Chronic Wasting Disease Transmission in Cervidae Study Act H. R. 6272
Abraham bill aims to stop Chronic Wasting Disease in deer
CWD is spreading in wild, free-ranging deer, caribou, elk and moose herds (Cervids) and in captive cervid herds across the United States. It has been found in 25 states, including in Mississippi, Arkansas and Texas. It has not been found in Louisiana, according to the state Department of Wildlife and Fisheries.
CWD is 100 percent fatal. There is no cure and no reliable live animal test to detect the disease and stop it before it spreads to other animals. The only known measure for reducing the spread of CWD is the complete depopulation of herds that test positive for the disease. It is unknown whether the disease can spread to non-cervid wildlife, livestock or humans.
Dr. Abraham, a former veterinarian, has introduced a bill that requires the Secretary of Agriculture to partner with the National Research Council of the National Academies of Science to study and identify the ways CWD is transmitted between wild, captive and farmed cervids. This will provide a credible and scientifically-based foundation of understanding of the disease that can help end its spread.
“CWD could have devastating effects on Louisiana deer populations and, possibly, other mammals. The best hope we have for controlling CWD begins with understanding how it spreads. We don’t have that right now. Since so little information exists on this topic, my bill would instruct some of the brightest scientists in the country to study and learn more about CWD so that we can stop it,” Dr. Abraham said.
The bill, HR 6272, has four original cosponsors: U.S. Reps. Glen Thompson, R-Pa.; Ryan Costello, R-Pa.; Tom Marino, R-Pa.; and Paul Gosar, R-Ariz. It has been referred to the House Agriculture Committee, of which Dr. Abraham is a member.
From: Legislation <Legislation@fda.hhs.gov>
To: Terry Singeltary <flounder9@verizon.net>
Cc: Legislation <Legislation@fda.hhs.gov>
Sent: Wed, Jul 11, 2018 8:38 am
Subject: RE: CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS FDA EMERGENCY REQUEST FOR RULE CHANGE
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Subject: CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS FDA EMERGENCY REQUEST FOR RULE CHANGE
From: Terry Singeltary <flounder9@verizon.net>
Date: July 10, 2018 at 11:21:06 AM CDT
To: bse-l@lists.aegee.org
Cc: cjdvoice@yahoogroups.com, bloodcjd@yahoogroups.com
Subject: CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS
*** ''but feeding of other ruminant protein, including scrapie-infected sheep, can continue to pigs.''CONFIDENTIAL SPONGIFORM ENCEPHALOPATHY OF PIGSCONFIDENTIALRef: Pigs10iIN CONFIDENCEDr. MettersFrom Dr. H Pickles Med ISD/3Date 10 September 1990Copy: Dr G Jones Mr D Hagger Mr T Murray (o/r) Dr D Harper Dr Richardson Mrs ShersbySPONGIFORM ENCEPHALOPATHY OF PIGS1. There has been a preliminary meeting of the Tyrrell committee today to discuss the significance of the pig experiment in the light of other evidence, for example on feline spongiform encephalopathy.2. The preliminary conclusions were:we now know pigs are capable of expressing spongiform encephalopathy. Previously this had been doubted.the clinical picture in pigs exposed to agent by these doses/routes is fairly distinctive and unlikely to have gone unrecognised.even so improved monitoring/surveillance of neurological disease in older pigs should be considered.feeding of the "specified offal" (ie nervous/lymphoid tissue from cattle) should no longer be permitted, to pigs or to any other species.*** but feeding of other ruminant protein, including scrapie-infected sheep, can continue to pigs.if one natural field case of spongiform encephalopathy were described in a pig, we would need a ban on offal from for human consumption.we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.90/9.10/7.1whilst any such action on pharmaceuticals/devices is for others to decide, this group (which includes 4 key members of the CSM group) suggests non-UK sources should now be used, at least for "high risk" pharmaceuticals and devices (ie for those from nervous or RE System)3. The full committee will meet on the 19th to confirm these conclusions, to review experimental protocols of transmission experiments, to reconsider the cat position in the light of additional cases and to consider scrapie in sheep and goats. In view of Mr Gummer's earlier commitments, we assume he willI want to go public on the pig soon after, so the Tyrrell committee will also prepare a brief written statement.4. You may want to consider with the MCA and the Medical Device Agency what preparatory action is appropriate in anticipation of the formal advice from the Tyrrell group. The CSM subgroup not due to meet until the 31 October.Hilary Pickles Room 414 Eileen House Ext: 22832Search advanced searchDetection of PrPres in peripheral tissue in pigs with clinical disease induced by intracerebral challenge with sheep-passaged bovine spongiform encephalopathy agentCarlos Hedman ,Alicia Otero ,Jean-Yves Douet,Caroline Lacroux,Séverine Lugan,Hicham Filali,Fabien Corbière,Naima Aron,Juan José Badiola,Olivier Andréoletti,Rosa BoleaPublished: July 5, 2018Abstract
Bovine spongiform encephalopathy (BSE) can be efficiently transmitted to pigs via intracerebral inoculation. A clear link has been established between the consumption of products of bovine origin contaminated with the BSE agent and the development of variant Creutzfeldt-Jakob disease in humans. Small ruminants can also naturally develop BSE, and sheep-adapted BSE (Sh-BSE) propagates more efficiently than cattle BSE in pigs and in mouse models expressing porcine prion protein. In addition, Sh-BSE shows greater efficiency of transmission to human models than original cow BSE. While infectivity and/or abnormal PrP accumulation have been reported in the central nervous system in BSE-infected pigs, the ability of the agent to replicate in peripheral tissues has not been fully investigated. We previously characterized the presence of prions in a panel of tissues collected at the clinical stage of disease from pigs experimentally infected with Sh-BSE. Western blot revealed low levels of PrPres accumulation in lymphoid tissues, nerves, and skeletal muscles from 4 of the 5 animals analysed. Using protein misfolding cyclic amplification (PMCA), which we found to be 6 log fold more sensitive than direct WB for the detection of pig BSE, we confirmed the presence of the Sh-BSE agent in lymphoid organs, nerves, ileum, and striated muscles from all 5 inoculated pigs. Surprisingly, PrPres positivity was also detected in white blood cells from one pig using this method. The presence of infectivity in lymphoid tissues, striated muscles, and peripheral nerves was confirmed by bioassay in bovine PrP transgenic mice. These results demonstrate the ability of BSE-derived agents to replicate efficiently in various peripheral tissues in pigs. Although no prion transmission has been reported in pigs following oral BSE challenge, our data support the continuation of the Feed Ban measure implemented to prevent entry of the BSE agent into the feed chain.Singeltary's comment;cwd and scrapie transmits to pigs orally and the USA Section 21 C.F.R. 589.2000, Animal Proteins Prohibited in Ruminant Feed ban WARNING
Posted by flounder on 08 Jul 2018 at 21:05 GMT
>>>Although no prion transmission has been reported in pigs following oral BSE challenge, our data support the continuation of the Feed Ban measure implemented to prevent entry of the BSE agent into the feed chain.<<<
I would kindly like to bring urgent awareness to PLOS and the authors of this study, and the globe, the USA Section 21 C.F.R. 589.2000, Animal Proteins Prohibited in Ruminant Feed ban has been a failed policy since inception imo (see DEFRA report below), also, cervid that are potentially at risk of Chronic Wasting Disease CWD TSE Prion, are still allowed to be used as protein feed for livestock. But foremost, CWD and Scrapie TRANSMITS TO PIGS BY ORAL ROUTE. please see many many more tonnages of 589.2000, Animal Proteins Prohibited in Ruminant Feed right up to 2017. this is an extremely dangerous situation for the globe, especially with this new outbreak of TSE Prion disease in a new livestock species, i.e. camels in Nigeria, this is an extremely dangerous situation that has global ramifications and needs to be addressed asap, or risk spreading cwd tse prion from the USA and Canada further around the globe. please see;Scrapie Transmits To Pigs By Oral Route, what about the terribly flawed USA tse prion feed ban?Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform EncephalopathiesLocation: Virus and Prion Research2017 Annual Report1a. Objectives (from AD-416):Objective 1: Investigate the mechanisms of protein misfolding in prion disease, including the genetic determinants of misfolding of the prion protein and the environmental influences on protein misfolding as it relates to prion diseases. Subobjective 1.A: Investigate the differences in the unfolded state of wild-type and disease associated prion proteins to better understand the mechanism of misfolding in genetic prion disease. Subobjective 1.B: Investigate the influence of metal ions on the misfolding of the prion protein in vitro to determine if environmental exposure to metal ions may alter disease progression. Objective 2: Investigate the pathobiology of prion strains in natural hosts, including the influence of prion source genotype on interspecies transmission and the pathobiology of atypical transmissible spongiform encephalopathies (TSEs). Subobjective 2.A: Investigate the pathobiology of atypical TSEs. Subobjective 2.B: Investigate the influence of prion source genotype on interspecies transmission. Objective 3: Investigate sampling methodologies for antemortem detection of prion disease, including the utility of blood sampling as a means to assess prion disease status of affected animals and the utility of environmental sampling for monitoring herd prion disease status. Subobjective 3.A: Investigate the utility of blood sampling as a means to assess prion disease status of affected animals. Subobjective 3.B: Investigate the utility of environmental sampling for monitoring herd prion disease status.1b. Approach (from AD-416):The studies will focus on three animal transmissible spongiform encephalopathy (TSE) agents found in the United States: bovine spongiform encephalopathy (BSE); scrapie of sheep and goats; and chronic wasting disease (CWD) of deer, elk, and moose. The research will address sites of protein folding and misfolding as it relates to prion disease, accumulation of misfolded protein in the host, routes of infection, and ante mortem diagnostics with an emphasis on controlled conditions and natural routes of infection. Techniques used will include spectroscopic monitoring of protein folding/misfolding, clinical exams, histopathology, immunohistochemistry, and biochemical analysis of proteins. The enhanced knowledge gained from this work will help understand the underlying mechanisms of prion disease and mitigate the potential for unrecognized epidemic expansions of these diseases in populations of animals that could either directly or indirectly affect food animals.3. Progress Report:All 8 project plan