TAHC Adopts Chronic Wasting Disease Movement Requirements and Trichomoniasis Program Rules

Media Contacts:

Callie Ward, Texas Animal Health Commission, 512-719-0743, callie.ward@tahc.texas.gov;

Friday, December 30, 2016 TAHC Adopts Chronic Wasting Disease Movement Requirements and Trichomoniasis Program Rules Media Contacts: Callie Ward, Texas Animal Health Commission, 512-719-0743, callie.ward@tahc.texas.gov; FOR IMMEDIATE RELEASE December 30, 2016 TAHC Adopts Chronic Wasting Disease Movement Requirements and Trichomoniasis Program Rules  Austin, TX - The Texas Animal Health Commission (TAHC) held a regularly scheduled Commission meeting on December 13, 2016, at its headquarters in Austin, Texas. The following rules were adopted during the meeting and will go into effect on January 2, 2016: Chapter 40, Chronic Wasting Disease, Repeal & Replace Movement Restriction Zone/Carcass Entry Requirements The adopted rule creates a new Section 40.6 CWD Movement Restriction Zone, which defines CWD movement restrictions in Containment Zones, Surveillance Zones, and interstate entry requirements. The Containment and Surveillance Zones are located in the Panhandle and Trans-Pecos regions, and Medina County. The implementation of the Medina County Containment and Surveillance Zone will be delayed until March 1, 2017. Chapter 38, Trichomoniasis, Certification Period & Sample Submission Timeframe The adopted rule extends the certification period of veterinarians certified to perform Trichomoniasis (Trich) program functions from 3 years to 5 years. The definition of cattle and associated Trich testing requirements now exclude bison. Lastly, veterinarians must ship Trich samples and have them arrive at the lab within 96 hours of collection instead of 120 hours. The following rules were proposed: Chapter 40, Chronic Wasting Disease, Surveillance Testing Requirements The purpose of the amendment is to add surveillance, movement reporting, identification, and record keeping requirements for Exotic CWD Susceptible Species. Chapter 41, Fever Ticks, Dipping, Treatment and Vaccination of Animals The proposed amendment will provide the Designated Fever Tick Epidemiologist (DFTE), with the approval of the Executive Director, the discretion to approve inspections, dipping, treatments and/or vaccination requirements that are less stringent than those currently prescribed. Chapter 59, General Practices and Procedures, HUB/Enhanced Contract Monitoring The new rule is proposed in response to Texas Government Code §2261.253 enacted by the 84th Texas Legislature, which requires each state agency by rule to establish a procedure to identify contracts that require enhanced contract or performance monitoring and prescribes certain reporting requirements. The TAHC will begin accepting public comments for the proposals on December 30. The deadline for comment submissions on proposed rules is January 30, 2017. Complete details of the rule proposals are available on the TAHC website at http://www.tahc.texas.gov/regs/proposals.html. The TAHC encourages and appreciates all comments. Comments on the proposed regulations must be submitted in writing to Amanda Bernhard, Texas Animal Health Commission, 2105 Kramer Lane, Austin, Texas 78758, by fax at (512) 719-0719, or by email to comments@tahc.texas.gov. ### http://www.tahc.texas.gov/news/2016/2016-12-30_CommissionMeeting.pdf Rules proposed at the December 13, 2016 Commission meeting — Open for comment 12/30/2016 - 01/30/2017 Chapter 40, Chronic Wasting Disease - Add surveillance, movement reporting, identification, and mortality record keeping requirements for Exotic CWD Susceptible Species View rule proposal. Comment The Texas Animal Health Commission (commission) proposes amendments to §40.5, concerning Movement Requirements for CWD Susceptible Species, in Chapter 40, which is entitled “Chronic Wasting Disease”. The purpose of the amendments is to add surveillance, movement reporting, identification, and mortality record keeping requirements pertaining to Exotic CWD Susceptible Species. Chronic Wasting Disease (CWD) is a transmissible spongiform encephalopathy (TSE). CWD is a progressive, fatal, degenerative neurological disease of farmed and free-ranging deer, elk, and moose. TSEs include a number of different diseases affecting animals or humans including bovine spongiform encephalopathy (BSE) in cattle, scrapie in sheep and goats, and CreutzfeldtJacob disease (CJD) in humans. Although CWD shares certain features with other TSEs, it is a distinct disease affecting only deer, elk, and moose. The species known to be susceptible to CWD are North American elk or wapiti (Cervus Canadensis), red deer (Cervus elaphus), mule deer (Odocoileus hemionus), black-tailed deer (Odocoileus hemionus), white-tailed deer (Odocoileus virginianus), Sika deer (Cervus Nippon), and moose (Alces alces). The species that are found in Texas are white-tailed deer, mule deer, elk, red deer, and Sika deer. The agent that causes CWD and other TSEs has not been completely characterized; however, the theory supported by most scientists is that TSE diseases are caused by proteins called prions. The exact mechanism of transmission is unclear; however, evidence suggests CWD is transmitted directly from one animal to another through saliva, feces, and urine containing abnormal prions shed in those body fluids and tissues. Because the disease has a long incubation period, animals infected with CWD may not produce any visible signs of the disease for a number of years after they become infected. The disease can be passed through contaminated environmental conditions and has been known to persist for a long period of time. The “official” diagnostic test for CWD is the Immunohistochemistry (IHC) test performed on the obex tissue of the brain and specific lymphoid tissues. This is a postmortem test in which the animal must be dead to be tested. There is no known treatment or vaccine for CWD. CWD was first recognized in 1967 in captive mule deer in Colorado. The disease has since been documented in captive and/or free-ranging deer and elk in 24 states, including Texas, and 2 Canadian provinces. In 2012, CWD was first discovered in Texas in a free-ranging mule deer in the Hueco Mountains along the New Mexico border in far West Texas. The commission and Texas Parks and Wildlife Department (TPWD) created a restricted zone that has required testing of susceptible species in that area and restricted movement of live animals. On June 30, 2015, a 2-year old white-tailed deer in a Medina County breeding facility was confirmed positive for CWD. Through testing requirements associated with tracing of deer either moved from or to this facility, CWD has also been discovered in other white-tailed deer, which includes four other facilities in Medina and Lavaca counties. A free-ranging mule deer buck, harvested in Hartley County, was confirmed positive for CWD on March 3, 2016. Hartley County is located in the Texas Panhandle and borders New Mexico. On December 6, 2016, a free-ranging elk harvested in Dallam County, was confirmed positive for CWD. Dallam County is also located in the Texas Panhandle and borders New Mexico and Oklahoma.   The commission works in coordination and collaboration with the TPWD to address CWD issues and concerns and to assess and mitigate the risks to the Texas cervid industries. All mule deer, white-tailed deer, and native species are generally under the jurisdiction of TPWD. They are classified as property of the state of Texas and TPWD manages them as a valuable and important resource of the state. TPWD through specific statutory authorization does allow individuals to breed, trade, sell, move, release, and hunt white-tailed or mule deer that meet certain legal requirements.  Elk, Sika deer, and red deer are also classified as CWD susceptible species, but are not indigenous to the state and therefore, not subject to the jurisdiction of TPWD. They are classified as exotic livestock which are privately owned. Texas has an unknown number of exotic cervid species that are free-ranging or maintained on private property behind high fences. Many of these facilities are hunting ranches, which are not subject to the seasonal and regulatory hunting restrictions of TPWD. Surveillance testing is a key, critical component to early detection of the disease and also the monitoring of the disease presence and prevalence in all areas of the state where CWD susceptible species exist. A strong surveillance system also supports Texas’ animal industries and their marketability because it provides more assurance and confidence that these animals are healthy.    The United States Department of Agriculture (USDA) Animal Plant Health Inspection Service (APHIS) has federal standards requiring participation in a National CWD Herd Certification Program (HCP) which is designed to be a voluntary federal-state cooperative program implemented by participating states. The HCP’s objective is to achieve a national approach that minimizes the risk of spreading CWD in cervid populations through uniform national herd certification standards. States must be approved by USDA to participate and these animals must be in an accepted program for the movement of these species interstate. Texas has an approved HCP program. Though Texas’ white-tailed deer population has had significant historical surveillance, very few elk, red deer or sika herds have participated in the CWD certification program.  