First Detection of Chronic Wasting Disease in a Wild Red Deer (Cervus elaphus) in Europe
First Detection of Chronic Wasting Disease in a Wild Red Deer (Cervus elaphus) in Europe
Turid Vikøren,1,4 Jørn Vage, ˚ 1 Knut I. Madslien,1 Knut H. Røed,2 Christer M. Rolandsen,3 Linh Tran,1 Petter Hopp,1 Vebjørn Veiberg,3 Marianne Heum,1 Torfinn Moldal,1 Carlos G. das Neves,1 Kjell Handeland,1 Bjørnar Ytrehus,3 Øyvor Kolbjørnsen,1 Helene Wisløff,1 Randi Terland,1 Britt Saure,1 Kine M. Dessen,1 Solveig Gjerden Svendsen,1 Brit S. Nordvik,1 and Sylvie L. Benestad1 1
Norwegian Veterinary Institute, PO Box 750 Sentrum, NO-0106 Oslo, Norway; 2 Faculty of Veterinary Medicine, Norwegian University of Life Sciences, PO Box 8146 Department, NO-0033 Oslo, Norway; 3 Norwegian Institute for Nature Research, PO Box 5685 Torgarden, NO-7485 Trondheim, Norway; 4 Corresponding author (email: turid.vikoren@vetinst.no)
ABSTRACT:
Chronic wasting disease (CWD) is a fatal contagious prion disease naturally occurring in cervids in North America. In 2016, CWD was detected in wild reindeer (Rangifer tarandus) and moose (Alces alces) in Norway. Here, we report the first known naturally infected wild Norwegian red deer (Cervus elaphus).
Chronic wasting disease (CWD) is a fatal neurodegenerative disorder that affects wild and farmed cervids. It is a prion disease belonging to the transmissible spongiform encephalopathies. The main distribution is North America, and natural infections occur in mule deer (Odocoileus hemionus), whitetailed deer (Odocoileus virginianus), elk (Cervus canadensis), and less frequently in moose (Alces alces; Williams 2005; Baeten et al. 2007). Recently, CWD was detected in Europe in wild reindeer (Rangifer tarandus) (Benestad et al. 2016) and moose (Pirisinu et al. 2018) from Norway and in one moose from Finland (Evira 2018). In captive red deer (Cervus elaphus), natural CWD has been reported in a single animal in Minnesota (Schwabenlander et al. 2013) and recently in a farm in Quebec, Canada (Canadian Food Inspection Agency 2018), respectively. Experimentally, CWD has been transmitted to various cervids, including red deer (Balachandran et al. 2010; Haley and Hoover 2015).
Norway has an estimated winter population of 335,000 wild red deer, moose, roe deer (Capreolus capreolus), and reindeer, in total (Austrheim et al. 2011), and approximately 120 deer farms, keeping mainly red deer and some fallow deer (Dama dama). The red deer inhabit southern Norway up to 668N, with the main population along the west coast, and 42,541 were harvested by hunters in 2017 (Statistics Norway 2018). Here, we report the first case of CWD in a wild red deer worldwide.
An adult female red deer was shot by a hunter in October 2017 in Gjemnes municipality in western Norway (Fig. 1). Before being shot, she was grazing alone on farmland with no signs of disease. She was field dressed, and the head and carcass were delivered to a game slaughterhouse. A spoon sample of the medulla oblongata (MO) was submitted to the Norwegian Veterinary Institute (NVI, Oslo, Norway) as part of a national CWD surveillance program. After the initial positive CWD result by routine TeSeE SAP ELISA (BioRad, Hercules, California, USA) for detection of abnormal prion protein (PrPres), the available remains of the animal were examined at NVI.
The deer was estimated to be 16 yr old based on cementum annuli in the first incisor root (Hamlin et al. 2000). Necropsy of the head, carcass, and hide revealed good body condition and no gross pathologic lesions. Half of the brain tissue remaining after the spoon sample, half of various lymph nodes (LN), and the tonsils were frozen, and the other halves were fixed in 10% buffered formalin. Samples of brain, LN, and tonsil were processed routinely for immunohistochemical (IHC) and histologic examination.
The MO and five LNs (retropharyngeal, mandibular, parotid, prescapular, popliteal) were analyzed using TeSeE SAP ELISA. Both the initial sample and second sample of MO at the obex area were positive (OD values 3.5 and 0.330), whereas all LNs were negative. The presence of CWD also was confirmed by the detection of PrPres in MO by using the TeSeE western Blot test (Bio-Rad, Hercules, California, USA). Histopathologic examination of MO was inconclusive for spongiform degeneration due to autolysis. No intraneuronal vacuolation was observed.
Sections of MO, LNs, and tonsil were prepared for IHC to demonstrate accumulation of PrPres as in Benestad et al. (2016) using the antibodies mAb L42, F99/97.6.1, and 12B2. In MO, F99/97.6.1 and L42 gave similar staining, with coarse granular deposits in the neuropil, and perineuronal, intraneuronal, and linear staining in several nuclei and axonal tracts. The immunostaining obtained with 12B2 was weaker and gave no intraneuronal staining. The LNs and tonsils showed no PrPres staining. Genomic DNA was extracted from brain tissue, and the prion protein gene open reading frame was amplified and sequenced (Applied Biosystems 35003L genetic analyzer with Big Dye Terminator chemistry, Foster City, California, USA), showing glutamic acid (E) homozygosity in codon 226.
Based on brain tissue being found positive for PrPres in three diagnostic tests, we concluded that this represented the first detection of CWD in wild red deer. Elk and red deer are closely related species (Cervus spp.). Experimentally, red deer were found to be susceptible to CWD after oral inoculation of prions from elk (Balachandran et al. 2010), accumulating PrPres in brain, lymphoreticular, and other peripheral tissues. Natural CWD was reported in a young captive red deer from Minnesota having PrPres positive brain tissue and LNs (Schwabenlander et al. 2013). This contrasts with our case, where no detectable PrPres was found in the LNs and tonsils. However, some elk infected with CWD show deposits of PrPres only in the brainstem and not in lymphoid tissues (Spraker et al. 2004, 2015).
Comprehensive surveillance was implemented after detecting CWD in Norway in 2016. Of 59,533 cervids tested from 2016 to 29 October 2018, CWD was diagnosed in 19 reindeer (all from Nordfjella mountain area), three moose (two from Selbu municipality, one from Lierne municipality), and the herein reported red deer from Gjemnes municipality (Fig. 1). In total, 11,398 wild red deer were tested, including 236 from Gjemnes (Norwegian Veterinary Institute 2018).
All of Norway is populated by one or more cervid species with varying degrees of overlapping distribution range. A relevant question is whether there is any migration of cervids between the CWD-positive populations. Gjemnes is located about 200 km north of Nordfjella, 170 km west of Selbu, and 335 km southwest of Lierne (Fig. 1). Seasonal migration is common, and distances may exceed 150 km, but migration distances for red deer in western Norway are usually in the range of 20–40 km (Meisingset et al. 2018).
The origin of CWD in Norwegian wild cervids is unknown. A major question is whether the CWD detected in reindeer, moose, and red deer represents different CWD strains. The CWD from moose in Norway was characterized as an atypical CWD identified as Nor16CWD (Pirisinu et al. 2018). In this context, to better understand the red deer isolate, further molecular analysis and bioassays are currently being done. The prevalence, epidemiology, and implications of the type of CWD discovered in this red deer remain to be determined.
