Results 1 to 5 of 5

Thread: First evidence intracranial and peroral transmission of CWD into Cynomolgus macaques

  1. #1
    Distinguished Community Member
    Join Date
    Oct 2006
    Location
    Bacliff, Texas
    Posts
    496

    Exclamation First evidence intracranial and peroral transmission of CWD into Cynomolgus macaques

    10:30 First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress

    Dr Stefanie Czub University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency Canada

    http://prion2017.org/programme/

    seems if my primitive education does not fail me, intracranial means inside the skull, and peroral means by the mouth. seems the price of tse prion poker just keeps going up...terry

    Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES

    Location: Virus and Prion Research

    Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease

    Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin

    Submitted 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 month challenge groups). The remaining pigs (>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. 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 month group was positive by EIA. PrPSc was detected by QuIC in at least one of the lymphoid tissues examined in 5/6 pigs in the intracranial <6 months group, 6/7 intracranial >6 months group, 5/6 pigs in the oral <6 months group, and 4/6 oral >6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%).

    Conclusions:

    This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.

    CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period.

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

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

    https://www.ars.usda.gov/research/pu...eqNo115=337105

    CONFIDENTIAL

    EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY

    While 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. ...

    http://web.archive.org/web/200310260...8/23004001.pdf

    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.

    http://web.archive.org/web/200308220...9/10007001.pdf

    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.

    http://web.archive.org/web/200308220...9/11005001.pdf

    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.

    http://web.archive.org/web/200308220...9/12002001.pdf

    But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all.

    http://web.archive.org/web/200305181...9/13004001.pdf

    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.....

    http://web.archive.org/web/200308220...9/21009001.pdf

    snip...see much more here ;

    WEDNESDAY, APRIL 05, 2017

    Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease

    http://chronic-wasting-disease.blogs...n-protein.html

    SUNDAY, APRIL 23, 2017

    FDA Sec. 589.1 589.2 Substances prohibited from use in animal food or feed Animal, proteins prohibited in ruminant feed current of April 1 2016

    http://madcowfeed.blogspot.com/2017/...rohibited.html

    SPONTANEOUS ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY

    ***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***

    http://www.nature.com/articles/srep11573

    *** 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 2

    The species barriers and public health threat of CWD and BSE prions

    Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr. Edward Hoover1 1Colorado State University

    Chronic 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 stakeholders

    http://www.wda2016.org/uploads/5/8/6...gs_low_res.pdf

    PRION 2016 TOKYO

    Zoonotic Potential of CWD Prions: An Update

    Chronic wasting disease (CWD) is a widespread and highly transmissible prion disease in free-ranging and captive cervid species in North America. The zoonotic potential of CWD prions is a serious public health concern, but the susceptibility of human CNS and peripheral organs to CWD prions remains largely unresolved. We reported earlier that peripheral and CNS infections were detected in transgenic mice expressing human PrP129M or PrP129V. Here we will present an update on this project, including evidence for strain dependence and influence of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of experimental human CWD prions.

    PRION 2016 TOKYO In Conjunction with Asia Pacific Prion Symposium 2016 PRION 2016 Tokyo Prion 2016

    http://prion2016.org/dl/newsletter_03.pdf

    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.

    http://grantome.com/grant/NIH/R01-NS088604-01A1

    Key Molecular Mechanisms of TSEs

    Zabel, Mark D.