As such, the commission has limited CWD surveillance testing for these cervid species as a result of this program.  In 2009, legislation was passed that authorized the commission to establish a disease surveillance program for elk. This authority is found in §161.0541 of the Texas Agriculture Code. Under this statute, the commission may require each person who moves elk in this state to have elk participate in a disease surveillance program.   Pursuant to this legislation, the commission adopted rules that require elk to participate in a CWD surveillance program in 2010, however, the rules were held in abeyance until 2012 to encourage voluntary participation. Elk producers wishing to sell or move elk are required to either enroll in a CWD herd monitoring programs or have 20% of their mortalities tested to quality animals for movement. This program is found in Title 4, Texas Administrative Code, Chapter 40, §40.5. The commission received a total of 243 CWD tests results for elk and red deer from 2003 to September of 2016.  The detection of CWD in different locations in Texas creates a risk for CWD exposure or infection to other susceptible species throughout the state. The commission believes it is necessary to conduct enhanced surveillance of Exotic CWD Susceptible Species to protect against the spread of CWD.Without adequate and equitable testing throughout Texas, the risk only increases for spreading CWD in the state, This only poses a greater disease risk to the cervid industries, as well as creates greater opportunity for negative economic impact for those industries. The commission has historically used a group of CWD stakeholders to provide guidance, along with recommendations to the commission staff regarding the CWD program and improving surveillance in the exotic CWD susceptible species. These stakeholders include members of USDA, TPWD, Texas Deer Association, Exotic Wildlife Association, Deer Breeder Corporation, Texas Wildlife Association, Texas Veterinary Medical Diagnostic Laboratory, Texas Southwest Cattle Feeders, Texas Veterinary Medical Association, AgriLife, along with noted private veterinary practitioners and wildlife biologists. The group discussed the need to modify the intrastate program for the Exotic CWD Susceptible Species to make it a more successful surveillance program. Section 40.5(a) provides definitions specific to this section. They include Eligible Mortality; Exotic CWD Susceptible Species; Premises; and Movement of an Exotic CWD Susceptible Species from one non-contiguous property or premises to another.  Section 40.5(b) provides for CWD surveillance requirements to require that all eligible mortalities be CWD tested until such time that three animals are tested and valid test results are obtained.  Section 40.5(c) provides for movement reporting and identification requirements for live Exotic CWD Susceptible Species moved or transported within the state. It requires the owner to obtain a Premises Identification Number and that an annual inventory be created and maintained by owners of Exotic CWD Susceptible Species and submitted to the commission, either in hard or electronic copy on forms provided or authorized by the commission.  Section 40.5(d) provides for the CWD testing requirements in terms of age, official test requirement.  Section 40.5(e) provides that the owner shall report all test results to the commission  Section 40.5(f) provides that the owner of a premises where an eligible mortality occurs must maintain mortality records. Section 40.5(g) provides that a premises where Exotic CWD Susceptible Species are located may be inspected by the commission or authorized agents of the commission. Section 40.5(h) provides that a dealer is a person engaged in the business of buying or selling Exotic CWD Susceptible Species and must maintain records for all Exotic CWD Susceptible Species transported within the state or where there is a transfer of ownership, and provide these to commission personnel upon request. Records required to be kept under the provisions of this section shall be maintained for not less than five years.  FISCAL NOTE Ms. Larissa Schmidt, Chief of Staff, Texas Animal Health Commission, has determined for the first five-year period the rule is in effect, there will be no significant fiscal implication initially to state and local governments as a result of enforcing or administering the rule as proposed. The work and associated costs will be done with existing resources. To curtail costs, manual resources will initially be used for data capture and program tracking, but if funds become available, a more robust database may be developed that allows producers to enter data through a web-based portal that also link to the Texas Veterinary Medical Diagnostic Laboratory (TVMDL) for direct transfer of laboratory results. The cost of such a database has not been fleshed out completely, but the cost is believed to be significant. The commission has requested an exceptional item for the upcoming budget cycle for CWD related staffing and expenses. The full amount requested through the Legislative Appropriations Request is $1,141,796 for Fiscal Years 2018 and 2019. It is anticipated that a portion of this request could be used to administer the proposed rule if the exceptional item is funded. The commission believes there will be no significant adverse economic implications on persons, or small and micro-businesses. It is estimated that compliance with the proposed amendments will cost a small or micro-business at or around $300.00 per year to comply with the requirements stated in the proposal. Small and Micro-business Impact Analysis Under the provisions of Government Code, Chapter 2006, a state agency must prepare an economic impact statement and a regulatory flexibility analysis for a rule that may have an adverse economic effect on small businesses and micro-businesses. As required by Government Code, §2006.002(g), in April 2008, the Office of the Attorney General issued guidelines to assist state agencies in determining a proposed rule's potential adverse economic impact on small businesses. These guidelines state that “[g]enerally, there is no need to examine the indirect effects of a proposed rule on entities outside of an agency's regulatory jurisdiction.” The guidelines state that an agency need only consider a proposed rule's “direct adverse economic impacts” to small businesses and micro-businesses to determine if any further analysis is required. The guidelines also list examples of the types of costs that may result in a “direct economic impact.” Such costs may include costs associated with additional recordkeeping or reporting requirements; new taxes or fees; lost sales or profits; changes in market competition; or the need to purchase or modify equipment or services. Government Code, §2006.001(1), defines a small or micro-business as a legal entity “formed for the purpose of making a profit” and “independently owned and operated.” A micro-business is a business with 20 or fewer employees. A small business is defined as a business with fewer than 100 employees, or less than $6 million in annual gross receipts. Although the commission is not able to adequately identify all the variations in which a business may be required to test tissue samples from an Exotic CWD Susceptible Species mortality, it is believed that most of these operations would qualify as a small or micro-business. Since the rule, as proposed, could impact these operations that engage in business activities for the purposes of generating a profit, the commission has carefully considered the rule and its impact on a business’s profitability. Because of the variety of business models within the state that may potentially be involved in a business enterprise that will be required to test eligible mortalities of Exotic CWD Susceptible Species, meaningful estimates of potential adverse economic impacts are difficult to assess.  It should also be noted that some aspects of this analysis are based on anticipated marketplace behavior which cannot be accurately predicted. In addition, to the extent that any marketplace analysis can be conducted, it is difficult, if not impossible, to accurately separate and distinguish marketplace behavior that is the result of the proposed new rule from marketplace behavior that is the result of the discovery of CWD in Texas. The purpose of this rule is not to adversely affect small business, but rather to protect valuable statewide resources through surveillance, which assesses the risk of further CWD being discovered. Surveillance testing is a key, critical component to determine to early detection of the disease and also the monitoring of the disease presence and prevalence in all areas of the state where CWD susceptible species exist. A strong surveillance system also supports Texas’ animal industries and their marketability. An inadequate surveillance program promotes the unnoticed spread of disease and ultimately makes the task of disease containment exponentially more difficult. In the current environment, the mobility and transportation of agricultural animals throughout the state and country has greatly increased the spread of disease and makes risk mitigation more difficult and complex. The commission has a voluntary CWD Certified Status Program which requires 100% testing of all mortalities in order to maintain and advance in status. The cost of testing is assumed by the herd owner. The requirements for this program are located in §40.3. Though the white-tailed deer population in Texas has had significant historical surveillance, fewer than 10 elk, red deer or Sika deer herds have participated in a CWD monitoring program in the past.   