Friday, October 23, 2015

Ohio Wildlife Council Passes Rule to Help Monitor CWD

 

 
Sent: Friday, October 23, 2015 4:39 PM
Subject: Ohio Wildlife Council Passes Rule to Help Monitor CWD
 

Ohio Wildlife Council Passes Rule to Help Monitor CWD
 
Posted on 10/22/2015 by Division of Wildlife COLUMBUS, OH - The Ohio Wildlife Council passed a rule change that will allow the creation of disease surveillance areas to monitor chronic wasting disease (CWD) at its regularly scheduled meeting Wednesday, Oct. 21, according to the Ohio Department of Natural Resources (ODNR).
 
The rule permits the ODNR Division of Wildlife to establish a disease surveillance area when CWD has been detected. This designation, when enacted, will include all areas within a minimum of 6 miles surrounding a location where the disease has been detected. The designation will remain in effect for a minimum of three years and will be posted at wildohio.gov.
 
These regulations would apply within any CWD designated surveillance area:
 
• Required submission of harvested deer carcasses to ODNR Division of Wildlife inspection stations for sampling during the deer-gun and deer-muzzleloading seasons; • Prohibit the placement of or use of salt, mineral supplement, grain, fruit, vegetables or other feed to attract or feed deer; • Prohibit the hunting of deer by the aid of salt, mineral supplement, grain, fruit, vegetables or other feed; and • Prohibit the removal of a deer carcass killed by a motor vehicle, unless the carcass complies with the deer carcass regulations.
 
Normal agricultural activities, including feeding of domestic animals would not be affected. Hunting deer over food plots, naturally occurring or cultivated plants and agriculture crops would still be allowed.
 
Also on Wednesday, the council passed a rule to include the Eurasian collared-dove in the definition of migratory game birds and game birds. The council also amended a rule to permit the possession of Eurasian collared-doves in the field, consistent with the exemption for mourning doves. The Eurasian collared-dove is a non-native species that has spread rapidly across North America. In flight, it is very similar in appearance to mourning doves.
 
The council also voted to amend rules to require trotlines used in the inland fishing district, and all float lines used statewide, be tagged by the user with their name and address or their unique ODNR Division of Wildlife customer identification number.
 
In addition, rules were amended to update the list of areas owned by American Electric Power that require a special permit to fish under an agreement with the ODNR Division of Wildlife, and amend the language for possession of fish and fish fillets at Pymatuning Lake.
 
The council voted to establish a daily bag limit of 30 fish, combined for striped bass, hybrid-striped bass or white bass from waters other than in the Lake Erie sport fishing district. Of these 30 fish, a daily limit of four fish longer than 15 inches in length was approved. The location specific daily bag limits for hybrid-striped bass taken from East Fork Lake, and striped bass from Senecaville Lake and Kiser Lake were removed.
 
The northern long-eared bat is now listed as threatened in Ohio because of a change in its federal status to threatened.
 
The next Ohio Wildlife Council meeting will be on Wednesday, Nov. 18. Council meetings are open to the public. Individuals who want to provide comments to the council should preregister at least two days prior to the meeting by calling 614-265-6304. All comments must be three minutes or less. The next ODNR Division of Wildlife public open house will be Saturday, March 5, 2016. ODNR Division of Wildlife staff will be available to answer questions and listen to concerns. For more information, visit wildohio.gov or call 800-WILDLIFE (945-3543).
 
The Ohio Wildlife Council is an eight-member board that approves all ODNR Division of Wildlife proposed rules and regulations. Appointed by the Governor, no more than four members may be of the same political party, and two of the council members must represent agriculture. Each term of office is four years.
 
ODNR ensures a balance between wise use and protection of our natural resources for the benefit of all. Visit the ODNR website at ohiodnr.gov.
 
 
PrPSc Detection and Infectivity in Semen from Scrapie-Infected Sheep
 
Richard Rubenstein1,5, Marie S Bulgin2, Binggong Chang1, Sharon Sorensen-Melson2, Robert B Petersen3 and Giuseppe LaFauci4 + Author Affiliations
 
1 SUNY Downstate Medical Center, Brooklyn, NY, USA; 2 University of Idaho, Caldwell, ID, USA; 3 Case Western Reserve University, Cleveland, OH, USA; 4 NYS Institute for Basic Research in Developmental Disabilities, Staten Island, NY, USA ↵5 E-mail: richard.rubenstein@downstate.edu Received 13 October 2011. Accepted 3 February 2012.
 
Abstract
 
A scrapie-positive ewe was found in a flock that had been scrapie free for 13 years, but housed adjacent to scrapie-positive animals, separated by a wire fence. Live animal testing of the entire flock of 24 animals revealed 7 more subclinical scrapie-positive ewes. We hypothesized that they may have contracted the disease from scrapie-positive rams used for breeding four months prior, possibly through the semen. The genotypes of the ewe flock were highly scrapie-susceptible and the rams were infected with the "Caine" Scrapie Strain having a short incubation time of 4.3-14.6 mo. in sheep with 136/171 VQ/VQ and AQ/VQ genotypes. PrPSc accumulates in a variety of tissues in addition to the central nervous system. Although transmission of prion diseases, or transmissible spongiform encephalopathies, has been achieved via peripheral organ or tissue homogenates as well as by blood transfusion, neither infectivity nor PrPSc have been found in semen from scrapie-infected animals. Using serial protein misfolding cyclic amplification followed by a surround optical fiber immunoassay, we demonstrate that semen from rams infected with a short incubation time scrapie strain contains prion disease-associated seeding activity that generated PrPSc in sPMCA. Injection of the ovinized transgenic mouse line TgSShpPrP with semen from scrapie-infected sheep resulted in PrPSc seeding activity in clinical and, probably as a result of the low titer, nonclinical mouse brain. These results suggest that the transmissible agent, or at least the seeding activity, for sheep scrapie is present in semen. This may be a strain specific phenomenon.
 
 
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
 
 
$$$ PRICE OF CWD TSE PRION mad cow POKER GOES UP $$$
 
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
 
Title: Transmission of chronic wasting disease to sentinel reindeer (Rangifer tarandus tarandus)
 
Authors
 
item Moore, S - item Kunkle, Robert item Nicholson, Eric item Richt, Juergen item Hamir, Amirali item Waters, Wade item Greenlee, Justin
 
Submitted to: American College of Veterinary Pathologists Meeting Publication Type: Abstract Only Publication Acceptance Date: August 12, 2015 Publication Date: N/A
 
Technical Abstract: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of North American cervids. Reindeer (Rangifer tarandus tarandus) are susceptible to CWD following oral challenge, but CWD has not been reported in free-ranging caribou (Rangifer tarandus caribou) or farmed reindeer. Potential contact between CWD-affected cervids and Rangifer species that are free-ranging or co-housed on farms presents a potential risk of CWD transmission. The aims of this study were to 1) investigate the transmission of CWD from white-tailed deer (Odocoileus virginianus; CWD-wtd), mule deer (Odocoileus hemionus; CWD-md), or elk (Cervus elaphus nelsoni; CWD-elk) to reindeer via the intracranial route, and 2) to assess for direct and indirect horizontal transmission to non-inoculated sentinels. Three groups of 5 reindeer fawns were challenged intracranially with CWD-wtd, CWD-md, or CWD-elk. Two years after challenge of inoculated reindeer, non-inoculated control reindeer were introduced into the same pen as the CWD-wtd inoculated reindeer (n=4) or into a pen adjacent to the CWD-md inoculated reindeer (n=2). Reindeer were allowed to develop clinical disease. At death/euthanasia a complete necropsy examination was performed, including immunohistochemical testing of tissues for disease-associated CWD prion protein (PrP-CWD). Intracranially challenged reindeer developed clinical disease from 21 months post-inoculation (MPI). ***PrP-CWD was detected in 5/6 sentinel reindeer although only 2/6 developed clinical disease during the study period (<57 and="" are="" both="" can="" cervid="" cwd="" directly="" div="" from="" have="" indirectly.="" mpi="" naive="" reindeer="" shown="" sources="" susceptible="" that="" to="" transmit="" various="" we="">
 
 
***PrP-CWD was detected in 5/6 sentinel reindeer although only 2/6 developed clinical disease during the study period (<57 and="" are="" both="" can="" cervid="" cwd="" directly="" div="" from="" have="" indirectly.="" mpi="" naive="" reindeer="" shown="" sources="" susceptible="" that="" to="" transmit="" various="" we="">
 
HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES
 
snip...see more here;
 
Tuesday, September 29, 2015
 
*** Transmission of chronic wasting disease to sentinel reindeer (Rangifer tarandus tarandus) can transmit CWD to naive reindeer both directly and indirectly
 
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
 
 
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
 
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
 
 
*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
 
 
HIGHEST INFECTION RATE ON SEVERAL CWD CONFIRMED CAPTIVES
 
CHRONIC WASTING DISEASE CWD WISCONSIN Almond Deer (Buckhorn Flats) Farm Update DECEMBER 2011
 
The CWD infection rate was nearly 80%, the highest ever in a North American captive herd.
 
