Wednesday, June 26, 2019

HOUSE COMMITTEE ON NATURAL RESOURCES SUBCOMMITTEE ON OVERSIGHT AND INVESTIGATIONS TESTIMONY TEXAS TPWD

''CWD has also been diagnosed in several free-ranging white-tailed deer harvested on ranches in close proximity to the remaining CWD positive breeding facilities within Medina County in central Texas. Genetic tests performed on those hunter-harvested deer found that the genetic composition of the subject animals were more closely related to deer in nearby captive facilities, as opposed to those in the surrounding free-range population.''

HOUSE COMMITTEE ON NATURAL RESOURCES SUBCOMMITTEE ON OVERSIGHT AND INVESTIGATIONS

Testimony Provided By: Carter P. Smith

Texas Parks and Wildlife Department

25 June, 2019

Washington, D.C.

__________________________________________________________________________

Introduction

Thank you Mr. Chairman and members of this Committee. I appreciate the chance to come before you today to share a few observations from a state perspective surrounding the management of chronic wasting disease (CWD), a serious and far reaching wildlife based issue that has become front and center for our agency since the disease’s unwelcome discovery in far west Texas in 2012. With the emergence of CWD has come considerable impacts, not only from the increased cost of containing the disease’s spread, but just as importantly, from the implications of how best to attenuate its impacts on social, cultural, recreational, and economic values that Texas and Texans hold dear.

We have learned from other states that in the absence of a targeted, proactive, and comprehensive disease management approach, CWD has the potential to directly and indirectly impact the management of Texas’ bountiful deer herds and other wildlife; the recreational pursuits of sportsmen and women; the livelihoods of people and businesses in rural communities;

the economic value of farm, ranch, and timberland properties; and the sale of hunting licenses, which have long been a primary driver of funding to support conservation of all species, not just game animals. Moreover, the ramifications of CWD for Texas and its multi-billion-dollar ranching, hunting, real estate, and wildlife management affiliated economies are expected to be significant, unless the disease can be successfully contained and controlled.

In short, with so much at stake for so many, complacency with this disease is not an option. 

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Deer and Deer Hunting in Texas

By way of background, Texas boasts a white-tailed and mule deer population in excess of 4.5 million deer. Each fall, approximately 840,000 deer hunters, including tens of thousands of nonresidents, take to the woods in pursuit of their favorite quarry and in fulfillment of time honored outdoor passions and heritage. These activities have a significant bearing on our state’s rural economies and communities, many of whom are dependent upon a seasonal influx of deer hunters who infuse in excess of $2 billion in direct expenditures on travel, goods, supplies, equipment, and other purchases that support their hunting-related activities. The vast majority of hunting in Texas occurs on private land. In fact, approximately 95 percent of lands are privately owned, where they are held in a patchwork of over 250,000 individual farms, ranches, timber and forest land, and other interests. For decades, the Real Estate Center at Texas A & M University has tracked rural land trends across the state, including land values (Figure 1) and motivations for owning and enjoying rural land. Since the mid-1990s, the primary motivations for people buying rural land in Texas have been an interest in hunting, wildlife enjoyment, and family recreation in the outdoors, a trend that continues today. Figure 1. Trend in Texas land values, 1971-2016.

$0 $500 $1,000 $1,500 $2,000 $2,500 $3,000

Texas Land Price Data - Nominal Median Price per Acre

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For the majority of Texas landowners, the wildlife species of greatest interest is deer, an emphasis that is reflected in voluntary wildlife management plans that Texas Parks and Wildlife Department (TPWD) holds with landowners across tens of millions of acres of privately managed properties.

Ensuring the health and vitality of our state’s deer populations on those lands, both free-range and captive, and the public’s confidence in the health and management of those deer herds, is foundational to the future of our state’s rural land values, our real estate markets, the voluntary cooperation of landowners in managing wildlife on private lands, and the local communities who depend upon the value of those lands for their tax base.

Management of Chronic Wasting Disease in Texas

State Authority

State fish and wildlife agencies are charged with managing and conserving public trust resources for the enjoyment and use of the states’ citizens, present and future. Given this important responsibility, these agencies are on the front lines in confronting the real and insidious threats associated with CWD. In Texas, TPWD has jurisdiction over native cervid species, i.e., whitetailed deer and mule deer, including approximately 1,000 captive deer breeding facilities containing around 75,000 deer.

Other cervids susceptible to CWD including elk, red deer, and sika deer are considered exotic livestock and fall under the jurisdiction of our sister agency, the Texas Animal Health Commission (TAHC), which administers the voluntary Herd Certification Program for interstate movement of captive cervids. Because of the important interface in Texas between free-range and captive native and exotic cervids, TPWD and TAHC work very closely in our efforts to combat further spread of CWD in Texas.

Landowner Cooperation

Any successful and sustainable CWD management strategy in Texas must be initiated and implemented with the trust and cooperation of private landowners. Because of the state’s 

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predominant make-up as a private lands dominated state, any effective wildlife and conservation related measure carried out at any kind of scale must be done through collaborative partnerships with landowners.

These landowners, in many cases, derive a significant amount of income from hunting leases, or simply enjoy having and observing deer on their property. This is particularly relevant given the adverse impacts this disease can have on white-tailed deer (Edmunds et al. 2016, Foley et al. 2016), mule deer (Miller at al. 2008, DeVivo 2015, and elk populations (Monello et al. 2014), as well as the adverse impacts this disease can have on hunters’ behavior (Needham et al. 2007, Vaske 2009, Zimmer 2012, Haus et al. 2017). For example, human dimensions research indicates that hunters will avoid hunting in areas of high CWD prevalence (Haus et al. 2017). Aside from this information, it stands to reason that if CWD is allowed to become established, increase through time, and ultimately result in deer population declines, the simple absence of sufficient numbers of deer would also negatively impact deer hunting participation. Such factors would have very detrimental impacts on landowner interest, participation, and support of deer, deer management, deer hunting, and other affiliated activities and economies.

Actively engaging landowners about the gravity of CWD and sharing options available to them to help with the arrest of the disease’s spread and prevalence are therefore essential in obtaining and maintaining their support and confidence in agency disease management efforts. Some of the adaptive management strategies for CWD control involving targeted removal of animals and/or substantially limiting concentration of animals in free range settings on private land are not as easily instituted in Texas as they may be in states that have larger areas of public land. That being said, many Texas landowners fully expect, and in fact demand, TPWD take appropriate action to control the disease and are supportive of measures that help minimize further risk of spread, particularly from areas that are high risk and/or are already known to possess the disease. To that end, TPWD has enjoyed strong support in its CWD management efforts from the state’s largest landowner organizations including the Texas and Southwestern Cattle Raiser’s Association and the Texas Wildlife Association.

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Factors Further Compounding and Influencing the Management of CWD

In attempting to arrest the further spread of CWD, Texas faces the same significant obstacles faced by other states, including the lack of a known treatment and effective prevention measures, disease persistence in the environment, inconspicuous progression of the disease, lack of proven management methods, the lack of funds (along with other limitations) to conduct sound research, and the always-fatal nature of the disease.

Data generated from other states has validated that CWD is an additional mortality factor in deer populations, and data indicate that mortality rates can surpass fawn recruitment in local populations with high CWD prevalence. Several research projects in Colorado (Miller at al. 2008, Monello et al. 2014), Wyoming (DeVivo 2015, Edmunds et al. 2016), and South Texas (Foley et al. 2016) have demonstrated that this additive mortality can have population-level impacts including a shift in age structure (to younger-aged animals) and a declining population. CWD does not have the immediate short-term impacts to deer populations that we see with some other diseases such as anthrax or epizootic hemorrhagic disease (EHD); however, insidious, persistent diseases that increase in prevalence in early years with no noticeable impacts, such as CWD, may be more likely to influence long-term population dynamics. CWD prevalence is much higher and has increased more rapidly in some populations than what is often proclaimed. In a publication describing the lessons learned from CWD management attempts during the first five decades of its known existence, Miller and Fischer (2016) concluded that heavily-infected cervid populations will not thrive.

Once CWD becomes established in a free-ranging deer population, it is unlikely that it can be eradicated, and containment and control at the local scale will depend on numerous variables that include deer densities and deer movement barriers. However, CWD can be contained in a specific area (i.e., not moved to other areas) or within a captive deer breeding facility by ceasing the movement of live deer, as well as the transport of those carcass parts that are likely to contain the prions from these infected populations. Efficacious sampling must occur to determine if a population or populations are infected with CWD. Early detection is critical for disease containment, but effective sampling can and has put a severe strain on already lean state budgets. 

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History and Distribution of CWD in Texas

In Texas, CWD was first discovered in 2012 in free-ranging mule deer in the Hueco Mountains near the Texas–New Mexico border. It has since been detected in free-ranging elk, mule deer, and white-tailed deer in the northwest Panhandle, and in five (5) captive white-tailed deer breeding facilities in central and south-central Texas (Figure 2). To date, three (3) of those facilities have been depopulated and closed, leaving only two (2) CWD-positive deer breeding facilities operating under the guidance of a TAHC CWD Herd and Facilities Management Plan. CWD has also been diagnosed in several free-ranging white-tailed deer harvested on ranches in close proximity to the remaining CWD positive breeding facilities within Medina County in central Texas. Genetic tests performed on those hunter-harvested deer found that the genetic composition of the subject animals were more closely related to deer in nearby captive facilities, as opposed to those in the surrounding free-range population. These findings highlight the important disease nexus between captive and free-ranging cervids and underscore the criticality of comprehensive CWD management strategies that address all CWD risk on the landscape. As of June 20, 2019, there have been 144 CWD-positives detected in Texas (Table 1).

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Figure 2. CWD Zones in Texas.