It is also impossible to properly estimate the number of small businesses subject to the proposed rule. Elk, Sika deer, and red deer are classified as exotic livestock and there is no registration, which makes it pragmatically impossible for the commission to properly estimate who owns or maintains these species. Texas has an estimated 2,000 animals which are considered Exotic CWD Susceptible Species that are maintained on private property behind high fences. The proposed amendments would result in no significant adverse economic implications to someone who must undertake the disease-testing requirements to continue certain activities. The estimated cost of meeting the testing requirements is $100 per animal or $300 per year. This cost includes submission of two tissue samples to the TVMDL in College Station, Texas, submission fee, head disposal fee (if whole head submitted), plus veterinary or sample collector fees, and the costs associated with record keeping.  Proposed Methods of Reducing Adverse Economic Impact on Small and Micro-businesses In the development of the proposed rule, there was significant discussions among stakeholder groups and commission staff. Several alternatives were raised, discussed and/or considered to achieve the goals of the proposed new rules while reducing potential adverse economic implications on small and micro-businesses and persons required to comply. One alternative that was actively discussed by the group was the use of antemortem testing of these species in order to obtain adequate surveillance. This is a live animal test that has not yet been properly validated and there is no data on this type of test for Sika and red deer. Additionally, test sensitivity for antemortem testing was discussed, which means early cases of the disease will likely be missed by the test. Trapping of these animals for testing is difficult, particularly when they must be held before movement to await test results. To capture these animals they would need to utilize anesthesia, which also raises the concern of Capture Myopathy. This type of test would increase the adverse economic impact on small and microbusinesses because it is more expensive than the postmortem official test. The second alternative considered was to increase surveillance efforts by authorizing movement between high fences only and requiring a certain number of test samples before animals could be moved. This would require a herd size determination or a herd inventory estimate before the number of required samples could be determined. This alternative would not eliminate the economic implications because testing would be required and record keeping would be increased. Another alternative considered was to initiate a slaughter testing requirement. If this alternative was used, it was discussed that the first 15 animals/carcasses sent to slaughter would be CWD tested. The group determined that this alternative would not be an effective surveillance effort because of the small numbers of Exotic CWD Susceptible Species that are sent to slaughter each year would not provide an adequate statewide surveillance that is both equitable and epidemiologically sound. The proposed model for disease surveillance as included in this proposed rule is proven. The commission has used this type model to identify other species of animals that have been potentially exposed to a disease of concern, but in the vast majority of disease efforts, the testing is performed on a live animal with results disclosed in a relatively short period of time. Live animal testing allows the agency to identify the disease exposure and accordingly take appropriate veterinary response. Because the official test for CWD is postmortem based, the commission has no control or alternative in testing eligible mortalities. PUBLIC BENEFIT NOTE Ms. Schmidt has also determined that for each of the first five years the rule is in effect, the public benefit anticipated as a result of enforcing the rule will be a reduction of the probability of CWD being spread from locations where it might currently exist by having increased surveillance, which will protect Exotic CWD Susceptible Species from a serious disease risk. The commission believes that there is also a collateral benefit of protection from disease spread in captive herds, thus helping to maintain the economic viability of captive herd owners and allowing for the continued enjoyment of the resource. LOCAL EMPLOYMENT IMPACT STATEMENT In accordance with Texas Government Code §2001.022, this agency has determined that the proposed rule will not impact local economies and, therefore, did not file a request for a local employment impact statement with the Texas Workforce Commission. TAKINGS ASSESSMENT The agency has determined that the proposed governmental action will not affect private real property. The proposed amendments are an activity related to the handling of animals, including requirements for testing, movement, inspection, identification, reporting of disease, and treatment, in accordance with 4 TAC §59.7, and are, therefore, compliant with the Private Real Property Preservation Act in Government Code, Chapter 2007. REQUEST FOR COMMENT Comments regarding the proposal may be submitted to Amanda Bernhard, Texas Animal Health Commission, 2105 Kramer Lane, Austin, Texas 78758, by fax at (512) 719-0719 or by email at “comments@tahc.texas.gov”. STATUTORY AUTHORITY The amendments are proposed under the following statutory authority as found in Chapter 161 of the Texas Agriculture Code. The commission is vested by statute, §161.041(a), with the requirement to protect all livestock, domestic animals, and domestic fowl from disease. The commission is authorized, through §161.041(b), to act to eradicate or control any disease or agent of transmission for any disease that affects livestock. Pursuant to §161.005, entitled “Commission Written Instruments”, the commission may authorize the executive director or another employee to sign written instruments on behalf of the commission.  A written instrument, including a quarantine or written notice signed under that authority, has the same force and effect as if signed by the entire commission. Pursuant to §161.006, entitled “Documents to Accompany Shipment”, if  required that a certificate or permit accompany animals or commodities moved in this state, the document must be in the possession of the person in charge of the animals or commodities, if the movement is made by any other means. Pursuant to §161.0415, entitled “Disposal of Diseased or Exposed Livestock”, the commission by order may require the slaughter of livestock, under the direction of the commission, or the sale of livestock for immediate slaughter. Pursuant to §161.0417, entitled “Authorized Personnel for Disease Control”, a person, including a veterinarian, must be authorized by the commission in order to engage in an activity that is part of a state or federal disease control or eradication program for animals. Section 161.0417 requires the commission to adopt necessary rules for the authorization of such persons and, after reasonable notice, to suspend or revoke a person's authorization if the commission determines that the person has substantially failed to comply with Chapter 161 or rules adopted under that chapter. Section 161.0417 does not affect the requirement for a license or an exemption under Chapter 801, Occupations Code, to practice veterinary medicine. Pursuant to §161.046, entitled “Rules”, the commission may adopt rules as necessary for the administration and enforcement of this chapter. Pursuant to §161.048, entitled “Inspection of Shipment of Animals or Animal Products”, the commission may require testing, vaccination, or another epidemiologically sound procedure before or after animals are moved. An agent of the commission is entitled to stop and inspect a shipment of animals or animal products being transported in this state in order to determine if the shipment originated from a quarantined area or herd; or determine if the shipment presents a danger to the public health or livestock industry through insect infestation or through a communicable or noncommunicable disease. Pursuant to §161.049, entitled “Dealer Records”, the commission may require a livestock, exotic livestock, domestic fowl, or exotic fowl dealer to maintain records of all livestock, exotic livestock, domestic fowl, or exotic fowl bought and sold by the dealer. Pursuant to §161.054, entitled “Regulation of Movement of Animals”, the commission, by rule, may regulate the movement of animals.  