Tennessee Republican representative Bud Hulsey wants to weaken CWD Carcass Ban rule and put other states at risk
Tennessee Lawmaker Looks
to Loosen Restricitons on CWD-Influenced Carcass Ban
16 hours ago
Tennessee law could negatively affect taxidermists in the state.
TN lawmaker wants to
ease restrictions on out-of-state deer carcass importation
More and more states are beginning to enforce deer carcass importation bans as wildlife officials continue to work to combat the spread of chronic wasting disease or CWD.
But there are some unseen side effects to these types of bans and one Tennessee lawmaker is working to help out some taxidermists that could be hit hard the state’s new ban on importing deer, moose and elk carcasses from CWD-positive states.
CWD is not currently in Tennessee, so it’s easy to see why authorities would like to keep it that way. But less obvious was how the ban might affect some people’s livelihood. “Probably 50 to 60 percent of my business is out of state,” taxidermist Jason Roberts told WJHL.
The solution being suggested by Republican representative Bud Hulsey in many ways mirrors what has been done in other states. “One, you can have it de-boned and processed where you killed it and then bring it in,” he told the news station. “Or you can bring it in the state but you have to take it immediately to a taxidermist or meat processing place.”
Such carcass importation bans aren’t exclusive to Tennessee as more and more states try to crack down on hunters bringing in out of state animals.
In one case in Alabama this past hunting season, an Alabama man was caught and hit with charges for bringing a deer carcass into the state from Illinois.
Back in 2015, Michigan authorities actually conducted a sting operation in which several people were charged for illegally bringing carcasses into the great lakes state.
As long as CWD keeps being an issue, it’s likely these types of legal problems will continue as well.
so, another stupid
lawmaker wishes to risk exporting Tennessee cervid, potentially infected with
Chronic Wasting Disease CWD TSE Prion aka mad cow type disease, to every other
state it exports it's cervid or cervid products too, or via interstate movement
of cervid carcass parts, just because of money. it's the damn lawmakers, lobbyist,
industry, is why we are in this cwd tse prion mess. the Honorable
Tennessee Republican representative Bud Hulsey is probably clueless to the
science behind the Chronic Wasting Disease Transmissible Spongiform
Encephalopathy TSE Prion aka mad cow type disease, and all it's ramification
and recent science there from. but that will not stop this guy from potentially
exposing every other state in the USA to CWD from Tennessee, because the
state of Tennessee is clueless as to whether or not it has CWD, due to it's
failed CWD testing surveillance efforts.
I have said it before,
and I will say it again, until every state and Nation is on the same page, with
the same rules, mandatory rules, not voluntary, voluntary rules DO NOT WORK, we
will never stop CWD from spreading, and this bill is another fine example
of why, ignorance, fueled by greed and money.
looks like every state
out there will have to ban any cervid product coming out of Tennessee if this
bill passes.
remember, just because
Tennessee does not have a documented case of CWD TSE Prion in it's cervid yet,
does not mean CWD is not already in Tennessee, of the contrary, from the CWD
surveillance efforts in Tennessee, the likelihood of that surveillance effort
of detecting any CWD, is very unlikely to date...I remember, I believe it was
NY, see;
***The most likely
origin of the agent was introduction through taxidermy specimens. Fawns were
exposed prior to weaning in the same area. ***
Dr. John Huntley, New
York State Veterinarian, discussed New York’s Chronic Wasting Disease (CWD)
program. The program goals are to;
1) detect existing
infection;
2) prevent introduction;
and
3) eradicate CWD
infection in captive deer populations.
There are two types of
captive cervid herds in New York. CWD monitored herds are usually deer held on
a shooting or nature preserve. It is usually impractical to perform an
annual inventory. CWD certified herds can be inventoried on an annual
basis and may be permitted to move animals. Requirements for a CWD
certified herd include herd enrollment, requirements for fencing and
facilities, individual animal identification, sampling of clinical cases and
all natural deaths for CWD testing, and requirements that all animal additions
come from CWD certified herds. Requirements for CWD monitored herds include
herd enrollment, fencing, and surveillance of 10% or 30 animals (whichever is
less) for CWD,
CAPTIVE WILDLIFE & ALTERNATIVE LIVESTOCK
303
with additions of new animals coming from CWD certified herds. New York requires that all captive cervid herds perform CWD surveillance at one of the two levels.
In early March 2005, the
WTD from the index herd were sampled as part of the monitoring program.
In mid-March, a WTD from a second farm died and was sampled as part of the
surveillance program. CWD was detected in both samples and both herds were
depopulated. In total, there were 100 herd contacts in 8 herds.
