Tuesday, October 03, 2017

MISSOURI MANDATORY CWD SAMPLING IN 25 COUNTIES NOV. 11 AND 12 2017

MANDATORY SAMPLING IN 25 COUNTIES NOV. 11 AND 12

  • Hunters who harvest deer in 25 select counties among the 41 counties of the MDC CWD management zone must present their deer to MDC staff for CWD mandatory sampling.
  • Mandatory sampling is only required during opening weekend of firearms deer season, Nov. 11 and 12.
  • MDC will provide 56 sampling stations throughout the 25 select counties.
  • Sampling locations will be open 7:30 a.m. until at least 8 p.m.
  • Deer must be presented by the hunter who harvested the animal.
  • Deer may be field dressed before being taken to a sampling station.
  • Hunters can also present just the deer head with about six inches of neck attached.
  • For bucks bound to a taxidermist, the cape may be removed prior to being taken to a sampling station as long as about six inches of the neck is left attached.


2017

Subject: ***CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat

CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat 

Chronic Wasting Disease (CWD) 

Prevention 

If CWD could spread to people, it would most likely be through eating of infected deer and elk. In a 2006-2007 CDC survey of U.S. residents, nearly 20 percent of those surveyed said they had hunted deer or elk and more than two-thirds said they had eaten venison or elk meat. However, to date, no CWD infections have been reported in people. 

Hunters must consider many factors when determining whether to eat meat from deer and elk harvested from areas with CWD, including the level of risk they are willing to accept. Hunters harvesting wild deer and elk from areas with reported CWD should check state wildlife and public health guidance to see whether testing of animals is recommended or required in a given state or region. In areas where CWD is known to be present, CDC recommends that hunters strongly consider having those animals tested before eating the meat. 

Tests for CWD are monitoring tools that some state wildlife officials use to look at the rates of CWD in certain animal populations. Testing may not be available in every state, and states may use these tests in different ways. A negative test result does not guarantee that an individual animal is not infected with CWD, but it does make it considerably less likely and may reduce your risk of exposure to CWD. 

To be as safe as possible and decrease their potential risk of exposure to CWD, hunters should take the following steps when hunting in areas with CWD: 

Do not shoot, handle or eat meat from deer and elk that look sick or are acting strangely or are found dead (road-kill). When field-dressing a deer: Wear latex or rubber gloves when dressing the animal or handling the meat. Minimize how much you handle the organs of the animal, particularly the brain or spinal cord tissues. Do not use household knives or other kitchen utensils for field dressing. Check state wildlife and public health guidance to see whether testing of animals is recommended or required. Recommendations vary by state, but information about testing is available from many state wildlife agencies. Strongly consider having the deer or elk tested for CWD before you eat the meat. If you have your deer or elk commercially processed, consider asking that your animal be processed individually to avoid mixing meat from multiple animals. If your animal tests positive for CWD, do not eat meat from that animal. The U.S. Department of Agriculture’s Animal and Plant Health Inspection Service regulates commercially farmed deer and elk. The agency operates a national CWD herd certification program. As part of the voluntary program, states and individual herd owners agree to meet requirements meant to decrease the risk of CWD in their herds. Privately owned herds that do not participate in the herd certification program may be at increased risk for CWD. 

Page last reviewed: August 17, 2017 Page last updated: August 17, 2017 Content source: Centers for Disease Control and Prevention National Center for Emerging and Zoonotic Infectious Diseases (NCEZID) Division of High-Consequence Pathogens and Pathology (DHCPP) 


 > However, to date, no CWD infections have been reported in people. 

key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry 

LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ 

*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).*** 



Molecular Barriers to Zoonotic Transmission of Prions 

*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein. 

*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype. 