The commission may restrict the intrastate movement of animals even though the movement of the animals is unrestricted in interstate or international commerce. Pursuant to §161.0541, entitled “Elk Disease Surveillance Program”, the commission by rule may establish a disease surveillance program for elk. Pursuant to §161.0545, entitled “Movement of Animal Products”, the commission may adopt rules that require the certification of persons who transport or dispose of inedible animal products, including carcasses, body parts, and waste material. The commission by rule may provide terms and conditions for the issuance, renewal, and revocation of a certification under this section. Pursuant to §161.055, entitled “Slaughter Plant Collection”, the commission may require slaughter plants to collect and submit blood samples and other diagnostic specimens for testing for disease. Pursuant to §161.056(a), entitled “Animal Identification Program”, the commission, in order to provide for disease control and enhance the ability to trace disease-infected animals or animals that have been exposed to disease, may develop and implement an animal identification program that is no more stringent than a federal animal disease traceability or other federal animal identification program. Section 161.056(d) authorizes the commission to by a two-thirds vote adopt rules to provide for an animal identification program more stringent than a federal program only for control of a specific animal disease or for animal emergency management. Pursuant to §161.057, entitled “Classification of Areas”, the commission by rule may prescribe criteria for classifying areas in the state for disease control. The criteria must be based on sound epidemiological principles. The commission may prescribe different control measures and procedures for areas with different classifications. Pursuant to §161.061, entitled “Establishment”, if the commission determines that a disease listed in §161.041 of this code or an agency of transmission of one of those diseases exists in a place in this state or among livestock, exotic livestock, domestic animals, domestic fowl, or exotic fowl, or that a place in this state or livestock, exotic livestock, domestic animals, domestic fowl, or exotic fowl are exposed to one of those diseases or an agency of transmission of one of those diseases. Pursuant to §161.101, entitled “Duty to Report”, a veterinarian, a veterinary diagnostic laboratory, or a person having care, custody, or control of an animal shall report the existence of the diseases, if required by the commission,  among livestock, exotic livestock, bison, domestic fowl, or exotic fowl to the commission within 24 hours after diagnosis of the disease. No other statutes, articles or codes are affected by the proposal. 40.5. Surveillance and Movement Requirements for Exotic CWD Susceptible Species. (a) Definitions: snip...see full text ; http://www.tahc.texas.gov/regs/proposed/2016-12_Ch40ChronicWastingDisease.pdf http://www.tahc.texas.gov/regs/proposals.html TSE PRION REFRESHER TME FIRST Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. snip... The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle... http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/mb/m09/tab05.pdf http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/mb/m09a/tab01.pdf http://collections.europarchive.org/tna/20090505194948/http://bseinquiry.gov.uk/files/yb/1987/06/10004001.pdf In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells 3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ... http://web.archive.org/web/20060307063531/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf ”The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite it’s subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province!” ...page 26. http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf *** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep. http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf http://bse-atypical.blogspot.com/2016/07/atypical-bovine-spongiform.html SPONTANEOUS ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY    ***Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.*** http://www.nature.com/articles/srep11573 Primate Biol., 3, 47–50, 2016 www.primate-biol.net/3/47/2016/ doi:10.5194/pb-3-47-2016 © Author(s) 2016. CC Attribution 3.0 License. Prions Walter Bodemer German Primate Center, Kellnerweg 4, 37077 Göttingen, Germany Correspondence to: Walter Bodemer (wbodemer@dpz.eu) Received: 15 June 2016 – Revised: 24 August 2016 – Accepted: 30 August 2016 – Published: 7 September 2016 Abstract. Prions gained widespread public and scientific interest in the year 2000. At that time, the human neurological Creutzfeldt–Jakob disease (CJD) was known. However, new CJD cases were diagnosed but they could not be ascribed to one of the classical CJD categories i.e. sporadic (sCJD), hereditary or acquired. Hence, they were classified as variant CJD (vCJD). Later on, experimental evidence suggested that vCJD was caused by prions postulated as unique novel infectious agents and, for example, responsible for bovine spongiform encephalopathy (BSE) also known as mad cow disease. The infection of humans by transmission of BSE prions also defined vCJD as a zoonotic disease. Prions, especially those associated with scrapie in sheep had been known for quite some time and misleadingly discussed as a slow virus. Therefore, this enigmatic pathogen and the transmission of this unusual infectious agent was a matter of a controversial scientific debate. An agent without nucleic acid did not follow the current dogma postulating DNA or RNA as inheritable information encoding molecules. Although numerous experimental results clearly demonstrated the infectious capacity of prions in several animal species, a model close to human was not readily available. Therefore, the use of rhesus monkeys (Macaca mulatta) served as a non-human primate model to elucidate prion infection under controlled experimental conditions. Not the least, transmission of BSE, human vCJD, and sCJD prions could be confirmed in our study. Any prion infection concomitant with progression of disease in humans, especially vCJD, could be analyzed only retrospectively and at late stages of disease. In contrast, the prion-infected rhesus monkeys were accessible before and after infection; the progression from early stage to late clinical stages – and eventually death of the animal–could be traced. Because of the phylogenetic proximity to humans, the rhesus monkey was superior to any rodent or other animal model. For these reasons an experimental approach had been conceived by J. Collinge in London and A. Aguzzi in Zurich and performed in a cooperative study with both research groups in the pathology unit of the German Primate Center (DPZ). The study in the DPZ lasted from 2001 until 2012. Our research in the pathology unit provided a temporal monitoring of how an initial prion infection develops eventually into disease; an approach that would have never been possible in humans since the time point of infection with prions from, for example, BSE is always unknown. Telemetry revealed a shift in sleep– wake cycles early on, long before behavioral changes or clinical symptoms appeared. Pathology confirmed nonneuronal tissue as hidden places where prions exist. The rhesus model also allowed first comparative studies of epigenetic modifications on RNA in peripheral blood and brain tissue collected from uninfected and prion infected animals. To conclude, our studies clearly demonstrated that this model is valid since progression to disease is almost identical to human CJD. Published by Copernicus Publications on behalf of the Deutsches Primatenzentrum GmbH (DPZ). SNIP... 2 Methods and results 2.1 Animals The reason to perform prion research in rhesus monkeys was to monitor infection and the temporal progression of prion infection in the rhesus monkey. In contrast to studies of human CJD cases, we could decide on the infectious dose. We also could control behavior immediately after prion inoculation and during the rather long time until animals died from the prion infection. Hidden places where prions might exist were found. Even epigenetic modifications on RNA could be detected. Taken together, these experimental approaches depended on animals. Using rhesus monkeys as a model system required thorough ethic reasoning and consultation with authorities before we actually turned to conduct the experiments. The Number of animals was limited just to fulfill statistical conditions. The individual health status was obtained and health care was provided throughout the study. The animals underwent daily inspection to monitor any changes in health and behavior. The experiments were conceived with the aim of reducing pain, suffering, and harm. Groups of animals were preferred in order to keep them in a social environment. The animals were originally kept in Vienna at Baxter and transferred to the German Primate Center (DPZ) in 2001. J. Collinge, A. Aguzzi, and C. Weissmann were the scientists who recommended this well-controlled prion infection study, and financial support was provided by an EU grant.To ensure statistical significance four groups consisting of four rhesus macaques each were formed: one uninfected control group, one group infected with BSE prions, one with vCJD prions, and one with sCJD prions. Health of animals, infection, and progression to disease was looked at in our pathology department and in cooperation with W. Schulz-Schaeffer at the UMG (University Medicine, Göttingen). Besides, neurologists from the UMG also observed the animals whenever clinical symptoms seemed to appear. This close observation and comparison with human CJD cases demonstrated how close clinical progression of human disease resembles the experimental infection in the non-human primate. 