https://youtu.be/aoPDeGL6mpQ?t=1384
Commission Agenda Item No. 5 Exhibit B
DISEASE DETECTION AND RESPONSE RULES
PROPOSAL PREAMBLE
1. Introduction.
snip...
A third issue is the accuracy of mortality reporting. Department records indicate that for each of the last five years an average of 26 deer breeders have reported a shared total of 159 escapes. Department records for the same time period indicate an average of 31 breeding facilities reported a shared total of 825 missing deer (deer that department records indicate should be present in the facility, but cannot be located or verified).
https://tpwd.texas.gov/business/feedback/meetings/2022/1104/agenda/item.phtml?item=5
On January 21, 2017 a tornado took down thousands of feet of fence for a 420-acre illegal deer enclosure in Lamar County that had been subject to federal and state investigation for illegally importing white-tailed deer into Mississippi from Texas (a CWD positive state). Native deer were free to move on and off the property before all of the deer were able to be tested for CWD. Testing will be made available for a period of three years for CWD on the property and will be available for deer killed within a 5-mile radius of the property on a voluntary basis.
https://www.mdwfp.com/media/254796/2016-17-deer-report.pdf
“It is interesting to note that, in 2001, the State of Texas shifted its deer management strategies toward the same leanings that Kroll has suggested for Wisconsin. In Texas, the change was brought about via heavy lobbying from the high-fence deer ranching industry. This pressure helped convince the Texas Parks and Wildlife to change their regulations and allow private landowners to select the own deer biologists.”
http://www.texasmonthly.com/story/which-side-fence-are-you
Chronic Wasting Disease in Texas
A Real Disease with Proven Impacts
Produced by a coalition of concerned hunters, landowners, & conservationists (last update 08/2023)
Snip…
Since 2012, CWD has been detected in wild deer in just 7 counties in Texas and is only established in the western panhandle and far west Texas.
In that same period of time, captive deer breeders have exposed almost half of Texas counties to CWD.
Deer held in captive breeding facilities are confined to much tighter spaces, and have intimate contact with many more animals on a daily basis. By far the greatest factor in amplifying the spread of CWD is the artificial movement of these animals, shipped in livestock trailers hundreds of miles, far outside of their natural home range, and ultimately released to co-mingle with wild deer.
Each year, Texas captive deer breeders liberate 20,000-30,000 deer from their pens to the wild.
For every deer breeding facility where a CWD positive deer is discovered, an epidemiological investigation is conducted by the Texas Parks & Wildlife Department and the Texas Animal Health Commission to determine how many other deer may have been exposed to the disease and where they have been shipped. Because of the prolific artificial movement of captive deer, one deer with CWD can impact hundreds of other facilities and ranches across the state.
Unfortunately, released deer in Texas are not required to retain any kind of visible identification (an ear tag), and for this reason, the vast majority of released deer cannot be relocated for testing.
As of August 2023, 116 Texas counties have received possibly infected breeder deer that cannot be located, putting more than 140,000 landowners at risk of the disease.
Snip
The state of Texas has been testing for CWD since 2002. Since that time, more than 302,360 captive and free range deer have been tested.
From 2015-2022, more than 127,000 samples were collected from hunter-harvested and roadkill deer. This sampling rate and risk-based distribution provides scientists confidence that they would have detected the disease if it existed at a very low prevalence (<1%) in any given region at the time sampling began.
Snip…
We have learned from other states where CWD has been present the longest, that a constant increase in the prevalence of the disease may lead to a significant decline in the deer population. When disease prevalence exceeds 20%, deer populations have declined by up to 50%. In some areas of Colorado, where CWD has been present since 1985, mule deer abundance has declined by 45% since that time, despite adequate habitat and no hunting ( Miller et al. 2008 ). Similarly, the South Converse Game Unit in Wyoming has documented CWD prevalence exceeding 50% and has seen an approximate 50% decline in mule deer populations.
Snip…
Rural Economies
Deer hunting is the lifeblood of rural Texas. White-tailed deer hunting is by far the most impactful segment of the hunting economy, representing $4.3 billion, according to a recent Texas A&M Study. And while deer breeders represent a very small segment of that economy (less than 5%), they represent one of the greatest risks. ( Full Texas A&M Report )
Real Estate
Rural land prices are largely driven by recreational buyers with hunting as a top land amenity. Without deer hunting, many of these properties will be worth much less.