TUESDAY, SEPTEMBER 12, 2017 

CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat 



Subject: Prion 2017 Conference Abstracts CWD

 2017 PRION CONFERENCE 

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

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

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

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

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

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

PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS 

Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO 

PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS 

*** PRION 2017 CONFERENCE VIDEO 



 TUESDAY, JUNE 13, 2017

PRION 2017 CONFERENCE ABSTRACT 

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


TUESDAY, JULY 04, 2017

*** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***


TUESDAY, JUNE 13, 2017

PRION 2017 CONFERENCE ABSTRACT Chronic Wasting Disease in European moose is associated with PrPSc features different from North American CWD


Wednesday, May 24, 2017 

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


SATURDAY, JULY 29, 2017 

Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC 


TUESDAY, MARCH 28, 2017 

*** Passage of scrapie to deer results in a new phenotype upon return passage to sheep ***


URINE

SUNDAY, JULY 16, 2017

*** Temporal patterns of chronic wasting disease prion excretion in three cervid species ***



TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION 

 

*** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSION 

 

*** INFECTIOUS AGENT OF SHEEP SCRAPIE MAY PERSIST IN THE ENVIRONMENT FOR AT LEAST 16 YEARS *** 

GUDMUNDUR GEORGSSON1, SIGURDUR SIGURDARSON2 AND PAUL BROWN3 



the tse prion aka mad cow type disease is not your normal pathogen. 

The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit. 

you cannot cook the TSE prion disease out of meat. 

you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE. 

Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well. 

the TSE prion agent also survives Simulated Wastewater Treatment Processes. 

IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades. 

you can bury it and it will not go away. 

The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area. 

it’s not your ordinary pathogen you can just cook it out and be done with. 

that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.


1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8 

Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery. 

Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. 

Laboratory of Central Nervous System Studies, National Institute of 

Neurological Disorders and Stroke, National Institutes of Health, 

Bethesda, MD 20892. 

Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them. 

PMID: 8006664 [PubMed - indexed for MEDLINE] 



New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication 



Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production 



Detection of protease-resistant cervid prion protein in water from a CWD-endemic area 



A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing 



Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals 



PPo4-4: 

Survival and Limited Spread of TSE Infectivity after Burial 




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. 
 
***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. 
 
 
 
In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes. 
 
Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification 
 
 
Wednesday, December 16, 2015 
 
*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission *** 
 
 
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years *** 
 
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3 
 
 
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
 
 
 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.
 
 
tse prion soil
 
 
 
 
 
Wednesday, December 16, 2015
 
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
 
 
The sources of dust borne prions are unknown but it seems reasonable to assume that faecal, urine, skin, parturient material and saliva-derived prions may contribute to this mobile environmental reservoir of infectivity. This work highlights a possible transmission route for scrapie within the farm environment, and this is likely to be paralleled in CWD which shows strong similarities with scrapie in terms of prion dissemination and disease transmission. The data indicate that the presence of scrapie prions in dust is likely to make the control of these diseases a considerable challenge.
 
 
>>>Particle-associated PrPTSE molecules may migrate from locations of deposition via transport processes affecting soil particles, including entrainment in and movement with air and overland flow. <<<
 
Fate of Prions in Soil: A Review
 
Christen B. Smith, Clarissa J. Booth, and Joel A. Pedersen*
 
Several reports have shown that prions can persist in soil for several years. Significant interest remains in developing methods that could be applied to degrade PrPTSE in naturally contaminated soils. Preliminary research suggests that serine proteases and the microbial consortia in stimulated soils and compost may partially degrade PrPTSE. Transition metal oxides in soil (viz. manganese oxide) may also mediate prion inactivation. Overall, the effect of prion attachment to soil particles on its persistence in the environment is not well understood, and additional study is needed to determine its implications on the environmental transmission of scrapie and CWD.
 
 
P.161: Prion soil binding may explain efficient horizontal CWD transmission
 
Conclusion. Silty clay loam exhibits highly efficient prion binding, inferring a durable environmental reservoir, and an efficient mechanism for indirect horizontal CWD transmission.
 