CWD Zone Species Total

Trans Pecos Mule Deer - Free Range 19

Panhandle

Mule Deer - Free Range 7

Elk - Free Range 1

White-tailed Deer - Free Range 4

South-Central Texas

White-tailed Deer - Free Range 3

White-tailed Deer - Breeder Pen 94

White-tailed Deer - Breeder Release Site 14

Elk - Breeder Release Site 2

Grand Total 144

Table 1. Number of CWD-positive deer or elk in Texas by geographic region, as of June 20, 2019.

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Texas CWD Management Plan Implementation

Keeping CWD contained within the three existing geographic nodes where it currently is known to exist is a high priority for both TPWD and TAHC, as well as sportsmen, landowners, wildlife managers, and others concerned about its further spread. To that end, precautionary and proactive disease management principles of early detection and rapid containment have been guiding tenets of the state’s philosophy and response in combating the disease.

Consistent with our state’s culture and circumstances, Texas has implemented what we believe are the most tenable, balanced, and prudent measures available to manage CWD. The three primary goals of our CWD management plan are:

• Minimize CWD risks to free-ranging and captive white-tailed deer, mule deer, and other susceptible species in Texas;

• Establish and maintain support for prudent CWD management with hunters, landowners, and other stakeholders; and

• Minimize direct and indirect impacts of CWD to hunting, hunting related economies, and conservation in Texas.

The principle strategy of early detection includes adequate surveillance, as well as enhanced testing requirements for individuals permitted to move live deer, all designed to increase the probability of detecting CWD where it exists and before it is moved. With the initial detection of CWD in 2012 in far west Texas, the Texas Parks and Wildlife (TPW) Commission, the governing board for TPWD, adopted regulations for this area of the state designed to increase CWD testing efforts through mandatory hunter harvest testing and restrictions on live deer movement. When CWD was detected in a captive deer breeding facility in Medina County in the summer of 2015 TPWD enacted measures statewide in an effort to arrest the spread of this disease.

To further understand the geographic extent and prevalence of the disease, TPWD intensified surveillance efforts beginning with the 2015-16 hunting season. As a point of reference, TPWD collected CWD samples from an average of just over 2,100 free-ranging deer per year between 2002-2015. Surveillance efforts increased in the fall of 2015 resulting in approximately 10,000 samples per year being collected from hunter-harvested deer and road kills during each of the last 4 years.

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In response to the 2015 discovery in a captive breeding facility, TPWD also adopted a comprehensive CWD management rules package to include the establishment of additional CWD Containment Zones and Surveillance Zones, CWD testing requirements for deer harvested within those zones, a suite of enhanced testing options for captive deer breeders to include antemortem (“live”) testing options, and restrictions on movement of live deer and specific carcass parts from regions or facilities of relatively high risk for CWD. Table 2 provides a summary of CWD tests collected from various sources over the last 16 years.

Fiscal Year TPWD Tests Deer Breeder (Post mortem) Deer Breeder (Ante mortem) TTT1 TTP2 Release Site Tests Totals FY 2003 810 ++ N/A 4,351 Not Required Not Required 810 FY 2004 2,920 ++ 2,920 FY 2005 2,782 ++ 2,782 FY 2006 2,594 517 3,111 FY 2007 2,393 886 3,279 FY 2008 2,026 978 3,004 FY 2009 2,218 1,148 3,366 FY 2010 1,973 1,279 3,252 FY 2011 2,571 2,034 4,605 FY 2012 2,069 1,821 329 4,219 FY 2013 2,079 2,153 757 4,989 FY 2014 1,921 2,378 569 4,868 FY 2015 1,847 3,787 561 6,195 FY 2016 10,726 5,314 8,841 548 340 3,798 29,567 FY 2017 9,820 5,058 16,065 287 199 2,996 34,425 FY 2018 9,634 2,183 1,900 309 0 1,302 15,328 Grand 58,383 29,536 26,806 7,711 539 8,096 131,071 Table 2. "Not Detected" CWD Test Results in Texas, FY 2003-2018. 1. Translocation permits 2. Trap and process permits * Subtotals for FY 2003 - FY 2011 do not include TTT test results. * This table presents only Not Detected results (for all FYs), and excludes all inconclusive, location, and positive results from all categories displayed. Breeder deer values include only eligible aged deer, 16 months of age or older.

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The increased testing that resulted from these programmatic and regulatory changes, as well as implementation of TAHC CWD Herd and Facilities Management Plans resulted in the detection of CWD in areas of the state and in facilities where it may not have otherwise been discovered for some time. TAHC CWD Herd and Facilities Management Plan sampling resulted in the detection of two (2) additional captive facilities after the initial discovery in 2015. Ante-mortem testing detected the disease in another captive deer facility, and increased testing of hunterharvested deer by TPWD staff discovered the presence of CWD in the western Panhandle region.

All of these new detections triggered additional TPW Commission approved regulatory changes to prevent the further spread of this disease.

TPWD has had to divert significant financial and personnel resources from other important conservation efforts to support our battle against CWD. Table 3 shows CWD expenditures since 2014, and depicts the seven-fold increase in annual expenditures. Expenditures towards CWD research are expected to increase in coming years so that we can better understand factors that enhance the spread of the disease or strategies that control its spread, but all of these costs pale in comparison to the potential economic ramifications that could occur if CWD gets a more expansive foothold in Texas.

CWD Expenditures FY 14 FY 15 FY 16 FY 17 FY 18 Salary & Fringe $133,001.15 $236,406.51 $1,040,054.87 $948,705.84 $917,463.86 Operating Expenditures $75,784.16 $30,147.16 $512,269.57 $624,636.10 $531,514.59 $208,785.31 $266,553.67 $1,552,324.44 $1,573,341.94 $1,448,978.45 Table 3. TPWD expenditures for CWD Surveillance by Fiscal Year.

More Must Be Done

CWD is a very unique, challenging, and trans-boundary disease that requires thoughtful, targeted, and coordinated investments in surveillance, research and education. And while states must continue to serve as leaders in enacting disease management measures appropriate to their site specific circumstances, the disease must also be addressed more holistically across the nation. To that end, it is imperative that federal and state agencies invest the necessary attention and targeted resources to enhance our understanding of this disease and to develop effective 

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management strategies to arrest its spread and prevalence. Key areas where additional emphasis and support in the management of CWD are needed include:

Research – The scientific community must work more collaboratively to set priorities and to design research projects which ensure investigations are well-designed and translate into effective, practical, and applied solutions. Currently, CWD research is deficient in understanding transmission routes through direct and indirect sources, measuring effective adaptive management strategies, improving diagnostic testing options, specifically for live animal (ante-mortem) testing, and human dimensions work that better assesses stakeholder perspectives about the disease and elements of its risk, threat, and management.

Education – Heightened and coordinated outreach/education strategies are needed to provide the necessary level of awareness to ensure all stakeholders understand the seriousness of this disease and its potential impacts to the public’s big game resources. Information based on science and facts, not fear mongering, that resonates with key audiences is essential. Although messages may need to be tailored for unique CWD management situations facing specific states, developing consistent messages across the nation is necessary.

Testing Methodologies and Lab Capacity – Developing more sensitive and rapid diagnostic tests and/or investing in additional diagnostic facilities to process hunters’ samples more expeditiously is very important to gain hunters’ support for CWD surveillance and management. Receiving test results after hunters have consumed their venison, or after having incurred additional expenses to keep unprocessed venison in edible condition while awaiting test results for extended periods of time are factors leading to hunter frustration and apathy. Such slow processing of samples can leave hunters with the impression that the disease must not be a serious threat.

Detection and Surveillance Capacity – Understanding that early detection is critical for successful CWD containment strategies, additional resources are necessary to conduct adequate CWD surveillance to provide sufficient confidence that the disease would be detected when a small proportion of the population is infected. This requires increased staffing as well as operating funds to cover costs associated with sampling and diagnostic testing.

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Conclusion

In Texas, as in other states across the nation, our proud outdoor and hunting heritage, robust outdoor based economies, wildlife conservation funding, private and public lands conservation, rural land values, and the vitality of our rural communities are of immense importance to our citizens. The continued spread of CWD is a sober and compelling reminder of what is at stake if we fail to take the requisite measures and actions necessary to protect those important values. That responsibility, while best carried out primarily by the states at local levels, would undoubtedly benefit from a more comprehensive focus, as well as certain targeted federal investments in research, education/outreach, and fiscal support to the states.

References

snip...see;


''CWD has also been diagnosed in several free-ranging white-tailed deer harvested on ranches in close proximity to the remaining CWD positive breeding facilities within Medina County in central Texas. Genetic tests performed on those hunter-harvested deer found that the genetic composition of the subject animals were more closely related to deer in nearby captive facilities, as opposed to those in the surrounding free-range population.''

TAHC CWD Scrapie TSE Prion SUMMARY MINUTES OF THE 403 rd COMMISSION MEETING Texas Animal Health Commission May 21, 2019

Summary Minutes of the 403rd Commission Meeting – 5/21/2019

▪ Chronic Wasting Disease • Traces received from affected elk herd in Oklahoma

(SEE UPDATE ON RECENT CAPTIVE CWD OKLAHOMA WEDNESDAY, APRIL 24, 2019 Oklahoma Farmed Elk Lincoln County has tested positive for chronic wasting disease CWD TSE Prion https://chronic-wasting-disease.blogspot.com/2019/04/oklahoma-farmed-elk-lincoln-county-has.html )

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V. Sheep and Goats

A. Scrapie: The first positive scrapie case in Texas since 2008 was identified in the Panhandle in April 2016 and the flock and premises remains under quarantine.

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Summary Minutes of the 403rd Commission Meeting – 5/21/2019

VI. Cervids

A. Chronic Wasting Disease (CWD): Five positive captive breeder herds have been disclosed since July 2015. Three herds are depopulated and two larger herds are managed under a herd plan. In addition, Texas Parks and Wildlife, Texas Veterinary Medical Diagnostic Laboratory, and Texas Animal Health Commission provided a CWD Symposium to address the disease status and current research in diagnostic as well as management strategies to mitigate the disease in Texas. As the state epidemiologist, I had the opportunity to provide the epidemiology of the disease in the 5 captive herds as well as the status of the data collected in collaboration with researchers on the subject. The summary of CWD in Texas by species is provided in Table 3.