milestones for FY17 were fully met. Research efforts directed toward meeting objective 1 of our project plan center around the production of recombinant prion protein from either bacteria or mammalian tissue culture systems and collection of thermodynamic data on the folding of the recombinant prion protein produced. Both bacterial and mammalian expression systems have been established. Thermodynamic data addressing the denatured state of wild-type and a disease associated variant of bovine prion protein has been collected and a manuscript is in preparation. In research pertaining to objective 2, all studies have been initiated and animals are under observation for the development of clinical signs. The animal studies for this objective are long term and will continue until onset of clinical signs. In vitro studies planned in parallel to the animals studies have similarly been initiated and are ongoing. Objective 3 of the project plan focuses on the detection of disease associated prion protein in body fluids and feces collected from a time course study of chronic wasting disease inoculated animals. At this time samples are being collected as planned and methods for analysis are under development.4. Accomplishments1. Showed that swine are potential hosts for the scrapie agent. A naturally occurring prion disease has not been recognized in swine, but the agent of bovine spongiform encephalopathy does transmit to swine by experimental routes. Swine are thought to have a robust species barrier when exposed to the naturally occurring prion diseases of other species, but the susceptibility of swine to the agent of sheep scrapie has not been thoroughly tested. ARS researchers at Ames, Iowa conducted this experiment to test the susceptibility of swine to U.S. scrapie isolates by intracranial and oral inoculation. Necropsies were done on a subset of animals at approximately 6 months post inoculation (PI): the time the pigs were expected to reach market weight. Remaining pigs were maintained and monitored for clinical signs of transmissible spongiform encephalopathies (TSE) until study termination at 80 months PI or when removed due to intercurrent disease. Brain samples were examined by multiple diagnostic approaches, and for a subset of pigs in each inoculation group, bioassay in mice expressing porcine prion protein. At 6 months PI, no evidence of scrapie infection was noted by any diagnostic method.***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.2. Determined that pigs naturally exposed to chronic wasting disease (CWD) may act as a reservoir of CWD infectivity. Chronic wasting disease is a naturally occurring, fatal, neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of CWD disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Pigs were assigned to 1 of 3 groups: intracranially inoculated; orally inoculated; or non-inoculated. At market weight age, half of the pigs in each group were tested ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by multiple diagnostic methods. Brain samples from selected pigs were bioassayed in mice expressing porcine prion protein. Some pigs from each inoculated group were positive by one or more tests. Bioassay was positive in 4 out of 5 pigs assayed. Although only small amounts of PrPSc were detected using sensitive methods, this study demonstrates that pigs can serve as hosts for CWD. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds.***These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.3. Developed a method for amplification and discrimination of the 3 forms of BSE in cattle. The prion protein (PrP) is a protein that is the causative agent of transmissible spongiform encephalopathies (TSEs). The disease process involves conversion of the normal cellular PrP to a pathogenic misfolded conformation. This conversion process can be recreated in the lab using a misfolding amplification process known as real-time quaking induced conversion (RT-QuIC). RT-QuIC allows the detection of minute amounts of the abnormal infectious form of the prion protein by inducing misfolding in a supplied substrate. Although RT-QuIC has been successfully used to detect pathogenic PrP with substrates from a variety of host species, prior to this work bovine prion protein had not been proven for its practical uses for RT-QuIC. We demonstrated that prions from transmissible mink encephalopathy (TME) and BSE-infected cattle can be detected with using bovine prion proteins with RT-QuIC, and developed an RT-QuIC based approach to discriminate different forms of BSE. This rapid and robust method, both to detect and discriminate BSE types, is of importance as the economic implications for different types of BSE vary greatly.Review PublicationsHwang, S., Greenlee, J.J., Nicholson, E.M. 2017. Use of bovine recombinant prion protein and real-time quaking-induced conversion to detect cattle transmissible mink encephalopathy prions and discriminate classical and atypical L- and H-type bovine spongiform encephalopathy. PLoS One. 12(2):e0172391.Moore, S., Kunkle, R., Greenlee, M., Nicholson, E., Richt, J., Hamir, A., Waters, W., Greenlee, J. 2016. Horizontal transmission of chronic wasting disease in reindeer. Emerging Infectious Diseases. 22(12):2142-2145. doi:10.3201/eid2212.160635.Moore, S.J., West Greenlee, M.H., Smith, J.D., Vrentas, C.E., Nicholson, E.M., Greenlee, J.J. 2016. A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211 cattle following intracranial inoculation. Frontiers in Veterinary Science. 3:78.Greenlee, J.J., Kunkle, R.A., Smith, J.D., West Greenlee, M.H. 2016. Scrapie in swine: a diagnostic challenge. Food Safety. 4(4):110-114. Kondru, N., Manne, S., Greenlee, J., West Greenlee, H., Anantharam, V., Halbur, P., Kanthasamy, A., Kanthasamy, A. 2017. Integrated organotypic slice cultures and RT-QuIC (OSCAR) assay: implications for translational discovery in protein misfolding diseases. Scientific Reports. 7:43155. doi:10.1038/srep43155.Mammadova, N., Ghaisas, S., Zenitsky, G., Sakaguchi, D.S., Kanthasamy, A.G., Greenlee, J.J., West Greenlee, M.H. 2017. Lasting retinal injury in a mouse model of blast-induced trauma. American Journal of Pathology. 187(7):1459-1472. doi:10.1016/j.ajpath.2017.03.005.***> 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. <******> CWD TO PIGS <***Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIESLocation: Virus and Prion ResearchTitle: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting diseaseAuthor item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, JustinSubmitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.6>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%). 6>6>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.CONFIDENTIALEXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHYWhile this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....snip...It was not until . . . August 1990, that the result from the pig persuaded both SEAC and us to change our view and to take out of pig rations any residual infectivity that might have arisen from the SBOs.4.303 The minutes of the meeting record that:It was very difficult to draw conclusions from one experimental result for what may happen in the field. However it would be prudent to exclude specified bovine offals from the pig diet. Although any relationship between BSE and the finding of a spongiform encephalopathy in cats had yet to be demonstrated, the fact that this had occurred suggested that a cautious view should be taken of those species which might be susceptible. The 'specified offals' of bovines should therefore be excluded from the feed of all species. 17IN CONFIENCEEXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY1. CMO should be aware that a pig inoculated experimentally (ic, iv, and ip) with BSE brain suspension has after 15 months developed an illness, now confirmed as a spongiform encephalopathy. This is the first ever description of such a disease in a pig, although it seems there ar no previous attempts at experimental inoculation with animal material. The Southwood group had thought igs would not be susceptible. Most pigs are slaughtered when a few weeks old but there have been no reports of relevant neurological illness in breeding sows or other elderly pigs. ...see full text ;IN CONFIDENCESo it is plausible pigs could be preclinically affected with BSE but since so few are allowed to reach adulthood this has not been recognised through clinical disease. ...CONFIDENTIALEXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHYWhile this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....BSE TO PIGS NEWS RELEASECONFIDENTIALBSE: PRESS PRESENTATIONINDUSTRY RESPONSE TYPICALDEFENSIVE BRIEFINGCONFIDENTIALpigs & pharmaceuticalsCOMMERCIAL IN CONFIDENCE COMMITTEE ON SAFETY OF MEDICINE NOT FOR PUBLICATION BOVINE SPONGIFORM ENCEPHALOPATHY WORKING GROUPThere are only two products using porcine brain and these use corticotrophin BP, made from porcine pituitary, source from outside the UK.............snip...7 OF 10 LITTLE PIGGIES WENT ON TO DEVELOP BSE;1: J Comp Pathol. 2000 Feb-Apr; 122(2-3): 131-43. Related Articles,The neuropathology of experimental bovine spongiform encephalopathy in the pig.Ryder SJ, Hawkins SA, Dawson M, Wells GA.Veterinary Laboratories Agency Weybridge, Woodham Lane, New Haw, Addlestone, Surrey, KT15 3NB, UK.In an experimental study of the transmissibility of BSE to the pig, seven of 10 pigs, infected at 1-2 weeks of age by multiple-route parenteral inoculation with a homogenate of bovine brain from natural BSE cases developed lesions typical of spongiform encephalopathy. The lesions consisted principally of severe neuropil vacuolation affecting most areas of the brain, but mainly the forebrain. In addition, some vacuolar change was identified in the rostral colliculi and hypothalamic areas of normal control pigs. PrP accumulations were detected immunocytochemically in the brains of BSE-infected animals. PrP accumulation was sparse in many areas and its density was not obviously related to the degree of vacuolation. The patterns of PrP immunolabelling in control pigs differed strikingly from those in the infected animals.PMID: 10684682 [PubMed - indexed for MEDLINE]snip...In the United States, feeding of ruminant by-products to ruminants is prohibited, but feeding of ruminant materials to swine and poultry still occurs. The potential for swine to have access to scrapie-contaminated feedstuffs exists, but the potential for swine to serve as a host for replication/accumulation of the agent of scrapie is unknown. The purpose of this study was to perform oral and intracerebral inoculation of the U.S. scrapie agent to determine the potential of swine as a host for the scrapie agent and their clinical susceptibility.see full text and more transmission studies here ;Transgenic mice expressing porcine prion protein resistant to classical scrapie but susceptible to sheep bovine spongiform encephalopathy and atypical scrapie.Emerg Infect Dis. 2009 Aug; [Epub ahead of print]NEW TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE (MAD CAMEL DISEASE) IN A NEW SPECIES
NEW OUTBREAK OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE IN A NEW SPECIES
Subject: Prion Disease in Dromedary Camels, Algeria
Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.