 
>>>Another alternative would be an absolute prohibition on the movement of deer within the state for any purpose. While this alternative would significantly reduce the potential spread of CWD, it would also have the simultaneous effect of preventing landowners and land managers from implementing popular management strategies involving the movement of deer, and would deprive deer breeders of the ability to engage in the business of buying and selling breeder deer. Therefore, this alternative was rejected because the department determined that it placed an avoidable burden on the regulated community.<<<
 
Wednesday, December 16, 2015
 
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
 
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4, Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
 
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge, Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK
 
Classical scrapie is an environmentally transmissible prion disease of sheep and goats. Prions can persist and remain potentially infectious in the environment for many years and thus pose a risk of infecting animals after re-stocking. In vitro studies using serial protein misfolding cyclic amplification (sPMCA) have suggested that objects on a scrapie affected sheep farm could contribute to disease transmission. This in vivo study aimed to determine the role of field furniture (water troughs, feeding troughs, fencing, and other objects that sheep may rub against) used by a scrapie-infected sheep flock as a vector for disease transmission to scrapie-free lambs with the prion protein genotype VRQ/VRQ, which is associated with high susceptibility to classical scrapie. When the field furniture was placed in clean accommodation, sheep became infected when exposed to either a water trough (four out of five) or to objects used for rubbing (four out of seven). This field furniture had been used by the scrapie-infected flock 8 weeks earlier and had previously been shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of 23) through exposure to contaminated field furniture placed within pasture not used by scrapie-infected sheep for 40 months, even though swabs from this furniture tested negative by PMCA. This infection rate decreased (1 out of 12) on the same paddock after replacement with clean field furniture. Twelve grazing sheep exposed to field furniture not in contact with scrapie-infected sheep for 18 months remained scrapie free. The findings of this study highlight the role of field furniture used by scrapie-infected sheep to act as a reservoir for disease re-introduction although infectivity declines considerably if the field furniture has not been in contact with scrapie-infected sheep for several months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental contamination.
 
snip...
 
Discussion
 
Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23).
 
Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier.
 
This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.
 
PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.
 
In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.
 
Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification
 
 
Wednesday, December 16, 2015
 
*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***
 
 
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
 
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
 
 
MONDAY, JUNE 12, 2017
 
Rethinking Major grain organizations opposition to CFIA's control zone approach to Chronic Wasting CWD TSE Prion Mad Deer Type Disease 2017?
 
