Wisconsin CWD TSE PRION PLAN preferred option disposal in a landfill OR public land is acceptable to leave the carcass in the spot of the kill
Wisconsin CWD TSE PRION PLAN preferred option disposal in a landfill OR public land is acceptable to leave the carcass in the spot of the kill
The preferred option is disposal in a landfill that accepts deer waste if you can do so within the CWD-affected county of harvest. Landfills are a safe and cost-effective option for disposing of carcass waste potentially contaminated with CWD-causing prions. Leaving deer carcass waste back on the landscape as close to where the deer was harvested as possible is less of a disease transmission risk than this waste being discarded in a location where CWD has not been detected. If hunting on public land, it is acceptable to leave the carcass in the spot of the kill.
To try and make things easier and prevent carcasses from being left all over public land, our waste management division has been working to compile a list of deer carcass waste disposal sites. The hope is that this list will help hunters find a place other than the woods to dispose of the carcass within the county of harvest. We are also working on an "Adopt-A-Dumpster" program to add more of these sites throughout the state. You can view the current list here: https://dnr.wi.gov/topic/hunt/landfillmap.html
>>> The preferred option is disposal in a landfill that accepts deer waste if you can do so within the CWD-affected county of harvest. Landfills are a safe and cost-effective option for disposing of carcass waste potentially contaminated with CWD-causing prions. Leaving deer carcass waste back on the landscape as close to where the deer was harvested as possible is less of a disease transmission risk than this waste being discarded in a location where CWD has not been detected. If hunting on public land, it is acceptable to leave the carcass in the spot of the kill. <<<
WOW, just wow...tss
Transmissible Spongiform Encephalopathy TSE Prion BSE, CWD, SCRAPIE, report on carcass incineration
>>>Consider the potential role of predators and scavengers to remove CWD infected animals and carcasses to reduce CWD transmission (Krumm, 2010; Wild, 2011).<<<
ABSOLUTELY A BAD DECISION, BASED ON THE FACT THAT THE CANINE AND FELINE SPECIES ARE SUSCEPTIBLE TO THE TSE PRION, AND THE FACT THAT THE TSE PRION SURVIVES THE Digestive System OF THE American crows (Corvus brachyrhynchos) AND THE Coyotes (Canis latrans).
ALSO, it was well documented that domestic feline and big cage cats in zoos contracted the TSE Prion disease.
ALSO, it was well documented that HOUNDS were susceptible to a TSE PRION, and later science shows the same thing for canines.
THIS CONSIDERATION SHOULD BE TABLED AND NEVER MENTIONED AGAIN FOR THE FOLLOWING REASONS ;
Saturday, December 05, 2015
CWD Prions Remain Infectious after Passage Through the Digestive System of Coyotes (Canis latrans)
Sunday, July 07, 2013
Could avian scavengers translocate infectious prions to disease-free areas initiating new foci of chronic wasting disease?
Prion. 2013 Jul 3;7(4). [Epub ahead of print]
Wednesday, October 17, 2012
Prion Remains Infectious after Passage through Digestive System of American Crows (Corvus brachyrhynchos)
Monday, February 14, 2011
THE ROLE OF PREDATION IN DISEASE CONTROL: A COMPARISON OF SELECTIVE AND NONSELECTIVE REMOVAL ON PRION DISEASE DYNAMICS IN DEER
NO, NO, NOT NO, BUT HELL NO !
Journal of Wildlife Diseases, 47(1), 2011, pp. 78-93 © Wildlife Disease Association 2011
Sunday, November 01, 2009
AS THE CROW FLIES, SO DOES CWD
American crows (Corvus brachyrhynchos) and potential spreading of CWD through feces of digested infectious carcases
Monday, July 13, 2009
Deer Carcass Decomposition and Potential Scavenger Exposure to Chronic Wasting Disease
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]
***> CONGRESSIONAL ABSTRACTS PRION CONFERENCE 2018
P69 Experimental transmission of CWD from white-tailed deer to co-housed reindeer
Mitchell G (1), Walther I (1), Staskevicius A (1), Soutyrine A (1), Balachandran A (1)
(1) National & OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada.
Chronic wasting disease (CWD) continues to be detected in wild and farmed cervid populations of North America, affecting predominantly white-tailed deer, mule deer and elk. Extensive herds of wild caribou exist in northern regions of Canada, although surveillance has not detected the presence of CWD in this population. Oral experimental transmission has demonstrated that reindeer, a species closely related to caribou, are susceptible to CWD. Recently, CWD was detected for the first time in Europe, in wild Norwegian reindeer, advancing the possibility that caribou in North America could also become infected. Given the potential overlap in habitat between wild CWD-infected cervids and wild caribou herds in Canada, we sought to investigate the horizontal transmissibility of CWD from white-tailed deer to reindeer.
Two white-tailed deer were orally inoculated with a brain homogenate prepared from a farmed Canadian white-tailed deer previously diagnosed with CWD. Two reindeer, with no history of exposure to CWD, were housed in the same enclosure as the white-tailed deer, 3.5 months after the deer were orally inoculated. The white-tailed deer developed clinical signs consistent with CWD beginning at 15.2 and 21 months post-inoculation (mpi), and were euthanized at 18.7 and 23.1 mpi, respectively. Confirmatory testing by immunohistochemistry (IHC) and western blot demonstrated widespread aggregates of pathological prion protein (PrPCWD) in the central nervous system and lymphoid tissues of both inoculated white-tailed deer. Both reindeer were subjected to recto-anal mucosal associated lymphoid tissue (RAMALT) biopsy at 20 months post-exposure (mpe) to the white-tailed deer. The biopsy from one reindeer contained PrPCWD confirmed by IHC. This reindeer displayed only subtle clinical evidence of disease prior to a rapid decline in condition requiring euthanasia at 22.5 mpe. Analysis of tissues from this reindeer by IHC revealed widespread PrPCWD deposition, predominantly in central nervous system and lymphoreticular tissues. Western blot molecular profiles were similar between both orally inoculated white-tailed deer and the CWD positive reindeer. Despite sharing the same enclosure, the other reindeer was RAMALT negative at 20 mpe, and PrPCWD was not detected in brainstem and lymphoid tissues following necropsy at 35 mpe. Sequencing of the prion protein gene from both reindeer revealed differences at several codons, which may have influenced susceptibility to infection.
Natural transmission of CWD occurs relatively efficiently amongst cervids, supporting the expanding geographic distribution of disease and the potential for transmission to previously naive populations. The efficient horizontal transmission of CWD from white-tailed deer to reindeer observed here highlights the potential for reindeer to become infected if exposed to other cervids or environments infected with CWD.
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
*** Nine of these recurrences occurred 14–21 years after culling
Gudmundur Georgsson,1 Sigurdur Sigurdarson2 and Paul Brown3
Correspondence Gudmundur Georgsson ggeorgs@hi.is
1 Institute for Experimental Pathology, University of Iceland, Keldur v/vesturlandsveg, IS-112 Reykjavı´k, Iceland
2 Laboratory of the Chief Veterinary Officer, Keldur, Iceland
3 Bethesda, Maryland, USA Received 7 March 2006 Accepted 6 August 2006
In 1978, a rigorous programme was implemented to stop the spread of, and subsequently eradicate, sheep scrapie in Iceland. Affected flocks were culled, premises were disinfected and, after 2–3 years, restocked with lambs from scrapie-free areas. Between 1978 and 2004, scrapie recurred on 33 farms. Nine of these recurrences occurred 14–21 years after culling, apparently as the result of environmental contamination, but outside entry could not always be absolutely excluded. Of special interest was one farm with a small, completely self-contained flock where scrapie recurred 18 years after culling, 2 years after some lambs had been housed in an old sheephouse that had never been disinfected. Epidemiological investigation established with near certitude that the disease had not been introduced from the outside and it is concluded that the agent may have persisted in the old sheep-house for at least 16 years.
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
Using in vitro Prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission.
Claudio Soto Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston.
Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.
=========================
***>>> Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.
========================
Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.
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
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 ***
161: Prion soil binding may explain efficient horizontal CWD transmission
Nathaniel Denkers1, Davin Henderson1, Shannon Bartelt-Hunt2, Jason Bartz3 and Edward Hoover1
1Colorado State University; Fort Collins, Colorado USA
2University of Nebraska-Lincoln; Omaha, Nebraska USA
3Creighton University; Omaha, Nebraska USA
Background Chronic wasting disease (CWD) is unique due to the facile spread in nature. The interaction of excreted CWD prions and soil is a hypothesized contributor in environmental transmission. The present study examines whether and to what degree CWD prions bind to silty clay loam (SCL) using an adapted version of real-time quaking-induced conversion (RT-QuIC) methodology.
Materials and Methods Varying amounts (50–3.12 mg) of SCL were incubated with 1 mL-serial dilutions of CWD (+), CWD (−), or no brain homogenate (BH). Samples were centrifuged, washed, diluted 1:10 in 0.1% SDS, and 2.5 uL seeded in RT-QuIC assays employing recombinant Syrian hamster prion PrP substrate. Multiple well replicates of sample and supernatant fractions were assayed for positive seeding activity (recorded as thioflavin T fluorescence emission; 480 nm). Samples were considered positive if they crossed a threshold of 25,000. Reaction rates (RR) were calculated, averaged, and expressed as 1/RR.
Results Positive seeding activity was detected for most SCL samples incubated with CWD (+) BH dilutions. Higher SCL concentrations (50 mg) produced low fluorescent readings due to optical interference. Lower SCL concentrations (6.25 mg) produced minimal optical interference and removed the vast majority of seeding activity from CWD+ BH in a concentration-dependent manner; determined by seeding activity in residual BH supernatants. Control SCL and supernatants produced minimal false-positive reactions (8 of 240 replicates; 3.3%). We estimated the prion binding capacity of SCL to be 0.16 ng/mg.
Conclusion Silty clay loam exhibits highly efficient prion binding, inferring a durable environmental reservoir, and an efficient mechanism for indirect horizontal CWD transmission.
