DNR Study Finds CWD-Infected Deer Die At 3 Times Rate Of Healthy Animals
5-Year Study In Southwestern Wisconsin Hopes To Understand Role CWD Plays In Deer Mortality, Population Thursday, March 1, 2018, 6:30am By Rich Kremer Share: Forward logo Print HTML logo Facebook logo Twitter logo Google+ logo ListenDownload WisContext: Chronic Wasting Disease In Wisconsin's Deer A five-year study on how chronic wasting disease impacts the state's deer population has found infected animals died at three times the rate of healthy deer.
While it's been known for decades that CWD is fatal, there hasn't been a comprehensive look at the specific role it plays in the deer population as a whole.
Since January 2017, Wisconsin Department of Natural Resources research scientists have been trapping deer and fitting them with radio collars that alert them when the animal has died. DNR Research Scientist Dan Storm said researchers would then locate the animals and test them for CWD.
In the first year, the agency put radio collars on 148 deer, 122 of which died, Storm said. Of those who died, he said 12 tested positive for the fatal brain disease. Storm said three quarters of deer testing positive for CWD died in the first year, while only one quarter of healthy deer died.
"We found that deer that have chronic wasting disease have significantly lower survival than those that do not," said Storm. "So we can say that with confidence but what we will learn more about is the magnitude of the difference."
Storm said he would have liked to get a bigger sample size but the findings are still significant. And he said with four more years of data they’ll have a better understanding of the role CWD plays in Wisconsin’s deer herd.
"We’re going to be better able to manage the deer population in the face of the disease," said Storm. "Now whether our research gives us any strong notions of how to manage deer differently to manage the disease ... I’m not certain about that yet."
There are two study areas in southwestern Wisconsin, both around 200 square miles. A low-CWD prevalence zone is in northeastern Grant and northwestern Iowa counties while a high-CWD prevalence study area is located in northeastern Iowa and northwestern Dane counties.
Similar studies have been conducted in western states on elk and mule deer. According to the DNR, those studies have found that CWD negatively impacts survival and population size.
Wisconsin Public Radio, © Copyright 2018, Board of Regents of the University of Wisconsin System and Wisconsin Educational Communications Board.
Deer Survival: Digging into Year-One Numbers
In January 2017, the Office of Applied Science began a comprehensive study of deer mortality in southwestern Wisconsin as part of the Governor’s Initiative on Chronic Wasting Disease (CWD). In this article, we report the results of our first year of monitoring deer survival. Since these are early results, we’re going to focus on broad differences between CWD positive and negative deer. We’ll report the percentage of deer that survived over the course of the year and how that differed between CWD-infected deer and uninfected deer. We’ll also break down the causes of mortality. More focused analysis, including sex, age and geographic differences will become possible as we gather more data.
Katie Luukonen prepares to collar a whitetail
doe captured in a clover net.
The primary way CWD could influence deer populations is by reducing survival at the population level. This leads to the question ‘are CWD-infected deer less likely to survive over the course of the year than uninfected deer and if so, by how much?’ It is important to note that there is more to population impacts than just this survival difference - which we will explain in a future article - but for now, let’s focus on the question of CWD and deer survival.
One way CWD can reduce survival, of course, is for the disease itself to kill the deer. To the best of our knowledge, CWD is always fatal. Thus, it is not unusual or unexpected to observe deer dying from CWD. But what does it actually mean to say a deer has died from CWD? Like many diseases, dying from CWD means dying from complications related to CWD infection. As the prions accumulate and damage the nervous system, they disrupt the deer’s natural physical and physiological processes. In addition to what we normally expect when we think of deer with end-stage CWD (emaciation, drooling, drooping head and ears), infected deer often have difficulty swallowing, leading to aspiration pneumonia. These complications may be the direct cause of death of an infected deer.
Study crew prepare to collar a doe restrained in a clover net.
While individual deer deaths directly from CWD are noteworthy and interesting, they are only a part of the story of how CWD may reduce deer survival. CWD may significantly negatively impact deer populations whether the final mortality event is directly or indirectly related to the disease. It could do this by making deer more vulnerable to other sources of mortality (predation, vehicle collisions, hunting etc.), because infected deer become less aware of their surroundings, responsive to stimuli, and physically coordinated. The ultimate cause of death is less important to understanding the impact of CWD than the difference in survival between infected and uninfected deer, regardless of cause. Therefore, we shouldn’t focus directly on CWD-specific mortality but on the more basic question of whether CWD is leading to an overall reduction of deer survival. It is this question that is most important to evaluating how best to manage deer in the face of this disease.
In January 2017, the Office of Applied Science began a comprehensive study of deer mortality in southwestern Wisconsin as part of the Governor’s Initiative on Chronic Wasting Disease (CWD). In this article, we report the results of our first year of monitoring deer survival. Since these are early results, we’re going to focus on broad differences between CWD positive and negative deer. We’ll report the percentage of deer that survived over the course of the year and how that differed between CWD-infected deer and uninfected deer. We’ll also break down the causes of mortality. More focused analysis, including sex, age and geographic differences will become possible as we gather more data.
Katie Luukonen prepares to collar a whitetail
doe captured in a clover net.
doe captured in a clover net.
The primary way CWD could influence deer populations is by reducing survival at the population level. This leads to the question ‘are CWD-infected deer less likely to survive over the course of the year than uninfected deer and if so, by how much?’ It is important to note that there is more to population impacts than just this survival difference - which we will explain in a future article - but for now, let’s focus on the question of CWD and deer survival.
One way CWD can reduce survival, of course, is for the disease itself to kill the deer. To the best of our knowledge, CWD is always fatal. Thus, it is not unusual or unexpected to observe deer dying from CWD. But what does it actually mean to say a deer has died from CWD? Like many diseases, dying from CWD means dying from complications related to CWD infection. As the prions accumulate and damage the nervous system, they disrupt the deer’s natural physical and physiological processes. In addition to what we normally expect when we think of deer with end-stage CWD (emaciation, drooling, drooping head and ears), infected deer often have difficulty swallowing, leading to aspiration pneumonia. These complications may be the direct cause of death of an infected deer.
Study crew prepare to collar a doe restrained in a clover net.
While individual deer deaths directly from CWD are noteworthy and interesting, they are only a part of the story of how CWD may reduce deer survival. CWD may significantly negatively impact deer populations whether the final mortality event is directly or indirectly related to the disease. It could do this by making deer more vulnerable to other sources of mortality (predation, vehicle collisions, hunting etc.), because infected deer become less aware of their surroundings, responsive to stimuli, and physically coordinated. The ultimate cause of death is less important to understanding the impact of CWD than the difference in survival between infected and uninfected deer, regardless of cause. Therefore, we shouldn’t focus directly on CWD-specific mortality but on the more basic question of whether CWD is leading to an overall reduction of deer survival. It is this question that is most important to evaluating how best to manage deer in the face of this disease.
Findings by the numbers
We collared 138 deer during the 2016-2017 winter, and we successfully tested 122 of these for CWD. Twelve of the 122 (9.8%) returned positive CWD test results.
The plot below shows survival of CWD-positive and CWD-negative deer through time. The vertical axis shows the percentage of animals alive (referred to scientifically as survival probability) and the horizontal axis is time. We can use this plot to see what survival is at any point in time, and to compare survival between infected and uninfected deer. (Note the vertical dotted line that denotes the beginning of the archery season and the 2 vertical shaded areas that denote the 9-day firearm and Holiday hunting seasons).
The two trend lines show the survival estimates and the shaded areas around the lines show the amount of uncertainty around those estimates. We can see that almost 90% of deer that tested negative for CWD at capture survived to the beginning of archery season, while only about 50% of CWD-positive deer survived over that period.
As expected, survival drops more sharply later in the year for both CWD-positive and -negative deer as hunting begins, and by the end of 2017, less than 25% of CWD-positive deer were still alive and about 75% of deer that didn’t test positive were still alive.
Year-One Survival Graph
This graph shows the difference in rate of survival between CWD-negative (blue) and CWD-positive deer (orange) over one year. It’s important to remember that this graph does not show mortality causes, only whether the deer survived.
The shaded areas around the two lines represent how certain we are that our line is correct. Certainty is determined by the size of our sample. This year, we observed many more CWD-negative deer than CWD-positive deer, so our sample size for negative deer is much larger than our sample size for positive deer. The larger our sample, the more certain we can be in our analysis, and the narrower the shaded area becomes around the line.
Right now, our estimation of CWD-negative deer survival is more certain than our estimation for CWD-positive deer. As our sample size continues to grow over the course of the study, the shaded regions will shrink around the solid lines, which may move up or down some as we collect more data.
Significantly, the shaded regions for CWD-negative deer survival and CWD-positive deer survival do not overlap. This makes us confident that the survival difference between positive and negative deer is statistically significant. We will need many more years of data to understand how big that difference actually is.]
We collared 138 deer during the 2016-2017 winter, and we successfully tested 122 of these for CWD. Twelve of the 122 (9.8%) returned positive CWD test results.
The plot below shows survival of CWD-positive and CWD-negative deer through time. The vertical axis shows the percentage of animals alive (referred to scientifically as survival probability) and the horizontal axis is time. We can use this plot to see what survival is at any point in time, and to compare survival between infected and uninfected deer. (Note the vertical dotted line that denotes the beginning of the archery season and the 2 vertical shaded areas that denote the 9-day firearm and Holiday hunting seasons).
The two trend lines show the survival estimates and the shaded areas around the lines show the amount of uncertainty around those estimates. We can see that almost 90% of deer that tested negative for CWD at capture survived to the beginning of archery season, while only about 50% of CWD-positive deer survived over that period.
As expected, survival drops more sharply later in the year for both CWD-positive and -negative deer as hunting begins, and by the end of 2017, less than 25% of CWD-positive deer were still alive and about 75% of deer that didn’t test positive were still alive.
Year-One Survival Graph
This graph shows the difference in rate of survival between CWD-negative (blue) and CWD-positive deer (orange) over one year. It’s important to remember that this graph does not show mortality causes, only whether the deer survived.
The shaded areas around the two lines represent how certain we are that our line is correct. Certainty is determined by the size of our sample. This year, we observed many more CWD-negative deer than CWD-positive deer, so our sample size for negative deer is much larger than our sample size for positive deer. The larger our sample, the more certain we can be in our analysis, and the narrower the shaded area becomes around the line.
Right now, our estimation of CWD-negative deer survival is more certain than our estimation for CWD-positive deer. As our sample size continues to grow over the course of the study, the shaded regions will shrink around the solid lines, which may move up or down some as we collect more data.
Significantly, the shaded regions for CWD-negative deer survival and CWD-positive deer survival do not overlap. This makes us confident that the survival difference between positive and negative deer is statistically significant. We will need many more years of data to understand how big that difference actually is.]