2.2 Infection Infectious prions from brain tissue of one sCJD and one vCJD case (provided by J. Collinge) as well as BSE prions (from a “German” madcow case and provided by W. Schulz Schaeffer) were intraperitoneally administered into the rhesus monkeys. 2.3 Monitoring of behavior and telemetry Early behavioral monitoring was carried out by the ethologists I. Machatschke and J. Dittami from Vienna University. Transmitters were used to record changes in the circadian rhythms. Body temperature, sleep–wake cycles, and activity profiles could be obtained over a time span of 2 years. Up to half a year after infection animals did not show any signs of prion infection. However, after 6 months and persisting for another few months some animals had some disturbances in circadian rhythms which disappeared and then never appeared again(I. Machatschke, personal communication,2006).For a rather long time of about 4–5 years animals seemed to be healthy. But then, almost all animals rapidly progressed to symptoms. Symptoms were highly similar or even identical to those seen in human CJD. 2.4 Pathology Blood and necropsy specimens from the animals served as a valuable source to detect pathologically associated prion protein even in non-neuronal skeletal and cardiac tissue. These “hidden places” of prion pathology and replication were clearly demonstrated and extended our view where prions might spread within an organism. Not only leukocytes and neuronal tissue harbor abnormal prion protein isoforms but also other tissues can propagate prion protein isoforms leading to toxicity, cell degeneration, and eventually transmissible prions (Krasemann et al., 2010, 2013). SNIP... 3 Conclusion Most importantly, early signs of an altered circadian rhythm, sleep–wake cycle, and activity and body temperature were recorded in prion-infected animals. This experimental approach would have never been feasible in studies with human CJD cases. After 4–6 years animals developed clinical symptoms highly similar to those typical for CJD. Clinicians confirmed how close the animal model and the human disease matched. Non-neuronal tissue like cardiac muscle and peripheral blood with abnormal, disease-related prion protein were detected in rhesus monkey tissues.  Molecular changes in RNA from repetitive Alu and BC200 DNA elements were identified and found to be targets of epigenetic editing mechanisms active in prion disease. To conclude, our results with the rhesus monkey model for prion disease proved to be a valid model and increased our knowledge of pathogenic processes that are distinctive to prion disease. SEE FULL TEXT ; http://www.primate-biol.net/3/47/2016/pb-3-47-2016.pdf    *** WDA 2016 NEW YORK ***  We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions.  Student Presentations Session 2  The species barriers and public health threat of CWD and BSE prions  Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr. Edward Hoover1 1Colorado State University  Chronic wasting disease (CWD) is spreading rapidly through cervid populations in the USA. Bovine spongiform encephalopathy (BSE, mad cow disease) arose in the 1980s because cattle were fed recycled animal protein. These and other prion diseases are caused by abnormal folding of the normal prion protein (PrP) into a disease causing form (PrPd), which is pathogenic to nervous system cells and can cause subsequent PrP to misfold. CWD spreads among cervids very efficiently, but it has not yet infected humans. On the other hand, BSE was spread only when cattle consumed infected bovine or ovine tissue, but did infect humans and other species. The objective of this research is to understand the role of PrP structure in cross-species infection by CWD and BSE. To study the propensity of each species’ PrP to be induced to misfold by the presence of PrPd from verious species, we have used an in vitro system that permits detection of PrPd in real-time. We measured the conversion efficiency of various combinations of PrPd seeds and PrP substrate combinations. We observed the cross-species behavior of CWD and BSE, in addition to feline-adapted CWD and BSE. We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. CWD is unique among prion diseases in its rapid spread in natural populations. BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species. This adaptation has consequences for surveillance of humans exposed to CWD. Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders http://www.wda2016.org/uploads/5/8/6/1/58613359/wda_2016_conference_proceedings_low_res.pdf  PRION 2016 TOKYO Zoonotic Potential of CWD Prions: An Update Ignazio Cali1, Liuting Qing1, Jue Yuan1, Shenghai Huang2, Diane Kofskey1,3, Nicholas Maurer1, Debbie McKenzie4, Jiri Safar1,3,5, Wenquan Zou1,3,5,6, Pierluigi Gambetti1, Qingzhong Kong1,5,6 1Department of Pathology, 3National Prion Disease Pathology Surveillance Center, 5Department of Neurology, 6National Center for Regenerative Medicine, Case Western Reserve University, Cleveland, OH 44106, USA. 4Department of Biological Sciences and Center for Prions and Protein Folding Diseases, University of Alberta, Edmonton, Alberta, Canada, 2Encore Health Resources, 1331 Lamar St, Houston, TX 77010 Chronic wasting disease (CWD) is a widespread and highly transmissible prion disease in free-ranging and captive cervid species in North America. The zoonotic potential of CWD prions is a serious public health concern, but the susceptibility of human CNS and peripheral organs to CWD prions remains largely unresolved. We reported earlier that peripheral and CNS infections were detected in transgenic mice expressing human PrP129M or PrP129V. Here we will present an update on this project, including evidence for strain dependence and influence of cervid PrP polymorphisms on CWD zoonosis as well as the characteristics of experimental human CWD prions. PRION 2016 TOKYO In Conjunction with Asia Pacific Prion Symposium 2016 PRION 2016 Tokyo Prion 2016 http://prion2016.org/dl/newsletter_03.pdf   http://grantome.com/grant/NIH/R01-NS088604-01A1   Monday, May 02, 2016 *** Zoonotic Potential of CWD Prions: An Update Prion 2016 Tokyo *** http://chronic-wasting-disease.blogspot.com/2016/05/zoonotic-potential-of-cwd-prions-update.html   Saturday, April 23, 2016 PRION 2016 TOKYO Saturday, April 23, 2016  SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016  Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online Taylor & Francis Prion 2016 Animal Prion Disease Workshop Abstracts WS-01: Prion diseases in animals and zoonotic potential Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a, Natalia Fernandez-Borges a. and Alba Marin-Moreno a "Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France  Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion. Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.  To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents. These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.  Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with ef?ciency comparable to that of cattle BSE. While the ef?ciency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice. Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.   http://www.tandfonline.com/doi/abs/10.1080/19336896.2016.1163048?journalCode=kprn20  why do we not want to do TSE transmission studies on chimpanzees $ 5. A positive result from a chimpanzee challenged severly would likely create alarm in some circles even if the result could not be interpreted for man. I have a view that all these agents could be transmitted provided a large enough dose by appropriate routes was given and the animals kept long enough. Until the mechanisms of the species barrier are more clearly understood it might be best to retain that hypothesis.  snip...  R. BRADLEY http://collections.europarchive.org/tna/20080102222950/http://www.bseinquiry.gov.uk/files/yb/1990/09/23001001.pdf   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 SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online http://scrapie-usa.blogspot.com/2016/04/scrapie-ws-01-prion-diseases-in-animals.html http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article  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 LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ *** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).