Wyoming National Elk Refuge CWD forum update December 8, 2016
CWD forum planned for December 7, 2016
The National Elk Refuge is co-hosting a CWD forum in Jackson, Wyoming on Wednesday, December 7, 2016. The forum will be held at the National Museum of Wildlife Art.
December 8, 2016 Update:
The CWD Forum was held on December 7, with approximately 100 people attending all or part of the presentations. Our sincere thanks to all who attended the forum.
The entire conference was videotaped. Each session title listed in the Schedule section below is a hotlink to view the individual talk. Each video may take a moment to load.
The National Elk Refuge, along with State and other Federal land and wildlife managers and other non-profit organizations, will co-host a Chronic Wasting Disease (CWD) forum on Wednesday, December 7, 2016. The forum will be held at the National Museum of Wildlife Art, located 2.5 miles north of the Town Square in Jackson, Wyoming.
The forum is dedicated to highlighting CWD research and management considerations. The goal of the event is to share current science-based information with the general public and all organizations concerned with the long-term health of area elk and deer populations.
The event is open to the public and free of charge. A $15 lunch will be available for purchase on the day of the event; an evening social includes complimentary hors d'oeuvres and a cash bar.
Attendees need to register for planning purposes. Please use the online registration form provided at this link.
Additional information will be posted here as organizers finalize the schedule and event details. Anyone interested in attending the forum is encouraged to bookmark this web link and check back for updates.
Schedule
8:00 - 8:30 am
Welcome table: pick up name tags, obtain a printed agenda, ask questions about the forum, etc.
Morning Presentations
8:30 - 8:45 am
National Elk Refuge Manager Steve Kallin: Welcome and introductions
The morning and afternoon sessions were moderated by Tom Segerstrom, who serves as the Executive Director of the Teton Conservation District. He is a certified wildlife biologist and historically worked in several agencies with important experience in the mining industry. Segerstrom also worked as a Land Steward and Staff Biologist for the Jackson Hole Land Trust for 15 years.
8:45 - 9:30 am
Dr. Mary Wood: Wyoming CWD Surveillance
Dr. Mary Wood is the Wyoming State Wildlife Veterinarian and supervises the Veterinary Services Branch of the Wyoming Game and Fish Department (WGFD). She oversees the Wyoming Game and Fish Wildlife Health Laboratory, wildlife disease surveillance programs, and the Thorne-Williams Wildlife Research Center. Additionally, she participates in both free ranging and captive wildlife disease research across the state with focuses in CWD and respiratory disease in bighorn sheep. Dr. Wood charis the WGFD Chronic Wasting Disease Management team and is actively engaged in regional and international CWD collaborations.
9:30 - 10:15 am
Dr. Davin Henderson: Studies of CWD Transmission and Shedding Using Rapid Sensitive Amplification Assays
Dr. Davin Henderson received his Ph.D. from the University of Minnesota in Biochemistry, Molecular Biology and Biophysics. He is currently a Research Scientist at the Prion Research Center at Colorado State University where he works with Edward Hoover to understand the pathogenesis and replication potential of Chronic Wasting Disease prions affecting deer and elk. He has 5 years of experience working with the RT-QuIC assay and over 15 years of experience in protein biochemistry. He is an author on over 10 manuscripts utilizing the RT-QuIC assay and has pioneered the detection of CWD prions in excreta.
10:15 - 10:30 am
Break
10:30 - 11:15 am
Dr. Joel Pedersen: Soil and Environmental Transmission of CWD
Dr. Joel Pedersen is the Rothermel Bascom Professor of Soil Science at the University of Wisconsin – Madison. He holds appointments in the Departments of Soil Science, Chemistry, and Civil & Environmental Engineering. He is a faculty member in the Environmental Chemistry and Technology program and the Molecular and Environmental Toxicology Center. Prof. Pedersen earned his B.S. degree at University of California Irvine, his M.S. degree at California Institute of Technology, and his doctorate at University of California Los Angeles. The Pedersen research group studies physicochemical and biophysical processes in terrestrial and aquatic environments and has pioneered work in understanding the environmental transmission of prion diseases. His group’s research emphasizes mechanistic studies of the interaction of organic contaminants and macromolecules with environmental interfaces. Prof. Pedersen received the National Science Foundation’s CAREER award and the Early Career Award from ASA-CSSA-SSSA (Agronomy Society of America-Crop Science Society of America-Soil Science Society of America).