 WEDNESDAY, MAY 17, 2017
 
*** Chronic Wasting Disease CWD TSE Prion aka Mad Deer Disease and the Real Estate Market Land Values ***
 
*** 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. 


WEDNESDAY, JUNE 28, 2017

Missouri MDC EXPANDS DEER FEEDING BAN TO 41 COUNTIES IN RESPONSE TO CWD


SATURDAY, MAY 20, 2017

Missouri CWD TSE PRION Surveillance and Monitoring


THURSDAY, MARCH 09, 2017 

Missouri MDC REPORTS TWO CASES OF CWD IN ST. CLAIR COUNTY 


TUESDAY, JANUARY 31, 2017 
Missouri Captive Cervid Industry and Legislation Set To Spread More CWD as it did in Texas
Tuesday, January 10, 2017
Missouri MDC reports three new cases of CWD from mandatory sampling
Saturday, December 24, 2016
Missouri MDC reports halfway mark on results of deer samples being tested for CWD confirm two positive to date
SUNDAY, MARCH 06, 2016
Missouri 2015-2016 CWD Surveillance Summary to Date, with confirmed cases mounting
Thursday, December 03, 2015
Missouri MDC reports CWD found in Franklin County
MONDAY, SEPTEMBER 28, 2015
MISSOURI CHRONIC WASTING DISEASE CWD TSE PRION UPDATE
Saturday, September 05, 2015
Missouri Captive Cervid Industry, CWD TSE Prion, and Procrastinating for Money, while mad deer and elk disease silently spreads
Tuesday, June 16, 2015
Missouri MDC changes deer hunting regs to help slow CWD
Wednesday, March 11, 2015
MDC reports 11 new cases of Chronic Wasting Disease CWD in Missouri deer
Monday, January 26, 2015
Missouri MDC reports two new cases of CWD found in Adair and Macon counties
Tuesday, December 09, 2014
Missouri MDC reports one new case of CWD, found in Adair County
Friday, October 17, 2014
Missouri Final action on Orders of Rule making Breeders and Big Game Hunting Preserves
Thursday, September 11, 2014
Missouri Nixon's Veto Stands Overide Fails on Agriculture Legislation
How they voted: attempt to override veto of ag bill fails in the House
Thursday, May 01, 2014
Missouri DNR CWD prevention and captive cervid farming Update
Tuesday, March 26, 2013
CWD Missouri remains confined to Linn-Macon-County Core Area with four new cases
Wednesday, January 23, 2013
Missouri sixth case CWD documented northwest Macon County
Tuesday, January 24, 2012
CWD found in two free-ranging deer from Macon County Missouri
Friday, February 26, 2010
Chronic wasting disease found in Missouri deer
Sunday, March 25, 2012
Three more cases of CWD found in free-ranging deer in Macon County
From: Terry S. Singeltary Sr.
Sent: Thursday, March 29, 2012 6:26 PM
Subject: re-Missouri officials seek states' advice on chronic wasting disease in deer
Thursday, May 31, 2012
Missouri MDC staff will provide information on five recently found cases of CWD in free-ranging deer in northwest Macon County June 2, 2012
Wednesday, September 05, 2012
Missouri MDC seeks hunters’ help when processing harvested deer and preventing CWD
Thursday, December 20, 2012
MISSOURI Initial CWD sampling test results available online from MDC so far one adult buck has tested positive for the disease
Friday, October 21, 2011
Chronic Wasting Disease Found in Captive Deer Missouri
The Missouri Department of Agriculture discovers the state's first case of CWD in a captive white-tailed deer.
Friday, February 26, 2010
Chronic wasting disease found in Missouri deer February 25, 2010
Chronic Wasting Disease Found in Captive Deer
The Missouri Departments of Agriculture, Conservation and Health and Senior Services and the U.S. Department of Agriculture announced today that a captive white-tailed deer in Linn County, Missouri has tested positive for Chronic Wasting Disease (CWD). CWD is a neurological disease found in deer, elk and moose.
"There is no evidence that CWD poses a risk to domestic animals or humans," said State Veterinarian Dr. Taylor Woods. "We have protocols in place to quickly and effectively handle these situations."
The animal that tested positive for CWD was a white-tailed deer inspected as part of the State's CWD surveillance and testing program. Preliminary tests were conducted by the USDA National Veterinary Services Laboratory in Ames, Iowa.
Upon receiving the confirmed CWD positive, Missouri's departments of Agriculture, Conservation and Health and Senior Services initiated their CWD Contingency Plan. The plan was developed in 2002 by the Cervid Health Committee, a task force comprised of veterinarians, animal health officers and conservation officers from USDA, MDA, MDC and DHSS working together to mitigate challenges associated with CWD.
CWD is transmitted by live animal to animal contact or soil to animal contact. The disease was first recognized in 1967 in captive mule deer in the Colorado Division of Wildlife captive wildlife research facility in Fort Collins, Colorado. CWD has been documented in deer and/or elk in Colorado, Illinois, Kansas, Michigan, Minnesota, Montana, Nebraska, New Mexico, New York, Oklahoma, South Dakota, Utah, Virginia, West Virginia, Wisconsin, and the Canadian Provinces of Alberta and Saskatchewan. There has been no evidence that the disease can be transmitted to humans.
"Missouri's proactive steps to put a testing protocol in place and create a contingency plan years ago is proving beneficial. We are in a solid position to follow pre-established steps to ensure Missouri's valuable whitetail deer resource remains healthy and strong," said Jason Sumners Missouri's Deer Biologist.
For more information regarding CWD, please contact Dr. Taylor Woods at (573) 751-3377.
Friday, September 20, 2013
*** Missouri State records show gaps in oversight of captive deer farms, ranches ***
MONDAY, SEPTEMBER 25, 2017