    Colorado State University-Fort Collins, Fort Collins, CO, United States

    Abstract Prion diseases, or transmissible spongiform encephalopathies (TSEs), are fatal neurodegenerative diseases affecting humans, cervids, bovids, and ovids. The absolute requirement of PrPC expression to generate prion diseases and the lack of instructional nucleic acid define prions as unique infectious agents. Prions exhibit species-specific tropism, inferring that unique prion strains exist that preferentially infct certain host species and confront transmission barriers to heterologous host species. However, transmission barriers are not absolute. Scientific consensus agrees that the sheep TSE scrapie probably breached the transmission barrier to cattle causing bovine spongiform encephalopathy that subsequently breached the human transmission barrier and likely caused several hundred deaths by a new-variant form of the human TSE Creutzfeldt-Jakob disease in the UK and Europe. The impact to human health, emotion and economies can still be felt in areas like farming, blood and organ donations and the threat of a latent TSE epidemic. This precedent raises the real possibility of other TSEs, like chronic wasting disease of cervids, overcoming similar human transmission barriers. A groundbreaking discovery made last year revealed that mice infected with heterologous prion strains facing significant transmission barriers replicated prions far more readily in spleens than brains6. Furthermore, these splenic prions exhibited weakened transmission barriers and expanded host ranges compared to neurogenic prions. These data question conventional wisdom of avoiding neural tissue to avoid prion xenotransmission, when more promiscuous prions may lurk in extraneural tissues. Data derived from work previously funded by NIH demonstrate that Complement receptors CD21/35 bind prions and high density PrPC and differentially impact prion disease depending on the prion isolate or strain used. Recent advances in live animal and whole organ imaging have led us to generate preliminary data to support novel, innovative approaches to assessing prion capture and transport. We plan to test our unifying hypothesis for this proposal that CD21/35 control the processes of peripheral prion capture, transport, strain selection and xenotransmission in the following specific aims.

    1. Assess the role of CD21/35 in splenic prion strain selection and host range expansion.

    2. Determine whether CD21/35 and C1q differentially bind distinct prion strains

    3. Monitor the effects of CD21/35 on prion trafficking in real time and space

    4. Assess the role of CD21/35 in incunabular prion trafficking

    Public Health Relevance Transmissible spongiform encephalopathies, or prion diseases, are devastating illnesses that greatly impact public health, agriculture and wildlife in North America and around the world. The impact to human health, emotion and economies can still be felt in areas like farming, blood and organ donations and the threat of a latent TSE epidemic. This precedent raises the real possibility of other TSEs, like chronic wasting disease (CWD) of cervids, overcoming similar human transmission barriers. Early this year Canada reported its first case of BSE in over a decade audits first case of CWD in farmed elk in three years, underscoring the need for continued vigilance and research. Identifying mechanisms of transmission and zoonoses remains an extremely important and intense area of research that will benefit human and other animal populations.

    http://grantome.com/grant/NIH/R56-AI122273-01A1

    PMCA Detection of CWD Infection in Cervid and Non-Cervid Species

    Hoover, Edward Arthur

    Colorado State University-Fort Collins, Fort Collins, CO, United States

    http://grantome.com/grant/NIH/R01-NS061902-07

    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).***

    https://www.landesbioscience.com/jou...ache=112223249

    Monday, May 02, 2016

    *** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***

    http://chronic-wasting-disease.blogs...ns-update.html

    Saturday, April 23, 2016

    PRION 2016 TOKYO Saturday, April 23, 2016

    SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online Taylor & Francis Prion 2016 Animal Prion Disease Workshop

    Abstracts

    WS-01: Prion diseases in animals and zoonotic potential

    Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a, Natalia Fernandez-Borges a. and Alba Marin-Moreno a "Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France

    Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier. To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents. These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant. Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.

    ***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.

    http://www.tandfonline.com/doi/abs/1...nalCode=kprn20

    why do we not want to do TSE transmission studies on chimpanzees $

    5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.

    snip...

    R. BRADLEY

    http://collections.europarchive.org/...9/23001001.pdf

    Title: Transmission of scrapie prions to primate after an extended silent incubation period) ***

    In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.

    *** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.

    *** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.

    http://www.ars.usda.gov/research/pub..._NO_115=313160

    SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016

    Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online

    http://scrapie-usa.blogspot.com/2016...n-animals.html

    http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article

    O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations

    Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France

    Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.

    *** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,

    ***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),

    ***is the third potentially zoonotic PD (with BSE and L-type BSE),

    ***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.

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

    ***thus questioning the origin of human sporadic cases***

    ***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.

    https://prion2015.files.wordpress.co...5abstracts.pdf

    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).***

    https://www.landesbioscience.com/jou...ache=112223249

    *** 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.

    http://cdmrp.army.mil/prevfunded/npr...nal_Report.pdf

    SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016

    Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online

    http://scrapie-usa.blogspot.com/2016...n-animals.html

    http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article

    http://scrapie-usa.blogspot.com/

    FRIDAY, APRIL 21, 2017

    URGENT GLOBAL UPDATE BLOOD, TISSUE, CJD, nvCJD, GSS, BSE, CWD, SCRAPIE, TSE, PRION

    http://creutzfeldt-jakob-disease.blo...issue-cjd.html

    MONDAY, MAY 1, 2017

    Congress ignores Trump and his proposal to cut funding of medical research by $1.2 billion, instead they approved $1.39 billion for Alzheimer’s disease research, an increase of $400 million

    http://betaamyloidcjd.blogspot.com/2...-proposal.html


    Terry S. Singeltary Sr.


