Texas Officials Are Taking A Big Risk To Fight A Devastating Deer Disease
Texas Officials Are Taking A Big Risk To Fight A Devastating Deer Disease
Large-scale PMCA screening of retropharyngeal lymph nodes and in white-tailed deer and comparisons with ELISA and IHC: the Texas CWD study
Rebeca Benaventea, Paulina Sotoa, Mitch Lockwoodb, and Rodrigo Moralesa
aDepartment of Neurology, McGovern Medical School, University of Texas Health Science Center at Houston, Texas, USA; bTexas Park and Wildlife Department, Texas, USA
Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy that affects various species of cervids, and both free-ranging and captive animals. Until now, CWD has been detected in 3 continents: North America, Europe, and Asia. CWD prevalence in some states may reach 30% of total animals. In Texas, the first case of CWD was reported in a free-range mule deer in Hudspeth and now it has been detected in additional 14 counties.
Currently, the gold standard techniques used for CWD screening and detection are ELISA and immunohistochemistry (IHC) of obex and retropharyngeal lymph nodes (RPLN). Unfortunately, these methods are known for having a low diagnostic sensitivity. Hence, many CWD-infected animals at pre-symptomatic stages may be misdiagnosed. Two promising in vitro prion amplification techniques, including the real-time quaking-induced conversion (RT-QuIC) and the protein misfolding cyclic amplification (PMCA) have been used to diagnose CWD and other prion diseases in several tissues and bodily fluids. Considering the low cost and speed of RT-QuIC, two recent studies have communicated the potential of this technique to diagnose CWD prions in RPLN samples. Unfortunately, the data presented in these articles suggest that identification of CWD positive samples is comparable to the currently used ELISA and IHC protocols. Similar studies using the PMCA technique have not been reported.
Aims: Compare the CWD diagnostic potential of PMCA with ELISA and IHC in RPLN samples from captive and free-range white-tailed deer.
Material and Methods: In this study we analyzed 1,003 RPLN from both free-ranging and captive white-tailed deer collected in Texas. Samples were interrogated with the PMCA technique for their content of CWD prions. PMCA data was compared with the results obtained through currently approved techniques.
Results: Our results show a 15-fold increase in CWD detection in free-range deer compared with ELISA. Our results unveil the presence of prion infected animals in Texas counties with no previous history of CWD. In the case of captive deer, we detected a 16% more CWD positive animals when compared with IHC. Interestingly, some of these positive samples displayed differences in their electroforetic mobilities, suggesting the presence of different prion strains within the State of Texas.
Conclusions: PMCA sensitivity is significantly higher than the current gold standards techniques IHC and ELISA and would be a good tool for rapid CWD screening.
Funded by: USDA
Grant number: AP20VSSPRS00C143
Stable and highly zoonotic cervid prion strain is possible
Manuel Camacho, Xu Qi, Liuting Qing, Sydney Smith, Jieji Hu, Wanyun Tao, Ignazio Cali, and Qingzhong Kong
Department of Pathology, Case Western Reserve University, Cleveland, USA
Aims: Whether CWD prions can infect humans remains unclear despite the very substantial scale and long history of human exposure of CWD in some areas. Multiple in vitro conversion experiments and in vivo animal studies suggest that the CWD-to-human transmission barrier is not unbreakable. A major public health concern on CWD zoonosis is the emergence of highly zoonotic CWD strains. We aim to address the question of whether highly zoonotic CWD strains are possible.
Material and Methods: We inoculated a few sCJD brain samples into cervidized transgenic mice, which were intended as negative controls for bioassays of brain tissues from sCJD cases who had hunted or consumed vension from CWD-endemic states. Some of these mice became infected and their brain tissues were further examined by serial passages in humanized or cervidized mice.
Results: Passage of sCJDMM1 in transgenic mice expressing elk PrP (Tg12) resulted in a ‘cervidized’ CJD strain that we termed CJDElkPrP. We observed 100% transmission of CJDElkPrPin transgenic mice expressing human PrP (Tg40h). We passaged CJDElkPrPtwo more times in the Tg12 mice. We found that such second and third passage CJDElkPrPprions also led to 100% infection in the Tg40h mice. In contrast, we and others found zero or poor transmission of natural elk CWD isolates in humanized mice, despite that natural elk CWD isolates and CJDElkPrPshare the same elk PrP sequence.
Conclusions: Our data demonstrate that highly zoonotic cervid prion strains are not only possible but also can be stably maintained in cervids and that CWD zoonosis is prion strain-dependent.