Conservation Funding
Deer hunters are the largest funders of wildlife conservation in Texas through excise taxes on firearms, ammunition, and gear along with active membership supporting and funding conservation organizations. If deer hunting suffers due to CWD, all wildlife in Texas lose.
Culture & Health
Texas’ native deer herd has iconic value for all Texans. Deer hunting brings families together, creates camaraderie in communities, and serves to connect Texans to nature. There is no better protein than wild, locally harvested, non-GMO and totally organic venison. A healthy deer herd leads to healthy Texans and a healthy and prosperous Texas.
Snip…
This isn't a disease for our lifetime. It's a disease for our grandchildren's lifetime.
- Dr. Bob Dittmar, Former Texas State Wildlife Veterinarian
Snip…
See the full text with maps, graphs, much more, excellent data…
https://bit.ly/3xL16Gm
Since 2012, CWD has been detected in wild deer in just 7 counties in Texas and is only established in the western panhandle and far west Texas.
In that same period of time, captive deer breeders have exposed almost half of Texas counties to CWD.
https://bit.ly/3xL16Gm
As of August 2023, 116 Texas counties have received possibly infected breeder deer that cannot be located, putting more than 140,000 landowners at risk of the disease.
https://bit.ly/3xL16Gm
ECONOMIC VALUES OF WHITE-TAILED DEER IN TEXAS
2022 SURVEY: PART I
http://web.archive.org/web/20230809171452/https://nri.tamu.edu/media/3702/economic-values-of-white-tailed-deer-in-texas-2022-survey-part-i.pdf
Don't mess Texas, or with Mother Nature in Texas, but, seems things went terribly wrong down here in Texas with CWD, be careful what you ask for;
TEXAS CWD STRAIN
“Wow,” he said. “Unlike anything we've seen before.”
The disease devastating deer herds may also threaten human health
Scientists are exploring the origins of chronic wasting disease before it becomes truly catastrophic.
Rae Ellen Bichell
Image credit: David Parsons/Istock
April 8, 2019
This story was published in collaboration with the Mountain West News Bureau, a collaboration between Wyoming Public Media, Boise State Public Radio in Idaho, KUER in Salt Lake City and KRCC and KUNC in Colorado.
SNIP...
One day in late February, in their laboratory in Fort Collins, Colorado, Wagner and Zabel compared the prions from the brains of CWD-infected deer in Texas with those of elk in Colorado. They want to know if the proteins were all mangled in the same way, or not. “If they are different, this would suggest that we have different strain properties, which is evidence as we're building our case that we might have multiple strains of CWD circulating in the U.S.,” says Wagner.
Step one is to see if they’re equally easy to destroy using a chemical called guanidine. The shape of a prion dictates everything, including the way it interacts with an animal’s cells and the ease with which chemicals can unfold it.
“Moment of truth,” said Wagner, as she and Zabel huddled around a computer, waiting for results to come through. When they did, Zabel was surprised.
“Wow,” he said. “Unlike anything we've seen before.”
The prions from the Texas deer were a lot harder to destroy than the ones from the Colorado elk. In fact, the guanidine barely damaged them at all. “We’ve never seen that before in any prion strain, which means that it has a completely different structure than we've ever seen before,” says Zabel. And that suggests that it might be a very different kind of chronic wasting disease. The researchers ran the same test on another Texas deer, with the same results.
Now, these are only the preliminary results from a few animals. Wagner and Zabel have a lot more experiments to do. But if future tests come to the same conclusion, it would support their hypothesis that there are multiple strains of chronic wasting disease out there, all with different origins. That, in turn, could mean that this disease will become even trickier to manage than it already is.
And, Zabel adds, there’s something else. “If it's still evolving, it may still evolve into a form that could potentially, eventually affect humans,” he says.
Zabel is not the only one worried about that possibility.
OSTERHOLM, THE EPIDEMIOLOGIST from Minnesota, is also concerned. He directs the Center for Infectious Disease Research and Policy at the University of Minnesota, and is serving a one-year stint as a “Science Envoy for Health Security” with the U.S. State Department. In February, he told Minnesota lawmakers that when it comes to chronic wasting disease, we are playing with fire. “You are going to hear from people that this is not going to be a problem other than a game farm issue. You're going to hear from people that it's not going to transmit to people, and I hope they're right, but I wouldn't bet on it,” he said. “And if we lose this one and haven’t done all we can do, we will pay a price.”