    WEDNESDAY, MAY 03, 2017

    First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques

    http://chronic-wasting-disease.blogs...anial-and.html

  2. #2
    Distinguished Community Member
    Join Date
    Oct 2006
    Location
    Bacliff, Texas
    Posts
    496

    Default

    Chronic Wasting Disease: CFIA Research Summary

    Embargoed until May 23, 2017

    (OCR of a scanned original)

    Research Findings

    Chronic Wasting Disease (CWD) is a progressive, fatal disease of the nervous system of cervids including deer, elk, moose, and reindeer that is caused by abnormal proteins called prions. It is known as a transmissible spongiform encephalopathy (TSE). Other TSEs include scrapie in sheep, bovine spongiform encephalopathy (BSE) in cattle, and Creutzfeldt-Jakob disease (CJD) in humans.

    A limited number of experimental studies have demonstrated that non-human primates, specifically squirrel monkeys, are susceptible to CWD prions. An ongoing research study has now shown that CWD can also be transmitted to macaques, which are genetically closer to humans.

    The study led by Dr. Stefanie Czub, a scientist at the Canadian Food Inspection Agency (CFIA), and funded by the Alberta Prion Research institute has demonstrated that by orally administering material under experimental conditions from cervids (deer and elk) naturally infected with CWD, the disease can be transmitted to macaques.

    in this project, which began in 2009, 18 macaques were exposed to CWD in a variety of ways: by injecting into the brain, through contact with skin, oral administration, and intravenously (into the bloodstream through veins). So far, results are available from 5 animals. At this point, two animals that were exposed to CWD by direct introduction into the brain, one that was administered infected brain material by oral administration and two that were given infected muscle by oral administration have become infected with CWD. The study is ongoing and testing continues in the remaining animals. The early results will be presented at PRlON 2017, the annual international conference on prion diseases, in Edinburgh, Scotland, May 23 to 26, 2017.

    Potential impacts of the new finding

    Since 2003 Canada has a policy that recommends that animals and materials known to be infected with prions be removed from the food chain and from health products. Although no direct evidence of CWD prion transmission to humans has ever been recorded, the policy advocates a precautionary approach to managing CWD and potential human exposure to prions. These initial findings do not change Health Canada’s Health Products and Food Branch (HPFB) position on food and health products. A precautionary approach is still recommended to manage the potential risks of exposure to prions through food and health products. Measures are in place at federal, provincial and territorial levels to reduce human exposure to products potentially contaminated by CWD by preventing known infected animals from entering the marketplace.

    While Federal and P/T government’s animal disease control policies continue to divert known CWD-infected animals away from entering the food and feed supply, research and development of sensitive detection methods including live-animal sampling techniques remain crucial for ensuring an accurate diagnosis. In addition, consistent federal, provincial and territorial communications of appropriate precautionary measures for hunters and indigenous communities are required.

    Next Steps

    The CFlA will continue to collaborate with national and international partners to develop and validate new diagnostic techniques. The CFlA will also continue to offer confirmatory testing services and reference laboratory expertise to provincial and territorial partners on demand.

    Currently, CFlA laboratories are leading or collaborating on several research projects to understand the potential for CWD to infect humans. These projects use non‐human primates, genetically modified mice, and cell-free amplification approaches. Given the present findings, CFiA encourages continued research into TSEs.

    The results of this study reinforce the need to redesign the federal program to foster greater adoption of risk mitigation measures for farmed cervids. Federal and provincial government collaboration will continue as new program options are assessed.

    The results of Dr. Czub’s research into CWD will be of interest to scientists, governments, industry and people who consume cervid products. After the presentation at PRION 2017, the research will follow the normal steps of completion, peer review and publication. The Government of Canada will monitor the response to this research and determine whether further review of the science is required. Other studies underway by other researchers may also become public as a result of the presentation of Dr. Czub’s research.