Funded by: NIH
Grant number: R01NS052319, R01NS088604, R01NS109532
Acknowledgement: We want to thank the National Prion Disease Pathology Surveillance Center and Drs. Allen Jenny and Katherine O’Rourke for providing the sCJD samples and the CWD samples, respectively.
Transmission of prion infectivity from CWD-infected macaque tissues to rodent models demonstrates the zoonotic potential of chronic wasting disease.
Samia Hannaouia, Ginny Chenga, Wiebke Wemheuerb, Walter J. Schulz-Schaefferb, Sabine Gilcha, and Hermann M. Schätzla
aDepartment of Comparative Biology and Experimental Medicine, Faculty of Veterinary Medicine & Hotchkiss Brain Institute; University of Calgary, Calgary, Canada; bInstitute of Neuropathology, Medical Faculty, Saarland University, Homburg/Saar, Germany
Aims: Chronic wasting disease (CWD) is a prion disease of cervids. Its rapid geographic expansion, shedding of infectivity and persistence in the environment for many years are of concern for humans. Here, we provide the first evidence by transmission experiments to different transgenic mouse models and bank voles that Cynomolgus macaques inoculated via different routes with CWD-positive cervid tissues harbor infectious prions that elicit clinical disease in rodents.
Material and Methods: We used tissue materials from macaques inoculated with CWD to inoculate transgenic mice overexpressing cervid PrPCfollowed by transmission into bank voles. We used RT-QuIC, immunoblot and PET blot analysis to assess brains, spinal cords, and tissues of the gastrointestinal tract (GIT) for the presence of prions.
Results: Our results show that of the macaque materials that induced clinical disease in transgenic mice,73% were from the CNS (46% spinal cord and 27% brain), and 27% were from the spleen, although attack rates were low around 20%. Clinical mice did not display PK-resistant PrPSc(PrPres) in immunoblot, but showed low-levels of prion seeding activity. Transmission into bank voles from clinical transgenic mice led to a 100% attack rate with typical PrPressignature in immunoblot, which was different from that of voles inoculated directly with CWD or scrapie prions. High-level prion seeding activity in brain and spinal cord and PrPresdeposition in the brain were present. Remarkably, we also found prion seeding activity in GIT tissues of inoculated voles. Second passage in bank voles led to a 100% attack rate in voles inoculated with brain, spinal cord and small intestine material from first round animals, with PrPresin immunoblot, prion seeding activity, and PrPresdeposition in the brain. Shortened survival times indicate adaptation in the new host. This also shows that prions detected in GIT tissues are infectious and transmissible. Transmission of brain material from sick voles back to cervidized mice revealed transmission in these mice with a 100% attack rate, and interestingly, with different biochemical signature and distribution in the brain.
Conclusions: Our findings demonstrate that macaques, considered the best model for the zoonotic potential of prions, were infected upon CWD challenge, including oral one. The disease manifested as atypical in macaques and transgenic mice, but with infectivity present at all times, as unveiled in the bank vole model with an unusual tissue tropism.
Funded by: The National Institutes of Health, USA, and the Alberta Prion Research Institute/Alberta Innovates Canada.
Grant number: 1R01NS121016-01; 201,600,023
Acknowledgement: We thank Umberto Agrimi, Istituto Superiore di Sanità, Rome, Italy, and Michael Beekes, Robert-Koch Institute Berlin, Germany, for providing the bank vole model. We thank the University of Calgary animal facility staff and Dr. Stephanie Anderson for animal care.
Transmission of Cervid Prions to Humanized Mice Demonstrates the Zoonotic Potential of CWD
Samia Hannaouia, Irina Zemlyankinaa, Sheng Chun Changa, Maria Immaculata Arifina, Vincent Béringueb, Debbie McKenziec, Hermann M. Schatzla, and Sabine Gilcha
aDepartment of Comparative Biology and Experimental Medicine, Faculty of Veterinary Medicine; Hotchkiss Brain Institute; University of Calgary, Calgary, Canada; bUniversité Paris-Saclay, INRAE, UVSQ, VIM, Jouy-en-Josas, France; cDepartment of Biological Sciences, Center for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Canada
Aims: Chronic wasting disease (CWD), a prion disease of cervids, spreads efficiently among wild and farmed animals. Potential transmission to humans of CWD is a growing concern due to its increasing prevalence. Here, we aimed to determine the zoonotic potential of CWD using a mouse model for human prion diseases.