RECOMMENDATION: That the Board approve the purchase of 80 acres of land for $465,000 for the Statewide Wildlife Habitat Program in Portage County and approve the restrictions on public use of the site.
 
SUMMARY:
 
 
For Immediate Release Thursday, October 2, 2014
 
Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov
 
*** TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease
 
DES MOINES – The Iowa Department of Agriculture and Land Stewardship today announced that the test results from the depopulation of a quarantined captive deer herd in north-central Iowa showed that 284 of the 356 deer, or 79.8% of the herd, tested positive for Chronic Wasting Disease (CWD).
 
 
*** see history of this CWD blunder here ;
 
 
On June 5, 2013, DNR conducted a fence inspection, after gaining approval from surrounding landowners, and confirmed that the fenced had been cut or removed in at least four separate locations; that the fence had degraded and was failing to maintain the enclosure around the Quarantined Premises in at least one area; that at least three gates had been opened;and that deer tracks were visible in and around one of the open areas in the sand on both sides of the fence, evidencing movement of deer into the Quarantined Premises.
 
 
The overall incidence of clinical CWD in white-tailed deer was 82%
 
Species (cohort) CWD (cases/total) Incidence (%) Age at CWD death (mo)
 
 
”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province!” page 26.
 
 
Sunday, January 06, 2013
 
USDA TO PGC ONCE CAPTIVES ESCAPE
 
*** "it‘s no longer its business.”
 
 
CWD, spreading it around...
 
for the game farm industry, and their constituents, to continue to believe that they are _NOT_, and or insinuate that they have _NEVER_ been part of the problem, will only continue to help spread cwd. the game farming industry, from the shooting pens, to the urine mills, the antler mills, the sperm mills, velvet mills, shooting pens, to large ranches, are not the only problem, but it is painfully obvious that they have been part of the problem for decades and decades, just spreading it around, as with transportation and or exportation and or importation of cervids from game farming industry, and have been proven to spread cwd. no one need to look any further than South Korea blunder ;
 
===========================================
 
spreading cwd around...
 
Between 1996 and 2002, chronic wasting disease was diagnosed in 39 herds of farmed elk in Saskatchewan in a single epidemic. All of these herds were depopulated as part of the Canadian Food Inspection Agency’s (CFIA) disease eradication program. Animals, primarily over 12 mo of age, were tested for the presence CWD prions following euthanasia. Twenty-one of the herds were linked through movements of live animals with latent CWD from a single infected source herd in Saskatchewan, 17 through movements of animals from 7 of the secondarily infected herds.
 
***The source herd is believed to have become infected via importation of animals from a game farm in South Dakota where CWD was subsequently diagnosed (7,4). A wide range in herd prevalence of CWD at the time of herd depopulation of these herds was observed. Within-herd transmission was observed on some farms, while the disease remained confined to the introduced animals on other farms.
 
 
spreading cwd around...
 
Friday, May 13, 2011
 
Chronic Wasting Disease (CWD) outbreaks and surveillance program in the Republic of Korea
 
Hyun-Joo Sohn, Yoon-Hee Lee, Min-jeong Kim, Eun-Im Yun, Hyo-Jin Kim, Won-Yong Lee, Dong-Seob Tark, In- Soo Cho, Foreign Animal Disease Research Division, National Veterinary Research and Quarantine Service, Republic of Korea
 
Chronic wasting disease (CWD) has been recognized as an important prion disease in native North America deer and Rocky mountain elks. The disease is a unique member of the transmissible spongiform encephalopathies (TSEs), which naturally affects only a few species. CWD had been limited to USA and Canada until 2000.
 
On 28 December 2000, information from the Canadian government showed that a total of 95 elk had been exported from farms with CWD to Korea. These consisted of 23 elk in 1994 originating from the so-called “source farm” in Canada, and 72 elk in 1997, which had been held in pre export quarantine at the “source farm”.Based on export information of CWD suspected elk from Canada to Korea, CWD surveillance program was initiated by the Ministry of Agriculture and Forestry (MAF) in 2001.
 
All elks imported in 1997 were traced back, however elks imported in 1994 were impossible to identify. CWD control measures included stamping out of all animals in the affected farm, and thorough cleaning and disinfection of the premises. In addition, nationwide clinical surveillance of Korean native cervids, and improved measures to ensure reporting of CWD suspect cases were implemented.
 
Total of 9 elks were found to be affected. CWD was designated as a notifiable disease under the Act for Prevention of Livestock Epidemics in 2002.
 
Additional CWD cases - 12 elks and 2 elks - were diagnosed in 2004 and 2005.
 
Since February of 2005, when slaughtered elks were found to be positive, all slaughtered cervid for human consumption at abattoirs were designated as target of the CWD surveillance program. Currently, CWD laboratory testing is only conducted by National Reference Laboratory on CWD, which is the Foreign Animal Disease Division (FADD) of National Veterinary Research and Quarantine Service (NVRQS).
 
In July 2010, one out of 3 elks from Farm 1 which were slaughtered for the human consumption was confirmed as positive. Consequently, all cervid – 54 elks, 41 Sika deer and 5 Albino deer – were culled and one elk was found to be positive. Epidemiological investigations were conducted by Veterinary Epidemiology Division (VED) of NVRQS in collaboration with provincial veterinary services.
 
Epidemiologically related farms were found as 3 farms and all cervid at these farms were culled and subjected to CWD diagnosis. Three elks and 5 crossbreeds (Red deer and Sika deer) were confirmed as positive at farm 2.
 
All cervids at Farm 3 and Farm 4 – 15 elks and 47 elks – were culled and confirmed as negative.
 
Further epidemiological investigations showed that these CWD outbreaks were linked to the importation of elks from Canada in 1994 based on circumstantial evidences.
 
In December 2010, one elk was confirmed as positive at Farm 5. Consequently, all cervid – 3 elks, 11 Manchurian Sika deer and 20 Sika deer – were culled and one Manchurian Sika deer and seven Sika deer were found to be positive. This is the first report of CWD in these sub-species of deer. Epidemiological investigations found that the owner of the Farm 2 in CWD outbreaks in July 2010 had co-owned the Farm 5.
 
In addition, it was newly revealed that one positive elk was introduced from Farm 6 of Jinju-si Gyeongsang Namdo. All cervid – 19 elks, 15 crossbreed (species unknown) and 64 Sika deer – of Farm 6 were culled, but all confirmed as negative.
 
 
 
 
 
New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication
 
The infectious agents responsible for transmissible spongiform encephalopathy (TSE) are notoriously resistant to most physical and chemical methods used for inactivating pathogens, including heat. It has long been recognized, for example, that boiling is ineffective and that higher temperatures are most efficient when combined with steam under pressure (i.e., autoclaving). As a means of decontamination, dry heat is used only at the extremely high temperatures achieved during incineration, usually in excess of 600°C. It has been assumed, without proof, that incineration totally inactivates the agents of TSE, whether of human or animal origin.
 
 
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production
 
Histochemical analysis of hamster brains inoculated with the solid residue showed typical spongiform degeneration and vacuolation. Re-inoculation of these brains into a new cohort of hamsters led to onset of clinical scrapie symptoms within 75 days, suggesting that the specific infectivity of the prion protein was not changed during the biodiesel process. The biodiesel reaction cannot be considered a viable prion decontamination method for MBM, although we observed increased survival time of hamsters and reduced infectivity greater than 6 log orders in the solid MBM residue. Furthermore, results from our study compare for the first time prion detection by Western Blot versus an infectivity bioassay for analysis of biodiesel reaction products. We could show that biochemical analysis alone is insufficient for detection of prion infectivity after a biodiesel process.
 
