Wednesday, December 31, 2014

NASDA BSE, CWD, SCRAPIE, TSE, PRION, Policy Statements updated with amendments passed during the NASDA Annual Meeting Updated September 18, 2014

NASDA BSE, CWD, SCRAPIE, TSE, PRION, Policy Statements updated with amendments passed during the NASDA Annual Meeting Updated September 18, 2014

 

 

Greetings NASDA et al,

 

 

with regards to ;

 

 

NASDA Policy Statements

 

Updated September 18, 2014 Downloaded September 18, 2014 NASDA Policy Statements updated with amendments passed during the 2014 NASDA Annual Meeting

 

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1.2.6 Wild and Exotic Animals

 

The unregulated, or inadequately regulated importation, commercialization, interstate movement and reintroduction of wild and exotic animals, including Cervidae and other wild and exotic ungulate species, poses a disease risk to domestic livestock. Even the barter and sale of surplus animals from quarantined zoos could result in the dissemination of diseases presently foreign to the domestic livestock. There is a need within the United States to address all 11 NASDA Policy Statements

 

susceptible animal species in disease control regulations. USDA should obtain authority over all animal species in order to provide for adequate control measures. The failure to do so will jeopardize the success of national disease eradication programs.

 

Non-indigenous ticks are entering the United States with imported “wildlife” such as lizards, snakes and tortoises, which are imported for the pet trade. These ticks threaten cattle and wildlife by possible transmission of diseases that could cause great economic hardships to agriculture and inhibit foreign trade. Apparently no federal agency has responsibility for the inspection and control of these invasive pests as they arrive on “wildlife” from countries with known infestations of dangerous foreign diseases. Few acaricides have been approved for treatment inside the United States of these “wildlife” for the pests. NASDA encourages the USDA and all other agencies to work closely with foreign governments, with frequent interchanges of information and technical assistance between countries, so that the prevention/eradication efforts and elimination from all animals being exported can be coordinated with prevention/eradication of these pests in the United States. NASDA urges that APHIS and the U.S. Fish and Wildlife Service take all necessary measures to prevent the introduction of non-indigenous ticks into the United States.

 

1.2.7 Disposal of Animal Carcasses and Animal Parts

 

Significant animal mortalities from natural disasters as well as recent outbreaks of infectious animal diseases such as Avian influenza demand expeditious and appropriate disposal of animal carcasses in a manner that will prevent disease spread, prevent excessive air emissions and prevent ground water and environmental contamination by infectious agents or by the byproducts of decomposition. State and federal agencies must have protocols, authorities and approvals in place for appropriate animal carcass disposal prior to, and not after, emergency disease or emergency mortality events. NASDA supports the development of a national coordinated carcass and SRM disposal / utilization plan / guidance that will enable states to be better prepared to address emergency and routine livestock disposal while protecting both public health and the environment.

 

Accurate identification of animals and products, traceability, and documentation of events is essential to ensure appropriate measures. In addition, adequate laboratory and diagnostic capabilities as well as essential interagency real time communication of critical information are important elements for animal carcass disposal. States must have necessary statutory authorities to deal with proper disposal of affected agricultural materials from either disease or other disaster incidences whether from imported or domestic animal production.

 

NASDA will work to formulate and gain approval from all agriculture and environmental agencies of appropriate protocols for permit sanitary carcass disposal; to provide effective systems of identification; to promulgate needed authority in model language; to authorize needed resources and laboratory and diagnostics capacities; and to effectively incorporate interagency communication agreements. 12

 

NASDA Policy Statements

 

1.2.8 Emergency Disease Preparedness/Response

 

Government infrastructure for emergency animal disease preparedness has decreased significantly at both the state and national levels. This has led to serious concerns regarding our ability to control and eradicate foreign animal and poultry diseases in the United States. The economic and trade implications are enormous.

 

Successful strategies for emergency disease preparedness will require the combined cooperative effort of industry, government, and academia. USDA, the states, and regional groups must work in concert to improve communications and to prepare for dealing with emergencies involving the introduction of foreign animal or poultry diseases. NASDA supports the Animal Health Protection Act (AHPA) introduced in Congress in 2000. The AHPA would be a powerful tool for safeguarding the United States from dangerous incursions by granting the USDA broader authority. Appropriate funding must be available to carry out an effective emergency disease response program.

 

The National Veterinary Services Laboratory (NVSL) provides vital support for the animal health programs of the Animal & Plant Health Inspection Service (APHIS). The NVSL plays a crucial role in safeguarding the agriculture of the United States from harmful disease events. Because of its importance in protecting American agriculture, NASDA supports funding for necessary upgrades to the NVSL Ames, Iowa, facility.

 

The heightened awareness of foreign animal diseases due to natural events as well as intentional introductions has been met with like attention to the needs of appropriate funding and infrastructure to implement an effective emergency disease response program.

 

Although the threat for introducing any foreign animal disease into the US is high, the spread of Chronic Wasting Disease (CWD) poses the most immediate threat in the US, as well as multifaceted challenges that impact State Departments of Agriculture, Natural Resources, animal diagnostic laboratories, the farmed cervid industry, deer processors and hunters:

 

• The health of captive herds must be carefully monitored to protect the economic future of the captive cervid industry

 

• Surveillance of the free roaming cervid population must be conducted to determine the prevalence and spread of the disease.

 

• Hunters must have a means of determining whether the animals they harvest are free of disease.

 

• The annual deer harvest must be sufficient to control population.

 

• Licensed deer processors require assurance of the disease status of hunter-killed deer in order to protect conditions in their facilities. 13

 

NASDA Policy Statements

 

Central to the challenges is the need for reliable, rapid diagnostic testing for CWD. Current restrictions on state testing do not promote the broad-based, rapid testing necessary to meet potential demand. USDA’s National Veterinary Services Laboratory (NVSL) conducts CWD surveillance, but is not equipped to provide the fast-turn around testing service required by hunters and processors and necessary to support programs of the Departments of Agriculture and Natural Resources. The current timetable for CWD results at NVSL is two to four weeks.

 

State laboratories must be able to provide CWD testing service.

 

The majority of state-run diagnostic laboratories are prohibited from possessing reagents necessary to run the tests. A limited number of laboratories recently authorized under contract with NVSL are required to use specific equipment (Ventana) and protocols established by NVSL. Non-contract laboratories that own and use quality immunohistochemistry stainers capable of producing accurate CWD test results must purchase a $45,000 Ventana immunohistochemistry stainer and a host of expensive commodities to be recognized by NVSL. NASDA acknowledges that prevention, containment and eradication of foreign animal diseases will require cooperative efforts of federal and state governments, industry, and academia. Further, NASDA urges USDA to:

 

• Expand the authorities of state-run diagnostic labs to conduct tests for foreign animal diseases, including CWD:

 

• Implementation of appropriate protocols to enhance the nation’s infrastructure to address foreign animal diseases, including accepting test results from laboratories that utilize systems other than Ventana, which produce accurate foreign animal disease test results.