Table 3. CWD in Texas by Species and State Fiscal Year (Dec 3, 2018)

Fiscal Year Freeranging Mule Deer Captive WTD Freeranging WTD Capt Ex CWD Susceptible Species Freeranging Elk Total by year

2012 2 0 0 0 0 2

2013 4 0 0 0 0 4

2014 0 0 0 0 0 0

2015 1 4 0 0 0 5

2016 2 21 0 0 0 23

2017 10 8 2 0 1 21

2018 5 69 4 2 0 80

2019 2 6 1 0 0 9

Total 26 108 7 2 1 144

TAHC continues to encourage exotic producers or owners to submit samples on any natural mortalities or hunter harvested exotics annually for CWD sampling. Since May 1, 2018 there has been at total of 215 samples from elk, red stag, or sika deer tested for CWD in Texas. This is a decrease of about 100 total sampled in the previous year (see Table 4 and Figure 3). In addition, Figure 4 was shared by TPWD and provides the numbers of exotics tested through TPWD check stations, road kills, or management areas. To note, the total number of permitted movements of exotics from other states into Texas is provided in Table 5. 

Table 4. Exotic CWD Susceptible Species Surveillance since May 1, 2018

Total Elk Red Deer Sika

General Surveillance 155 46 74 35

Zone Surveillance 16 6 7 3

Positive Herds 44 27 15 2

Total 215 79 96 40

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Summary Minutes of the 403rd Commission Meeting – 5/21/2019

Figure 3. Exotic CWD testing since May 1, 2018

Figure 4. 2018-19 TPWD Exotic Sampling (courtesy of Alan Cain)

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Summary Minutes of the 403rd Commission Meeting – 5/21/2019

Table 5. Number of Exotic CWD Species entering Texas by Fiscal Year

Species 2014 2015 2016 2017 2018 2019

Elk 106 142 104 134 121 102

Red Deer 114 81 172 239 273 347

Sika 0 11 12 0 14 9

Total 220 234 288 373 408 458

Elk Traces outs: In April, Texas was notified by the Oklahoma Department of Agriculture of a newly identified positive CWD elk herd that was in the herd certification program for 20 years. Four Texas elk herds have received elk from this herd dating back to 2014 including herds in Collingsworth, Gillespie, Young, and Bosque counties. Individual herd plans are under development for each one of these premises which will include surveillance on elk, WTD, and/or Mule deer on the premises.

VII. Program Records Activities:

Table 6. Total CVIs received in TX by type

2018 Totals Incoming Outgoing TX to TX

Paper 22353 18255 15895

17-30's 1205 15 2117

GVL 8896 13318 12035

CO/KS 1970 0 0

mCVI / AgView 3057 182 120

TAHC eCVI 0 1600 652

VSPS 1233 1351 417

New Planet Technologies 12 0 0

other state's electronic 236 0 0

Vet Sentry 37 0 0

total electronic 15441 16451 13224

total paper 23558 18270 18012

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Summary Minutes of the 403rd Commission Meeting – 5/21/2019

Figure 5 and 6. Proportions by state of imports and exports into Texas. The total imports were 6,001 movements of 213,889 animals, whereas the total exports was 3,726 movements of 133,405 animals.

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Summary Minutes of the 403rd Commission Meeting – 5/21/2019 

snip...


WEDNESDAY, MAY 15, 2019 

TAHC CWD TSE Prion Summary Minutes of the 402nd Commission Meeting – 12/11/2018



TEXAS CWD TSE PRION STRAIN UNLIKE ANYTHING EVER SEEN

“Wow,” he said. “Unlike anything we've seen before.”

The prions from the Texas deer were a lot harder to destroy than the ones from the Colorado elk. In fact, the guanidine barely damaged them at all. “We’ve never seen that before in any prion strain, which means that it has a completely different structure than we've ever seen before,” says Zabel. And that suggests that it might be a very different kind of chronic wasting disease. The researchers ran the same test on another Texas deer, with the same results.

One day in late February, in their laboratory in Fort Collins, Colorado, Wagner and Zabel compared the prions from the brains of CWD-infected deer in Texas with those of elk in Colorado. They want to know if the proteins were all mangled in the same way, or not. “If they are different, this would suggest that we have different strain properties, which is evidence as we're building our case that we might have multiple strains of CWD circulating in the U.S.,” says Wagner.

Step one is to see if they’re equally easy to destroy using a chemical called guanidine. The shape of a prion dictates everything, including the way it interacts with an animal’s cells and the ease with which chemicals can unfold it.

“Moment of truth,” said Wagner, as she and Zabel huddled around a computer, waiting for results to come through. When they did, Zabel was surprised.

“Wow,” he said. “Unlike anything we've seen before.”

The prions from the Texas deer were a lot harder to destroy than the ones from the Colorado elk. In fact, the guanidine barely damaged them at all. “We’ve never seen that before in any prion strain, which means that it has a completely different structure than we've ever seen before,” says Zabel. And that suggests that it might be a very different kind of chronic wasting disease. The researchers ran the same test on another Texas deer, with the same results.

Now, these are only the preliminary results from a few animals. Wagner and Zabel have a lot more experiments to do. But if future tests come to the same conclusion, it would support their hypothesis that there are multiple strains of chronic wasting disease out there, all with different origins. That, in turn, could mean that this disease will become even trickier to manage than it already is.

And, Zabel adds, there’s something else. “If it's still evolving, it may still evolve into a form that could potentially, eventually affect humans,” he says.

Zabel is not the only one worried about that possibility. 

 OSTERHOLM, THE EPIDEMIOLOGIST from Minnesota, is also concerned. He directs the Center for Infectious Disease Research and Policy at the University of Minnesota, and is serving a one-year stint as a “Science Envoy for Health Security” with the U.S. State Department. In February, he told Minnesota lawmakers that when it comes to chronic wasting disease, we are playing with fire. “You are going to hear from people that this is not going to be a problem other than a game farm issue. You're going to hear from people that it's not going to transmit to people, and I hope they're right, but I wouldn't bet on it,” he said. “And if we lose this one and haven’t done all we can do, we will pay a price.”

If that wasn’t warning enough, he added: “Just remember what happened in England.”

SUNDAY, APRIL 14, 2019 

Chronic Wasting Disease TSE Prion Strains everything in Texas is bigger, better, and badder


FRIDAY, APRIL 05, 2019 

TPWD CWD Sampling Effort Leads to Proposed Containment Zone Expansion


TUESDAY, MARCH 05, 2019 

TAHC CWD TSE PRION AT 144 POSITIVE MINUTES OF THE 401st COMMISSION MEETING Texas Animal Health Commission August 7, 2018 


TUESDAY, FEBRUARY 26, 2019 

TEXAS CWD TSE PRION CASES RISE TO 144 CASES WITH 1 WILD, 1 BREEDER, AND 1 BREEDER RELEASE 


SUNDAY, JUNE 10, 2018 

TEXAS SUMMARY MINUTES OF THE 400th COMMISSION MEETING CWD TSE PRION TAHC April 17, 2018


SATURDAY, DECEMBER 02, 2017

TEXAS TAHC CWD TSE PRION Trace Herds INs and OUTs Summary Minutes of the 399th and 398th Commission Meeting – 8/22/2017 5/9/2017


TEXAS BREEDER DEER ESCAPEE WITH CWD IN THE WILD, or so the genetics would show?

OH NO, please tell me i heard this wrong, a potential Texas captive escapee with cwd in the wild, in an area with positive captive cwd herd?

apparently, no ID though. tell me it ain't so please...

23:00 minute mark

''Free Ranging Deer, Dr. Deyoung looked at Genetics of this free ranging deer and what he found was, that the genetics on this deer were more similar to captive deer, than the free ranging population, but he did not see a significant connection to any one captive facility that he analyzed, so we believe, Ahhhhhh, this animal had some captive ahhh, whatnot.''


Wyoming CWD Dr. Mary Wood

''first step is admitting you have a problem''

''Wyoming was behind the curve''

wyoming has a problem...


the other part, these tissues and things in the body then shed or secrete prions which then are the route to other animals into the environment, so in particular, the things, the secretions that are infectious are salvia, feces, blood and urine. so pretty much anything that comes out of a deer is going to be infectious and potential for transmitting disease.
Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS See Wisconsin update...terrible news, right after Texas updated map around 5 minute mark...
WISCONSIN CWD CAPTIVE CWD UPDATE VIDEO
cwd update on Wisconsin from Tammy Ryan...
Wyoming CWD Dr. Mary Wood ''first step is admitting you have a problem'' ''Wyoming was behind the curve'' wyoming has a problem...

SATURDAY, JANUARY 19, 2019 

Texas Chronic Wasting Disease CWD TSE Prion Symposium 2018 posted January 2019 VIDEO SET 18 CLIPS 


TEXAS SUMMARY MINUTES OF THE 400th COMMISSION MEETING CWD TSE PRION TAHC April 17, 2018

V. SHEEP AND GOATS

A. Scrapie: The first positive scrapie case in Texas since 2008 was identified in the Panhandle in April 2016 and the flock and premises remains under quarantine.

Chronic Wasting Disease – NOT Approved – denied waiver to allow twin moose calves to enter Texas from a non-CWD monitored herd. According to Texas Administrative Code Title 4, Part 2, Chapter 51.10 all CWD susceptible species must meet federal requirements for interstate movements. Additionally, observation of an animal does not provide sufficient evidence of disease freedom, especially when applied to CWD.