    The Public Health Agency of Canada, Health Canada, CFlA and other Federal partners are working together to assess what policies or programs need further review as well as preparing other communications about the research and health policy and advice to Canadian. 2017/04/28

    ===end...UNOFFICIAL...NO URL LINK...TSS===

    0:30 First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress

    Dr Stefanie Czub University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency Canada

    http://prion2017.org/programme/

    WEDNESDAY, MAY 03, 2017

    *** First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques

    http://chronic-wasting-disease.blogs...anial-and.html


    kind regards, terry

  3. #3
    Distinguished Community Member
    Join Date
    Oct 2006
    Location
    Bacliff, Texas
    Posts
    496

    Default

    PRION 2017 - A-Z of Abstracts

    http://prion2017.org/wp-content/uplo...resenter_2.pdf

    Greetings BSE-L et al,

    it looks like Prion 2017 conference is going to be interesting for sure. i can't wait until i get my hands on the Congressional Abstracts. i have been very lucky in receiving the Abstracts in the past from various sources. Japan Prion 2016 and Japan was gracious enough to send me the full package last year. i have been fishing for several days seeking out a source for the PRION2017 abstracts with no luck. T and F or anybody else so far will not even acknowledge my request to even know if this will all be made available freely to the public, which imo it should be. i'm not saying we're special, but myself and many others that try to keep up with the science every year are finding it more and more difficult, and it is some of us that have donated our loved ones brain or tissue samples to science freely to research to find the causes and cure. i hope T and F will find it in their hearts all abstracts online free to the public, or send me a copy so i can. if i must buy one i will, if i can find it. this is just to damn important...

    p.s., i gonna cast a bait here in the BSE-L, to any of the old...young folks here that might want to send me a copy and especially Dr. Czub findings in totality, it would surely be appreciated, and kept in total secret if need be.thanks!

    Notice to Members Regarding Chronic Wasting Disease (CWD)

    Posted on: May 31st, 2017

    To: MNA Members

    From: Métis Nation of Alberta

    Date: Wednesday, May 31, 2017

    Métis Nation of Alberta (MNA) was made aware of a recent Canadian research study examining the transmission of Chronic Wasting Disease. The initial results of the study indicate that macaque monkeys (genetically similar to humans) can be infected with Chronic Wasting Disease (CWD) after eating deer that is infected with CWD. CWD is a prion disease, which are fatal, transmissible diseases characterized by abnormal proteins in the brain and nervous system. To date no research has shown that CWD can be passed on to humans, and no human cases of CWD have ever been identified. However, this new research indicates that it is a possibility. The Deputy Chief Medical Officer of Health has reached out to us to share with our Métis harvesters this important information.
    For more information you can visit:

    http://aep.alberta.ca/fish-wildlife/...s/default.aspx

    and

    http://www.nwhc.usgs.gov/disease_inf...ease/index.jsp.

    What the Alberta Government knows:

    CWD is present in southeastern Alberta, with the area slowly spreading westward over time (introduced into Alberta from Saskatchewan) – see map for more information at

    http://aep.alberta.ca/fish-wildlife/...Heads-2016.pdf

    CWD circulates in deer populations, particularly mule deer; it has been found in about 4% of deer tested in 2016;

    Elk can be infected in areas where CWD has been present in deer for a long period of time;
    Moose can also be infected, but this would be fairly rare.

    Necessary Precautions for Harvesters:

    Hunters and others who handle carcasses follow basic handling precautions (available here

    http://aep.alberta.ca/fish-wildlife/...ng-Oct2009.pdf

    All deer, moose and elk harvested from CWD mandatory submission wildlife management units (WMUs) be tested for CWD; and

    A negative result (no CWD detected by the test) must be obtained before any part of an animal is eaten.