 

1.2.9 Bovine Spongiform Encephalopathy Bovine Spongiform Encephalopathy (BSE) in livestock has gained much of the world’s attention with its identification in Western and Eastern Europe, Israel, Japan and North America. BSE and other TSEs are considered serious animal health concerns. BSE has also become a public health issue as a result of the connection that has been made between BSE in cattle and variant Creutzfeld-Jakob Disease (vCJD) in humans. Public confidence in the beef supply is potentially affected each time another case of BSE in cattle is identified. Many questions remain that can only be resolved through further research, on-going evaluation and assessing the risks involved. Maintaining an adequate food safety system while additional knowledge is obtained remains a primary objective.

 

NASDA supports a policy which assures that the U. S. actions are supported by the best available science–a policy that embraces research as a method to advance current knowledge and understanding, is based on risk analysis, is able to assure the consuming public that the beef supply is safe because of the actions taken by U. S. public agencies and is fair to U. S. beef producers.

 

Within this context, NASDA supports—

 

• Development of a feed ban based on the best available science and is enforceable. 14 NASDA Policy Statements

 

• Increased research – especially to develop an in vitro testing procedure that is rapid, accurate, and cost efficient, further analysis of other possible methods of transmission of the disease in cattle (e. g., blood/tissue), other possible avenues of transmission to humans, disposal options for SRM, infectivity of tissue from animals under 30 months of age, develop and implement effective methods for inactivation of transmissible spongiform encephalopathy (TSE) agents, further determination of pathways by which the agent causes the disease.

 

• Risk assessment – determine options for proper actions based on risk assessment.

 

• Normalization of trade and consideration of regionalized barriers, where appropriate, to minimize the overall effect on U. S. producers while regional issues are worked out. Regionalization areas may be across international borders. • An emphasis on developing whatever is needed to allow the U. S. to qualify for better than minimal risk status with our trading partners. • The need for an animal ID system that is operational as soon as practical. • Harmonization of all animal health standards. Harmonization of BSE Standards while avoiding reaching agreement on other standards is not generally recognized as free trade in the U. S. No feeder cattle should be allowed to be imported until agreement is reached on harmonization of other animal health standards, especially bluetongue, anaplasmosis, brucellosis, and tuberculosis.

 

• NASDA realizes there is no such thing as a no cost policy-if the U. S. needs to take actions to assure eradication in a reasonable timeframe, NASDA believes that affected sectors of the industry (e.g., renderers, perhaps others) should be assisted to assure compliance is reached as reasonably as possible.

 

• Surveillance programs that assure the U. S. is compliant with OIE Standards and that go beyond compliance where such actions can lead to the removal of infected animals from the U. S. herd (e.g., due diligence on trace-forwards, trace-backs and cohorts). 1.2.10 Animal Disease Eradication and Control The completion of several disease control programs of significance to the economic viability of livestock production agriculture in the United States is nearing. Bovine tuberculosis, bovine brucellosis, swine brucellosis and pseudorabies are examples of diseases that will likely be eradicated from domestic livestock. Funding cuts and other resource constraints threaten the ability of USDA, specifically the Animal and Plant Health Inspection Service (APHIS), to complete these important programs. As international trade has increased, the threat of an outbreak of a foreign animal disease in the United States has also increased. Such an outbreak would disrupt production of food animals, 15 NASDA Policy Statements interrupt the domestic meat and poultry supply, adversely affect food processing, marketing and the distribution chain, and cause the loss of export markets for United States livestock and livestock products. The loss to the United States would be billions of dollars in trade of agricultural products. NASDA encourages APHIS to accept the DNA test in sheep, proven by ARS researchers as well as scientists in Great Britain as reliable, in determining scrapie susceptibility. NASDA believes that disease control programs are essential if eradication of animal and poultry diseases and the prevention of the introduction or outbreak of foreign or domestic diseases is to be successful. Priority should be given to programs whose efforts are aimed at preventing the outbreak of animal health diseases and protecting our nation’s domestic livestock from foreign diseases. Valid tests should also be developed to properly detect diseases that pose a risk to animal health. Some animal health diseases that require specific attention are:

 

• Avian Influenza

 

• Bluetongue

 

• Brucellosis

 

• Johnes Disease

 

• Pseudorabies

 

• Raccoon Strain Rabies

 

• Scrapie

 

• Tuberculosis

 

• Vesicular Stomatitis

 

• Chronic Wasting Disease

 

• Anaplasmosis

 

• West Nile Viral Encephalitis

 

Sufficient resources should be made available for such programs so that the appropriate agencies can provide indemnity to owners of diseased livestock, which will encourage the elimination of remaining infected herds, and maintain an adequate number of animal health professionals able to respond to animal health issues.

 

NASDA believes that any comprehensive program to control or eradicate disease from domestic livestock should include provisions for testing, quarantining exposed animals, and indemnifying diseased animals. All susceptible species should be included in regulations addressing disease control, including non-livestock species that can harbor and/or transmit diseases of concern. 16

 

NASDA Policy Statements Historically, animal disease eradication and control programs have been cooperative state/federal programs and should continue to be cooperative state/federal programs. APHIS has published a proposed rule that would codify a standardized cost sharing formula for animal disease and plant pest and disease emergency eradication programs that are conducted cooperatively with states. Unfortunately, expanding world trade and the threat of bioterrorism have increased the risk of destructive pests and diseases being introduced into the United States.

 

The United States Department of Agriculture (USDA) is the federal agency statutorily charged with preventing the introduction, spread and establishment of plant pests and diseases, noxious weeds and pests and diseases of livestock in the United States. States are not federally mandated to partner with USDA in this endeavor yet have historically done so with great success. Developing a plan on how the United States Department of Agriculture should respond to emergencies is not without merit. In fact, NASDA's Animal Health Safeguarding Review and the Safeguarding American Plant Resources Review conducted by the National Plant Board contain recommendations that would facilitate the kind of out year planning envisioned in the proposed rule. Emergency programs relating to animal and plant health by their very nature, however, do not accommodate a "one size fits all" approach. While some suggest a cost share formula would yield savings to the Federal Government in future years, it will actually result in quite the opposite for states, who are already bearing significant costs associated with plant and animal pest and diseases that are not detected at the border. NASDA urges USDA to withdraw the proposed rule and work with states toward the development of a joint system for the early detection and eradication of plant and animal pests and diseases.