Colorado Chronic Wasting Disease CWD TSE Prion Mandatory Submission of test samples in some areas and zoonosis

(see origin of cwd in Colorado debate and evidence there from...tss)


TUESDAY, OCTOBER 03, 2017

Wisconsin CWD-positive white-tailed deer found on Shawano County hunting ranch


THURSDAY, AUGUST 03, 2017

Wisconsin CWD Showing Up in Northern Wisconsin Deer Farms


Wednesday, February 10, 2016

*** Wisconsin Two deer that escaped farm had chronic wasting disease CWD ***


MONDAY, OCTOBER 02, 2017

Michigan 3 ½-year-old female deer likely to be the 10th free-ranging deer Chronic Wasting Disease CWD TSE Prion


THURSDAY, SEPTEMBER 28, 2017

Pennsylvania GAME COMMISSION OFFERS FREE CWD TESTS FOR DMA-HARVESTED DEER


THURSDAY, SEPTEMBER 21, 2017

Pennsylvania Game Commission has scheduled a series of public meetings to ensure Pennsylvanians remain informed about chronic wasting disease CWD TSE Prion


SATURDAY, AUGUST 12, 2017

Pennsylvania 27 deer from Bedford County farm test positive for chronic wasting disease


WEDNESDAY, JULY 12, 2017

PENNSYLVANIA CWD FOUND IN THE WILD IN CLEARFIELD COUNTY


MONDAY, AUGUST 28, 2017

Minnesota CWD tests mandatory for deer harvested in central, north-central and southeast


WEDNESDAY, JULY 26, 2017

Wyoming CWD found in new elk hunt area in Southeast Washakie County


WEDNESDAY, SEPTEMBER 27, 2017

TEXAS, TPWD, WIN CWD COURT CASE AGAINST DEER BREEDERS CAUSE NO. D-1-GN-15-004391


THURSDAY, SEPTEMBER 21, 2017

TEXAS TPWD CWD mandatory check stations for Chronic Wasting Disease in the South Central, Panhandle, and Trans-Pecos areas


MONDAY, AUGUST 14, 2017

*** Texas Chronic Wasting Disease CWD TSE Prion History


THURSDAY, SEPTEMBER 21, 2017

Arkansas AGFC Video Public CWD Meeting in Clinton


WEDNESDAY, AUGUST 16, 2017
ARKANSAS CWD TSE PRION 214 CASES CONFIRMED TO DATE AS OF AUGUST 9, 2017
Iowa Supreme Court rules law allows quarantine of CWD deer, not land

This is very, very concerning imo. 

IF this ruling is upheld as such ;

''The Iowa Supreme Court upheld the district court ruling — saying the law gives the DNR only the authority to quarantine the deer — not the land. The ruling says if the Iowa Legislature wants to expand the quarantine powers as suggested by the DNR, then it is free to do so.''

IF a 'precedent' is set as such, by the Legislature not intervening to expand quarantine powers to the DNR for CWD TSE Prion, and the precedent is set as such that the cervid industry and land there from, once contaminated with the CWD TSE Prion, are free to repopulate, sell the land, etc, imo, this will blow the lid off any containment efforts of this damn disease CWD TSE Prion. The Iowa Supreme Court did not just pass the cwd buck down the road, the Supreme Court of Iowa just threw the whole state of Iowa under the bus at 100 MPH. what about the exposure to the other species that come across that land, and then off to some other land? this makes no sense to me, if this is set in stone and the Legislation does not stop it, and stop if fast, any containment of the cwd tse prion will be futile, imo...terry

FRIDAY, JUNE 16, 2017

Iowa Supreme Court rules law allows quarantine of CWD deer, not land


WEDNESDAY, AUGUST 16, 2017 

THURSDAY, AUGUST 10, 2017

NORWAY MAKES CHANGES TO NATIONAL CHRONIC WASTING DISEASE CWD TSE PRION RULES




Terry S. Singeltary Sr.



posted by Terry S. Singeltary Sr. at 5:07 PM

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