Causes of mortality
Of CWD-positive deer that have died so far, at least 4 died directly from CWD, meaning they were found dead and were obviously emaciated and were unconsumed or with small amounts of scavenging. These deer were taken in for laboratory necropsy, except for 1 deer that was too decomposed. Laboratory necropsies confirmed CWD-infection and found substantial emaciation, muscle wasting, and 2 had pneumonia.
Three CWD-positive deer had been significantly consumed by coyotes, though it was not clear whether these were the result of scavenging or predation. One of these was captured on a trail-camera just prior to death looking extremely emaciated and with a bloated abdomen, suggesting late stage CWD symptoms.
Another CWD-positive deer was harvested by a hunter during the 9-day firearm season. For those deer that were not CWD-positive at capture, most mortality was due to hunting. A handful of additional deer died from other causes (vehicle collisions, coyote predation, etc.).
The survival difference between CWD-positive and CWD-negative deer is notable, but we must keep in mind that 12 CWD-positive animals is a relatively small number. Referring back to the survival plot, you’ll see the shaded area around the line is relatively wide. What this means is that there is a lot of uncertainty in the survival estimates of the CWD-positive deer, final survival estimates of CWD-positive deer could be higher or lower but likely fall within the shaded band. This level of uncertainty is a direct consequence of the relatively small number of CWD-positive deer we collared so far.
Despite this level of uncertainty, the estimated survival rates are already significantly different from each other by statistical standards. Therefore, we can now say with confidence that the survival rate of CWD positive deer is lower than for negative animals, which was expected.
A whitetail doe looks out from the woods.She was collared in Winter 2018.
As the study continues, we will gather much more information from both positive and negative deer. which will allow for more conclusive statements about the magnitude of difference in survival rates and the overall impact of CWD on the population. This preliminary analysis suggests CWD may be negatively impacting deer survival in Wisconsin and it certainly warrants paying attention to as the study moves forward.
DNR announces updated CWD Response
Plan By Central Office March 2, 2018 Contact(s): Tami Ryan, DNR wildlife health section chief, 608-266-3143
MADISON--Increased surveillance, increased sampling, carcass movement restrictions and local community involvement are just some the goals outlined in the recently updated Wisconsin Department of Natural Resources CWD Response Plan.
The updated plan, the result of a collaborative effort between DNR, Wisconsin Department of Agriculture Trade and Consumer Protection, the Wisconsin Conservation Congress and key stakeholders, will be the guide for CWD response and management over the next five years. Implementation of the plan as part of Gov. Scott Walker's Chronic Wasting Disease Initiative has already begun.
Among the key points in the plan is the work of County Deer Advisory Councils and local communities. The citizen based CDACs set the deer population goals for their counties, which is an important factor in those counties where CWD has been detected.
"We can't emphasize enough the importance of the work carried out by the County Deer Advisory Councils, hunters and citizens," said DNR Secretary Dan Meyer. "They know more about the deer herd in their counties than anyone and their contribution is a valuable tool in addressing CWD."
When a detection is found in a new area, DNR in collaboration with the CDAC and local landowners will launch a rapid response Citizen Advisory Team to determine the extent of CWD, share the information widely, and collectively determine the appropriate response.
Team members will host citizen-based informational meetings in several locations in the county. They will go "door-to-door" visiting landowners within a 2-mile radius of the positive detection to help develop and promote voluntary landowner surveillance testing permits, encourage the reporting of "sick deer" at the local level, and educate landowners on the current feeding and baiting regulations.
This approach was first used after the 2011 CWD discovery in Washburn County where there hasn't been a positive CWD detection since. The same idea is now being deployed in Lincoln County where the first case of CWD was announced in January.
Hunters play a vital role in tracking and managing the disease. The updated plan calls for making more CWD sampling opportunities available to hunters through sampling kiosks around the state and making more hunters aware of self-sampling testing kits. The department will continue to encourage hunters to get their harvested deer tested not only for their own piece of mind but to help us track the disease.
Realizing that deer carcass movement around the state and carcass disposal practices may play a role in the spread of CWD, there will be increased efforts to make hunters aware of the risks of moving carcasses from CWD positive counties to other counties where CWD has not been reported. Proper carcass disposal will also be stressed. New information on proper disposal can be found on the DNR website, dnr.wi.gov, by searching for "deer carcass disposal sites."
DATCP, which has authority over deer farms, is working closely with stakeholders to address biosecurity measures through rule language that will result in enhanced fencing requirements at game farms where a CWD positive has been found.
There is no single solution to eradicating CWD but it will take a collaborative effort of state agencies, Conservation Congress, CDACs, hunters and the public to better manage it.
Find out more about this updated CWD Response plan by going to the DNR website, dnr.wi.gov, and search keywords "CWD Response Plan."
Last Revised: Friday, March 02, 2018
SNIP...see more;
Southwest Wisconsin CWD, Deer and Predator Study Investigating the relationships between deer, predators and disease
Deer with CWD have a lower survival rate than deer without CWD Uncertainty remains exactly how much lower the survival rate is between CWD+ and CWD- deer More data from this 5 year study will provide more certainty Survival one important piece of the puzzle in determining the impact of CWD on deer populations Thanks to the many landowners who’ve allowed us to access their properties!
WISCONSIN CHRONIC WASTING DISEASE CWD TSE PRION 2017 POSITIVE FIGURES
Wisconsin CWD 2017 9685 testd, with 593 CWD POSITIVE.
Wisconsin CWD total to date, 209,615 tested since 2002, with 4,175 CWD POSITIVE to date.
WHILE we all await for more from this study and others about the cwd tse prion, i still wait for results of this study, and when they might be posted so the public can see;
''Results: We assessed archived human biopsy tissues from CWD endemic and non-endemic regions for the presence of abnormal PrP by RT-QuIC. Formalin-fixed, paraffin-embedded histology blocks were processed to extract tissue homogenates. Our study focused on analyzing appendix biopsy samples due to their previous use in surveillance studies and accessibility, but we also show the methodology can be applied to additional lymphoreticular tissues such as tonsils, spleen and lymph nodes. We compared 100 appendix biopsies from patients residing within the chronic wasting disease (CWD) endemic region to 100 appendix biopsies from patients residing outside the CWD endemic region.''
P143 Toward estimating sub-clinical human prion prevalence: Development of high-throughput amplification and detection methodologies.
Jeffrey Christiansen1, Sam Mellentine1, Clare Hoover1, Patrick Bosque2, James Ironside3, Edward Hoover1, Candace Mathiason1
1Colorado State University, Fort Collins, United States, 2University of Colorado School of Medicine, Aurora, United States, 3University of Edinburgh , Edinburgh, Scotland
Aims: The ability to determine the prevalence of subclinical diseases is of utmost importance to public health management. In the case of variant Creutzfeldt-Jakob disease (vCJD), determining subclinical prevalence has proven difficult. Foremost, the tissue tropism and time-course of abnormal prion protein (PrP) accumulation is not well characterized during the protracted asymptomatic phase of disease, making conclusive identification difficult. A recent study conducted in the UK identified 1 in 2000 subclinical vCJD carriers by assessing archived paraffin-embedded appendix tissues by immunohistochemistry (IHC). While vCJD exemplifies the dangers of TSE zoonosis, the unknown zoonotic potential of CWD and atypical scrapie cannot be neglected. Compounding the difficulty in diagnosing new zoonotic TSEs is the unknown clinical presentation and potential to manifest in an asymptomatic carrier state.
Methods: Detection of prions, especially during the asymptomatic phase of disease, has proven to be challenging and requires time consuming and expensive methods such as bioassay, IHC and Western blotting. The real time-quaking induced conversion assay (RT-QuIC) permits the amplification of low levels of prion seeding activity through cycles of shaking recombinant PrP substrate with a prion seed. The generation of nascent amyloid fibrils is measured in real-time through incorporation of thioflavin T, in a 96-well plate format for high-throughput.
Results: We assessed archived human biopsy tissues from CWD endemic and non-endemic regions for the presence of abnormal PrP by RT-QuIC. Formalin-fixed, paraffin-embedded histology blocks were processed to extract tissue homogenates. Our study focused on analyzing appendix biopsy samples due to their previous use in surveillance studies and accessibility, but we also show the methodology can be applied to additional lymphoreticular tissues such as tonsils, spleen and lymph nodes. We compared 100 appendix biopsies from patients residing within the chronic wasting disease (CWD) endemic region to 100 appendix biopsies from patients residing outside the CWD endemic region.
Conclusions: Our method offers an opportunity to identify abnormal PrP in archived biopsy specimens from health centers across the country to perform retrospective analysis on a statistically significant number of anonymized samples. Identification of subclinical disease prevalence is critical to limiting the spread of human prion disease through transfusions and iatrogenic transfer.
=====
''Results: We assessed archived human biopsy tissues from CWD endemic and non-endemic regions for the presence of abnormal PrP by RT-QuIC. Formalin-fixed, paraffin-embedded histology blocks were processed to extract tissue homogenates. Our study focused on analyzing appendix biopsy samples due to their previous use in surveillance studies and accessibility, but we also show the methodology can be applied to additional lymphoreticular tissues such as tonsils, spleen and lymph nodes. We compared 100 appendix biopsies from patients residing within the chronic wasting disease (CWD) endemic region to 100 appendix biopsies from patients residing outside the CWD endemic region.''
???
Of CWD-positive deer that have died so far, at least 4 died directly from CWD, meaning they were found dead and were obviously emaciated and were unconsumed or with small amounts of scavenging. These deer were taken in for laboratory necropsy, except for 1 deer that was too decomposed. Laboratory necropsies confirmed CWD-infection and found substantial emaciation, muscle wasting, and 2 had pneumonia.
Three CWD-positive deer had been significantly consumed by coyotes, though it was not clear whether these were the result of scavenging or predation. One of these was captured on a trail-camera just prior to death looking extremely emaciated and with a bloated abdomen, suggesting late stage CWD symptoms.
Another CWD-positive deer was harvested by a hunter during the 9-day firearm season. For those deer that were not CWD-positive at capture, most mortality was due to hunting. A handful of additional deer died from other causes (vehicle collisions, coyote predation, etc.).
The survival difference between CWD-positive and CWD-negative deer is notable, but we must keep in mind that 12 CWD-positive animals is a relatively small number. Referring back to the survival plot, you’ll see the shaded area around the line is relatively wide. What this means is that there is a lot of uncertainty in the survival estimates of the CWD-positive deer, final survival estimates of CWD-positive deer could be higher or lower but likely fall within the shaded band. This level of uncertainty is a direct consequence of the relatively small number of CWD-positive deer we collared so far.
Despite this level of uncertainty, the estimated survival rates are already significantly different from each other by statistical standards. Therefore, we can now say with confidence that the survival rate of CWD positive deer is lower than for negative animals, which was expected.
A whitetail doe looks out from the woods.She was collared in Winter 2018.