***The most likely
origin of the agent was introduction through taxidermy specimens. Fawns were
exposed prior to weaning in the same area.
Surveillance of
free-ranging deer in a 10 mile radius around the two index farms revealed 2
positive cases out of 292 samples. Genetic testing revealed that the isolates
from the free-ranging WTD were different than those from the index herd. New
York based their program and information on that obtained from Wisconsin and
Colorado. They continue implementation of their captive deer surveillance
program that includes both CWD and TB. There is rigorous enforcement of the
program and continued development of additional techniques and procedures. Dr.
Thomas Gidlewski, USDA-APHIS-VS, presented an update on the USDA-APHIS Chronic
Wasting Disease program as well as the status of CWD in North America with
particular emphasis on the events of last year. The proposed rule on CWD
has almost cleared departmental review and is about to enter the
extra-departmental clearance process. As soon as the rule is finalized,
the Uniform Methods and Rules will be reconciled with the rule and the
grandfathering process of existing state CWD programs will begin.
Appropriate sample collection includes obex, medial retropharyngeal lymph nodes
and tonsil and the relative importance of each kind of tissue varies by
species. The quality assurance measures that the USDA-APHIS-VS, National
Veterinary Services Laboratory (NVSL) uses to verify internal and contract
laboratory results involve verification of the positive results by two
pathologists followed by completely repeating the test starting with the
originally submitted samples. A review of the current status of the
long term CWD interspecies transmission experiments suggests that a relatively
strong species barrier exists even when the direct intracerebral inoculation
route is utilized. Primary passage in a non-cervid species does appear to
make the agent more virulent in subsequent passage in that same species.
They have demonstrated positive rectal biopsies in three of the four LL
(leucine/leucine) elk homozygous at codon 132 providing further evidence that
this genotype does not convey absolute resistance. In 2005, CWD was
discovered in New York, West Virginia and in free ranging deer in Alberta,
Canada, as well as in a free ranging Colorado moose.
Tennessee Wildlife
Resources Agency Chronic Wasting Disease Response Plan 2016
TWRA Wildlife Technical
Report 15-12
snip...
Chronological Overview
of TWRA’s Response to the Threat of CWD
Beginning in 2002, due to increasing national concerns over CWD and the serious nature of the disease, Tennessee Wildlife Resources Agency (TWRA) began CWD monitoring of white-tailed deer and elk. As of 2016, a total of 9,394 free-ranging white-tailed deer and 80 freeranging elk have been tested for the disease. CWD has not been detected in Tennessee.
Beginning in 2002, due to increasing national concerns over CWD and the serious nature of the disease, Tennessee Wildlife Resources Agency (TWRA) began CWD monitoring of white-tailed deer and elk. As of 2016, a total of 9,394 free-ranging white-tailed deer and 80 freeranging elk have been tested for the disease. CWD has not been detected in Tennessee.
It is well documented that the movement of infected, live cervids and infected carcasses by humans has resulted in broad geographic expansion in the nationwide distribution of CWD. Fortunately, the TWRA has implemented various regulations helping to minimize these threats. In 2009, the TWRA adopted regulations imposing a moratorium on new facilities possessing and/or harvesting big game species under the authority of a Private Wildlife Preserve Permit (Appendix B). The regulation requires that Cervidae being held or harvested in wildlife preserves and imported from a herd outside of Tennessee be obtained only from a herd which has been certified CWD-free for the previous five years and which is authorized for import by the Tennessee Department of Agriculture. Cervidae being held or harvested in wildlife preserves and obtained from a Tennessee source also must be from a herd which has been certified CWD-free continuously for the previous five years. In 2012, the TWRA adopted a regulation that no person may import, transport, or possess a cervid carcass or cervid part from any CWD positive area unless it meets certain criteria that prevent introduction of prions from CWD positive areas (Appendix C). The state ban on possession of live white-tailed deer also helps in limiting the threat of CWD in Tennessee (Appendix D).
The TWRA recognizes the detection of CWD in Tennessee would have significant biological, ecological, economic and sociological implications. CWD represents a serious longterm threat to cervid populations in the state. The purpose of this response plan is to provide direction, guidelines and a specific course of action for monitoring and managing CWD in Tennessee if it were to occur.
This plan includes goals that outline:
• Appropriate preventive measures to keep CWD from entering the state. • Appropriate levels of CWD testing throughout the state to ensure early detection. • Methods to determine prevalence and spatial distribution of CWD if detected. • Management actions that will limit the spread of CWD if detected. • Determining the origin of any CWD positive cervid. • Distribution of accurate and effective information on CWD to the public, Agency staff, the Tennessee Fish and Wildlife Commission (TFWC) and other stakeholders. • Guiding research on CWD to support future management and control efforts.