TSE Scrapie, CWD, BSE, Prion, Soil
Clay content and pH: soil characteristic associations with the persistent presence of chronic wasting disease in northern Illinois
Sheena J. Dorak, Michelle L. Green, Michelle M. Wander, Marilyn O. Ruiz, Michael G. Buhnerkempe, Ting Tian, Jan E. Novakofski & Nohra E. Mateus-Pinilla
Scientific Reportsvolume 7, Article number: 18062(2017) doi:10.1038/s41598-017-18321-x
Download Citation
Ecological epidemiology Ecological modelling Infectious diseases Prions
Received: 21 August 2017
Accepted: 08 December 2017
Published online: 22 December 2017
Abstract
Environmental reservoirs are important to infectious disease transmission and persistence, but empirical analyses are relatively few. The natural environment is a reservoir for prions that cause chronic wasting disease (CWD) and influences the risk of transmission to susceptible cervids. Soil is one environmental component demonstrated to affect prion infectivity and persistence. Here we provide the first landscape predictive model for CWD based solely on soil characteristics. We built a boosted regression tree model to predict the probability of the persistent presence of CWD in a region of northern Illinois using CWD surveillance in deer and soils data. We evaluated the outcome for possible pathways by which soil characteristics may increase the probability of CWD transmission via environmental contamination. Soil clay content and pH were the most important predictive soil characteristics of the persistent presence of CWD. The results suggest that exposure to prions in the environment is greater where percent clay is less than 18% and soil pH is greater than 6.6. These characteristics could alter availability of prions immobilized in soil and contribute to the environmental risk factors involved in the epidemiological complexity of CWD infection in natural populations of white-tailed deer.
Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil 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
cwd tse prion and soil, see more ;
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 ***
MONDAY, MARCH 05, 2018
TRUCKING AROUND AND SPREADING CHRONIC WASTING DISEASE CWD TSE PRION VIA MOVEMENT OF CERVID AND TRANSPORTATION VEHICLES
old days, with the less infectious typical c-type BSE aka mad cow disease...tss
PAUL BROWN SCRAPIE SOIL TEST
http://www.bseinquiry.gov.uk/files/sc/seac07/tab03.pdf
some unofficial info. from a source on the inside looking out;
Confidential!!!!
As early as 1992-3 there had been long studies conducted on small pastures containing scrapie infected sheep at the sheep research station associated with the Neuropathogenesis Unit in Edinburgh, Scotland. Whether these are documented...I don't know. But personal recounts both heard and recorded in a daily journal indicate that leaving the pastures free and replacing the topsoil completely at least 2 feet of thickness each year for SEVEN years....and then when very clean (proven scrapie free) sheep were placed on these small pastures.... the new sheep also broke with scrapie and passed it to offspring. I am not sure that TSE contaminated ground could ever be free of the agent!! A very frightening revelation!!!
xxxxxxxxxxx
you can take that with however many grains of salt you wish, and we can debate these issues all day long, but bottom line, this is not rocket-science, all one has to do is some experiments and case studies, but for the life of me, i don't know what they are waiting on?
kind regards, Terry S. Singeltary Sr., Bacliff, Texas USA
report on bovine carcass incineration
INCINERATION TEMPS
Requirements include:
a. after burning to the range of 800 to 1000*C to eliminate smell;
well heck, this is just typical public relations fear factor control. do you actually think they would spend the extra costs for fuel, for such extreme heat, just to eliminate smell, when they spread manure all over your veg's. i think not. what they really meant were any _TSE agents_.
b. Gas scrubbing to eliminate smoke -- though steam may be omitted;
c. Stacks to be fitted with grit arreaters;
snip...
1.2 Visual Imact
It is considered that the requirement for any carcase incinerator disign would be to ensure that the operations relating to the reception, storage and decepitation of diseased carcasses must not be publicly visible and that any part of a carcase could not be removed or interfered with by animals or birds.
see full text;
OPINION ON THE USE OF BURIAL FOR DEALING WITH ANIMAL CARCASSES AND OTHER ANIMAL MATERIALS THAT MIGHT CONTAIN BSE/TSE
ADOPTED BY THE SCIENTIFIC STEERING COMMITTEE MEETING OF 16-17 JANUARY 2003
OPINION
On 17 May 2002, the Scientific Steering Committee (SSC) was invited by Commission Services to advice on the examples of conditions under which safe burial of potentially TSE-infected (animal) materials can be achieved.
The details of the SSC’s evaluation are provided in the attached report. The SSC concludes as follows:
(1) The term “burial” includes a diversity of disposal conditions. Although burial is widely used for disposal of waste the degradation process essential for BSE/TSE infectivity reduction is very difficult to control. The extent to which such an infectivity reduction can occur as a consequence of burial is poorly characterised. It would appear to be a slow process in various circumstances.
(2) A number of concerns have been identified including potential for groundwater contamination, dispersal/transmission by birds/animals/insects, accidental uncovering by man.
(3) In the absence of any new data the SSC confirms its previous opinion that animal material which could possibly be contaminated with BSE/TSEs, burial poses a risk except under highly controlled conditions (e.g., controlled landfill).
The SSC reiterates the consideration made in its opinion of 24-25 June 1999 on “Fallen Stock”1
. The limited capacity for destruction of animal wastes in certain countries or regions in the first place justifies the installation of the required facilities; it should not be used as a justification for unsafe disposal practices such as burial. However, the SSC recognises that for certain situations or places or for certain diseases (including animals killed and recycled or disposed of as a measure to control notifiable diseases), the available rendering or incinerator or disposal capacity within a region or country could be a limiting factor in the control of a disease. Thus if hundreds or even millions of animals need to be rendered after killing or if the transport of a material to a rendering or disposal plant proved to be impractical, an appropriate case by case risk assessment2 should be carried out before deciding upon the most appropriate way of disposal. In principle, the risk is expected to be the lower for small incinerators3 as compared to burial. As such decisions in practice may have to be taken at very short notice, risk management scenarios according to various possible risks should be prepared in advance to allow for a rapid decision when the need arises.
1 Scientific Opinion on The risks of non conventional transmissible agents, conventional infectious agents or other hazards such as toxic substances entering the human food or animal feed chains via raw material from fallen stock and dead animals (including also: ruminants, pigs, poultry, fish, wild/exotic/zoo animals, fur animals, cats, laboratory animals and fish) or via condemned materials. Adopted By the Scientific Steering Committee at its meeting of 24-25 June 1999. (and re-edited at its meeting of 22-23 July 1999).
2 See also the relevant sections and footnotes on risk assessment in the report accompanying the SSC opinion of 24-25 June 1999.
3 See SSC opinion of 16-17 January 2003 on the use of small incinerators for BSE risk reduction.
THE USE OF BURIAL FOR DEALING WITH CARCASSES AND OTHER MATERIALS THAT MIGHT CONTAIN BSE/TSE
REPORT
1. MANDATE
On 17 May 2002, the Scientific Steering Committee (SSC) was invited by Commission Services to advice on the examples of conditions under which safe burial of potentially TSE-infected animal materials can be achieved. The SSC appointed Prof.J.Bridges as rapporteur. His report was discussed and amended by the TSE/BSE ad hoc Group at its meeting of 9 January 2003 and by the SSC at its meeting of 16-17 January 2003.
2. GENERAL CONSIDERATIONS
“Burial” covers a range of disposal situations ranging from the practice of burying animals on farms and other premises in a relatively shallow trench (with or without treatment such as lining) to deep disposal to a lined and professionally managed landfill site (SSC 2001).
Buried organic material is normally decomposed by microbial and chemical processes. However this is not a process amenable to control measures. As noted by the SSC “Opinion on Fallen Stock” (SSC 25th June 1999) there is little reliable information on the extent and rate of infectivity reduction of BSE/TSEs following burial. An old paper by Brown and Gajdusek 1991 assumed a reduction of 98% over 3 years. However it is noted that the rate of degradation of materials following burial can vary very considerably between sites. This is not surprising because the degradation process is strongly influenced by factors such as water content of the site, temperature inside the site, nature of adsorptive “material” present etc. The previous SSC opinion noted that BSE/TSEs appear to be resistant to degradation when stored at room temperature over several years. It also raised concerns that mites could serve as a vector and/or reservoir for the infected scrapie material. Burial sites may have a thriving animal population. Uncovering of risk material that is not deeply buried is therefore possible.
The SSC in its opinion of 28th-29th June 2001 set out a framework for assessing the risk from different waste disposal processes. These criteria may be applied to burial as follows:
(1) Characterisation of the risk materials involved.
Unlike many other waste disposal options there are no technical or economic factors that would limit the nature of the material that can be disposed of by burial. Moreover in many cases the location of burial sites is uncertain. The potential for transmission of BSE/TSEs for SRM that is buried near the surface is also poorly characterised.
3
(2) Risk reduction
The extent to which the infectivity is reduced is likely to vary substantially according to the nature of the site depth of burial whether pre-treatment by burning or through the addition of lime is used etc. There appears to be no scientific basis at present for the prediction of the rate of loss of infectivity. In the absence of such data, as a worst case, it has to be assumed that over a three-five year period the loss of infectivity may be slight. In principle on a well-managed fully contained landfill the risks from infective material can approach zero. However this requires rigorous management over many years. This is difficult to guarantee.
(3) Degree to Which the Risks can be Contained
The principal concerns are:
Prevention of access to the SRM by animals that could result in the transmission (directly or indirectly) of the BSE/TSE.
Penetration of prions into the leachate/groundwater. It is noted that on some landfill sites leachate is sprayed into the air to facilitate oxidation of some organic components. Such a practice could in principle lead to dispersal of BSE/TSEs. It is also noted that it is not uncommon for landfill sites to be re-engineered to increase their stability, gas and leachate flow and/or total capacity. If this re-engineering involved an area where previous burial of BSE/TSE contaminated material had taken place and additional risk could accrue. The possibility of contaminated material being dug up in shallow and unmarked burial sites on farms etc constitutes a considerably greater risk.
3. FURTHER INVESTIGATIONS
Research is needed on specific aspects of the behaviour of prion like molecules in controlled landfills i.e.:
Potential for adsorption to other material present in the waste that might limit their mobility.
Principal factors influencing rates of degradation.
Effectiveness of encasement in cement in controlling/reducing the risk.
4. CONCLUSION
In the absence of new evidence the opinion of the SSC “Opinion on Fallen Stock” (SSC 25th June 1999) must be endorsed strongly that land burial of all animals and material derived from them for which there is a possibility that they could incorporate BSE/TSEs poses a significant risk. Only in exceptional circumstances where there could be a considerable delay in implementing a safe means of disposal should burial of such materials be considered. Guidelines should be made available to aid on burial site selection.