VI. CERVIDS

A. Chronic Wasting Disease (CWD) in white-tailed deer (WTD): There are 5 positive WTD breeding facilities in Texas. The total number of positive WTD and current status of each facility is listed below:

Facility Current Status Number Positive

1 Depopulated in 2015 4

2 Depopulated in early 2016 5

3 Quarantined January 2016, managed on herd plan 28, 12 suspects, 2 elk

4 Quarantined March 2016, recently depopulated ~100 does and managed on a herd plan, 25

5 Quarantined May 2017, depopulated herd October 2017 2

In late FY 2017, USDA informed TAHC that some end of year CWD indemnity funds were designated to Texas for the current positive herds. USDA required complete depopulation of the newest facility (Facility #5) based on the smaller size. The herd was depopulated in October and one additional positive doe was disclosed. The remaining available funds were allocated to use on facility 4 to remove deer in high risk pens. Of the 100 deer depopulated in facility #4, 9 were positive and all 9 were in pens in the same section as the index pen. In addition, a hunter harvested buck at facility #4 was positive that was harvested in November 2017.

In facility #3, since January 2016, there are a total of 28 positives and 12 suspects (tonsil biopsy confirmed positive only at this time) WTD. Of those, 31 are from the breeder pens or grower pens (17 bucks and 14 does). In addition, there were 9 positives disclosed from hunter harvested samples from 4 different pastures (6 bucks, 3 does). And there were 2 positive elk cows disclosed from 117 samples in 1 pasture. Both cows were natural additions to the elk herd.

The free ranging summary for the 2017-2018 hunting season include 2 positive mule deer from Hudspeth County, 2 mule deer from Hartley County, and 1 WTD from Hartley County. The WTD was on the Containment Zone border and a slight adjustment to that zone will be addressed before the next hunting season.

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Summary Minutes of the 400th Commission Meeting – 4/17/2018

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Statewide exotic CWD susceptible species surveillance monitoring in ongoing. General surveillance includes any facility that is testing CWD susceptible species for their annual premise requirement. Hunter harvest samples include samples collected at check stations in one of the 3 zones (the Panhandle, West Texas, or Medina area). Samples collected on positive premises include testing to meet requirements for a positive premise herd plan.

CWD Susceptible Species Surveillance 2017-18

Exotic Species General Statewide Surveillance Positive PremiseContainment Zone* Hunter Harvest in Zones for ’17-18

Positive Negative Positive Negative Positive Negative

Red Deer 0 70 0 14 0 8

Elk 0 30 2 (cows) 115 0 19

Sika 26 0 1 0 4

Total 0 126 2 130 0 31 


TUESDAY, JANUARY 29, 2019 

TEXAS REPORTS 2 MORE CWD TSE PRION ALL WILD CERVID TOTAL TO DATE 141


*** Hartley County Sheep with Scrapie, and CWD in Hartley county ??? 

*** Friday, April 22, 2016 

*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in a Mule Deer 


CWD TSE PRION PAYING TO PLAY PROGRAM $$$

SUNDAY, MAY 14, 2017 

85th Legislative Session 2017 AND THE TEXAS TWO STEP Chronic Wasting Disease CWD TSE Prion, and paying to play


Wednesday, May 04, 2016 

TPWD proposes the repeal of §§65.90 -65.94 and new §§65.90 -65.99 Concerning Chronic Wasting Disease - Movement of Deer Singeltary Comment Submission 


TUESDAY, DECEMBER 16, 2014

Texas 84th Legislature 2015 H.R. No. 2597 Kuempel Deer Breeding Industry TAHC TPWD CWD TSE PRION 


SUNDAY, DECEMBER 14, 2014

TEXAS 84th Legislature commencing this January, deer breeders are expected to advocate for bills that will seek to further deregulate their industry


TEXAS HISTORY OF CWD Singeltary telling TAHC, that CWD was waltzing into Texas from WSMR around Trans Pecos region, starting around 2001, 2002, and every year, there after, until New Mexico finally shamed TAHC et al to test where i had been telling them to test for a decade. 2012 cwd was detected first right there where i had been trying to tell TAHC for 10 years. 

***> Singeltary on Texas Chronic Wasting Disease CWD TSE Prion History <***


WEDNESDAY, JUNE 19, 2019 

Experts urge immediate action to contain the epidemic Chronic Wasting Disease CWD TSE Prion


SUNDAY, JUNE 16, 2019 

Pennsylvania Release of chronic wasting disease CWD TSE plan delayed, what's the hurry now after floundering since 2012

Pennsylvania, here's what CWD TSE Prion on steroids in slow motion looks like, it's kinda like compounding interest, and Pennsylvania should get a a hefty return on their floundering with CWD TSE PRION...terry


SATURDAY, JUNE 15, 2019 

Montana Second Deer Suspected of Testing Positive for Chronic Wasting Disease in Libby


THURSDAY, JUNE 06, 2019 

Missouri MDC proposes new efforts to limit spread of CWD TSE Prion To Date 116 Cases Confirmed


THURSDAY, JUNE 06, 2019 

Arkansas AGFC identified 241 new positive cases of CWD TSE Prion in white-tailed deer and five elk during the 2018-19 deer hunting season WD Management Zone expands to include Baxter, Scott and Stone counties


MONDAY, JUNE 03, 2019 

Tennessee NEW CWD UNIT HUNTING REGULATIONS ESTABLISHED TO AID IN EFFORTS FOR DISEASE MANAGEMENT


THURSDAY, JUNE 06, 2019 

Wisconsin After a Total of 7 Confirmed Cases The Depopulated Portage County Hunting Ranch Tests Negative for CWD TSE Prion


FRIDAY, MAY 10, 2019 

Wisconsin Portage County Deer Farm Depopulated due to CWD TSE Prion ​6 Cases Confirmed


THURSDAY, MAY 09, 2019 

Minnesota Seven deer test positive for CWD at Crow Wing County deer farm


THURSDAY, MAY 09, 2019 

Michigan CWD TSE Prion increases to 120 Cases to Date


THURSDAY, MARCH 28, 2019 

Michigan CWD Identified in a Montcalm County Farmed Deer


WEDNESDAY, APRIL 24, 2019 

Oklahoma Farmed Elk Lincoln County has tested positive for chronic wasting disease CWD TSE Prion 

JOINT RELEASE FROM THE OKLAHOMA DEPARTMENT OF AGRICULTURE, FOOD & FORESTRY AND THE OKLAHOMA DEPARTMENT OF WILDLIFE CONSERVATION 

Chronic Wasting Disease Confirmed in One Farmed Oklahoma Elk 


THURSDAY, MARCH 21, 2019 

South Dakota Chronic wasting disease (CWD) has been identified in a captive elk in Clark County


WEDNESDAY, MARCH 20, 2019 

North Dakota Deer Found Near Williston Tests Positive for CWD


THURSDAY, APRIL 25, 2019 

Missouri MDC reports 41 new positive test results for CWD have been confirmed following its sampling


TUESDAY, APRIL 23, 2019 

Virginia DGIF CWD TSE Prion As April 2019 the Department has diagnosed 68 positive cases since 2009 


THURSDAY, APRIL 11, 2019 

Montana Chronic Wasting Disease CWD TSE Prion 2018 Report 26 New Cases


THURSDAY, FEBRUARY 21, 2019 
Tennessee officials concerned after 183 deer test positive for CWD TSE Prion
FRIDAY, MAY 10, 2019 

Alabama Officially Invites CWD TSE Prion Into Their State When Bait Bill Becomes Law

WEDNESDAY, APRIL 03, 2019 

Estimating the amount of Chronic Wasting Disease infectivity passing through abattoirs and field slaughter


WEDNESDAY, MARCH 13, 2019 

CWD, TSE, PRION, MATERNAL mother to offspring, testes, epididymis, seminal fluid, and blood


THURSDAY, MARCH 14, 2019

USDA APHIS CDC Cervids: Chronic Wasting Disease Specifics Updated 2019


SATURDAY, MARCH 16, 2019

Chronic Wasting Disease CWD TSE Prion United States of America Update March 16, 2019


TUESDAY, MARCH 26, 2019

USDA ARS 2018 USAHA RESOLUTIONS Investigation of the Role of the Prion Protein Gene in CWD Resistance and Transmission of Disease


TUESDAY, APRIL 30, 2019 

Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies 2018 Annual Report


FRIDAY, MARCH 29, 2019

First Detection of Chronic Wasting Disease in a Wild Red Deer (Cervus elaphus) in Europe


let's review some recent science on the environmental effects of the exposure of the cwd tse prion, it's not pretty...

P-147 Infection and detection of PrPCWD in soil from CWD infected farm in Korea

Hyun Joo Sohn, Kyung Je Park, In Soon Roh, Hyo Jin Kim, Hoo Chang Park, Byounghan Kim

Animal and Plant Quarantine Agency (QIA), Korea

Transmissible spongiform encephalopathy (TSE) is a fatal neurodegenerative disorder, which is so-called as prion diseases due to the causative agents (PrPSc). TSEs are believed to be due to the template-directed accumulation of disease-associated prion protein, generally designated PrPSc. Chronic wasting disease (CWD) is the prion disease that is known spread horizontally. CWD has confirmed last in Republic of Korea in 2010 since first outbreak of CWD in 2001. The environmental reservoirs mediate the transmission of this disease. The significant levels of infectivity have been detected in the saliva, urine, and feces of TSE-infected animals. Using serial protein misfolding cyclic amplification (sPMCA), we developed a detection method for CWD PrPSc in soil from CWD affected farm in 2010. We found to detect PrPSc in soil from CWD infected farm, but not detect PrPSc in soil of wild cervid habitats and normal cervid farm in Korea. We also tried the bioassay on transgenic mice overexpressing elk prion protein (TgElk mice) to confirm infectivity of CWD-infected farm soil and washing solution of it. As the results, there was the presence of infectious prions in them. The attack rates were each 12.5% (1/8, soil) and 100% (6/6, soil washing solution). Our method appears to be a very useful technique for monitoring PrPSc levels in environmental conditions. 


see full text;


2018 - 2019

***> This is very likely to have parallels with control efforts for CWD in cervids.

Rapid recontamination of a farm building occurs after attempted prion removal


Kevin Christopher Gough, BSc (Hons), PhD1, Claire Alison Baker, BSc (Hons)2, Steve Hawkins, MIBiol3, Hugh Simmons, BVSc, MRCVS, MBA, MA3, Timm Konold, DrMedVet, PhD, MRCVS3 and Ben Charles Maddison, BSc (Hons), PhD2

Abstract

The transmissible spongiform encephalopathy scrapie of sheep/goats and chronic wasting disease of cervids are associated with environmental reservoirs of infectivity. 