Material and Methods: Transgenic mice overexpressing human PrPChomozygous for methionine at codon 129 (tg650) were inoculated intracerebrally with brain homogenates of white-tailed deer infected with Wisc-1/CWD1 or 116AG CWD strains. Mice were monitored for clinical signs and were euthanized at terminal disease. Brains were tested by RT-QuIC, western blot upon PK digestion, and immunohistochemistry; fecal homogenates were analyzed by RT-QuIC. Brain/spinal cord and fecal homogenates of CWD-inoculated tg650 mice were inoculated into tg650 mice or bank voles. Brain homogenates of bank voles inoculated with fecal homogenates of CWD-infected tg650 mice were used for second passage in bank voles.
Results: Here, we provide the strongest evidence supporting the zoonotic potential of CWD prions, and their possible phenotype in humans. Inoculation of mice expressing human PrPCwith deer CWD isolates (strains Wisc-1 and 116AG) resulted in atypical clinical manifestations in > 75% of the mice, with myoclonus as leading clinical sign. Most of tg650 brain homogenates were positive for seeding activity in RT-QuIC. Clinical disease and presentation was transmissible to tg650 mice and bank voles. Intriguingly, protease-resistant PrP in the brain of tg650 mice resembled that found in a familial human prion disease and was transmissible upon passage. Abnormal PrP aggregates upon infection with Wisc-1 were detectable in thalamus, hypothalamus, and midbrain/pons regions.
Unprecedented in human prion disease, feces of CWD-inoculated tg650 mice harbored prion seeding activity and infectious prions, as shown by inoculation of bank voles and tg650 with fecal homogenates.
Conclusions: This is the first evidence that CWD can infect humans and cause disease with a distinctive clinical presentation, signature, and tropism, which might be transmissible between humans while current diagnostic assays might fail to detect it. These findings have major implications for public health and CWD-management.
Funded by: We are grateful for financial support from the Natural Sciences and Engineering Research Council of Canada, the National Institutes of Health, Genome Canada, and the Alberta Prion Research Institute. SG is supported by the Canada Research Chairs program.
Acknowledgement: We thank Dr. Trent Bollinger, WCVM, University of Saskatchewan, Saskatoon, Canada, for providing brain tissue from the WTD-116AG isolate, Dr. Stéphane Haïk, ICM, Paris, France, for providing brain tissue from vCJD and sCJD cases, and Dr. Umberto Agrimi, Istituto Superiore di Sanità, Italy, for the bank vole model. We thank animal facility staff for animal care, Dr. Stephanie Anderson for veterinary oversight, and Yo-Ching Cheng for preparing recombinant PrP substrates. Thank you to Dr. Stephanie Booth and Jennifer Myskiw, Public Health Agency of Canada, Canada.
The chronic wasting disease agent from white-tailed deer is infectious to humanized mice after passage through raccoons
Eric Cassmanna, Xu Qib, Qingzhong Kongb, and Justin Greenleea
aNational Animal Disease Center, Agricultural Research Service, US Department of Agriculture, Ames, IA, USA
bDepartments of Pathology, Neurology, National Center for Regenerative Medicine, and National Prion Disease Pathology Surveillance Center, Case Western Reserve University, Cleveland, Ohio, USA
Aims: Evaluate the zoonotic potential of the raccoon passaged chronic wasting disease (CWD) agent in humanized transgenic mice in comparison with the North American CWD agent from the original white-tailed deer host.
Material and Methods: Pooled brain material (GG96) from a CWD positive herd was used to oronasally inoculate two white-tailed deer with wild-type prion protein genotype and intracranially inoculate a raccoon. Brain homogenates (10% w/v) from the raccoon and the two white-tailed deer were used to intracranially inoculate separate groups of transgenic mice that express human prion protein with methionine (M) at codon 129 (Tg40h). Brains and spleens were collected from mice at experimental endpoints of clinical disease or approximately 700 days post-inoculation. Tissues were divided and homogenized or fixed in 10% buffered neutral formalin. Immunohistochemistry, enzyme immunoassay, and western blot were used to detect misfolded prion protein (PrPSc) in tissue.
Results: Humanized transgenic mice inoculated with the raccoon passaged CWD agent from white-tailed deer exhibited a 100% (12/12) attack rate with an average incubation period of 605 days. PrPScwas detected in brain tissue by enzyme immunoassay with an average optical density of 3.6/4.0 for positive brains. PrPScalso was detected in brain tissue by western blot and immunohistochemistry. No PrPScwas detected in the spleens of mice inoculated with the raccoon passaged CWD agent. Humanized mice inoculated with the CWD agent from white-tailed deer did not have detectable PrPScusing conventional immunoassay techniques.