OPINION ON OPEN BURNING OF POTENTIALLY TSE-INFECTED ANIMAL MATERIALS
ADOPTED BY THE SCIENTIFIC STEERING COMMITTEE AT ITS MEETING OF 16-17 JANUARY 2003
OPINION
On 17 May 2002, the Scientific Steering Committee (SSC) was invited by Commission Services to advice on the examples of conditions under which safe burning of potentially TSE-infected (animal) materials can be achieved.
The details of the SSC’s evaluation are provided in the attached report. The SSC concludes as follows:
(1) “Burning” covers a wide variety of combustion conditions. This opinion is concerned with the process of open burning e.g. bonfires.
(2) There are serious concerns regarding the use of open burning for the destruction of pathogen contaminated animal waste, particularly for waste which may be contaminated with relatively heat stable pathogens. Issues include: the potentially very high variability of the pathogen inactivation, the nature of the gaseous and particulate emissions, and the risks from the residual ash.
(3) The SSC recommends that open burning is only considered for pathogen destruction under exceptional circumstances following a specific risk assessment. In the case of animal waste possibly contaminated with BSE/TSE in view of the uncertainty of the risk open burning should be considered a risk. Suitable monitoring methods for TSE contamination of both air and ash are needed.
Protocols for safe burning in emergency situations need to be established.
The SSC reiterates the consideration made in its opinion of 24-25 June 1999 on “Fallen Stock”1. The limited capacity for destruction of animal wastes in certain countries or regions in the first place justifies the installation of the required facilities; it should not be used as a justification for unsafe disposal practices such as burial. However, the SSC recognises that for certain situations or places or for certain diseases (including animals killed and recycled or disposed of as a measure to control notifiable diseases), the available rendering or incinerator or disposal capacity within a region or country could be a limiting factor in the control of a disease. Thus if hundreds or even millions of animals need to be rendered after killing or if the transport of a material to a rendering or disposal plant proved to be impractical, an appropriate case by case risk assessment2 should be carried out before deciding upon the most appropriate way of disposal. In principle, the risk is expected to be the lower for small incinerators3 as compared to open burning. As such decisions in practice may have to be taken at very short notice, risk management scenarios according to various possible risks should be prepared in advance to allow for a rapid decision when the need arises.
1 Scientific Opinion on The risks of non conventional transmissible agents, conventional infectious agents or other hazards such as toxic substances entering the human food or animal feed chains via raw material from fallen stock and dead animals (including also: ruminants, pigs, poultry, fish, wild/exotic/zoo animals, fur animals, cats, laboratory animals and fish) or via condemned materials. Adopted By the Scientific Steering Committee at its meeting of 24-25 June 1999. (and re-edited at its meeting of 22-23 July 1999).
2 See also the relevant sections and footnotes on risk assessment in the report accompanying the SSC opinion of 24-25 June 1999.
3 See SSC opinion of 16-17 January 2003 on the use of small incinerators for BSE risk reduction.
3
OPEN BURNING OF POTENTIALLY TSE-INFECTED ANIMAL MATERIALS REPORT
1. MANDATE
On 17 May 2002, the Scientific Steering Committee (SSC) was invited by Commission Services to advice on the examples of conditions under which safe burning of potentially TSE-infected animal materials can be achieved. The SSC appointed Prof.J.Bridges as rapporteur. His report was discussed and amended by the TSE/BSE ad hoc Group at its meeting of 9 January 2003 and by the SSC at its meeting of 16-17 January 2003.
2. GENERAL CONSIDERATIONS
Burning is a combustion process to which a range of control measures may be applied to contain emissions and to ensure the completeness of the degradation process for organic matter. Depending on the source (waste) material the burning process may or may not require addition of other energy sources. Incineration/pyrolysis are contained combustion processes are contained combustion processes and therefore have the potential for a high level of control. (However see opinion on small incinerators). At the other end of the control spectrum is open burning; such as bonfires.
Typically combustion of animal waste requires the addition of a high calorific fuel in order to initiate (and for some materials to sustain) the process. It is recognised that open burning of animal waste is a very cheap and convenient method of disposal. However uncontained burning has a number of problems in terms of the potential risks involved:
(1) In the open burning situation a range of temperatures will be encountered. It is difficult therefore to ensure complete combustion of the animal waste. If the waste is contaminated with pathogens there will remain considerable uncertainty as to the degree of their inactivation.
(2) Gaseous and particulate emissions to the atmosphere will occur and consequently worker and public exposure is likely. There is very little data to indicate whether or not some pathogens could be dispersed to air as a consequence of open burning.
(3) The supporting/secondary fuel may be a source of contamination itself. For example in the recent foot and mouth disease outbreak in the UK timbers were used at some sites that were heavily contaminated with pentachlorophenol.
(4) The residual ash must be considered to be a risk source. Its safe disposal needs to be assured (see opinion on small incinerators) to prevent human and animal contact and protect from groundwater contamination. While careful selection of burning sites can reduce the risks open burning should only be considered in emergency situations. For each such emergency situation a specific risk assessment should be conducted which must include the risk
4
from the pathogen of immediate concern but also other pathogens that might be present.
3. RISK ASSESSMENT OF OPEN BURNING FOR BSE
The SSC, at its meeting of 28th-29th June 2001, recommended “a framework for the assessment of the risk from different options for the safe disposal or use of meat and bone meal (MBM) and other products which might be contaminated with TSEs and other materials. Applying the framework to the practice of open burning, the following conclusions can be drawn:
3.1. Nature of the materials handled
Potentially a wide variety of materials can be used provided suitable secondary fuel is available. The burning process is very simple in principle and difficult in practice to regulate effectively.
3.2. Risk reduction due to open burning
There is no reliable data to indicate the extent of risk reduction that could be achieved by open burning. It is reasonable however to assume that overall it will be rather less effective in reducing the infectivity of BSE/TSE than well conducted incineration. Moreover the reproducibility of the risk reduction is likely to be very variable even at a single location.
3.3. Airborne emissions and residue ash
The composition of airborne emissions and residue ash is rarely monitored. From a risk assessment viewpoint particular attention needs to be given to the potential for the airborne dispersal of relatively heat stable pathogens as a consequence of open burning. In the absence of reliable data both airborne emissions and residual ash must be considered to constitute a significant risk if animal waste that might be contaminated with TSEs is being burnt.
4. FURTHER INVESTIGATION
Research is needed particularly on:
The potential for airborne dispersal of relatively heat stable pathogens.
Methodologies to improve the efficacy of the combustion process to ensure the inactivation of pathogen contaminated animal waste.
5. CONCLUSION
Open burning potentially represents a significant risk where the animal waste has the possibility of being contaminated with BSEs/TSEs. Suitable monitoring methods for TSE contamination of both air and ash are needed. Protocols for safe burning in emergency situations need to be established.
OPINION ON THE USE OF SMALL INCINERATORS FOR BSE RISK REDUCTION
SCIENTIFIC STEERING COMMITTEE MEETING OF 16-17 JANUARY 2003
OPINION On 17 May 2002, the Scientific Steering Committee (SSC) was invited by Commission Services to (i) evaluate a risk assessment1 prepared for the UK’s Spongiform Encephalopathy Advisory Committee (SEAC), on the potential risk arising from the use of small incinerators to dispose of specified risk materials and (ii) to advise on the safety with regard to TSE risks of the use of such small incinerators.
The details of the SSC’s evaluation are provided in the attached report. The SSC concludes as follows:
(i) The SSC, at its meeting of 28th -29th June 2001, recommended “a framework for the assessment of the risk from different options for the safe disposal or use of meat and bone meal (MBM) and other products which might be contaminated with TSEs and other materials.” This framework comprised five components:
(1) Identification and characterisation of the risk materials involved, the possible means for their transmission and potential at risk groups.
(2) The risk reduction achieved by the particular process.
(3) The degree to which the risks can be contained under both normal and emergency operating conditions. This inevitably includes consideration of the effectiveness of control measures.
(4) Identification of interdependent processes for example transport, storage, loading of any TSE related risk materials.
(5) The intended end-use of the products for example disposal, recycling etc. The risk assessment prepared for SEAC focuses on the risks involved steps 1 and 2 in respect of BSE/TSEs only and is based on a visit to 10 incinerators out of a total of 263 in the UK of which 60% had after burners.
The risk assessment is also using a number of assumptions and data that may be valid for certain incinerator types under certain conditions, but are not necessarily applicable either for all types of materials to be disposed of, or to the whole range of types of small incinerators in use the EU and the UK.
(ii) Small incinerators are widely used to meet the needs of local communities. These incinerators vary greatly in their design, nature of use and performance characteristics and the quality of their management. As a consequence of this variability there are many uncertainties in identifying risks posed by small incinerators that are used to treat SRM materials and each type should eventually receive its own assessment. Also, general operating and control criteria should be established for safe incineration, a s it has been done for large incinerators.
1 DNV Consulting (Det Norske Veritas), 2001. Risk assessment of SRM incinerators. Prepared for the UK Ministry of Agriculture, Fisheries and Food. Revision 2 of the Draft report, February 2001. 24 pages.
3
Potential risk sources arising from the incineration process include: gaseous emissions and residual ash. Research is currently ongoing mimicking incineration of TSE-infected brain tissue to assess the infectivity clearance level under various scenarios2 . However, there are no final reported measurements that enable the risk to be assessed from either the emissions or the ash from small incinerators. It has been argued that the protein content of the ash is a reasonable surrogate measure of the degree of risk deduction caused by the incineration process. This assumption is questionable in view of the resistance to heat of prions as compared to other proteins. Protein measurements in ash are however probably a useful general measure of the overall efficiency and reproducibility of the incineration process.
Results in the aforementioned report1 indicate a large degree of variability in performance among the small incinerators in the UK that have been evaluated. It is anticipated that small incinerators, used by other Member States will also show a considerable variation in performance. In evaluating the risk of small incinerators, consideration should be given to the risk of potential contamination of the ash and of the gaseous emissions.
In the absence of generally accepted and enforced performance standards for small incinerators handling SRMs each such facility therefore needs to be the subject of a specific risk assessment. The SSC considers that the standards set up by the new Waste Incinerator Directive (2000/76/EC) and in its opinion of June 1999 on waste disposal should serve as guidance.