 

NASDA's Animal Health Safeguarding Review and the Safeguarding American Plant Resources Review would provide a sound footing for the development of a science based rule that combines the unique abilities of each partner. NASDA discourages attempts to construct meaningful eradication programs around budgetary decisions.

 

1.2.11 Homeland Security and Agriculture NASDA strongly supports the pest exclusion mission area known as Agricultural Quarantine Inspection (AQI) at the nation’s ports of entry that serve to protect our domestic agriculture industry from a foreign pest or disease incursion. After the events of September 11, 2001 and the anthrax incidents that followed, AQI functions were transferred from the United States Department of Agriculture (USDA) to the newly created Department of Homeland Security ("DHS") in an effort to consolidate all governmental functions that protect the nation against threats to the homeland into one agency.

 

NASDA strongly supports the mission and efforts of DHS to prevent terrorists and terrorist weapons from entering the United States. While the prevention of terrorists and terrorist weapons from entering the United States is vital to the security of the nation, so too, is the protection of the nation's food supply, our agricultural economy, and animal health. Introductions of foreign animal diseases, such as Exotic Newcastle Disease and emerging diseases, such as West Nile Virus, Avian Influenza and Chronic Wasting 17

 

NASDA Policy Statements

 

Disease, are of great concern to the nation’s livestock and animal producers and could cause significant impacts to the nation’s agricultural economy. Unfortunately, since the AQI transfer, pest and disease introductions have increased dramatically. It is clear that DHS’ administration of the AQI program lacks efficacy and currently there are no performance measures relative to AQI functions that DHS must meet to ensure the resources that DHS receives to protect the U.S. domestic agriculture sector are being utilized for this purpose. In addition, in order for AQI to remain effective while housed at DHS, it was essential that DHS and APHIS establish a consistent and clear communication structure that provides for problem resolution with built-in accountability in order to provide the greatest degree of risk reduction. Unfortunately, DHS’ mission is so broad that AQI is not viewed within the agency as a critical function either in terms of staffing or funding. Therefore, NASDA supports the re-assignment of the AQI mission area back to USDA APHIS given that they have the expertise to carry out a focused, coordinated and effective agricultural safeguarding effort and are statutorily charged with managing exotic pests and diseases.

 

NASDA urges that increased emphasis be placed on the mission of safeguarding agriculture and strongly supports the immediate adoption of quantifiable performance measures for AQI functions to ensure the program is meeting the statutory mission for which it was created – protecting American agriculture from a foreign plant or animal pest or disease. These performance measures should consider the interdiction, control, eradication and suppression costs borne by state and local governments for foreign pests and diseases that AQI fails to interdict at the ports of entry. These costs shall be assessed to the budget of the parent department of AQI. In addition, NASDA urges DHS’ Office of Domestic Preparedness to provide specific funding opportunities to state departments of agriculture for local preparedness similar to grants provided to state departments of health.

 

1.3 APHIS REORGANIZATION AND CONSOLIDATION

 

USDA’s Animal and Plant Health Inspection Service (APHIS) consolidated the following offices — Veterinary Services (VS), Plant Protection and Quarantine (PPQ), Wildlife Services, Animal Care, and Investigations and Enforcement Services — into two regional offices. The consolidation streamlined the administration of programs, permitted cross utilization of personnel, and made the agency more responsive to the needs of the states and their constituencies. NASDA commends APHIS for its efforts to seek efficiency within the federal government and to improve satisfaction of its constituencies. We recognize the importance of the consolidation of APHIS programs into eastern and western regional offices as a cost savings measure, while maintaining accessibility by customers and partners. NASDA recommends that, to prevent negative impacts on services, costs for future reorganizations should not be taken from operational programs, but from agency overhead savings. Further, NASDA recognizes that plant and animal health issues may not be similar within the consolidated regions and that current funding levels of programs in a particular region may be diminished due to priority setting as a result of the regional consolidation.

 

NASDA urges APHIS 18 NASDA Policy Statements to consider the plant and animal health needs of the states within the current regional composition when allocating program funding.

 

NASDA strongly supports increasing funding to PPQ Unit for the purpose of interception of illegal and smuggled food products that pose a direct threat to the food security of the United States of America and to homeland security.

 

NASDA also strongly supports increasing APHIS’s ability to fine and prosecute offenders of United States’ agricultural import laws.

 

NASDA also recognizes that the 48 inspectors that the PPQ Smuggling and Interdiction Program has for inspection of all imported food and agricultural products into the United States is severely inadequate and further poses a direct flaw in the United States’ ability to ensure food security and homeland security.

 

1.4 ANIMAL DAMAGE CONTROL

 


 

 

I kindly submit the following scientific update on the Transmissible Spongiform Encephalopathy TSE prion disease ;

 

 

DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012

 

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In the USA, under the Food and Drug Administration’s BSE Feed Regulation (21 CFR 589.2000) most material (exceptions include milk, tallow, and gelatin) from deer and elk is prohibited for use in feed for ruminant animals. With regards to feed for non-ruminant animals, under FDA law, CWD positive deer may not be used for any animal feed or feed ingredients. For elk and deer considered at high risk for CWD, the FDA recommends that these animals do not enter the animal feed system. However, this recommendation is guidance and not a requirement by law.

 

Animals considered at high risk for CWD include:

 

1) animals from areas declared to be endemic for CWD and/or to be CWD eradication zones and

 

2) deer and elk that at some time during the 60-month period prior to slaughter were in a captive herd that contained a CWD-positive animal.

 

Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.

 

The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.

 

Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.

 

There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.

 

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36% in 2007 (Almberg et al., 2011). In such areas, population declines of deer of up to 30 to 50% have been observed (Almberg et al., 2011). In areas of Colorado, the prevalence can be as high as 30% (EFSA, 2011).

 

The clinical signs of CWD in affected adults are weight loss and behavioural changes that can span weeks or months (Williams, 2005). In addition, signs might include excessive salivation, behavioural alterations including a fixed stare and changes in interaction with other animals in the herd, and an altered stance (Williams, 2005). These signs are indistinguishable from cervids experimentally infected with bovine spongiform encephalopathy (BSE).

 

Given this, if CWD was to be introduced into countries with BSE such as GB, for example, infected deer populations would need to be tested to differentiate if they were infected with CWD or BSE to minimise the risk of BSE entering the human food-chain via affected venison.

 

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The rate of transmission of CWD has been reported to be as high as 30% and can approach 100% among captive animals in endemic areas (Safar et al., 2008).