Conclusions: The host range of the CWD agent from white-tailed deer was expanded in our experimental model after one passage through raccoons.
Funded by: This research was funded in its entirety by congressionally appropriated funds to the United States Department of Agriculture, Agricultural Research Service. The funders of the work did not influence study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Acknowledgement: We thank Quazetta Brown, Lexi Frese, Rylie Frese, Kevin Hassall, Leisa Mandell, and Trudy Tatum for providing excellent technical support to this project.
Shedding of Chronic Wasting Disease Prions in Multiple Excreta Throughout Disease Course in White-tailed Deer
Nathaniel D. Denkersa, Erin E. McNultya, Caitlyn N. Krafta, Amy V. Nallsa, Joseph A. Westricha, Wilfred Goldmannb, Candace K. Mathiasona, and Edward A. Hoovera
aPrion Research Center, College of Veterinary Medicine and Biological Sciences, Department of Microbiology, Immunology, and Pathology; Colorado State University, Fort Collins, CO, USA; bDivision of Infection and Immunity, The Roslin Institute and the Royal Dick School of Veterinary Studies, University of Edinburgh, Midlothian, UK
Aims: Chronic wasting disease (CWD) now infects cervids in South Korea, North America, and Scandinavia. CWD is unique in its efficient transmission and shedding of prions in body fluids throughout long course infections. Questions remain as to the magnitude of shedding and the route of prion acquisition. As CWD continues to expand, the need to better understand these facets of disease becomes more pertinent. The purpose of the studies described was to define the longitudinal shedding profile of CWD prions in urine, saliva, and feces throughout the course of infection in white-tailed deer.
Material and Methods: Twelve (12) white-tailed deer were inoculated with either 1 mg or 300ng of CWD. Urine, saliva, and feces were collected every 3-month post-inoculation (MPI) throughout the study duration. Cohorts were established based on PNRP genotype: codon 96 GG (n = 6) and alternate codons 96 GS (n = 5) & 103NT (n = 1). Urine and saliva were analyzed using iron-oxide magnetic extraction (IOME) and real-time quaking induced conversion (RT-QuIC)(IQ). Feces were subjected to IOME, followed by 4 rounds protein misfolding cyclic amplification (PMCA) with products analyzed by RT-QuIC (IPQ). To determine whether IPQ may be superior to IQ, a subset of urine and saliva were also tested by IPQ. Results were compared with clinical disease status.
Results: Within the 96 GG cohort, positive seeding activity was detected in feces from all deer (100%), in saliva from 5 of 6 (83%), and in urine from 4 of 6 (66%). Shedding in all excreta occurred at, or just after, the first positive tonsil biopsy result. In the 96 GS/103NT cohort, positive seeding activity could be detected in feces from 3 of 6 (50%) deer, saliva in 2 of 6 (33%), and urine in 1 of 6 (16%). Shedding in excreta was detected >5 months after the first tonsil positive result. Four of six 96 GG deer developed clinical signs of CWD, whereas only 2 of the 96 GS/103NT did. Shedding was more frequently detected in deer with clinical disease. The IPQ protocol did not significantly improve detection in saliva or urine samples, however, it significantly augmented detection in feces by eliminating non-specific background commonly experienced with IQ. Negative control samples remained negative in samples tested.
Conclusions: These studies demonstrate: (a) CWD prion excretion occurs throughout infection; (2) PRNP genotype (GG≫GS/NT) influences the excreta shedding; and (3) detection sensitivity in excreta can vary with different RT-QuIC protocols. These results provide a more complete perspective of prion shedding in deer during the course of CWD infection.
Funded by: National Institutes of Health (NIH)
Grant number: RO1-NS061902-09 R to EAH, PO1-AI077774 to EAH, and R01-AI112956-06 to CKM
Acknowledgement: We abundantly thank Sallie Dahmes at WASCO and David Osborn and Gino D’Angelo at the University of Georgia Warnell School of Forestry and Natural Resources for their long-standing support of this work through provision of the hand-raised, CWD-free, white-tailed deer used in these studies
https://www.tandfonline.com/doi/full/10.1080/19336896.2022.2091286
https://www.nature.com/articles/srep11573
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.
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***thus questioning the origin of human sporadic cases***
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***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.
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https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf
***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.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
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
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.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
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.