    For more information, contact:
    Amy Quintal
    Métis Nation of Alberta
    Métis Harvesting Liaison
    Tel: (780) 455 – 2200
    aquintal@metis.org

    http://albertametis.com/2017/05/noti...g-disease-cwd/

    FRIDAY, JUNE 02, 2017

    Alberta Canada Chronic Wasting Disease (CWD) Surveillance Update: 2016/17 Final

    http://chronic-wasting-disease.blogs...g-disease.html

    Chronic Wasting Disease: CFIA Research Summary

    Embargoed until May 23, 2017

    (OCR of a scanned original)

    Research Findings

    Chronic Wasting Disease (CWD) is a progressive, fatal disease of the nervous system of cervids including deer, elk, moose, and reindeer that is caused by abnormal proteins called prions. It is known as a transmissible spongiform encephalopathy (TSE). Other TSEs include scrapie in sheep, bovine spongiform encephalopathy (BSE) in cattle, and Creutzfeldt-Jakob disease (CJD) in humans.

    A limited number of experimental studies have demonstrated that non-human primates, specifically squirrel monkeys, are susceptible to CWD prions. An ongoing research study has now shown that CWD can also be transmitted to macaques, which are genetically closer to humans.

    The study led by Dr. Stefanie Czub, a scientist at the Canadian Food Inspection Agency (CFIA), and funded by the Alberta Prion Research institute has demonstrated that by orally administering material under experimental conditions from cervids (deer and elk) naturally infected with CWD, the disease can be transmitted to macaques.

    in this project, which began in 2009, 18 macaques were exposed to CWD in a variety of ways: by injecting into the brain, through contact with skin, oral administration, and intravenously (into the bloodstream through veins). So far, results are available from 5 animals. At this point, two animals that were exposed to CWD by direct introduction into the brain, one that was administered infected brain material by oral administration and two that were given infected muscle by oral administration have become infected with CWD. The study is ongoing and testing continues in the remaining animals. The early results will be presented at PRlON 2017, the annual international conference on prion diseases, in Edinburgh, Scotland, May 23 to 26, 2017.

    Potential impacts of the new finding

    Since 2003 Canada has a policy that recommends that animals and materials known to be infected with prions be removed from the food chain and from health products. Although no direct evidence of CWD prion transmission to humans has ever been recorded, the policy advocates a precautionary approach to managing CWD and potential human exposure to prions. These initial findings do not change Health Canada’s Health Products and Food Branch (HPFB) position on food and health products. A precautionary approach is still recommended to manage the potential risks of exposure to prions through food and health products. Measures are in place at federal, provincial and territorial levels to reduce human exposure to products potentially contaminated by CWD by preventing known infected animals from entering the marketplace.

    While Federal and P/T government’s animal disease control policies continue to divert known CWD-infected animals away from entering the food and feed supply, research and development of sensitive detection methods including live-animal sampling techniques remain crucial for ensuring an accurate diagnosis. In addition, consistent federal, provincial and territorial communications of appropriate precautionary measures for hunters and indigenous communities are required.

    Next Steps

    The CFlA will continue to collaborate with national and international partners to develop and validate new diagnostic techniques. The CFlA will also continue to offer confirmatory testing services and reference laboratory expertise to provincial and territorial partners on demand.

    Currently, CFlA laboratories are leading or collaborating on several research projects to understand the potential for CWD to infect humans. These projects use non‐human primates, genetically modified mice, and cell-free amplification approaches. Given the present findings, CFiA encourages continued research into TSEs.

    The results of this study reinforce the need to redesign the federal program to foster greater adoption of risk mitigation measures for farmed cervids. Federal and provincial government collaboration will continue as new program options are assessed.

    The results of Dr. Czub’s research into CWD will be of interest to scientists, governments, industry and people who consume cervid products. After the presentation at PRION 2017, the research will follow the normal steps of completion, peer review and publication. The Government of Canada will monitor the response to this research and determine whether further review of the science is required. Other studies underway by other researchers may also become public as a result of the presentation of Dr. Czub’s research.

    The Public Health Agency of Canada, Health Canada, CFlA and other Federal partners are working together to assess what policies or programs need further review as well as preparing other communications about the research and health policy and advice to Canadian. 2017/04/28

    ===end...UNOFFICIAL...NO URL LINK...TSS===

    0:30 First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress

    Dr Stefanie Czub University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency Canada

    http://prion2017.org/programme/


    WEDNESDAY, MAY 03, 2017

    *** First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques

    http://chronic-wasting-disease.blogs...anial-and.html

    Wednesday, May 24, 2017

    PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh UPDATE 1

    Subject: PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh

    *see archives of previous Prion Conferences, the ones that are still available, scroll down towards bottom in this link.