FIGURE 1. Map of Norway showing the location of wild cervids found positive for chronic wasting disease (CWD) in the period from 2016 through 29 October 2018. The CWD-positive red deer (Cervus elaphus) was in Gjemnes municipality (blue filled circle). The CWD-positive moose (Alces alces) were in the municipalities of Selbu, 2016 (n¼2) and Lierne, 2017 (n¼1; green filled circles). The Nordfjella reindeer area is functionally divided into two zones, and all (n¼19) the CWD-positive wild reindeer (Rangifer tarandus) were found in the northern zone, referred to as zone 1 (red).
WEDNESDAY, MARCH 06, 2019
Norway The Madness Continues in Nordfjella Chronic Wasting Disease CWD TSE Prion
hay, straw, grains...and cwd tse prion
***> NORWAY CWD UPDATE December 2018 Report from the Norwegian Scientific Committee for Food and Environment (VKM) 2018: 16
Factors that can contribute to spread of CWD – an update on the situation in Nordfjella, Norway
Opinion of Panel on biological hazards of the Norwegian Scientific Committee for Food and Environment 13.12.2018 ISBN: 978-82-8259-316-8 ISSN: 2535-4019 Norwegian Scientific Committee for Food and Environment (VKM) Po 222 Skøyen 0213 Oslo Norway FRIDAY, DECEMBER 14, 2018 Norway, Nordfjella VKM 2018 16
Factors that can contribute to spread of CWD TSE Prion UPDATE December 14, 2018
FRIDAY, NOVEMBER 16, 2018
Norway atypical TSE Prion found in Fourth Moose
Greetings TSE prion world,
i am seeing more and more references to the atypical Nor-98-type CWD TSE Prion in Norway as being of the non-infectious or non-infective variant. with science documented to date, i do not believe that any CWD Skrantesjuke TSE Prion typical or atypical in Norway or anywhere else can be classified as ''non-infective variant''. IF, Norway takes the USDA OIE views and makes atypical Nor-98 type CWD in Deer a International trading commodity fueled by junk science, as they did with sheep, i.e. no trade restrictions for Nor-98 in sheep, the world should then weep...terry
Nor-98 atypical Scrapie Transmission Studies Review
MONDAY, APRIL 25, 2011
Experimental Oral Transmission of Atypical Scrapie to Sheep
Volume 17, Number 5–May 2011
Research
Experimental Oral Transmission of Atypical Scrapie to Sheep
Marion M. Simmons, S. Jo Moore,1 Timm Konold, Lisa Thurston, Linda A. Terry, Leigh Thorne, Richard Lockey, Chris Vickery, Stephen A.C. Hawkins, Melanie J. Chaplin, and John Spiropoulos –Weybridge, Addlestone, UK
Suggested citation for this article
Abstract
To investigate the possibility of oral transmission of atypical scrapie in sheep and determine the distribution of infectivity in the animals' peripheral tissues, we challenged neonatal lambs orally with atypical scrapie; they were then killed at 12 or 24 months. Screening test results were negative for disease-specific prion protein in all but 2 recipients; they had positive results for examination of brain, but negative for peripheral tissues. Infectivity of brain, distal ileum, and spleen from all animals was assessed in mouse bioassays; positive results were obtained from tissues that had negative results on screening. These findings demonstrate that atypical scrapie can be transmitted orally and indicate that it has the potential for natural transmission and iatrogenic spread through animal feed. Detection of infectivity in tissues negative by current surveillance methods indicates that diagnostic sensitivity is suboptimal for atypical scrapie, and potentially infectious material may be able to pass into the human food chain.
SNIP...
Discussion This study is still ongoing and will not be completed until 2012. However, the current interim report documents the successful oral transmission of atypical scrapie, confirms that the disease phenotype is retained following transmission by this route in AHQ/AHQ sheep, and indicates that infectivity can be demonstrated in the gut in the absence of detectable PrPSc at least as early as 12 months after exposure.
One sheep (animal 12) culled at 24 months post inoculation displayed abnormalities in behavior and movement suggestive of atypical scrapie. Signs like ataxia with head tremor and circling have been described in experimental (19) and natural (3,30) disease, which was attributed to lesions in the cerebellum and forebrain, respectively, corresponding with PrPSc accumulation in these areas (20,24).
By contrast, animal 11, which had confirmed atypical scrapie based on postmortem tests, was considered clinically normal. The less severe and limited PrPSc accumulation in the brain of this sheep than in animal 12 may explain the absence of clinical abnormalities, which is supported by our findings in goats with scrapie in which more extensive PrPSc accumulation in the brain was usually associated with a more severe clinical disease (25).
Although all TSEs are transmissible after intracerebral challenge to a susceptible host, only some are infectious under natural conditions. Therefore, it was important from a pathogenesis and disease control perspective to establish whether or not oral transmission can be successful. However, the challenge model in this study exposed animals as neonates, when the esophageal groove is operational and the lambs are physiologically monogastric. Exposure of 3-month-old ruminating animals to similar amounts of positive brain by the oral route have so far not resulted in any clinical disease, with all animals still alive >1,500 days post challenge (M.M. Simmons, unpub. data), but most natural cases have been recorded in animals older than this, so these animals may still progress to disease in the next few years. Since this challenge study in older animals has no time-kill component, and no losses caused by unrelated disease have occurred, whether any of these sheep are in a preclinical phase of disease is unknown. Unfortunately, the absence of detectable PrPSc in lymphoreticular tissues of sheep with atypical scrapie precludes the use of biopsies to ascertain early infection in these animals.
Transmission may be more efficient in newborn animals; the incubation periods of sheep orally infected with classical scrapie were significantly shorter in sheep challenged at 14 days of age than those challenged at 6 months of age (31). If, however, oral transmission is only effective in such young animals, then field exposure would most likely have to be through milk, which is known to be a highly effective route of transmission for classical scrapie (32). No data are currently available on the potential infectivity of milk from animals with atypical scrapie.
Successful oral transmission also raises questions regarding the pathogenesis of this form of disease. There must be passage of the infectious agent from the alimentary canal to the brain through one of several possible routes, most likely those that have been suggested and discussed in detail for other TSEs, for example, retrograde neuronal transportation either directly (33–35) or through lymphoid structures or hematogenously (36). Infectivity in the absence of readily demonstrable PrPSc has been reported (37–39), and although the mouse bioassay may detect evidence of disease in other tissues, these data may not be available for at least another 2 years. More protease-sensitive forms of PrPSc may be broken down more efficiently within cells and thus do not accumulate in peripheral tissues (19), enabling atypical PrPSc to transit the digestive tract and disseminate through other systems in small amounts before accumulating detectably in the central nervous system.
Although we do not have epidemiologic evidence that supports the efficient spread of disease in the field, these data imply that disease is potentially transmissible under field situations and that spread through animal feed may be possible if the current feed restrictions were to be relaxed. Additionally, almost no data are available on the potential for atypical scrapie to transmit to other food animal species, certainly by the oral route. However, work with transgenic mice has demonstrated the potential susceptibility of pigs, with the disturbing finding that the biochemical properties of the resulting PrPSc have changed on transmission (40). The implications of this observation for subsequent transmission and host target range are currently unknown.
How reassuring is this absence of detectable PrPSc from a public health perspective? The bioassays performed in this study are not titrations, so the infectious load of the positive gut tissues cannot be quantified, although infectivity has been shown unequivocally. No experimental data are currently available on the zoonotic potential of atypical scrapie, either through experimental challenge of humanized mice or any meaningful epidemiologic correlation with human forms of TSE. However, the detection of infectivity in the distal ileum of animals as young as 12 months, in which all the tissues tested were negative for PrPSc by the currently available screening and confirmatory diagnostic tests, indicates that the diagnostic sensitivity of current surveillance methods is suboptimal for detecting atypical scrapie and that potentially infectious material may be able to pass into the human food chain undetected.