 

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In summary, in endemic areas, there is a medium probability that the soil and surrounding environment is contaminated with CWD prions and in a bioavailable form. In rural areas where CWD has not been reported and deer are present, there is a greater than negligible risk the soil is contaminated with CWD prion.

 

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In summary, given the volume of tourists, hunters and servicemen moving between GB and North America, the probability of at least one person travelling to/from a CWD affected area and, in doing so, contaminating their clothing, footwear and/or equipment prior to arriving in GB is greater than negligible. For deer hunters, specifically, the risk is likely to be greater given the increased contact with deer and their environment. However, there is significant uncertainty associated with these estimates.

 

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Therefore, it is considered that farmed and park deer may have a higher probability of exposure to CWD transferred to the environment than wild deer given the restricted habitat range and higher frequency of contact with tourists and returning GB residents.

 

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NEW URL LINK ;

 


 

Docket APHIS-2007-0033 Docket Title Agricultural Bioterrorism Protection Act of 2002; Toxin List Docket Type Rulemaking APHIS Posted Apr 09 2009 7:13pm Docket APHIS-2007-0033 Docket Title Agricultural Bioterrorism Protection Act of 2002; Biennial Review and Republication of the Select Agent and Toxin List Docket Type Rulemaking Document APHIS-2007-0033-0001 Document Title Agricultural Bioterrorism Protection Act of 2002; Biennial Review and Republication of the Select Agent and Toxin List Public Submission APHIS-2007-0033-0002.1 Public Submission Title Attachment to Singeltary comment

 

Comment DOCKET APHIS-2007-0033 Agricultural Bioterrorism Protection Act of 2002; Biennial Review and Republication of the Select Agent and Toxin List

 

August, 29, 2007

 

Greetings APHIS,

 

I would kindly like to submit the following to ;

 

DEPARTMENT OF AGRICULTURE Animal and Plant Health Inspection Service

 

7 CFR Part 331 9 CFR Part 121

 

Docket No. APHIS-2007-0033 RIN 0579-AC53

 

This is my second submission to APHIS about Bioterrorism and the Transmissible Spongiform Encephalopathy TSE agent. My first submission was Mon, 27 Jan 2003 15:54:57 -0600 Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of 2002 (see my old submission at bottom dated Subject: Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of 2002; Date: Mon, 27 Jan 2003 15:54:57 -0600 From: "Terry S. Singeltary Sr." To: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000328/!x-usc:mailto:reg ).

 

WHAT I am most concerned about is that ONLY BSE is listed as a dangerous toxin in the family of TSE. With the ever growing list of atypical TSE like atypical BSE BASE, and the atypical Scrapie Nor-98, and also the typical scrapie strains, and Chronic Wasting Disease CWD, why is it only BSE is listed ?

 

I think that all of these TSE's should be listed with the BSE agent as a potential Biological weapon. With these atypical TSE, even more so, due to the fact the possibility of vertical and lateral transmission, unlike BSE (not documented to date to transmit that way). With the atypical BSE BASE being more virulent to humans than the typical BSE, why is it not listed ?

 

WHY is the atypical Scrapie Nor-98, with this being a potential threat to not only animals, but humans as well, why is this not listed ?

 

WHY is Chronic Wasting Disease CWD of deer and elk not listed, especially since CWD has transmitted to the bovine by inoculation to date, with oral studies still ongoing, and the fact the oral route would take much longer, would CWD wreck havoc on a countries economy too, let alone the very real potential for CWD to transmit to humans, why is CWD not listed as a Bio-toxin ?

 

IF these terrorist are willing to walk into a mall and blow themselves up as a walking bomb, what is to keep them from exposing themselves to one of these deadly TSEs, and then going to a hospital and exposing many with CJD somehow. This may seem far fetched, but very possible. Why is CJD not listed ?

 

IN short, and very simple, all you would have to do is change the BSE, to human and animal TSE, thus all bases would be covered. but in only including the BSE strain of TSE agent, I think you are only fooling yourselves, again. ...

 

SOURCES

 

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 Elsevier Editorial System(tm) for The Lancet Infectious DiseasesManuscript DraftManuscript Number:Title: HUMAN and ANIMAL TSE Classifications i.e. mad cowdisease and the UKBSEnvCJD only theoryArticle Type: Personal ViewCorresponding Author: Mr. Terry S. Singeltary,Corresponding Author's Institution: naFirst Author: Terry S Singeltary, noneOrder of Authors: Terry S Singeltary, none; Terry S. SingeltaryAbstract: TSEs have been rampant in the USA for decades in manyspecies, and they all have been rendered and fed backto animals for human/animal consumption. I propose thatthe current diagnostic criteria for human TSEs onlyenhances and helps the spreading of human TSE from thecontinued belief of the UKBSEnvCJD only theory in 2007.

 

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 Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of 2002; [TSS SUBMISSION ON POTENTIAL FOR BSE/TSE & FMD 'SUITCASE BOMBS'] - TSS 1/27/03 (0)

 

Docket Management

 

Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food Facilities, Section 305 Comment Number: EC-254 [TSS SUBMISSION]

 

Subject: Docket No: 02-088-1 RE-Agricultural Bioterrorism Protection Act of 2002; Date: Mon, 27 Jan 2003 15:54:57 -0600 From: "Terry S. Singeltary Sr." To: [log in to unmask] Docket No: 02-088-1

 

Title: Agricultural Bioterrorism Protection Act of 2002; Possession, Use, and Transfer of Biological Agents and Toxins

 


 

 Greetings,

 

i would like to kindly submit to this docket and warn of the potential for biological 'suitcase bombs' from civilian air-traffic populations from known BSE/FMD and other exotic animal disease pathogens coming into the USA.

 

please be warned;

 

Date: Thu, 21 Mar 2002 08:42:56 -0800 Reply-To: Bovine Spongiform Encephalopathy Sender: Bovine Spongiform Encephalopathy From: "Terry S. Singeltary Sr." Subject: USA SEALED BORDERS AND THE ''USCS'' (unspecified species coding system) MORE POTENTIAL B.S.eee

 

Change in Disease Status of Greece With Regard to Foot-and-Mouth

 

[Federal Register: March 21, 2002 (Volume 67, Number 55)]

 

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Under Sec. 94.11, meat and other animal products of ruminants and swine, including ship stores, airplane meals, and baggage containing these meat or animal products, may not be imported into the United States except in accordance with Sec. 94.11 and the applicable requirements of the U.S. Department of Agriculture's Food Safety and Inspection Service at 9 CFR chapter III.

 

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From an economic standpoint, the proposed rule would have little or no impact on U.S. animal stock and commodities. There are two reasons. First, the proposed rule would not remove other disease-based restrictions on the importation of ruminants or swine (and certain meat and other products from those animals) from Greece into the United States. Because bovine spongiform encephalopathy is considered to exist in Greece, the importation of ruminants and meat, meat products, and certain other products of ruminants that have been in Greece is prohibited.