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160
Author
Submitted to: North American Deer Farmer Publication Type: Trade Journal Publication Acceptance Date: 7/1/2022 Publication Date: 7/20/2022 Citation: Cassmann, E.D., Greenlee, J.J. 2022. Exploring the possibility of CWD transmission through artificial insemination of semen from CWD positive bucks. North American Deer Farmer. p. 107-109. Interpretive Summary: Technical Abstract: Artificial insemination is a popular method for herd management and reproduction in the cervid farming industry. There are numerous benefits including increased access to superior genetics, convenience, and increased farm revenue. In this article, we summarize the research that is underway to determine if semen from a CWD infected buck can transmit the disease. Some research has already been performed on the reproductive transmission of CWD in cervids. Scientists from Colorado State University used Muntjac deer to demonstrate that CWD positive does could transmit CWD to their fawns (1). In the study, Muntjac does were bred to CWD negative bucks. At the time of breeding, does were either in the early or late stage of CWD infection. Fawns from both doe groups were positive for CWD. More recent laboratory experiments on semen from CWD positive bucks have demonstrated the presence of CWD prions (2). Researchers used an amplification technique called PMCA (protein misfolding cyclic amplification). The technique amplifies low levels of CWD prions to a point where conventional antibody methods can detect them. The caveat to the discovery of CWD prions in semen is that we’re unsure if the amount of CWD prions in semen is biologically relevant. In other words, is the level of CWD prions in semen sufficient to be infectious and cause disease in deer? In our present study, we are trying to answer that question. We obtained semen from a CWD positive buck. The semen was confirmed to be PMCA positive. For the study, we used the transcervical insemination method in three does. As of June 19th, a single fawn was born. Shortly after birth the fawn was separated to prevent environment CWD exposure. We are assessing both the does and the fawn for the development of CWD. The experiment is expected to last several years, and periodic sampling will help monitor progress. A second phase of the study will investigate the absolute susceptibility of white-tailed deer does to CWD after transcervical and/or vaginal exposure to large amounts of CWD prions. We plan to expose two does to brain suspension from a CWD positive deer. These does will also be monitored long term for the development of disease. If these does remain negative, it would indicate that CWD transmission to the dam is highly unlikely via reproductive tract exposure. TUESDAY, DECEMBER 31, 2019 In Vitro detection of Chronic Wasting Disease (CWD) prions in semen and reproductive tissues of white tailed deer bucks (Odocoileus virginianus TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super ovulation, and the potential TSE Prion connection, what if? SUNDAY, FEBRUARY 16, 2020 ***> Jerking for Dollars, Are Texas Politicians and Legislators Masturbating Deer For Money, and likely spreading CWD TSE Prion? THURSDAY, JULY 10, 2014 supercalifragilisticexpialidocious or superovulationcwdtsepriondocious ? (It was noted with concern that hormone extracts could be manufactured by a veterinary surgeon for administration to animals under his care without any Medicines Act Control.) PITUITARY EXTRACT This was used to help cows super ovulate. *** This tissue was considered to be of greatest risk of containing BSE and consequently transmitting the disease. *** Proposed Amendments to CWD Zone Rules Your opinions and comments have been submitted successfully. Thank you for participating in the TPWD regulatory process. THURSDAY, AUGUST 04, 2022 Texas Proposed Amendments to CWD Zone Rules Singeltary Submission FRIDAY, APRIL 30, 2021 Should Property Evaluations Contain Scrapie, CWD, TSE PRION Environmental Contamination of the land? ***> 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 WEDNESDAY, MAY 17, 2017 *** Chronic Wasting Disease CWD TSE Prion aka Mad Deer Disease and the Real Estate Market Land Values *** MONDAY, MARCH 05, 2018 TRUCKING AROUND AND SPREADING CHRONIC WASTING DISEASE CWD TSE PRION VIA MOVEMENT OF CERVID AND TRANSPORTATION VEHICLES TUESDAY, JUNE 28, 2022 TAHC PROPOSES CHANGES TO VOLUNTARY CWD PROGRAM CHAPTER 40, CHRONIC WASTING DISEASE SINGELTARY SUBMISSION JUNE 28, 2022 ***> 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 <*** “Regrettably, the gravity of this situation continues to mount with these new CWD positive discoveries, as well as with the full understanding of just how many other facilities and release sites across Texas were connected to the CWD positive sites in Uvalde and Hunt Counties,” said Carter Smith, Executive Director of TPWD. ***> 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.'' FRIDAY, JUNE 04, 2021 Texas Breeder Deer May Have Spread Brain Disease CWD TSE Prion Into The Wild Governor Abbott on HOW TO LEGISLATE SPREADING CWD TO HELL AND BACK IN TEXAS $$$ i picked up on something that was said, there were several folks complaining that the breeders were gettingpicked on, and someone said something about trying to 