 
Detection of protease-resistant cervid prion protein in water from a CWD-endemic area
 
The data presented here demonstrate that sPMCA can detect low levels of PrPCWD in the environment, corroborate previous biological and experimental data suggesting long term persistence of prions in the environment2,3 and imply that PrPCWD accumulation over time may contribute to transmission of CWD in areas where it has been endemic for decades. This work demonstrates the utility of sPMCA to evaluate other environmental water sources for PrPCWD, including smaller bodies of water such as vernal pools and wallows, where large numbers of cervids congregate and into which prions from infected animals may be shed and concentrated to infectious levels.
 
 
A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing
 
Keywords:Abattoir;bovine spongiform encephalopathy;QRA;scrapie;TSE
 
In this article the development and parameterization of a quantitative assessment is described that estimates the amount of TSE infectivity that is present in a whole animal carcass (bovine spongiform encephalopathy [BSE] for cattle and classical/atypical scrapie for sheep and lambs) and the amounts that subsequently fall to the floor during processing at facilities that handle specified risk material (SRM). BSE in cattle was found to contain the most oral doses, with a mean of 9864 BO ID50s (310, 38840) in a whole carcass compared to a mean of 1851 OO ID50s (600, 4070) and 614 OO ID50s (155, 1509) for a sheep infected with classical and atypical scrapie, respectively. Lambs contained the least infectivity with a mean of 251 OO ID50s (83, 548) for classical scrapie and 1 OO ID50s (0.2, 2) for atypical scrapie. The highest amounts of infectivity falling to the floor and entering the drains from slaughtering a whole carcass at SRM facilities were found to be from cattle infected with BSE at rendering and large incineration facilities with 7.4 BO ID50s (0.1, 29), intermediate plants and small incinerators with a mean of 4.5 BO ID50s (0.1, 18), and collection centers, 3.6 BO ID50s (0.1, 14). The lowest amounts entering drains are from lambs infected with classical and atypical scrapie at intermediate plants and atypical scrapie at collection centers with a mean of 3 × 10−7 OO ID50s (2 × 10−8, 1 × 10−6) per carcass. The results of this model provide key inputs for the model in the companion paper published here.
 
 
PL1
 
Using in vitro prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission.
 
Claudio Soto
 
Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston.
 
Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases.
 
=========================
 
***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease.
 
========================
 
Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.
 
 
see ;
 
 
 
 
 
 
98 | Veterinary Record | January 24, 2015
 
EDITORIAL
 
Scrapie: a particularly persistent pathogen
 
Cristina Acín
 
Resistant prions in the environment have been the sword of Damocles for scrapie control and eradication. Attempts to establish which physical and chemical agents could be applied to inactivate or moderate scrapie infectivity were initiated in the 1960s and 1970s,with the first study of this type focusing on the effect of heat treatment in reducing prion infectivity (Hunter and Millson 1964). Nowadays, most of the chemical procedures that aim to inactivate the prion protein are based on the method developed by Kimberlin and collaborators (1983). This procedure consists of treatment with 20,000 parts per million free chlorine solution, for a minimum of one hour, of all surfaces that need to be sterilised (in laboratories, lambing pens, slaughterhouses, and so on). Despite this, veterinarians and farmers may still ask a range of questions, such as ‘Is there an official procedure published somewhere?’ and ‘Is there an international organisation which recommends and defines the exact method of scrapie decontamination that must be applied?’
 
From a European perspective, it is difficult to find a treatment that could be applied, especially in relation to the disinfection of surfaces in lambing pens of affected flocks. A 999/2001 EU regulation on controlling spongiform encephalopathies (European Parliament and Council 2001) did not specify a particular decontamination measure to be used when an outbreak of scrapie is diagnosed. There is only a brief recommendation in Annex VII concerning the control and eradication of transmissible spongiform encephalopathies (TSE s).
 
Chapter B of the regulation explains the measures that must be applied if new caprine animals are to be introduced to a holding where a scrapie outbreak has previously been diagnosed. In that case, the statement indicates that caprine animals can be introduced ‘provided that a cleaning and disinfection of all animal housing on the premises has been carried out following destocking’.
 
Issues around cleaning and disinfection are common in prion prevention recommendations, but relevant authorities, veterinarians and farmers may have difficulties in finding the specific protocol which applies. The European Food and Safety Authority (EFSA ) published a detailed report about the efficacy of certain biocides, such as sodium hydroxide, sodium hypochlorite, guanidine and even a formulation of copper or iron metal ions in combination with hydrogen peroxide, against prions (EFSA 2009). The report was based on scientific evidence (Fichet and others 2004, Lemmer and others 2004, Gao and others 2006, Solassol and others 2006) but unfortunately the decontamination measures were not assessed under outbreak conditions.
 
The EFSA Panel on Biological Hazards recently published its conclusions on the scrapie situation in the EU after 10 years of monitoring and control of the disease in sheep and goats (EFSA 2014), and one of the most interesting findings was the Icelandic experience regarding the effect of disinfection in scrapie control. The Icelandic plan consisted of: culling scrapie-affected sheep or the whole flock in newly diagnosed outbreaks; deep cleaning and disinfection of stables, sheds, barns and equipment with high pressure washing followed by cleaning with 500 parts per million of hypochlorite; drying and treatment with 300 ppm of iodophor; and restocking was not permitted for at least two years. Even when all of these measures were implemented, scrapie recurred on several farms, indicating that the infectious agent survived for years in the environment, even as many as 16 years after restocking (Georgsson and others 2006).
 
In the rest of the countries considered in the EFSA (2014) report, recommendations for disinfection measures were not specifically defined at the government level. In the report, the only recommendation that is made for sheep is repopulation with sheep with scrapie-resistant genotypes. This reduces the risk of scrapie recurrence but it is difficult to know its effect on the infection.
 
Until the EFSA was established (in May 2003), scientific opinions about TSE s were provided by the Scientific Steering Committee (SSC) of the EC, whose advice regarding inactivation procedures focused on treating animal waste at high temperatures (150°C for three hours) and high pressure alkaline hydrolysis (SSC 2003). At the same time, the TSE Risk Management Subgroup of the Advisory Committee on Dangerous Pathogens (ACDP) in the UK published guidance on safe working and the prevention of TSE infection. Annex C of the ACDP report established that sodium hypochlorite was considered to be effective, but only if 20,000 ppm of available chlorine was present for at least one hour, which has practical limitations such as the release of chlorine gas, corrosion, incompatibility with formaldehyde, alcohols and acids, rapid inactivation of its active chemicals and the stability of dilutions (ACDP 2009).
 
In an international context, the World Organisation for Animal Health (OIE) does not recommend a specific disinfection protocol for prion agents in its Terrestrial Code or Manual. Chapter 4.13 of the Terrestrial Code, General recommendations on disinfection and disinsection (OIE 2014), focuses on foot-and-mouth disease virus, mycobacteria and Bacillus anthracis, but not on prion disinfection. Nevertheless, the last update published by the OIE on bovine spongiform encephalopathy (OIE 2012) indicates that few effective decontamination techniques are available to inactivate the agent on surfaces, and recommends the removal of all organic material and the use of sodium hydroxide, or a sodium hypochlorite solution containing 2 per cent available chlorine, for more than one hour at 20ºC.
 
The World Health Organization outlines guidelines for the control of TSE s, and also emphasises the importance of mechanically cleaning surfaces before disinfection with sodium hydroxide or sodium hypochlorite for one hour (WHO 1999).
 
Finally, the relevant agencies in both Canada and the USA suggest that the best treatments for surfaces potentially contaminated with prions are sodium hydroxide or sodium hypochlorite at 20,000 ppm. This is a 2 per cent solution, while most commercial household bleaches contain 5.25 per cent sodium hypochlorite. It is therefore recommended to dilute one part 5.25 per cent bleach with 1.5 parts water (CDC 2009, Canadian Food Inspection Agency 2013).
 
So what should we do about disinfection against prions? First, it is suggested that a single protocol be created by international authorities to homogenise inactivation procedures and enable their application in all scrapie-affected countries. Sodium hypochlorite with 20,000 ppm of available chlorine seems to be the procedure used in most countries, as noted in a paper summarised on p 99 of this issue of Veterinary Record (Hawkins and others 2015). But are we totally sure of its effectiveness as a preventive measure in a scrapie outbreak? Would an in-depth study of the recurrence of scrapie disease be needed?
 