Accomplishing these goals will minimize the impact of CWD on white-tailed deer and elk in the state. The management of CWD will require a multi-year adaptive management approach that can be refined as the science of CWD detection and management advances.
Prevention is the only cure for CWD due to the persistence of prions (the infectious agent) in the environment (Williams and Miller 2002). This plan focuses on prevention, early detection
4
and control of the disease with major efforts focused on containing the disease and monitoring its prevalence within a defined area.
Response and support teams are identified with specific responsibilities outlined. The TWRA will rely on partnerships with private citizens and other governmental agencies to manage CWD if it were to occur in Tennessee.
Authority
Tennessee Wildlife Resources Agency
Tennessee Code Annotated Title 70 provides the overall authority to the TWRA for all native wildlife (e.g., white-tailed deer, wild elk, etc.) and its management, conservation, protection and propagation. Pursuant to TCA 70-1-302(a)(5), the Agency has the authority to exercise control measures of undesirable species. Pursuant to TCA 70-4-107, the Tennessee Fish and Wildlife Commission (TFWC) has the authority to issue proclamations in order to set seasons, manner, means, etc. TCA 70-4-107(c)(3) authorizes the Commission to summarily close, reopen and/or extend seasons during emergency conditions.
Additionally, pursuant to TCA 70-4-113 the Executive Director and his designees have the authority to use any device to capture or kill any animal for specific purposes, or when it is considered necessary by the Executive Director to reduce or control any species that may be detrimental to human safety, health or property.
Importation and possession of live white-tailed deer is illegal in Tennessee. However, white-tailed deer may be incidentally contained within a property with high enough fencing to prevent escape and there is no restriction on high-fencing of properties. Although white-tailed deer are likely contained within these properties, the ownership of these deer remains with the state. TWRA is also responsible for permitting private big game wildlife preserves, but the regulatory authority of cervids other than white-tailed deer in these enclosures rests with the Tennessee Department of Agriculture (TDA) (Appendix D). Currently, there is a moratorium on the establishment of new private big game wildlife preserves (Appendix B).
Tennessee Department of Agriculture
Live importation and live possession of cervids other than white-tailed deer and wild elk is legal in Tennessee (Appendix D). The regulatory authority over these activities (i.e., live possession and importation of captive cervids) is the TDA, including the State Veterinarian. More specifically, the State Veterinarian has authority over sanitary disposition of any dead animal and disease related issues with all live animals. Furthermore, the State Veterinarian can order vaccination, quarantine and destruction of any animal. It is not entirely known how many captive cervid facilities exist in the state since they are not required to be registered or permitted unless they are involved in interstate movement of CWD-susceptible cervids. Operators of cervid facilities involved in interstate movement of
5
CWD-susceptible species are required to participate in TDA’s CWD Herd Certification Program (HCP) (Appendix E). Participating in the CWD HCP is only voluntary for those facilities not involved in interstate movement of Cervidae. Therefore, some captive cervid facilities are unknown by TDA and TWRA. As a result, TWRA is working to identify the locations of all captive cervid facilities in Tennessee and map them to assist with CWD prevention and/or control efforts (Appendix F).
United States Department of Agriculture Veterinary Services
If CWD is found in a captive cervid herd, the United States Department of Agriculture (USDA) Veterinary Services will work in concert with the State Veterinarian to develop a herd plan outlining protocol for animal movement into and out of the facility and possible euthanasia, disposal, indemnity, etc. In a case where white-tailed deer have been incidentally contained within a CWD-positive captive cervid facility, TWRA will work with USDA and the State Veterinarian to properly manage these whitetails following a USDA herd plan.
II. PRE-DETECTION PREPARATION
Regulatory Action
Prevention is the only cure for CWD. Thus, if CWD is detected in Tennessee, the focus will be on containing its spread.
If CWD is ever detected in Tennessee, the following regulatory options exist to help prevent its spread:
• A ban on feeding and rehabilitating wild cervids in defined TWRA CWD Containment and Enhanced Surveillance Areas. • Ban on removal of cervid carcasses and parts from defined TWRA CWD Containment and Enhanced Surveillance Areas. • Mandatory sampling of hunter-harvested deer and elk from within TWRA CWD Containment and Enhanced Surveillance Areas at physical checking stations. • Increase deer bag limits, extended deer seasons and/or allow additional weapon types in TWRA established CWD Containment Area(s). • Mandate disposal requirements for hunter-killed cervids taken in TWRA established CWD Containment and Enhanced Surveillance Areas.
In order to expedite implementation of these regulatory options, draft language (i.e., wording) for potential regulations will be developed.