 

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 ========================

 

What are the U.S. imports of affected animals or animal products from the country?

 

Very few products that would be of risk for transmission of BSE were imported into the US from Greece during 2000 or 2001 (January - April). Due to the above mentioned import ban, no live ruminants, ruminant meat, meal made from ruminants, or other high risk products from ruminants were imported from Greece during this time period. In 2001 (January - April), 3000 kg of enzymes and prepared enzymes and 5 kg of medicants containing antibiotics for veterinary use were imported. The data do not provide a species of origin code for these products, therefore they may not contain any ruminant product.

 

Sources: World Trade Atlas

 

What is the level of passenger traffic arriving in the United States from the affected country?

 

Approximately 185,000 direct flights from Greece arrived to US airports in fiscal year 2000. Also, an unknown number of passengers from Greece arrived via indirect flights.

 

Under APHIS-PPQ's agriculture quarantine inspection monitoring, 584 air passengers from Greece were sampled for items of agricultural interest in fiscal year 2000. Of these passengers, 14 carried meat (non-pork) items that could potentially transmit pathogens that cause BSE; most passengers carried from one to two kilograms (kg) of meat, although one passenger in November 1999 carried 23 kg of meat in a suitcase. Florida, Massachusetts, and New York were the reported destinations of these passengers. None of the passengers with meat items reported plans to visit or work on a ranch or farm while in the US.

 

Source: US Department of Transportation, and APHIS-PPQ Agricultural Quarantine Inspection data base

 


 

 Greetings list members,

 

i just cannot accept this;

 

23 kg of meat in a suitcase (suitcase bomb...TSS)

 

The data do not provide a species of origin code for these

 

products, therefore they may not contain any ruminant product.

 

what kind of statement is this?

 

how stupid do they think we are?

 

it could also very well mean that _all_ of it was ruminant based products !

 

Terry S. Singeltary Sr., Bacliff, Texas USA

 

What is the level of passenger traffic arriving in the United States from Slovenia?

 

There were no direct flights from Slovenia to the US in fiscal year 2000.

 

APHIS-PPQ’s agriculture quarantine inspection monitoring sampled 27 air passengers from Slovenia for items of agricultural interest in fiscal year 2000. One of these 27 passengers was carrying two kilograms of a meat item that could potentially harbor pathogens that cause BSE. This passenger arrived to Elizabeth, New York, in June 2000 and declared no intention to visit a farm or ranch in the US.

 

Source: US Department of Transportation, and APHIS-PPQ Agricultural Quarantine Inspection data base

 


 

 What is the level of passenger traffic arriving in the United States from the affected country?

 

A total of 45,438 passengers arrived in the US on direct flights from the Czech Republic in fiscal year 2000. It is likely that additional passengers originating in the Czech Republic traveled to the US on non-direct flights.

 

As part of APHIS-PPQ’s Agriculture Quarantine Inspection Monitoring, 238 air passengers from the Czech Republic were inspected for items of agricultural interest in fiscal year 2000. Of these, 10, or 4.2%, were found to be carrying a total of 17 kg of items that could potentially present a risk for BSE. None of the passengers with items reported plans to visit or work on a farm or ranch while in the US.

 

Source: US Department of Transportation, and APHIS-PPQ Agricultural Quarantine Inspection data base

 


 

 What are the US imports of affected animals or animal products from Austria?

 

Between 1998 and June 2001, US imports from Austria included goat meat, animal feeds, and sausage. The sausage and animals feeds were from unspecified species.

 

Source: World Trade Atlas

 

snip...

 

What is the level of passenger traffic arriving in the United States from Austria?

 

A total of 168,598 passengers on direct flights from Austria arrived at US airports in fiscal year 2000. An undetermined number of passengers from Austria arrived in the US via indirect flights.

 

Under APHIS-PPQ’s agricultural quarantine inspection monitoring, 565 air passengers from Austria were sampled for items of agricultural interest in fiscal year 2000. Ten (10) of these passengers, or 1.7 percent, carried a total of 23 kg meat (non-pork) items that could potentially harbor the pathogen(s) that cause BSE. None of these passengers from whom meat items were confiscated reported plans to visit or work on a ranch or farm during their visit to the US.

 

Source: US Dept. of Transportation; APHIS-PPQ

 


 

 Greetings FDA and public,

 

if you go to the below site, and search all BSE known countries and check out their air traffic illegal meat they have confiscated, and check out the low number checked, compared to actual passenger traffic, would not take too much for some nut to bring in FMD/TSEs into the USA as a 'suitcase bomb'.

 

[[Under APHIS-PPQ's agricultural quarantine inspection monitoring, 284 air passengers from Israel were sampled for items of agricultural interest in fiscal year 2001. Seven of these passengers, or 2 percent, carried a total of 11 kg of meat items that could potentially harbor the pathogen that causes BSE. None of these passengers from whom meat items were confiscated reported plans to visit or work on a ranch or farm during their visit to the U.S.]]

 

if they were to have questioned the terrorist that bombed the Twin Towers with jets, if they were to have questioned them at flight school in the USA, i am sure that they would have said they did not intend to visit the Twin Towers as a flying bomb either. what am i thinking, they probably did ask this? stupid me.

 

[[In 1999 a small amount of non-species specific meat and offal was imported and a small amount of fetal bovine serum (FBS) was also imported. FBS is considered to have a relatively low risk of transmitting BSE.]]

 

more of the USA infamous 'non-species coding system', wonder how many of these species are capable of carrying a TSE?

 

snip...

 

A total of 524,401 passengers arrived on direct flights to the U.S. from Israel in fiscal year 2000. This number does not include passengers who arrived in the U.S. from Israel via indirect flights.

 

Under APHIS-PPQ's agricultural quarantine inspection monitoring, 284 air passengers from Israel were sampled for items of agricultural interest in fiscal year 2001. Seven of these passengers, or 2 percent, carried a total of 11 kg of meat items that could potentially harbor the pathogen that causes BSE. None of these passengers from whom meat items were confiscated reported plans to visit or work on a ranch or farm during their visit to the U.S.

 


 

 Source: U.S. Department of Transportation and APHIS-PPQ Agricultural Quarantine Inspection data base.

 

What is the level of passenger traffic arriving in the United States from Japan?

 

Approximately 6.84 million passengers on 29,826 direct flights from Japan arrived at US airports in fiscal year 2000. An undetermined number of passengers from Japan arrived in the US via indirect flights.