What we can conclude is that, if we want to fight prion diseases, and specifically classical scrapie, we must focus on the accuracy of diagnosis, monitoring and surveillance; appropriate animal identification and control of movements; and, in the end, have homogeneous and suitable protocols to decontaminate and disinfect lambing barns, sheds and equipment available to veterinarians and farmers. Finally, further investigations into the resistance of prion proteins in the diversity of environmental surfaces are required.
 
References
 
snip...
 
98 | Veterinary Record | January 24, 2015
 
 
Persistence of ovine scrapie infectivity in a farm environment following cleaning and decontamination
 
Steve A. C. Hawkins, MIBiol, Pathology Department1, Hugh A. Simmons, BVSc MRCVS, MBA, MA Animal Services Unit1, Kevin C. Gough, BSc, PhD2 and Ben C. Maddison, BSc, PhD3 + Author Affiliations
 
1Animal and Plant Health Agency, Woodham Lane, New Haw, Addlestone, Surrey KT15 3NB, UK 2School of Veterinary Medicine and Science, The University of Nottingham, Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK 3ADAS UK, School of Veterinary Medicine and Science, The University of Nottingham, Sutton Bonington, Loughborough, Leicestershire LE12 5RD, UK E-mail for correspondence: ben.maddison@adas.co.uk Abstract Scrapie of sheep/goats and chronic wasting disease of deer/elk are contagious prion diseases where environmental reservoirs are directly implicated in the transmission of disease. In this study, the effectiveness of recommended scrapie farm decontamination regimens was evaluated by a sheep bioassay using buildings naturally contaminated with scrapie. Pens within a farm building were treated with either 20,000 parts per million free chorine solution for one hour or were treated with the same but were followed by painting and full re-galvanisation or replacement of metalwork within the pen. Scrapie susceptible lambs of the PRNP genotype VRQ/VRQ were reared within these pens and their scrapie status was monitored by recto-anal mucosa-associated lymphoid tissue. All animals became infected over an 18-month period, even in the pen that had been subject to the most stringent decontamination process. These data suggest that recommended current guidelines for the decontamination of farm buildings following outbreaks of scrapie do little to reduce the titre of infectious scrapie material and that environmental recontamination could also be an issue associated with these premises.
 
SNIP...
 
Discussion
 
Thorough pressure washing of a pen had no effect on the amount of bioavailable scrapie infectivity (pen B). The routine removal of prions from surfaces within a laboratory setting is treatment for a minimum of one hour with 20,000 ppm free chlorine, a method originally based on the use of brain macerates from infected rodents to evaluate the effectiveness of decontamination (Kimberlin and others 1983). Further studies have also investigated the effectiveness of hypochlorite disinfection of metal surfaces to simulate the decontamination of surgical devices within a hospital setting. Such treatments with hypochlorite solution were able to reduce infectivity by 5.5 logs to lower than the sensitivity of the bioassay used (Lemmer and others 2004). Analogous treatment of the pen surfaces did not effectively remove the levels of scrapie infectivity over that of the control pens, indicating that this method of decontamination is not effective within a farm setting. This may be due to the high level of biological matrix that is present upon surfaces within the farm environment, which may reduce the amount of free chlorine available to inactivate any infectious prion. Remarkably 1/5 sheep introduced into pen D had also became scrapie positive within nine months, with all animals in this pen being RAMALT positive by 18 months of age. Pen D was no further away from the control pen (pen A) than any of the other pens within this barn. Localised hot spots of infectivity may be present within scrapie-contaminated environments, but it is unlikely that pen D area had an amount of scrapie contamination that was significantly different than the other areas within this building. Similarly, there were no differences in how the biosecurity of pen D was maintained, or how this pen was ventilated compared with the other pens. This observation, perhaps, indicates the slower kinetics of disease uptake within this pen and is consistent with a more thorough prion removal and recontamination. These observations may also account for the presence of inadvertent scrapie cases within other studies, where despite stringent biosecurity, control animals have become scrapie positive during challenge studies using barns that also housed scrapie-affected animals (Ryder and others 2009). The bioassay data indicate that the exposure of the sheep to a farm environment after decontamination efforts thought to be effective in removing scrapie is sufficient for the animals to become infected with scrapie. The main exposure routes within this scenario are likely to be via the oral route, during feeding and drinking, and respiratory and conjunctival routes. It has been demonstrated that scrapie infectivity can be efficiently transmitted via the nasal route in sheep (Hamir and others 2008), as is the case for CWD in both murine models and in white-tailed deer (Denkers and others 2010, 2013). Recently, it has also been demonstrated that CWD prions presented as dust when bound to the soil mineral montmorillonite can be infectious via the nasal route (Nichols and others 2013). When considering pens C and D, the actual source of the infectious agent in the pens is not known, it is possible that biologically relevant levels of prion survive on surfaces during the decontamination regimen (pen C). With the use of galvanising and painting (pen D) covering and sealing the surface of the pen, it is possible that scrapie material recontaminated the pens by the movement of infectious prions contained within dusts originating from other parts of the barn that were not decontaminated or from other areas of the farm.
 
Given that scrapie prions are widespread on the surfaces of affected farms (Maddison and others 2010a), irrespective of the source of the infectious prions in the pens, this study clearly highlights the difficulties that are faced with the effective removal of environmentally associated scrapie infectivity. This is likely to be paralleled in CWD which shows strong similarities to scrapie in terms of both the dissemination of prions into the environment and the facile mode of disease transmission. These data further contribute to the understanding that prion diseases can be highly transmissible between susceptible individuals not just by direct contact but through highly stable environmental reservoirs that are refractory to decontamination.
 
The presence of these environmentally associated prions in farm buildings make the control of these diseases a considerable challenge, especially in animal species such as goats where there is lack of genetic resistance to scrapie and, therefore, no scope to re-stock farms with animals that are resistant to scrapie.
 
Scrapie Sheep Goats Transmissible spongiform encephalopathies (TSE) Accepted October 12, 2014. Published Online First 31 October 2014
 
 
Monday, November 3, 2014
 
Persistence of ovine scrapie infectivity in a farm environment following cleaning and decontamination
 
 
PPo3-22:
 
Detection of Environmentally Associated PrPSc on a Farm with Endemic Scrapie
 
Ben C. Maddison,1 Claire A. Baker,1 Helen C. Rees,1 Linda A. Terry,2 Leigh Thorne,2 Susan J. Belworthy2 and Kevin C. Gough3 1ADAS-UK LTD; Department of Biology; University of Leicester; Leicester, UK; 2Veterinary Laboratories Agency; Surry, KT UK; 3Department of Veterinary Medicine and Science; University of Nottingham; Sutton Bonington, Loughborough UK
 
Key words: scrapie, evironmental persistence, sPMCA
 
Ovine scrapie shows considerable horizontal transmission, yet the routes of transmission and specifically the role of fomites in transmission remain poorly defined. Here we present biochemical data demonstrating that on a scrapie-affected sheep farm, scrapie prion contamination is widespread. It was anticipated at the outset that if prions contaminate the environment that they would be there at extremely low levels, as such the most sensitive method available for the detection of PrPSc, serial Protein Misfolding Cyclic Amplification (sPMCA), was used in this study. We investigated the distribution of environmental scrapie prions by applying ovine sPMCA to samples taken from a range of surfaces that were accessible to animals and could be collected by use of a wetted foam swab. Prion was amplified by sPMCA from a number of these environmental swab samples including those taken from metal, plastic and wooden surfaces, both in the indoor and outdoor environment. At the time of sampling there had been no sheep contact with these areas for at least 20 days prior to sampling indicating that prions persist for at least this duration in the environment. These data implicate inanimate objects as environmental reservoirs of prion infectivity which are likely to contribute to disease transmission.
 
 
Willingham, Erin McNulty, Kelly Anderson, Jeanette Hayes-Klug, Amy Nalls, and Candace Mathiason Colorado State University; Fort Collins, CO USA
 
Chronic wasting disease (CWD) is the transmissible spongiform encephalopathy (TSE), of free-ranging and captive cervids (deer, elk and moose).
 
The presence of infectious prions in the tissues, bodily fluids and environments of clinical and preclinical CWD-infected animals is thought to account for its high transmission efficiency. Recently it has been recognized that mother to offspring transmission may contribute to the facile transmission of some TSEs. Although the mechanism behind maternal transmission is not yet known, the extended asymptomatic TSE carrier phase (lasting years to decades) suggests that it may have implications in the spread of prions.
 