https://wwwnc.cdc.gov/eid/article/24/6/17-2007_article
http://camelusprp.blogspot.com/2018/04/tse-prion-disease-in-dromedary-camels.html
***> IMPORTS AND EXPORTS <***
http://camelusprp.blogspot.com/2018/04/dromedary-camels-algeria-prion-mad.html2017 USAHA RESOLUTION
RESOLUTION NUMBER: 1 Combined with 6, 13, 16, and 22 APPROVED
SUBJECT MATTER: Adequate Funding for Prevention, Diagnosis, and Response for Foreign Animal Disease Outbreaks
http://www.usaha.org/upload/Resolution/2017/Resolution_1_6_13_16_22_FAD_Sup..pdf
http://camelusprp.blogspot.com/2018/04/genetic-variation-of-prion-protein-gene.htmlO.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populationsEmmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, FrancePrion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),***is the third potentially zoonotic PD (with BSE and L-type BSE),***thus questioning the origin of human sporadic cases.We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.===============***thus questioning the origin of human sporadic cases***===============***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.==============***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.PRION 2016 TOKYOSaturday, April 23, 2016SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X onlineTaylor & FrancisPrion 2016 Animal Prion Disease Workshop AbstractsWS-01: Prion diseases in animals and zoonotic potentialJuan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,Natalia Fernandez-Borges a. and Alba Marin-Moreno a"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. FranceDietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.why do we not want to do TSE transmission studies on chimpanzees $5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.snip...R. BRADLEYTitle: Transmission of scrapie prions to primate after an extended silent incubation period)*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.I urge everyone to watch this video closely...terry*** you can see video here and interview with Jeff's Mom, and scientist telling you to test everything and potential risk factors for humans ***ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE ???
here is the latest;SEE CZUB CWD TSE Prion Zoonosis to squirrel monkey by oral route to macaque, RACE et al study, and other studies that show that indeed CWD is a increasingly zoonosis risk factor for humans...terry9:35 Candace Mathiason (Colorado State University): An Overview-Chronic WastingDisease mother to offspring transmission studies conducted at Colorado State University.10:05 Hermann Schätzl/Sandor Dudas (University of Calgary): Oral transmission of CWDinto Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity inmacaques and bio-assayed transgenic mice.16:30 Jo Moore (USDA, Ames): The agent of chronic wasting disease from pigs is infectiousin transgenic mice expressing human PRNP.***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. CWD is unique among prion diseases in its rapid spread in natural populations. BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species. This adaptation has consequences for surveillance of humans exposed to CWD. Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholdersCDC CWD 2018 TRANSMISSION*** 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.see more cwd zoonosis risk factors from updated science below...terry
Cervid to human prion transmission
Kong, Qingzhong
Case Western Reserve University, Cleveland, OH, United States
Abstract
Prion disease is transmissible and invariably fatal. Chronic wasting disease (CWD) is the prion disease affecting deer, elk and moose, and it is a widespread and expanding epidemic affecting 22 US States and 2 Canadian provinces so far. CWD poses the most serious zoonotic prion transmission risks in North America because of huge venison consumption (>6 million deer/elk hunted and consumed annually in the USA alone), significant prion infectivity in muscles and other tissues/fluids from CWD-affected cervids, and usually high levels of individual exposure to CWD resulting from consumption of the affected animal among often just family and friends. However, we still do not know whether CWD prions can infect humans in the brain or peripheral tissues or whether clinical/asymptomatic CWD zoonosis has already occurred, and we have no essays to reliably detect CWD infection in humans. 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.
Aim 1 will prove that the classical CWD strain may infect humans in brain or peripheral lymphoid tissues at low levels by conducting systemic bioassays in a set of "humanized" Tg mouse lines expressing common human PrP variants using a number of CWD isolates at varying doses and routes. Experimental "human CWD" samples will also be generated for Aim 3.
Aim 2 will test the hypothesis that the cervid-to-human prion transmission barrier is dependent on prion strain and influenced by the host (human) PrP sequence by examining and comparing the transmission efficiency and phenotypes of several atypical/unusual CWD isolates/strains as well as a few prion strains from other species that have adapted to cervid PrP sequence, utilizing the same panel of humanized Tg mouse lines as in Aim 1.
Aim 3 will establish reliable essays for detection and surveillance of CWD infection in humans by examining in details the clinical, pathological, biochemical and in vitro seeding properties of existing and future experimental "human CWD" samples generated from Aims 1-2 and compare them with those of common sporadic human Creutzfeldt-Jakob disease (sCJD) prions.
Aim 4 will attempt to detect clinical CWD-affected human cases by examining a significant number of brain samples from prion-affected human subjects in the USA and Canada who have consumed venison from CWD-endemic areas utilizing the criteria and essays established in Aim 3. The findings from this proposal will greatly advance our understandings on the potential and characteristics of cervid prion transmission in humans, establish reliable essays for CWD zoonosis and potentially discover the first case(s) of CWD infection in humans.
Public Health Relevance There are significant and increasing human exposure to cervid prions because chronic wasting disease (CWD, a widespread and highly infectious prion disease among deer and elk in North America) continues spreading and consumption of venison remains popular, but our understanding on cervid-to-human prion transmission is still very limited, raising public health concerns. This proposal aims to define the zoonotic risks of cervid prions and set up and apply essays to detect CWD zoonosis using mouse models and in vitro methods. The findings will greatly expand our knowledge on the potentials and characteristics of cervid prion transmission in humans, establish reliable essays for such infections and may discover the first case(s) of CWD infection in humans.
Funding Agency Agency National Institute of Health (NIH)
Institute National Institute of Neurological Disorders and Stroke (NINDS)
Type Research Project (R01)
Project # 1R01NS088604-01A1
Application # 9037884
Study Section Cellular and Molecular Biology of Neurodegeneration Study Section (CMND)
Program Officer Wong, May
Project Start 2015-09-30
Project End 2019-07-31
Budget Start 2015-09-30
Budget End 2016-07-31
Support Year 1
Fiscal Year 2015
Total Cost $337,507
Indirect Cost $118,756
Institution
Name Case Western Reserve University
Department Pathology
Type Schools of Medicine
DUNS # 077758407
City Cleveland
State OH
Country United States
Zip Code 44106
http://grantome.com/grant/NIH/R01-NS088604-01A1 http://grantome.com/grant/NIH/R01-NS088604-01A1CWD TSE Prion Zoonosis to squirrel monkey and macaquePrion 2017 Conference Abstracts CWD2017 PRION CONFERENCEFirst evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progressStefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/GoettingenThis is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves.Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice.At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERSSubject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEOPRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS*** PRION 2017 CONFERENCE VIDEOTUESDAY, JUNE 13, 2017PRION 2017 CONFERENCE ABSTRACTFirst evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress9:35 Candace Mathiason (Colorado State University): An Overview-Chronic WastingDisease mother to offspring transmission studies conducted at Colorado State University.10:05 Hermann Schätzl/Sandor Dudas (University of Calgary): Oral transmission of CWDinto Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity inmacaques and bio-assayed transgenic mice.16:30 Jo Moore (USDA, Ames): The agent of chronic wasting disease from pigs is infectiousin transgenic mice expressing human PRNP.SATURDAY, JULY 29, 2017Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFCZOONOTIC, ZOONOSIS, CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION10. ZOONOTIC, ZOONOSIS, CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION AKA MAD DEER ELK DISEASE IN HUMANS, has it already happened, that should be the question...''In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II)EFSA Panel on Biological Hazards (BIOHAZ) Antonia Ricci Ana Allende Declan Bolton Marianne Chemaly Robert Davies Pablo Salvador Fernández Escámez ... See all authorsFirst published: 17 January 2018 https://doi.org/10.2903/j.efsa.2018.5132 ;also, see;8. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data. In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available.snip...The tissue distribution of infectivity in CWD‐infected cervids is now known to extend beyond CNS and lymphoid tissues. While the removal of these specific tissues from the food chain would reduce human dietary exposure to infectivity, exclusion from the food chain of the whole carcass of any infected animal would be required to eliminate human dietary exposure.zoonosis zoonotic cervid tse prion cwd to humans, preparing for the storm***An alternative to modeling the species barrier is the cell-free conversion assay which points to CWD as the animal prion disease with the greatest zoonotic potential, after (and very much less than) BSE.116***Volume 2: Science