Preventing environmental prions acting as a source of infectivity to healthy animals is of major concern to farms that have had outbreaks of scrapie and also to the health management of wild and farmed cervids. 

Here, an efficient scrapie decontamination protocol was applied to a farm with high levels of environmental contamination with the scrapie agent. 

Post-decontamination, no prion material was detected within samples taken from the farm buildings as determined using a sensitive in vitro replication assay (sPMCA). 

A bioassay consisting of 25 newborn lambs of highly susceptible prion protein genotype VRQ/VRQ introduced into this decontaminated barn was carried out in addition to sampling and analysis of dust samples that were collected during the bioassay. 

Twenty-four of the animals examined by immunohistochemical analysis of lymphatic tissues were scrapie-positive during the bioassay, samples of dust collected within the barn were positive by month 3. 

The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease.

snip...

As in the authors' previous study,12 the decontamination of this sheep barn was not effective at removing scrapie infectivity, and despite the extra measures brought into this study (more effective chemical treatment and removal of sources of dust) the overall rates of disease transmission mirror previous results on this farm. With such apparently effective decontamination (assuming that at least some sPMCA seeding ability is coincident with infectivity), how was infectivity able to persist within the environment and where does infectivity reside? Dust samples were collected in both the bioassay barn and also a barn subject to the same decontamination regime within the same farm (but remaining unoccupied). Within both of these barns dust had accumulated for three months that was able to seed sPMCA, indicating the accumulation of scrapie-containing material that was independent of the presence of sheep that may have been incubating and possibly shedding low amounts of infectivity.

This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapiepositive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.

Acknowledgements The authors thank the APHA farm staff, Tony Duarte, Olly Roberts and Margaret Newlands for preparation of the sheep pens and animal husbandry during the study. The authors also thank the APHA pathology team for RAMALT and postmortem examination.

Funding This study was funded by DEFRA within project SE1865. 

Competing interests None declared. 


Saturday, January 5, 2019 

Rapid recontamination of a farm building occurs after attempted prion removal 


THURSDAY, FEBRUARY 28, 2019 

BSE infectivity survives burial for five years with only limited spread



***> CONGRESSIONAL ABSTRACTS PRION CONFERENCE 2018

P69 Experimental transmission of CWD from white-tailed deer to co-housed reindeer 

Mitchell G (1), Walther I (1), Staskevicius A (1), Soutyrine A (1), Balachandran A (1) 

(1) National & OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada. 

Chronic wasting disease (CWD) continues to be detected in wild and farmed cervid populations of North America, affecting predominantly white-tailed deer, mule deer and elk. Extensive herds of wild caribou exist in northern regions of Canada, although surveillance has not detected the presence of CWD in this population. Oral experimental transmission has demonstrated that reindeer, a species closely related to caribou, are susceptible to CWD. Recently, CWD was detected for the first time in Europe, in wild Norwegian reindeer, advancing the possibility that caribou in North America could also become infected. Given the potential overlap in habitat between wild CWD-infected cervids and wild caribou herds in Canada, we sought to investigate the horizontal transmissibility of CWD from white-tailed deer to reindeer. 

Two white-tailed deer were orally inoculated with a brain homogenate prepared from a farmed Canadian white-tailed deer previously diagnosed with CWD. Two reindeer, with no history of exposure to CWD, were housed in the same enclosure as the white-tailed deer, 3.5 months after the deer were orally inoculated. The white-tailed deer developed clinical signs consistent with CWD beginning at 15.2 and 21 months post-inoculation (mpi), and were euthanized at 18.7 and 23.1 mpi, respectively. Confirmatory testing by immunohistochemistry (IHC) and western blot demonstrated widespread aggregates of pathological prion protein (PrPCWD) in the central nervous system and lymphoid tissues of both inoculated white-tailed deer. Both reindeer were subjected to recto-anal mucosal associated lymphoid tissue (RAMALT) biopsy at 20 months post-exposure (mpe) to the white-tailed deer. The biopsy from one reindeer contained PrPCWD confirmed by IHC. This reindeer displayed only subtle clinical evidence of disease prior to a rapid decline in condition requiring euthanasia at 22.5 mpe. Analysis of tissues from this reindeer by IHC revealed widespread PrPCWD deposition, predominantly in central nervous system and lymphoreticular tissues. Western blot molecular profiles were similar between both orally inoculated white-tailed deer and the CWD positive reindeer. Despite sharing the same enclosure, the other reindeer was RAMALT negative at 20 mpe, and PrPCWD was not detected in brainstem and lymphoid tissues following necropsy at 35 mpe. Sequencing of the prion protein gene from both reindeer revealed differences at several codons, which may have influenced susceptibility to infection. 

Natural transmission of CWD occurs relatively efficiently amongst cervids, supporting the expanding geographic distribution of disease and the potential for transmission to previously naive populations. The efficient horizontal transmission of CWD from white-tailed deer to reindeer observed here highlights the potential for reindeer to become infected if exposed to other cervids or environments infected with CWD. 



***> Infectious agent of sheep scrapie may persist in the environment for at least 16 years


***> Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. 


Gudmundur Georgsson,1 Sigurdur Sigurdarson2 and Paul Brown3

Correspondence

Gudmundur Georgsson ggeorgs@hi.is

1 Institute for Experimental Pathology, University of Iceland, Keldur v/vesturlandsveg, IS-112 Reykjavı´k, Iceland

2 Laboratory of the Chief Veterinary Officer, Keldur, Iceland

3 Bethesda, Maryland, USA

Received 7 March 2006 Accepted 6 August 2006

In 1978, a rigorous programme was implemented to stop the spread of, and subsequently eradicate, sheep scrapie in Iceland. Affected flocks were culled, premises were disinfected and, after 2–3 years, restocked with lambs from scrapie-free areas. Between 1978 and 2004, scrapie recurred on 33 farms. Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. Of special interest was one farm with a small, completely self-contained flock where scrapie recurred 18 years after culling, 2 years after some lambs had been housed in an old sheephouse that had never been disinfected. Epidemiological investigation established with near certitude that the disease had not been introduced from the outside and it is concluded that the agent may have persisted in the old sheep-house for at least 16 years.

 
 
TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION 

 

 *** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSION 

 

SEE;

Back around 2000, 2001, or so, I was corresponding with officials abroad during the bse inquiry, passing info back and forth, and some officials from here inside USDA aphis FSIS et al. In fact helped me get into the USA 50 state emergency BSE conference call way back. That one was a doozy. But I always remember what “deep throat” I never knew who they were, but I never forgot;

Some unofficial information from a source on the inside looking out -

Confidential!!!!

As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke out with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!

---end personal email---end...tss



Infectivity surviving ashing to 600*C is (in my opinion) degradable but infective. based on Bown & Gajdusek, (1991), landfill and burial may be assumed to have a reduction factor of 98% (i.e. a factor of 50) over 3 years. CJD-infected brain-tissue remained infectious after storing at room-temperature for 22 months (Tateishi et al, 1988). Scrapie agent is known to remain viable after at least 30 months of desiccation (Wilson et al, 1950). and pastures that had been grazed by scrapie-infected sheep still appeared to be contaminated with scrapie agent three years after they were last occupied by sheep (Palsson, 1979).



Dr. Paul Brown Scrapie Soil Test BSE Inquiry Document



Using in vitro Prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission. 

Claudio Soto Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston. 

Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.

=========================

***>>> Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.

========================

Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis. 



New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication 



Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production 



Detection of protease-resistant cervid prion protein in water from a CWD-endemic area 



A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing 



Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals 



PPo4-4: 

Survival and Limited Spread of TSE Infectivity after Burial 




Discussion Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). 

Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). 

Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23). 

Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. 

Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. 

Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). 

The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. 

When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier. 

This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. 

Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. 

It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. 

Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. 

Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. 

Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions. 

PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. 

In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. 

In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). 

As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. 

False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). 

This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. 

This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. 

In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. 

Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. 

The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. 

In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). 

A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). 

This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. 

Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions. 

In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. 

These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes. 

Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification 


Wednesday, December 16, 2015 

*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission *** 


WEDNESDAY, MARCH 13, 2019 

CWD, TSE, PRION, MATERNAL mother to offspring, testes, epididymis, seminal fluid, and blood


MONDAY, FEBRUARY 25, 2019

MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019


THURSDAY, OCTOBER 04, 2018

Cervid to human prion transmission 5R01NS088604-04 Update


MONDAY, APRIL 01, 2019 

PUBLIC HEALTH U of M launches Chronic Wasting Disease Program to address potential health crisis



> 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).***
Chronic Wasting Disease CWD TSE Prion aka mad deer disease zoonosis
We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence;
(3) Reliable essays can be established to detect CWD infection in humans; and
(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.
ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE
here is the latest;
PRION 2018 CONFERENCE
Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice
Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge).
To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years.
After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles.
Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate.
The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.
Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP.
The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD..
***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***
READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT from this study ;
P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States
Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1) (1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA..
SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD
states.
AND ANOTHER STUDY;
P172 Peripheral Neuropathy in Patients with Prion Disease
Wang H(1), Cohen M(1), Appleby BS(1,2) (1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio..
IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017,
AND
included 104 patients. SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%),
AND
THAT The Majority of cases were male (60%), AND half of them had exposure to wild game.
snip…
see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below…terry
THURSDAY, OCTOBER 04, 2018
Cervid to human prion transmission 5R01NS088604-04 Update
snip…full text;
SATURDAY, FEBRUARY 09, 2019
Experts: Yes, chronic wasting disease in deer is a public health issue — for people
Date: May 4, 2018 at 12:39:00 PM EDT 

Mineral licks as environmental reservoirs of chronic wasting disease prions 

Ian H. Plummer, Chad J. Johnson, Alexandra R. Chesney, Joel A. Pedersen, Michael D. Samuel 

CONCLUSIONS

We used mb-PMCA to detect CWD in soil and water from mineral licks naturally contaminated with prions and used by free-ranging deer, livestock, and non-cervid wildlife species. Detection of prions in environmental reservoirs represents an important first step in understanding the contribution of environmental transmission to CWD epizootics and potential for cross-species transmission. The present study characterized an environmental prion reservoir by (1) identifying an apparent “hot spot” of deposition and potential exposure to both cervid and non-cervid species; (2) indicating CWD prions shed by free-ranging cervids are present in areas of frequent use leading to environmental contamination and potentially plant uptake; and (3) motivating investigation of the exposure and susceptibility of non-cervid species to CWD contaminated soil, water, and plant materials. Future research should be directed at quantifying CWD prion concentrations at mineral licks and other areas where cervids congregate, determining the persistence of prion infectivity at these sites, delineating spatial-temporal patterns of environmental prion deposition and accumulation, and assessing consumption by susceptible animals. Identifying additional environmental reservoirs of CWD prions and determining the contributions of direct and indirect transmission over the course of CWD outbreaks represent key aims in advancing understanding of long-term CWD infection dynamics.




SUNDAY, DECEMBER 29, 2013 

Impacts of wildlife baiting and supplemental feeding on infectious disease transmission risk: A synthesis of knowledge


Friday, October 26, 2012 

CHRONIC WASTING DISEASE CWD PENNSYLVANIA GAME FARMS, URINE ATTRACTANT PRODUCTS, BAITING, AND MINERAL LICKS 


CWD, GAME FARMS, BAITING, AND POLITICS 



cattle, pigs, sheep, cwd, tse, prion, oh my!

***> In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). 

Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable.



cwd scrapie pigs oral routes

***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <*** 

 >*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <*** 

***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). 

***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. 

This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. 

Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains. 




Friday, December 14, 2012

DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012

snip.....

In the USA, under the Food and Drug Administration's BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.

Animals considered at high risk for CWD include:

1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and

2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.

Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.

The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.

Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.

There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.

snip.....

36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).

The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).

Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.

snip.....

The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).

snip.....

In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.

snip.....

In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible... For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.

snip.....

Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.

snip.....


TUESDAY, APRIL 18, 2017 

*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***


WEDNESDAY, JUNE 26, 2019 

Subcommittee Hearing: Chronic Wasting Disease: The Threats to Wildlife, Public Lands, Hunting, and Health

video


MONDAY, JUNE 24, 2019 

APHIS, FSIS, USDA, FDA, Transmissible Spongiform Encephalopathy TSE, BSE, CWD, Scrapie, Camel TSE Prion Disease, CJD Humans


WEDNESDAY, JUNE 19, 2019 

Experts urge immediate action to contain the epidemic Chronic Wasting Disease CWD TSE Prion


SUNDAY, JUNE 16, 2019 

Pennsylvania Release of chronic wasting disease CWD TSE plan delayed, what's the hurry now after floundering since 2012

Pennsylvania, here's what CWD TSE Prion on steroids in slow motion looks like, it's kinda like compounding interest, and Pennsylvania should get a a hefty return on their floundering with CWD TSE PRION...terry


MONDAY, JUNE 24, 2019 

Pennsylvania JOYCE AMENDMENT ALLOCATING $15 MILLION FOR NEW CWD STUDY CLEARS HOUSE


FRIDAY, JUNE 21, 2019 

CJD TSE Prion cases update USA, Texas, Canada, and UK


Prion Conference 2018

O5 Prion Disease in Dromedary Camels 

Babelhadj B (1), Di Bari MA (2), Pirisinu L (2), Chiappini B (2), Gaouar SB (3), Riccardi G (2), Marcon S (2), Agrimi U (2), Nonno R (2), Vaccari G (2) (1) École Normale Supérieure Ouargla. Laboratoire de protection des écosystèmes en zones arides et semi arides University Kasdi Merbah Ouargla, Ouargla, Algeria; (2) Istituto Superiore di Sanità, Department of Food Safety, Nutrition and Veterinary Public Health, Rome, Italy (3) University Abou Bekr Bélkaid, Tlemcen, Algeria. 

Prions are responsible for fatal and transmissible neurodegenerative diseases including CreutzfeldtJakob disease in humans, scrapie in small ruminants and bovine spongiform encephalopathy (BSE). Following the BSE epidemic and the demonstration of its zoonotic potential, general concerns have been raised on animal prions. 

Here we report the identification of a prion disease in dromedary camels (Camelus dromedarius) in Algeria and designate it as Camel Prion Disease (CPD). In the last years, neurological symptoms have been observed in adult male and female dromedaries presented for slaughter at the Ouargla abattoir. The symptoms include weight loss, behavioral abnormalities and neurological symptoms such as tremors, aggressiveness, hyper-reactivity, typical down and upwards movements of the head, hesitant and uncertain gait, ataxia of the hind limbs, occasional falls and difficult getting up. During 2015 and 2016, symptoms suggestive of prion disease were observed in 3.1% of 2259 dromedaries presented at ante-mortem examination. Laboratory diagnosis was obtained in three symptomatic dromedaries, sampled in 2016 and 2017, by the detection of typical neurodegeneration and disease-specific prion protein (PrPSc) in brain tissues. 

Histopathological examination revealed spongiform change, gliosis and neuronal loss preferentially in grey matter of subcortical brain areas. Abundant PrPSc deposition was detected in the same brain areas by immunohistochemistry and PET-blot. Western blot analysis confirmed the presence of PK-resistant PrPSc, whose N-terminal cleaved PK-resistant core was characterized by a mono-glycosylated dominant form and by a distinctive N-terminal cleavage, different from that observed in BSE and scrapie. 

PrPSc was also detected, by immunohistochemistry, in all sampled lymph nodes (cervical, prescapular and lumbar aortic) of the only animal from which they were collected. 

The PRNP sequence of the two animals for which frozen material was available, showed 100% nucleotide identity with the PRNP sequence already reported for dromedary camel. 

Overall, these data demonstrate the presence of a prion disease in dromedary camelswhose nature, origin and spread need further investigations. However, our preliminary observations on the rather high prevalence of symptomatic dromedaries and the involvement of lymphoid tissues, are consistent with CPD being an infectious disease. In conclusion, the emergence of a new prion disease in a livestock species of crucial importance for millions of people around the world, makes urgent to assess the risk for humans and to develop policies able to control the spread of the disease in animals and to minimize human exposure. 


CDC

New Outbreak of TSE Prion in NEW LIVESTOCK SPECIES

Mad Camel Disease

Volume 24, Number 6—June 2018 Research 

Prion Disease in Dromedary Camels, Algeria
Abstract

Prions cause fatal and transmissible neurodegenerative diseases, including Creutzfeldt-Jakob disease in humans, scrapie in small ruminants, and bovine spongiform encephalopathy (BSE). After the BSE epidemic, and the associated human infections, began in 1996 in the United Kingdom, general concerns have been raised about animal prions. We detected a prion disease in dromedary camels (Camelus dromedarius) in Algeria. Symptoms suggesting prion disease occurred in 3.1% of dromedaries brought for slaughter to the Ouargla abattoir in 2015–2016. We confirmed diagnosis by detecting pathognomonic neurodegeneration and disease-specific prion protein (PrPSc) in brain tissues from 3 symptomatic animals. Prion detection in lymphoid tissues is suggestive of the infectious nature of the disease. PrPSc biochemical characterization showed differences with BSE and scrapie. Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.

SNIP...

The possibility that dromedaries acquired the disease from eating prion-contaminated waste needs to be considered.
Tracing the origin of prion diseases is challenging. In the case of CPD, the traditional extensive and nomadic herding practices of dromedaries represent a formidable factor for accelerating the spread of the disease at long distances, making the path of its diffusion difficult to determine. Finally, the major import flows of live animals to Algeria from Niger, Mali, and Mauritania (27) should be investigated to trace the possible origin of CPD from other countries.
Camels are a vital animal species for millions of persons globally. The world camel population has a yearly growth rate of 2.1% (28). In 2014, the population was estimated at ≈28 million animals, but this number is probably underestimated.. Approximately 88% of camels are found in Africa, especially eastern Africa, and 12% are found in Asia. Official data reported 350,000 dromedaries in Algeria in 2014 (28).
On the basis of phenotypic traits and sociogeographic criteria, several dromedary populations have been suggested to exist in Algeria (29). However, recent genetic studies in Algeria and Egypt point to a weak differentiation of the dromedary population as a consequence of historical use as a cross-continental beast of burden along trans-Saharan caravan routes, coupled with traditional extensive/nomadic herding practices (30).
Such genetic homogeneity also might be reflected in PRNP. Studies on PRNP variability in camels are therefore warranted to explore the existence of genotypes resistant to CPD, which could represent an important tool for CPD management as it was for breeding programs for scrapie eradication in sheep.
In the past 10 years, the camel farming system has changed rapidly, with increasing setup of periurban dairy farms and dairy plants and diversification of camel products and market penetration (13). This evolution requires improved health standards for infectious diseases and, in light of CPD, for prion diseases.
The emergence of another prion disease in an animal species of crucial importance for millions of persons worldwide makes it necessary to assess the risk for humans and develop evidence-based policies to control and limit the spread of the disease in animals and minimize human exposure. The implementation of a surveillance system for prion diseases would be a first step to enable disease control and minimize human and animal exposure. Finally, the diagnostic capacity of prion diseases needs to be improved in all countries in Africa where dromedaries are part of the domestic livestock.