11:15 am - 12:00 pm
Amy Girard: Modeling the Effects of CWD on a Rocky Mountain Elk Population Using Genotype-Specific Mortality Rates
Amy Girard recently received her master’s degree from the University of Wyoming through the Department of Animal and Veterinary Sciences. While focused on wildlife disease, she studied the transmission dynamics of the parasite Eleaophora schneideri and the effects of genotype on CWD driven mortality in elk herds of Wyoming. Amy has used her education and interest in wildlife to study a wide variety of species including birds and fish. Prior to graduate school, Amy worked with the Wyoming Game and Fish Department studying brucellosis on elk feedgrounds. Amy currently works with Teton County Weed and Pest.
12:00 - 1:30 pm: Lunch break. A $15 lunch will be available on site.
Afternoon Presentations
1:30 - 2:15 pm
Dr. Melia DeVivo: Endemic CWD and Mule Deer Populations Decline in Wyoming
Dr. Melia DeVivo received her bachelor’s and master’s degrees from Indiana University of Pennsylvania, where she studied the habitat use characteristics of parturient elk and survival of calves in northcentral PA. She graduated from the University of Wyoming receiving a Ph.D. in Veterinary Sciences, where she studied the population effects of chronic wasting disease of free ranging mule deer in southeastern Wyoming. Her research has focused on cervid ecology, demography, and disease. Dr. DeVivo is currently working on publications regarding her work on CWD and collaborating with local wildlife and habitat experts on a project for the Jackson Hole Conservation Alliance identifying conservation targets for the Jackson Hole region.
2:15 - 3:00 pm
Nathan Galloway and Jenny Powers: Lessons Learned about CWD in Elk at Rocky Mountain and Wind Cave National Parks
Nathan Galloway joined the Wildlife Health Branch in 2015. He is trained as a microbiologist, a disease ecologist and a Bayesian modeler and attempts to use his diverse background to facilitate conversation between interested collaborators who often lack a common vocabulary. Nathan is concurrently finishing his PhD at Colorado State University on chronic wasting disease in free-ranging populations and is thrilled to have the opportunity with the NPS to contribute to knowledge about the dynamics and management of wildlife diseases. When not analyzing data and discussing the community ecology of wildlife disease, Nathan can be found riding his bike, hiking, and trying to pay attention to the worthwhile.
Jenny Powers joined the National Park Service Wildlife Health program in 2002 as a wildlife veterinarian. With a background in large animal medicine and reproductive physiology, Jenny works with parks on wildlife health issues ranging from capture and anesthesia projects to disease outbreak investigations. She has studied chronic wasting disease (CWD) related questions from both management and research perspectives since joining the NPS. As the CWD coordinator for the NPS Jenny has assisted parks to learn about the epidemiology, ecology, and transmission of the disease as well as develop deer and elk management plans which accommodate CWD surveillance, disinfection, and disposal. Jenny received her DVM from the University of California, Davis and her PhD from Colorado State University. She enjoys working through "thorny" wildlife management problems with a variety of state, federal, university, and other conservation partners.
3:00 - 3:15 pm
Break
3:15 - 4:00 pm
Dr. Tom Hobbs: Using Models and Data to Support Adaptive Management of the Jackson Elk Herd
Dr. Tom Hobbs has worked on population and community ecology of large mammals for the last three decades. Virtually all of his work uses models of ecological process to gain insight from data. He has particular expertise in building demographic models on populations, models that now widely used to support management and policy in North America and Europe. He has been on the faculty at Colorado State since 2001 and before that he worked for 20 years as a research scientist for Colorado Division of Wildlife. He has served as a rotating Program Director in the Population and Community Ecology Cluster of the Division of Environmental Biology at the National Science Foundation. He is a member of the Editorial Board of Ecological Applications. Princeton University Press recently published his book (co-authored with Mevin Hooten), Bayesian Modeling: a Statistical Primer for Ecologists. Tom has a degree in general biology from Grinnell College and an MS. and Ph.D. in wildlife ecology from Colorado State University.