6
Sampling
The TWRA Disease Coordinator will be responsible for keeping an inventory of equipment and supplies for CWD sampling (Appendix G) and a CWD response (Appendix H). These items will be distributed to each Region as needed or upon request.
Pre-CWD Beginning in 2016, TWRA’s sampling efforts will be more targeted, focusing on hunterkilled white-tailed deer and wild elk in counties within a 5-mile radius of known captive cervid facilities (Appendix F). Obex samples will be taken from elk while retropharyngeal lymph node samples will be taken from both white-tailed deer and elk. Sampling in these counties will likely have to occur on a rotation to ensure every county is sampled within a certain number of years. Facilities of interest are high-fenced private properties containing white-tailed deer, big game wildlife preserves, captive elk facilities, and captive nonnative cervid facilities (Appendix F). The rationale for focusing sampling efforts around captive cervid facilities is the high potential for CWD spread from captive cervids (Miller 2012). If a sufficient number of samples from these areas cannot be obtained by TWRA alone, taxidermists and meat processors receiving cervids and/or cervid parts from these areas may be enlisted to provide additional animals for sampling. Additionally, more intensive sampling will occur in counties bordering CWD-positive counties in adjoining states. More intensive sampling of roadkill and reportedly sick deer and elk will also occur statewide beginning in 2016. To facilitate this and increase awareness of sick deer and elk, the Agency will encourage the public to report cervids appearing unhealthy and whenever possible these animals will be sampled and tested. In cases where sampling cannot occur, the location of the reportedly sick cervid will be documented. Post-CWD In the event of a confirmed positive detection of CWD, retropharyngeal lymph node samples will be taken from white-tailed deer according to procedures outlined in Appendix I. The cornerstone of this sampling strategy is maintaining an estimate of the deer population.
Regarding elk, obex and retropharyngeal lymph nodes will be taken from hunter-harvested animals and any other elk carcasses available to TWRA within the Containment Area.
7
III. RESPONSE TO A CWD POSITIVE
While CWD has potentially serious consequences, there is currently no evidence it can be transmitted to humans or domestic animals. Consequently, it is important the response to an outbreak of CWD be proportional to the health risks and economic impact.
Notification Process
snip...see full report
here 44 pages;
''Beginning in 2002, due
to increasing national concerns over CWD and the serious nature of the disease,
Tennessee Wildlife Resources Agency (TWRA) began CWD monitoring of white-tailed
deer and elk.
As of 2016, a total of
9,394 free-ranging white-tailed deer and 80 freeranging elk have been tested
for the disease. CWD has not been detected in Tennessee. ''
deer population in
Tennessee ?
Deer hunting in
Tennessee remains strong for good reason; there are plenty of deer to go around
with an estimated population of about 600,000 animals.
http://www.gameandfishmag.com/forecasts/tennessee-deer-hunting-forecast-2016/
http://www.gameandfishmag.com/forecasts/tennessee-deer-hunting-forecast-2016/
cwd tse prion disease
surveillance testing Tennessee to date...LOL!
V. 2015 CHRONIC WASTING
DISEASE (CWD) SURVEILLANCE
Even though CWD has never been detected in
Tennessee, TWRA personnel have conducted CWD surveillance since 2002.
Initially, TWRA personnel sampled over 1,000 white tailed deer annually, but
biologists realized these sampling efforts were likely insufficient to detect
CWD in wild cervid populations. However, TWRA personnel have continued to test
a minimum of 200 white-tailed deer per year. In regards to elk, CWD testing of
hunter-harvested elk has continued since the first elk hunting season in 2009.
TWRA personnel sampled 286 whitetails and four
elk in 2015. All samples were submitted to the Southeastern Cooperative
Wildlife Disease Study College of Veterinary Medicine for analysis and none
tested positive for CWD.
https://www.tn.gov/assets/entities/twra/attachments/16-2_2015-16_Deer_and_elk_annual_report_final.pdf
https://www.tn.gov/assets/entities/twra/attachments/16-2_2015-16_Deer_and_elk_annual_report_final.pdf
sadly, if you don't
look, you don't find, and Tennessee very own biologists realized these sampling
efforts were likely insufficient to detect CWD in wild cervid populations and
they admitted it in the above report, and that's why it is critical for
states that do not want to import cwd into their state, to be very aware of
other states that do not look to find cwd tse prion. ...terry
Inactivation of the TSE
Prion disease
Chronic Wasting Disease
CWD, and other TSE prion disease, these TSE prions know no borders.
these TSE prions know no
age restrictions.
The TSE prion disease
survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit.
you cannot cook the TSE
prion disease out of meat.
you can take the ash and
mix it with saline and inject that ash into a mouse, and the mouse will go down
with TSE.