'legislate' there way out of this. folks, this is terrible, ihave seen this in other states, and it just spreads cwd even more. hell, it happened right here in Texas in theearly days, that's why we are where were at now, you cannot let a bunch of Austin Legislative Socialites regulateCWD, just look what happened in Wisconsin. but i bet this attempted swaying of regulatory power shift fromTPWD et al to the Texas Legislature in Austin is happening as we speak. we can't let this happen... SUNDAY, JANUARY 22, 2017 Texas 85th Legislative Session 2017 Chronic Wasting Disease CWD TSE Prion Cervid Captive Breeder Industry FRIDAY, JANUARY 27, 2017 TEXAS, Politicians, TAHC, TPWD, and the spread of CWD TSE Prion in Texas SUNDAY, MAY 14, 2017 85th Legislative Session 2017 AND THE TEXAS TWO STEP Chronic Wasting Disease CWD TSE Prion, and paying to play $$$ Powerful Abbott appointee's lobbying sparks blowback in Legislature In an ironic twist for Gov. Greg Abbott, who has made ethics reform an urgent political priority, the Texas House is taking aim at what critics call a "pay to play" culture among his appointees. BY JAY ROOT MAY 12, 2017 12 AM Houston billionaire Dan Friedkin is chairman of the Texas Parks and Wildlife Commission. Texas Parks and Wildlife Commission When Gov. Greg Abbott tapped one of his top campaign donors to become chairman of the Texas Parks and Wildlife Commission, he didn’t get a part-time appointee who would merely draft rules and implement conservation laws passed by the Legislature. In Dan Friedkin, the governor got a Houston billionaire — with a team of privately funded lobbyists — willing to use his influence to ensure his wildlife interests are taken into account by the Legislature before they pass those laws, interviews and records show. On the receiving end of that influence, and not in a happy way, is state Rep. Chris Paddie, R-Marshall. Paddie said a lobbyist working for Friedkin’s business empire, which includes a massive South Texas hunting ranch, has been working against his deer breeder management bill, which many large ranchers oppose. The state Parks and Wildlife Department oversees deer breeding regulations in Texas. “Many times these appointees are well-heeled, very influential people,” Paddie said. “Overall, I feel that it’s inappropriate for an appointee of a board or commission to have personal lobbyists lobbying on issues related to that board or commission.” Under Texas law, state agencies are barred from lobbying the Legislature. But the powerful people who oversee them aren’t. If Paddie and dozens of his colleagues get their way, that practice soon will be a Class A misdemeanor. Last weekend, Paddie attached a ban on appointee lobbying — which would apply to any issues intersecting with their state responsibilities — to an ethics bill that already had powerful friends of the governor in its crosshairs. The provision was adopted unanimously and the bill sailed out of the Texas House on a 91-48 vote Saturday. The ethics bill, authored by Rep. Lyle Larson, R-San Antonio, would bar big campaign donors from getting appointed by governors in the first place. Anyone who contributed over $2,500 would be barred from serving on state boards and commissions. Larson pointed to news articles documenting the amount of campaign money appointees have collectively given governors. Last year the San Antonio Express-News calculated that Abbott had received nearly $9 million from people he’s picked for appointed office; before that, a widely cited report from Texans for Public Justice found former Gov. Rick Perry had received $17 million from his own appointees. Larson said 20 years from now, Texans will be reading the same stories about a future governor unless the Legislature does something about it now. “We’ve read that article for the last three decades,” Larson said during a brief floor speech. “This is your opportunity to say, 'We need to stop this.' The most egregious ethics violation we’ve got in the state is the pay to play in the governor’s office.” A prodigious fundraiser, Abbott has put plenty of big donors on prestigious boards and commissions. On the Parks and Wildlife Commission alone, he has installed three mega-donors — pipeline mogul Kelcy Warren, who’s given Abbott more than $800,000 over his statewide political career; Houston businessman S. Reed Morian, who has given $600,000; and Friedkin, who personally donated more than $700,000 — while his Gulf States Toyota PAC gave Abbott another $100,000, according to Ethics Commission records. Passage of Larson’s HB 3305 represents an ironic twist for Abbott, who for the second session in a row has made ethics reform an urgent political priority — resulting in a bill that's now taking aim at his gubernatorial appointments. Abbott, who has made a habit of ignoring tough questions, hasn't made any public statements about the bill, and his office did not respond to multiple requests for comment. Friedkin — whose wealth is estimated at $3.4 billion by Forbes — is the owner and CEO of Gulf States Toyota, founded in 1969, which has had the exclusive rights to distribute new Toyotas in Texas and four nearby states. He’d also been a mega-donor to former Gov. Rick Perry, who first appointed Friedkin to the Parks and Wildlife Commission in 2005. Abbott made Friedkin