Placental trafficking and/or secretion in milk are 2 means by which maternal prion transmission may occur. In these studies we explore these avenues during early and late infection using a transgenic mouse model expressing cervid prion protein. Na€ıve and CWD-infected dams were bred at both timepoints, and were allowed to bear and raise their offspring. Milk was collected from the dams for prion analysis, and the offspring were observed for TSE disease progression. Terminal tissues harvested from both dams and offspring were analyzed for prions.
 
We have demonstrated that
 
(1) CWDinfected TgCerPRP females successfully breed and bear offspring, and
 
(2) the presence of PrPCWD in reproductive and mammary tissue from CWD-infected dams.
 
We are currently analyzing terminal tissue harvested from offspring born to CWD-infected dams for the detection of PrPCWD and amplification competent prions. These studies will provide insight into the potential mechanisms and biological significance associated with mother to offspring transmission of TSEs.
 
==============
 
P.157: Uptake of prions into plants
 
Christopher Johnson1, Christina Carlson1, Matthew Keating1,2, Nicole Gibbs1, Haeyoon Chang1, Jamie Wiepz1, and Joel Pedersen1 1USGS National Wildlife Health Center; Madison, WI USA; 2University of Wisconsin - Madison; Madison, WI USA
 
Soil may preserve chronic wasting disease (CWD) and scrapie infectivity in the environment, making consumption or inhalation of soil particles a plausible mechanism whereby na€ıve animals can be exposed to prions. Plants are known to absorb a variety of substances from soil, including whole proteins, yet the potential for plants to take up abnormal prion protein (PrPTSE) and preserve prion infectivity is not known. In this study, we assessed PrPTSE uptake into roots using laser scanning confocal microscopy with fluorescently tagged PrPTSE and we used serial protein misfolding cyclic amplification (sPMCA) and detect and quantify PrPTSE levels in plant aerial tissues. Fluorescence was identified in the root hairs of the model plant Arabidopsis thaliana, as well as the crop plants alfalfa (Medicago sativa), barley (Hordeum vulgare) and tomato (Solanum lycopersicum) upon exposure to tagged PrPTSE but not a tagged control preparation. Using sPMCA, we found evidence of PrPTSE in aerial tissues of A. thaliana, alfalfa and maize (Zea mays) grown in hydroponic cultures in which only roots were exposed to PrPTSE. Levels of PrPTSE in plant aerial tissues ranged from approximately 4 £ 10 ¡10 to 1 £ 10 ¡9 g PrPTSE g ¡1 plant dry weight or 2 £ 105 to 7 £ 106 intracerebral ID50 units g ¡1 plant dry weight. Both stems and leaves of A. thaliana grown in culture media containing prions are infectious when intracerebrally-injected into mice. ***Our results suggest that prions can be taken up by plants and that contaminated plants may represent a previously unrecognized risk of human, domestic species and wildlife exposure to prions.
 
===========
 
***Our results suggest that prions can be taken up by plants and that contaminated plants may represent a previously unrecognized risk of human, domestic species and wildlife exposure to prions.***
 
SEE ;
 
Friday, May 15, 2015
 
Grass Plants Bind, Retain, Uptake, and Transport Infectious Prions
 
Report
 
 
============
 
P.19: Characterization of chronic wasting disease isolates from freeranging deer (Odocoileus sp) in Alberta and Saskatchewan, Canada
 
Camilo Duque Velasquez1, Chiye Kim1, Nathalie Daude1, Jacques van der Merwe1, Allen Herbst1, Trent Bollinger2, Judd Aiken1, and Debbie McKenzie1 1Centre for Prions and Protein Folding Diseases; University of Alberta; Edmonton, Canada; 2Western College of Veterinary Medicine; University of Saskatchewan; Saskatoon, Canada
 
Chronic wasting disease (CWD) is an emerging prion disease of free ranging and captive species of Cervidae. In North America, CWD is enzootic in some wild cervid populations and can circulate among different deer species. The contagious nature of CWD prions and the variation of cervid PRNP alleles, which influence host susceptibility, can result in the emergence and adaptation of different CWD strains. These strains may impact transmission host range, disease diagnosis, spread dynamics and efficacy of potential vaccines. We are characterizing different CWD agents by biochemical analysis of the PrPCWD conformers, propagation in vitro cell assays1 and by comparing transmission properties and neuropathology in Tg33 (Q95G96) and Tg60 (Q95S96) mice.2 Although Tg60 mice expressing S96- PrPC have been shown resistant to CWD infectivity from various cervid species,2,3
 
***these transgenic mice are susceptible to H95 C CWD, a CWD strain derived from experimental infection of deer expressing H95G96-PrPC. The diversity of strains present in free-ranging mule deer (Odocoileus hemionus) and white-tailed deer (Odocoileus virginianus) from Alberta and Saskatchewan is being determined and will allow us to delineate the properties of CWD agents circulating in CWD enzootic cervid populations of Canada.
 
References
 
1. van der Merwe J, Aiken J, Westaway D, McKenzie D. The standard scrapie cell assay: Development, utility and prospects. Viruses 2015; 7(1):180–198; PMID:25602372; http://dx.doi.org/10.3390/v7010180
 
2. Meade-White K, Race B, Trifilo M, Bossers A, Favara C, Lacasse R, Miller M, Williams E, Oldstone M, Race R, Chesebro B. Resistance to chronic wasting disease in transgenic mice expressing a naturally occurring allelic variant of deer prion protein. J Virol 2007; 81(9):4533–4539; PMID: 17314157; http://dx. doi.org/10.1128/JVI.02762-06
 
3. Race B, Meade-White K, Miller MW, Fox KA, Chesebro B. In vivo comparison of chronic wasting disease infectivity from deer with variation at prion protein residue 96. J Virol 2011; 85(17):9235–9238; PMID: 21697479; http://dx.doi.org/10.1128/JVI.00790-11
 
=========
 
***these transgenic mice are susceptible to H95 C CWD, a CWD strain derived from experimental infection of deer expressing H95G96-PrPC.
 
==========
 
P.136: Mother to offspring transmission of CWD—Detection in fawn tissues using the QuIC assay
 
Amy Nalls, Erin McNulty, Clare Hoover, Jeanette Hayes-Klug, Kelly Anderson, Edward Hoover, and Candace Mathiason Colorado State University; Fort Collins, CO USA
 
To investigate the role mother to offspring transmission plays in chronic wasting disease (CWD), we have employed a small, polyestrous breeding, indoor maintainable cervid model, the Reeves’ muntjac deer. Muntjac doe were inoculated with CWD and tested positive by lymphoid biopsy at 4 months post inoculation. From these CWD-infected doe, we obtained 3 viable fawns. These fawns tested IHC-positive for CWD by lymphoid biopsy as early as 40 d post birth, and all have been euthanized due to clinical disease at 31, 34 and 59 months post birth. The QuIC assay demonstrates sensitivity and specificity in the detection of conversion competent prions in peripheral IHC-positive tissues including tonsil, mandibular, partotid, retropharyngeal, and prescapular lymph nodes, adrenal gland, spleen and liver. In summary, using the muntjac deer model, we have demonstrated CWD clinical disease in offspring born to CWD-infected doe and found that the QuIC assay is an effective tool in the detection of prions in peripheral tissues. ***Our findings demonstrate that transmission of prions from mother to offspring can occur, and may be underestimated for all prion diseases.
 
===============
 
***Our findings demonstrate that transmission of prions from mother to offspring can occur, and may be underestimated for all prion diseases.
 
===============
 
 
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. ***
 
P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification
 
Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama National Institute of Animal Health; Tsukuba, Japan
 
To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplification (PMCA).
 
Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.
 
Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, ***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.
 
================
 
 
 
P.97: Scrapie transmits to white-tailed deer by the oral route and has a molecular profile similar to chronic wasting disease and distinct from the scrapie inoculum
 
Justin Greenlee1, S Jo Moore1, Jodi Smith1, M Heather West Greenlee2, and Robert Kunkle1 1National Animal Disease Center; Ames, IA USA; 2Iowa State University; Ames, IA USA
 
The purpose of this work was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and chronic wasting disease (CWD). We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n D 5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. In cervidized mice, the 2 inocula have distinct incubation times. Sheep inoculated intranasally with WTD derived scrapie developed disease, but only after inoculation with the inoculum that had a scrapie-like profile. The WTD study is ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, 2 distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.
 