 

Under APHIS-PPQ's agriculture quarantine inspection monitoring, 801 air passengers from Japan were sampled for items of agricultural interest in fiscal year 2000. Of these 801 passengers, 10 carried meat (non-pork) items that could potentially harbor the pathogen(s) that cause BSE; most passengers carried an average of 1.7 kilograms of meat. None of these passengers from whom meat items were confiscated reported plans to visit or work on a ranch or farm during their visit to the US.

 

Source: US Department of Transportation, and APHIS-PPQ Agricultural Quarantine Inspection data base

 


 

 What is the level of passenger traffic arriving in the United States from the affected country?

 

A total of 3.3 million passengers arrived in the US on direct flights from Germany in 1998, although many of these passengers would not have originated in Germany. As part of APHIS-PPQ's Agriculture Quarantine Inspection Monitoring, 8,247 air passengers from Germany were inspected for items of agricultural interest. Of these, 198, or 2.3%, were found to be carrying a total of 304 kg of items that could potentially present a risk for BSE. Thirty (30) of the passengers with items reported plans to visit or work on a farm or ranch while in the US. Reported destination states of these 30 passengers were CA, CO, DE, FL, LA, MT, OH, VA, and WY.

 

Source: US Department of Transportation, and APHIS-PPQ Agricultural Quarantine Inspection data base

 


 

 search archives at bottom of page of each BSE Country;

 


 

 more on non-species coding system and TSEs and potential 'suitcase bombs';

 

To: Bovine Spongiform Encephalopathy Subject: Re: POLAND FINDS 4TH MAD COW CASE/USA IMPORTS FROM POLAND/non-species coding system strikes again References:< [log in to unmask]> Content-Type: text/plain; charset=ISO-8859-1; format=flowed Content-Transfer-Encoding: 8bit X-Virus-Scanner: Found to be clean

 

Greetings again List Members,

 

let me kick a madcow around here a bit.

 

on the imports from Poland and the infamous USA 'non-species' coding system.

 

the USDA/APHIS states;

 

During the past four years (1998 - 2001), US imports from Poland included non-species specific animal products used in animal feeds and non-species specific sausage and offal products (Table 3). Given US restrictions on ruminant product imports, these US imports should not have contained ruminant material.

 

NOW, if you read Polands GBR risk assessment and opinion on BSE, especially _cross-contamination_, it states;

 

ANNEX 1

 

Poland - Summary of the GBR-Assessment, February 2001

 

EXTERNAL CHALLENGE STABILITY INTERACTION OF EXTERNAL CHALLENGE AND STABILITY

 

The very high to extremely high external challenge met a very unstable system and could have led to contamination of domestic cattle in Poland from 1987 onwards.

 

This internal challenge again met the still very unstable system and increased over time.

 

The continuing very high external challenge supported this development.

 

Not OK MBM-ban since 1997, but no feed controls. Reasonably OK Heat treatment equivalent to 133°C / 20min / 3 bar standards, but no evidence provided on compliance.

 

Not OK. No SRM-ban, SRM are rendered and included in cattle feed.

 

BSE surveillance:

 

Not sufficient before 2001.

 

Cross-contamination:

 

Lines for ruminant and non-ruminant feed in feed-mills only separated in time and no analytical controls carried out. Likely present since 1987 and growing.

 

see full text and ANNEX 1 at;

 


 

 so in my humble opinion, the statement by the USDA/APHIS that ''these US imports _should_ not have contained ruminant materials, is a joke. a sad joke indeed.

 

* POLAND BSE GBR RISK ASSESSMENT

 


 

 BSE ISRAEL change in disease status, AND THE DAMN NON-SPECIES CODING SYSTEM $$$

 

Subject: BSE ISRAEL change in disease status, AND THE DAMN NON-SPECIES CODING SYSTEM $$$ Date: November 1, 2002 at 8:03 am PST

 

[Federal Register: November 1, 2002 (Volume 67, Number 212)]

 

DEPARTMENT OF AGRICULTURE

 

Animal and Plant Health Inspection Service

 

9 CFR Part 94

 

[Docket No. 02-072-2]

 

Change in Disease Status of Israel Because of BSE

 

AGENCY: Animal and Plant Health Inspection Service, USDA.

 

ACTION: Affirmation of interim rule as final rule.

 

-----------------------------------------------------------------------

 

SUMMARY: We are adopting as a final rule, without change, an interim rule that amended the regulations by adding Israel to the list of regions where bovine spongiform encephalopathy exists because the disease had been detected in a native-born animal in that region. The effect of the interim rule was a restriction on the importation of ruminants, meat, meat products, and certain other products of ruminants that had been in Israel. The interim rule was necessary to help prevent the introduction of bovine spongiform encephalopathy into the United States.

 

EFFECTIVE DATE: The interim rule became effective on June 4, 2002.

 

FOR FURTHER INFORMATION CONTACT: Dr. Gary Colgrove, Chief Staff Veterinarian, Sanitary Trade Issues Team, National Center for Import and Export, VS, APHIS, 4700 River Road Unit 38, Riverdale, MD 20737- 1231; (301) 734-4356.

 

SUPPLEMENTARY INFORMATION:

 

Background

 

The regulations in 9 CFR parts 93, 94, 95, and 96 (referred to below as the regulations) govern the importation of certain animals, birds, poultry, meat, other animal products and byproducts, hay, and straw into the United States in order to prevent the introduction of various animal diseases, including bovine spongiform encephalopathy (BSE). In an interim rule effective June 4, 2002, and published in the Federal Register on July 18, 2002 (67 FR 47243-47244, Docket No. 02- 072-1), we amended the regulations in Sec. 94.18 (a)(1) by adding Israel to the list of regions where BSE exists due to the detection of BSE in a native-born animal in that region. Comments on the interim rule were required to be received on or before September 16, 2002. We did not receive any comments. Therefore, for the reasons given in the interim rule, we are adopting the interim rule as a final rule. This action also affirms the information contained in the interim rule concerning Executive Orders 12866 and 12988 and the Paperwork Reduction Act. Further, for this action, the Office of Management and Budget has waived its review under Executive Order 12866.