As the study continues, we will gather much more information from both positive and negative deer. which will allow for more conclusive statements about the magnitude of difference in survival rates and the overall impact of CWD on the population. This preliminary analysis suggests CWD may be negatively impacting deer survival in Wisconsin and it certainly warrants paying attention to as the study moves forward.
P143 Toward estimating sub-clinical human prion prevalence: Development of high-throughput amplification and detection methodologies.
Jeffrey Christiansen1, Sam Mellentine1, Clare Hoover1, Patrick Bosque2, James Ironside3, Edward Hoover1, Candace Mathiason1
1Colorado State University, Fort Collins, United States, 2University of Colorado School of Medicine, Aurora, United States, 3University of Edinburgh , Edinburgh, Scotland
Aims: The ability to determine the prevalence of subclinical diseases is of utmost importance to public health management. In the case of variant Creutzfeldt-Jakob disease (vCJD), determining subclinical prevalence has proven difficult. Foremost, the tissue tropism and time-course of abnormal prion protein (PrP) accumulation is not well characterized during the protracted asymptomatic phase of disease, making conclusive identification difficult. A recent study conducted in the UK identified 1 in 2000 subclinical vCJD carriers by assessing archived paraffin-embedded appendix tissues by immunohistochemistry (IHC). While vCJD exemplifies the dangers of TSE zoonosis, the unknown zoonotic potential of CWD and atypical scrapie cannot be neglected. Compounding the difficulty in diagnosing new zoonotic TSEs is the unknown clinical presentation and potential to manifest in an asymptomatic carrier state.
Methods: Detection of prions, especially during the asymptomatic phase of disease, has proven to be challenging and requires time consuming and expensive methods such as bioassay, IHC and Western blotting. The real time-quaking induced conversion assay (RT-QuIC) permits the amplification of low levels of prion seeding activity through cycles of shaking recombinant PrP substrate with a prion seed. The generation of nascent amyloid fibrils is measured in real-time through incorporation of thioflavin T, in a 96-well plate format for high-throughput.
Results: We assessed archived human biopsy tissues from CWD endemic and non-endemic regions for the presence of abnormal PrP by RT-QuIC. Formalin-fixed, paraffin-embedded histology blocks were processed to extract tissue homogenates. Our study focused on analyzing appendix biopsy samples due to their previous use in surveillance studies and accessibility, but we also show the methodology can be applied to additional lymphoreticular tissues such as tonsils, spleen and lymph nodes. We compared 100 appendix biopsies from patients residing within the chronic wasting disease (CWD) endemic region to 100 appendix biopsies from patients residing outside the CWD endemic region.
Conclusions: Our method offers an opportunity to identify abnormal PrP in archived biopsy specimens from health centers across the country to perform retrospective analysis on a statistically significant number of anonymized samples. Identification of subclinical disease prevalence is critical to limiting the spread of human prion disease through transfusions and iatrogenic transfer.
=====
''Results: We assessed archived human biopsy tissues from CWD endemic and non-endemic regions for the presence of abnormal PrP by RT-QuIC. Formalin-fixed, paraffin-embedded histology blocks were processed to extract tissue homogenates. Our study focused on analyzing appendix biopsy samples due to their previous use in surveillance studies and accessibility, but we also show the methodology can be applied to additional lymphoreticular tissues such as tonsils, spleen and lymph nodes. We compared 100 appendix biopsies from patients residing within the chronic wasting disease (CWD) endemic region to 100 appendix biopsies from patients residing outside the CWD endemic region.''
???
Conclusions
The appendix prevalence data raise legitimate concerns about the prevalence of prionaemia because a large number of individuals with presumably subclinical vCJD prion infection are blood donors and are undergoing invasive dentistry and surgery. Based on observations of several mammalian species, abnormal PrP immunoreactivity in peripheral lymphoreticular tissue is likely to be an accurate surrogate for prionaemia.16-19 Although there is a clear and pressing need for a donor blood screening assay, a proportion of vCJD-infected individuals may pose lower risks for secondary transmission of prion infection. The Direct Detection Assay result was negative in this case. The published sensitivity of this assay in a blinded series of vCJD blood samples is 71%; therefore, a negative result in a single case is not surprising. Although this test is the only assay proven to detect vCJD infection from clinical cases, there are several other experimental blood tests for vCJD in different stages of development. Our data suggest that it may be impossible to achieve sensitivity approaching 100% using available validation samples because some patients with vCJD may have no or very little prionaemia. Apparently modest sensitivity results in blinded studies of test validity should be interpreted with caution.
''Results: We assessed archived human biopsy tissues from CWD endemic and non-endemic regions for the presence of abnormal PrP by RT-QuIC. Formalin-fixed, paraffin-embedded histology blocks were processed to extract tissue homogenates. Our study focused on analyzing appendix biopsy samples due to their previous use in surveillance studies and accessibility, but we also show the methodology can be applied to additional lymphoreticular tissues such as tonsils, spleen and lymph nodes. We compared 100 appendix biopsies from patients residing within the chronic wasting disease (CWD) endemic region to 100 appendix biopsies from patients residing outside the CWD endemic region.''
???
PRION CONFERENCE 2015, 2016, 2017, ON potential for CWD TSE PRION ZOONOSIS, if it has not happened already...
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly 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.
snip...
R. BRADLEY
Title: Transmission of scrapie prions to primate after an extended silent incubation period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
*** WDA 2016 NEW YORK ***
*** We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions.
Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders
Volume 23, Number 9—September 2017
Research Letter Chronic Wasting Disease Prion Strain Emergence and Host Range Expansion
***Thus, emergent CWD prion strains may have higher zoonotic potential than common strains.
2017
Subject: ***CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
Chronic Wasting Disease (CWD)
Prevention
* Strongly consider having the deer or elk tested for CWD before you eat the meat.
* If you have your deer or elk commercially processed, consider asking that your animal be processed individually to avoid mixing meat from multiple animals.
* If your animal tests positive for CWD, do not eat meat from that animal.
> 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).***
TUESDAY, SEPTEMBER 12, 2017
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
SATURDAY, JANUARY 27, 2018
CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018
Prion 2017 Conference Abstracts CWD
2017 PRION CONFERENCE
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1
University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen
This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves.
Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice.
At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS
Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO
PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS
*** PRION 2017 CONFERENCE VIDEO
TUESDAY, JUNE 13, 2017
PRION 2017 CONFERENCE ABSTRACT
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
TUESDAY, JULY 04, 2017
*** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***
***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***
SATURDAY, JULY 29, 2017
Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC
Tuesday, December 20, 2011
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in a North American captive herd. RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.
SUMMARY:
captive deer farmers breeders entitlement program, i.e. indemnity program, why?
how many states have $465,000., and can quarantine and purchase there from, each cwd said infected farm, but how many states can afford this for all the cwd infected cervid game ranch type farms, and why do tax payers have to pay for it ???
For Immediate Release Thursday, October 2, 2014
Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov
*** TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease ***
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD).
For Immediate Release
Thursday, October 2, 2014
Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov Share on facebook Share on twitter Share on email Share on print More Sharing Services 1
TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD). The owners of the quarantined herd have entered into a fence maintenance agreement with the Iowa Department of Agriculture and Land Stewardship, which requires the owners to maintain the 8’ foot perimeter fence around the herd premises for five years after the depopulation was complete and the premises had been cleaned and disinfected
CWD is a progressive, fatal, degenerative neurological disease of farmed and free-ranging deer, elk, and moose. There is no known treatment or vaccine for CWD. CWD is not a disease that affects humans.
On July 18, 2012, USDA Animal and Plant Health Inspection Service’s (APHIS) National Veterinary Services Lab in Ames, IA confirmed that a male white tail deer harvested from a hunting preserve in southeast IA was positive for CWD. An investigation revealed that this animal had just been introduced into the hunting preserve from the above-referenced captive deer herd in north-central Iowa.
The captive deer herd was immediately quarantined to prevent the spread of CWD. The herd has remained in quarantine until its depopulation on August 25 to 27, 2014.
The Iowa Department of Agriculture and Land Stewardship participated in a joint operation to depopulate the infected herd with USDA Veterinary Services, which was the lead agency, and USDA Wildlife Services.
Federal indemnity funding became available in 2014. USDA APHIS appraised the captive deer herd of 376 animals at that time, which was before depopulation and testing, at $1,354,250. At that time a herd plan was developed with the owners and officials from USDA and the Iowa Department of Agriculture and Land Stewardship.
Once the depopulation was complete and the premises had been cleaned and disinfected, indemnity of $917,100.00 from the USDA has been or will be paid to the owners as compensation for the 356 captive deer depopulated.
The Iowa Department of Agriculture and Land Stewardship operates a voluntary CWD program for farms that sell live animals. Currently 145 Iowa farms participate in the voluntary program. The above-referenced captive deer facility left the voluntary CWD program prior to the discovery of the disease as they had stopped selling live animals. All deer harvested in a hunting preserve must be tested for CWD.
-30-
79.8 percent of the deer tested positive for the disease
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD). The owners of the quarantined herd have entered into a fence maintenance agreement with the Iowa Department of Agriculture and Land Stewardship, which requires the owners to maintain the 8’ foot perimeter fence around the herd premises for five years after the depopulation was complete and the premises had been cleaned and disinfected
CWD is a progressive, fatal, degenerative neurological disease of farmed and free-ranging deer, elk, and moose. There is no known treatment or vaccine for CWD. CWD is not a disease that affects humans.
On July 18, 2012, USDA Animal and Plant Health Inspection Service’s (APHIS) National Veterinary Services Lab in Ames, IA confirmed that a male white tail deer harvested from a hunting preserve in southeast IA was positive for CWD. An investigation revealed that this animal had just been introduced into the hunting preserve from the above-referenced captive deer herd in north-central Iowa.
The captive deer herd was immediately quarantined to prevent the spread of CWD. The herd has remained in quarantine until its depopulation on August 25 to 27, 2014.
The Iowa Department of Agriculture and Land Stewardship participated in a joint operation to depopulate the infected herd with USDA Veterinary Services, which was the lead agency, and USDA Wildlife Services.
Federal indemnity funding became available in 2014. USDA APHIS appraised the captive deer herd of 376 animals at that time, which was before depopulation and testing, at $1,354,250. At that time a herd plan was developed with the owners and officials from USDA and the Iowa Department of Agriculture and Land Stewardship.
Once the depopulation was complete and the premises had been cleaned and disinfected, indemnity of $917,100.00 from the USDA has been or will be paid to the owners as compensation for the 356 captive deer depopulated.
The Iowa Department of Agriculture and Land Stewardship operates a voluntary CWD program for farms that sell live animals. Currently 145 Iowa farms participate in the voluntary program. The above-referenced captive deer facility left the voluntary CWD program prior to the discovery of the disease as they had stopped selling live animals. All deer harvested in a hunting preserve must be tested for CWD.