 
Saturday, January 31, 2015
 
European red deer (Cervus elaphus elaphus) are susceptible to Bovine Spongiform Encephalopathy BSE by Oral Alimentary route
 
 
I strenuously once again urge the FDA and its industry constituents, to make it MANDATORY that all ruminant feed be banned to all ruminants, and this should include all cervids as soon as possible for the following reasons...
 
======
 
In the USA, under the Food and Drug Administrations BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system.
 
***However, this recommendation is guidance and not a requirement by law.
 
======
 
31 Jan 2015 at 20:14 GMT
 
*** Ruminant feed ban for cervids in the United States? ***
 
31 Jan 2015 at 20:14 GMT
 
 
Saturday, September 12, 2015
 
In utero transmission and tissue distribution of chronic wasting disease-associated prions in free-ranging Rocky Mountain elk
 
>>>Interestingly, five of fifteen sPMCA positive dams showed no evidence of PrPCWD in either CNS or LRS, sites typically assessed in diagnosing CWD. Analysis of fetal tissues harvested from the fifteen sPMCA positive dams revealed PrPCWD in 80% of fetuses (12/15), regardless of gestational stage. These findings demonstrate that PrPCWD is more abundant in peripheral tissues of CWD exposed elk than current diagnostic methods suggest, and that transmission of prions from mother to offspring may contribute to the efficient transmission of the CWD in naturally exposed cervid populations.<<<
 
 
***S P O N T A N E O U S***S P O R A D I C***
 
spontaneous atypical BSE ???
 
if that's the case, then France is having one hell of an epidemic of atypical BSE, probably why they stopped testing for BSE, problem solved $$$
 
As of December 2011, around 60 atypical BSE cases have currently been reported in 13 countries, *** with over one third in France.
 
 
so 20 cases of atypical BSE in France, compared to the remaining 40 cases in the remaining 12 Countries, divided by the remaining 12 Countries, about 3+ cases per country, besides Frances 20 cases. you cannot explain this away with any spontaneous BSe. ...TSS
 
Sunday, October 5, 2014
 
France stops BSE testing for Mad Cow Disease
 
 
*** spontaneous TSE prion, that's wishful thinking. on the other hand, if spontaneous did ever happen (never once documented in the field), it would be our worst nightmare, due to feed. just saying.
 
*** We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes. ***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.***
 
***>>> 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. <<<***
 
 
 
PRION 2015 CONFERENCE FT. COLLINS CWD RISK FACTORS TO HUMANS
 
*** LATE-BREAKING ABSTRACTS PRION 2015 CONFERENCE ***
 
O18
 
Zoonotic Potential of CWD Prions
 
Liuting Qing1, Ignazio Cali1,2, Jue Yuan1, Shenghai Huang3, Diane Kofskey1, Pierluigi Gambetti1, Wenquan Zou1, Qingzhong Kong1 1Case Western Reserve University, Cleveland, Ohio, USA, 2Second University of Naples, Naples, Italy, 3Encore Health Resources, Houston, Texas, USA
 
***These results indicate that the CWD prion has the potential to infect human CNS and peripheral lymphoid tissues and that there might be asymptomatic human carriers of CWD infection.***
 
P.105: RT-QuIC models trans-species prion transmission
 
Kristen Davenport, Davin Henderson, Candace Mathiason, and Edward Hoover Prion Research Center; Colorado State University; Fort Collins, CO USA
 
Additionally, human rPrP was competent for conversion by CWD and fCWD.
 
***This insinuates that, at the level of protein:protein interactions, the barrier preventing transmission of CWD to humans is less robust than previously estimated.***
 
 
From: Terry S. Singeltary Sr.
 
Sent: Saturday, November 15, 2014 9:29 PM
 
To: Terry S. Singeltary Sr.
 
Subject: THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE R. G. WILL 1984
 
THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE
 
R. G. WILL
 
1984
 
*** 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). (SEE LINK IN REPORT HERE...TSS) PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;
 
snip...
 
 
*** 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).***
 
 
*** 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.
 
 
now, let’s see what the authors said about this casual link, personal communications years ago. 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 ;
 
 
July's Milwaukee Journal Sentinel article did prod state officials to ask CDC to investigate the cases of the three men who shared wild game feasts. The two men the CDC is still investigating were 55 and 66 years old. But there's also Kevin Boss, a Minnesota hunter who ate Barron County venison and died of CJD at 41. And there's Jeff Schwan, whose Michigan Tech fraternity brothers used to bring venison sausage back to the frat house. His mother, Terry, says that in May 2001, Jeff, 26, began complaining about his vision. A friend noticed misspellings in his e-mail, which was totally unlike him. Jeff began losing weight. He became irritable and withdrawn. By the end of June, he couldn't remember the four-digit code to open the garage door or when and how to feed his parents' cats. At a family gathering in July, he stuck to his parents and girlfriend, barely talking. "On the night we took him to the hospital, he was speaking like he was drunk or high and I noticed his pupils were so dilated I couldn't see the irises," his mother says. By then, Jeff was no longer able to do even simple things on his computer at work, and "in the hospital, he couldn't drink enough water." When he died on September 27, 2001, an autopsy confirmed he had sporadic CJD.
 
In 2000, Belay looked into three CJD cases reported by The Denver Post, two hunters who ate meat from animals killed in Wyoming and the daughter of a hunter who ate venison from a plant that processed Colorado elk. All three died of CJD before they were 30 years old. The CDC asked the USDA to kill 1,000 deer and elk in the area where the men hunted. Belay and others reported their findings in the Archives of Neurology, writing that although "circumstances suggested a link between the three cases and chronic wasting disease, they could find no 'causal' link." Which means, says Belay, "not a single one of those 1,000 deer tested positive for CWD. For all we know, these cases may be CWD. What we have now doesn't indicate a connection. That's reassuring, but it would be wrong to say it will never happen."
 
So far, says NIH researcher Race, the two Wisconsin cases pinpointed by the newspaper look like spontaneous CJD. "But we don't know how CWD would look in human brains. It probably would look like some garden-variety sporadic CJD." What the CDC will do with these cases and four others (three from Colorado and Schwan from Upper Michigan), Race says, is "sequence the prion protein from these people, inject it into mice and wait to see what the disease looks like in their brains. That will take two years."
 
CJD is so rare in people under age 30, one case in a billion (leaving out medical mishaps), that four cases under 30 is "very high," says Colorado neurologist Bosque. "Then, if you add these other two from Wisconsin [cases in the newspaper], six cases of CJD in people associated with venison is very, very high." Only now, with Mary Riley, there are at least seven, and possibly eight, with Steve, her dining companion. "It's not critical mass that matters," however, Belay says. "One case would do it for me." The chance that two people who know each other would both contact CJD, like the two Wisconsin sportsmen, is so unlikely, experts say, it would happen only once in 140 years.
 
Given the incubation period for TSEs in humans, it may require another generation to write the final chapter on CWD in Wisconsin. "Does chronic wasting disease pass into humans? We'll be able to answer that in 2022," says Race. Meanwhile, the state has become part of an immense experiment.
 
 
I urge everyone to watch this video closely...terry
 
*** you can see video here and interview with Jeff's Mom, and scientist telling you to test everything and potential risk factors for humans ***
 
 
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, Val erie 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 longe 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...TSS
 
===============
 
 
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.
 
 
Tuesday, May 26, 2015
 
*** Minimise transmission risk of CJD and vCJD in healthcare settings ***
 
Last updated 15 May 2015
 
 
 
*** Creutzfeldt-Jakob Disease *** Public Health Crisis VIDEO
 
 
 
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
 
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
 
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
 
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
 
Terry S. Singeltary, Sr Bacliff, Tex
 
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.
 
 
 
cwd to humans, consumption, exposure, sub-clinical, iatrogenic, what if ?
 