In the absence of reliable data on the possible residual infectivity of the ash, it should be disposed of, i.e., in controlled landfills as described in the SSC opinion of June 1999 on safe disposal of waste.
The SSC finally wishes to emphasise the need for suitable monitoring methods in order that risks can be assessed readily for individual types of small incinerators.
2 P.Brown, pers.comm., December 2002. Publication in progress.
4
THE USE OF SMALL INCINERATORS FOR BSE RISK REDUCTION REPORT
1. MANDATE
On 17 May 2002, the Scientific Steering Committee (SSC) was invited by Commission Services to (i) evaluate a risk assessment3 prepared for the UK’s
Spongiform Encephalopathy Advisory Committee (SEAC), on the potential risk arising from the use of small incinerators to dispose of specified risk materials and (ii) to advise on the safety with regard to TSE risks of the use of such small incinerators.
The SSC appointed Prof.J.Bridges as rapporteur. His report was discussed and amended by the TSE/BSE ad hoc Group at its meeting of 9 January 2003 and by the SSC at its meeting of 16-17 January 2003.
2. CURRENT LEGISLATIVE FRAMEWORK
Until 2000, small incinerators were exempt from the emission limits set by the EC for MSW and hazardous waste incinerators with throughputs greater than 50 kg/hour. An “incineration plant” is defined by the new Incineration of Waste Directive (2000/76/EC) as “any stationary or mobile technical equipment dedicated to the thermal treatment of waste with or without recovery of the combustion heat generated”. This definition would appear to exclude open burning of waste. The new Directive, which must be transposed into the legislation of each Member State by December 2002, replaces a range of previous directives on incineration. It applies to all new incinerator installations from December 28th 2002 and all existing installations from December 28th 2005. The principal aim of the Directive is to prevent and/or limit negative environmental effects due to emissions into air, soil, surface and ground water and the resulting risks to human health from the incineration and co-incineration of waste. It covers many aspects from a requirement for afterburners to airborne emission limits and criteria for the composition of residual ash. Previous EC legislation has exempted small incinerators (i.e. those operating at less than 50 kg per hour). The Waste Incinerator Directive (WID) (2000) allows such small incinerators to be exempt from licensing at the national level however they will still be subjected to the same onerous requirements of the WID as larger incinerators.
In the UK it is proposed that in future incinerators dealing with non-hazardous waste but with a throughput of less than 1 tonne per hour will be regulated by local authorities whereas those with a larger throughput will be regulated by the national authority. It is possible that different regulatory mechanisms may result in differences in the rigour with which the new standards are enforced. The position on the disposal of animal waste is complicated. Animal carcass incineration use not covered by the WID and therefore the existing regulatory framework (90/66/EEC which covers animal and public health requirements to ensure destruction of pathogens) will continue to be applied. A new Animal By-Products Regulation
3 DNV Consulting (Det Norske Veritas), 2001. Risk assessment of SRM incinerators. Prepared for the UK Ministry of Agriculture, Fisheries and Food. Revision 2 of the Draft report, February 2001. 24 pages.
5
(ABPR) will apply in Member States during the first part of 2003. The relationship to WID has been included in the ABPR. It is important that it does not result in less strict standards being applied for animal carcass incineration. In contrast to whole carcasses WID will apply to the burning of meat and bone meal, tallow or other material (even if they burn animal carcasses too). Additional specific directives will continue to apply to waste that could be contaminated with BSE/TSEs. (96/449/EC)
3. CURRENT USE OF SMALL INCINERATORS TO DISPOSE OF ANIMAL WASTE Small incinerators are used for a variety of purposes and in a range of locations among Member States. Many are located alongside small abattoirs, knackers, hunt kennels, or laboratories. Thus they meet the needs of relatively small communities. Across Member States these small incinerators include a variety of designs and operating conditions (as indicated above in principle they will probably be required to meet specific standards for emissions and for the composition of the residual ash by December 28th 2005).
In the UK there are indications (see DNV Report 2001) that a considerable quantity of SRM which would have previously been sent for rendering is now being incinerated directly in small incinerators. Thus evaluation of the risks from such incinerators is of increasing importance.
4. RISK ASSESSMENT FOR SMALL INCINERATORS
The SSC, at its meeting of 28th -29th June 2001, recommended “a framework for the assessment of the risk from different options for the safe disposal or use of meat and bone meal (MBM) and other products which might be contaminated with TSEs and other materials.
This framework comprised five components:
(1) Identification and characterisation of the risk materials involved, the possible means for their transmission and potential at risk groups.
(2) The risk reduction achieved by the particular process.
(3) The degree to which the risks can be contained under both normal and emergency operating conditions. This inevitably includes consideration of the effectiveness of control measures.
(4) Identification of interdependent processes for example transport, storage, loading of any TSE related risk materials.
(5) The intended end-use of the products for example disposal, recycling etc. Recently a report has been prepared by DNV consulting (2001) for the UK Ministry of Agriculture, Fisheries and Food (now known as DEFRA) that assesses the risks from small incinerators in the UK that receive SRMs. This report focuses on the risks involved steps 1 and 2 in respect of BSE/TSEs only. 10 incinerators out of a total of 263 in the UK were visited of which 60% had after burners.
(1) Nature of the materials handled
The DNV report 2001 starts with the assumption that “the materials incinerated at small abattoirs will be mainly SRM and bones from animals that are fit for human consumption. It may also include material from animals failed by meat inspectors. The likelihood of there being an animal
6
with significant BSE infectivity is very small and certainly much less than for the fallen stock handled by hunt kennels and knackers4 . For this reason the study has concentrated on the latter type of operation”.
The Report notes that “the material handled by both knacker and hunt kennels is highly variable and difficult to characterise”. In terms of input the key factors to consider are:
The number of adult bovines processed and the proportion of these carcasses that are likely to be infected.
The extent of infectivity (in terms of human oral Infectious Units) that may occur (average and worst case).
In the DNV (2001) risk assessment only the BSE risk from processing bovine SRMs was considered. For quantitative risk assessment purposes the mean value of the oral ID50 for cattle was taken as 0.1 gram. A range of values was taken to cover uncertainty in the inter-species barrier from 104 to 1 (as recommended by the SSC 2000). In order to assess the likelihood that a particular carcass could be infected, UK and Swiss monitoring data was used. An incidence rate based on Prionics test findings of between 0.013 and 0.0025 was calculated. The DNV Report notes that prevalence rates are progressively reducing from these 1998/99 figures. Finally the report concludes that the SRM from an infected bovine could contribute 700 Infectious Units.
(2) Risk reduction due to incineration
Once a carcass/SRM has been introduced into a small incinerator there are two main sources for the potential release of BSE infectivity
(a) Airborne emissions
(b) Residual ash
There is no direct data on the TSE levels that may occur in those two media. The SSC however is aware of currently ongoing heat studies mimicking various incineration conditions and scenarios and aiming at assessing the TSE clearance efficacy of these processes (P.Brown, pers.comm., 16.01.03) on both the residual ash and the trapped emission gases.
In the absence of final data from such experiments for individual (small) incinerator types, the DNV Report (2001) assumes that measurement of the total protein content of ash is a relevant surrogate for BSE/TSE material. Protein content is a useful indicator of the general performance of an incinerator. However it is much more problematic whether it is also a valid marker for possible BSE/TSE contamination as it known that BSE/TSE are relatively heat resistant as compared to other proteins. Failure to detect certain amino acids present in prions is encouraging but the sensitivity limits for amino acids are relatively poor for reassurance purposes. Equally important, the data provided in the DNV report shows moderate split sample
4 It may be mentioned that this assumption may be valid for the UK as a whole, but note necessarily for all other Member States.
7
variation but often substantial inter sampling variation (up to 600 fold). This indicates a wide span of performance standards among the small SRM incinerators in the UK and most likely across the whole of the EU. Typically performance was substantially poorer than is the case for larger incinerators. Unburned material is not uncommonly noted in the ash from small incinerators. If the reduction in protein content due to incineration is accepted as a valid indicator, typical infectivity reduction can be calculated to be of the order of 1600 (DNV Report 2001).
Incinerators are known to emit particulate matter from their stacks. Larger incinerators have much higher stacks to facilitate disposal of emissions, they also have gas cleaning equipment to minimise the emission of particulate matter, metals and acidic gases. Small incinerators generally do not have any gas cleaning equipment. It can be speculated (as in the DNV Report 2001) that unburned materials (and therefore potentially infections is much less likely to be emitted in the form of particulate matter than burnt material. Nonetheless there is no data to support this assumption.
(3) Other considerations
(a) Disposal of ash
In the case of small incinerators ash is often dispersed of locally to a trench, which is typically neither lined, nor is the residue buried deeply. In contrast for larger incinerators in the UK ash is normally disposed of to a contained landfill. The risk from disposal to a trench is difficult to gauge in the absence of reliable data on the possible infectivity of the ash.
(b) Management factors
Almost inevitably the level of expertise available for the management of small incinerators is highly variable because few such facilities can afford to employ specialists in incineration. This is also likely to be often the case for the inspectors as well. While such considerations cannot formally be taken into account in a risk assessment, they are not the less relevant factors that need to be considered in assessing the risk from a particular plant.
(c) Benchmarking
The DNV 2001 risk assessment relies greatly on the assumption that BSE/TSE contaminated material is very unlikely to be processed. The Report seeks to compare the risks from a small incinerator with that from large SRM incinerators which the author had assessed previously (DNV, 1997). It identifies that the risk is four-five –fold less from a typical small incinerator because the scale of activities is much lower. However it is noted that the amount of experimental data to back this conclusion is extremely limited and does not take into account either risks from the residual ash or any consequences of a substantially lower stack height limiting the dilution of the emitted particulate and gaseous matter.
8
5. FURTHER INVESTIGATIONS
In view of the uncertainty regarding the risks due to BSE/TSE contamination of the fly and bottom ash and airborne emissions it is recommended that further research is conducted to identify the residual risks (along with attendant uncertainties) from the burial of ash (without further treatment,) in uncontained sites. It is essential that suitable monitoring methods are developed.
6. LITERATURE
EC (European Commission), 1999. Opinion on The risks of non conventional transmissible agents, conventional infectious agents or other hazards such as toxic substances entering the human food or animal feed chains via raw material from fallen stock and dead animals (including also: ruminants, pigs, poultry, fish, wild/exotic/zoo animals, fur animals, cats, laboratory animals and fish) or via condemned materials. Adopted By the Scientific Steering Committee at its meeting of 24-25 June 1999 and re-edited at its meeting of 22-23 July 1999.