Prion Infected
Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well.
the TSE prion agent also
survives Simulated Wastewater Treatment Processes.
IN fact, you should also
know that the TSE Prion agent will survive in the environment for years, if not
decades.
you can bury it and it
will not go away.
The TSE agent is capable
of infected your water table i.e. Detection of protease-resistant cervid prion
protein in water from a CWD-endemic area.
it’s not your ordinary
pathogen you can just cook it out and be done with. that’s what’s so worrisome
about Iatrogenic mode of transmission, a simple autoclave will not kill this
TSE prion agent.
HORIZONTAL TRANSMISSION
OF THE CWD TSE PRION DISEASE AND ENVIRONMENTAL RISK FACTORS
*** Title: Pathological
features of chronic wasting disease in reindeer and demonstration of horizontal
transmission ***
https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261
https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261
PLEASE SEE DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE
Volume 22, Number 12—December 2016
Dispatch
Horizontal Transmission
of Chronic Wasting Disease in Reindeer
http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article
http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article
Monday, September 05, 2016
Pathological features of chronic wasting disease in reindeer and demonstration of horizontal transmission Major Findings for Norway
http://chronic-wasting-disease.blogspot.com/2016/09/pathological-features-of-chronic.html
Thursday, September 22,
2016
NORWAY DETECTS 5TH CASE OF CHRONIC WASTING DISEASE CWD TSE PRION Skrantesjuke
http://chronic-wasting-disease.blogspot.com/2016/09/norway-detects-5th-case-of-chronic.html
NORWAY DETECTS 5TH CASE OF CHRONIC WASTING DISEASE CWD TSE PRION Skrantesjuke
http://chronic-wasting-disease.blogspot.com/2016/09/norway-detects-5th-case-of-chronic.html
SUNDAY, OCTOBER 02, 2016
*** What is the risk of a cervid TSE being introduced from Norway into Great Britain? Qualitative Risk Assessment September 2016
http://chronic-wasting-disease.blogspot.com/2016/10/what-is-risk-of-cervid-tse-being.html
*** What is the risk of a cervid TSE being introduced from Norway into Great Britain? Qualitative Risk Assessment September 2016
http://chronic-wasting-disease.blogspot.com/2016/10/what-is-risk-of-cervid-tse-being.html
Sunday, December 11, 2016
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
Increased Abundance of M Cells in the Gut Epithelium Dramatically Enhances Oral Prion Disease Susceptibility
http://prionprp.blogspot.com/2016/12/increased-abundance-of-m-cells-in-gut.html
***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
http://prion2016.org/dl/newsletter_03.pdf
Saturday, May 28, 2016
*** Infection and detection of PrPCWD in soil from CWD infected farm in Korea Prion 2016 Tokyo ***
http://chronic-wasting-disease.blogspot.com/2016/05/infection-and-detection-of-prpcwd-in.html
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
http://jgv.sgmjournals.org/content/87/12/3737.full
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.
https://prion2015.files.wordpress.com/2015/05/programguide1.pdf
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.
https://prion2015.files.wordpress.com/2015/05/programguide1.pdf
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
Wednesday, December 16,
2015
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full
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.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4397813/pdf/13567_2015_Article_176.pdf
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4397813/pdf/13567_2015_Article_176.pdf
>>>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.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3160281/
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.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3160281/
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.
https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf
Conclusion. Silty clay loam exhibits highly efficient prion binding, inferring a durable environmental reservoir, and an efficient mechanism for indirect horizontal CWD transmission.
https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf
>>>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
http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full
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
http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full
Wednesday, December 16,
2015
*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***
http://scrapie-usa.blogspot.com/2015/12/objects-in-contact-with-classical.html
*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***
http://scrapie-usa.blogspot.com/2015/12/objects-in-contact-with-classical.html
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 ;
http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf
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 ;
http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf
Thursday, June 09, 2016
Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie TSE Prion Experiment 1964
How Did CWD Get Way Down In Medina County, Texas?
http://chronic-wasting-disease.blogspot.com/2016/06/how-did-cwd-get-way-down-in-medina.html
Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie TSE Prion Experiment 1964
How Did CWD Get Way Down In Medina County, Texas?