Sunday, August 23, 2015
 
TAHC Chronic Wasting Disease CWD TSE Prion and how to put lipstick on a pig and take her to the dance in Texas
 
from the other side of the fence... today’s Singeltary Sunday School class ‘thinking outside of the box, God’s Wrath’ at the bottom. ...tss
 
 
TEXAS DEER CZAR SENT TO WISCONSIN TO SOLVE CWD CRISIS, WHILE ROME (TEXAS) BURNS
 
Tuesday, August 11, 2015
 
Wisconsin doing what it does best, procrastinating about CWD yet again thanks to Governor Walker
 
 
Wednesday, March 18, 2015
 
*** Chronic Wasting Disease CWD Confirmed Texas Trans Pecos March 18, 2015
 
 
Wednesday, March 25, 2015
 
*** Chronic Wasting Disease CWD Cases Confirmed In New Mexico 2013 and 2014 UPDATE 2015
 
 
Wednesday, July 01, 2015
 
*** TEXAS Chronic Wasting Disease Detected in Medina County Captive Deer
 
 
Tuesday, July 21, 2015
 
*** Texas CWD Medina County Herd Investigation Update July 16, 2015 ***
 
 
Thursday, August 06, 2015
 
*** WE HAVE LOST TEXAS TO CWD TASK FORCE CATERING TO INDUSTRY
 
 
Friday, August 07, 2015
 
*** Texas CWD Captive, and then there were 4 ?
 
 
Thursday, September 24, 2015
 
TEXAS Hunters Asked to Submit Samples for Chronic Wasting Disease CWD TSE Prion Testing
 
*** I cannot stress enough to all of you, for the sake of your family and mine, before putting anything in the freezer, have those deer tested for CWD. ...terry
 
 
Saturday, October 03, 2015
 
TEXAS CHRONIC WASTING DISEASE CWD TSE PRION GOD MUST NOT BE A TEXAN 2002 TO 2015
 
 
Friday, October 09, 2015
 
Texas TWA Chronic Wasting Disease TSE Prion Webinars and Meeting October 2015
 
 
Monday, August 24, 2015
 
Ohio wildlife officials ramp up fight against fatal deer brain disease after 17 more positive tests CWD
 
 
Sunday, October 18, 2015
 
*** Pennsylvania Game Commission Law and Law Makers CWD TSE PRION Bans Singeltary 2002 from speaking A smelly situation UPDATED 2015
 
 
Monday, August 31, 2015
 
Illinois Loosing Ground to Chronic Wasting Disease CWD cases mounting with 71 confirmed in 2015 and 538 confirmed cases to date
 
 
Saturday, September 05, 2015
 
Missouri Captive Cervid Industry, CWD TSE Prion, and Procrastinating for Money, while mad deer and elk disease silently spreads
 
 
Friday, August 14, 2015
 
*** Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation
 
 
Friday, August 14, 2015
 
Carcass Management During a Mass Animal Health Emergency Draft Programmatic Environmental Impact Statement—August 2015
 
 
Tuesday, September 22, 2015
 
*** Host Determinants of Prion Strain Diversity Independent of Prion Protein Genotype
 
 
Friday, August 28, 2015
 
Chronic Wasting Disease CWD TSE Prion Diagnostics and subclinical infection
 
 
 
Sunday, October 18, 2015
 
*** World Organisation for Animal Health (OIE) and the Institut Pasteur Cooperating on animal disease and zoonosis research ***
 
 
Wednesday, August 05, 2015
 
*** Ohio confirms to me Chronic Wasting Disease CWD Spreads 19 confirmed cases to date ***
 
Just got off the phone with Christy Clevenger of Ohio
 
Ohio Department of Agriculture March 2012 – Present (3 years 6 months)Reynoldsburg, Ohio CWD program
 
Ms. Clevenger confirmed, to date, from the Yoder debacle, 1 confirmed case of CWD from the Hunting Preserve, 2 confirmed cases from the Breeding Farm, and 16 confirmed cases of CWD from the Breeder Depopulation, with a total to date of 19 cases of CWD in Ohio...
 
Terry
 
 
Thursday, April 02, 2015
 
OHIO CONFIRMS SECOND POSTIVE CHRONIC WASTING DISEASE CWD on Yoder's properties near Millersburg
 
Second Ohio white-tailed deer tests positive for deadly brain disease
 
Print Email D'Arcy Egan, The Plain Dealer By D'Arcy Egan, The Plain Dealer Email the author | Follow on Twitter on April 01, 2015 at 2:10 PM, updated April 01, 2015 at 3:09 PM
 
Ohio Dept. of Agriculture.jpg CLEVELAND, Ohio -- As state officials try to legally force Holmes County deer farmer Daniel Yoder to euthanize a herd of expensive white-tailed deer, a second deer has tested positive for chronic wasting disease (CWD) on Yoder's properties near Millersburg.
 
The first positive test ever for CWD in Ohio was from a deer killed Oct. 22 at Yoder's hunting preserve, World Class Whitetails. The second positive result came a few days ago while testing another Yoder deer that had died.
 
The National Veterinary Services Laboratories in Ames, Iowa confirmed the results.
 
"It has always been a case of not if, but when another deer would test positive on those properties," said Communications Director Erica Hawkins of the Ohio Department of Agriculture. "This wasn't unexpected. We expected to find positives at his facilities and, with de-population, we expect to find more."
 
Yoder's two breeding farms and hunting preserve were quarantined a year ago after it was discovered an infected Pennsylvania deer had been shipped there. It has become common for the breeding and hunting operations to ship deer to other states.
 
In Ohio, the ODA manages captive deer herds. The Ohio Division of Wildlife manages the wild deer herd.
 
Breeding large-antlered deer to supply the fenced deer-hunting operations has become a booming business. The price for a deer sporting trophy antlers can range from a few thousands dollars to more than $50,000.
 
Because the disease is highly contagious and almost impossible to eradicate, Yoder's breeding farms and fenced deer hunting operation was shut down and all deer 12 months and older that die on the properties were required to be tested for CWD, regardless of the circumstances, said Hawkins.
 
While CWD has become a major problem in Wisconsin and many western states, Yoder's captive deer have been the only Ohio animals to test positive for the always-fatal brain disease. CWD is found in the wild, but spreads far more quickly among crowded herds of captive deer or elk.
 
The ODOW constantly tests road-killed deer and deer killed by hunters for the disease. Because of the positive test in Holmes County, wildlife officials focused on deer harvested from that area during the recent hunting seasons.
 
The disease is related to mad cow disease, but has never been contracted by humans, according to the Centers for Disease Control and Prevention.
 
The ODOW reported last fall at least two deer had escaped from Yoder's farms and were killed by sport hunters. There have also been other instances of deer escaping from fenced hunting operations around state.
 
Hawkins said discussions are still underway to determine the best way to eliminate the herd because of the high cost of destruction and disposal of the deer.
 
"A lot of questions still need to be answered," Hawkins said. "This is the first situation like this in Ohio."
 
Yoder was charged in Holmes County Common Pleas Court on Feb. 25 with two counts of tampering with evidence, reported the Wooster Daily Record. Yoder had given a customer packages of venison obtained from a doe after the trophy buck he had killed appeared to be ill. The customer received the antlers, but Yoder disposed of the buck's head and carcass without performing the required tests, charged ODA enforcement agent William Lesho.
 
Three West Virginia hunters had paid to kill three deer on the preserve on another date and the required samples of the deer were not collected. In order to determine if a deer has CWD, the brain or brain stem must be tested
 
 
First Case of Chronic Wasting Disease Confirmed in Ohio on Private Preserve
 
10/23/2014 Ohio DNR in Wildlife
 
Active steps taken to control further spread; no evidence the disease affects humans
 
REYNOLDSBURG, OHIO – The Ohio Department of Agriculture (ODA) and the Ohio Department of Natural Resources (ODNR) today confirmed the first positive case of Chronic Wasting Disease (CWD) in the state in a captive deer herd in Holmes County. The state continues to take quarantine action to control the further spread of the disease. There is no evidence that CWD has affected the wild deer population in the state.
 
The positive sample was taken from a single buck on a hunting preserve in Millersburg and tested as part of Ohio’s CWD monitoring program for captive white-tailed deer operations. The preserve had been under quarantine since April 24, 2014, and was subject to intensive monitoring and sampling protocols because of a known connection to a captive deer operation in Pennsylvania that tested positive for CWD earlier this year. The quarantine will remain enforced until the state is satisfied that disease transference can no longer occur.
 
“Ohio’s captive white-tail deer licensing program was enacted two years ago for the purpose of continuously monitoring the heath of the captive deer populations in the state to manage the spread of and exposure to diseases such as CWD. We have worked closely with the Pennsylvania Department of Agriculture to identify and trace back positive cases,” said State Veterinarian Dr. Tony Forshey. “We will continue to take aggressive steps to ensure that CWD does not pose a threat to the state’s wild deer population.”
 