4:00 - 4:45 pm
Dr. Chad Bishop: Role of Habitat Treatments and Related Mitigation Strategies to Offset Impacts of Altered Feedground Management
Chad Bishop is Director of the Wildlife Biology Program at University of Montana. As Director, Chad is responsible for a wide array of functions tied to running the Program, with an emphasis on faculty and student support and Program outreach and development. He received a Bachelor’s of Science degree in Biology (Fish and Wildlife Management Option) from Montana State University (1995), a Master’s of Science degree in Wildlife Resources from University of Idaho (1998), and a Doctorate degree in Wildlife Biology from Colorado State University (2007). Prior to University of Montana, he spent nearly 16 years working for Colorado Division of Wildlife (now Colorado Parks and Wildlife), where he held positions as an ungulate researcher (1999-2009), Mammals Research Leader (2009-2012), and Assistant Director (2012-2015).
4:45 - 6:30 pm: Social Hour; hors d'oeuvres and cash bar provided.
Evening Presentation
6:30 - 8:00 pm
Round Table Discussion, moderated by John Turner
Among his many accomplishments, John Turner served as the Director of the U.S. Fish and Wildlife Service from 1989-1993 and Assistant Secretary of State for the Bureau of Oceans and International Environmental and Scientific Affairs from 2001 through 2005. Turner received a Master of Science degree in Wildlife Ecology from the University of Michigan and a Bachelor of Arts degree in Biology from the University of Notre Dame. A native of Moose, Wyoming, Turner is a third-generation rancher who, with his brothers, operates the Triangle X Ranch in Grand Teton National Park.
https://www.fws.gov/nwrs/threecolumn.aspx?id=2147595622
SEE VIDEOS ;
INTRODUCTION
https://www.youtube.com/watch?v=iJN8hg9wzWA
Published on Dec 13, 2016
Jackson Hole Chronic Wasting Disease Forum
December 7, 2016
Dr. Mary Wood
https://www.youtube.com/watch?v=JfTsWH-aaQg
Jackson Hole Chronic Wasting Disease Forum
December 7, 2016
Dr. Davin Henderson
https://www.youtube.com/watch?v=cX-yKanZYBM
December 7, 2016
Dr. Mary Wood
https://www.youtube.com/watch?v=JfTsWH-aaQg
Jackson Hole Chronic Wasting Disease Forum
December 7, 2016
Dr. Davin Henderson
https://www.youtube.com/watch?v=cX-yKanZYBM
Published on Dec 13, 2016
Jackson Hole Chronic Wasting Disease Forum
December 7, 2016
*** Dr. Melia Devivo ***
December 7, 2016
*** Dr. Melia Devivo ***
https://www.youtube.com/watch?v=-5RoabC4BL4
Published on Dec 14, 2016
Jackson Hole Chronic Wasting Disease Forum
December 7, 2016
Dr. Chad Bishop
December 7, 2016
Dr. Chad Bishop
https://www.youtube.com/watch?v=TZWQi9Fqk6g
Jackson Hole Chronic Wasting Disease Forum
December 7, 2016
Dr. Joel Pedersen
https://www.youtube.com/watch?v=qrCE6Ah-fPE
Jackson Hole Chronic Wasting Disease Forum
December 7, 2016
Amy Girard
https://www.youtube.com/watch?v=TNN-CyeC0Aw
7 Dr Powers:Galloway
https://www.youtube.com/watch?v=OZzkO3UKYWw
8 Dr Tom Hobbs
https://www.youtube.com/watch?v=WsN8dPPz2GA
9 Dr Chad Bishop
https://www.youtube.com/watch?v=TZWQi9Fqk6g
10 Evening Presentation
https://www.youtube.com/watch?v=TpG9WBVRZCs
please remember, to date ;
***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 CWO
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
PLUS, PROLONGED INCUBATION OF CWD TSE PRION VIA GENETIC MANIPULATION, WILL GIVE RISE TO LONGER LIFE, AND LONGER TIME TO SPREAD THE CWD TSE PRION AGENT...TSS
Saturday, May 28, 2016
*** Infection and detection of PrPCWD in soil from CWD infected farm in Korea Prion 2016 Tokyo ***
Clay Components in Soil Dictate Environmental Stability and Bioavailability of Cervid Prions in Mice
http://chronic-wasting-disease.blogspot.com/2016/12/clay-components-in-soil-dictate.html
Wednesday, December 14, 2016
*** 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/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf
PRION 2016 TOKYO
Zoonotic Potential of CWD Prions: An Update
Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3, Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6, Pierluigi Gambetti1, Qingzhong Kong1,5,6 1Department of Pathology, 3National Prion Disease Pathology Surveillance Center, 5Department of Neurology, 6National Center for Regenerative Medicine, Case Western Reserve University, Cleveland, OH 44106, USA. 4Department of Biological Sciences and Center for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Alberta, Canada, 2Encore Health Resources, 1331 Lamar St, Houston, TX 77010
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.