Increased Atypical Scrapie Detections
Press reports indicate that increased surveillance is catching what otherwise would have been unreported findings of atypical scrapie in sheep. In 2009, five new cases have been reported in Quebec, Ontario, Alberta, and Saskatchewan. With the exception of Quebec, all cases have been diagnosed as being the atypical form found in older animals. Canada encourages producers to join its voluntary surveillance program in order to gain scrapie-free status. The World Animal Health will not classify Canada as scrapie-free until no new cases are reported for seven years. The Canadian Sheep Federation is calling on the government to fund a wider surveillance program in order to establish the level of prevalence prior to setting an eradication date. Besides long-term testing, industry is calling for a compensation program for farmers who report unusual deaths in their flocks.
Atypical scrapie in Australia
RW Cook,a* J Bingham,bAS Besier,cCL Bayley,dM Hawes,ePL Shearer,fM Yamada,bJ Bergfeld,bDT Williamsband DJ Middletonb Background Since its initial detection in Norway in 1998, atypical scrapie (‘atypical/Nor98 scrapie’) has been reported in sheep in the majority of European countries (including in regions free of classical scrapie) and in the Falkland Islands, the USA, Canada,New Zealand and Australia.
Case series The diagnosis in Australia of atypical scrapie in four Merino and one Merino-cross sheep showing clinical signs of neurological disease was based on the detection of grey matter neuropil vacuolation (spongiform change) in the brain (particularly inthe molecular layer of the cerebellar cortex) and associated abnormal prion protein (PrPSc) deposition in both grey and white matter. Changes were minimal in the caudal brainstem, the predilection site for lesions of classical scrapie.Conclusion The distinctive lesion profile of atypical scrapie in these five sheep highlights the diagnostic importance of routine histological evaluation of the cerebellum for evidence of neuropil vacuolation and associated PrPSc deposition in adult sheep with suspected neurological disease.
Keywords atypical scrapie; prion disease; sheep; transmissible spongiform encephalopathy
Abbreviations ANZSDP, Australian and New Zealand StandardDiagnostic Procedure; CNS, central nervous system; DMNV, dorsalmotor nucleus of the vagus nerve; H&E, haematoxylin and eosin;IHC, immunohistochemistry; NTSESP, National TSE SurveillanceProgram; PrPSc, abnormal prion protein isomer; TSE, transmissiblespongiform encephalopathy. Aust Vet J 2016;94:452–455 doi: 10.1111/avj.12529
Friday, February 11, 2011
Atypical/Nor98 Scrapie Infectivity in Sheep Peripheral Tissues
snip...
The presence of infectivity in peripheral tissues that enter the food chain clearly indicates that the risk of dietary exposure to Atypical/Nor98 scrapie cannot be disregarded. However, according to our observations, in comparison to the brain, the infectious titres in the peripheral tissues were five log10 lower in Atypical/Nor98 scrapie than in classical scrapie. Therefore, the reduction of the relative exposure risk following SRM removal (CNS, head, spleen and ileum) is probably significantly higher in Atypical/Nor98 scrapie cases than in classical scrapie cases. However, considering the currently estimated prevalence of Atypical/Nor98 scrapie in healthy slaughtered EU population [10], it is probable that atypical scrapie infectivity enters in the food chain despite the prevention measures in force.
Finally, the capacity of Atypical/Nor98 scrapie agent (and more generally of small ruminants TSE agents) to cross species barrier that naturally limits the transmission risk is insufficiently documented. Recently, the transmission of an Atypical/Nor98 scrapie isolate was reported into transgenic mice over-expressing the porcine PrP [47]. Such results cannot directly be extrapolated to natural exposure conditions and natural hosts. However, they underline the urgent need for further investigations on the potential capacity of Atypical/Nor98 scrapie to propagate in other species than small ruminants.
snip...please see full text thanks to the Authors and plospathogens.org/
PR-26
NOR98 SHOWS MOLECULAR FEATURES REMINISCENT OF GSS
R. Nonno1, E. Esposito1, G. Vaccari1, E. Bandino2, M. Conte1, B. Chiappini1, S. Marcon1, M. Di Bari1, S.L. Benestad3, U. Agrimi1 1 Istituto Superiore di Sanità, Department of Food Safety and Veterinary Public Health, Rome, Italy (romolo.nonno@iss.it); 2 Istituto Zooprofilattico della Sardegna, Sassari, Italy; 3 National Veterinary Institute, Department of Pathology, Oslo, Norway
Molecular variants of PrPSc are being increasingly investigated in sheep scrapie and are generally referred to as “atypical” scrapie, as opposed to “classical scrapie”. Among the atypical group, Nor98 seems to be the best identified. We studied the molecular properties of Italian and Norwegian Nor98 samples by WB analysis of brain homogenates, either untreated, digested with different concentrations of proteinase K, or subjected to enzymatic deglycosylation. The identity of PrP fragments was inferred by means of antibodies spanning the full PrP sequence. We found that undigested brain homogenates contain a Nor98-specific PrP fragment migrating at 11 kDa (PrP11), truncated at both the C-terminus and the N-terminus, and not N-glycosylated. After mild PK digestion, Nor98 displayed full-length PrP (FL-PrP) and N-glycosylated C-terminal fragments (CTF), along with increased levels of PrP11. Proteinase K digestion curves (0,006-6,4 mg/ml) showed that FL-PrP and CTF are mainly digested above 0,01 mg/ml, while PrP11 is not entirely digested even at the highest concentrations, similarly to PrP27-30 associated with classical scrapie. Above 0,2 mg/ml PK, most Nor98 samples showed only PrP11 and a fragment of 17 kDa with the same properties of PrP11, that was tentatively identified as a dimer of PrP11. Detergent solubility studies showed that PrP11 is insoluble in 2% sodium laurylsorcosine and is mainly produced from detergentsoluble, full-length PrPSc. Furthermore, among Italian scrapie isolates, we found that a sample with molecular and pathological properties consistent with Nor98 showed plaque-like deposits of PrPSc in the thalamus when the brain was analysed by PrPSc immunohistochemistry. Taken together, our results show that the distinctive pathological feature of Nor98 is a PrP fragment spanning amino acids ~ 90-155. This fragment is produced by successive N-terminal and C-terminal cleavages from a full-length and largely detergent-soluble PrPSc, is produced in vivo and is extremely resistant to PK digestion. Intriguingly, these conclusions suggest that some pathological features of Nor98 are reminiscent of Gerstmann-Sträussler-Scheinker disease.
119
P03.141
Aspects of the Cerebellar Neuropathology in Nor98
Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute,
Norway Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.