***> IMPORTS AND EXPORTS <***

***SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN ***


ZOONOSIS OF SCRAPIE TSE PRION

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. 


***> 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. <***

Transmission of scrapie prions to primate after an extended silent incubation period 

Emmanuel E. Comoy, Jacqueline Mikol, Sophie Luccantoni-Freire, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Valérie Durand, Capucine Dehen, Olivier Andreoletti, Cristina Casalone, Juergen A. Richt, Justin J. Greenlee, Thierry Baron, Sylvie L. Benestad, Paul Brown & Jean-Philippe Deslys Scientific Reports volume 5, Article number: 11573 (2015) | Download Citation

Abstract 

Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.

SNIP...

Discussion We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes. 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.

The second possibility is a laboratory cross-contamination. Three facts make this possibility equally unlikely. First, handling of specimens in our laboratory is performed with fastidious attention to the avoidance of any such cross-contamination. Second, no laboratory cross-contamination has ever been documented in other primate laboratories, including the NIH, even between infected and uninfected animals housed in the same or adjacent cages with daily intimate contact (P. Brown, personal communication). Third, the cerebral lesion profile is different from all the other prion diseases we have studied in this model19, with a correlation between cerebellar lesions (massive spongiform change of Purkinje cells, intense PrPres staining and reactive gliosis26) and ataxia. The iron deposits present in the globus pallidus are a non specific finding that have been reported previously in neurodegenerative diseases and aging27. Conversely, the thalamic lesion was reminiscent of a metabolic disease due to thiamine deficiency28 but blood thiamine levels were within normal limits (data not shown). The preferential distribution of spongiform change in cortex associated with a limited distribution in the brainstem is reminiscent of the lesion profile in MM2c and VV1 sCJD patients29, but interspecies comparison of lesion profiles should be interpreted with caution. It is of note that the same classical scrapie isolate induced TSE in C57Bl/6 mice with similar incubation periods and lesional profiles as a sample derived from a MM1 sCJD patient30.

We are therefore confident that the illness in this cynomolgus macaque represents a true transmission of a sheep c-scrapie isolate directly to an old-world monkey, which taxonomically resides in the primate subdivision (parvorder of catarrhini) that includes humans. With an homology of its PrP protein with humans of 96.4%31, cynomolgus macaque constitutes a highly relevant model for assessing zoonotic risk of prion diseases. Since our initial aim was to show the absence of transmission of scrapie to macaques in the worst-case scenario, we obtained materials from a flock of naturally-infected sheep, affecting animals with different genotypes32. This c-scrapie isolate exhibited complete transmission in ARQ/ARQ sheep (332 ± 56 days) and Tg338 transgenic mice expressing ovine VRQ/VRQ prion protein (220 ± 5 days) (O. Andreoletti, personal communication). From the standpoint of zoonotic risk, it is important to note that sheep with c-scrapie (including the isolate used in our study) have demonstrable infectivity throughout their lymphoreticular system early in the incubation period of the disease (3 months-old for all the lymphoid organs, and as early as 2 months-old in gut-associated lymph nodes)33. In addition, scrapie infectivity has been identified in blood34, milk35 and skeletal muscle36 from asymptomatic but scrapie infected small ruminants which implies a potential dietary exposure for consumers.

Two earlier studies have reported the occurrence of clinical TSE in cynomolgus macaques after exposures to scrapie isolates. In the first study, the “Compton” scrapie isolate (derived from an English sheep) and serially propagated for 9 passages in goats did not transmit TSE in cynomolgus macaque, rhesus macaque or chimpanzee within 7 years following intracerebral challenge1; conversely, after 8 supplementary passages in conventional mice, this “Compton” isolate induced TSE in a cynomolgus macaque 5 years after intracerebral challenge, but rhesus macaques and chimpanzee remained asymptomatic 8.5 years post-exposure8. However, multiple successive passages that are classically used to select laboratory-adapted prion strains can significantly modify the initial properties of a scrapie isolate, thus questioning the relevance of zoonotic potential for the initial sheep-derived isolate. The same isolate had also induced disease into squirrel monkeys (new-world monkey)9. A second historical observation reported that a cynomolgus macaque developed TSE 6 years post-inoculation with brain homogenate from a scrapie-infected Suffolk ewe (derived from USA), whereas a rhesus macaque and a chimpanzee exposed to the same inoculum remained healthy 9 years post-exposure1. This inoculum also induced TSE in squirrel monkeys after 4 passages in mice. Other scrapie transmission attempts in macaque failed but had more shorter periods of observation in comparison to the current study. Further, it is possible that there are differences in the zoonotic potential of different scrapie strains.

The most striking observation in our study is the extended incubation period of scrapie in the macaque model, which has several implications. Firstly, our observations constitute experimental evidence in favor of the zoonotic potential of c-scrapie, at least for this isolate that has been extensively studied32,33,34,35,36. The cross-species zoonotic ability of this isolate should be confirmed by performing duplicate intracerebral exposures and assessing the transmissibility by the oral route (a successful transmission of prion strains through the intracerebral route may not necessarily indicate the potential for oral transmission37). However, such confirmatory experiments may require more than one decade, which is hardly compatible with current general management and support of scientific projects; thus this study should be rather considered as a case report.

Secondly, transmission of c-BSE to primates occurred within 8 years post exposure for the lowest doses able to transmit the disease (the survival period after inoculation is inversely proportional to the initial amount of infectious inoculum). The occurrence of scrapie 10 years after exposure to a high dose (25 mg) of scrapie-infected sheep brain suggests that the macaque has a higher species barrier for sheep c-scrapie than c-BSE, although it is notable that previous studies based on in vitro conversion of PrP suggested that BSE and scrapie prions would have a similar conversion potential for human PrP38.

Thirdly, prion diseases typically have longer incubation periods after oral exposure than after intracerebral inoculations: since humans can develop Kuru 47 years after oral exposure39, an incubation time of several decades after oral exposure to scrapie would therefore be expected, leading the disease to occur in older adults, i.e. the peak age for cases considered to be sporadic disease, and making a distinction between scrapie-associated and truly sporadic disease extremely difficult to appreciate.

Fourthly, epidemiologic evidence is necessary to confirm the zoonotic potential of an animal disease suggested by experimental studies. A relatively short incubation period and a peculiar epidemiological situation (e.g., all the first vCJD cases occurring in the country with the most important ongoing c-BSE epizootic) led to a high degree of suspicion that c-BSE was the cause of vCJD. Sporadic CJD are considered spontaneous diseases with an almost stable and constant worldwide prevalence (0.5–2 cases per million inhabitants per year), and previous epidemiological studies were unable to draw a link between sCJD and classical scrapie6,7,40,41, even though external causes were hypothesized to explain the occurrence of some sCJD clusters42,43,44. However, extended incubation periods exceeding several decades would impair the predictive values of epidemiological surveillance for prion diseases, already weakened by a limited prevalence of prion diseases and the multiplicity of isolates gathered under the phenotypes of “scrapie” and “sporadic CJD”.

Fifthly, considering this 10 year-long incubation period, together with both laboratory and epidemiological evidence of decade or longer intervals between infection and clinical onset of disease, no premature conclusions should be drawn from negative transmission studies in cynomolgus macaques with less than a decade of observation, as in the aforementioned historical transmission studies of scrapie to primates1,8,9. Our observations and those of others45,46 to date are unable to provide definitive evidence regarding the zoonotic potential of CWD, atypical/Nor98 scrapie or H-type BSE. The extended incubation period of the scrapie-affected macaque in the current study also underscores the limitations of rodent models expressing human PrP for assessing the zoonotic potential of some prion diseases since their lifespan remains limited to approximately two years21,47,48. This point is illustrated by the fact that the recently reported transmission of scrapie to humanized mice was not associated with clinical signs for up to 750 days and occurred in an extreme minority of mice with only a marginal increase in attack rate upon second passage13. The low attack rate in these studies is certainly linked to the limited lifespan of mice compared to the very long periods of observation necessary to demonstrate the development of scrapie. Alternatively, one could estimate that a successful second passage is the result of strain adaptation to the species barrier, thus poorly relevant of the real zoonotic potential of the original scrapie isolate of sheep origin49. The development of scrapie in this primate after an incubation period compatible with its lifespan complements the study conducted in transgenic (humanized) mice; taken together these studies suggest that some isolates of sheep scrapie can promote misfolding of the human prion protein and that scrapie can develop within the lifespan of some primate species.

In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free... Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.