INFORM: Cervid Health and States Indemnity FY 2015
USDA Animal and Plant Health Inspection Service sent this bulletin at 09/19/2014 05:22 PM EDT
Animal and Plant Health Inspection Service (APHIS), Veterinary Services (VS) received a total of $3 million in appropriated funding to support cervid health activities in fiscal year (FY) 2014, and made approximately $1.0 million of this funding available for indemnity of chronic wasting disease (CWD) positive, suspect, and exposed farmed cervids. All of the available FY2014 indemnity funding was used to depopulate three CWD-infected herds. However, several States have asked about the availability of Federal indemnity funds for CWD-exposed animals in the future.
VS plans to offer Federal indemnity for CWD-exposed cervids beginning in FY2015. Briefly, we will prioritize the highest risk CWD-exposed animals for indemnity based on the availability of funding. Any newly reported CWD-positive herds will be considered for indemnity as they are identified, based first on funding availability and secondly on the risk presented by the herd.
We will reassess our fiscal year funding on a quarterly basis so that providing indemnity for exposed animals does not exhaust available funding early in the fiscal year. By taking this fiscally cautious approach, we hope to provide indemnity for positive herds identified later in the fiscal year while removing high-risk animals from the landscape as soon as possible to minimize the risk for disease spread. Further, removal and testing of these exposed animals will provide a better understanding of the disease risk presented by these animals/herds.
VS plans to work with our State and industry stakeholders on the criteria to assess the risk and on the process through which States can request this indemnity. These will be finalized in a VS Guidance Document in the near future. We look forward to working with you to implement this process in the coming year.
***
FRIDAY, FEBRUARY 23, 2018
Pennsylvania NEW CWD MANAGEMENT AREA TO BE ANNOUNCED
MONDAY, FEBRUARY 12, 2018
Pennsylvania CWD TSE Prion has been found in captive deer in Huntingdon and Lancaster counties
WEDNESDAY, FEBRUARY 21, 2018
Maryland Chronic Wasting Disease CWD TSE Prion Found In Ten Deer Allegany and Washington Counties
SATURDAY, FEBRUARY 17, 2018
Montana Special Hunts 9 more cases CWD TSE Prion to date, more samples still pending
FRIDAY, FEBRUARY 09, 2018
Mississippi Chronic Wasting Disease confirmed in a White-tailed Deer
TUESDAY, FEBRUARY 13, 2018
*** MISSISSIPPI STATE DEPARTMENT OF HEALTH Chronic Wasting Disease: Public Health Recommendations ***
WEDNESDAY, NOVEMBER 22, 2017
Minnesota Chronic Wasting Disease discovered in Winona County farm
FRIDAY, NOVEMBER 24, 2017
Todd Robbins-Miller President of Minnesota Deer Farmers Association is oblivious to Chronic Wasting CWD TSE PRION DISEASE risk factors
WEDNESDAY, FEBRUARY 21, 2018
TEXAS TPWD CWD TSE PRION 2 MORE FROM BREEDER RELEASE SITE TOTALS 81 CASES TO DATE
WEDNESDAY, JANUARY 24, 2018
TEXAS CHRONIC WASTING DISEASE CWD TSE PRION MOUNTING, JUMPS TO 79 CASES TO DATE
FRIDAY, FEBRUARY 16, 2018
Texas Deer Breeders Continue fight against the state’s wildlife agency and its regulations trying to contain CWD TSE Prion
WEDNESDAY, FEBRUARY 07, 2018
New Mexico Bans All Live Cervid Importation Due To CWD TSE Prion still NO Final 2017 Positives Update for N.M.
FRIDAY, FEBRUARY 09, 2018
Virginia 2017 Hunt Confirms 16 Cases Chronic Wasting Disease CWD TSE Prion
MONDAY, FEBRUARY 05, 2018
Nebraska Chronic Wasting Disease CWD TSE Prion 2017 Survey Confirms 203 Positives From 1,807 Deer Sampled
SATURDAY, FEBRUARY 03, 2018
Arkansas Reports 346 Positive CWD TSE Prion cases found as of January 8, 2018
THURSDAY, FEBRUARY 08, 2018
Utah Chronic Wasting Disease CWD TSE Prion Update to date from 2017 Hunting Season
TUESDAY, JANUARY 30, 2018
Colorado Chronic Wasting Disease CWD TSE Prion 7/2015-6/2016 Results (2017?)
THURSDAY, JANUARY 25, 2018
Ohio Chronic Wasting Disease CWD TSE Prioin aka mad deer update 2016-2017 SEASON SUMMARY
SATURDAY, JANUARY 20, 2018
Pennsylvania CWD TSE Prion Cases Explodes 51 deer from the 2017-18 hunting seasons have tested positive for CWD majority of samples collected still are being analyzed
WEDNESDAY, JANUARY 24, 2018
Illinois Chronic Wasting Disease CWD TSE Prion cases mounting with 75 confirmed 2017 and 685 total to date
THURSDAY, FEBRUARY 08, 2018
Iowa DNR Wayne County Confirms CWD with 7 additional CWD positive tests so far from deer in northeast from 2017 season
SATURDAY, FEBRUARY 10, 2018
Chronic wasting disease management in ranched elk using rectal biopsy testing Research Paper 09 Feb 2018
January 14, 2018
Michigan’s Chronic Wasting Disease Working Group Recommendations Report to the Natural Resources Commission Prepared December 2017 CWD Confirmed Cases holding for now at 57 cases
Michigan UPDATE, see also ;
Addressing deer disease: DNR, MSU collaborate on deer movement study in south-central Michigan
Contact: Dwayne Etter (DNR), 517-284-4725 or David Williams (MSU), 517-917-0716 Agency: Natural Resources
Jan. 30, 2018
Michigan State University and the Michigan Department of Natural Resources will be placing location-tracking collars on white-tailed deer in south-central Michigan as part of a multiyear study of deer disease, including chronic wasting disease.
January 14, 2018
Missouri MDC REPORTS 15 NEW CASES OF CWD TSE Prion in Deer
MONDAY, JANUARY 29, 2018
Wyoming, Hanna, WGFD diagnosed chronic wasting disease (CWD) for the first time in Deer Hunt Area 161
MONDAY, JANUARY 29, 2018
North Dakota CWD Confirmed whitetail buck and a mule deer doe 2017 deer gun season from unit 3F2
SUNDAY, FEBRUARY 18, 2018
Chronic Wasting Disease CWD TSE Prion RoundUp February 18, 2018
TUESDAY, DECEMBER 12, 2017
*** Chronic Wasting Disease CWD TSE Prion (aka mad deer disease) Update USA December 14, 2017 ***
(zoonosis and environmental risk factors towards the bottom, after state by state reports)
MONDAY, MARCH 13, 2017
CHRONIC WASTING DISEASE CWD TSE PRION UDATE March 13, 2017
SATURDAY, JANUARY 14, 2017
CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL UPDATE JANUARY 14, 2017
Sunday, June 23, 2013
National Animal Health Laboratory Network Reorganization Concept Paper (Document ID APHIS-2012-0105-0001)
***Terry S. Singeltary Sr. submission
Singeltary submission ;
Program Standards: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose
DOCUMENT ID: APHIS-2006-0118-0411
***Singeltary submission
Singeltary submission ;
Program Standards: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose
*** DOCUMENT ID: APHIS-2006-0118-0411
SUNDAY, FEBRUARY 11, 2018
Experimental sheep BSE prions generate the vCJD phenotype when serially passaged in transgenic mice expressing human prion protein
Detection of PrPBSE and prion infectivity in the ileal Peyer’s patch of young calves as early as 2 months after oral challenge with classical bovine spongiform encephalopathy
Ivett Ackermann, Anne Balkema-Buschmann, Reiner Ulrich, Kerstin Tauscher, James C. Shawulu, Markus Keller, Olanrewaju I. Fatola, Paul Brown and Martin H. GroschupEmail authorView ORCID ID profile
Veterinary Research201748:88
https://doi.org/10.1186/s13567-017-0495-5© The Author(s) 2017
Received: 22 August 2017Accepted: 1 December 2017Published: 19 December 2017
Abstract
In classical bovine spongiform encephalopathy (C-BSE), an orally acquired prion disease of cattle, the ileal Peyer’s patch (IPP) represents the main entry port for the BSE agent. In earlier C-BSE pathogenesis studies, cattle at 4–6 months of age were orally challenged, while there are strong indications that the risk of infection is highest in young animals. In the present study, unweaned calves aged 4–6 weeks were orally challenged to determine the earliest time point at which newly formed PrPBSE and BSE infectivity are detectable in the IPP. For this purpose, calves were culled 1 week as well as 2, 4, 6 and 8 months post-infection (mpi) and IPPs were examined for BSE infectivity using a bovine PrP transgenic mouse bioassay, and for PrPBSE by immunohistochemistry (IHC) and protein misfolding cyclic amplification (PMCA) assays. For the first time, BSE prions were detected in the IPP as early as 2 mpi by transgenic mouse bioassay and PMCA and 4 mpi by IHC in the follicular dendritic cells (FDCs) of the IPP follicles. These data indicate that BSE prions propagate in the IPP of unweaned calves within 2 months of oral uptake of the agent.
snip...
In summary, our study demonstrates for the first time PrPBSE (by PMCA) and prion infectivity (by mouse bioassay) in the ileal Peyer’s patch (IPP) of young calves as early as 2 months after infection. From 4 mpi nearly all calves showed PrPBSE positive IPP follicles (by IHC), even with PrPBSE accumulation detectable in FDCs in some animals. Finally, our results confirm the IPP as the early port of entry for the BSE agent and a site of initial propagation of PrPBSE and infectivity during the early pathogenesis of the disease. Therefore, our study supports the recommendation to remove the last four metres of the small intestine (distal ileum) at slaughter, as designated by current legal requirements for countries with a controlled BSE risk status, as an essential measure for consumer and public health protection.