 

Regulatory Flexibility Act

 

This action affirms an interim rule that amended the regulations by adding Israel to the list of regions where BSE exists. The effect of the interim rule was a restriction on the importation of ruminants, meat, meat products, and certain other products of ruminants that had been in Israel. The interim rule was necessary to help prevent the introduction of BSE into the United States. The following analysis addresses the economic effects of the interim rule on small entities, as required by the Regulatory Flexibility Act. The interim rule's restrictions on the importation of ruminants and ruminant products and byproducts from Israel are not expected to have a significant impact on a substantial number of small entities due to the fact that the restricted items are either not imported from Israel or are imported in very small amounts. There are three categories of imports that may be affected, but Israel's share of U.S. imports is small in each case. The first category of affected imported commodities is ``Meat and edible meat offal, salted in brine, dried or smoked; edible flours and meals of meat or meat offal.'' Average total yearly imports of these products by the United States over the 3-year period 1999-2001 were valued at $24.6 million. Imports from Israel in 1999 were valued at $26,000. No imports of these products from Israel were reported for 2000 or 2001. The second category of affected commodities is ``Preparations of a kind used in animal feeding.'' Average total yearly imports of these products, 1999-2001, were valued at $93.5 million. Imports from Israel had an average yearly value over this period of about $76,000. The final category of affected commodities is ``Other prepared or preserved meat, meat offal or blood.'' Average yearly imports of these products, 1999-2001, were valued at $101.2 million. Imports from Israel had an average yearly value over this period of about $2.7 million. It is apparent that Israel is a minor supplier to the United States of the ruminant products and byproducts affected by the BSE-related restrictions resulting from the interim rule. Therefore, we do not expect that the interim rule's restrictions on ruminants and ruminant products and byproducts from Israel will substantially affect any U.S. importers, large or small, of those commodities. Under these circumstances, the Administrator of the Animal and Plant Health Inspection Service has determined that this action will not have a significant economic impact on a substantial number of small entities.

 

List of Subjects in 9 CFR Part 94

 

Animal diseases, Imports, Livestock, Meat and meat products, Milk, Poultry and poultry products, Reporting and recordkeeping requirements.

 

PART 94--RINDERPEST, FOOT-AND-MOUTH DISEASE, FOWL PEST (FOWL PLAGUE), EXOTIC NEWCASTLE DISEASE, AFRICAN SWINE FEVER, HOG CHOLERA, AND BOVINE SPONGIFORM ENCEPHALOPATHY: PROHIBITED AND RESTRICTED IMPORTATIONS

 

Accordingly, we are adopting as a final rule, without change, the interim rule that amended 9 CFR part 94 and that was published at 67 FR 47243-47244 on July 18, 2002.

 

Authority: 7 U.S.C. 450, 7711-7714, 7751, 7754, 8303, 8306, 8308, 8310, 8311, and 8315; 21 U.S.C 136 and 136a; 31 U.S.C. 9701; 42 U.S.C. 4331 and 4332; 7 CFR 2.22, 2.80, and 371.4.

 

Done in Washington, DC, this 28th day of October, 2002. Bobby R. Acord, Administrator, Animal and Plant Health Inspection Service. [FR Doc. 02-27812 Filed 10-31-02; 8:45 am] BILLING CODE 3410-34-P

 


 

 greetings List members,

 

MORE OF THE INFAMOUS USA NON-SPECIES CODING SYSTEM.

 

as long as the exporting country and the importing country know not what they are exporting (play dumb/stupid), this non-species coding system allows potential BSE/TSE materials to be imported and exported freely and legally...

 

TSS

 

What are the U.S. imports of affected animals or animal products from Israel ?

 

The U.S. imported no live ruminants or ruminant meat from Israel since 1999. In 1999 a small amount of non-species specific meat and offal was imported and a small amount of fetal bovine serum (FBS) was also imported. FBS is considered to have a relatively low risk of transmitting BSE. Other imports from Israel during the period 1998-2001 included non-species specific preparations used in animal feeds and other non-food products of unspecified animals. For the category "preparations used in animal feeding, NESOI" that was imported into the U.S., it is possible that bovine meat or bovine byproducts could have been included in this category. However, the US Food and Drug Administration prohibits feeding of meat-and-bone meal to ruminants in the U.S.

 

HS Code

 

Description

 

Unit

 

1998

 

1999

 

2000

 

2001

 

Feed - non species specific

 

Total

 

45,030

 

48,000

 

50,649

 

43,000

 

2309909500

 

Preparations Used in Animal Feedings, NESOI

 

KG

 

45,030

 

48,000

 

50,649

 

43,000

 

Meat & offal- non species specific

 

Total

 

5

 

0

 

0

 

0

 

300110

 

Dried Organs

 

KG

 

5

 

0

 

0

 

0

 

Other animal products - ruminants

 

Total

 

24

 

0

 

0

 

0

 

3002100040

 

Fetal Bovine Serum (FBS)

 

KG

 

24

 

0

 

0

 

0

 

Source: World Trade Atlas

 

What is the level of passenger traffic arriving in the United States from Israel?

 

A total of 524,401 passengers arrived on direct flights to the U.S. from Israel in fiscal year 2000. This number does not include passengers who arrived in the U.S. from Israel via indirect flights.

 

Under APHIS-PPQ?s agricultural quarantine inspection monitoring, 284 air passengers from Israel were sampled for items of agricultural interest in fiscal year 2001. Seven of these passengers, or 2 percent, carried a total of 11 kg of meat items that could potentially harbor the pathogen that causes BSE. None of these passengers from whom meat items were confiscated reported plans to visit or work on a ranch or farm during their visit to the U.S.

 

Source: U.S. Department of Transportation and APHIS-PPQ Agricultural Quarantine Inspection data base.

 


 

 TSS

 

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

 

Docket Management Docket: 02N-0276 - Bioterrorism Preparedness; Registration of Food Facilities, Section 305 Comment Number: EC -254 Accepted - Volume 11

 


 


 

Infectivity surviving ashing to 600*C is (in my opinion) degradable but infective. based on Bown & Gajdusek, (1991), landfill and burial may be assumed to have a reduction factor of 98% (i.e. a factor of 50) over 3 years. CJD-infected brain-tissue remained infectious after storing at room-temperature for 22 months (Tateishi et al, 1988). Scrapie agent is known to remain viable after at least 30 months of desiccation (Wilson et al, 1950). and pastures that had been grazed by scrapie-infected sheep still appeared to be contaminated with scrapie agent three years after they were last occupied by sheep (Palsson, 1979).

 


 

PAUL BROWN SCRAPIE SOIL TEST

 


 

 snip...

 

please see full text ;

 

Thursday, February 17, 2011

 

Environmental Sources of Scrapie Prions

 


 

2014

 

*** We conclude that TSE infectivity is likely to survive burial for long time periods with minimal loss of infectivity and limited movement from the original burial site. However PMCA results have shown that there is the potential for rainwater to elute TSE related material from soil which could lead to the contamination of a wider area. These experiments reinforce the importance of risk assessment when disposing of TSE risk materials.