A newly identified type of scrapie agent can naturally infect sheep with resistant PrP genotypes
Annick Le Dur*,?, Vincent Béringue*,?, Olivier Andréoletti?, Fabienne Reine*, Thanh Lan Laï*, Thierry Baron§, Bjørn Bratberg¶, Jean-Luc Vilotte?, Pierre Sarradin**, Sylvie L. Benestad¶, and Hubert Laude*,?? +Author Affiliations
*Virologie Immunologie Moléculaires and ?Génétique Biochimique et Cytogénétique, Institut National de la Recherche Agronomique, 78350 Jouy-en-Josas, France; ?Unité Mixte de Recherche, Institut National de la Recherche Agronomique-Ecole Nationale Vétérinaire de Toulouse, Interactions Hôte Agent Pathogène, 31066 Toulouse, France; §Agence Française de Sécurité Sanitaire des Aliments, Unité Agents Transmissibles Non Conventionnels, 69364 Lyon, France; **Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, 37380 Nouzilly, France; and ¶Department of Pathology, National Veterinary Institute, 0033 Oslo, Norway
Edited by Stanley B. Prusiner, University of California, San Francisco, CA (received for review March 21, 2005)
Abstract Scrapie in small ruminants belongs to transmissible spongiform encephalopathies (TSEs), or prion diseases, a family of fatal neurodegenerative disorders that affect humans and animals and can transmit within and between species by ingestion or inoculation. Conversion of the host-encoded prion protein (PrP), normal cellular PrP (PrPc), into a misfolded form, abnormal PrP (PrPSc), plays a key role in TSE transmission and pathogenesis. The intensified surveillance of scrapie in the European Union, together with the improvement of PrPSc detection techniques, has led to the discovery of a growing number of so-called atypical scrapie cases. These include clinical Nor98 cases first identified in Norwegian sheep on the basis of unusual pathological and PrPSc molecular features and "cases" that produced discordant responses in the rapid tests currently applied to the large-scale random screening of slaughtered or fallen animals. Worryingly, a substantial proportion of such cases involved sheep with PrP genotypes known until now to confer natural resistance to conventional scrapie. Here we report that both Nor98 and discordant cases, including three sheep homozygous for the resistant PrPARR allele (A136R154R171), efficiently transmitted the disease to transgenic mice expressing ovine PrP, and that they shared unique biological and biochemical features upon propagation in mice. These observations support the view that a truly infectious TSE agent, unrecognized until recently, infects sheep and goat flocks and may have important implications in terms of scrapie control and public health.
Monday, December 1, 2008
When Atypical Scrapie cross species barriers
Authors
Andreoletti O., Herva M. H., Cassard H., Espinosa J. C., Lacroux C., Simon S., Padilla D., Benestad S. L., Lantier F., Schelcher F., Grassi J., Torres, J. M., UMR INRA ENVT 1225, Ecole Nationale Veterinaire de Toulouse.France; ICISA-INlA, Madrid, Spain; CEA, IBiTec-5, DSV, CEA/Saclay, Gif sur Yvette cedex, France; National Veterinary Institute, Postboks 750 Sentrum, 0106 Oslo, Norway, INRA IASP, Centre INRA de Tours, 3738O Nouzilly, France.
Content
Atypical scrapie is a TSE occurring in small ruminants and harbouring peculiar clinical, epidemiological and biochemical properties. Currently this form of disease is identified in a large number of countries. In this study we report the transmission of an atypical scrapie isolate through different species barriers as modeled by transgenic mice (Tg) expressing different species PRP sequence.
The donor isolate was collected in 1995 in a French commercial sheep flock. inoculation into AHQ/AHQ sheep induced a disease which had all neuro-pathological and biochemical characteristics of atypical scrapie. Transmitted into Transgenic mice expressing either ovine or PrPc, the isolate retained all the described characteristics of atypical scrapie.
Surprisingly the TSE agent characteristics were dramatically different v/hen passaged into Tg bovine mice. The recovered TSE agent had biological and biochemical characteristics similar to those of atypical BSE L in the same mouse model. Moreover, whereas no other TSE agent than BSE were shown to transmit into Tg porcine mice, atypical scrapie was able to develop into this model, albeit with low attack rate on first passage.
Furthermore, after adaptation in the porcine mouse model this prion showed similar biological and biochemical characteristics than BSE adapted to this porcine mouse model. Altogether these data indicate.
(i) the unsuspected potential abilities of atypical scrapie to cross species barriers
(ii) the possible capacity of this agent to acquire new characteristics when crossing species barrier
These findings raise some interrogation on the concept of TSE strain and on the origin of the diversity of the TSE agents and could have consequences on field TSE control measures.
SUNDAY, NOVEMBER 23, 2008
PRION October 8th - 10th 2008 Book of Abstracts
***> snip...see full text;
WEDNESDAY, NOVEMBER 01, 2017
Norway detects CWD Skrantesjuke Deer possibly atypical Nor-98-type TSE?
TUESDAY, MARCH 28, 2017
*** Passage of scrapie to deer results in a new phenotype upon return passage to sheep ***
SPONTANEOUS ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY
***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.***
THURSDAY, OCTOBER 25, 2018
***> Norway New additional requirements for imports of hay and straw for animal feed from countries outside the EEA due to CWD TSE Prion
THURSDAY, FEBRUARY 14, 2019
Norway Eradication of Chronic Wasting Disease is not completed
FINLAND MOOSE FOUND DEAD IN FOREST WITH CHRONIC WASTING DISEASE 8.3.2018 12:56
The chronic wasting disease (CWD) has been found in a moose or European elk (Alces alces) for the first time ever in Finland. The disease was diagnosed in Kuhmo in a 15-year old moose that had died naturally. The results of the analyses carried out by Finnish Food Safety Authority Evira have been verified by a EU reference laboratory. Species of the deer family, known as “cervids”, can suffer from the chronic wasting disease, and it is always fatal. The disease is not known to have been contracted by people.
Norway was before this case the only European country where CWD has been diagnosed. The monitoring of the occurrence of the disease was intensified from the beginning of 2018 in Finland and five other EU Member States.
In Finland, the occurrence of the disease has been studied already since 2003. None of the ca. 2 500 samples analysed so far had tested positive for the disease. The monitoring of the disease will now be further intensified in the Kuhmo and Kainuu region. Hunters are going to be provided with more instructions before the start of the next hunting season, if appropriate.
The chronic wasting disease is not known to have been contracted by people. Moose meat is safe to eat and no restrictions are imposed on the sales and exportation of meat of animals of the deer family. As a precautionary measure the export of live animals of the deer family to other countries will be discontinued for now.
CWD is a slowly progressing disease of deer, elk, reindeer, and moose which always leads to death. The chronic wasting disease is a prion disease and related to the BSE (bovine spongiform encephalopathy) and other TSE diseases (transmissible spongiform encephalopathy). The disease is common in North America. The moose found in Kuhmo did not suffer from the North American, highly contagious form of the chronic wasting disease. The disease seems to resemble most the form of cervid TSE diagnosed in Norway, which appears to be found incidentally in individual animals of the deer family.
For more information, please contact:
Leena Räsänen, Director, tel. +358 50 388 6518 (Food Safety)
Terhi Laaksonen, Head of Unit, tel. +358 40 159 5812 (Control of Animal Diseases)
Sirkka-Liisa Korpenfelt, Senior Resarcher, tel. + 358 50 351 0308 (Laboratory Analyses)
Antti Oksanen, Research Professor, tel. +358 44 561 6491 (Wild Animal Diseases)
Kajsa Hakulin, Ministerial Advisor, Ministry of Agriculture and Forestry, tel. +358 295 162361 (National and EU Legislation)
SATURDAY, MARCH 10, 2018
Chronic Wasting Disease CWD TSE Prion Goes Global Finland Falls, Behind Norway and S. Korea
FINLAND REPORTS FIRST CASE OF CHRONIC WASTING DISEASE CWD TSE PRION IN A moose or European elk (Alces alces)
TUESDAY, JULY 03, 2018
Chronic Wasting Disease CWD TSE Prion Global Report Update, USA, CANADA, KOREA, NORWAY, FINLAND, Game Farms and Fake news
***> 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
***> 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 ***
MONDAY, JANUARY 14, 2019
Evaluation of iatrogenic risk of CJD transmission associated with Chronic Wasting Disease TSE Prion in Texas TAHC TPWD
It is a dimension as vast as space and as timeless as infinity. It is the middle ground between light and shadow, between science and superstition, and it lies between the pit of man's fears and the summit of his knowledge. This is the dimension of imagination. It is NOT, an area which we call the Twilight Zone, but an area that believes junk science, and the very industries and lobbyist some Texas Hunters, the cervid industry, that insist on shoving the fake news down their throats, we call this ted nugent junk science, and in TEXAS, sometimes you just can't fix stupid, this is where the rubber meets the road, here's your sign!
chronic wasting disease cwd tse prion aka mad deer elk disease, if you consume a cwd tse prion positive cervid, then months, years, decades later, go on to have surgery, dental, ophthalmology, endoscopy, donate tissue, blood, organs, you then expose those medical theaters and tissue, blood, organs, that are incubating the infectious cwd tse prion disease, to everyone that comes in contact.
these are not memes, these are actual statements from hunters/industry in Texas about CWD tse prion.