FRIDAY, DECEMBER 22, 2017
Detection of PrPBSE and prion infectivity in the ileal Peyer’s patch of young calves as early as 2 months after oral challenge with classical bovine spongiform encephalopathy
Thursday, November 16, 2017
Texas Natural Meats Recalls Beef Products Due To Possible Specified Risk Materials Contamination
*** Subject: USA CJD, BSE, SCRAPIE, CWD, TSE PRION END OF YEAR REPORTS 2017
TUESDAY, DECEMBER 12, 2017
Bovine Spongiform Encephalopathy BSE TSE Prion (aka mad cow disease) Report December 14, 2017 2017
TUESDAY, DECEMBER 12, 2017
Chronic Wasting Disease CWD TSE Prion (aka mad deer disease) Update USA December 14, 2017
FRIDAY, DECEMBER 15, 2017
Canada CFIA updating its national CWD TSE PRION efforts to eradicate disease farmed cervid NOT successful December 14, 2017
TUESDAY, DECEMBER 12, 2017
SCRAPIE TSE PRION UPDATE USA DECEMBER 14, 2017
USAHA 2017 RESOLUTIONS
RESOLUTION NUMBER: 23
APPROVED AS AMENDED SOURCE: COMMITTEE ON WILDLIFE AND CAPTIVE WILDLIFE
SUBJECT MATTER: Annual Reporting on Chronic Wasting Disease Epidemiological Data
BACKGROUND INFORMATION: Chronic wasting disease (CWD) has been recognized in wild cervids since the 1980’s. Availability of complete epidemiological information is critical for evaluating the effectiveness of science-based disease control programs. Access to pertinent information from epidemiological investigations across the country in wild populations is imperative to developing success strategies for managing the disease. More comprehensive information is needed on CWD epidemiology in the affected wild populations. Analysis of data from CWD affected populations across the country will improve risk assessment. Comprehensive epidemiological data evaluation may potentially identify factors contributing to the detection of CWD, enhance mitigation strategies to reduce the likelihood of CWD in new populations, and facilitate its earliest detection when it is present.
RESOLUTION: The United States Animal Health Association (USAHA) requests the United States Department of Agriculture (USDA), Animal and Plant Health Inspection Service, Veterinary Services and other appropriate federal and state agencies to work cooperatively to assemble, analyze, summarize, and make available annually to the Committee on Wildlife and Captive Wildlife at the USAHA meeting all pertinent information from epidemiological investigations of Chronic Wasting Disease (CWD) in cervid populations (including wild, free-ranging, and captive).
Specific information requested may include:
1) Compiled CWD testing data from each state to include:
a) Overall state testing numbers of each susceptible species tested;
b) Number of CWD positive tests found annually in each state;
c) Overall state testing in wild populations;
d) Prevalence of CWD in positive populations;
e) Population totals for each susceptible species of wild herds in each state;
f) Demography of positive and negative animals in infected herds;
g) Results from all tissues that were tested;
h) Duration of monitoring prior to detection of the first case - including numbers of animals in the herd, numbers tested, and numbers not tested;
i) Results of trace-forward and trace-back investigations; and
j) All other pertinent data that will enhance risk assessment of CWD in cervids and identification of effective mitigation measures.
2) Compiled data should also be posted on the USDA website.
http://www.usaha.org/upload/Resolution/2017/Resolution_23_CWD_Data.pdf
RESOLUTION NUMBER: 21 APPROVED SOURCE: COMMITTEE ON SHEEP, GOATS AND CAMELIDS SUBJECT MATTER: National Scrapie Eradication Program Funding
BACKGROUND INFORMATION: Due to the success of the cooperative National Scrapie Eradication Program, no new cases of scrapie have been identified in the United States (US) in the past 18 months. There are key components of the program that have been critical to this success and the effort to have the US be recognized internationally as free from scrapie, which would open new markets to US sheep and goat products. Surveillance and traceability are vital to this eradication program. Program use of sheep and goat official tags have demonstrated that official plastic tags are preferred over metal tags for readability and to reduce safety concerns. Funding for tags that are readable, acceptable to producers and efficient for regulators is essential to continue identification compliance and progress of the program.
RESOLUTION: The United States Animal Health Association urges the United States Secretary of Agriculture to request a congressional appropriation of five million additional dollars of new money to be added to the Equine, Cervid and Small Ruminant health line for the purpose of supporting Small Ruminant Health Programs to complete the eradication of scrapie and assure program success. It is vital that this new funding does not reduce other current United States Department of Agriculture, Animal and Plant Health Inspection Service, Veterinary Services program funding lines.
lol, drop in the bucket and a band-aid approach to something that needed a tourniquet decades ago...
TUESDAY, DECEMBER 12, 2017
Creutzfeldt Jakob Disease CJD National Prion Disease Pathology Surveillance Center Cases Examined to December 14, 2017
THURSDAY, FEBRUARY 15, 2018
Iatrogenic Creutzfeldt-Jakob disease with Amyloid-β pathology: an international study
WEDNESDAY, NOVEMBER 1, 2017
Blood-derived amyloid-β protein induces Alzheimer’s disease pathologies
http://betaamyloidcjd.blogspot.com/2017/11/blood-derived-amyloid-protein-induces.html
Alzheimer’s disease, iatrogenic, and Transmissible Spongiform Encephalopathy TSE Prion disease, that is the question ???
>>> The only tenable public line will be that "more research is required’’ <<<
>>> possibility on a transmissible prion remains open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?
[9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. There are also results to be made available shortly (1) concerning a farmer with CJD who had BSE animals, (2) on the possible transmissibility of Alzheimer’s and (3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.]
https://web.archive.org/web/20170126060344/http://collections.europarchive.org/tna/20080102232842/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf
https://web.archive.org/web/20040315075058/http://www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf
https://web.archive.org/web/20040315075058/www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf
snip...see full Singeltary Nature comment here;
http://www.nature.com/nature/journal/v525/n7568/full/nature15369.html#/comments
see Singeltary comments to Plos ;
Subject: 1992 IN CONFIDENCE TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES POSSIBILITY ON A TRANSMISSIBLE PRION REMAINS OPEN
BSE101/1 0136
IN CONFIDENCE
CMO
From: . Dr J S Metiers DCMO 4
November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognised the public sensitivity of these findings and intend to report them in their proper context. 'This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed". As the report emphasises the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible. what are the implications for public health?
3. The route 'of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk.
However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed. 1
92/11.4/1.1
BSE101/1 0137 4.
The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion.
The only tenable public line will be that "more research is required’’ before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.
J S METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832 llllYc!eS 2 92/11.4/1.2
https://web.archive.org/web/20160320084827/http://collections.europarchive.org/tna/20081106170650/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf
>>> The only tenable public line will be that "more research is required’’ <<<
>>> possibility on a transmissible prion remains open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?
Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015)
snip...see full Singeltary Nature comment here;
Alzheimer's disease
let's not forget the elephant in the room. curing Alzheimer's would be a great and wonderful thing, but for starters, why not start with the obvious, lets prove the cause or causes, and then start to stop that. think iatrogenic, friendly fire, or the pass it forward mode of transmission. think medical, surgical, dental, tissue, blood, related transmission. think transmissible spongiform encephalopathy aka tse prion disease aka mad cow type disease...
Commentary: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
http://journals.plos.org/plosone/article/comment?id=info:doi/10.1371/annotation/933cc83a-a384-45c3-b3b2-336882c30f9d
https://www.frontiersin.org/articles/10.3389/fnagi.2016.00005/full
Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease
*** Singeltary comment PLoS ***
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
http://www.plosone.org/annotation/listThread.action?root=82860
Ann N Y Acad Sci. 1982;396:131-43.
Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).
Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.
Abstract
Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD.
http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.1982.tb26849.x/abstract
Sunday, November 22, 2015
*** Effect of heating on the stability of amyloid A (AA) fibrils and the intra- and cross-species transmission of AA amyloidosis
Abstract
Amyloid A (AA) amyloidosis is a protein misfolding disease characterized by extracellular deposition of AA fibrils. AA fibrils are found in several tissues from food animals with AA amyloidosis. For hygienic purposes, heating is widely used to inactivate microbes in food, but it is uncertain whether heating is sufficient to inactivate AA fibrils and prevent intra- or cross-species transmission. We examined the effect of heating (at 60 °C or 100 °C) and autoclaving (at 121 °C or 135 °C) on murine and bovine AA fibrils using Western blot analysis, transmission electron microscopy (TEM), and mouse model transmission experiments. TEM revealed that a mixture of AA fibrils and amorphous aggregates appeared after heating at 100 °C, whereas autoclaving at 135 °C produced large amorphous aggregates. AA fibrils retained antigen specificity in Western blot analysis when heated at 100 °C or autoclaved at 121 °C, but not when autoclaved at 135 °C. Transmissible pathogenicity of murine and bovine AA fibrils subjected to heating (at 60 °C or 100 °C) was significantly stimulated and resulted in amyloid deposition in mice. Autoclaving of murine AA fibrils at 121 °C or 135 °C significantly decreased amyloid deposition. Moreover, amyloid deposition in mice injected with murine AA fibrils was more severe than that in mice injected with bovine AA fibrils. Bovine AA fibrils autoclaved at 121 °C or 135 °C did not induce amyloid deposition in mice. These results suggest that AA fibrils are relatively heat stable and that similar to prions, autoclaving at 135 °C is required to destroy the pathogenicity of AA fibrils. These findings may contribute to the prevention of AA fibril transmission through food materials to different animals and especially to humans.
Purchase options Price * Issue Purchase USD 511.00 Article Purchase USD 54.00
http://www.tandfonline.com/doi/abs/10.3109/13506129.2015.1095735?journalCode=iamy20
http://betaamyloidcjd.blogspot.com/2015/11/effect-of-heating-on-stability-of.html
Sunday, February 25, 2018
PRION ROUND TABLE CONFERENCE 2018 MAY, 22-25 A REVIEW
Terry S. Singeltary Sr.
The appendix prevalence data raise legitimate concerns about the prevalence of prionaemia because a large number of individuals with presumably subclinical vCJD prion infection are blood donors and are undergoing invasive dentistry and surgery. Based on observations of several mammalian species, abnormal PrP immunoreactivity in peripheral lymphoreticular tissue is likely to be an accurate surrogate for prionaemia.16-19 Although there is a clear and pressing need for a donor blood screening assay, a proportion of vCJD-infected individuals may pose lower risks for secondary transmission of prion infection. The Direct Detection Assay result was negative in this case. The published sensitivity of this assay in a blinded series of vCJD blood samples is 71%; therefore, a negative result in a single case is not surprising. Although this test is the only assay proven to detect vCJD infection from clinical cases, there are several other experimental blood tests for vCJD in different stages of development. Our data suggest that it may be impossible to achieve sensitivity approaching 100% using available validation samples because some patients with vCJD may have no or very little prionaemia. Apparently modest sensitivity results in blinded studies of test validity should be interpreted with caution.
''Results: We assessed archived human biopsy tissues from CWD endemic and non-endemic regions for the presence of abnormal PrP by RT-QuIC. Formalin-fixed, paraffin-embedded histology blocks were processed to extract tissue homogenates. Our study focused on analyzing appendix biopsy samples due to their previous use in surveillance studies and accessibility, but we also show the methodology can be applied to additional lymphoreticular tissues such as tonsils, spleen and lymph nodes. We compared 100 appendix biopsies from patients residing within the chronic wasting disease (CWD) endemic region to 100 appendix biopsies from patients residing outside the CWD endemic region.''
???
PRION CONFERENCE 2015, 2016, 2017, ON potential for CWD TSE PRION ZOONOSIS, if it has not happened already...