If that wasn’t warning enough, he added: “Just remember what happened in England.”
He was talking about mad cow disease. Decades ago, Osterholm got involved in studying the potential for the newly emerging condition — bovine spongiform encephalopathy, or BSE for short — to be transmitted to humans.
At that point, researchers had yet to document a prion disease in animals that could infect people. They did, however, have a few pieces of the puzzle. For one, work in Papua New Guinea had shown that people could transmit prion diseases to each other if they practiced cannibalism, especially of the brain-eating variety. They also knew that BSE was spreading quickly between cattle. Osterholm says he and others worried that the more widespread it became, the more chances it might have to change into something that could sicken people.
“A lot of people thought that it was an overreaction,” says Osterholm. “Then, of course, in 1996, 10 years later, we recognized that in fact transmission had occurred.” Variant Creutzfeldt-Jakob disease, as the illness is called when it appears in human beings, has infected about 230 people worldwide. Osterholm says he feels like he’s having déjà vu, except that instead of mad cow, now it’s chronic wasting disease that’s spreading in animals, with the potential to cross the species barrier to infect humans.
SNIP...SEE FULL TEXT;
https://www.hcn.org/articles/wildlife-the-disease-devastating-deer-herds-may-also-threaten-human-health-science
TEXAS CWD STRAIN
77. Assessing chronic wasting disease strain differences in free-ranging cervids across the United States
Kaitlyn M. Wagnera, Caitlin Ott-Connb, Kelly Strakab, Bob Dittmarc, Jasmine Battend, Robyn Piercea, Mercedes Hennessya, Elizabeth Gordona, Brett Israela, Jenn Ballarde and Mark D Zabela
aPrion Research Center at Colorado State University; bMichigan Department of Natural Resources; cTexas Parks and Wildlife Department; dMissouri Department of Conservation, 5. Arkansas Game and Fish Commission CONTACT Kaitlyn M. Wagner miedkait@rams.colostate.edu
ABSTRACT
Background/Introduction: Chronic wasting disease (CWD) is an invariably fatal prion disease affecting captive and free-ranging cervids, including white-tailed deer, mule deer, moose, elk, and reindeer. Since the initial description of the disease in the 1960’s, CWD has spread to 23 states, 3 Canadian Provinces, South Korea, Norway and, most recently, Finland. While some outbreaks of CWD were caused by transport of infected animals from endemic regions, the origin of CWD in other epizootics is unclear and has not been characterized. Previous studies have shown that there are two distinct strains of CWD. However, the continuous spread and the unclear origin of several outbreaks warrant continued surveillance and further characterization of strain diversity.
Materials and Methods: To address these knowledge gaps, we used biochemical tests to assess strain differences between CWD outbreaks in Michigan, Texas, Missouri, and Colorado, USA. Brain or lymph node samples were homogenized and digested in 50 µg/mL proteinase K (PK). These samples were then run on a Western blot to assess glycoform ratio and electrophoretic mobility. Texas samples were digested in 100 µg/mL PK. To assess conformational stability, brain or lymph node homogenates were incubated in increasing concentrations of guanidine hydrochloride from 0 M to 4 M in 0.5 M increments. Samples were then precipitated in methanol overnight, washed and PK digested in 50 µg/mL PK before slot blotting.
Results: Our results have found significant differences in glycoform ratio between CWD from Michigan and Colorado, but no differences were observed in conformational stability assays. Interestingly, when testing our CWD isolates from Texas to analyse electrophoretic mobility and glycoform ratio, we found that these samples did not exhibit the characteristic band shift when treated with PK, but PK resistant material remained. Additionally, results from our conformational stability assay demonstrate a unique profile of these Texas isolates. Testing of samples from Missouri is currently underway.
Conclusions: Thus far, our data indicate that there are strain differences between CWD circulating in Michigan and CWD in Colorado and provide important insight into CWD strain differences between two non-contiguous outbreaks. We have also identified a unique strain of CWD in Texas with biochemical strain properties not seen in any of our other CWD isolates. These results highlight the importance of continued surveillance to better understand this devastating disease. These results have important implications for CWD emergence, evolution and our understanding of prion strain heterogeneity on the landscape.
http://www.tandfonline.com/doi/full/10.1080/19336896.2019.1615197
Texas Game Wardens Bust Illegal Deer Operations Across the State Feb. 27, 2025
Media Contact: TPWD News, Business Hours, 512-389-8030
AUSTIN – A recent investigation by Texas Game Wardens resulted in approximately 1,200 pending charges and 22 suspects from across the state involved in the deer breeding industry and black-market wildlife trade.