God help them, and us...terry
''Got a call today from TPWD, I’ve got a mule deer that tested early positive for CWD. I’m soon to turn into a zombie because I have already been eating it. They advised not to consume any of the meat...too late! They want to come confiscate what meat is left once they get more results back from another lab.''
snip...
MONDAY, FEBRUARY 25, 2019
MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019
BSE INQUIRY EVIDENCE
Why did the appearance of new TSEs in animals matter so much? It has always been known that TSEs will transfer across species boundaries. The reason for this was never known until the genetic nature of the prion gene was fully investigated and found to be involved. The gene is found to have well preserved sites and as such there is a similar gene throughout the animal kingdom...and indeed a similar gene is found in insects! It is NOT clear that the precise close nature of the PrP gene structure is essention for low species barriers. Indeed it is probably easier to infect cats with BSE than it is to infect sheep. As such it is not clear that simply because it is possible to infect BSE from cattle into certain monkeys then other apes will necessarily be infectable with the disease. One factor has stood out, however, and that is that BSE, when inoculated into mice would retain its apparent nature of disease strain, and hence when it was inoculated back into cattle, then the same disease was produced. Similarly if the TSE from kudu was inoculated into mice then a similar distribution of disease in the brain of the mouse is seen as if BSE had been inoculated into the mouse. This phenomenon was not true with scrapie, in which the transmission across a species barrier was known to lose many of the scrapie strain phenomena in terms of incubation period or disease histopathology. This also suggested that BSE was not derived from scrapie originally but we probably will never know.
------------------------------------------------------------------------
TSE in wild UK deer? The first case of BSE (as we now realise) was in a nyala in London zoo and the further zoo cases in ungulates were simply thought of as being interesting transmissions of scrapie initially. The big problem started to appear with animals in 1993-5 when it became clear that there was an increase in the CJD cases in people that had eaten deer although the statistics involved must have been questionable. The reason for this was that the CJD Surveillance was well funded to look into the diet of people dying of CJD. This effect is not clear with vCJD...if only because the numbers involved are much smaller and hence it is difficult to gain enough statistics. They found that many other foods did not appear to have much association at all but that deer certainly did and as years went by the association actually became clearer. The appearance of vCJD in 1996 made all this much more difficult in that it was suddenly clearer that the cases of sporadic CJD that they had been checking up until then probably had nothing to do with beef...and the study decreased. During the period there was an increasing worry that deer were involved with CJD..
see references:
DEER BRAIN SURVEY
Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY
Date: Fri, 18 Oct 2002 23:12:22 +0100
From: Steve Dealler
Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member
To: BSE-L@ References: <3daf5023 .4080804="" a="" class="yiv7114294437linkified" href="http://wt.net/" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">WT.NET
Dear Terry,
An excellent piece of review as this literature is desparately difficult to get back from Government sites.
What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported. Well, if you dont look adequately like they are in USA currenly then you wont find any!
Steve Dealler ===============
BSE Inquiry Steve Dealler
Management In Confidence
BSE: Private Submission of Bovine Brain Dealler
reports of sheep and calf carcasses dumped...
re-scrapie to cattle GAH Wells BSE Inquiry
https://web.archive.org/web/20090506043931/http://www.bseinquiry.gov.uk/files/yb/1993/12/09001001.pdf
Dr. Dealler goes rogue to confirm BSE
Confirmation BSE Dealler's mad cow
BSE vertical transmission
1993 cjd report finds relationship with eat venison and cjd increases 9 fold, let the cover up begin...tss
FINDINGS
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02)..
The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
GAME FARM INDUSTRY WANTS TO COVER UP FINDINGS OF INCREASE RISK TO CJD FROM CERVID
BSE INQUIRY
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane
BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended.. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
MONDAY, FEBRUARY 25, 2019
MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019
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.
(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. <***
https://prion2018.org/
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
https://prion2018.org/wp-content/uploads/2018/05/program.pdf
https://prion2018.org/
THURSDAY, OCTOBER 04, 2018
Cervid to human prion transmission 5R01NS088604-04 Update
http://grantome.com/grant/NIH/R01-NS088604-04
http://chronic-wasting-disease.blogspot.com/2018/10/cervid-to-human-prion-transmission.html
snip...full text;
SATURDAY, FEBRUARY 09, 2019
Experts: Yes, chronic wasting disease in deer is a public health issue — for people
***> 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
*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.
you can see more evidence here ;
Wednesday, May 24, 2017
PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh UPDATE 1
WEDNESDAY, SEPTEMBER 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
PRION 2010
International Prion Congress: From agent to disease September 8–11, 2010 Salzburg, Austria
Transmission Studies
Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}....TSS
resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.
snip....
Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿
Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations
In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease
Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.
*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.
see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM .......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
snip... full text ;
> 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).***
SEE; Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey
Monday, May 23, 2011
CDC Assesses Potential Human Exposure to Prion Diseases Travel Warning
Public release date: 23-May-2011
Contact: Francesca Costanzo adajmedia@elsevier.com 215-239-3249 Elsevier Health Sciences
CDC assesses potential human exposure to prion diseases Study results reported in the Journal of the American Dietetic Association
Philadelphia, PA, May 23, 2011 – Researchers from the Centers for Disease Control and Prevention (CDC) have examined the potential for human exposure to prion diseases, looking at hunting, venison consumption, and travel to areas in which prion diseases have been reported in animals. Three prion diseases in particular – bovine spongiform encephalopathy (BSE or “Mad Cow Disease”), variant Creutzfeldt-Jakob disease (vCJD), and chronic wasting disease (CWD) – were specified in the investigation. The results of this investigation are published in the June issue of the Journal of the American Dietetic Association.
“While prion diseases are rare, they are generally fatal for anyone who becomes infected. More than anything else, the results of this study support the need for continued surveillance of prion diseases,” commented lead investigator Joseph Y. Abrams, MPH, National Center for Emerging and Zoonotic Infectious Diseases, CDC, Atlanta.”But it’s also important that people know the facts about these diseases, especially since this study shows that a good number of people have participated in activities that may expose them to infection-causing agents.”
Although rare, human prion diseases such as CJD may be related to BSE. Prion (proteinaceous infectious particles) diseases are a group of rare brain diseases that affect humans and animals. When a person gets a prion disease, brain function is impaired. This causes memory and personality changes, dementia, and problems with movement. All of these worsen over time. These diseases are invariably fatal. Since these diseases may take years to manifest, knowing the extent of human exposure to possible prion diseases could become important in the event of an outbreak.