*** https://www.landesbioscience.com/journals/prion/article/28124/?nocache=112223249    *** 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 ***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified. P-145 Estimating chronic wasting disease resistance in cervids using real time quaking- induced conversion Nicholas J Haley1, Rachel Rielinqer2, Kristen A Davenport3, W. David Walter4, Katherine I O'Rourke5, Gordon Mitchell6, Juergen A Richt2 1 Department of Microbiology and Immunology, Midwestern University, United States; 2Department of Diagnostic Medicine and Pathobiology, Kansas State University; 3Prion Research Center; Colorado State University; 4U.S. Geological Survey, Pennsylvania Cooperative Fish and Wildlife Research Unit; 5Agricultural Research Service, United States Department of Agriculture; 6Canadian Food Inspection Agency, National and OlE Reference Laboratory for Scrapie and CWO In mammalian species, the susceptibility to prion diseases is affected, in part, by the sequence of the host's prion protein (PrP). In sheep, a gradation from scrapie susceptible to resistant has been established both in vivo and in vitro based on the amino acids present at PrP positions 136, 154, and 171, which has led to global breeding programs to reduce the prevalence of scrapie in domestic sheep. In cervids, resistance is commonly characterized as a delayed progression of chronic wasting disease (CWD); at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified. To model the susceptibility of various naturally-occurring and hypothetical cervid PrP alleles in vitro, we compared the amplification rates and efficiency of various CWD isolates in recombinant PrPC using real time quaking-induced conversion. We hypothesized that amplification metrics of these isolates in cervid PrP substrates would correlate to in vivo susceptibility - allowing susceptibility prediction for alleles found at 10 frequency in nature, and that there would be an additive effect of multiple resistant codons in hypothetical alleles. Our studies demonstrate that in vitro amplification metrics predict in vivo susceptibility, and that alleles with multiple codons, each influencing resistance independently, do not necessarily contribute additively to resistance. Importantly, we found that the white-tailed deer 226K substrate exhibited the slowest amplification rate among those evaluated, suggesting that further investigation of this allele and its resistance in vivo are warranted to determine if absolute resistance to CWD is possible. ***at present, no cervid PrP allele conferring absolute resistance to prion infection has been identified. PRION 2016 CONFERENCE TOKYO http://prion2016.org/dl/newsletter_03.pdf Saturday, May 28, 2016 *** Infection and detection of PrPCWD in soil from CWD infected farm in Korea Prion 2016 Tokyo *** http://chronic-wasting-disease.blogspot.com/2016/05/infection-and-detection-of-prpcwd-in.html *** Infectious agent of sheep scrapie may persist in the environment for at least 16 years *** Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3 http://jgv.sgmjournals.org/content/87/12/3737.full Using in vitro prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission.  Claudio Soto Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston.  Prion and prion-like proteins are misfolded protein aggregates with the ability to selfpropagate to spread disease between cells, organs and in some cases across individuals. I n T r a n s m i s s i b l e s p o n g i f o r m encephalopathies (TSEs), prions are mostly composed by a misfolded form of the prion protein (PrPSc), which propagates by transmitting its misfolding to the normal prion protein (PrPC). The availability of a procedure to replicate prions in the laboratory may be important to study the mechanism of prion and prion-like spreading and to develop high sensitive detection of small quantities of misfolded proteins in biological fluids, tissues and environmental samples. Protein Misfolding Cyclic Amplification (PMCA) is a simple, fast and efficient methodology to mimic prion replication in the test tube. PMCA is a platform technology that may enable amplification of any prion-like misfolded protein aggregating through a seeding/nucleation process. In TSEs, PMCA is able to detect the equivalent of one single molecule of infectious PrPSc and propagate prions that maintain high infectivity, strain properties and species specificity. Using PMCA we have been able to detect PrPSc in blood and urine of experimentally infected animals and humans affected by vCJD with high sensitivity and specificity. Recently, we have expanded the principles of PMCA to amplify amyloid-beta (Aβ) and alphasynuclein (α-syn) aggregates implicated in Alzheimer's and Parkinson's diseases, respectively. Experiments are ongoing to study the utility of this technology to detect Aβ and α-syn aggregates in samples of CSF and blood from patients affected by these diseases. ========================= ***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease. ======================== Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis. https://prion2015.files.wordpress.com/2015/05/programguide1.pdf  see ;  with CWD TSE Prions, I am not sure there is any absolute yet, other than what we know with transmission studies, and we know tse prion kill, and tse prion are bad. science shows to date, that indeed soil, dirt, some better than others, can act as a carrier. same with objects, farm furniture. take it with how ever many grains of salt you wish, or not. if load factor plays a role in the end formula, then everything should be on the table, in my opinion...tss see ;  ***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease. Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis.  https://prion2015.files.wordpress.com/2015/05/programguide1.pdf  see ; http://www.tandfonline.com/doi/pdf/10.4161/pri.28467  Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil Particles  Author Summary Transmissible spongiform encephalopathies (TSEs) are a group of incurable neurological diseases likely caused by a misfolded form of the prion protein. TSEs include scrapie in sheep, bovine spongiform encephalopathy (‘‘mad cow’’ disease) in cattle, chronic wasting disease in deer and elk, and Creutzfeldt-Jakob disease in humans. Scrapie and chronic wasting disease are unique among TSEs because they can be transmitted between animals, and the disease agents appear to persist in environments previously inhabited by infected animals. Soil has been hypothesized to act as a reservoir of infectivity and to bind the infectious agent. In the current study, we orally dosed experimental animals with a common clay mineral, montmorillonite, or whole soils laden with infectious prions, and compared the transmissibility to unbound agent. We found that prions bound to montmorillonite and whole soils remained orally infectious, and, in most cases, increased the oral transmission of disease compared to the unbound agent. The results presented in this study suggest that soil may contribute to environmental spread of TSEs by increasing the transmissibility of small amounts of infectious agent in the environment.  https://www.aphis.usda.gov/emergency_response/downloads/tools/johnson%20et%20al%20prions%20in%20soil.pdf  tse prion soil  http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0058630  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3567181/pdf/ppat.1003113.pdf  http://www.nature.com/srep/2015/150210/srep08358/full/srep08358.html?WT.ec_id=SREP-639-20150217  http://www.cell.com/cell-reports/pdfExtended/S2211-1247(15)00437-4  Wednesday, December 16, 2015  Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission  http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full The sources of dust borne prions are unknown but it seems reasonable to assume that faecal, urine, skin, parturient material and saliva-derived prions may contribute to this mobile environmental reservoir of infectivity. This work highlights a possible transmission route for scrapie within the farm environment, and this is likely to be paralleled in CWD which shows strong similarities with scrapie in terms of prion dissemination and disease transmission. The data indicate that the presence of scrapie prions in dust is likely to make the control of these diseases a considerable challenge.  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4397813/pdf/13567_2015_Article_176.pdf >>>Particle-associated PrPTSE molecules may migrate from locations of deposition via transport processes affecting soil particles, including entrainment in and movement with air and overland flow. <<< Fate of Prions in Soil: A Review Christen B. Smith, Clarissa J. Booth, and Joel A. Pedersen* Several reports have shown that prions can persist in soil for several years. Significant interest remains in developing methods that could be applied to degrade PrPTSE in naturally contaminated soils. Preliminary research suggests that serine proteases and the microbial consortia in stimulated soils and compost may partially degrade PrPTSE. Transition metal oxides in soil (viz. manganese oxide) may also mediate prion inactivation. Overall, the effect of prion attachment to soil particles on its persistence in the environment is not well understood, and additional study is needed to determine its implications on the environmental transmission of scrapie and CWD. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3160281/ P.161: Prion soil binding may explain efficient horizontal CWD transmission Conclusion. Silty clay loam exhibits highly efficient prion binding, inferring a durable environmental reservoir, and an efficient mechanism for indirect horizontal CWD transmission.  https://prion2015.files.wordpress.com/2015/05/prion2015abstracts.pdf >>>Another alternative would be an absolute prohibition on the movement of deer within the state for any purpose. While this alternative would significantly reduce the potential spread of CWD, it would also have the simultaneous effect of preventing landowners and land managers from implementing popular management strategies involving the movement of deer, and would deprive deer breeders of the ability to engage in the business of buying and selling breeder deer. Therefore, this alternative was rejected because the department determined that it placed an avoidable burden on the regulated community.<<<  Wednesday, December 16, 2015  Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission  Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4, Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1  1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge, Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK  Classical scrapie is an environmentally transmissible prion disease of sheep and goats. Prions can persist and remain potentially infectious in the environment for many years and thus pose a risk of infecting animals after re-stocking. In vitro studies using serial protein misfolding cyclic amplification (sPMCA) have suggested that objects on a scrapie affected sheep farm could contribute to disease transmission. This in vivo study aimed to determine the role of field furniture (water troughs, feeding troughs, fencing, and other objects that sheep may rub against) used by a scrapie-infected sheep flock as a vector for disease transmission to scrapie-free lambs with the prion protein genotype VRQ/VRQ, which is associated with high susceptibility to classical scrapie. When the field furniture was placed in clean accommodation, sheep became infected when exposed to either a water trough (four out of five) or to objects used for rubbing (four out of seven). This field furniture had been used by the scrapie-infected flock 8 weeks earlier and had previously been shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of 23) through exposure to contaminated field furniture placed within pasture not used by scrapie-infected sheep for 40 months, even though swabs from this furniture tested negative by PMCA. This infection rate decreased (1 out of 12) on the same paddock after replacement with clean field furniture. Twelve grazing sheep exposed to field furniture not in contact with scrapie-infected sheep for 18 months remained scrapie free. The findings of this study highlight the role of field furniture used by scrapie-infected sheep to act as a reservoir for disease re-introduction although infectivity declines considerably if the field furniture has not been in contact with scrapie-infected sheep for several months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental contamination. snip...  Discussion  Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23).  Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier.  This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.  PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.  In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.  Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification  http://journal.frontiersin.org/article/10.3389/fvets.2015.00032/full  Wednesday, December 16, 2015  *** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***  http://scrapie-usa.blogspot.com/2015/12/objects-in-contact-with-classical.html   Sunday, December 11, 2016 Clay Components in Soil Dictate Environmental Stability and Bioavailability of Cervid Prions in Mice http://chronic-wasting-disease.blogspot.com/2016/12/clay-components-in-soil-dictate.html Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie Experiment 1964 How Did CWD Get Way Down In Medina County, Texas? Confucius ponders... Could the Scrapie experiments back around 1964 at Moore Air Force near Mission, Texas, could this area have been ground zero for CWD TSE Prion (besides the CWD cases that have waltzed across the Texas, New Mexico border near WSMR Trans Pecos region since around 2001)? Epidemiology of Scrapie in the United States 1977 snip... Scrapie Field Trial Experiments Mission, Texas A Scrapie Field Trial was developed at Mission, Texas, to provide additional information for the eradication program on the epidemiology of natural scrapie. The Mission Field Trial Station is located on 450 acres of pastureland, part of the former Moore Air Force Base, near Mission, Texas. It was designed to bring previously exposed, and later also unexposed, sheep or goats to the Station and maintain and breed them under close observation for extended periods to determine which animals would develop scrapie and define more closely the natural spread and other epidemiological aspects of the disease. The 547 previously exposed sheep brought to the Mission Station beginning in 1964 were of the Cheviot, Hampshire, Montadale, or Suffolk breeds. They were purchased as field outbreaks occurred, and represented 21 bloodlines in which scrapie had been diagnosed. Upon arrival at the Station, the sheep were maintained on pasture, with supplemental feeding as necessary. The station was divided into 2 areas: (1) a series of pastures and-pens occupied by male animals only, and (2) a series of pastures and pens occupied by females and young progeny of both sexes. ... snip...see full text ; http://web.archive.org/web/20030513212324/http://www.bseinquiry.gov.uk/files/mb/m08b/tab64.pdf   Thursday, June 09, 2016 Scrapie Field Trial Experiments Mission, Texas, The Moore Air Force Base Scrapie TSE Prion Experiment 1964 How Did CWD Get Way Down In Medina County, Texas?  http://chronic-wasting-disease.blogspot.com/2016/06/how-did-cwd-get-way-down-in-medina.html http://scrapie-usa.blogspot.com/2016/06/scrapie-field-trial-experiments-mission.html    Friday, April 22, 2016 *** Texas Scrapie Confirmed in a Hartley County Sheep where CWD was detected in a Mule Deer   http://scrapie-usa.blogspot.com/2016/04/texas-scrapie-confirmed-in-hartley.html  Thursday, December 08, 2016 USDA APHIS National Scrapie Eradication Program October 2016 Monthly Report Fiscal Year 2017 atypical NOR-98 Scrapie http://scrapie-usa.blogspot.com/2016/12/usda-aphis-national-scrapie-eradication.html *** Title: Pathological features of chronic wasting disease in reindeer and demonstration of horizontal transmission *** https://www.ars.usda.gov/research/publications/publication/?seqNo115=328261 PLEASE SEE DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE Volume 22, Number 12—December 2016 Dispatch Horizontal Transmission of Chronic Wasting Disease in Reindeer http://wwwnc.cdc.gov/eid/article/22/12/16-0635_article Monday, September 05, 2016 Pathological features of chronic wasting disease in reindeer and demonstration of horizontal transmission Major Findings for Norway http://chronic-wasting-disease.blogspot.com/2016/09/pathological-features-of-chronic.html Thursday, September 22, 2016 NORWAY DETECTS 5TH CASE OF CHRONIC WASTING DISEASE CWD TSE PRION Skrantesjuke http://chronic-wasting-disease.blogspot.com/2016/09/norway-detects-5th-case-of-chronic.html SUNDAY, OCTOBER 02, 2016 *** What is the risk of a cervid TSE being introduced from Norway into Great Britain? Qualitative Risk Assessment September 2016 http://chronic-wasting-disease.blogspot.com/2016/10/what-is-risk-of-cervid-tse-being.html Sunday, December 11, 2016 Clay Components in Soil Dictate Environmental Stability and Bioavailability of Cervid Prions in Mice http://chronic-wasting-disease.blogspot.com/2016/12/clay-components-in-soil-dictate.html Wednesday, December 14, 2016 Increased Abundance of M Cells in the Gut Epithelium Dramatically Enhances Oral Prion Disease Susceptibility http://prionprp.blogspot.com/2016/12/increased-abundance-of-m-cells-in-gut.html some of you may be interested in these videos presented recently at the WYOMING CWD FORUM. Thursday, December 15, 2016 Wyoming National Elk Refuge CWD forum update December 8, 2016 http://chronic-wasting-disease.blogspot.com/2016/12/wyoming-national-elk-refuge-cwd-forum.html Friday, November 18, 2016 Missouri MDC Collected 19,200 Tissue Samples for CWD Testing MDC thanks hunters for help in collecting 19,200 tissue samples for CWD testing https://huntfish.mdc.mo.gov/hunting-trapping/wildlife-diseases/chronic-wasting-disease-cwd/cwd-surveillance-and-monitoring http://chronic-wasting-disease.blogspot.com/2016/11/missouri-mdc-collected-19200-tissue.html Friday, June 01, 2012 TEXAS DEER CZAR