DNV Consulting (Det Norske Veritas), 1997. Risks from disposing of BSE infected cattle in animal carcass incinerators. Report prepared for the UK Environment Agency.
DNV Consulting (Det Norske Veritas), 2001. Risk assessment of SRM incinerators. Prepared for the UK Ministry of Agriculture, Fisheries and Food. Revision 2 of the Draft report, February 2001. 24 pages.
SEAC (Spongiform Encephalopathy Advisory Committee, UK), 2001. Public summary of the SEAC meeting of 25 April 2001.
2003
From: TSS
Subject: ONLY DUMB AND DUMBER DISPOSE OF DEER/ELK CARCASS IN GARBAGE !!!
Date: November 5, 2003 at 2:05 pm PST
Properly dispose of your deer carcass
The Pine Journal Last Updated: Wednesday, November 05th, 2003 02:00:56 PM
The Western Lake Superior Sanitary District (WLSSD) reminds residents about the procedures for the proper management and handling of deer carcasses and waste that results from deer processing.
Deer carcasses disposed of by individuals are exempt from any special handling requirements. these carcasses may be disposed of in the trash within the Western Lake Superior Sanitary District, unless they are known to have Chronic Wasting Disease (CWD). Carcasses from deer known to be infected with CWD must be disposed of in an alternate manner.
If a resident knows or suspects that a deer carcass may be infected with CWD, they should contact their local Department of Natural Resources wildlife manager for recommended disposal alternatives.
Deer carcasses generated either commercially or in bulk are subject to further disposal regulation. Businesses are directed to contact their waste haulers for information.
http://www.cloquetmn.com/journal/index.php?sect_rank=3&story_id=156416
-------- Original Message --------
Subject: RE-Properly dispose of your deer carcass
Date: Wed, 05 Nov 2003 16:02:22 -0600
From: "Terry S. Singeltary Sr."
To: journal@cloquetmn.com
no concern here over any CWD or worse yet, sub-clinical CWD. Dumb and Dumber just throw the carcass in the garbage and let the smaller critters just spread this agent to high Heaven, or just dump in your local land fill and let it leech to the water tables, no problem for dumb and dumber...
(105KB) - Opinion on a treatment of animal waste by means of high temperature (150°c, 3 hours) and high pressure alkaline hydrolysis. (adopted on 10 April 2003) (327KB)
http://europa.eu.int/comm/food/fs/sc/ssc/out358_en.pdf
Opinion on six alternative methods for safe disposal of animal by-products (adopted on 10-11 april 2003) (303KB)
http://europa.eu.int/comm/food/fs/sc/ssc/out352_en.pdf
Opinion on Chronic Wasting Disease and tissues that might carry a risk for human and animal feed chains (Scientific Steering Committee Meeting of 6 7 March 2003) (116KB)
http://europa.eu.int/comm/food/fs/sc/ssc/out323_en.pdf
- -
re-CWD/TSEs & ENVIRONMENT CONTAMINATION
i believe it to be very irresponsible to dispose of clinical/sub-clinial cases of CWD in landfill...
TSS
Aguzzi warns of CWD danger
The TSE family of diseases also includes chronic wasting disease (CWD) in deer, a condition that has spread in the US in recent years (Nature 416, 569; 2002). Speaking at the Days of Molecular Medicine conference in La Jolla in March, prion expert Adriano Aguzzi issued a strong warning against underestimating this form of TSE.
"For more than a decade, the US has by-and-large considered mad cows to be an exquisitely European problem. The perceived need to protect US citizens from this alien threat has even prompted the deferral of blood donors from Europe," he said. "Yet the threat-from-within posed by CWD needs careful consideration, since the evidence that CWD is less dangerous to humans than BSE is less-than-complete. Aguzzi went on to point out that CWD is arguably the most mysterious of all prion diseases.
"Its horizontal spread among the wild population is exceedingly efficient, and appears to have reached a prevalence unprecedented even by BSE in the UK at its peak. The pathogenesis of CWD, therefore, deserves a vigorous research effort. Europeans also need to think about this problem, and it would be timely and appropriate to increase CWD surveillance in Europe too." Aguzzi has secured funding from the National Institutes of Health to investigate CWD, and the effort will be lead by Christina Sigurdson in his department at the University of Zurich. KAREN BIRMINGHAM, LONDON
This quote from Dr. Gambetti is especially significant since he is the rather cautious TSE researcher under contract with the Centers for Disease Control to examine the brains of individuals who have died of CJD.
-----------------
Pierluigi Gambetti, director of the National Prion Disease Pathology Surveillance Center at Case Western Reserve University in Cleveland, said all deer should be tested for chronic wasting disease before any processing is done.
"There is no way around it," he said. "Nobody should touch that meat unless it has been tested."
--------------------------------------
http://www.ledger-enquirer.com/mld/...ion/3954298.htm
======================================================
TSEs & ENVIRONMENT
LANCET
Volume 351, Number 9110 18 April 1998 [Previous] [Next]
BSE: the final resting place
How to dispose of dangerous waste is a question that has vexed the human race for hundreds of years. The answer has usually been to get it out of sight--burn it or bury it. In Periclean Athens, victims of the plague were incinerated in funeral pyres; in 14th century Venice, a law stipulated that Black Death corpses should be buried to a minimum depth of 5 feet; and now, as the 20th century draws to a close, we are challenged by everything from industrial mercury to the smouldering reactors of decommissioned atomic submarines.
The Irish Department of Agriculture will convene an expert panel on April 27-29 to discuss the disposal of tissues from animals with bovine spongiform encephalopathy (BSE). Proper disposal of tissues from infected cattle has implications for both human and animal safety. Safety for human beings is an issue because there is now unassailable if still indirect evidence that BSE causes infections in man in the form of "new variant" Creutzfeld-Jakob disease (nvCJD).1-3 Safety for animals is also an issue because BSE-affected cattle could possibly transmit disease to species other than cattle, including sheep, the species that was almost surely the unwitting source of the BSE epidemic.
The first matter to consider is the distribution of infectivity in the bodies of infected animals. The brain (and more generally, the central nervous system) is the primary target in all transmissible spongiform encephalopathies (TSE), and it contains by far the highest concentration of the infectious agent. In naturally occuring disease, infectivity may reach levels of up to about one million lethal doses per gram of brain tissue, whether the disease be kuru, CJD, scrapie, or BSE. The infectious agent in BSE-infected cattle has so far been found only in brain, spinal cord, cervical and thoracic dorsal root ganglia, trigeminal ganglia, distal ileum, and bone marrow.4 However, the much more widespread distribution of low levels of infectivity in human beings with kuru or CJD, and in sheep and goats with scrapie, suggests that caution is advisable in prematurely dismissing as harmless other tissues of BSE-infected cattle.
A second consideration relates to the routes by which TSE infection can occur. Decades of accumulated data, both natural and experimental, have shown clearly that the most efficient method of infection is by direct penetration of the central nervous system; penetration of peripheral sites is less likely to transmit disease. Infection can also occur by the oral route, and the ingestion of as little as 1 g of BSE brain tissue can transmit disease to other cattle.5 Infection by the respiratory route does not occur (an important consideration with respect to incineration), and venereal infection either does not occur or is too rare to be detected.
How can tissue infectivity be destroyed before disposal? The agents that cause TSE have been known almost since their discovery to have awesome resistance to methods that quickly and easily inactivate most other pathogens. Irradiation, chemicals, and heat are the three commonest inactivating techniques. Irradiation has proved entirely ineffective, and only a handful of a long catalogue of chemicals have produced more than modest reduction in infectivity. The most active of these are concentrated solutions of sodium hypochlorite (bleach) or sodium hydroxide (lye). As for heat, even though the agent shares with most other pathogens the feature of being more effectively damaged by wet heat than by dry heat, boiling has little effect, and steam heat under pressure (autoclaving) at temperatures of 121à ºC is not always sterilising. To date, the most effective heat kill requires exposure of infectious material to steam heat at 134à ºC for 1 h in a porous-load autoclave.6 Exposure to dry heat even at temperatures of up to 360à ºC for 1 h may leave a small amount of residual infectivity.7 The standard method of incineration, heating to about 1000à ºC for at least several seconds, has been assumed to achieve total sterilisation, but needs experimental verification in the light of suggestions that rendered tissue waste might find some useful purpose as a source of heating fuel.
Thus, TSE agents are very resistant to virtually every imaginable method of inactivation, and those methods found to be most effective may, in one test or another, fail to sterilise. It seems that even when most infectious particles succumb to an inactivating process, there may remain a small subpopulation of particles that exhibit an extraordinary capacity to withstand inactivation, and that, with appropriate testing, will be found to retain the ability to transmit disease. Also, almost all available inactivation data have come from research studies done under carefully controlled laboratory conditions, and it is always difficult to translate these conditions to the world of commerce. Even when the data are applied in the commercial process, the repetitive nature of the process requires vigilance in quality control and inspection to ensure adherence to its regulations.
The final issue that must be addressed is the "lifespan" of the infectious agent after disposal if it has been only incompletely inactivated beforehand. Given the extraordinary resistance of the agent to decontamination measures, the epidemiological and experimental evidence indicating that TSE agents may endure in nature for a long time should come as no surprise. The first real clue to this possibility came from the Icelandic observation that healthy sheep contracted scrapie when they grazed on pastures that had lain unused for 3 years after having been grazed by scrapie-infected sheep.8
Support for this observation was obtained from an experiment in which scrapie-infected brain material was mixed with soil, placed in a container, and then allowed to "weather" in a semi-interred state for 3 years.9 A small amount of residual infectivity was detected in the contaminated soil, and most of the infectivity remained in the topmost layers of soil, where the tissue had originally been placed--in other words, there had been no significant leaching of infectivity to deeper soil layers.
It is therefore plausible for surface or subsurface disposal of TSE-contaminated tissue or carcasses to result in long-lasting soil infectivity. Uncovered landfills are a favourite feeding site for seagulls, which could disperse the infectivity.10 Other animals might do likewise, and if the landfill site were later used for herbivore grazing, or tilled as arable land, the potential for disease transmission might remain. A further question concerns the risk of contamination of the surrounding water table, or even surface waste-water channels, by effluents and discarded solid waste from treatment plants.