http://chronic-wasting-disease.blogspot.com/2016/06/how-did-cwd-get-way-down-in-medina.html
Friday, April 22, 2016
*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in a Mule Deer
http://scrapie-usa.blogspot.com/2016/04/texas-scrapie-confirmed-in-hartley.html
*** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in a Mule Deer
http://scrapie-usa.blogspot.com/2016/04/texas-scrapie-confirmed-in-hartley.html
Thursday, December 08,
2016
USDA APHIS National Scrapie Eradication Program October 2016 Monthly Report Fiscal Year 2017 atypical NOR-98 Scrapie
http://scrapie-usa.blogspot.com/2016/12/usda-aphis-national-scrapie-eradication.html
USDA APHIS National Scrapie Eradication Program October 2016 Monthly Report Fiscal Year 2017 atypical NOR-98 Scrapie
http://scrapie-usa.blogspot.com/2016/12/usda-aphis-national-scrapie-eradication.html
Monday, April 04, 2016
Limited amplification of chronic wasting disease prions in the peripheral tissues of intracerebrally inoculated cattle
Limited amplification of chronic wasting disease prions in the peripheral tissues of intracerebrally inoculated cattle
”The occurrence of CWD
must be viewed against the contest of the locations in which it occurred. It
was an incidental and unwelcome complication of the respective wildlife
research programmes. Despite it’s subsequent recognition as a new disease of
cervids, therefore justifying direct investigation, no specific research
funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently
not their province!” page 26.
http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
Evidence That
Transmissible Mink Encephalopathy Results from Feeding Infected Cattle
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/mb/m09/tab05.pdf
Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
snip...
The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...
http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/mb/m09/tab05.pdf
In Confidence -
Perceptions of unconventional slow virus diseases of animals in the USA -
APRIL-MAY 1989 - G A H Wells
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...
http://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...
http://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
The occurrence of CWD
must be viewed against the contest of the locations in which it occurred. It
was an incidental and unwelcome complication of the respective wildlife
research programmes. Despite its subsequent recognition as a new disease of
cervids, therefore justifying direct investigation, no specific research
funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently
not their province!...page 26.
http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
*** Spraker suggested an
interesting explanation for the occurrence of CWD. The deer pens at the Foot
Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut
that time, allegedly, some scrapie work was conducted at this site. When deer
were introduced to the pens they occupied ground that had previously been
occupied by sheep.
http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
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
***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
Primate Biol., 3, 47–50,
2016 www.primate-biol.net/3/47/2016/ doi:10.5194/pb-3-47-2016 © Author(s) 2016.
CC
Attribution 3.0 License.
Attribution 3.0 License.
Prions
Walter Bodemer German
Primate Center, Kellnerweg 4, 37077 Göttingen, Germany Correspondence to:
Walter Bodemer (wbodemer@dpz.eu)
Received: 15 June 2016 –
Revised: 24 August 2016 – Accepted: 30 August 2016 – Published: 7 September
2016
Abstract.
Prions gained widespread public and scientific interest in the year 2000. At that time, the human neurological Creutzfeldt–Jakob disease (CJD) was known. However, new CJD cases were diagnosed but they could not be ascribed to one of the classical CJD categories i.e. sporadic (sCJD), hereditary or acquired. Hence, they were classified as variant CJD (vCJD). Later on, experimental evidence suggested that vCJD was caused by prions postulated as unique novel infectious agents and, for example, responsible for bovine spongiform encephalopathy (BSE) also known as mad cow disease. The infection of humans by transmission of BSE prions also defined vCJD as a zoonotic disease. Prions, especially those associated with scrapie in sheep had been known for quite some time and misleadingly discussed as a slow virus. Therefore, this enigmatic pathogen and the transmission of this unusual infectious agent was a matter of a controversial scientific debate. An agent without nucleic acid did not follow the current dogma postulating DNA or RNA as inheritable information encoding molecules. Although numerous experimental results clearly demonstrated the infectious capacity of prions in several animal species, a model close to human was not readily available. Therefore, the use of rhesus monkeys (Macaca mulatta) served as a non-human primate model to elucidate prion infection under controlled experimental conditions. Not the least, transmission of BSE, human vCJD, and sCJD prions could be confirmed in our study. Any prion infection concomitant with progression of disease in humans, especially vCJD, could be analyzed only retrospectively and at late stages of disease. In contrast, the prion-infected rhesus monkeys were accessible before and after infection; the progression from early stage to late clinical stages – and eventually death of the animal–could be traced. Because of the phylogenetic proximity to humans, the rhesus monkey was superior to any rodent or other animal model. For these reasons an experimental approach had been conceived by J. Collinge in London and A. Aguzzi in Zurich and performed in a cooperative study with both research groups in the pathology unit of the German Primate Center (DPZ). The study in the DPZ lasted from 2001 until 2012. Our research in the pathology unit provided a temporal monitoring of how an initial prion infection develops eventually into disease; an approach that would have never been possible in humans since the time point of infection with prions from, for example, BSE is always unknown. Telemetry revealed a shift in sleep– wake cycles early on, long before behavioral changes or clinical symptoms appeared. Pathology confirmed nonneuronal tissue as hidden places where prions exist. The rhesus model also allowed first comparative studies of epigenetic modifications on RNA in peripheral blood and brain tissue collected from uninfected and prion infected animals. To conclude, our studies clearly demonstrated that this model is valid since progression to disease is almost identical to human CJD.