The suspects and charges are associated with three deer breeding facilities, ten release sites, one deer management pen and three illegal facilities not registered in the Texas Wildlife Information Management Services (TWIMS) database, meaning they were operating or receiving deer in violation of registration requirements and disease monitoring protocols.
https://tpwd.texas.gov/newsmedia/releases/?req=20250227b
Texas Game Wardens Bust Illegal Deer Operations Across the State Feb. 27, 2025
https://chronic-wasting-disease.blogspot.com/2025/02/texas-game-wardens-bust-illegal-deer.html
TUESDAY, FEBRUARY 25, 2025
TEXAS ANIMAL HEALTH COMMISSION 423rd Commission Meeting CWD Update February 25, 2025
https://chronic-wasting-disease.blogspot.com/2025/02/texas-animal-health-commission-423rd.html
SUNDAY, MAY 04, 2025
Texas Senate Bill 2649 creation of a statewide Chronic Wasting Disease plan
https://chronic-wasting-disease.blogspot.com/2025/05/texas-senate-bill-2649-creation-of.html
SUNDAY, MAY 04, 2025
Texas Senate Bill 2651 establishment of a pilot program to breed deer resistant to CWD TSE Prion, what could go wrong?
https://chronic-wasting-disease.blogspot.com/2025/05/texas-senate-bill-2651-establishment-of_4.html
Texas S.B. 2843 Directs TPWD to conduct a comprehensive study of current measures to control chronic wasting disease (CWD) in deer
Trying to legislate CWD is what got Texas in this CWD mess to begin with, how did that work out$$$ Legislators and Politicians need to stay away and let TPWD and TAHC et try and contain this mess that Legislators and Politicians got us in, called CWD TSE Prion…terry
https://chronic-wasting-disease.blogspot.com/2025/04/texas-sb-2843-directs-tpwd-to-conduct.html
THURSDAY, APRIL 10, 2025
CWD TSE Prion, Politics, Friendly Fire, Unforeseen Consequences, What If?
https://chronic-wasting-disease.blogspot.com/2025/04/cwd-tse-prion-politics-friendly-fire.html
Friday, February 21, 2025
Deer don’t die from CWD, it’s the insurance companies, or it's a Government conspiracy?
https://chronic-wasting-disease.blogspot.com/2025/02/deer-dont-die-from-cwd-its-insurance.html
THURSDAY, APRIL 24, 2025
***> US Captive CWD Positive Herds Update April 2025
https://chronic-wasting-disease.blogspot.com/2025/04/us-captive-cwd-positive-herds-update.html
Captive CHRONIC WASTING DISEASE CASES Update August 2025
https://www.aphis.usda.gov/sites/default/files/status-of-captive-herds.pdf
I can’t imagine trying to regulate CWD, and any human zoonosis there from, as they tried to do with BSE TSE Prion aka mad cow disease, especially with CWD TSE being more virulent and more infectious…a terrible worst case scenario, are we there yet?