A reasonable conclusion from existing data is that there is a potential for human infection to result from environmental contamination by BSE-infected tissue residues. The potential cannot be quantified because of the huge number of uncertainties and assumptions that attend each stage of the disposal process.
On the positive side, spongiform encephalopathy can be said to be not easily transmissible. Although the level of infectivity to which creatures are exposed is not known, it is probably very low, since sheep that die from scrapie, cattle that die from BSE, and human beings who die from nvCJD represent only a small proportion of their respective exposed populations.
Whatever risk exists is therefore extremely small, but not zero, hence all practical steps that might reduce the risk to the smallest acceptable level must be considered. What is practical and what is acceptable are concepts that will be hammered out on the anvil of politics: scientific input, such as it is, already waits in the forge. A fairly obvious recommendation, based on the science, would be that all material that is actually or potentially contaminated by BSE, whether whole carcasses, rendered solids, or waste effluents, should be exposed to lye and thoroughly incinerated under strictly inspected conditions. Another is that the residue is buried in landfills to a depth that would minimise any subsequent animal or human exposure, in areas that would not intersect with any potable water-table source. Certainly, it has been, and will continue to be, necessary in many instances to accept less than the ideal.
Paul Brown
Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892, USA
1 Will RG, Ironside JW, Zeidler M, et al. A new variant of Creutzfeldt-Jakob disease in the UK. Lancet 1996; 347: 921-25 [PubMed].
2 Bruce M, Will RG, Ironside JW, et al. Transmissions to mice indicate that 'new variant' CJD is caused by the BSE agent. Nature 1997: 389: 498-501.
3 Collinge J, Sidle KCL, Heads J, Ironside J, Hill AF. Molecular analysis of prion strain variation and the aetiology of 'new variant' CJD. Nature 1996; 383: 685-90 [PubMed].
4 Wells GAH, Hawkins SAC, Green RB, et al. Preliminary observations on the pathogenesis of experimental bovine spongiform encephalopathy (BSE): an update. Vet Rec 1998; 142: 103-06 [PubMed].
5 Collee JG, Bradley R. BSE: a decade on--part 2. Lancet 1997; 349: 715-21 [PubMed].
6 Taylor DM. Exposure to, and inactivation of, the unconventional agents that cause transmissible degenerative encephalopathies. In: Baker HF, Ridley RM, eds. Methods in molecular medicine: prion diseases. Totawa NJ: Humana Press, 1996: 105-18.
7 Brown P, Liberski PP, Wolff A, Gajdusek DC. Resistance of scrapie infectivity to steam autoclaving after formaldehyde fixation and limited survival after ashing at 360à °C: practical and theoretical implications, J Infect Dis 1990; 161: 467-72 [PubMed].
8 Palsson PA. Rida (scrapie) in Iceland and its epidemiology. In: Prusiner SB, Hadlow WJ, eds. Slow transmissible diseases of the nervous system, vol I. New York: Academic Press, 1979: 357-66.
9 Brown P, Gajdusek DC. Survival of scrapie virus after 3 years' interment. Lancet 1991; 337; 269-70.
10 Scrimgoeur EM, Brown P, Monaghan P. Disposal of rendered specified offal. Vet Rec 1996; 139: 219-20 [PubMed].
http://www.thelancet.com/newlancet/sub/issues/vol351no9110/body.commentary1146.html
snip...END...TSS
WISCONSIN CWD TSE PRION 2018
LISTEN TO THIS NICE LITTLE CWD BLUES DIDDY BY TAMI ABOUT WISCONSIN CWD TSE PRION. WOW, ANNUAL UPDATES NOW, FROM HERE ON OUT, ABOUT CWD...200,000 CWD TESTS, WITH OVER 3500 CWD POSITIVE CASES, SEEING INCREASING TRENDS IN PREVALENCE AND DISTRIBUTION...CARCASS DISPOSAL SIGNIFICANT CHALLENGE...CWD SAMPLING EFFORTS GONE DONE, WHILE CWD POSITIVES HAVE GONE UP...ALSO, 40 SELF SERVING KIOSKS ACROSS STATE AND FREE HUNTER SERVICE CWD TESTING AND SICK DEER POLICY REPORTING AND TESTING ACROSS STATE!
MONDAY, JUNE 25, 2018
Wisconsin DATCP Confirms CWD-Positive Elk in Sauk County Breeding Farm
MONDAY, JUNE 18, 2018
Wisconsin DATCP Confirms CWD-Positive Deer in Marinette County farm has been quarantined
WEDNESDAY, JUNE 13, 2018
Wisconsin DATCP NVSL confirmed 21 WTD from a deer farm Iowa County tested positive for chronic wasting disease (CWD)
SATURDAY, MARCH 03, 2018
WISCONSIN CHRONIC WASTING DISEASE TSE Prion DNR Study Finds CWD-Infected Deer Die At 3 Times Rate Of Healthy Animals
FRIDAY, FEBRUARY 16, 2018
Wisconsin Deer from Now-Quarantined PA Lancaster County Farm Tests Positive for Chronic Wasting Disease CWD TSE Prion
FRIDAY, JANUARY 26, 2018
WISCONSIN REPORTS 588 CWD TSE PRION POSITIVE CASES FOR 2017 WITH 4170 CASES CONFIRMED TO DATE
TSE PRION UPDATE September 4, 2018
TUESDAY, AUGUST 28, 2018
USDA finds BSE infection in Florida cow 08/28/18 6:43 PM
WEDNESDAY, AUGUST 29, 2018
USDA Announces Atypical Bovine Spongiform Encephalopathy Detection USDA 08/29/2018 10:00 AM EDT
WEDNESDAY, AUGUST 29, 2018
Transmissible Spongiform Encephalopathy TSE Prion Atypical BSE Confirmed Florida Update USA August 28, 2018
WEDNESDAY, AUGUST 29, 2018
OIE Bovine spongiform encephalopathy, United States of America Information received on 29/08/2018 from Dr John Clifford, Official Delegate, Chief Trade Advisor, APHIS USDA
''The event is resolved. No more reports will be submitted.''
well, so much for those herd mates exposed to this atypical BSE cow, and all those trace in and trace outs.
The OIE, USDA, and the BSE MRR policy is a joke, a sad, very sad joke...
THURSDAY, AUGUST 30, 2018
Florida Department of Agriculture and Consumer Services announced it is working closely with U.S. Department of Agriculture regarding an atypical case of Bovine Spongiform Encephalopathy BSE
THURSDAY, AUGUST 30, 2018
TRACKING HERD MATES USDA MAD COW DISEASE, TRACE FORWARD, TRACE BACK RECORDS, WHO CARES, NOT THE OIE
USDA ONLY TESTING 20k HEAD OF CATTLE A YEAR FOR MAD COW DISEASE ...LOL!
WEDNESDAY, AUGUST 29, 2018
USDA Announces Atypical Bovine Spongiform Encephalopathy Detection USDA 08/29/2018 10:00 AM EDT
WEDNESDAY, AUGUST 29, 2018
USDA DROPS MAD COW TESTING FROM 40K A YEAR TO JUST 20K A YEAR, IMPOSSIBLE TO FIND BSE, BUT THEY DID, IN FLORIDA!
SUNDAY, SEPTEMBER 23, 2018
Low-volume goat milk transmission of classical scrapie to lambs and goat kids
WEDNESDAY, SEPTEMBER 5, 2018
APHIS Concurrence With OIE Risk Designations for Bovine Spongiform Encephalopathy [Docket No. APHIS-2018-0012]
TUESDAY, SEPTEMBER 4, 2018
TUESDAY, SEPTEMBER 25, 2018
USDA Outlines Next Steps for Advancing Animal Disease Traceability LOL!
TUESDAY, JULY 03, 2018
Chronic Wasting Disease CWD TSE Prion Global Report Update, USA, CANADA, KOREA, NORWAY, FINLAND, Game Farms and Fake news
SUNDAY, APRIL 8, 2018
Transmissible Spongiform Encephalopathy TSE Prion Disease Global Pandemic Urgent Update April 9, 2018
TUESDAY, AUGUST 07, 2018
Passage of scrapie to deer results in a new phenotype upon return passage to sheep
***> NEW TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE (MAD CAMEL DISEASE) IN A NEW SPECIES <***
NEW OUTBREAK OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE IN A NEW SPECIES
Subject: Prion Disease in Dromedary Camels, Algeria
Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.
Wednesday, May 30, 2018
Dromedary camels in northern Africa have a neurodegenerative prion disease that may have originated decades ago
***> IMPORTS AND EXPORTS <***
SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN
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
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/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 efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/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
https://web.archive.org/web/20170126051158/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
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
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/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 efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
http://www.tandfonline.com/doi/abs/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
https://web.archive.org/web/20170126051158/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
ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE ???
here is the latest;
PRION 2018 CONFERENCE
Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice
Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge).
To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys.
Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years. After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles.
Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate. The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology. Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP. The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD.
***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***
READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT from this study ;
P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States
Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1) (1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA.
SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD states.
AND ANOTHER STUDY;
P172 Peripheral Neuropathy in Patients with Prion Disease
Wang H(1), Cohen M(1), Appleby BS(1,2) (1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio.
IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017, AND included 104 patients.
SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%), AND THAT The Majority of cases were male (60%), AND half of them had exposure to wild game.
snip...see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below...terry
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
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
just out CDC...see;
Research
Susceptibility of Human Prion Protein to Conversion by Chronic Wasting Disease Prions
Marcelo A. BarriaComments to Author , Adriana Libori, Gordon Mitchell, and Mark W. Head Author affiliations: National CJD Research and Surveillance Unit, University of Edinburgh, Edinburgh, Scotland, UK (M.A. Barria, A. Libori, M.W. Head); National and OIE Reference Laboratory for Scrapie and CWD, Canadian Food Inspection Agency, Ottawa, Ontario, Canada (G. Mitchell)
M. A. Barria et al.
ABSTRACT
Chronic wasting disease (CWD) is a contagious and fatal neurodegenerative disease and a serious animal health issue for deer and elk in North America. The identification of the first cases of CWD among free-ranging reindeer and moose in Europe brings back into focus the unresolved issue of whether CWD can be zoonotic like bovine spongiform encephalopathy. We used a cell-free seeded protein misfolding assay to determine whether CWD prions from elk, white-tailed deer, and reindeer in North America can convert the human prion protein to the disease-associated form. We found that prions can convert, but the efficiency of conversion is affected by polymorphic variation in the cervid and human prion protein genes. In view of the similarity of reindeer, elk, and white-tailed deer in North America to reindeer, red deer, and roe deer, respectively, in Europe, a more comprehensive and thorough assessment of the zoonotic potential of CWD might be warranted.