TO WISCONSIN ASK TO EXPLAIN COMMENTS Deer expert asked to explain comments http://chronic-wasting-disease.blogspot.com/2012/06/texas-deer-czar-to-wisconsin-ask-to.html Sunday, May 08, 2016 WISCONSIN CHRONIC WASTING DISEASE CWD TSE PRION UPDATE WISCONSIN CHRONIC WASTING DISEASE CWD TSE PRION SPIRALING FURTHER INTO THE ABYSS UPDATE Wisconsin Chronic Wasting Disease CWD TSE Prion http://chronic-wasting-disease.blogspot.com/2016/05/wisconsin-chronic-wasting-disease-cwd.html Sunday, July 26, 2015 TEXAS IN MELT DOWN MODE OVER CAPTIVE CWD AND THEY ARE PUTTING LIPSTICK ON THAT PIG AND TAKING HER TO THE DANCE LIKE MAD COW DISEASE http://chronic-wasting-disease.blogspot.com/2015/07/texas-in-melt-down-mode-over-captive.html Saturday, December 03, 2016 TEXAS CHRONIC WASTING DISEASE CWD TSE PRION UPDATE 35 CASES TO DATE http://chronic-wasting-disease.blogspot.com/2016/12/texas-chronic-wasting-disease-cwd-tse.html Sunday, January 24, 2016 IOWA CHRONIC WASTING TSE PRION DISEASE UPDATE http://chronic-wasting-disease.blogspot.com/2016/01/iowa-chronic-wasting-tse-prion-disease.html 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. http://www.iowadnr.gov/Portals/idnr/uploads/Hunting/060613_consent_order.pdf  ***79.8 percent of the deer tested positive for the disease ***  ***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). ***  For Immediate Release  Thursday, October 2, 2014  Dustin Vande Hoef 515/281-3375 or 515/326-1616 (cell) or Dustin.VandeHoef@IowaAgriculture.gov Share on facebook Share on twitter Share on email Share on print More Sharing Services 1  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). The owners of the quarantined herd have entered into a fence maintenance agreement with the Iowa Department of Agriculture and Land Stewardship, which requires the owners to maintain the 8’ foot perimeter fence around the herd premises for five years after the depopulation was complete and the premises had been cleaned and disinfected  CWD is a progressive, fatal, degenerative neurological disease of farmed and free-ranging deer, elk, and moose. There is no known treatment or vaccine for CWD. CWD is not a disease that affects humans.  On July 18, 2012, USDA Animal and Plant Health Inspection Service’s (APHIS) National Veterinary Services Lab in Ames, IA confirmed that a male white tail deer harvested from a hunting preserve in southeast IA was positive for CWD. An investigation revealed that this animal had just been introduced into the hunting preserve from the above-referenced captive deer herd in north-central Iowa.  The captive deer herd was immediately quarantined to prevent the spread of CWD. The herd has remained in quarantine until its depopulation on August 25 to 27, 2014.  The Iowa Department of Agriculture and Land Stewardship participated in a joint operation to depopulate the infected herd with USDA Veterinary Services, which was the lead agency, and USDA Wildlife Services.  Federal indemnity funding became available in 2014. USDA APHIS appraised the captive deer herd of 376 animals at that time, which was before depopulation and testing, at $1,354,250. At that time a herd plan was developed with the owners and officials from USDA and the Iowa Department of Agriculture and Land Stewardship.  Once the depopulation was complete and the premises had been cleaned and disinfected, indemnity of $917,100.00 from the USDA has been or will be paid to the owners as compensation for the 356 captive deer depopulated.  The Iowa Department of Agriculture and Land Stewardship operates a voluntary CWD program for farms that sell live animals. Currently 145 Iowa farms participate in the voluntary program. The above-referenced captive deer facility left the voluntary CWD program prior to the discovery of the disease as they had stopped selling live animals. All deer harvested in a hunting preserve must be tested for CWD.   -30-  http://www.iowaagriculture.gov/press/2014press/press10022014.asp  *** Federal indemnity funding became available in 2014. USDA APHIS appraised the captive deer herd of 376 animals at that time, which was before depopulation and testing, at $1,354,250.  *** At that time a herd plan was developed with the owners and officials from USDA and the Iowa Department of Agriculture and Land Stewardship.  *** Once the depopulation was complete and the premises had been cleaned and disinfected, indemnity of $917,100.00 from the USDA has been or will be paid to the owners as compensation for the 356 captive deer depopulated.  SEE A FEW OF WISCONSIN CWD ENTITLEMENT PAYOUTS TO CAPTIVE OWNERS ;  $298,770 + $465,000  Sunday, January 17, 2016  Wisconsin Captive CWD Lotto Pays Out Again indemnity payment of $298,770 for 228 white-tailed deer killed on farm  http://chronic-wasting-disease.blogspot.com/2016/01/wisconsin-captive-cwd-lotto-pays-out.html this does not look good ; snip...see full text ; http://chronic-wasting-disease.blogspot.com/2016/01/iowa-chronic-wasting-tse-prion-disease.html Tuesday, December 20, 2016 IOWA CHRONIC WASTING DISEASE FOUND AT A DEER FARM IN BUCHANAN COUNTY http://chronic-wasting-disease.blogspot.com/2016/12/iowa-chronic-wasting-disease-found-at.html Tuesday, December 27, 2016 Minnesota 3rd CWD infected deer identified in southeast http://chronic-wasting-disease.blogspot.com/2016/12/minnesota-3rd-cwd-infected-deer.html Tuesday, November 22, 2016 Minnesota Tests confirm 2 CWD-positive deer near Lanesboro http://chronic-wasting-disease.blogspot.com/2016/11/minnesota-tests-confirm-2-cwd-positive.html Friday, August 05, 2016 MINNESOTA CHRONIC WASTING DISEASE SURVEILLANCE AND TESTING CWD TSE PRION UPDATE http://chronic-wasting-disease.blogspot.com/2016/08/minnesota-chronic-wasting-disease.html http://chronic-wasting-disease.blogspot.com/ Comment Comment Period Closed Mar 31 2014, at 11:59 PM ET ID: APHIS-2006-0118-0411 Docket No. 00-108-10 Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose; Program Standards >>>The CWD herd certification program is a voluntary, cooperative program that establishes minimum requirements for the interstate movement of farmed or captive cervids, provisions for participating States to administer Approved State CWD Herd Certification Programs, and provisions for participating herds to become certified as having a low risk of being infected with CWD<<< Greetings USDA/APHIS et al, I kindly would like to comment on Docket No. 00-108-10 Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose; Program Standards. https://www.regulations.gov/document?D=APHIS-2006-0118-0411 Comment Comment Period Closed Jun 1 2009, at 11:59 PM ET ID: APHIS-2006-0118-0100 APHIS-2006-0118-0096 Greetings APHIS et al, I would kindly like to comment on ; Docket ID APHIS-2006-0118 Docket Title Chronic Wasting Disease Herd Certification Program Document ID APHIS-2006-0118-0096 Document Title Chronic Wasting Disease Herd Certification Program and Interstate Movement of Farmed or Captive Deer, Elk, and Moose with great sadness, my comments are as follows ;  https://www.regulations.gov/document?D=APHIS-2006-0118-0100 Comment Comment Period Closed Jun 13 2016, at 11:59 PM ET Docket No. FDA-2013-N-0764 for Animal Feed Regulatory Program Standards. Singeltary Comment, Greetings FDA et al, I would kindly like to comment on ; Docket No. FDA-2013-N-0764 for Animal Feed Regulatory Program Standards. https://www.regulations.gov/document?D=FDA-2013-N-0764-0008 Comment Greetings FDA et al, I kindly would like to make comment submission to ; Docket No. FDA-2016-N-0321 Risk Assessment of Foodborne Illness Associated with Pathogens from Produce Grown in Fields Amended with Untreated Biological Soil Amendments of Animal Origin; Request for Comments, Scientific Data, and Information A Notice by the Food and Drug Administration on 03/04/2016 MY comment as follows, https://www.regulations.gov/document?D=FDA-2016-N-0321-0005 related information, Open Docket Folder Comment Docket No. APHIS-2014-0107 Bovine Spongiform Encephalopathy; Importation of Animals and Animal Products Singeltary Submission ; Comment Period Closed Mar 2 2015, at 11:59 PM ET ID: APHIS-2014-0107-0003 https://www.regulations.gov/document?D=APHIS-2014-0107-0003 Wednesday, December 21, 2016 TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES 2016 ANNUAL REPORT ARS RESEARCH http://transmissiblespongiformencephalopathy.blogspot.com/2016/12/transmission-differentiation-and.html Thursday, December 08, 2016 USDA APHIS National Scrapie Eradication Program October 2016 Monthly Report Fiscal Year 2017 atypical NOR-98 Scrapie http://scrapie-usa.blogspot.com/2016/12/usda-aphis-national-scrapie-eradication.html http://scrapie-usa.blogspot.com/2016/06/scrapie-field-trial-experiments-mission.html

Friday, December 30, 2016

General Hospital’ actress Barbara Tarbuck dies at 74 from Creutzfeldt Jakob Disease CJD

http://creutzfeldt-jakob-disease.blogspot.com/2016/12/general-hospital-actress-barbara.html

Wednesday, December 14, 2016

Diagnosis of Human Prion Disease Using Real-Time Quaking-Induced Conversion Testing of Olfactory Mucosa and Cerebrospinal Fluid Samples

http://creutzfeldt-jakob-disease.blogspot.com/2016/12/diagnosis-of-human-prion-disease-using.html

Terry S. Singeltary Sr.