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
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/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf
PRION 2016 TOKYO
Zoonotic Potential of CWD Prions: An Update
Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3, Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6, Pierluigi Gambetti1, Qingzhong Kong1,5,6 1Department of Pathology, 3National Prion Disease Pathology Surveillance Center, 5Department of Neurology, 6National Center for Regenerative Medicine, Case Western Reserve University, Cleveland, OH 44106, USA. 4Department of Biological Sciences and Center for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Alberta, Canada, 2Encore Health Resources, 1331 Lamar St, Houston, TX 77010
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.
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
Monday, May 02, 2016
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
http://chronic-wasting-disease.blogspot.com/2016/05/zoonotic-potential-of-cwd-prions-update.html
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=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/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_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/2016/04/scrapie-ws-01-prion-diseases-in-animals.html
*** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo ***
http://chronic-wasting-disease.blogspot.com/2016/05/zoonotic-potential-of-cwd-prions-update.html
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=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/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_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/2016/04/scrapie-ws-01-prion-diseases-in-animals.html
Thursday, June 09, 2016
Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie TSE Prion Experiment 1964
Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie Experiment 1964
How Did CWD Get Way Down In Medina County, Texas?
Confucius ponders...
Could the Scrapie experiments back around 1964 at Moore Air Force near Mission, Texas, could this area have been ground zero for CWD TSE Prion (besides the CWD cases that have waltzed across the Texas, New Mexico border near WSMR Trans Pecos region since around 2001)?
Epidemiology of Scrapie in the United States 1977
snip...
Scrapie Field Trial Experiments Mission, Texas
A Scrapie Field Trial was developed at Mission, Texas, to provide additional information for the eradication program on the epidemiology of natural scrapie. The Mission Field Trial Station is located on 450 acres of pastureland, part of the former Moore Air Force Base, near Mission, Texas. It was designed to bring previously exposed, and later also unexposed, sheep or goats to the Station and maintain and breed them under close observation for extended periods to determine which animals would develop scrapie and define more closely the natural spread and other epidemiological aspects of the disease.
The 547 previously exposed sheep brought to the Mission Station beginning in 1964 were of the Cheviot, Hampshire, Montadale, or Suffolk breeds. They were purchased as field outbreaks occurred, and represented 21 bloodlines in which scrapie had been diagnosed. Upon arrival at the Station, the sheep were maintained on pasture, with supplemental feeding as necessary. The station was divided into 2 areas: (1) a series of pastures and-pens occupied by male animals only, and (2) a series of pastures and pens occupied by females and young progeny of both sexes. ...
snip...see full text ;
Mission, Texas Scrapie transmission to cattle study
Wilbur Clarke (reference the Mission, Texas scrapie transmission transmission to cattle study) is now the State Veterinarian for Montana based at Helena.
I was given confidential access to sections from the Clarke scrapie-cattle transmission experiment. Details of the experimental design were as supplied previously by Dr. Wrathall (copy of relevant information appended). Only 3 animals (2 inoculated with 2nd pass Suffolk scrapie and 1 inoculated with Angora goat passaged scrapie) showed clinical signs. Clinical signs were characterised by weakness, ''a stilted hindlimb gait'', disorientation, ataxia and, terminally, lateral recumbency. The two cattle from which I examined material were inocluated at 8 months of age and developed signs 36 months pi (goat scrapie inoculum) and 49 months pi (one of the Suffolk scrapie inoculated) respectively. This latter animal was killed at 58 months of age and so the clinical duration was only 1 month. The neuropathology was somewhat different from BSE or the Stetsonville TME in cattle. Vacuolar changes were minimal, to the extent that detection REQUIRED CAREFUL SEARCHING. Conversely astrocyte hypertrophy was a widespread and prominent feature. The material requires DETAILED NEUROPATHOLOGICAL ASSESSMENT BUT WHETHER OR NOT THIS WILL BE DONE REMAINS A QUESTION.