Molecular Barriers to Zoonotic Transmission of Prions
Marcelo A. Barria, Aru Balachandran, Masanori Morita, Tetsuyuki Kitamoto, Rona Barron, Jean Manson, Richard Knight, James W. Ironside, and Mark W. Headcorresponding author
snip...
The conversion of human PrPC by CWD brain homogenate in PMCA reactions was less efficient when the amino acid at position 129 was valine rather than methionine.
***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.
snip...
However, we can say with confidence that under the conditions used here, none of the animal isolates tested were as efficient as C-type BSE in converting human PrPC, which is reassuring.
***Less reassuring is the finding that there is no absolute barrier to the conversion of human PrPC by CWD prions in a protocol using a single round of PMCA and an entirely human substrate prepared from the target organ of prion diseases, the brain.
ZOONOTIC, ZOONOSIS, CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION
10. ZOONOTIC, ZOONOSIS, CHRONIC WASTING DISEASE CWD TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION AKA MAD DEER ELK DISEASE IN HUMANS, has it already happened, that should be the question...
''In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids.'' Scientific opinion on chronic wasting disease (II)
EFSA Panel on Biological Hazards (BIOHAZ) Antonia Ricci Ana Allende Declan Bolton Marianne Chemaly Robert Davies Pablo Salvador Fernández Escámez ... See all authors
First published: 17 January 2018 https://doi.org/10.2903/j.efsa.2018.5132 ;
also, see;
8. Even though human TSE‐exposure risk through consumption of game from European cervids can be assumed to be minor, if at all existing, no final conclusion can be drawn due to the overall lack of scientific data. In particular the US data do not clearly exclude the possibility of human (sporadic or familial) TSE development due to consumption of venison. The Working Group thus recognizes a potential risk to consumers if a TSE would be present in European cervids. It might be prudent considering appropriate measures to reduce such a risk, e.g. excluding tissues such as CNS and lymphoid tissues from the human food chain, which would greatly reduce any potential risk for consumers. However, it is stressed that currently, no data regarding a risk of TSE infections from cervid products are available.
snip...
The tissue distribution of infectivity in CWD‐infected cervids is now known to extend beyond CNS and lymphoid tissues. While the removal of these specific tissues from the food chain would reduce human dietary exposure to infectivity, exclusion from the food chain of the whole carcass of any infected animal would be required to eliminate human dietary exposure.
https://efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2018.5132
zoonosis zoonotic cervid tse prion cwd to humans, preparing for the storm
***An alternative to modeling the species barrier is the cell-free conversion assay which points to CWD as the animal prion disease with the greatest zoonotic potential, after (and very much less than) BSE.116***
https://www.tandfonline.com/doi/pdf/10.4161/pri.29237
To date there is no direct evidence that CWD has been or can be transmitted from animals to humans.
However, initial findings from a laboratory research project funded by the Alberta Prion Research Institute (APRI) and Alberta Livestock Meat Agency (ALMA), and led by a Canadian Food Inspection Agency (CFIA) scientist indicate that CWD has been transmitted to cynomolgus macaques (the non-human primate species most closely related to humans that may be used in research), through both the intracranial and oral routes of exposure.
Both infected brain and muscle tissues were found to transmit disease.
Health Canada’s Health Products and Food Branch (HPFB) was asked to consider the impact of these findings on the Branch’s current position on CWD in health products and foods.
Summary and Recommendation:
snip...
Health Portfolio partners were recently made aware of initial findings from a research project led by a CFIA scientist that have demonstrated that cynomolgus macaques can be infected via intracranial exposure and oral gavage with CWD infected muscle.
These findings suggest that CWD, under specific experimental conditions, has the potential to cross the human species barrier, including by enteral feeding of CWD infected muscle.
https://www.thetyee.ca/Documents/2017/06/24/Risk-Advisory-Opinion-CWD-2017.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
CDC CWD 2018 TRANSMISSION
https://www.cdc.gov/prions/cwd/transmission.html
TUESDAY, SEPTEMBER 12, 2017
CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat
http://chronic-wasting-disease.blogspot.com/2017/09/cdc-now-recommends-strongly-consider.html
SATURDAY, JANUARY 27, 2018
CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018
http://chronic-wasting-disease.blogspot.com/2018/01/cdc-chronic-wasting-disease-cwd-tse.html
Subject: CDC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE REPORT USA JANUARY 2018
CHRONIC WASTING DISEASE CWD TSE PRION IS THE USA AND NORTH AMERICA'S MAD COW DISEASE.
THE USDA INC ET AL WORKED VERY HARD CONCEALING BSE TSE PRION IN CATTLE. they almost succeeded $$$
BUT CWD TSE PRION IN CERVIDS IS A DIFFERENT BEAST, THE COVER UP THERE, USDA INC COULD NOT CONTAIN.
SPORADIC CJD IS 85%+ OF ALL HUMAN TSE PRION DISEASE.
SPORADIC CJD HAS NOW BEEN LINKED TO TYPICAL AND ATYPICAL BSE, SCRAPIE, AND CWD.
SPORADIC/SPONTANEOUS TSE HAS NEVER BEEN PROVEN.
***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.***
https://www.nature.com/articles/srep11573
CDC CWD TSE PRION UPDATE USA JANUARY 2018
As of January 2018, CWD in free-ranging deer, elk and/or moose has been reported in at least 22 states in the continental United States, as well as two provinces in Canada. In addition, CWD has been reported in reindeer and moose in Norway, and a small number of imported cases have been reported in South Korea. The disease has also been found in farmed deer and elk. CWD was first identified in captive deer in the late 1960s in Colorado and in wild deer in 1981. By the 1990s, it had been reported in surrounding areas in northern Colorado and southern Wyoming. Since 2000, the area known to be affected by CWD in free-ranging animals has increased to at least 22 states, including states in the Midwest, Southwest, and limited areas on the East Coast.. It is possible that CWD may also occur in other states without strong animal surveillance systems, but that cases haven’t been detected yet. Once CWD is established in an area, the risk can remain for a long time in the environment. The affected areas are likely to continue to expand. Nationwide, the overall occurrence of CWD in free-ranging deer and elk is relatively low. However, in several locations where the disease is established, infection rates may exceed 10 percent (1 in 10), and localized infection rates of more than 25 percent (1 in 4) have been reported. The infection rates among some captive deer can be much higher, with a rate of 79% (nearly 4 in 5) reported from at least one captive herd. As of January 2018, there were 186 counties in 22 states with reported CWD in free-ranging cervids..
Chronic Wasting Disease Among Free-Ranging Cervids by County, United States, January 2018
snip....
https://www.cdc.gov/prions/cwd/occurrence.html
*** 2017-2018 CWD TSE Prion UPDATE
https://www.cdc.gov/prions/cwd/occurrence.html
*** 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
Transmission Studies
Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}...TSS
resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.
snip...
https://web.archive.org/web/20090506002237/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf
Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿
Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations
In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.
http://jvi.asm.org/content/83/18/9608.full
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease
Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.
http://science.sciencemag.org/content/311/5764/1117.long
*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.
see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV
Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS
Thursday, April 03, 2008
A prion disease of cervids: Chronic wasting disease 2008 1: Vet Res. 2008 Apr 3;39(4):41 A prion disease of cervids: Chronic wasting disease Sigurdson CJ.
snip...
*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,
snip... full text ;
http://chronic-wasting-disease.blogspot.com/2008/04/prion-disease-of-cervids-chronic.html
> 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).***
http://www.tandfonline.com/doi/full/10.4161/pri.28124?src=recsys
http://www.tandfonline.com/doi/pdf/10.4161/pri.28124?needAccess=true
https://wwwnc.cdc.gov/eid/article/20/1/13-0858_article
SEE; Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey
Monday, May 23, 2011
CDC Assesses Potential Human Exposure to Prion Diseases Travel Warning
Public release date: 23-May-2011
Contact: Francesca Costanzo adajmedia@elsevier.com 215-239-3249 Elsevier Health Sciences
CDC assesses potential human exposure to prion diseases Study results reported in the Journal of the American Dietetic Association Philadelphia, PA, May 23, 2011 – Researchers from the Centers for Disease Control and Prevention (CDC) have examined the potential for human exposure to prion diseases, looking at hunting, venison consumption, and travel to areas in which prion diseases have been reported in animals. Three prion diseases in particular – bovine spongiform encephalopathy (BSE or “Mad Cow Disease”), variant Creutzfeldt-Jakob disease (vCJD), and chronic wasting disease (CWD) – were specified in the investigation. The results of this investigation are published in the June issue of the Journal of the American Dietetic Association.
“While prion diseases are rare, they are generally fatal for anyone who becomes infected. More than anything else, the results of this study support the need for continued surveillance of prion diseases,” commented lead investigator Joseph Y. Abrams, MPH, National Center for Emerging and Zoonotic Infectious Diseases, CDC, Atlanta.”But it’s also important that people know the facts about these diseases, especially since this study shows that a good number of people have participated in activities that may expose them to infection-causing agents.”
Although rare, human prion diseases such as CJD may be related to BSE. Prion (proteinaceous infectious particles) diseases are a group of rare brain diseases that affect humans and animals. When a person gets a prion disease, brain function is impaired. This causes memory and personality changes, dementia, and problems with movement. All of these worsen over time. These diseases are invariably fatal. Since these diseases may take years to manifest, knowing the extent of human exposure to possible prion diseases could become important in the event of an outbreak.
CDC investigators evaluated the results of the 2006-2007 population survey conducted by the Foodborne Diseases Active Surveillance Network (FoodNet). This survey collects information on food consumption practices, health outcomes, and demographic characteristics of residents of the participating Emerging Infections Program sites. The survey was conducted in Connecticut, Georgia, Maryland, Minnesota, New Mexico, Oregon, and Tennessee, as well as five counties in the San Francisco Bay area, seven counties in the Greater Denver area, and 34 counties in western and northeastern New York.