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
why do we not want to do TSE transmission studies on chimpanzees $
5. A positive result from a chimpanzee challenged severly 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.
snip...
R. BRADLEY
Title: Transmission of scrapie prions to primate after an extended silent incubation period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
*** WDA 2016 NEW YORK ***
*** We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions.
Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders
Volume 23, Number 9—September 2017
Research Letter Chronic Wasting Disease Prion Strain Emergence and Host Range Expansion
***Thus, emergent CWD prion strains may have higher zoonotic potential than common strains.
2017
Subject: ***CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
Chronic Wasting Disease (CWD)
Prevention
* Strongly consider having the deer or elk tested for CWD before you eat the meat.
* If you have your deer or elk commercially processed, consider asking that your animal be processed individually to avoid mixing meat from multiple animals.
* If your animal tests positive for CWD, do not eat meat from that animal.
> 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).***
TUESDAY, SEPTEMBER 12, 2017
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
SATURDAY, JANUARY 27, 2018
CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018
Prion 2017 Conference Abstracts CWD
2017 PRION CONFERENCE
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1
University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen
This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves.
Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice.
At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.
PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS
Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO
PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS
*** PRION 2017 CONFERENCE VIDEO
TUESDAY, JUNE 13, 2017
PRION 2017 CONFERENCE ABSTRACT
First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress
TUESDAY, JULY 04, 2017
*** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***
***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***
SATURDAY, JULY 29, 2017
Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC
Tuesday, December 20, 2011
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011
The CWD infection rate was nearly 80%, the highest ever in a North American captive herd. RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.
SUMMARY:
captive deer farmers breeders entitlement program, i.e. indemnity program, why?
how many states have $465,000., and can quarantine and purchase there from, each cwd said infected farm, but how many states can afford this for all the cwd infected cervid game ranch type farms, and why do tax payers have to pay for it ???
For Immediate Release Thursday, October 2, 2014
Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov
*** TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease ***
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD).
For Immediate Release
Thursday, October 2, 2014
Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov Share on facebook Share on twitter Share on email Share on print More Sharing Services 1
TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD). The owners of the quarantined herd have entered into a fence maintenance agreement with the Iowa Department of Agriculture and Land Stewardship, which requires the owners to maintain the 8’ foot perimeter fence around the herd premises for five years after the depopulation was complete and the premises had been cleaned and disinfected
CWD is a progressive, fatal, degenerative neurological disease of farmed and free-ranging deer, elk, and moose. There is no known treatment or vaccine for CWD. CWD is not a disease that affects humans.
On July 18, 2012, USDA Animal and Plant Health Inspection Service’s (APHIS) National Veterinary Services Lab in Ames, IA confirmed that a male white tail deer harvested from a hunting preserve in southeast IA was positive for CWD. An investigation revealed that this animal had just been introduced into the hunting preserve from the above-referenced captive deer herd in north-central Iowa.
The captive deer herd was immediately quarantined to prevent the spread of CWD. The herd has remained in quarantine until its depopulation on August 25 to 27, 2014.
The Iowa Department of Agriculture and Land Stewardship participated in a joint operation to depopulate the infected herd with USDA Veterinary Services, which was the lead agency, and USDA Wildlife Services.
Federal indemnity funding became available in 2014. USDA APHIS appraised the captive deer herd of 376 animals at that time, which was before depopulation and testing, at $1,354,250. At that time a herd plan was developed with the owners and officials from USDA and the Iowa Department of Agriculture and Land Stewardship.
Once the depopulation was complete and the premises had been cleaned and disinfected, indemnity of $917,100.00 from the USDA has been or will be paid to the owners as compensation for the 356 captive deer depopulated.
The Iowa Department of Agriculture and Land Stewardship operates a voluntary CWD program for farms that sell live animals. Currently 145 Iowa farms participate in the voluntary program. The above-referenced captive deer facility left the voluntary CWD program prior to the discovery of the disease as they had stopped selling live animals. All deer harvested in a hunting preserve must be tested for CWD.
-30-
79.8 percent of the deer tested positive for the disease
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD). The owners of the quarantined herd have entered into a fence maintenance agreement with the Iowa Department of Agriculture and Land Stewardship, which requires the owners to maintain the 8’ foot perimeter fence around the herd premises for five years after the depopulation was complete and the premises had been cleaned and disinfected
CWD is a progressive, fatal, degenerative neurological disease of farmed and free-ranging deer, elk, and moose. There is no known treatment or vaccine for CWD. CWD is not a disease that affects humans.
On July 18, 2012, USDA Animal and Plant Health Inspection Service’s (APHIS) National Veterinary Services Lab in Ames, IA confirmed that a male white tail deer harvested from a hunting preserve in southeast IA was positive for CWD. An investigation revealed that this animal had just been introduced into the hunting preserve from the above-referenced captive deer herd in north-central Iowa.
The captive deer herd was immediately quarantined to prevent the spread of CWD. The herd has remained in quarantine until its depopulation on August 25 to 27, 2014.
The Iowa Department of Agriculture and Land Stewardship participated in a joint operation to depopulate the infected herd with USDA Veterinary Services, which was the lead agency, and USDA Wildlife Services.
Federal indemnity funding became available in 2014. USDA APHIS appraised the captive deer herd of 376 animals at that time, which was before depopulation and testing, at $1,354,250. At that time a herd plan was developed with the owners and officials from USDA and the Iowa Department of Agriculture and Land Stewardship.
Once the depopulation was complete and the premises had been cleaned and disinfected, indemnity of $917,100.00 from the USDA has been or will be paid to the owners as compensation for the 356 captive deer depopulated.
The Iowa Department of Agriculture and Land Stewardship operates a voluntary CWD program for farms that sell live animals. Currently 145 Iowa farms participate in the voluntary program. The above-referenced captive deer facility left the voluntary CWD program prior to the discovery of the disease as they had stopped selling live animals. All deer harvested in a hunting preserve must be tested for CWD.
INFORM: Cervid Health and States Indemnity FY 2015
USDA Animal and Plant Health Inspection Service sent this bulletin at 09/19/2014 05:22 PM EDT
Animal and Plant Health Inspection Service (APHIS), Veterinary Services (VS) received a total of $3 million in appropriated funding to support cervid health activities in fiscal year (FY) 2014, and made approximately $1.0 million of this funding available for indemnity of chronic wasting disease (CWD) positive, suspect, and exposed farmed cervids. All of the available FY2014 indemnity funding was used to depopulate three CWD-infected herds. However, several States have asked about the availability of Federal indemnity funds for CWD-exposed animals in the future.
VS plans to offer Federal indemnity for CWD-exposed cervids beginning in FY2015. Briefly, we will prioritize the highest risk CWD-exposed animals for indemnity based on the availability of funding. Any newly reported CWD-positive herds will be considered for indemnity as they are identified, based first on funding availability and secondly on the risk presented by the herd.
We will reassess our fiscal year funding on a quarterly basis so that providing indemnity for exposed animals does not exhaust available funding early in the fiscal year. By taking this fiscally cautious approach, we hope to provide indemnity for positive herds identified later in the fiscal year while removing high-risk animals from the landscape as soon as possible to minimize the risk for disease spread. Further, removal and testing of these exposed animals will provide a better understanding of the disease risk presented by these animals/herds.
VS plans to work with our State and industry stakeholders on the criteria to assess the risk and on the process through which States can request this indemnity. These will be finalized in a VS Guidance Document in the near future. We look forward to working with you to implement this process in the coming year.
***
FRIDAY, FEBRUARY 23, 2018
Pennsylvania NEW CWD MANAGEMENT AREA TO BE ANNOUNCED
MONDAY, FEBRUARY 12, 2018
Pennsylvania CWD TSE Prion has been found in captive deer in Huntingdon and Lancaster counties
WEDNESDAY, FEBRUARY 21, 2018
Maryland Chronic Wasting Disease CWD TSE Prion Found In Ten Deer Allegany and Washington Counties
SATURDAY, FEBRUARY 17, 2018
Montana Special Hunts 9 more cases CWD TSE Prion to date, more samples still pending
FRIDAY, FEBRUARY 09, 2018
Mississippi Chronic Wasting Disease confirmed in a White-tailed Deer
TUESDAY, FEBRUARY 13, 2018
*** MISSISSIPPI STATE DEPARTMENT OF HEALTH Chronic Wasting Disease: Public Health Recommendations ***
WEDNESDAY, NOVEMBER 22, 2017
Minnesota Chronic Wasting Disease discovered in Winona County farm
FRIDAY, NOVEMBER 24, 2017
Todd Robbins-Miller President of Minnesota Deer Farmers Association is oblivious to Chronic Wasting CWD TSE PRION DISEASE risk factors
WEDNESDAY, FEBRUARY 21, 2018
TEXAS TPWD CWD TSE PRION 2 MORE FROM BREEDER RELEASE SITE TOTALS 81 CASES TO DATE
WEDNESDAY, JANUARY 24, 2018
TEXAS CHRONIC WASTING DISEASE CWD TSE PRION MOUNTING, JUMPS TO 79 CASES TO DATE
FRIDAY, FEBRUARY 16, 2018
Texas Deer Breeders Continue fight against the state’s wildlife agency and its regulations trying to contain CWD TSE Prion
WEDNESDAY, FEBRUARY 07, 2018
New Mexico Bans All Live Cervid Importation Due To CWD TSE Prion still NO Final 2017 Positives Update for N.M.
FRIDAY, FEBRUARY 09, 2018
Virginia 2017 Hunt Confirms 16 Cases Chronic Wasting Disease CWD TSE Prion
MONDAY, FEBRUARY 05, 2018
Nebraska Chronic Wasting Disease CWD TSE Prion 2017 Survey Confirms 203 Positives From 1,807 Deer Sampled
SATURDAY, FEBRUARY 03, 2018
Arkansas Reports 346 Positive CWD TSE Prion cases found as of January 8, 2018
THURSDAY, FEBRUARY 08, 2018
Utah Chronic Wasting Disease CWD TSE Prion Update to date from 2017 Hunting Season
TUESDAY, JANUARY 30, 2018
Colorado Chronic Wasting Disease CWD TSE Prion 7/2015-6/2016 Results (2017?)