4. The link between BSE and vCJD4.29 The evidence discussed above that vCJD is caused by BSE seems overwhelming. Uncertainties exist about the cause of CJD in farmers, their wives and in several abattoir workers. It seems that farmers at least might be at higher risk than others in the general population. 1 Increased ascertainment (ie, increased identification of cases as a result of greater awareness of the condition) seems unlikely, as other groups exposed to risk, such as butchers and veterinarians, do not appear to have been affected. The CJD in farmers seems to be similar to other sporadic CJD in age of onset, in respect to glycosylation patterns, and in strain-typing in experimental mice. Some farmers are heterozygous for the methionine/valine variant at codon 129, and their lymphoreticular system (LRS) does not contain the high levels of PrPSc found in vCJD. It remains a remote possibility that when older people contract CJD from BSE the resulting phenotype is like sporadic CJD and is distinct from the vCJD phenotype in younger people...BSE INQUIRYSummary and Recommendation:snip...Health Portfolio partners were recently made aware of initial findings from a research project led by a CFIA scientist that have demonstrated that cynomolgus macaques can be infected via intracranial exposure and oral gavage with CWD infected muscle.These findings suggest that CWD, under specific experimental conditions, has the potential to cross the human species barrier, including by enteral feeding of CWD infected muscle.*** WDA 2016 NEW YORK ***We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions.In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species.***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions.Student Presentations Session 2The species barriers and public health threat of CWD and BSE prionsMs. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr. Edward Hoover1 1Colorado State UniversityChronic wasting disease (CWD) is spreading rapidly through cervid populations in the USA. Bovine spongiform encephalopathy (BSE, mad cow disease) arose in the 1980s because cattle were fed recycled animal protein.These and other prion diseases are caused by abnormal folding of the normal prion protein (PrP) into a disease causing form (PrPd), which is pathogenic to nervous system cells and can cause subsequent PrP to misfold. CWD spreads among cervids very efficiently, but it has not yet infected humans. On the other hand, BSE was spread only when cattle consumed infected bovine or ovine tissue, but did infect humans and other species.The objective of this research is to understand the role of PrP structure in cross-species infection by CWD and BSE. To study the propensity of each species’ PrP to be induced to misfold by the presence of PrPd from verious species, we have used an in vitro system that permits detection of PrPd in real-time.We measured the conversion efficiency of various combinations of PrPd seeds and PrP substrate combinations.We observed the cross-species behavior of CWD and BSE, in addition to feline-adapted CWD and BSE. We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species.***We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. CWD is unique among prion diseases in its rapid spread in natural populations. BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species. This adaptation has consequences for surveillance of humans exposed to CWD. Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholdersCDC CWD 2018 TRANSMISSION*** 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.Transmission StudiesMule 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)}...TSSresulted 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 AffiliationsIn 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 DiseaseHere 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 PSTFrom: "Belay, Ermias"To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"Sent: Monday, September 30, 2002 9:22 AMSubject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERSDear 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 AMSubject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERSSunday, November 10, 2002 6:26 PM ......snip........end..............TSSThursday, April 03, 2008A 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).***TUESDAY, JULY 03, 2018***> Missouri Donald Hill, et al., Respondents, vs. Missouri Department of Conservation, et al., Appellants SC96739TUESDAY, JULY 03, 2018***> Chronic Wasting Disease CWD TSE Prion Global Report Update, USA, CANADA, KOREA, NORWAY, FINLAND, Game Farms and Fake newsTUESDAY, JULY 10, 2018CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS*** ''but feeding of other ruminant protein, including scrapie-infected sheep, can continue to pigs.''CONFIDENTIAL SPONGIFORM ENCEPHALOPATHY OF PIGSthe tse prion aka mad cow type disease is not your normal pathogen.The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.you cannot cook the TSE prion disease out of meat.you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE.Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.the TSE prion agent also survives Simulated Wastewater Treatment Processes.IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades.you can bury it and it will not go away.The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area.it’s not your ordinary pathogen you can just cook it out and be done with.that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery.Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC.Laboratory of Central Nervous System Studies, National Institute ofNeurological Disorders and Stroke, National Institutes of Health,Bethesda, MD 20892.Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.PMID: 8006664 [PubMed - indexed for MEDLINE]TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION*** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSIONInfectious agent of sheep scrapie may persist in the environment for at least 16 years*** Nine of these recurrences occurred 14–21 years after cullingGudmundur Georgsson,1 Sigurdur Sigurdarson2 and Paul Brown3Correspondence Gudmundur Georgsson ggeorgs@hi.is1 Institute for Experimental Pathology, University of Iceland, Keldur v/vesturlandsveg, IS-112 Reykjavı´k, Iceland2 Laboratory of the Chief Veterinary Officer, Keldur, Iceland3 Bethesda, Maryland, USA Received 7 March 2006 Accepted 6 August 2006In 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.*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3Using 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 replicationPrion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel ProductionDetection of protease-resistant cervid prion protein in water from a CWD-endemic areaA Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During ProcessingRapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone mealsPPo4-4:Survival and Limited Spread of TSE Infectivity after BurialDiscussion 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 amplificationWednesday, December 16, 2015*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***161: Prion soil binding may explain efficient horizontal CWD transmissionNathaniel Denkers1, Davin Henderson1, Shannon Bartelt-Hunt2, Jason Bartz3 and Edward Hoover11Colorado State University; Fort Collins, Colorado USA2University of Nebraska-Lincoln; Omaha, Nebraska USA3Creighton University; Omaha, Nebraska USABackground Chronic wasting disease (CWD) is unique due to the facile spread in nature. The interaction of excreted CWD prions and soil is a hypothesized contributor in environmental transmission. The present study examines whether and to what degree CWD prions bind to silty clay loam (SCL) using an adapted version of real-time quaking-induced conversion (RT-QuIC) methodology.Materials and Methods Varying amounts (50–3.12 mg) of SCL were incubated with 1 mL-serial dilutions of CWD (+), CWD (−), or no brain homogenate (BH). Samples were centrifuged, washed, diluted 1:10 in 0.1% SDS, and 2.5 uL seeded in RT-QuIC assays employing recombinant Syrian hamster prion PrP substrate. Multiple well replicates of sample and supernatant fractions were assayed for positive seeding activity (recorded as thioflavin T fluorescence emission; 480 nm). Samples were considered positive if they crossed a threshold of 25,000. Reaction rates (RR) were calculated, averaged, and expressed as 1/RR.Results Positive seeding activity was detected for most SCL samples incubated with CWD (+) BH dilutions. Higher SCL concentrations (50 mg) produced low fluorescent readings due to optical interference. Lower SCL concentrations (6.25 mg) produced minimal optical interference and removed the vast majority of seeding activity from CWD+ BH in a concentration-dependent manner; determined by seeding activity in residual BH supernatants. Control SCL and supernatants produced minimal false-positive reactions (8 of 240 replicates; 3.3%). We estimated the prion binding capacity of SCL to be 0.16 ng/mg.Conclusion Silty clay loam exhibits highly efficient prion binding, inferring a durable environmental reservoir, and an efficient mechanism for indirect horizontal CWD transmission.TSE Scrapie, CWD, BSE, Prion, SoilClay content and pH: soil characteristic associations with the persistent presence of chronic wasting disease in northern IllinoisSheena J. Dorak, Michelle L. Green, Michelle M. Wander, Marilyn O. Ruiz, Michael G. Buhnerkempe, Ting Tian, Jan E. Novakofski & Nohra E. Mateus-PinillaScientific Reportsvolume 7, Article number: 18062(2017) doi:10.1038/s41598-017-18321-xDownload CitationEcological epidemiology Ecological modelling Infectious diseases PrionsReceived: 21 August 2017Accepted: 08 December 2017Published online: 22 December 2017AbstractEnvironmental reservoirs are important to infectious disease transmission and persistence, but empirical analyses are relatively few. The natural environment is a reservoir for prions that cause chronic wasting disease (CWD) and influences the risk of transmission to susceptible cervids. Soil is one environmental component demonstrated to affect prion infectivity and persistence. Here we provide the first landscape predictive model for CWD based solely on soil characteristics. We built a boosted regression tree model to predict the probability of the persistent presence of CWD in a region of northern Illinois using CWD surveillance in deer and soils data. We evaluated the outcome for possible pathways by which soil characteristics may increase the probability of CWD transmission via environmental contamination. Soil clay content and pH were the most important predictive soil characteristics of the persistent presence of CWD. The results suggest that exposure to prions in the environment is greater where percent clay is less than 18% and soil pH is greater than 6.6. These characteristics could alter availability of prions immobilized in soil and contribute to the environmental risk factors involved in the epidemiological complexity of CWD infection in natural populations of white-tailed deer.Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil ParticlesAuthor SummaryTransmissible spongiform encephalopathies (TSEs) are a group of incurable neurological diseases likely caused by a misfolded form of the prion protein. TSEs include scrapie in sheep, bovine spongiform encephalopathy (‘‘mad cow’’ disease) in cattle, chronic wasting disease in deer and elk, and Creutzfeldt-Jakob disease in humans. Scrapie and chronic wasting disease are unique among TSEs because they can be transmitted between animals, and the disease agents appear to persist in environments previously inhabited by infected animals. Soil has been hypothesized to act as a reservoir of infectivity and to bind the infectious agent. In the current study, we orally dosed experimental animals with a common clay mineral, montmorillonite, or whole soils laden with infectious prions, and compared the transmissibility to unbound agent. We found that prions bound to montmorillonite and whole soils remained orally infectious, and, in most cases, increased the oral transmission of disease compared to the unbound agent. The results presented in this study suggest that soil may contribute to environmental spread of TSEs by increasing the transmissibility of small amounts of infectious agent in the environment.tse prion soilcwd tse prion and soil, see more ;MONDAY, JUNE 12, 2017Rethinking Major grain organizations opposition to CFIA's control zone approach to Chronic Wasting CWD TSE Prion Mad Deer Type Disease 2017?WEDNESDAY, MAY 17, 2017*** Chronic Wasting Disease CWD TSE Prion aka Mad Deer Disease and the Real Estate Market Land Values ***MONDAY, MARCH 05, 2018TRUCKING AROUND AND SPREADING CHRONIC WASTING DISEASE CWD TSE PRION VIA MOVEMENT OF CERVID AND TRANSPORTATION VEHICLESto date, there is no cervid that has been documented to be totally resistant to cwd tse prion.