    http://prionprp.blogspot.com/2017/05...ate-23-26.html

    WEDNESDAY, MAY 31, 2017

    Texas New Exotic CWD Susceptible Species Rules Now in Effect

    http://chronic-wasting-disease.blogs...sceptible.html

    WEDNESDAY, MAY 17, 2017

    CWD, TSE, PRION, Cattle, Pigs, Sheep, and Humans aka Mad Cow Disease

    http://chronic-wasting-disease.blogs...sheep-and.html

    Groups seek to save NIH brain collection

    By STEVE MITCHELL, Medical Correspondent | April 1, 2005 at 4:48 PM

    http://www.upi.com/Science_News/2005...32301112391588

    NIH may destroy human brain collection

    By STEVE MITCHELL, Medical Correspondent | March 24, 2005 at 8:42 AM

    http://www.upi.com/Science_News/2005...36201111698400

    NIH sends mixed signals on CJD brains

    By STEVE MITCHELL, Medical Correspondent | April 7, 2005 at 3:30 PM

    http://www.upi.com/Science_News/2005...32301112391588

    Groups seek to save NIH brain collection

    By STEVE MITCHELL, Medical Correspondent | April 1, 2005 at 4:48 PM

    http://www.upi.com/Science_News/2005...61321112921422


    JOHN CORNYN TEXAS UNITED STATES SENATE WASHINGTON, DC 20510-4305 April 26,2005

    Mr. Terry Singeltary P.O. Box 42 Bacliff, Texas 77518

    Dear Mr. Singeltary:

    In response to your recent request for my assistance, I have contacted the National Institutes of Health. I will write you again as soon as I receive a reply. I appreciate having the opportunity to represent you in the United States Senate and to be of service in this matter.

    Sincerely, JOHN CORNYN United States Senator JC:djl

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

    JOHN CORNYN TEXAS UNITED STATES SENATE WASHINGTON, DC 20510-4305 May 18,2005 Mr. Terry Singeltary P.O. Box 42 Bacliff, Texas 77518

    Dear Mr. Singeltary:

    Enclosed is the reply I received from the Department of Health and Human Services in response to my earlier inquiry on your behalf. I hope this will be useful to you. I appreciate having the opportunity to represent you in the United States Senate. Thank you for taking time to contact me.

    Sincerely, JOHN CORNYN United States Senate JC:djl Enclosure

    DEPARTMENT OF HEALTH & HUMAN SERVICES National Institutes of Health National Institute of Neurological Disorders and Stroke NINDS Building 31, Room 8A52 31 Center Dr., MSC 2540 Bethesda, Maryland 20892-2540 Phone: 301-496-9746 Fax: 301-496-0296 Email: [log in to unmask] May 10, 2005

    The Honorable John Cornyn United States Senator Occidental Tower 5005 LBJ Freeway, Suite 1150 Dallas, Texas 75244-6199

    Dear Senator Cornyn:

    Your letter to the National Institutes of Health (NIH) forwarding correspondence from Mr. Terry S. Singeltary, Sr., has been forwarded to me for reply. Mr. Singeltary is concerned about the preservation of Creutzfeldt-Jakob disease (CJD) brain samples that have been maintained by the National Institute of Neurological Disorders and Stroke (NINDS) Intramural Research program for many years. I am sorry to learn that Mr. Singeltary's mother died of CJD and can certainly understand his desire that any tissues that could help investigators unravel the puzzle of this deadly disease are preserved. I hope he will be pleased to learn that all the brains and other tissues with potential to help scientists learn about CJD are, and will continue to be, conserved. (The tissues that a red is carded are those that have either decayed to an extent that renders them no longer appropriate for research or those for which we do not have sufficient identification.) The purpose of gathering these brains and tissues is to help scientists learn about CJD. To that end, some of the NINDS-held samples are distributed to investigators who can demonstrate that they have a compelling research or public health need for such materials. For example, samples have been transferred to NIH grantee Dr. Pierluigi Gambetti, who heads the National Prion Diseases Pathology Surveillance Center at Case Western Reserve University in Ohio and works with the Centers for Disease Control and Prevention to monitor all cases of CJD in the United States. Dr. Gambetti studies the tissues to learn about the formation, physical and chemical properties, and pathogenic mechanisms of prion proteins, which are believed to be involved in the cause of CJD. Samples have also been transferred to Dr. David Asher, at the U.S. Food and Drug Administration, for use in assessing a potential diagnostic test for CJD.