Transmission Studies
Thursday, December 08, 2016
USDA APHIS National Scrapie Eradication Program October 2016 Monthly Report Fiscal Year 2017 atypical NOR-98 Scrapie
Title: Pathological features of chronic wasting disease in reindeer and demonstration of horizontal transmission
Tuesday, December 13, 2016
Norway Chronic Wasting Disease CWD TSE Prion disease Skrantesjuke December 2016 Update
Monday, September 05, 2016
Pathological features of chronic wasting disease in reindeer and demonstration of horizontal transmission Major Findings for Norway
Thursday, September 22, 2016
NORWAY DETECTS 5TH CASE OF CHRONIC WASTING DISEASE CWD TSE PRION Skrantesjuke
SUNDAY, OCTOBER 02, 2016
*** What is the risk of a cervid TSE being introduced from Norway into Great Britain? Qualitative Risk Assessment September 2016
Wednesday, September 7, 2016
*** An assessment of the long-term persistence of prion infectivity in aquatic environments
http://transmissiblespongiformencephalopathy.blogspot.com/2016/09/an-assessment-of-long-term-persistence.html
Friday, September 02, 2016
*** Chronic Wasting Disease Drives Population Decline of White-Tailed Deer
Chronic Wasting Disease (CWD) Susceptibility of Several North American Rodents That Are Sympatric with Cervid CWD Epidemics▿
MOUNTAIN LIONS, FELINE, CWD TSE PRION
AD.63:
Susceptibility of domestic cats to chronic wasting disease
Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1 1Colorado State University; Fort Collins, CO USA; 2University of Minnesota; Saint Paul, MN USA
Domestic and nondomestic cats have been shown to be susceptible to feline spongiform encephalopathy (FSE), almost certainly caused by consumption of bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and free-ranging nondomestic felids scavenge cervid carcasses, including those in areas affected by chronic wasting disease (CWD), we evaluated the susceptibility of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated cats developed signs consistent with prion disease, including a stilted gait, weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from these two cats were pooled and inoculated into cohorts of cats by IC, PO, and intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the symptomatic cats by western blotting and immunohistochemistry and abnormalities were seen in magnetic resonance imaging, including multifocal T2 fluid attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4 IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns consistent with the early stage of feline CWD.
*** These results demonstrate that CWD can be transmitted and adapted to the domestic cat, thus raising the issue of potential cervid-to- feline transmission in nature.
http://www.prion2013.ca/tiny_uploads/forms/Scientific-Program.pdf
www.landesbioscience.com
PO-081: Chronic wasting disease in the cat— Similarities to feline spongiform encephalopathy (FSE)
http://www.landesbioscience.com/journals/prion/04-Prion6-2-Pathogenesis-and-pathology.pdf
new link ;
http://www.tandfonline.com/doi/pdf/10.4161/pri.20609
http://chronic-wasting-disease.blogspot.com/2012/05/chronic-wasting-disease-cwd-prion2012.html
FELINE SPONGIFORM ENCEPHALOPATHY FSE
http://felinespongiformencephalopathyfse.blogspot.com/2009_04_01_archive.html
http://felinespongiformencephalopathyfse.blogspot.com/
3 further cheetah cases have occured, plus 1 lion, plus all the primates, and 20 additional house cats. Nothing has been published on any of these UK cases either. One supposes the problem here with publishing is that many unpublished cases were _born_ long after the feed "ban". Caught between a rock and a hard place: leaky ban or horizontal transmission (or both).
http://www.mad-cow.org/may99_zoo_news.html
http://www.mad-cow.org/00/aug00_late_news.html#ggg
Monday, February 14, 2011
THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER NO, NO, NOT NO, BUT CensoredCensoredCensoredCensored NO !
Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011
http://chronic-wasting-disease.blogspot.com/2011/02/role-of-predation-in-disease-control.html
Susceptibility of domestic cats to chronic wasting disease
Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1 1Colorado State University; Fort Collins, CO USA; 2University of Minnesota; Saint Paul, MN USA
Domestic and nondomestic cats have been shown to be susceptible to feline spongiform encephalopathy (FSE), almost certainly caused by consumption of bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and free-ranging nondomestic felids scavenge cervid carcasses, including those in areas affected by chronic wasting disease (CWD), we evaluated the susceptibility of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated cats developed signs consistent with prion disease, including a stilted gait, weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from these two cats were pooled and inoculated into cohorts of cats by IC, PO, and intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the symptomatic cats by western blotting and immunohistochemistry and abnormalities were seen in magnetic resonance imaging, including multifocal T2 fluid attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4 IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns consistent with the early stage of feline CWD.