CDC investigators evaluated the results of the 2006-2007 population survey conducted by the Foodborne Diseases Active Surveillance Network (FoodNet). This survey collects information on food consumption practices, health outcomes, and demographic characteristics of residents of the participating Emerging Infections Program sites. The survey was conducted in Connecticut, Georgia, Maryland, Minnesota, New Mexico, Oregon, and Tennessee, as well as five counties in the San Francisco Bay area, seven counties in the Greater Denver area, and 34 counties in western and northeastern New York.
Survey participants were asked about behaviors that could be associated with exposure to the agents causing BSE and CWD, including travel to the nine countries considered to be BSE-endemic (United Kingdom, Republic of Ireland, France, Portugal, Switzerland, Italy, the Netherlands, Germany, Spain) and the cumulative length of stay in each of those countries. Respondents were asked if they ever had hunted for deer or elk, and if that hunting had taken place in areas considered to be CWD-endemic (northeastern Colorado, southeastern Wyoming or southwestern Nebraska). They were also asked if they had ever consumed venison, the frequency of consumption, and whether the meat came from the wild.
The proportion of survey respondents who reported travel to at least one of the nine BSE endemic countries since 1980 was 29.5%. Travel to the United Kingdom was reported by 19.4% of respondents, higher than to any other BSE-endemic country. Among those who traveled, the median duration of travel to the United Kingdom (14 days) was longer than that of any other BSE-endemic country.. Travelers to the UK were more likely to have spent at least 30 days in the country (24.9%) compared to travelers to any other BSE endemic country. The prevalence and extent of travel to the UK indicate that health concerns in the UK may also become issues for US residents.
The proportion of survey respondents reporting having hunted for deer or elk was 18.5% and 1.2% reported having hunted for deer or elk in CWD-endemic areas. Venison consumption was reported by 67.4% of FoodNet respondents, and 88.6% of those reporting venison consumption had obtained all of their meat from the wild. These findings reinforce the importance of CWD surveillance and control programs for wild deer and elk to reduce human exposure to the CWD agent. Hunters in CWD-endemic areas are advised to take simple precautions such as: avoiding consuming meat from sickly deer or elk, avoiding consuming brain or spinal cord tissues, minimizing the handling of brain and spinal cord tissues, and wearing gloves when field-dressing carcasses.
According to Abrams, “The 2006-2007 FoodNet population survey provides useful information should foodborne prion infection become an increasing public health concern in the future. The data presented describe the prevalence of important behaviors and their associations with demographic characteristics. Surveillance of BSE, CWD, and human prion diseases are critical aspects of addressing the burden of these diseases in animal populations and how that may relate to human health.”
###
The article is “Travel history, hunting, and venison consumption related to prion disease exposure, 2006-2007 FoodNet population survey” by Joseph Y. Abrams, MPH; Ryan A. Maddox, MPH; Alexis R Harvey, MPH; Lawrence B. Schonberger, MD; and Ermias D. Belay, MD. It appears in the Journal of the American Dietetic Association, Volume 111, Issue 6 (June 2011) published by Elsevier.
In an accompanying podcast CDC’s Joseph Y. Abrams discusses travel, hunting, and eating venison in relation to prion diseases. It is available at http://adajournal.org/content/podcast. ;
Thursday, May 26, 2011
Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey
Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.
Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey
Joseph Y. Abrams, MPH, Ryan A. Maddox, MPH , Alexis R. Harvey, MPH , Lawrence B. Schonberger, MD , Ermias D. Belay, MD
Accepted 15 November 2010. Abstract Full Text PDF References .
Abstract
The transmission of bovine spongiform encephalopathy (BSE) to human beings and the spread of chronic wasting disease (CWD) among cervids have prompted concerns about zoonotic transmission of prion diseases. Travel to the United Kingdom and other European countries, hunting for deer or elk, and venison consumption could result in the exposure of US residents to the agents that cause BSE and CWD. The Foodborne Diseases Active Surveillance Network 2006-2007 population survey was used to assess the prevalence of these behaviors among residents of 10 catchment areas across the United States. Of 17,372 survey respondents, 19.4% reported travel to the United Kingdom since 1980, and 29.5% reported travel to any of the nine European countries considered to be BSE-endemic since 1980. The proportion of respondents who had ever hunted deer or elk was 18.5%, and 1.2% had hunted deer or elk in a CWD–endemic area. More than two thirds (67.4%) reported having ever eaten deer or elk meat. Respondents who traveled spent more time in the United Kingdom (median 14 days) than in any other BSE-endemic country. Of the 11,635 respondents who had consumed venison, 59.8% ate venison at most one to two times during their year of highest consumption, and 88.6% had obtained all of their meat from the wild. The survey results were useful in determining the prevalence and frequency of behaviors that could be important factors for foodborne prion transmission.
PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;
Thursday, May 26, 2011
Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey
Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.
NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;
Wednesday, March 18, 2009
Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II
Transmissible Spongiform Encephalopathies
Spongiform Encephalopathy in Captive Wild ZOO BSE INQUIRY
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
FRIDAY, MARCH 15, 2019
Saskatchewan Chronic Wasting Disease TSE Prion 349 Cases Positive for 2018
THURSDAY, MARCH 14, 2019
USDA APHIS CDC FDA BSE TSE PRION UPDATE 2019
FRIDAY, MARCH 15, 2019
USDA APHIS SCRAPIE TSE PRION Sheep and Goat Health Update 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
***> TEXAS CHRONIC WASTING DISEASE CWD TSE PRION 2019
Exotic CWD susceptible species forms due April 1 Surveillance is critical to early detection of CWD in exotic susceptible species PUBLISHED ON MARCH 18, 2019
TAHC rules state that owners of high-fenced premises where exotic CWD susceptible species are located must keep an annual inventory and submit the inventory form to TAHC on or before April 1 of each year. Above: Indochina Sika Deer. (Charles Barilleaux, Flickr/Creative Commons)
AUSTIN — The Texas Animal Health Commission (TAHC) would like to remind all owners of premises where exotic chronic wasting disease (CWD) susceptible species are located that annual mortality records and inventory forms are due on or before 12:00 AM, April 1, 2019.
Exotic CWD susceptible species include North American elk or wapiti, black-tailed deer, red deer, reindeer, sika deer, moose and any associated subspecies or hybrids. Axis deer are not classified as a susceptible species.
As part of the May 9, 2017 adopted amendments to §40.5 of the Texas Administrative Code, TAHC added identification and mortality record keeping requirements for exotic CWD susceptible species. A copy of the rule may be viewed at http://bit.ly/2Dky7KP.
Statewide surveillance provides valuable information that is critical to early detection of CWD in exotic susceptible species and protects the health and marketability of these animals.
Annual Inventory Form
TAHC rules state that owners of high-fenced premises where exotic CWD susceptible species are located must keep an annual inventory and submit the inventory form to TAHC on or before April 1 of each year.
TAHC rules state that owners of high-fenced premises where exotic CWD susceptible species are located must keep an annual inventory and submit the inventory form to TAHC on or before April 1 of each year.
You may obtain an inventory form on the TAHC website at:
https://www.tahc.texas.gov/animal_health/elk-deer/PDF/13-06_ExoticCWDSusceptibleSpeciesInventory.pdf
https://www.tahc.texas.gov/animal_health/elk-deer/PDF/13-06_ExoticCWDSusceptibleSpeciesInventory.pdf
Completed inventory forms may be submitted by email to CWD_reports@tahc.texas.gov; by fax to (512) 719-0729; or by mail to:
Texas Animal Health Commission
Attention: CWD Susceptible Species Reporting
P.O. Box 12966
Austin, Texas 78711-2966
Attention: CWD Susceptible Species Reporting
P.O. Box 12966
Austin, Texas 78711-2966
For further information, contact your local TAHC region office or call TAHC’s Traceability Department at 1-800-550-8242 x 777.