***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified.
P-145 Estimating chronic wasting disease resistance in cervids using real time quaking- induced conversion
Nicholas J Haley1, Rachel Rielinqer2, Kristen A Davenport3, W. David Walter4, Katherine I O'Rourke5, Gordon Mitchell6, Juergen A Richt2 1 Department of Microbiology and Immunology, Midwestern University, United States; 2Department of Diagnostic Medicine and Pathobiology, Kansas State University; 3Prion Research Center; Colorado State University; 4U.S. Geological Survey, Pennsylvania Cooperative Fish and Wildlife Research Unit; 5Agricultural Research Service, United States Department of Agriculture; 6Canadian Food Inspection Agency, National and OlE Reference Laboratory for Scrapie and CWD
In mammalian species, the susceptibility to prion diseases is affected, in part, by the sequence of the host's prion protein (PrP). In sheep, a gradation from scrapie susceptible to resistant has been established both in vivo and in vitro based on the amino acids present at PrP positions 136, 154, and 171, which has led to global breeding programs to reduce the prevalence of scrapie in domestic sheep. In cervids, resistance is commonly characterized as a delayed progression of chronic wasting disease (CWD); at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified. To model the susceptibility of various naturally-occurring and hypothetical cervid PrP alleles in vitro, we compared the amplification rates and efficiency of various CWD isolates in recombinant PrPC using real time quaking-induced conversion. We hypothesized that amplification metrics of these isolates in cervid PrP substrates would correlate to in vivo susceptibility - allowing susceptibility prediction for alleles found at 10 frequency in nature, and that there would be an additive effect of multiple resistant codons in hypothetical alleles. Our studies demonstrate that in vitro amplification metrics predict in vivo susceptibility, and that alleles with multiple codons, each influencing resistance independently, do not necessarily contribute additively to resistance. Importantly, we found that the white-tailed deer 226K substrate exhibited the slowest amplification rate among those evaluated, suggesting that further investigation of this allele and its resistance in vivo are warranted to determine if absolute resistance to CWD is possible.
***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified.
PRION 2016 CONFERENCE TOKYO
http://prion2016.org/dl/newsletter_03.pdf
''There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.''
c) The commonest form of CJD occurs as a sporadic disease, the cause of which is unknown, although genetic factors (particularly the codon 129 polymorphism in the prion protein gene (PRNP)) influence disease susceptibility. The familial forms of human TSEs (see Box 1) appear to have a solely genetic origin and are closely associated with mutations or insertions in the PRNP gene. Most, but not all, of the familial forms of human TSEs have been transmitted experimentally to animals. There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.
https://www.gov.uk/government/uploa...nt_data/file/209755/Part_1_-_Introduction.pdf
''There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.''
c) The commonest form of CJD occurs as a sporadic disease, the cause of which is unknown, although genetic factors (particularly the codon 129 polymorphism in the prion protein gene (PRNP)) influence disease susceptibility. The familial forms of human TSEs (see Box 1) appear to have a solely genetic origin and are closely associated with mutations or insertions in the PRNP gene. Most, but not all, of the familial forms of human TSEs have been transmitted experimentally to animals. There are no known familial or genetic TSEs of animals, although polymorphisms in the PRNP gene of some species (sheep for example) may influence the length of the incubation period and occurrence of disease.
https://www.gov.uk/government/uploa...nt_data/file/209755/Part_1_-_Introduction.pdf
Subject: cwd genetic susceptibility
Genetic susceptibility to chronic wasting disease in free-ranging white-tailed deer: Complement component C1q and Prnp polymorphisms§
Julie A. Blanchong a, *, Dennis M. Heisey b , Kim T. Scribner c , Scot V. Libants d , Chad Johnson e , Judd M. Aiken e , Julia A. Langenberg f , Michael D. Samuel g
snip...
Identifying the genetic basis for heterogeneity in disease susceptibility or progression can improve our understanding of individual variation in disease susceptibility in both free-ranging and captive populations. What this individual variation in disease susceptibility means for the trajectory of disease in a population, however, is not straightforward. For example, the greater, but not complete, resistance to CWD in deer with at least one Serine (S) at amino acid 96 of the Prnp gene appears to be associated with slower progression of disease (e.g., Johnson et al., 2006; Keane et al., 2008a). If slower disease progression results in longer-lived, infected deer with longer periods of infectiousness, resistance may lead to increased disease transmission rates, higher prion concentrations in the environment, and increased prevalence, as has been observed in some captive deer herds (Miller et al., 2006; Keane et al., 2008a). Alternatively, if the slower progression of disease in resistant deer is not associated with longer periods of infectiousness, but might instead indicate a higher dose of PrPCWD is required for infection, transmission rates in the population could decline especially if, as in Wisconsin, deer suffer high rates of mortality from other sources (e.g., hunting). Clearly, determining the relationship between genetic susceptibility to infection, dose requirements, disease progression, and the period of PrPCWD infectiousness are key components for understanding the consequences of CWD to free-ranging populations.
http:// http://forest.wisc.edu/files/pdfs/samuel/2009%20blanchong%20et%20al%20genetic%20susceptibility%20chronic%20wasting.pdf
http://lib.dr.iastate.edu/cgi/viewcontent.cgi?article=1083&context=nrem_pubs
http://onlinelibrary.wiley.com/doi/10.2903/j.efsa.2017.4667/epdf
http://www.tandfonline.com/doi/full/10.1080/19336896.2015.1115179
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4964855/pdf/kprn-09-06-1115179.pdf
http://www.sciencedirect.com/science/article/pii/S1567134809001956?via=ihub
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4964855/MONDAY, NOVEMBER 20, 2017*** What ever happened to 'LUCKY' the Wapiti cow elk thought to be immune from CWD with LL genotype MIA? ***Use of environmental sites by mule deer: a proxy for relative risk of chronic wasting disease exposure and transmissionMARIAFERNANDAMEJIA-SALAZAR,1,CHERYLL. WALDNER,2 YEENTENHWANG,1,3 AND TRENTK. BOLLINGER1,41 Department of Veterinary Pathology, University of Saskatchewan, 52 Campus Drive, Saskatoon, Saskatchewan S7N 5B4 Canada2 Department of Large Animal Clinical Sciences, University of Saskatchewan, 52 Campus Drive, Saskatoon,Saskatchewan S7N 5B4 Canada3 Fish and Wildlife Branch, Saskatchewan Ministry of Environment, Regina, Saskatchewan S4S 5W6 Canada4 Canadian Wildlife Health Cooperative (CWHC), 52 Campus Drive, Saskatoon, Saskatchewan S7N 5B4 Canada Citation:Mejıa-Salazar, M. F., C. L. Waldner, Y. T. Hwang, and T. K. Bollinger. 2018.Use of environmental sites by mule deer: a proxy for relative risk of chronic wasting disease exposure and transmission.Ecosphere 9(1):e02055.10.1002/ecs2.2055Abstract.Prions that cause chronic wasting disease (CWD) in cervids can remain infective for years out-side the host. Infectious cervids shed prions for a long time, consequently depositing prions in frequently used areas. These environmental prions are important in CWD epidemiology. Unfortunately, effective tools for quantifying CWD prions in soil, water, and other environmental sources are not currently available. Our goal was to investigate relative differences in visits by mule deer (Odocoileus hemionus hemionus) to various environmental site types as an indicator of the relative risk of prion contamination and disease transmission.For this, we deployed a system of triggered-by-movement cameras at eight site types in a CWD-endemic area in Saskatchewan, Canada. We first assessed whether the relative differences among site types in the frequency of visits by mule deer of any sex-and-age class, males, and females varied by season and site type.We then assessed whether the rate of behaviors with a high risk of environmental prion transmission (either contamination or acquisition) differed by season and site type. Finally, we assessed whether the intensity of visitation, based on the number of animals per picture, differed by season and site type. We found that grain sources and beds were key attractants for mule deer:(1) The greatest number of pictures with mule deer per camera-day occurred at grain sources across all seasons, except in fawning, when beds were the most visited sites;(2) during pre-rut and early gestation, mule deer visited grain sources at least twice as often as most other sites;(3) females were more likely to visit beds and grain sources, but there was no significant site preferences for males after accounting for season;(4) mule deer were most likely to be pictured contacting the environment at grain sources in early gestation; and(5) beds and grain sources were the most intensively visited sites. We also found that environmental contacts at waterholes were more frequent during spring.We discuss the potential importance of various sites in the transmission of CWD and how their modification could potentially reduce the risk of prion environmental exposure among mule deer.snip...CONCLUSIONSIn CWD-endemic areas, prion accumulation is most likely at environmental sites that are used frequently by large numbers of deer (Miller et al. 2004, Georgsson et al. 2006, Mathiason et al. 2009, Gough and Maddison 2010). The potential for CWD transmission both from prions in the environment and directly from infected deer is, therefore, also relatively higher at these locations. We demonstrated that mule deer in our study area preferentially and more intensively visited grain sources, particularly during pre-rut and early gestation, and that contacts with the environment occurred more commonly at such sites, especially during early gestation. Our findings suggest that grain sources could play a central role in the potential for CWD transmission and control. Based on these findings, limiting access to grain spills and other artificial feed sites during winter (mid-December to the end of March) is likely to help reduce CWD transmission in wild cervid populations in areas with similar characteristics to our study site. Similar recommendations have been made for management of tuberculosis in wild cervids (Miller et al. 2003).Moreover, as previously noted by Potapov et al.(2013) and Habib et al. (2011), the applicability of CWD dynamic models can be greatly improved by expanding these models by considering both the non-random social interactions between individuals (Mejıa-Salazar et al. 2017a) and the environmental dynamics of prion transmission. Until such time that analytical techniques are developed to detect concentrations of CWD prions in the environment, our results can be immediately used to rank the relative importance of various environmental sources of CWD prions in future epidemic models for this region. Without formal initiatives to address the unintentional creation of concentrated and localized attractive feeding sources for deer, such as grain spills, CWD will most likely be perpetuated, and the success of other suggested control efforts targeting population density or size (Uehlinger et al. 2016) will most likely be jeopardized.Key words:artificial feeding; bed sites; carcass; chronic wasting disease; disease management; environmental prion contamination; frequency of visitation; grain; intensity of visitation; mule deer; prion; remote photography.Received14 September 2017; accepted 17 November 2017. Corresponding Editor: Andrew W. Park.Copyright:©2018 Mejıa-Salazar et al. This is an open access article under the terms of the Creative Commons AttributionLicense, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.E-mail:mihicoltia@gmail.comDecember 2014, Volume 36, Issue 6, pp 1049–1061 | Cite as
Mineral licks: motivational factors for visitation and accompanying disease risk at communal use sites of elk and deer
Authors Authors and affiliations Michael J. LavelleEmail authorGregory E. PhillipsJustin W. FischerPatrick W. BurkeNathan W. SewardRandal S. StahlTracy A. NicholsBruce A. WunderKurt C. VerCauteren 1. 2. 3. 4.