SUNDAY, MARCH 19, 2023
Abandoned factory ‘undoubtedly’ contains dormant Mad Cow Disease that could threaten humans, Thruxted Mill, Queniborough CJD
https://bseinquiry.blogspot.com/2023/03/abandoned-factory-undoubtedly-contains.html
DFA Draft Factual Accounts
DFA 11 "The Touch Test"
DFA 14
Consideration of the Risk from Mechanically Recovered Meat (MRM) in 1989-1990 Draft Factual Accounts 9 July 1999
http://web.archive.org/web/20001219041200/http://www.bse.org.uk/dfa/dfa14.htm
DFA 15
Monitoring and Enforcement of the SBO Regulations Draft Factual Accounts 9 July 1999
http://web.archive.org/web/20001219080500/http://www.bse.org.uk/dfa/dfa15.htm
DFA 16: MID 1995 TO THE FINAL DAYS
http://web.archive.org/web/20001121091600/http://www.bse.org.uk/dfa/dfa16.htm
DFA 17
http://web.archive.org/web/20001219215500/http://www.bse.org.uk/dfa/dfa17.htm
DFA 26 Public Pronouncements by the CMO, May 1990 29 November 1999
https://web.archive.org/web/20001209084800/http://www.bse.org.uk/dfa/dfa26.pdf
DFA 25 Notification of the Ruminant Feed Ban to non-EC countries 4 November 1999
https://web.archive.org/web/20001209084800/http://www.bse.org.uk/dfa/dfa25.pdf
DFA 24 Public Pronouncements by the CMO on the human heath implications of BSE, March 1993 and June 1993. 6 December 1999
https://web.archive.org/web/20001209084800/http://www.bse.org.uk/dfa/dfa24.pdf
DFA 23 Maff statements in 1990 about a cat with a spongiform encephalopathy16 November 1999
https://web.archive.org/web/20001209084800/http://www.bse.org.uk/dfa/dfa23.pdf
DFA 22 MIADFA 21 Cattle Tracking 23 November 1999
https://web.archive.org/web/20001209084800/http://www.bse.org.uk/dfa/dfa21.pdf
DFA 20 Introduction of the ruminant feed ban and compulsory notification of BSE in Northern Ireland3 December 1999
https://web.archive.org/web/20001209084800/http://www.bse.org.uk/dfa/dfa20.pdf
DFA 19 Dissection of Bovine Eye balls 8 November 1999
https://web.archive.org/web/20001209084800/http://www.bse.org.uk/dfa/dfa19.pdf
DFA 18 Cosmetics 29 October 1999
https://web.archive.org/web/20001209084800/http://www.bse.org.uk/dfa/dfa18.pdf
DFA 17 Medicines and medical devices 7 October 1999
https://web.archive.org/web/20001209084800/http://www.bse.org.uk/dfa/dfa17.pdf
DFA 17
http://web.archive.org/web/20001219215500/http://www.bse.org.uk/dfa/dfa17.htm
DFA 16 Mid 1995 to the final days 7 July 1999
https://web.archive.org/web/20001209084800/http://www.bse.org.uk/dfa/dfa16.pdf
DFA 16: MID 1995 TO THE FINAL DAYS
http://web.archive.org/web/20001121091600/http://www.bse.org.uk/dfa/dfa16.htm
DFA 15 Monitoring and Enforcements of the SBO Regulations 9 July 1999
https://web.archive.org/web/20001209084800/http://www.bse.org.uk/dfa/dfa15.pdf
DFA 15
Monitoring and Enforcement of the SBO Regulations Draft Factual Accounts 9 July 1999
http://web.archive.org/web/20001219080500/http://www.bse.org.uk/dfa/dfa15.htm
DFA 14 Consideration of the Risk from Mechanically Recovered Meat (MRM) in 1989 9 July 1999
https://web.archive.org/web/20001209084800/http://www.bse.org.uk/dfa/dfa14.pdf
DFA 14
Consideration of the Risk from Mechanically Recovered Meat (MRM) in 1989-1990 Draft Factual Accounts 9 July 1999
http://web.archive.org/web/20001219041200/http://www.bse.org.uk/dfa/dfa14.htm
BSE Inquiry Issues Factual Accounts.
https://webarchive.nationalarchives.gov.uk/ukgwa/20090505205439mp_/http://www.bseinquiry.gov.uk/files/ia/ia2/tab11.pdf
BSE Inquiry Issues more Factual Accounts, 22nd January 1999.
https://webarchive.nationalarchives.gov.uk/ukgwa/20090505205439mp_/http://www.bseinquiry.gov.uk/files/ia/ia2/tab12.pdf
BSE Inquiry Issues more Factual Accounts, 26th January 1999.
https://webarchive.nationalarchives.gov.uk/ukgwa/20090505205439mp_/http://www.bseinquiry.gov.uk/files/ia/ia2/tab13.pdf
07 February 1997 A4-0020/97
(To obtain the full text of this report in DA, EL, ES, IT, NL, PT, FI or SV , please consult " Plenary sessions" in the language of your choice, select option "Reports - by A4 number" and search for "A4-0020/97")
REPORT
on alleged contraventions or maladministration in the implementation of Community law in relation to BSE, without prejudice to the jurisdiction of the Community and national courts
https://www.europarl.europa.eu/conferences/19981130/bse/a4002097_en.htm#:~:text=At%20its%20meetings%20of%2013,submitted%20on%207%20February%201997.
BSE Inquiry Draft Factual Accounts DFAs
https://bseinquiry.blogspot.com/2022/08/bse-inquiry-draft-factual-accounts-dfas.html
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
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