Annual Mortality Record Form
TAHC rules state that owners of high-fenced or low-fenced premises where exotic CWD susceptible species are located must submit eligible mortality records (defined in the rule as hunter-harvested or natural mortalities of animals 16 months of age or older) to TAHC on or before April 1 of each year.
TAHC rules state that owners of high-fenced or low-fenced premises where exotic CWD susceptible species are located must submit eligible mortality records (defined in the rule as hunter-harvested or natural mortalities of animals 16 months of age or older) to TAHC on or before April 1 of each year.
Please note that TAHC surveillance rules require the owner of a premises to CWD test all eligible mortalities until such time that three animals are tested each year.
You may obtain a mortality record form on TAHC’s website at:
https://www.tahc.texas.gov/animal_health/elk-deer/PDF/17-10_ExoticCWDSusceptibleSpeciesMortalityRecord.pdf
https://www.tahc.texas.gov/animal_health/elk-deer/PDF/17-10_ExoticCWDSusceptibleSpeciesMortalityRecord.pdf
Your own form is acceptable so long as it includes the following:
· Date the exotic CWD susceptible species died or was harvested
· Species, age and gender
· Any RFID or NUES tag number affixed to the animal
· Any other ID number, official or unofficial, on the animal
· The accession number and collection date if a CWD sample was collected
· Date the exotic CWD susceptible species died or was harvested
· Species, age and gender
· Any RFID or NUES tag number affixed to the animal
· Any other ID number, official or unofficial, on the animal
· The accession number and collection date if a CWD sample was collected
Completed mortality record forms may be submitted by email to CWD_reports@tahc.texas.gov; by fax to (512) 719-0729; and by mail to:
Texas Animal Health Commission
Attention: CWD Susceptible Species Reporting
P.O. Box 12966, Austin, Texas 78711-2966
Attention: CWD Susceptible Species Reporting
P.O. Box 12966, Austin, Texas 78711-2966
Estimated annual inventory and mortality records must be retained for one year from the date of submission.
Testing Requirements & Test Result Reporting
TAHC rules state that all CWD test samples be collected by a state or federal animal health official, accredited veterinarian or a certified CWD postmortem sample collector; and the samples must be submitted to an official laboratory for all eligible mortalities. The owner must report all test results to their TAHC region office within 30 days of receiving the results. For a list of certified CWD postmortem sample collectors, visit:
https://www.tahc.texas.gov/animal_health/elk-deer/PDF/TAHC_CertifiedCWDSampleCollectorContactList.pdf?1.1
TAHC rules state that all CWD test samples be collected by a state or federal animal health official, accredited veterinarian or a certified CWD postmortem sample collector; and the samples must be submitted to an official laboratory for all eligible mortalities. The owner must report all test results to their TAHC region office within 30 days of receiving the results. For a list of certified CWD postmortem sample collectors, visit:
https://www.tahc.texas.gov/animal_health/elk-deer/PDF/TAHC_CertifiedCWDSampleCollectorContactList.pdf?1.1
Exotic CWD Susceptible Species Test Submission forms are available on TAHC’s website at:
https://www.tahc.texas.gov/animal_health/elk-deer/PDF/17-11_ExoticCWDSusceptibleSpeciesTestSubmission.pdf
https://www.tahc.texas.gov/animal_health/elk-deer/PDF/17-11_ExoticCWDSusceptibleSpeciesTestSubmission.pdf
Texas A&M Veterinary Medical Diagnostic Laboratory (TVMDL) works with wildlife producers and wildlife/animal health agencies across the country to ensure the health of CWD susceptible cervid species through surveillance testing. Further information is available by following the link below:
https://tvmdl.tamu.edu/2016/08/19/tpwd-alerts-deer-breeders-tvmdl-usda-live-testing-approved-faster-elisa-testing-now-available/
https://tvmdl.tamu.edu/2016/08/19/tpwd-alerts-deer-breeders-tvmdl-usda-live-testing-approved-faster-elisa-testing-now-available/
More information about exotic CWD susceptible species is available at; www.tahc.texas.gov/animal_health/elk-deer/#cwdexotic; through your local TAHC region office; or by calling 1-800-550-8242 x777.
-----Original Message-----
From: Terry Singeltary <flounder9@verizon.net>
To: CWD_reports <CWD_reports@tahc.texas.gov>
Cc: public_info <public_info@tahc.texas.gov>; laura.leal <laura.leal@tahc.texas.gov>
Sent: Tue, Mar 5, 2019 12:07 pm
Subject: TAHC CWD TSE PRION AT 144 POSITIVE MINUTES OF THE 401st COMMISSION MEETING Texas Animal Health Commission August 7, 2018
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?
From: Terry Singeltary <flounder9@verizon.net>
To: CWD_reports <CWD_reports@tahc.texas.gov>
Cc: public_info <public_info@tahc.texas.gov>; laura.leal <laura.leal@tahc.texas.gov>
Sent: Tue, Mar 5, 2019 12:07 pm
Subject: TAHC CWD TSE PRION AT 144 POSITIVE MINUTES OF THE 401st COMMISSION MEETING Texas Animal Health Commission August 7, 2018
TAHC CWD TSE PRION MINUTES OF THE 401st COMMISSION MEETING Texas Animal Health Commission August 7, 2018
MINUTES OF THE 401st COMMISSION MEETING
Texas Animal Health Commission August 7, 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.
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.
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
• Waiver Report - April 17, 2018 to August 7th, 2018
§ Chronic Wasting Disease – NOT Approved – denied request that federal regulations on CWD fencing requirements be waived. TAHC has no jurisdiction to waive federal program requirements.
Exotic Susceptible CWD TSE Prion Species
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?
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
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
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 <***
Prion 2018 Conference
WA1 An overview— Chronic Wasting Disease mother to offspring transmission studies conducted at Colorado State
University Nalls AV1‡, McNulty EE1‡, Hoover C1, Hoover EA1, Wild M2, Powers J2, Selariu A1, Mathiason CK1 1Colorado State University, Fort Collins, CO USA, 2 National Park Services, Fort Collins, CO USA.
Chronic wasting disease (CWD) demonstrates remarkable transmission efficiency among captive and free-ranging cervid populations. Intrigued by this facile transmission, we designed a series of studies to determine the potential for CWD transmission from mother to offspring. Viable offspring born to early or late-stage CWD-infected Reeves‘ muntjac dams demonstrated lymphoid biopsy positivity as early as 40 days post birth and developed clinical disease in 2-5 years. Prion infectivity was validated in the milk and colostrum collected from these dams via oral infection studies in naïve fawns, providing a potential mechanism for maternal transmission. High nonviability (~60%) was noted in full-term offspring born to this cohort of CWD-infected muntjac dams. Tissues harvested from the nonviable offspring contained prion seeding activity, suggesting that CWD had been trafficked from mother-to- offspring during gestation. Gestational timing of CWD transfer was assessed by analysis of in utero harvested tissues from a second cohort of preclinical and clinical CWD-infected muntjac dams, and it was found that transmission can occur as early as the first trimester of pregnancy. The next series of studies were initiated to determine if this was a phenomenon of experimental infection, or whether it also occurs in naturally-infected cervids. In collaboration with the National Park Service we evaluated in utero derived tissues from healthy free-ranging elk dams whose habitat is a known CWD endemic region. Prion seeding activity was detected in fetal tissues harvested from several preclinical CWD positive naturally-infected dams in this population. To begin to unravel the biological relevance of these findings we initiated mouse bioassay to assess the infectivity of the pregnancy microenvironment of muntjac dams. Uterus, placenta, ovary and amniotic fluid contained prion infectivity. Ongoing mouse bioassay will further define infectivity in fetal and reproductive tissues harvested from free-ranging naturally-exposed elk dams. This work has led to a better understanding of the transmission dynamics of CWD, demonstrating that: (i) fetuses of preclinicalinfected cervid dams are exposed to CWD long before exposure to maternal saliva or contaminated environments, (ii) CWD mother-to- offspring transmission occurs in free-ranging naturally-exposed cervid populations, and (iii) the Reeves‘ muntjac deer can be used to further explore mechanisms of in utero prion trafficking and the potential for multigenerational CWD transmission.