Article First Online: 08 April 2014 258 Downloads 1 Citations
Abstract
Free-ranging cervids acquire most of their essential minerals through forage consumption, though occasionally seek other sources to account for seasonal mineral deficiencies. Mineral sources occur as natural geological deposits (i.e., licks) or as anthropogenic mineral supplements. In both scenarios, these sources commonly serve as focal sites for visitation. We monitored 11 licks in Rocky Mountain National Park, north-central Colorado, using trail cameras to quantify daily visitation indices (DVI) and soil consumption indices (SCI) for Rocky Mountain elk (Cervus elaphus) and mule deer (Odocoileus hemionus) during summer 2006 and documented elk, mule deer, and moose (Alces alces) visiting licks. Additionally, soil samples were collected, and mineral concentrations were compared to discern levels that explain rates of visitation. Relationships between response variables; DVI and SCI, and explanatory variables; elevation class, moisture class, period of study, and concentrations of minerals were examined. We found that DVI and SCI were greatest at two wet, low-elevation licks exhibiting relatively high concentrations of manganese and sodium. Because cervids are known to seek Na from soils, we suggest our observed association of Mn with DVI and SCI was a likely consequence of deer and elk seeking supplemental dietary Na. Additionally, highly utilized licks such as these provide an area of concentrated cervid occupation and interaction, thus increasing risk for environmental transmission of infectious pathogens such as chronic wasting disease, which has been shown to be shed in the saliva, urine, and feces of infected cervids.
Keywords Cervus elaphus Chronic wasting disease Elk Geophagy Mineral lick Mule deer Odocoileus hemionus
https://rd.springer.com/article/10.1007/s10653-014-9600-0
Elk and Deer Use of Mineral Licks: Implications for Disease Transmission
Kurt C. VerCauteren1*, Michael J. Lavelle1, Gregory E. Phillips1, Justin W. Fischer1, and Randal S. Stahl1 1United States Department of Agriculture, Animal and Plant Health Inspection Service, Wildlife Services, National Wildlife Research Center, 4101 LaPorte Avenue, Fort Collins, CO 80521-2154, USA *Cooresponding author e-mail: kurt.c.vercauteren@aphis.usda.gov
North American cervids require and actively seek out minerals to satisfy physiological requirements. Minerals required by free-ranging cervids exist within natural and artificial mineral licks that commonly serve as focal sites for cervids. Ingestion of soils contaminated with the agent that causes chronic wasting disease (CWD) may result in risk of contracting CWD. Our objective was to evaluate the extent and nature of use of mineral licks by CWD-susceptible cervid species. We used animal-activated cameras to monitor use of 18 mineral licks between 1 June and 16 October 2006 in Rocky Mountain National Park, north-central Colorado. We also assessed mineral concentrations at mineral licks to evaluate correlations between visitation rates and site-specific characteristics. We collected > 400,000 images of which 991 included elk, 293 included deer, and 6 included moose. We documented elk and deer participating in a variety of potentially risky behaviors (e.g., ingesting soil, ingesting water, defecating, urinating) while at mineral licks. Results from the mineral analyses combined with camera data revealed that visitation was highest at sodium-rich mineral licks. Mineral licks may play a role in disease transmission by acting as sites of increased interaction as well as reservoirs for deposition, accumulation, and ingestion of disease agents.
http://www.cwd-info.org/pdf/3rd_CWD_Symposium_utah.pdf
http://chronic-wasting-disease.blogspot.com/2009/08/third-international-cwd-symposium-july.htmlSunday, January 06, 2013
USDA TO PGC ONCE CAPTIVES ESCAPE
*** "it‘s no longer its business.”
http://chronic-wasting-disease.blogspot.com/2013/01/usda-to-pgc-once-captives-escape-its-no.htmlCOLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989
http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province!” page 26.ALSO, one of the most, if not the most top TSE Prion God in Science today is Professor Adriano Aguzzi, and he recently commented on just this, on a cwd post on my facebook page August 20 at 1:44pm, quote;''it pains me to no end to even comtemplate the possibility, but it seems entirely plausible that CWD originated from scientist-made spread of scrapie from sheep to deer in the colorado research facility. If true, a terrible burden for those involved.'' August 20 at 1:44pm ...end
https://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdfSHOOTING PENS (HIGH/LOW FENCE), CAPTIVE CERVID FARMING, BREEDING, SPERM MILLS, ANTLER MILLS, URINE MILLS, a petri dish for cwd tse prion disease...
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
https://web.archive.org/web/20170126060744/http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989
http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdfSubject: CWD TSE PRION 16 MONTH age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be RevisedSaturday, February 04, 2012Wisconsin 16 MONTH age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revisedalso see;Chronic Wasting Disease in a Wisconsin White-Tailed Deer Farm and 15 of 22 fawns aged 6 to 9 months (68.2%) were positive.specific susceptibility? 194. It is probable, based on age-class specific prevalence data from wild cervids and epidemiological evidence from captive cervids in affected research centres, that both adults and fawns may become infected with CWD (Miller, Wild & Williams, 1998; Miller et al., 2000). 198. In Odocoileus virginianus – white tailed deer, out of 179 white-tailed deer which had become enclosed by an elk farm fence, in Sioux County, northwestern Nebraska, four fawns only eight months old were among the 50% of CWD-positive animals; these fawns were not showing any clinical signs of CWD (Davidson, 2002).SCWDS BRIEFSVolume 17 January 2002 Number 4CWD News from Nebraska and KansasInfection with the chronic wasting disease (CWD) agent recently was found in 28 of 58 formerly wild white-tailed deer in a high-fenced enclosure adjacent to a pen containing CWDaffected captive elk in northern Sioux County, Nebraska.***Four of the positive deer were fawns approximately 8 months old, which is unusually young for animals testing positive for CWD.CWD in adult deer and fawns***Five of the CWD-positive deer were fawns, less than 1 year of age.Early CWD (PrPd detected in the tonsil or retropharyngeal node but not brain) was diagnosed in 14 deer (12 adults ranging from 1?5 to more than 5 years of age and two fawns). Late CWD (PrPd detectable in brain as well as lymphoid tissues) was diagnosed in 53 deer (50 adults ranging in age from 1?5 to 7 years of age and three fawns). None of the CWD-positive deer showed clinical signs of the disease (weight loss, hypersalivation, disorientation) or gross changes consistent with CWD (serous atrophy of fat) at necropsy.Illinois CWD, see where there 2003 sampling showed 2. % of fawns tested had CWD i.e. 1 positive out of 51 samples.2003Boone-Winnebago Unit Fawn 51 1 2.0%2011 FAWN CWD POSITIVE ILLINOIS1/26/11 WINNEBAGO 344N 2E S36 F FAWN SHARPSHOOTING2/10/11 OGLE 341N 1E S7 F FAWN SHARPSHOOTING3/9/11 OGLE 341N 1E S7 M FAWN SHARPSHOOTINGFor example, in 2008 a fawn tested positive and in 2010 an infected yearling buck was detected in Smith CountyP172 Multigenerational transmission of CWD prions from mother to offspringErin Mcnulty1, MS Amy Nalls1, Dr Clare Hoover1, Dr Jenny Powers2, Dr Edward Hoover1, Dr Candace Mathiason1 1Colorado State University, Fort Collins, United States, 2National Park Services, Fort Collins, United StatesAims: Chronic wasting disease (CWD) continues to demonstrate geographic expansion, now found in captive and/or free-range cervid populations in North America, South Korea and Norway. While horizontal transmission is credited for much of the spread of CWD, few studies have monitored the transmission of this disease from mother-to-offspring.CWD-infected muntjac dams are able to become pregnant, carry, deliver and rear offspring during the long asymptomatic phase of prion infection. We have demonstrated that CWD prions can be transmitted from mother to first-generation offspring leading to prion infection and subsequent development of TSE disease, and that transmission occurs during gestation (Nalls 2013). We have also observed fecundity in first-generation offspring. In fact, one first-generation female muntjac gave birth to two nonviable second-generation offspring. Tissues harvested from these nonviable second-generation offspring harbor protein misfolding cyclic amplification (PMCA) competent prions.Recently we revealed PrPC seeding activity and infectious prions within the reproductive milieu (uterus, ovaries, placentomes, amniotic fluid) of CWD-infected Reeve’s muntjac dams by PMCA, real time quaking-induced conversion (RT-QuIC) and bioassay. The presence of CWD prions in the pregnancy microenvironment begs the question: Is it possible CWD is transmitted from one generation to the next via intrauterine or germline exposure to infectious prions?Methods: To begin to address this question we assessed tissues harvested from full-term second-generation nonviable muntjac offspring for infectivity by mouse bioassay. Transgenic mice expressing the cervid prion protein, Tg(CerPrP-E226)5037+/- (n=6/cohort), were IP-inoculated with PMCA-amplified lung, mammary gland, kidney or uterus from nonviable 2nd generation muntjac offspring (n=2) born to a first generation dam (n=1), or PMCA-amplified age and tissue-matched negative control second-generation offspring (n=2). Mice from all cohorts were examined for prions by western blot and RTQuIC.Results: All mice (n=20) inoculated with PMCA-amplified tissue from “gestational CWD-exposed” second-generation offspring developed signs consistent with TSE disease, including severe ataxia and weight loss between 209-373 days pi, and were confirmed CWD positive by western blot and RT-QuIC. Negative control mice (n=9) receiving PMCA-amplified negative age and tissue-matched homogenates remained healthy and TSE-free for the same duration. Studies have been initiated to further assess the relationship between prions in ovaries and CWD transmission.Conclusions: Our data indicates that: (1) multigenerational transmission of infectious CWD prions from mother-to-offspring may be possible and (2) early and persistent exposure of the developing embryo to infectious CWD prions in the uterine microenvironment may help explain the facile transmission of CWD in the native host.