The state has quarantined 43 captive deer operations in Ohio since April 15, 2014, for receiving approximately 125 deer from operations in Pennsylvania that later tested positive for CWD. Twenty-two of those quarantines were lifted after negative CWD test results were confirmed in 53 of the suspect animals from Pennsylvania. ODA will continue to enforce quarantine restrictions on 21 operations, including five hunting preserves, until the department is satisfied that the threat of disease transference has passed.
 
The disease is fatal in deer, elk and moose, but there is no evidence CWD can be transmitted to humans, according to the Centers for Disease Control and Prevention (CDC) and The World Health Organization. Though no human disease has been associated with CWD, the CDC recommends, as a precaution, that people or other animals do not eat any part of an animal diagnosed with or showing signs of CWD.
 
“We have no reason to believe that there has been transference to the state’s wild deer population,” said Scott Zody, chief of the ODNR Division of Wildlife. “With hunting season in progress, there are no CWD concerns that should prevent anyone from enjoying wild deer hunting in Ohio or from consuming meat from healthy animals.”
 
The ODNR Division of Wildlife is recommending that hunters continue to take standard precautions such as shooting only animals that appear healthy, wearing rubber gloves when field-dressing their deer and washing thoroughly when finished. If hunters should observe a deer that appears unhealthy, they are encouraged to contact their local wildlife office or officer.
 
Since 2002, the state has conducted surveillance throughout Ohio for the disease. State and federal officials will continue this regular sampling and testing throughout the hunting season to continue to monitor the health of the state’s wild deer population. Tissue samples from 753 deer killed on Ohio’s roads were collected from September 2013 through March 2014 and were tested for CWD. An additional 88 hunter-harvested mature white-tailed deer and nine deer displaying symptoms consistent with CWD were tested as well and were all negative.
 
In response to this positive finding, the ODNR Division of Wildlife will increase sampling efforts in the wild deer population within six miles of the hunting preserve from which the CWD-positive deer came as well as near the other captive operations that are under quarantine. Those samples will include high-risk animals such as those killed on roads or exhibiting neurological symptoms as well as hunter-harvested deer in the area.
 
CWD, first discovered in captive mule deer in Colorado in 1967, attacks the brains of infected deer, elk and moose, producing small lesions that eventually result in death. It is transmitted by direct animal-to-animal contact through saliva, feces and urine. Signs of the disease include weight loss, excessive salivation, increased drinking and urination, and abnormal behavior like stumbling, trembling and depression. Infected deer and elk may also allow unusually close approach by humans or natural predators. The disease is fatal in deer, and there is no known treatment or vaccine.
 
 
FOR IMMEDIATE RELEASE
 
Media Contacts:
 
Erica Hawkins, ODA, (614) 752‐9817, erica.hawkins@agri.ohio.gov
 
Susie Vance, ODNR, (614) 265‐6335, susie.vance@dnr.state.oh.us
 
FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE PRESERVE
 
Active steps taken to control further spread; no evidence the disease affects humans
 
REYNOLDSBURG, Ohio (Oct. 23, 2014) – The Ohio Department of Agriculture and the Ohio Department of Natural Resources today confirmed the first positive case of Chronic Wasting Disease (CWD) in the state in a captive deer operation in Holmes County. The state continues to take quarantine action to control the further spread of the disease. There is no evidence that CWD has affected the wild deer population in the state.
 
The positive sample was taken from a single buck on a hunting preserve in Millersburg and tested as part of Ohio’s CWD monitoring program for captive white‐tailed deer operations. The preserve had been under quarantine since April 24, 2014, and was subject to intensive monitoring and sampling protocols because of a known connection to a captive deer operation in Pennsylvania that tested positive for CWD earlier this year. The quarantine will remain enforced until the state is satisfied that disease transference can no longer occur.
 
“Ohio’s captive white‐tail deer licensing program was enacted two years ago for the purpose of continuously monitoring the heath of the captive deer populations in the state to manage the spread of and exposure to diseases such as CWD. We have worked closely with the Pennsylvania Department of Agriculture to identify and trace back positive cases,” said State Veterinarian Dr. Tony Forshey. “We will continue to take aggressive steps to ensure that CWD does not pose a threat to the state’s wild deer population.”
 
The state has quarantined 43 captive deer operations in Ohio since April 15, 2014 for receiving approximately 125 deer from operations in Pennsylvania that later tested positive for CWD. Twenty‐two of those quarantines were lifted after negative CWD test results were confirmed in 53 of the suspect animals from Pennsylvania. ODA will continue to enforce quarantine restrictions on 21 operations, including five hunting preserves, until the department is satisfied that the threat of disease transference has passed.
 
The disease is fatal in deer, elk and moose, but there is no evidence CWD can be transmitted to humans, according to the Centers for Disease Control and Prevention (CDC) and The World Health Organization. Though no human disease has been associated with CWD, the CDC recommends, as a precaution, that people or other animals do not eat any part of an animal diagnosed with or showing signs of CWD. “We have no reason to believe that there has been transference to the state’s wild deer population,” said Scott Zody, Chief of the Ohio Department of Natural Resources’ Division of Wildlife. “With hunting season in progress, there are no CWD concerns that should prevent anyone from enjoying wild deer hunting in Ohio or from consuming meat from healthy animals.”
 
The Division of Wildlife is recommending that hunters continue to take standard precautions such as shooting only animals that appear healthy, wearing rubber gloves when field‐dressing their deer, and washing thoroughly when finished. If hunters should observe a deer that appears unhealthy, they are encouraged to contact their local wildlife office or officer.
 
Since 2002, the state has conducted surveillance throughout Ohio for the disease. State and federal officials will continue this regular sampling and testing throughout the hunting season to continue to monitor the health of the state’s wild deer population. Tissue samples from 753 deer killed on Ohio’s roads were collected from September 2013 through March 2014 and were tested for CWD. An additional 88 hunter‐harvested mature white‐tailed deer and nine deer displaying symptoms consistent with CWD were tested as well and were all negative.
 
In response to this positive finding, the Division of Wildlife will increase sampling efforts in the wild deer population within six miles of the hunting preserve from which the CWD‐positive deer came as well as near the other captive operations that are under quarantine. Those samples will include high‐risk animals such as those killed on roads or exhibiting neurological symptoms as well as hunter‐harvested deer in the area.
 
CWD, first discovered in captive mule deer in Colorado in 1967, attacks the brains of infected deer, elk and moose, producing small lesions that eventually result in death. It is transmitted by direct animal‐toanimal contact through saliva, feces and urine. Signs of the disease include weight loss, excessive salivation, increased drinking and urination, and abnormal behavior like stumbling, trembling and depression. Infected deer and elk may also allow unusually close approach by humans or natural predators. The disease is fatal in deer and there is no known treatment or vaccine.
 
‐‐ 30 ‐‐
 
 
 
Thursday, October 23, 2014
 
*** FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE PRESERVE
 
 
Wednesday, February 11, 2015
 
World Class Whitetails quarantined CWD deer Daniel M. Yoder charged with two counts of tampering with evidence
 
 
Sunday, October 18, 2015
 
*** Pennsylvania Game Commission Law and Law Makers CWD TSE PRION Bans Singeltary 2002 from speaking A smelly situation UPDATED 2015
 
 
Wednesday, October 21, 2015
 
TAHC CHRONIC WASTING DISEASE CWD TSE PRION REPORT OCTOBER 2015
 
 
Monday, August 31, 2015
 
*** Illinois Loosing Ground to Chronic Wasting Disease CWD cases mounting with 71 confirmed in 2015 and 538 confirmed cases to date ***
 
 
Saturday, September 05, 2015
 
Missouri Captive Cervid Industry, CWD TSE Prion, and Procrastinating for Money, while mad deer and elk disease silently spreads
 
 
Friday, August 14, 2015
 
*** Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation
 
 
Friday, August 14, 2015
 
Carcass Management During a Mass Animal Health Emergency Draft Programmatic Environmental Impact Statement—August 2015
 
 
Tuesday, September 22, 2015
 
*** Host Determinants of Prion Strain Diversity Independent of Prion Protein Genotype
 
 
Friday, August 28, 2015
 
Chronic Wasting Disease CWD TSE Prion Diagnostics and subclinical infection
 
 
Terry S. Singeltary Sr.

posted by Terry S. Singeltary Sr. at 4:40 PM

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