THURSDAY, JANUARY 25, 2018
Ohio Chronic Wasting Disease CWD TSE Prioin aka mad deer update 2016-2017 SEASON SUMMARY
SATURDAY, JANUARY 20, 2018
Pennsylvania CWD TSE Prion Cases Explodes 51 deer from the 2017-18 hunting seasons have tested positive for CWD majority of samples collected still are being analyzed
WEDNESDAY, JANUARY 24, 2018
Illinois Chronic Wasting Disease CWD TSE Prion cases mounting with 75 confirmed 2017 and 685 total to date
THURSDAY, FEBRUARY 08, 2018
Iowa DNR Wayne County Confirms CWD with 7 additional CWD positive tests so far from deer in northeast from 2017 season
SATURDAY, FEBRUARY 10, 2018
Chronic wasting disease management in ranched elk using rectal biopsy testing Research Paper 09 Feb 2018
January 14, 2018
Michigan’s Chronic Wasting Disease Working Group Recommendations Report to the Natural Resources Commission Prepared December 2017 CWD Confirmed Cases holding for now at 57 cases
Michigan UPDATE, see also ;
Addressing deer disease: DNR, MSU collaborate on deer movement study in south-central Michigan
Contact: Dwayne Etter (DNR), 517-284-4725 or David Williams (MSU), 517-917-0716 Agency: Natural Resources
Jan. 30, 2018
Michigan State University and the Michigan Department of Natural Resources will be placing location-tracking collars on white-tailed deer in south-central Michigan as part of a multiyear study of deer disease, including chronic wasting disease.
January 14, 2018
Missouri MDC REPORTS 15 NEW CASES OF CWD TSE Prion in Deer
MONDAY, JANUARY 29, 2018
Wyoming, Hanna, WGFD diagnosed chronic wasting disease (CWD) for the first time in Deer Hunt Area 161
MONDAY, JANUARY 29, 2018
North Dakota CWD Confirmed whitetail buck and a mule deer doe 2017 deer gun season from unit 3F2
SUNDAY, FEBRUARY 18, 2018
Chronic Wasting Disease CWD TSE Prion RoundUp February 18, 2018
TUESDAY, DECEMBER 12, 2017
*** Chronic Wasting Disease CWD TSE Prion (aka mad deer disease) Update USA December 14, 2017 ***
(zoonosis and environmental risk factors towards the bottom, after state by state reports)
MONDAY, MARCH 13, 2017
CHRONIC WASTING DISEASE CWD TSE PRION UDATE March 13, 2017
SATURDAY, JANUARY 14, 2017
CHRONIC WASTING DISEASE CWD TSE PRION GLOBAL UPDATE JANUARY 14, 2017
Sunday, June 23, 2013
National Animal Health Laboratory Network Reorganization Concept Paper (Document ID APHIS-2012-0105-0001)
***Terry S. Singeltary Sr. submission
Singeltary submission ;
Program Standards: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose
DOCUMENT ID: APHIS-2006-0118-0411
***Singeltary submission
Singeltary submission ;
Program Standards: Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose
*** DOCUMENT ID: APHIS-2006-0118-0411
SUNDAY, FEBRUARY 11, 2018
Experimental sheep BSE prions generate the vCJD phenotype when serially passaged in transgenic mice expressing human prion protein
Detection of PrPBSE and prion infectivity in the ileal Peyer’s patch of young calves as early as 2 months after oral challenge with classical bovine spongiform encephalopathy
Ivett Ackermann, Anne Balkema-Buschmann, Reiner Ulrich, Kerstin Tauscher, James C. Shawulu, Markus Keller, Olanrewaju I. Fatola, Paul Brown and Martin H. GroschupEmail authorView ORCID ID profile
Veterinary Research201748:88
https://doi.org/10.1186/s13567-017-0495-5© The Author(s) 2017
Received: 22 August 2017Accepted: 1 December 2017Published: 19 December 2017
Abstract
In classical bovine spongiform encephalopathy (C-BSE), an orally acquired prion disease of cattle, the ileal Peyer’s patch (IPP) represents the main entry port for the BSE agent. In earlier C-BSE pathogenesis studies, cattle at 4–6 months of age were orally challenged, while there are strong indications that the risk of infection is highest in young animals. In the present study, unweaned calves aged 4–6 weeks were orally challenged to determine the earliest time point at which newly formed PrPBSE and BSE infectivity are detectable in the IPP. For this purpose, calves were culled 1 week as well as 2, 4, 6 and 8 months post-infection (mpi) and IPPs were examined for BSE infectivity using a bovine PrP transgenic mouse bioassay, and for PrPBSE by immunohistochemistry (IHC) and protein misfolding cyclic amplification (PMCA) assays. For the first time, BSE prions were detected in the IPP as early as 2 mpi by transgenic mouse bioassay and PMCA and 4 mpi by IHC in the follicular dendritic cells (FDCs) of the IPP follicles. These data indicate that BSE prions propagate in the IPP of unweaned calves within 2 months of oral uptake of the agent.
snip...
In summary, our study demonstrates for the first time PrPBSE (by PMCA) and prion infectivity (by mouse bioassay) in the ileal Peyer’s patch (IPP) of young calves as early as 2 months after infection. From 4 mpi nearly all calves showed PrPBSE positive IPP follicles (by IHC), even with PrPBSE accumulation detectable in FDCs in some animals. Finally, our results confirm the IPP as the early port of entry for the BSE agent and a site of initial propagation of PrPBSE and infectivity during the early pathogenesis of the disease. Therefore, our study supports the recommendation to remove the last four metres of the small intestine (distal ileum) at slaughter, as designated by current legal requirements for countries with a controlled BSE risk status, as an essential measure for consumer and public health protection.
FRIDAY, DECEMBER 22, 2017
Detection of PrPBSE and prion infectivity in the ileal Peyer’s patch of young calves as early as 2 months after oral challenge with classical bovine spongiform encephalopathy
Thursday, November 16, 2017
Texas Natural Meats Recalls Beef Products Due To Possible Specified Risk Materials Contamination
*** Subject: USA CJD, BSE, SCRAPIE, CWD, TSE PRION END OF YEAR REPORTS 2017
TUESDAY, DECEMBER 12, 2017
Bovine Spongiform Encephalopathy BSE TSE Prion (aka mad cow disease) Report December 14, 2017 2017
TUESDAY, DECEMBER 12, 2017
Chronic Wasting Disease CWD TSE Prion (aka mad deer disease) Update USA December 14, 2017
FRIDAY, DECEMBER 15, 2017
Canada CFIA updating its national CWD TSE PRION efforts to eradicate disease farmed cervid NOT successful December 14, 2017
TUESDAY, DECEMBER 12, 2017
SCRAPIE TSE PRION UPDATE USA DECEMBER 14, 2017
USAHA 2017 RESOLUTIONS
RESOLUTION NUMBER: 23
APPROVED AS AMENDED SOURCE: COMMITTEE ON WILDLIFE AND CAPTIVE WILDLIFE
SUBJECT MATTER: Annual Reporting on Chronic Wasting Disease Epidemiological Data
BACKGROUND INFORMATION: Chronic wasting disease (CWD) has been recognized in wild cervids since the 1980’s. Availability of complete epidemiological information is critical for evaluating the effectiveness of science-based disease control programs. Access to pertinent information from epidemiological investigations across the country in wild populations is imperative to developing success strategies for managing the disease. More comprehensive information is needed on CWD epidemiology in the affected wild populations. Analysis of data from CWD affected populations across the country will improve risk assessment. Comprehensive epidemiological data evaluation may potentially identify factors contributing to the detection of CWD, enhance mitigation strategies to reduce the likelihood of CWD in new populations, and facilitate its earliest detection when it is present.
RESOLUTION: The United States Animal Health Association (USAHA) requests the United States Department of Agriculture (USDA), Animal and Plant Health Inspection Service, Veterinary Services and other appropriate federal and state agencies to work cooperatively to assemble, analyze, summarize, and make available annually to the Committee on Wildlife and Captive Wildlife at the USAHA meeting all pertinent information from epidemiological investigations of Chronic Wasting Disease (CWD) in cervid populations (including wild, free-ranging, and captive).
Specific information requested may include:
1) Compiled CWD testing data from each state to include:
a) Overall state testing numbers of each susceptible species tested;
b) Number of CWD positive tests found annually in each state;
c) Overall state testing in wild populations;
d) Prevalence of CWD in positive populations;
e) Population totals for each susceptible species of wild herds in each state;
f) Demography of positive and negative animals in infected herds;
g) Results from all tissues that were tested;
h) Duration of monitoring prior to detection of the first case - including numbers of animals in the herd, numbers tested, and numbers not tested;
i) Results of trace-forward and trace-back investigations; and
j) All other pertinent data that will enhance risk assessment of CWD in cervids and identification of effective mitigation measures.
2) Compiled data should also be posted on the USDA website.
http://www.usaha.org/upload/Resolution/2017/Resolution_23_CWD_Data.pdf
RESOLUTION NUMBER: 21 APPROVED SOURCE: COMMITTEE ON SHEEP, GOATS AND CAMELIDS SUBJECT MATTER: National Scrapie Eradication Program Funding
BACKGROUND INFORMATION: Due to the success of the cooperative National Scrapie Eradication Program, no new cases of scrapie have been identified in the United States (US) in the past 18 months. There are key components of the program that have been critical to this success and the effort to have the US be recognized internationally as free from scrapie, which would open new markets to US sheep and goat products. Surveillance and traceability are vital to this eradication program. Program use of sheep and goat official tags have demonstrated that official plastic tags are preferred over metal tags for readability and to reduce safety concerns. Funding for tags that are readable, acceptable to producers and efficient for regulators is essential to continue identification compliance and progress of the program.
RESOLUTION: The United States Animal Health Association urges the United States Secretary of Agriculture to request a congressional appropriation of five million additional dollars of new money to be added to the Equine, Cervid and Small Ruminant health line for the purpose of supporting Small Ruminant Health Programs to complete the eradication of scrapie and assure program success. It is vital that this new funding does not reduce other current United States Department of Agriculture, Animal and Plant Health Inspection Service, Veterinary Services program funding lines.
lol, drop in the bucket and a band-aid approach to something that needed a tourniquet decades ago...
TUESDAY, DECEMBER 12, 2017
Creutzfeldt Jakob Disease CJD National Prion Disease Pathology Surveillance Center Cases Examined to December 14, 2017
THURSDAY, FEBRUARY 15, 2018
Iatrogenic Creutzfeldt-Jakob disease with Amyloid-β pathology: an international study
WEDNESDAY, NOVEMBER 1, 2017
Blood-derived amyloid-β protein induces Alzheimer’s disease pathologies
http://betaamyloidcjd.blogspot.com/2017/11/blood-derived-amyloid-protein-induces.html
Alzheimer’s disease, iatrogenic, and Transmissible Spongiform Encephalopathy TSE Prion disease, that is the question ???
>>> The only tenable public line will be that "more research is required’’ <<<
>>> possibility on a transmissible prion remains open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?