=====P176 Infectious CWD prions at the fetal-maternal interfaceMs. Amy Nalls1, Ms. Erin McNulty1, Ms. Laura Pulscher1, Dr. Clare Hoover1, Dr. Edward Hoover1, Dr. Candace Mathiason1 1Colorado State University, Fort Collins, United StatesAims: Ample evidence exists for the trafficking of infectious agents across the placenta, often with grave outcomes to the developing fetus (i.e. zika, brucella, cytomegalovirus). While less studied, pregnancy-related transmissible spongiform encephalopathies (TSEs) have been implicated in several species, including humans.Our previous work demonstrated that prions can be transferred from mother-to-offspring resulting in the development of clinical TSE disease in offspring born to CWD-infected muntjac dams (Nalls 2013). We also revealed PMCA-prion seeding activity in maternal and fetal tissues harvested in utero from muntjac dams at various stages of pregnancy and CWD infection. What remained unknown was whether the prions detected at the fetal-maternal interface were infectious. In addition, we were interested to determine if the ultrasensitive RT-QuIC methodology may enhance our ability to detect prion seeding activity within the pregnancy microenvironment.We undertook this study to assess CWD infectivity and RT-QuIC PrPc seeding activity in in utero harvested— (1) female reproductive tissues and fluids associated with the pregnancy microenvironment; the ovary, uterus and birthing fluids, and (2) the semipermeable interface between cervid mother and fetus throughout pregnancy; the placentome.Methods: RT-QuIC: A total of 12 replicates/sample of ovary (n=6), uterus (n=6), placentome (n=5-6 placentomes each from n=2 pregnancies) and birthing fluids (n=4) were analyzed. Bioassay: Transgenic mice expressing the cervid prion protein, Tg(CerPrP-E226)5037+/- (n=9/cohort), were IC-inoculated with 30μl 10% homogenate of uterus (n=2), placentome (n=2) or 5-fold concentrated birthing fluids (n=3).Results: RT-QuIC: PrPC seeding activity was consistently detected in 5/6 ovary, 6/6 uterus, 9/11 placentomes, 2/2 amniotic and 0/2 allantoic fluids. Bioassay: Clinical TSE disease (ataxia, weight loss and stiff tail) was observed in mice inoculated with uterus, placentome and amniotic fluid, but not allantoic fluid between 180-343 day pi while negative control cohorts remained healthy. Bioassay mice were confirmed TSE positive: brain (uterus 7/8, placentome 8/8, amniotic fluid 1/9, allantoic fluid 0/9) and spleen (uterus 7/8, placentome 7/8, amniotic fluid 2/9, allantoic fluid 0/0) by western blot and RT-QuIC.Conclusions: Here, using a native CWD susceptible host, we have— for the first time— demonstrated infectious prions in the cervid pregnancy microenvironment and placental structure at the fetal-maternal interface. These findings reveal a source of infectious prions that the developing fetus is exposed to long before the birthing process, maternal grooming, or encounter with contaminated environments. Thus suggesting that CWD mother-to-offspring transmission may contribute to the facile transmission of CWD and be underappreciated for all TSEs.FRIDAY, MARCH 30, 2018Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary Submission March 30, 2018Terry S. Singeltary Sr., Bacliff, Texas USA 77518 flounder9@verizon..netAttachments (1) Docket No. APHIS-2018-0011 Chronic Wasting Disease Herd Certification Program Standards Singeltary View Attachment:View as format pdfhttps://www.regulations.gov/docketBrowser?rpp=25&so=DESC&sb=commentDueDate&po=0&dct=PS&D=APHIS-2018-0011SUNDAY, JUNE 10, 2018TEXAS SUMMARY MINUTES OF THE 400th COMMISSION MEETING CWD TSE PRION TAHC April 17, 2018SATURDAY, MARCH 31, 2018TEXAS DETECTS IT'S 101 CASE of CWD TSE PRION Breeder White-tailed Deer with no end in sight2018 03/27/18 Breeder Deer Uvalde Facility #3 White-tailed Deer M 2.5THURSDAY, MARCH 22, 2018TEXAS CWD TSE PRION JUMP TO 100 POSITIVE, NEW CASES 17 BREEDER, 1 BREEDER RELEASE, AND 1 WILD SINCE JAN 31, 2018WEDNESDAY, FEBRUARY 21, 2018TEXAS TPWD CWD TSE PRION 2 MORE FROM BREEDER RELEASE SITE TOTALS 81 CASES TO DATEFRIDAY, APRIL 22, 2016Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in a Mule Deer April 22, 2016TSS REPORT ON 2ND TEJAS MAD COW Mon, 22 Nov 2004 17:12:15 -0600 (the one that did NOT get away, thanks to the Honorable Phyllis Fong)-------- Original Message --------Subject: Re: BSE 'INCONCLUSIVE' COW from TEXAS ???Date: Mon, 22 Nov 2004 17:12:15 –0600From: "Terry S. Singeltary Sr." To: Carla Everett References: <[log in to unmask]> <[log in to unmask] us>Greetings Carla,still hear a rumor;Texas single beef cow not born in Canada no beef entered the food chain?and i see the TEXAS department of animal health is ramping up forsomething, but they forgot a url for update?I HAVE NO ACTUAL CONFIRMATION YET...can you confirm???terry==============================it took my letter to the GAO OIG the Honorable Phyllis Fong, many letters from many scientist around the globe, some of which i had written, to get them to finally confirm this mad cow, after sitting somewhere for months and months on a 48 hour turn around on BSE testing confirmations, by their own rules, via the BSE Red Books. ...tss*** Qualitative Analysis of BSE Risk Factors in the United StatesFebruary 13, 2000 at 3:37 pm PST (BSE red book)Tuesday, July 14, 2009 U.S.*** Emergency Bovine Spongiform Encephalopathy Response Plan Summary and BSE Red BookDate: February 14, 2000 at 8:56 am PSTWHERE did we go wrong $$$*** ALL iatrogenic cjd is, is sporadic cjd, until the iatrogenic event is discovered, traced back, documented in the Academic domain, and then put into the public domain and documented as an iatrogenic CJD event. that’s why 85%+ of all human TSE prion disease is still sporadic CJD. problem solved $$$PLEASE REMEMBER, IN 55 YEARS AND OLDER, THE RATE OF DOCUMENTED CJD JUMPS TO ONE IN 9,000.Diagnosis and Reporting of Creutzfeldt-Jakob DiseaseSingeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA Diagnosis and Reporting of Creutzfeldt-Jakob DiseaseTo the Editor:In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.Terry S. Singeltary, Sr Bacliff, Tex1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.Tracking spongiform encephalopathies in North AmericaXavier BoschPublished: August 2003Summary;“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.”49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD) the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). "I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source."Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk.Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE."Getting data on TSEs in the USA from the government is like pulling teeth", Singeltary argues. "You get it when they want you to have it, and only what they want you to have."Norman Foster, director of the Cognitive Disorders Clinic at the University of Michigan (Ann Arbor, MI, USA), says that "current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings"; adding that, "the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure". The USA should develop a system modelled on that established in the UK, he points out.Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunters "two of whom were friends" who died from pathologically confirmed CJD, says that "at present there are insufficient data to claim transmission of CWD into humans"; adding that "[only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further". Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison.CDC spokesman Ermias Belay says that the CDC "will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat". He notes that although "the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100%" and that "[we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited".26 March 2003Terry S. Singeltary, retired (medically) CJD WATCHI lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?***> 2001 FDA CJD TSE Prion Singeltary SubmissionSent: Monday, January 08,2001 3:03 PMWOW, my submission held up on the www for 17 years, and was proven to be true, and now, it has been removed from the www, the same url does not work anymore and it was just working this year. nothing like the FDA et al cleaning up any evidence of truth with their mad cow debacle and sporadic cjd cover up contineus...so sad$$$let's review the truth about sporadic cjd shall we;***> U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001[host Richard Barns] and now a question from Terry S. Singeltary of CJD Watch.
[TSS] yes, thank you, U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?
[no answer, you could hear in the back ground, mumbling and 'we can't. have him ask the question again.]
[host Richard] could you repeat the question?
[TSS] U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?
[not sure whom ask this] what group are you with?
[TSS] CJD Watch, my Mom died from hvCJD and we are tracking CJD world-wide.
[not sure who is speaking] could you please disconnect Mr. Singeltary
[TSS] you are not going to answer my question?