*** These results demonstrate that CWD can be transmitted and adapted to the domestic cat, thus raising the issue of potential cervid-to- feline transmission in nature.
http://www.prion2013.ca/tiny_uploads/forms/Scientific-Program.pdf
www.landesbioscience.com
PO-081: Chronic wasting disease in the cat— Similarities to feline spongiform encephalopathy (FSE)
http://www.landesbioscience.com/journals/prion/04-Prion6-2-Pathogenesis-and-pathology.pdf
new link ;
http://www.tandfonline.com/doi/pdf/10.4161/pri.20609
http://chronic-wasting-disease.blogspot.com/2012/05/chronic-wasting-disease-cwd-prion2012.html
FELINE SPONGIFORM ENCEPHALOPATHY FSE
http://felinespongiformencephalopathyfse.blogspot.com/2009_04_01_archive.html
http://felinespongiformencephalopathyfse.blogspot.com/
3 further cheetah cases have occured, plus 1 lion, plus all the primates, and 20 additional house cats. Nothing has been published on any of these UK cases either. One supposes the problem here with publishing is that many unpublished cases were _born_ long after the feed "ban". Caught between a rock and a hard place: leaky ban or horizontal transmission (or both).
http://www.mad-cow.org/may99_zoo_news.html
http://www.mad-cow.org/00/aug00_late_news.html#ggg
Monday, February 14, 2011
THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER NO, NO, NOT NO, BUT CensoredCensoredCensoredCensored NO !
Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011
http://chronic-wasting-disease.blogspot.com/2011/02/role-of-predation-in-disease-control.html
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
Using in vitro prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto
Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston.
Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.
=========================
***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.
========================
Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.
see ;
with CWD TSE Prions, I am not sure there is any absolute yet, other than what we know with transmission studies, and we know tse prion kill, and tse prion are bad. science shows to date, that indeed soil, dirt, some better than others, can act as a carrier. same with objects, farm furniture. take it with how ever many grains of salt you wish, or not. if load factor plays a role in the end formula, then everything should be on the table, in my opinion...tss
see ;
***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.
see ;
Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil Particles
Author Summary
Transmissible 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.
https://www.aphis.usda.gov/emergency_response/downloads/tools/johnson%20et%20al%20prions%20in%20soil.pdf
tse prion soil
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
The sources of dust borne prions are unknown but it seems reasonable to assume that faecal, urine, skin, parturient material and saliva-derived prions may contribute to this mobile environmental reservoir of infectivity. This work highlights a possible transmission route for scrapie within the farm environment, and this is likely to be paralleled in CWD which shows strong similarities with scrapie in terms of prion dissemination and disease transmission. The data indicate that the presence of scrapie prions in dust is likely to make the control of these diseases a considerable challenge.
>>>Particle-associated PrPTSE molecules may migrate from locations of deposition via transport processes affecting soil particles, including entrainment in and movement with air and overland flow. <<<
Fate of Prions in Soil: A Review
Christen B. Smith, Clarissa J. Booth, and Joel A. Pedersen*
Several reports have shown that prions can persist in soil for several years. Significant interest remains in developing methods that could be applied to degrade PrPTSE in naturally contaminated soils. Preliminary research suggests that serine proteases and the microbial consortia in stimulated soils and compost may partially degrade PrPTSE. Transition metal oxides in soil (viz. manganese oxide) may also mediate prion inactivation. Overall, the effect of prion attachment to soil particles on its persistence in the environment is not well understood, and additional study is needed to determine its implications on the environmental transmission of scrapie and CWD.
P.161: Prion soil binding may explain efficient horizontal CWD transmission
Conclusion. Silty clay loam exhibits highly efficient prion binding, inferring a durable environmental reservoir, and an efficient mechanism for indirect horizontal CWD transmission.