chairman of the commission in 2015. Requests for comment from Friedkin's office went unanswered. In addition to his public role as parks and wildlife chairman, a perch that gives him significant influence over deer management issues, Friedkin has private wildlife interests. He owns the sprawling Comanche Ranch in South Texas, according to published news accounts. The January 2014 edition of Texas Wildlife, published by the Texas Wildlife Association, described Friedkin’s Comanche Ranch as “privately owned and privately hunted” and said it’s “in the business to produce as many trophy bucks as possible, without damaging the native habitat.” The association, which advocates for private landowners and hunting rights, has locked horns with deer breeding interests at Parks and Wildlife and the Capitol. They compete against each other in the lucrative trophy deer hunting market — and the battle between them perennially spills into the rule-making process at the Parks and Wildlife Commission. One of their battles centers on how captive deer are tagged so that game wardens and others can distinguish them from native deer. Current law requires a combination of tags and tattoos, and the ranchers and large landowners want to keep it that way. The breeders, meanwhile, favor tagging deer with microchips, which they contend are more accurate and foolproof. The Wildlife Association said in a Facebook post that removing visible tag or tattoo requirements and allowing microchip tracking “creates real biosecurity risks and blurs ethical lines in the hunting community, as captive deer breeders are allowed to transport and release these animals to be co-mingled with pasture-born deer.” Proponents of the current system say tough rules on breeders are needed to keep out imported deer that may carry Chronic Wasting Disease, which has been found in Texas. On the other side of the issue is the Texas Deer Association, which represents breeder interests. Executive Director Patrick Tarlton said opposition to his $1.6 billion industry stems less from environmental and health concerns and more from wealthy ranch owners who want to boost profits from trophy-seeking hunters. He notes that Chronic Wasting Disease has been found in both free range and captive deer. Paddie sided with the breeders by filing House Bill 2855, which would allow breeders to track their deer with microchips instead of relying on physical tags that they say can be torn off. No one identifying themselves as a Friedkin corporate lobbyist opposed the deer breeding bills during public hearings, according to House and Senate committee records published online. Behind the scenes, it was a different story. Paddie said his chief of staff reached out to Laird Doran, one of several lobbyists for Friedkin’s Gulf States Toyota, after hearing that he was trying to convince other legislators to help defeat Paddie's deer microchip bill. “My chief called him and said, 'Hey, if you’ve got a problem with our bill why aren’t you talking to us?’ ” Paddie said. “He said he represented the Friedkin Group when that happened.” According to an email from an aide to Sen. Craig Estes, R-Wichita Falls, who is carrying the deer breeding bill in the Senate, Doran also identified himself as a representative of the “Friedkin Group.” That’s the name of the consortium that contains Friedkin's Gulf States Toyota, according to the company’s Linked-In page. He told Estes’ aide that the Friedkin group was opposed to any bill that would “remove requirements for (deer) ear tags,” the senator’s office confirmed. It’s not clear exactly which Friedkin interests Doran was advancing. Doran is registered at the Texas Ethics Commission with a single entity — Gulf States Toyota — and the agency has no record of a lobbyist working for an entity or individual with the name Friedkin in it, the commission confirmed Wednesday afternoon. However, Doran checked a variety of non-automotive subject areas in which he is lobbying during this legislative session on behalf of Friedkin’s lucrative distributorship, including “animals,” “parks & wildlife,” “state agencies, boards & commissions,” “environment” and more, his detailed lobby disclosures show. Doran, director of government relations and senior counsel at the Friedkin Group, did not return phone and email messages left by The Texas Tribune. Estes said he didn’t have a problem with a governor's appointee engaging in lobbying on issues that affected their private interests, as long as they keep that separate from their state roles. “I don’t think they should be barred from expressing their views as long as they’re careful to say these are my views, not the views of the agency I’m representing,” Estes said. But Tarlton, the deer association director, said Friedkin’s use of lobbyists to oppose deer breeders in the Legislature gives the breeders' opponents a huge advantage. “I think that if the commissioner of Texas Parks and Wildlife is actively lobbying against an industry which his department directly oversees, it absolutely sets up an unfair and closed system of government,” Tarlton said. “The commission is supposed to be the unbiased and equitable oversight for everything wildlife.” Paddie hopes his amendment to Larsen's ethics bill will even the playing field. He referred to the wealthy Parks