[not sure whom speaking] NO2 January 2000 British Medical Journal U.S.Scientist should be concerned with a CJD epidemic in the U.S., as well15 November 1999 British Medical Journal hvCJD in the USA * BSE in U.S.Singeltary on CWD TSE Prion videoRe-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy>>> The only tenable public line will be that "more research is required’’ <<<>>> possibility on a transmissible prion remains open<<<O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?Re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathyNature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015)snip...see full Singeltary Nature comment here;Alzheimer's diseaselet's not forget the elephant in the room. curing Alzheimer's would be a great and wonderful thing, but for starters, why not start with the obvious, lets prove the cause or causes, and then start to stop that. think iatrogenic, friendly fire, or the pass it forward mode of transmission. think medical, surgical, dental, tissue, blood, related transmission. think transmissible spongiform encephalopathy aka tse prion disease aka mad cow type disease...Commentary: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathySelf-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease*** Singeltary comment PLoS ***Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?Posted by flounder on 05 Nov 2014 at 21:27 GMTIN CONFIDENCE5 NOVEMBER 1992TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES[9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication.There are also results to be made available shortly(1) concerning a farmer with CJD who had BSE animals,(2) on the possible transmissibility of Alzheimer’s and(3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.]snip...see full Singeltary Nature comment here;re-Evidence for human transmission of amyloid-? pathology and cerebral amyloid angiopathy Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015)I would kindly like to comment on the Nature Paper, the Lancet reply, and the newspaper articles.First, I applaud Nature, the Scientist and Authors of the Nature paper, for bringing this important finding to the attention of the public domain, and the media for printing said findings.Secondly, it seems once again, politics is getting in the way possibly of more important Transmissible Spongiform Encephalopathy TSE Prion scientific findings. findings that could have great implications for human health, and great implications for the medical surgical arena. but apparently, the government peer review process, of the peer review science, tries to intervene again to water down said disturbing findings.where have we all heard this before? it's been well documented via the BSE Inquiry. have they not learned a lesson from the last time?we have seen this time and time again in England (and other Country's) with the BSE mad cow TSE Prion debacle.That 'anonymous' Lancet editorial was disgraceful. The editor, Dick Horton is not a scientist.The pituitary cadavers were very likely elderly and among them some were on their way to CJD or Alzheimer's. Not a bit unusual. Then the recipients, who got pooled extracts injected from thousands of cadavers, were 100% certain to have been injected with both seeds. No surprise that they got both diseases going after thirty year incubations.That the UK has a "system in place to assist science journalists" to squash embargoed science reports they find 'alarming' is pathetic.Sounds like the journalists had it right in the first place: 'Alzheimer's may be a transmissible infection' in The Independent to 'You can catch Alzheimer's' in The Daily Mirror or 'Alzheimer's bombshell' in The Daily Expressif not for the journalist, the layperson would not know about these important findings.where would we be today with sound science, from where we were 30 years ago, if not for the cloak of secrecy and save the industry at all cost mentality?when you have a peer review system for science, from which a government constantly circumvents, then you have a problem with science, and humans die.to date, as far as documented body bag count, with all TSE prion named to date, that count is still relatively low (one was too many in my case, Mom hvCJD), however that changes drastically once the TSE Prion link is made with Alzheimer's, the price of poker goes up drastically.so, who makes that final decision, and how many more decades do we have to wait?the iatrogenic mode of transmission of TSE prion, the many routes there from, load factor, threshold from said load factor to sub-clinical disease, to clinical disease, to death, much time is there to spread a TSE Prion to anywhere, but whom, by whom, and when, do we make that final decision to do something about it globally? how many documented body bags does it take? how many more decades do we wait? how many names can we make up for one disease, TSE prion?Professor Collinge et al, and others, have had troubles in the past with the Government meddling in scientific findings, that might in some way involve industry, never mind human and or animal health.FOR any government to continue to circumvent science for monetary gain, fear factor, or any reason, shame, shame on you.in my opinion, it's one of the reasons we are at where we are at to date, with regards to the TSE Prion disease science i.e. money, industry, politics, then comes science, in that order.greed, corporate, lobbyist there from, and government, must be removed from the peer review process of sound science, it's bad enough having them in the pharmaceutical aspect of healthcare policy making, in my opinion.my mother died from confirmed hvCJD, and her brother (my uncle) Alzheimer's of some type (no autopsy?). just made a promise, never forget, and never let them forget, before I do.I kindly wish to remind the public of the past, and a possible future we all hopes never happens again. ...2012Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Background
Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.
Methods
Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.
Results
I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.
Conclusions
There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.
end...tss
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
source references ...end...tss
Hello Nicole,
by all means, please do use my poster. but I thought this was already taken care of, and I could not attend for my poster presentation, therefore, it was not going to be presented. I have some health issues and could not make the trip.
please see old correspondence below...
From: Nicole Sanders Sent: Tuesday, April 10, 2012 5:37 PM To: Terry S. Singeltary Sr. Subject: RE: re-submission
Dear Terry,
The decline of proposal number 30756 is registered in the system.. Thank you for your consideration.
Best Regards,
Nicole
Nicole Sanders
Senior Specialist, Membership & Conference Programming
______________________________________
From: xxxx
To: Terry Singeltary
Sent: Saturday, December 05, 2009 9:09 AM
Subject: 14th ICID - abstract accepted for 'International Scientific Exchange'
Your preliminary abstract number: 670
Dear Mr. Singeltary,
On behalf of the Scientific Committee, I am pleased to inform you that your abstract
'Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009'
WAS accepted for inclusion in the INTERNATIONAL SCIENTIFIC EXCHANGE (ISE) section of the 14th International Congress on Infectious Diseases. Accordingly, your abstract will be included in the "Intl. Scientific Exchange abstract CD-rom" of the Congress which will be distributed to all participants.
Abstracts accepted for INTERNATIONAL SCIENTIFIC EXCHANGE are NOT PRESENTED in the oral OR poster sessions.
Your abstract below was accepted for: INTERNATIONAL SCIENTIFIC EXCHANGE
#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
Author: T. Singeltary; Bacliff, TX/US
Topic: Emerging Infectious Diseases Preferred type of presentation: International Scientific Exchange
This abstract has been ACCEPTED.
#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
Authors: T. Singeltary; Bacliff, TX/US
Title: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
Body: Background
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods
12 years independent research of available data
Results
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i..e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries.
I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
Keywords: Transmissible Spongiform Encephalopathy Creutzfeldt Jakob Disease Prion
page 114 ;
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
http://www.isid.org/14th_icid/
http://www.isid.org/publications/ICID_Archive.shtml
http://ww2.isid.org/Downloads/IMED2009_AbstrAuth.pdfWEDNESDAY, JULY 04, 2018CREUTZFELDT-JAKOB DISEASE: GUIDELINES FOR SOCIAL WORKERS IN ENGLAND June 2018SUNDAY, JUNE 24, 2018Validation and utilization of amended diagnostic criteria in Creutzfeldt-Jakob disease surveillanceSATURDAY, JUNE 23, 2018Diagnosis of Methionine/Valine Variant Creutzfeldt-Jakob Disease by Protein Misfolding Cyclic AmplificationVolume 24, Number 7—July 2018 Dispatch
*** Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States revisited 2017
Singeltary et al
http://creutzfeldt-jakob-disease.blogspot.com/2017/08/monitoring-occurrence-of-emerging-forms.html
[TSS] yes, thank you, U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?
[no answer, you could hear in the back ground, mumbling and 'we can't. have him ask the question again.]
[host Richard] could you repeat the question?
[TSS] U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?
[not sure whom ask this] what group are you with?
[TSS] CJD Watch, my Mom died from hvCJD and we are tracking CJD world-wide.
[not sure who is speaking] could you please disconnect Mr. Singeltary
[TSS] you are not going to answer my question?
[not sure whom speaking] NO
Background
Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.
Methods
Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.
Results
I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.
Conclusions
There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.
end...tss
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
source references ...end...tss
Hello Nicole,
by all means, please do use my poster. but I thought this was already taken care of, and I could not attend for my poster presentation, therefore, it was not going to be presented. I have some health issues and could not make the trip.
please see old correspondence below...
From: Nicole Sanders Sent: Tuesday, April 10, 2012 5:37 PM To: Terry S. Singeltary Sr. Subject: RE: re-submission
Dear Terry,
The decline of proposal number 30756 is registered in the system.. Thank you for your consideration.
Best Regards,
Nicole
Nicole Sanders
Senior Specialist, Membership & Conference Programming
______________________________________
From: xxxx
To: Terry Singeltary
Sent: Saturday, December 05, 2009 9:09 AM
Subject: 14th ICID - abstract accepted for 'International Scientific Exchange'
Your preliminary abstract number: 670
Dear Mr. Singeltary,
On behalf of the Scientific Committee, I am pleased to inform you that your abstract
'Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009'
WAS accepted for inclusion in the INTERNATIONAL SCIENTIFIC EXCHANGE (ISE) section of the 14th International Congress on Infectious Diseases. Accordingly, your abstract will be included in the "Intl. Scientific Exchange abstract CD-rom" of the Congress which will be distributed to all participants.
Abstracts accepted for INTERNATIONAL SCIENTIFIC EXCHANGE are NOT PRESENTED in the oral OR poster sessions.
Your abstract below was accepted for: INTERNATIONAL SCIENTIFIC EXCHANGE
#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
Author: T. Singeltary; Bacliff, TX/US
Topic: Emerging Infectious Diseases Preferred type of presentation: International Scientific Exchange
This abstract has been ACCEPTED.
#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
Authors: T. Singeltary; Bacliff, TX/US
Title: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
Body: Background
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods
12 years independent research of available data
Results
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i..e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries.
I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
Keywords: Transmissible Spongiform Encephalopathy Creutzfeldt Jakob Disease Prion
page 114 ;
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
http://www.isid.org/14th_icid/
http://www.isid.org/publications/ICID_Archive.shtml
http://ww2.isid.org/Downloads/IMED2009_AbstrAuth.pdf
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