    Page 2 - The Honorable John Cornyn

    in closing, we know that donating organs and tissue from loved ones is a very difficult and personal choice that must often be made at the most stressful of times. We at the NINDS are grateful to those stalwart family members who make this choice in the selfless hope that it will help others afflicted with CJD. We also know the invaluable contribution such donations make to the advancement of medical science, and we are dedicated to the preservation of all of the tissue samples that can help in our efforts to overcome CJD.

    I hope this information is helpful to you in responding to Mr. Singeltary. Sincerely, Story C. Landis, Ph.D. Director, National Institute of Neurological Disorders and Stroke

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


    http://creutzfeldt-jakob-disease.blo...withjames.html

    kind regards, terry
    Last edited by flatfish; 06-04-2017 at 01:14 PM.

  4. #4
    Distinguished Community Member
    Join Date
    Oct 2006
    Location
    Bacliff, Texas
    Posts
    496

    Default

    ''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.''

    First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress

    Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1

    University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen

    This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves.

    Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice.

    At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.

    PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS

    0:30 First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress

    Dr Stefanie Czub University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency Canada

    http://prion2017.org/programme/

    see science to date that the call should be made NOW, that cwd to humans is possible, and all precautions there fore, should be take will great urgency.

    WEDNESDAY, MAY 03, 2017

    *** First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques

    http://chronic-wasting-disease.blogs...anial-and.html

    WEDNESDAY, APRIL 05, 2017

    Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease

    http://chronic-wasting-disease.blogs...n-protein.html

    TUESDAY, APRIL 18, 2017

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

    http://usdameatexport.blogspot.com/2...rion-feed.html

    TUESDAY, JUNE 06, 2017

    CHRONIC WASTING DISEASE CWD TSE PRION ZOONOSIS ZOONOTIC INSIDIOUS AND DIRE CONSEQUENCES AHEAD

    http://chronic-wasting-disease.blogs...tse-prion.html

    SATURDAY, JUNE 10, 2017

    Chronic Wasting Disease CWD TSE Prion to Humans, who makes that final call, when, or, has it already happened?

    http://chronic-wasting-disease.blogs...-prion_10.html

    MONDAY, JUNE 12, 2017

    Rethinking Major grain organizations opposition to CFIA's control zone approach to Chronic Wasting CWD TSE Prion Mad Deer Type Disease 2017?

    http://chronic-wasting-disease.blogs...nizations.html

    Terry S. Singeltary Sr.

  5. #5
    Distinguished Community Member
    Join Date
    Oct 2006
    Location
    Bacliff, Texas
    Posts
    496

    Default

    Subject: PRION 2017 CONFERENCE ABSTRACT First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress

    First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress

    Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1

    University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen

    This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves.

    Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice.

    At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation.

    PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS

    TUESDAY, JUNE 13, 2017

    PRION 2017 CONFERENCE ABSTRACT First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress

    http://chronic-wasting-disease.blogs...act-first.html


    kind regards, terry

Similar Threads

  1. Replies: 1
    Last Post: 12-10-2015, 01:35 PM
  2. Replies: 0
    Last Post: 12-10-2015, 01:34 PM
  3. Replies: 0
    Last Post: 09-09-2015, 11:09 AM
  4. Blood reference materials from macaques infected with vCJD agent
    By flatfish in forum Creutzfeldt Jakobs Disease (CJD)
    Replies: 0
    Last Post: 08-28-2014, 09:45 AM
  5. Asynchronous Onset of Clinical Disease in BSE-Infected Macaques
    By flatfish in forum Creutzfeldt Jakobs Disease (CJD)
    Replies: 0
    Last Post: 05-24-2013, 01:54 PM

Tags for this Thread

Posting Permissions

  • You may not post new threads
  • You may not post replies
  • You may not post attachments
  • You may not edit your posts
  •  


BTC Inc's Disclaimer and Privacy Policy

The material on this site is for information & support purposes only, and is not a substitute for medical advice provided by a licensed health care provider. Always consult your doctor before trying anything that you find online.