[9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. There are also results to be made available shortly (1) concerning a farmer with CJD who had BSE animals, (2) on the possible transmissibility of Alzheimer’s and (3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.]
https://web.archive.org/web/20170126060344/http://collections.europarchive.org/tna/20080102232842/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf
https://web.archive.org/web/20040315075058/http://www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf
https://web.archive.org/web/20040315075058/www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf
snip...see full Singeltary Nature comment here;
http://www.nature.com/nature/journal/v525/n7568/full/nature15369.html#/comments
see Singeltary comments to Plos ;
Subject: 1992 IN CONFIDENCE TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES POSSIBILITY ON A TRANSMISSIBLE PRION REMAINS OPEN
BSE101/1 0136
IN CONFIDENCE
CMO
From: . Dr J S Metiers DCMO 4
November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognised the public sensitivity of these findings and intend to report them in their proper context. 'This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed". As the report emphasises the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible. what are the implications for public health?
3. The route 'of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk.
However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed. 1
92/11.4/1.1
BSE101/1 0137 4.
The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion.
The only tenable public line will be that "more research is required’’ before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.
J S METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832 llllYc!eS 2 92/11.4/1.2
https://web.archive.org/web/20160320084827/http://collections.europarchive.org/tna/20081106170650/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf
>>> The only tenable public line will be that "more research is required’’ <<<
>>> possibility on a transmissible prion remains open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?
Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015)
snip...see full Singeltary Nature comment here;
Alzheimer's disease
let's not forget the elephant in the room. curing Alzheimer's would be a great and wonderful thing, but for starters, why not start with the obvious, lets prove the cause or causes, and then start to stop that. think iatrogenic, friendly fire, or the pass it forward mode of transmission. think medical, surgical, dental, tissue, blood, related transmission. think transmissible spongiform encephalopathy aka tse prion disease aka mad cow type disease...
Commentary: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
http://journals.plos.org/plosone/article/comment?id=info:doi/10.1371/annotation/933cc83a-a384-45c3-b3b2-336882c30f9d
https://www.frontiersin.org/articles/10.3389/fnagi.2016.00005/full
Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease
*** Singeltary comment PLoS ***
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
http://www.plosone.org/annotation/listThread.action?root=82860
Ann N Y Acad Sci. 1982;396:131-43.
Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).
Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.
Abstract
Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD.
http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.1982.tb26849.x/abstract
Sunday, November 22, 2015
*** Effect of heating on the stability of amyloid A (AA) fibrils and the intra- and cross-species transmission of AA amyloidosis
Abstract
Amyloid A (AA) amyloidosis is a protein misfolding disease characterized by extracellular deposition of AA fibrils. AA fibrils are found in several tissues from food animals with AA amyloidosis. For hygienic purposes, heating is widely used to inactivate microbes in food, but it is uncertain whether heating is sufficient to inactivate AA fibrils and prevent intra- or cross-species transmission. We examined the effect of heating (at 60 °C or 100 °C) and autoclaving (at 121 °C or 135 °C) on murine and bovine AA fibrils using Western blot analysis, transmission electron microscopy (TEM), and mouse model transmission experiments. TEM revealed that a mixture of AA fibrils and amorphous aggregates appeared after heating at 100 °C, whereas autoclaving at 135 °C produced large amorphous aggregates. AA fibrils retained antigen specificity in Western blot analysis when heated at 100 °C or autoclaved at 121 °C, but not when autoclaved at 135 °C. Transmissible pathogenicity of murine and bovine AA fibrils subjected to heating (at 60 °C or 100 °C) was significantly stimulated and resulted in amyloid deposition in mice. Autoclaving of murine AA fibrils at 121 °C or 135 °C significantly decreased amyloid deposition. Moreover, amyloid deposition in mice injected with murine AA fibrils was more severe than that in mice injected with bovine AA fibrils. Bovine AA fibrils autoclaved at 121 °C or 135 °C did not induce amyloid deposition in mice. These results suggest that AA fibrils are relatively heat stable and that similar to prions, autoclaving at 135 °C is required to destroy the pathogenicity of AA fibrils. These findings may contribute to the prevention of AA fibril transmission through food materials to different animals and especially to humans.
Purchase options Price * Issue Purchase USD 511.00 Article Purchase USD 54.00
http://www.tandfonline.com/doi/abs/10.3109/13506129.2015.1095735?journalCode=iamy20
http://betaamyloidcjd.blogspot.com/2015/11/effect-of-heating-on-stability-of.html
Blood-derived amyloid-β protein induces Alzheimer’s disease pathologies
http://betaamyloidcjd.blogspot.com/2017/11/blood-derived-amyloid-protein-induces.html
Alzheimer’s disease, iatrogenic, and Transmissible Spongiform Encephalopathy TSE Prion disease, that is the question ???
>>> The only tenable public line will be that "more research is required’’ <<<
>>> possibility on a transmissible prion remains open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?
[9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. There are also results to be made available shortly (1) concerning a farmer with CJD who had BSE animals, (2) on the possible transmissibility of Alzheimer’s and (3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.]
https://web.archive.org/web/20170126060344/http://collections.europarchive.org/tna/20080102232842/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf
https://web.archive.org/web/20040315075058/http://www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf
https://web.archive.org/web/20040315075058/www.bseinquiry.gov.uk/files/yb/1992/12/16005001.pdf
snip...see full Singeltary Nature comment here;
http://www.nature.com/nature/journal/v525/n7568/full/nature15369.html#/comments
see Singeltary comments to Plos ;
Subject: 1992 IN CONFIDENCE TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES POSSIBILITY ON A TRANSMISSIBLE PRION REMAINS OPEN
BSE101/1 0136
IN CONFIDENCE
CMO
From: . Dr J S Metiers DCMO 4
November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have recognised the public sensitivity of these findings and intend to report them in their proper context. 'This hopefully will avoid misunderstanding and possible distortion by the media to portray the results as having more greater significance than the findings so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection) the researchers have demonstrated the transmission of a pathological process from two cases one of severe Alzheimer's disease the other of Gerstmann-Straussler disease to marmosets. However they have not demonstrated the transmission of either clinical condition as the "animals were behaving normally when killed". As the report emphasises the unanswered question is whether the disease condition would have revealed itself if the marmosets had lived longer. They are planning further research to see if the conditions, as opposed to the partial pathological process, is transmissible. what are the implications for public health?
3. The route 'of transmission is very specific and in the natural state of things highly unusual. However it could be argued that the results reveal a potential risk, in that brain tissue from these two patients has been shown to transmit a pathological process. Should therefore brain tissue from such cases be regarded as potentially infective? Pathologists, morticians, neuro surgeons and those assisting at neuro surgical procedures and others coming into contact with "raw" human brain tissue could in theory be at risk.
However, on a priori grounds given the highly specific route of transmission in these experiments that risk must be negligible if the usual precautions for handling brain tissue are observed. 1
92/11.4/1.1
BSE101/1 0137 4.
The other dimension to consider is the public reaction. To some extent the GSS case demonstrates little more than the transmission of BSE to a pig by intra-cerebral injection. If other prion diseases can be transmitted in this way it is little surprise that some pathological findings observed in GSS were also transmissible to a marmoset. But the transmission of features of Alzheimer's pathology is a different matter, given the much greater frequency of this disease and raises the unanswered question whether some cases are the result of a transmissible prion.
The only tenable public line will be that "more research is required’’ before that hypothesis could be evaluated. The possibility on a transmissible prion remains open. In the meantime MRC needs carefully to consider the range and sequence of studies needed to follow through from the preliminary observations in these two cases. Not a particularly comfortable message, but until we know more about the causation of Alzheimer's disease the total reassurance is not practical.
J S METTERS Room 509 Richmond House Pager No: 081-884 3344 Callsign: DOH 832 llllYc!eS 2 92/11.4/1.2
https://web.archive.org/web/20160320084827/http://collections.europarchive.org/tna/20081106170650/http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf
>>> The only tenable public line will be that "more research is required’’ <<<
>>> possibility on a transmissible prion remains open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?
Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015)
snip...see full Singeltary Nature comment here;
Alzheimer's disease
let's not forget the elephant in the room. curing Alzheimer's would be a great and wonderful thing, but for starters, why not start with the obvious, lets prove the cause or causes, and then start to stop that. think iatrogenic, friendly fire, or the pass it forward mode of transmission. think medical, surgical, dental, tissue, blood, related transmission. think transmissible spongiform encephalopathy aka tse prion disease aka mad cow type disease...
Commentary: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy
http://journals.plos.org/plosone/article/comment?id=info:doi/10.1371/annotation/933cc83a-a384-45c3-b3b2-336882c30f9d
https://www.frontiersin.org/articles/10.3389/fnagi.2016.00005/full
Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease
*** Singeltary comment PLoS ***
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
http://www.plosone.org/annotation/listThread.action?root=82860
Ann N Y Acad Sci. 1982;396:131-43.
Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease).
Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC.
Abstract
Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD.
http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.1982.tb26849.x/abstract
Sunday, November 22, 2015
*** Effect of heating on the stability of amyloid A (AA) fibrils and the intra- and cross-species transmission of AA amyloidosis
Abstract
Amyloid A (AA) amyloidosis is a protein misfolding disease characterized by extracellular deposition of AA fibrils. AA fibrils are found in several tissues from food animals with AA amyloidosis. For hygienic purposes, heating is widely used to inactivate microbes in food, but it is uncertain whether heating is sufficient to inactivate AA fibrils and prevent intra- or cross-species transmission. We examined the effect of heating (at 60 °C or 100 °C) and autoclaving (at 121 °C or 135 °C) on murine and bovine AA fibrils using Western blot analysis, transmission electron microscopy (TEM), and mouse model transmission experiments. TEM revealed that a mixture of AA fibrils and amorphous aggregates appeared after heating at 100 °C, whereas autoclaving at 135 °C produced large amorphous aggregates. AA fibrils retained antigen specificity in Western blot analysis when heated at 100 °C or autoclaved at 121 °C, but not when autoclaved at 135 °C. Transmissible pathogenicity of murine and bovine AA fibrils subjected to heating (at 60 °C or 100 °C) was significantly stimulated and resulted in amyloid deposition in mice. Autoclaving of murine AA fibrils at 121 °C or 135 °C significantly decreased amyloid deposition. Moreover, amyloid deposition in mice injected with murine AA fibrils was more severe than that in mice injected with bovine AA fibrils. Bovine AA fibrils autoclaved at 121 °C or 135 °C did not induce amyloid deposition in mice. These results suggest that AA fibrils are relatively heat stable and that similar to prions, autoclaving at 135 °C is required to destroy the pathogenicity of AA fibrils. These findings may contribute to the prevention of AA fibril transmission through food materials to different animals and especially to humans.
Purchase options Price * Issue Purchase USD 511.00 Article Purchase USD 54.00
http://www.tandfonline.com/doi/abs/10.3109/13506129.2015.1095735?journalCode=iamy20
http://betaamyloidcjd.blogspot.com/2015/11/effect-of-heating-on-stability-of.html
Sunday, February 25, 2018
PRION ROUND TABLE CONFERENCE 2018 MAY, 22-25 A REVIEW
Terry S. Singeltary Sr.
No comments:
Post a Comment
Note: Only a member of this blog may post a comment.