Prions gained widespread public and scientific interest in the year 2000. At that time, the human neurological Creutzfeldt–Jakob disease (CJD) was known. However, new CJD cases were diagnosed but they could not be ascribed to one of the classical CJD categories i.e. sporadic (sCJD), hereditary or acquired. Hence, they were classified as variant CJD (vCJD). Later on, experimental evidence suggested that vCJD was caused by prions postulated as unique novel infectious agents and, for example, responsible for bovine spongiform encephalopathy (BSE) also known as mad cow disease. The infection of humans by transmission of BSE prions also defined vCJD as a zoonotic disease. Prions, especially those associated with scrapie in sheep had been known for quite some time and misleadingly discussed as a slow virus. Therefore, this enigmatic pathogen and the transmission of this unusual infectious agent was a matter of a controversial scientific debate. An agent without nucleic acid did not follow the current dogma postulating DNA or RNA as inheritable information encoding molecules. Although numerous experimental results clearly demonstrated the infectious capacity of prions in several animal species, a model close to human was not readily available. Therefore, the use of rhesus monkeys (Macaca mulatta) served as a non-human primate model to elucidate prion infection under controlled experimental conditions. Not the least, transmission of BSE, human vCJD, and sCJD prions could be confirmed in our study. Any prion infection concomitant with progression of disease in humans, especially vCJD, could be analyzed only retrospectively and at late stages of disease. In contrast, the prion-infected rhesus monkeys were accessible before and after infection; the progression from early stage to late clinical stages – and eventually death of the animal–could be traced. Because of the phylogenetic proximity to humans, the rhesus monkey was superior to any rodent or other animal model. For these reasons an experimental approach had been conceived by J. Collinge in London and A. Aguzzi in Zurich and performed in a cooperative study with both research groups in the pathology unit of the German Primate Center (DPZ). The study in the DPZ lasted from 2001 until 2012. Our research in the pathology unit provided a temporal monitoring of how an initial prion infection develops eventually into disease; an approach that would have never been possible in humans since the time point of infection with prions from, for example, BSE is always unknown. Telemetry revealed a shift in sleep– wake cycles early on, long before behavioral changes or clinical symptoms appeared. Pathology confirmed nonneuronal tissue as hidden places where prions exist. The rhesus model also allowed first comparative studies of epigenetic modifications on RNA in peripheral blood and brain tissue collected from uninfected and prion infected animals. To conclude, our studies clearly demonstrated that this model is valid since progression to disease is almost identical to human CJD.
Published by Copernicus
Publications on behalf of the Deutsches Primatenzentrum GmbH (DPZ).
SNIP...
2 Methods and results
SNIP...
2 Methods and results
2.1 Animals The reason
to perform prion research in rhesus monkeys was to monitor infection and the
temporal progression of prion infection in the rhesus monkey. In contrast to
studies of human CJD cases, we could decide on the infectious dose. We also could
control behavior immediately after prion inoculation and during the rather long
time until animals died from the prion infection. Hidden places where prions
might exist were found. Even epigenetic modifications on RNA could be detected.
Taken together, these experimental approaches depended on animals. Using rhesus
monkeys as a model system required thorough ethic reasoning and consultation
with authorities before we actually turned to conduct the experiments. The
Number of animals was limited just to fulfill statistical conditions. The
individual health status was obtained and health care was provided throughout
the study. The animals underwent daily inspection to monitor any changes in
health and behavior. The experiments were conceived with the aim of reducing
pain, suffering, and harm. Groups of animals were preferred in order to keep
them in a social environment. The animals were originally kept in Vienna at
Baxter and transferred to the German Primate Center (DPZ) in 2001. J. Collinge,
A. Aguzzi, and C. Weissmann were the scientists who recommended this
well-controlled prion infection study, and financial support was provided by an
EU grant.To ensure statistical significance four groups consisting of four
rhesus macaques each were formed: one uninfected control group, one group
infected with BSE prions, one with vCJD prions, and one with sCJD prions.
Health of animals, infection, and progression to disease was looked at in our
pathology department and in cooperation with W. Schulz-Schaeffer at the UMG (University
Medicine, Göttingen). Besides, neurologists from the UMG also observed the
animals whenever clinical symptoms seemed to appear. This close observation and
comparison with human CJD cases demonstrated how close clinical progression of
human disease resembles the experimental infection in the non-human primate.