Survey participants were asked about behaviors that could be associated with exposure to the agents causing BSE and CWD, including travel to the nine countries considered to be BSE-endemic (United Kingdom, Republic of Ireland, France, Portugal, Switzerland, Italy, the Netherlands, Germany, Spain) and the cumulative length of stay in each of those countries. Respondents were asked if they ever had hunted for deer or elk, and if that hunting had taken place in areas considered to be CWD-endemic (northeastern Colorado, southeastern Wyoming or southwestern Nebraska). They were also asked if they had ever consumed venison, the frequency of consumption, and whether the meat came from the wild.
The proportion of survey respondents who reported travel to at least one of the nine BSE endemic countries since 1980 was 29.5%. Travel to the United Kingdom was reported by 19.4% of respondents, higher than to any other BSE-endemic country. Among those who traveled, the median duration of travel to the United Kingdom (14 days) was longer than that of any other BSE-endemic country. Travelers to the UK were more likely to have spent at least 30 days in the country (24.9%) compared to travelers to any other BSE endemic country. The prevalence and extent of travel to the UK indicate that health concerns in the UK may also become issues for US residents.
The proportion of survey respondents reporting having hunted for deer or elk was 18.5% and 1.2% reported having hunted for deer or elk in CWD-endemic areas. Venison consumption was reported by 67.4% of FoodNet respondents, and 88.6% of those reporting venison consumption had obtained all of their meat from the wild. These findings reinforce the importance of CWD surveillance and control programs for wild deer and elk to reduce human exposure to the CWD agent. Hunters in CWD-endemic areas are advised to take simple precautions such as: avoiding consuming meat from sickly deer or elk, avoiding consuming brain or spinal cord tissues, minimizing the handling of brain and spinal cord tissues, and wearing gloves when field-dressing carcasses.
According to Abrams, “The 2006-2007 FoodNet population survey provides useful information should foodborne prion infection become an increasing public health concern in the future. The data presented describe the prevalence of important behaviors and their associations with demographic characteristics. Surveillance of BSE, CWD, and human prion diseases are critical aspects of addressing the burden of these diseases in animal populations and how that may relate to human health.”
###
The article is “Travel history, hunting, and venison consumption related to prion disease exposure, 2006-2007 FoodNet population survey” by Joseph Y. Abrams, MPH; Ryan A. Maddox, MPH; Alexis R Harvey, MPH; Lawrence B. Schonberger, MD; and Ermias D. Belay, MD. It appears in the Journal of the American Dietetic Association, Volume 111, Issue 6 (June 2011) published by Elsevier.
In an accompanying podcast CDC’s Joseph Y. Abrams discusses travel, hunting, and eating venison in relation to prion diseases. It is available at http://adajournal.org/content/podcast.
http://www.eurekalert.org/pub_releases/2011-05/ehs-cap051811.php
Thursday, May 26, 2011
Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey
Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.
Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey
Joseph Y. Abrams, MPH, Ryan A. Maddox, MPH , Alexis R. Harvey, MPH , Lawrence B. Schonberger, MD , Ermias D. Belay, MD
Accepted 15 November 2010. Abstract Full Text PDF References .
Abstract
The transmission of bovine spongiform encephalopathy (BSE) to human beings and the spread of chronic wasting disease (CWD) among cervids have prompted concerns about zoonotic transmission of prion diseases. Travel to the United Kingdom and other European countries, hunting for deer or elk, and venison consumption could result in the exposure of US residents to the agents that cause BSE and CWD. The Foodborne Diseases Active Surveillance Network 2006-2007 population survey was used to assess the prevalence of these behaviors among residents of 10 catchment areas across the United States. Of 17,372 survey respondents, 19.4% reported travel to the United Kingdom since 1980, and 29.5% reported travel to any of the nine European countries considered to be BSE-endemic since 1980. The proportion of respondents who had ever hunted deer or elk was 18.5%, and 1.2% had hunted deer or elk in a CWD–endemic area. More than two thirds (67.4%) reported having ever eaten deer or elk meat. Respondents who traveled spent more time in the United Kingdom (median 14 days) than in any other BSE-endemic country. Of the 11,635 respondents who had consumed venison, 59.8% ate venison at most one to two times during their year of highest consumption, and 88.6% had obtained all of their meat from the wild. The survey results were useful in determining the prevalence and frequency of behaviors that could be important factors for foodborne prion transmission.
http://www.adajournal.org/article/S0002-8223(11)00278-1/abstract
PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;
Thursday, May 26, 2011
Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey
Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.
http://transmissiblespongiformencephalopathy.blogspot.com/2011/05/travel-history-hunting-and-venison.html
NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;
Wednesday, March 18, 2009
Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II
http://chronic-wasting-disease.blogspot.com/2009/03/noahs-ark-holding-llc-dawson-mn-recall.html
Transmissible Spongiform Encephalopathies
Spongiform Encephalopathy in Captive Wild ZOO BSE INQUIRY
https://web.archive.org/web/20090506001201/http://www.bseinquiry.gov.uk/files/mb/m09a/tab03.pdf
BSE INQUIRY
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane
BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended.. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
https://web.archive.org/web/20170126073306/http://collections..europarchive..org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf
Spongiform Encephalopathy in Captive Wild ZOO BSE INQUIRY
https://web.archive.org/web/20090506001201/http://www.bseinquiry.gov.uk/files/mb/m09a/tab03.pdf
BSE INQUIRY
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane
BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended.. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
http://web.archive.org/web/20030511010117/http://www.bseinquiry.gov.uk/files/yb/1994/10/00003001.pdf
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02).
The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
https://web.archive.org/web/20170126073306/http://collections..europarchive..org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1994/08/00004001.pdf
***> Prion 2018 P74 High Prevalence of CWD prions in male reproductive samples
Carlos Kramm (1,2), Ruben Gomez-Gutierrez (1,3), Tracy Nichols (4), Claudio Soto (1) and Rodrigo Morales (1)
READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT Protein Misfolding Cyclic Amplification PMCA results showed positive CWD prion detection in testes, epididymis and seminal fluid samples. seems also the scientists are worried about any potential mechanisms of CWD spreading and they want to decrease putative interindividual transmission associated to insemination using CWD contaminated specimens, if that might occur under natural conditions. i have been concerned about this for some time with BSE super-ovulation and since;
PrPSc detection and infectivity in semen from scrapie-infected sheep
PITUITARY EXTRACT
This was used to help cows super ovulate. This tissue was considered to be of greatest risk of containing BSE and consequently transmitting the disease...
This was used to help cows super ovulate. This tissue was considered to be of greatest risk of containing BSE and consequently transmitting the disease...
MANAGEMENT IN CONFIDENCE
CERTIFIED BSE-FREE HERDS FOR SOURCE OF MATERIAL FOR BIOLOGICAL PRODUCTS
Tuesday, February 8, 2011
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
HAVE YOU BEEN THUNDERSTRUCK?
SUNDAY, AUGUST 02, 2015
TEXAS CWD, Have you been ThunderStruck, deer semen, straw bred bucks, super ovulation, and the potential TSE Prion connection, what if?
Court papers state that in February 2007, Favero acquired 184 straws of whitetail deer semen valued at about $92,000 from a buck named “Diablo'” that he knew had been illegally taken out of Texas, and again in January 2008 took another 110 straws of semen from a buck named “Thunderstruck.” (Read more in the court paper posted at the bottom of this entry.)
TEXAS CONFIRMS 117TH CASE OF CWD TSE PRION
WEDNESDAY, AUGUST 22, 2018
TEXAS CWD TSE PRION 16 MORE CASES DETECTED TOTAL TO DATE 117 CONFIRMED NEW 14 BREEDERS 2 FREE RANGE
TUESDAY, SEPTEMBER 4, 2018
USA CJD, BSE, SCRAPIE, CWD, TSE PRION END OF YEAR REPORTS September 4, 2018
HUMAN MAD COW DISEASE nvCJD TEXAS CASE NOT LINKED TO EUROPEAN TRAVEL CDC
Sunday, November 23, 2014
Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas
Updated: October 7, 2014
CDC and the Texas Department of State Health Services (DSHS) have completed the investigation of the recently reported fourth vCJD case in the United States. It confirmed that the case was in a US citizen born outside the Americas and indicated that the patient's exposure to the BSE/vCJD agent most likely occurred before he moved to the United States; the patient had resided in Kuwait, Russia and Lebanon. The completed investigation did not support the patient's having had extended travel to European countries, including the United Kingdom, or travel to Saudi Arabia. The specific overseas country where this patient’s infection occurred is less clear largely because the investigation did not definitely link him to a country where other known vCJD cases likely had been infected.
https://www.cdc.gov/ncidod/dvrd/vcjd/other/confirmed-case-in-texas.htm
https://vcjd.blogspot.com/2014/11/confirmed-variant-creutzfeldt-jakob.html
Sunday, November 23, 2014
Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas
Updated: October 7, 2014
CDC and the Texas Department of State Health Services (DSHS) have completed the investigation of the recently reported fourth vCJD case in the United States. It confirmed that the case was in a US citizen born outside the Americas and indicated that the patient's exposure to the BSE/vCJD agent most likely occurred before he moved to the United States; the patient had resided in Kuwait, Russia and Lebanon. The completed investigation did not support the patient's having had extended travel to European countries, including the United Kingdom, or travel to Saudi Arabia. The specific overseas country where this patient’s infection occurred is less clear largely because the investigation did not definitely link him to a country where other known vCJD cases likely had been infected.
https://www.cdc.gov/ncidod/dvrd/vcjd/other/confirmed-case-in-texas.htm
https://vcjd.blogspot.com/2014/11/confirmed-variant-creutzfeldt-jakob.html
TUESDAY, JULY 31, 2018
USA CJD TSE Tables of Cases Examined National Prion Disease Pathology Surveillance Center Cases Examined May 1, 2018
http://prionunitusaupdate.blogspot.com/2018/07/usa-cjd-tse-tables-of-cases-examined.html
WEDNESDAY, SEPTEMBER 05, 2018
Edmonton woman one of the youngest diagnosed with CJD at 35 years old and pregnant
SATURDAY, SEPTEMBER 22, 2018
Emerging Diseases, Infection Control & California Dental Practice Act TSE PRION
Terry S. Singeltary Sr.
posted by Terry S. Singeltary Sr. at
3:31 PM
0 Comments:
Post a Comment
Subscribe to Post Comments [Atom]
<< Home