***> Wednesday, January 23, 2019 

***> CFIA SFCR Guidance on Specified risk material (SRM) came into force on January 15, 2019 <***


SATURDAY, MARCH 2, 2019 

MAD COW TSE PRION DISEASE AND THE PEER REVIEW PROCESS OF BSe Science $$$


friendly fire, pass it forward, they call it iatrogenic cjd, or what i call 'tse prion poker', are you all in $$$

SATURDAY, MARCH 16, 2019 

Medical Devices Containing Materials Derived from Animal Sources (Except for In Vitro Diagnostic Devices) Guidance for Industry and Food and Drug Administration Staff Document issued on March 15, 2019 Singeltary Submission


TUESDAY, APRIL 09, 2019 

Horizon Health Network Moncton Hospital notified more than 700 patients after two cases of CJD were diagnosed both patients had undergone cataracts surgery before being diagnosed


MONDAY, APRIL 8, 2019 

Studies Further Support Transmissibility of Alzheimer Disease–Associated Proteins


Scientific Advisors and Consultants Staff 2001 Advisory Committee TSE PRION Singeltary Submission Freas Monday, January 08,2001 3:03 PM FDA Singeltary submission 2001 

Greetings again Dr. Freas and Committee Members, 

I wish to submit the following information to the Scientific Advisors and Consultants Staff 2001 Advisory Committee (short version). I understand the reason of having to shorten my submission, but only hope that you add it to a copy of the long version, for members to take and read at their pleasure, (if cost is problem, bill me, address below). So when they realize some time in the near future of the 'real' risks i speak of from human/animal TSEs and blood/surgical products. I cannot explain the 'real' risk of this in 5 or 10 minutes at some meeting, or on 2 or 3 pages, but will attempt here: 

fda link is dead in the water; 


snip...see full text 


CHRONIC WASTING DISEASE CONGRESS Serial No. 107-117 May 16, 2002

CHRONIC WASTING DISEASE

JOINT OVERSIGHT HEARING BEFORE THE SUBCOMMITTEE ON FORESTS AND FOREST HEALTH JOINT WITH THE SUBCOMMITTEE ON FISHERIES CONSERVATION, WILDLIFE AND OCEANS OF THE COMMITTEE ON RESOURCES U.S. HOUSE OF REPRESENTATIVES ONE HUNDRED SEVENTH CONGRESS SECOND SESSION

May 16, 2002

Serial No. 107-117

snip...

Mr. MCINNIS. Today, this joint Subcommittee hearing will explore an issue of immeasurable importance to the growing number of communities in wide-ranging parts of this country, the growing incidence of Chronic Wasting Disease in North America’s wild and captive deer and elk populations. In a matter of just a few months, this once parochial concern has grown into something much larger and much more insidious than anyone could have imagined or predicted.

As each day passes, this problem grows in its size, scope, and consequence. One thing becomes clear. Chronic Wasting Disease is not a Colorado problem. It is a Wisconsin problem or a Nebraska or Wyoming problem. It is a national problem and anything short of a fully integrated, systematic national assault on this simply will not do, which is precisely why we brought our group together here today.

snip...

So this is a disease that is spreading throughout the continent and it is going to require a national response as well as the efforts that are currently taking place in States like Wisconsin, Colorado, Nebraska, Wyoming, the interest they now have down in Texas and some of the neighboring States that have large white-tailed deer population and also elk.

This is a huge issue for us, Mr. Chairman, in the State of Wisconsin. I want to commend Governor McCallum and your staff and the various agencies for the rapid response that you have shown, given the early detection of CWD after the last deer hunting season. The problem that we have, though, is just a lack of information, good science in regards to what is the best response, how dangerous is this disease. We cannot close the door, quite frankly, with the paucity of scientific research that is out there right now in regards to how the disease spreads, the exposure of other livestock herds—given the importance of our dairy industry in the State, that is a big issue—and also the human health effects.



Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018 Singeltary Submission

Comment from Terry Singeltary Sr. The is a Comment on the Animal and Plant Health Inspection Service (APHIS) Notice: Chronic Wasting Disease Herd Certification Program Standards

For related information, Open Docket Folder

Comment Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018

Greetings APHIS, USDA, Dr. Tracy Nichols, et al, 

I wish to kindly submit my comments on the Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards please. i have submitted online and sent a hard copy to Dr. Nichols via email. i know that my concern may not be the same concern as others, but ramifications from cwd tse prion can be long lasting, and science is still emerging. however, the science today warrants immediate and further actions be taken, especially about zoonosis potential for cwd tse prion, if it has not happened already. my comments, with reference materials, are as follows, and will be formatted in such a way, i will address issues by numbers 1-10, and under each one of my comments by each number, i will reference my comments with science to back up what i am stating/asking...thank you kindly, terry

1. I believe that immediately, there should be a 'DECLARATION OF EXTRAORDINARY EMERGENCY FOR FOREIGN ANIMAL DISEASE OF THE United States of America USA' due to Chronic Wasting Disease CWD Transmissible Spongiform Encephalopathy TSE Prion disease. All Intercontinental, International, Interstate movements of cervid should be banned immediately from the USA, and documented CWD TSE Prion Countries. ...

snip...

see full text Singeltary Submission for references.

2. Voluntary Chronic Wasting Disease Herd Certification Program should be made MANDATORY immediately, OR NO PERMIT TO FARM DEER OR ELK, PERIOD! you don't want to join, then fine, you don't farm cervid and or any product there from...see full text Singeltary Submission for references.

3. INDEMNITY, NO MORE Federal indemnity program, or what i call, ENTITLEMENT PROGRAM for game farm industry. NO MORE BAIL OUTS FROM TAX PAYERS. if the captive industry can't buy insurance to protect not only themselves, but also their customers, and especially the STATE, from Chronic Wasting Disease CWD TSE Prion or what some call mad deer disease and harm therefrom, IF they can't afford to buy that insurance that will cover all of it, then they DO NOT GET A PERMIT to have a game farm for anything. This CWD TSE Prion can/could/has caused property values to fall from some reports in some places. roll the dice, how much is a state willing to lose?...see full text Singeltary Submission for references.

4. QUARANTINE OF ALL CAPTIVE, BREEDERS, URINE, ANTLER, VELVET, SPERM, OR ANY FACILITY that has been confirmed to have Chronic Wasting Disease CWD TSE Prion, the QUARANTINE should be for 21 years due to science showing what scrapie can do. 5 years is NOT enough. see; Infectious agent of sheep scrapie may persist in the environment for at least 16 years...


snip...see full text Singeltary Submission for references.

PLEASE SEE Singeltary full text file DOWNLOAD ON GOVERNMENT SITE, OR GO TO THIS URL LINK FOR FULL TEXT OF SINGELTARY SUBMISSION TO Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018, PLEASE SEE;

FRIDAY, MARCH 30, 2018 

Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018


Terry S. Singeltary Sr., Bacliff, Texas USA 77518 flounder9@verizon.net Attachments (1) Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary


MONDAY, MAY 20, 2019 

APHIS, USDA, Announces the Finalized Chronic Wasting Disease Herd Certification Program Standards Singeltary Submissions






Comment from Terry Singeltary

The is a Comment on the Animal and Plant Health Inspection Service (APHIS) Notice: Concurrence with the World Organization for Animal Health's Risk Designation for Bovine Spongiform Encephalopathy
For related information, Open Docket Folder

Comment

APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary Submission

Greetings APHIS et al,

I would kindly like to comment on APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], and my comments are as follows, with the latest peer review and transmission studies as references of evidence.

THE OIE/USDA BSE Minimal Risk Region MRR is nothing more than free pass to import and export the Transmissible Spongiform Encephalopathy TSE Prion disease. December 2003, when the USDA et al lost it's supposedly 'GOLD CARD' ie BSE FREE STATUS (that was based on nothing more than not looking and not finding BSE), once the USA lost it's gold card BSE Free status, the USDA OIE et al worked hard and fast to change the BSE Geographical Risk Statuses i.e. the BSE GBR's, and replaced it with the BSE MRR policy, the legal tool to trade mad cow type disease TSE Prion Globally. The USA is doing just what the UK did, when they shipped mad cow disease around the world, except with the BSE MRR policy, it's now legal.

Also, the whole concept of the BSE MRR policy is based on a false pretense, that atypical BSE is not transmissible, and that only typical c-BSE is transmissible via feed. This notion that atypical BSE TSE Prion is an old age cow disease that is not infectious is absolutely false, there is NO science to show this, and on the contrary, we now know that atypical BSE will transmit by ORAL ROUTES, but even much more concerning now, recent science has shown that Chronic Wasting Disease CWD TSE Prion in deer and elk which is rampant with no stopping is sight in the USA, and Scrapie TSE Prion in sheep and goat, will transmit to PIGS by oral routes, this is our worst nightmare, showing even more risk factors for the USA FDA PART 589 TSE PRION FEED ban.

The FDA PART 589 TSE PRION FEED ban has failed terribly bad, and is still failing, since August 1997. there is tonnage and tonnage of banned potential mad cow feed that went into commerce, and still is, with one decade, 10 YEARS, post August 1997 FDA PART 589 TSE PRION FEED ban, 2007, with 10,000,000 POUNDS, with REASON, Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement. you can see all these feed ban warning letters and tonnage of mad cow feed in commerce, year after year, that is not accessible on the internet anymore like it use to be, you can see history of the FDA failure August 1997 FDA PART 589 TSE PRION FEED ban here, but remember this, we have a new outbreak of TSE Prion disease in a new livestock species, the camel, and this too is very worrisome.

WITH the OIE and the USDA et al weakening the global TSE prion surveillance, by not classifying the atypical Scrapie as TSE Prion disease, and the notion that they want to do the same thing with typical scrapie and atypical BSE, it's just not scientific.

WE MUST abolish the BSE MRR policy, go back to the BSE GBR risk assessments by country, and enhance them to include all strains of TSE Prion disease in all species. With Chronic Wasting CWD TSE Prion disease spreading in Europe, now including, Norway, Finland, Sweden, also in Korea, Canada and the USA, and the TSE Prion in Camels, the fact the the USA is feeding potentially CWD, Scrapie, BSE, typical and atypical, to other animals, and shipping both this feed and or live animals or even grains around the globe, potentially exposed or infected with the TSE Prion. this APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087], under it's present definition, does NOT show the true risk of the TSE Prion in any country. as i said, it's nothing more than a legal tool to trade the TSE Prion around the globe, nothing but ink on paper.

AS long as the BSE MRR policy stays in effect, TSE Prion disease will continued to be bought and sold as food for both humans and animals around the globe, and the future ramifications from friendly fire there from, i.e. iatrogenic exposure and transmission there from from all of the above, should not be underestimated. ...

https://bovineprp.blogspot.com/2019/06/aphis-concurrence-with-oie-risk.html

Attachments

  (1)

APHIS Concurrence With OIE Risk Designation for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0087] Singeltary...







Terry S. Singeltary Sr.

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