2.2 Infection Infectious
prions from brain tissue of one sCJD and one vCJD case (provided by J.
Collinge) as well as BSE prions (from a “German” madcow case and provided by W.
Schulz Schaeffer) were intraperitoneally administered into the rhesus monkeys.
2.3 Monitoring of
behavior and telemetry Early behavioral monitoring was carried out by the
ethologists I. Machatschke and J. Dittami from Vienna University. Transmitters
were used to record changes in the circadian rhythms. Body temperature,
sleep–wake cycles, and activity profiles could be obtained over a time span of 2
years. Up to half a year after infection animals did not show any signs of
prion infection. However, after 6 months and persisting for another few months
some animals had some disturbances in circadian rhythms which disappeared and
then never appeared again(I. Machatschke, personal communication,2006).For a
rather long time of about 4–5 years animals seemed to be healthy. But then,
almost all animals rapidly progressed to symptoms. Symptoms were highly similar
or even identical to those seen in human CJD.
2.4 Pathology Blood and
necropsy specimens from the animals served as a valuable source to detect
pathologically associated prion protein even in non-neuronal skeletal and
cardiac tissue. These “hidden places” of prion pathology and replication were
clearly demonstrated and extended our view where prions might spread within an
organism. Not only leukocytes and neuronal tissue harbor abnormal prion protein
isoforms but also other tissues can propagate prion protein isoforms leading to
toxicity, cell degeneration, and eventually transmissible prions (Krasemann et
al., 2010, 2013).
SNIP...
3 Conclusion
SNIP...
3 Conclusion
Most importantly, early
signs of an altered circadian rhythm, sleep–wake cycle, and activity and body
temperature were recorded in prion-infected animals. This experimental approach
would have never been feasible in studies with human CJD cases. After 4–6 years
animals developed clinical symptoms highly similar to those typical for CJD.
Clinicians confirmed how close the animal model and the human disease matched.
Non-neuronal tissue like cardiac muscle and peripheral blood with abnormal,
disease-related prion protein were detected in rhesus monkey tissues.
Molecular changes in RNA from repetitive Alu and BC200 DNA elements were identified and found to be targets of epigenetic editing mechanisms active in prion disease. To conclude, our results with the rhesus monkey model for prion disease proved to be a valid model and increased our knowledge of pathogenic processes that are distinctive to prion disease.
SEE FULL TEXT ;
http://www.primate-biol.net/3/47/2016/pb-3-47-2016.pdf
Molecular changes in RNA from repetitive Alu and BC200 DNA elements were identified and found to be targets of epigenetic editing mechanisms active in prion disease. To conclude, our results with the rhesus monkey model for prion disease proved to be a valid model and increased our knowledge of pathogenic processes that are distinctive to prion disease.
SEE FULL TEXT ;
http://www.primate-biol.net/3/47/2016/pb-3-47-2016.pdf
*** 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
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
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
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
*** 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
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 ef?ciency comparable to that of cattle BSE. While the ef?ciency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
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 ef?ciency comparable to that of cattle BSE. While the ef?ciency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20
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
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
Title: Transmission of
scrapie prions to primate after an extended silent incubation
period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
http://www.ars.usda.gov/research/publications/publications.htm?SEQ_NO_115=313160
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
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
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.com/2015/05/prion2015abstracts.pdf
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.com/2015/05/prion2015abstracts.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/journals/prion/article/28124/?nocache=112223249
*** 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/journals/prion/article/28124/?nocache=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/nprp/NPRP_Summit_Final_Report.pdf
http://cdmrp.army.mil/prevfunded/nprp/NPRP_Summit_Final_Report.pdf
see further science on
different species and risk factors there from spreading via CWD TSE Prion ;
http://chronic-wasting-disease.blogspot.com/2012/01/chronic-wasting-disease-cwd-cervids.html
http://chronic-wasting-disease.blogspot.com/
Wednesday, December 21, 2016
TRANSMISSION,
DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
2016 ANNUAL REPORT ARS RESEARCH
Thursday, December 08,
2016
USDA APHIS National
Scrapie Eradication Program October 2016 Monthly Report Fiscal Year 2017
atypical NOR-98 Scrapie
Wednesday, January 07,
2009
CWD to tighten taxidermy rules Hunters need to understand regulations
Saturday, April 13, 2013
Tennessee Launches CWD Herd Certification Program in the wake of legislation for game farms
Monday, November 12,
2012
Tennessee The White-tailed Deer Breeding and Farming Act pushes to legalize deer farming 2012
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
11:50 AM
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