and Wildlife chairman (see the 2:29:00 mark in this recorded exchange) when he tacked the appointee-lobbying provision onto Larson’s bill. Paddie said he’s not singling out anyone. He said it would apply to other powerful gubernatorial appointees in a position to do the same. “I could have named any number of examples as far as the agencies in particular,” Paddie said. “I want to stop it if anyone serving on any agency is doing this.” Ryan Murphy contributed to this report. Disclosure: The Texas Wildlife Association, Texas Parks and Wildlife Department and Gulf States Toyota have been financial supporters of The Texas Tribune. A complete list of Tribune donors and sponsors is available here. TUESDAY, AUGUST 02, 2016 TEXAS TPWD Sets Public Hearings on Deer Movement Rule Proposals in Areas with CWD Rule Terry S. Singeltary Sr. comment submission SUNDAY, MAY 22, 2016 TEXAS CWD DEER BREEDERS PLEA TO GOVERNOR ABBOTT TO CIRCUMVENT TPWD SOUND SCIENCE TO LET DISEASE SPREAD 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 Terry S. Singeltary Sr. Your opinions and comments have been submitted successfully. Thank you for participating in the TPWD regulatory process. Wednesday, October 28, 2015 Interim Chronic Wasting Disease Response Rules Comment online through 07:00 a.m. November 5, 2015 SUNDAY, AUGUST 23, 2015 Subject: Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig and take her to the dance in Texas I was listening to a radio show the other day here in the Galveston bay area, and outdoor show, they had a breeder or someone from the industry on, and I was amazed at the false information he was spewing. the part about the poor little girl with her pet deer crying in the breeder pen, ...... cry me a friggen river, they are raising the damn deer to put in a pen to slaughter, or to breed for that purpose, AND you ought to see a human die from this shit. my mother did everything Linda Blair did in that movie the exorcist except spin her head 360 degrees. she DID levitate in bed because she would jerk so bad, where it took three grown strong adults to hold her down to keep her from hurting herself, all the while screaming God why can’t I stop this. so cry me a fucking river on a damn deer they are raising to have slaughtered, but whine because the TPWD et al are going to kill it to try and prevent the spread of disease cwd. if the TPWD et al had a better way of confirming or not whether those cervid had CWD, they would do it. the live tests they have to date do not work 100%, so there for they have not been validated. oh that’s fine with the pen owners, but it’s not fine for Texas. you don’t want a cwd test that just works part of the time. it’s total ignorance out there now, and they will put lipstick on this pig and take her to the dance, just like TAHC did with mad cow disease, and that’s well documented. they will change what ever law to meet their needs$$$ I will agree with this much of what the industry said this morning, that cwd has been in Texas for a long time, and in the pens to, and that the TAHC has not tested enough, that much he got correct. I have been saying this year, after year, after year, since back to 2001, to the TAHC, and told them exactly where they should be testing back in 2001, and then year after year after year, up and until 2012, where they finally did test there in enough numbers to find it a decade later, exactly where I been saying it was. the cwd deer have been waltzing across Texas from there for over a decade. it does not matter if I am pro-pen or not. that will not and does not change the science. why in the hell did they speak about the 4 confirmed deer from that index herd, yes, I said 4 now. why is not the TAHC TPWD telling that to the public now. why did not that guy today speak of 4? all the newspapers are reporting it, and I ask about the 4th case weeks and weeks ago? where is that information at on TAHC site? I am a meat eater, I am pro-hunt, and extremely pro-gun, I am however anti-stupid and anti-prion, prions can kill you, I don’t want to eat prions, you should not either. but here is the kicker, you eat meat infected with CWD TSE prion, your exposed, however you never go clinical in your life........BBBUT, your exposed and if you go on to have surgical, dental, tissue, blood donations, etc. you risk exposing my family and others...I will simply post this one short abstract of an old study the late great Dr. Gibbs... Texas 84th Legislative Session 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 TUESDAY, DECEMBER 16, 2014 Texas 84th Legislature 2015 H.R. No. 2597 Kuempel Deer Breeding Industry TAHC TPWD CWD TSE PRION expand this to see all breeder cwd, and then think of what they have released at release sites... “Regrettably, the gravity of this situation continues to mount with these new CWD positive discoveries, as well as with the full understanding of just how many other facilities and release sites across Texas were connected to the CWD positive sites in Uvalde and Hunt Counties,” said Carter Smith, Executive Director of TPWD. TAHC Chapter 40, Chronic Wasting Disease Terry Singeltary Comment Submission Counties where CWD Exposed Deer were Released, September 2021 Number of CWD Exposed Deer Released by County, September 2021 |
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