>>>Another alternative would be an absolute prohibition on the movement of deer within the state for any purpose. While this alternative would significantly reduce the potential spread of CWD, it would also have the simultaneous effect of preventing landowners and land managers from implementing popular management strategies involving the movement of deer, and would deprive deer breeders of the ability to engage in the business of buying and selling breeder deer. Therefore, this alternative was rejected because the department determined that it placed an avoidable burden on the regulated community.<<<
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4, Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge, Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK
Classical scrapie is an environmentally transmissible prion disease of sheep and goats. Prions can persist and remain potentially infectious in the environment for many years and thus pose a risk of infecting animals after re-stocking. In vitro studies using serial protein misfolding cyclic amplification (sPMCA) have suggested that objects on a scrapie affected sheep farm could contribute to disease transmission. This in vivo study aimed to determine the role of field furniture (water troughs, feeding troughs, fencing, and other objects that sheep may rub against) used by a scrapie-infected sheep flock as a vector for disease transmission to scrapie-free lambs with the prion protein genotype VRQ/VRQ, which is associated with high susceptibility to classical scrapie. When the field furniture was placed in clean accommodation, sheep became infected when exposed to either a water trough (four out of five) or to objects used for rubbing (four out of seven). This field furniture had been used by the scrapie-infected flock 8 weeks earlier and had previously been shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of 23) through exposure to contaminated field furniture placed within pasture not used by scrapie-infected sheep for 40 months, even though swabs from this furniture tested negative by PMCA. This infection rate decreased (1 out of 12) on the same paddock after replacement with clean field furniture. Twelve grazing sheep exposed to field furniture not in contact with scrapie-infected sheep for 18 months remained scrapie free. The findings of this study highlight the role of field furniture used by scrapie-infected sheep to act as a reservoir for disease re-introduction although infectivity declines considerably if the field furniture has not been in contact with scrapie-infected sheep for several months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.
Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
Tuesday, November 29, 2016
Wyoming CWD Report monitoring efforts increase with focus on improving herd health
http://chronic-wasting-disease.blogspot.com/2016/11/wyoming-cwd-report-monitoring-efforts.html
Thursday, November 17, 2016
Wyoming Game and Fish Department confirmed CWD Deer Hunt Area 110 west of Cody
http://chronic-wasting-disease.blogspot.com/2016/11/wyoming-game-and-fish-department_17.html
Wednesday, November 09, 2016
Wyoming Game and Fish Department confirmed chronic wasting disease (CWD) in Deer Hunt Area 121, near Heart Mountain
http://chronic-wasting-disease.blogspot.com/2016/11/wyoming-game-and-fish-department.html
Tuesday, October 18, 2016
WYOMING Game and Fish finds CWD in new deer hunt area near Dubois and will more actively monitor elk feedgrounds
http://chronic-wasting-disease.blogspot.com/2016/10/wyoming-game-and-fish-finds-cwd-in-new_18.html
Sunday, October 16, 2016
Wyoming Game and Fish finds CWD in new deer hunt area near Osage
http://chronic-wasting-disease.blogspot.com/2016/10/wyoming-game-and-fish-finds-cwd-in-new.html
Tuesday, June 07, 2016
Wyoming For the first time in several years an ungulate has tested positive for Chronic Wasting Disease (CWD) on the west side of the continental divide
http://chronic-wasting-disease.blogspot.com/2016/06/wyoming-for-first-time-in-several-years.html
Wednesday, April 27, 2016
WYOMING GAME AND FISH DEPARTMENT CHRONIC WASTING DISEASE MANAGEMENT PLAN APRIL 22, 2016
http://chronic-wasting-disease.blogspot.com/2016/04/wyoming-game-and-fish-department.html
Thursday, March 10, 2016
WYOMING RIDE EM COWBOY HELICOPTER WRANGLING RAMBO STYLE DEER BULLDOGGING RODEO FOR CWD VIDEO
http://chronic-wasting-disease.blogspot.com/2016/03/wyoming-ride-em-cowboy-helicopter.html
Monday, March 07, 2016
Wyoming Game and Fish Department confirmed chronic wasting disease (CWD) in a buck mule deer that was found dead southeast of Lander
http://chronic-wasting-disease.blogspot.com/2016/03/wyoming-game-and-fish-department.html
Tuesday, January 12, 2016
Wyoming Game and Fish seeks additional public comments on draft of updated CWD plan Singeltary 2nd submission
From: Terry S. Singeltary Sr.
Sent: Tuesday, January 12, 2016 3:52 PM
To: daryl.lutz@wgf.state.wy.us
Cc: Tara.Hodges@wyo.gov ; wyomingwildlife@wyo.gov ; Carrie.Little@wyo.gov
Subject: Game and Fish seeks additional public comments on draft of updated CWD plan Singeltary 2nd submission
http://chronic-wasting-disease.blogspot.com/2016/01/game-and-fish-seeks-additional-public.html
Wednesday, December 14, 2016
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
1:48 PM
0 Comments:
Post a Comment
Subscribe to Post Comments [Atom]
<< Home