P74 High Prevalence of CWD prions in male reproductive samples
Carlos Kramm (1,2), Ruben Gomez-Gutierrez (1,3), Tracy Nichols (4), Claudio Soto (1) and Rodrigo Morales (1) (1) Mitchell Center for Alzheimer´s disease and Related Brain Disorders, Dept. of Neurology, University of Texas Houston Medical School, Houston, TX 77030, USA (2) Universidad de los Andes, Facultad de Medicina, Av. San Carlos de Apoquindo 2200, Las Condes, Santiago, Chile (3) Universidad de Málaga, Málaga, Spain (4) National Wildlife Research Center, United States Department of Agriculture, Fort Collins, CO 80521, USA.
Chronic wasting disease (CWD) is a highly infectious and fatal illness affecting captive and free-ranging cervids. Mother-to-offspring prion transmission has been described in some animal prion diseases, including CWD. However, few studies have been performed to analyze the prevalence of CWD prions in reproductive male tissues and fluids. Here, we optimized the Protein Misfolding Cyclic Amplification (PMCA) assay for the efficient detection of CWD prions in these samples. This study was done in collaboration with United States Department of Agriculture (USDA) scientists who provided blindly field-collected testes, epididymis and seminal fluid samples from 21 white-tailed deer that were analyzed for prion infection by post-mortem histological studies in brain stem and lymphoid tissues. The results showed positive CWD prion detection in testes, epididymis and seminal fluid samples. A high prevalence of CWD-PrPSc was found in samples collected at the late-presymptomatic stage of the disease. Our results showed a correlation between the presence of CWD-PrPSc in male reproductive organs and blood. These findings demonstrate a high efficiency of CWD prion detection by PMCA in testes, epididymis and seminal fluid, and offer a possibility for a routine screening of semen samples to be commercially distributed for artificial insemination. Our results may uncover new opportunities to understand the mechanisms of CWD spreading and decrease putative inter-individual transmission associated to insemination using CWD contaminated specimens.
SUNDAY, AUGUST 02, 2015
TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super ovulation, and the potential TSE Prion connection, what if?
how is Wisconsin and Texas doing after the Texas Deer Czar, aka Dr. Dough, went up to Wisconsin to fix the cwd tse prion problem, hows that working out???
THURSDAY, FEBRUARY 28, 2019
Wisconsin CWD TSE Prion Explodes To 1,048 Positive 2018-2019 With Total 5,234 Confirmed To Date
WEDNESDAY, MARCH 13, 2019
Wisconsin caves to cervid game farm industry and lets fencing requirements expire, which will allow CWD to spread even further
WEDNESDAY, MARCH 06, 2019
Wisconsin Continues to Ignore CWD TSE Prion, as the disease continues to mount, the Governor flounders, more wild deer positive
THURSDAY, MARCH 28, 2019
Michigan CWD Identified in a Montcalm County Farmed Deer
Colorado Chronic Wasting Disease Response Plan December 2018
I. Executive Summary Mule deer, white-tailed deer, elk and moose are highly valued species in North America. Some of Colorado’s herds of these species are increasingly becoming infected with chronic wasting disease (CWD). As of July 2018, at least 31 of Colorado's 54 deer herds (57%), 16 of 43 elk herds (37%), and 2 of 9 moose herds (22%) are known to be infected with CWD. Four of Colorado's 5 largest deer herds and 2 of the state’s 5 largest elk herds are infected. Deer herds tend to be more heavily infected than elk and moose herds living in the same geographic area. Not only are the number of infected herds increasing, the past 15 years of disease trends generally show an increase in the proportion of infected animals within herds as well. Of most concern, greater than a 10-fold increase in CWD prevalence has been estimated in some mule deer herds since the early 2000s; CWD is now adversely affecting the performance of these herds.
snip...
IMPORTANT PUBLIC HEALTH MESSAGE
Disease in humans resulting from CWD exposure has not been reported to date. However, public health officials cannot determine there is no risk from eating meat from infected animals. Consequently, officials recommend that people avoid exposure to CWD-infected animals. Please see the Colorado Department of Public Health and Environment website ( http://www.colorado.gov/pacific/cdphe/priondiseases ) for the most current recommendations on carcass testing and other preventive measures.
To minimize exposure to CWD and other diseases of potential concern, Colorado Parks and Wildlife (CPW) and state public health officials advise hunters not to shoot, handle or consume any deer, elk or moose that is acting abnormally or appears to be sick. When fielddressing game, wear rubber gloves and minimize the use of a bone saw to cut through the brain or spinal cord (backbone). Minimize contact with brain or spinal cord tissues, eyes, spleen or lymph nodes. Always wash hands and utensils thoroughly after dressing and processing game meat.
(the map on page 71, cwd marked in red, is shocking...tss)
snip...see full report and more updated science on cwd tse prion here;
TUESDAY, MARCH 12, 2019
Colorado Parks and Wildlife is addressing Chronic Wasting Disease with its CWD Response Plan
FRIDAY, DECEMBER 28, 2018
Chronic Wasting Disease CWD TSE Prion 2019 Where The Rubber Meets The Road
Six fawns tested positive for CWD, five fawns from the core study area, including the youngest (5 months) free-ranging cervid to test positive.
Approximately 4,200 fawns, defined as deer under 1 year of age, were sampled from the eradication zone over the last year. The majority of fawns sampled were between the ages of 5 to 9 months,
though some were as young as 1 month.
Two of the six fawns with CWD detected were 5 to 6 months old. All six of the positive fawns were taken from the core area of the CWD eradication zone where the highest numbers of positive deer have been identified.
the old 16 month old rule with cervids, as well as the 30 month rule with bovine, in terms of tse prion, should be trashed...imo...kind regards, terry
WEDNESDAY, MARCH 13, 2019
CWD, TSE, PRION, MATERNAL mother to offspring, testes, epididymis, seminal fluid, and blood
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.
TUESDAY, APRIL 18, 2017
*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***
***> Wednesday, January 23, 2019
***> CFIA SFCR Guidance on Specified risk material (SRM) came into force on January 15, 2019 <***
THURSDAY, FEBRUARY 07, 2019
CWD TSE Prion, and Processing your own meat
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.
TUESDAY, APRIL 18, 2017
*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***
***> 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 $$$
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.
WEDNESDAY, FEBRUARY 20, 2019
CHRONIC WASTING DISEASE CONGRESS Serial No. 107-117 May 16, 2002 Updated 2019
Terry S. Singeltary Sr., Bacliff, Texas USA 77518 flounder9@verizon.net Galveston Bay, on the bottom...
posted by Terry S. Singeltary Sr. at
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