 

*** The results show that even highly diluted PrPSc can bind efficiently to polypropylene, stainless steel, glass, wood and stone and propagate the conversion of normal prion protein. For in vivo experiments, hamsters were ic injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters, inoculated with 263K-contaminated implants of all groups, developed typical signs of prion disease, whereas control animals inoculated with non-contaminated materials did not.

 

PRION 2014 CONFERENCE

 

CHRONIC WASTING DISEASE CWD

 

A FEW FINDINGS ;

 

Conclusions. To our knowledge, this is the first established experimental model of CWD in TgSB3985. We found evidence for co-existence or divergence of two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice. Finally, we observed phenotypic differences between cervid-derived CWD and CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway to characterize these strains.

 

We conclude that TSE infectivity is likely to survive burial for long time periods with minimal loss of infectivity and limited movement from the original burial site. However PMCA results have shown that there is the potential for rainwater to elute TSE related material from soil which could lead to the contamination of a wider area. These experiments reinforce the importance of risk assessment when disposing of TSE risk materials.

 

The results show that even highly diluted PrPSc can bind efficiently to polypropylene, stainless steel, glass, wood and stone and propagate the conversion of normal prion protein. For in vivo experiments, hamsters were ic injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters, inoculated with 263K-contaminated implants of all groups, developed typical signs of prion disease, whereas control animals inoculated with non-contaminated materials did not.

 

Our data establish that meadow voles are permissive to CWD via peripheral exposure route, suggesting they could serve as an environmental reservoir for CWD. Additionally, our data are consistent with the hypothesis that at least two strains of CWD circulate in naturally-infected cervid populations and provide evidence that meadow voles are a useful tool for CWD strain typing.

 

Conclusion. CWD prions are shed in saliva and urine of infected deer as early as 3 months post infection and throughout the subsequent >1.5 year course of infection. In current work we are examining the relationship of prionemia to excretion and the impact of excreted prion binding to surfaces and particulates in the environment.

 

Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC) are shed in urine of infected deer as early as 6 months post inoculation and throughout the subsequent disease course. Further studies are in progress refining the real-time urinary prion assay sensitivity and we are examining more closely the excretion time frame, magnitude, and sample variables in relationship to inoculation route and prionemia in naturally and experimentally CWD-infected cervids.

 

Conclusions. Our results suggested that the odds of infection for CWD is likely controlled by areas that congregate deer thus increasing direct transmission (deer-to-deer interactions) or indirect transmission (deer-to-environment) by sharing or depositing infectious prion proteins in these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely controlled by separate factors than found in the Midwestern and endemic areas for CWD and can assist in performing more efficient surveillance efforts for the region.

 

Conclusions. During the pre-symptomatic stage of CWD infection and throughout the course of disease deer may be shedding multiple LD50 doses per day in their saliva. CWD prion shedding through saliva and excreta may account for the unprecedented spread of this prion disease in nature.

 

see full text and more ;

 

Monday, June 23, 2014

 

*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD

 


 


 

*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years***

 

Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3

 


 

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

 


 

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

 


 

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

 


 

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

 


 

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

 


 

*** Survival and Limited Spread of TSE Infectivity after Burial

 

Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute and R(D)SVS; University of Edinburgh; Roslin, Scotland UK

 

Scrapie and chronic wasting disease probably spread via environmental routes, and there are also concerns about BSE infection remaining in the environment after carcass burial or waste 3disposal. In two demonstration experiments we are determining survival and migration of TSE infectivity when buried for up to five years, as an uncontained point source or within bovine heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters containing either sandy or clay soil. Migration from the boluses is being assessed from soil cores taken over time. With the exception of a very small amount of infectivity found 25 cm from the bolus in sandy soil after 12 months, no other infectivity has been detected up to three years. Secondly, ten bovine heads were spiked with TSE infected mouse brain and buried in the two soil types. Pairs of heads have been exhumed annually and assessed for infectivity within and around them. After one year and after two years, infectivity was detected in most intracranial samples and in some of the soil samples taken from immediately surrounding the heads. The infectivity assays for the samples in and around the heads exhumed at years three and four are underway. These data show that TSE infectivity can survive burial for long periods but migrates slowly. Risk assessments should take into account the likely long survival rate when infected material has been buried.

 

The authors gratefully acknowledge funding from DEFRA.

 


 


 

Sunday, November 3, 2013

 

Environmental Impact Statements; Availability, etc.: Animal Carcass Management [Docket No. APHIS-2013-0044]

 


 

2012

 

PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer

 

Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA

 

snip...

 

The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.

 

*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.

 

Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.

 


 

2011

 

*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.

 


 

*** We hypothesize that both BSE prions and CWD prions passaged through felines will seed human recPrP more efficiently than BSE or CWD from the original hosts, evidence that the new host will dampen the species barrier between humans and BSE or CWD. The new host effect is particularly relevant as we investigate potential means of trans-species transmission of prion disease.

 


 

Veterinary Pathology Onlinevet.sagepub.com Published online before print February 27, 2014, doi: 10.1177/0300985814524798 Veterinary Pathology February 27, 2014 0300985814524798

 

Lesion Profiling and Subcellular Prion Localization of Cervid Chronic Wasting Disease in Domestic Cats

 

D. M. Seelig1⇑ A. V. Nalls1 M. Flasik2 V. Frank1 S. Eaton2 C. K. Mathiason1 E. A. Hoover1 1Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, CO, USA 2Department of Biomedical Sciences, Colorado State University, Fort Collins, CO, USA D. M. Seelig, University of Minnesota, Department of Veterinary Clinical Sciences, Room 339 VetMedCtrS, 6192A (Campus Delivery Code), 1352 Boyd Ave, St Paul, MN 55108, USA. Email address: dseelig@umn.edu

 

Abstract

 

Chronic wasting disease (CWD) is an efficiently transmitted, fatal, and progressive prion disease of cervids with an as yet to be fully clarified host range. While outbred domestic cats (Felis catus) have recently been shown to be susceptible to experimental CWD infection, the neuropathologic features of the infection are lacking. Such information is vital to provide diagnostic power in the event of natural interspecies transmission and insights into host and strain interactions in interspecies prion infection. Using light microscopy and immunohistochemistry, we detail the topographic pattern of neural spongiosis (the “lesion profile”) and the distribution of misfolded prion protein in the primary and secondary passage of feline CWD (FelCWD). We also evaluated cellular and subcellular associations between misfolded prion protein (PrPD) and central nervous system neurons and glial cell populations. From these studies, we (1) describe the novel neuropathologic profile of FelCWD, which is distinct from either cervid CWD or feline spongiform encephalopathy (FSE), and (2) provide evidence of serial passage-associated interspecies prion adaptation. In addition, we demonstrate through confocal analysis the successful co-localization of PrPD with neurons, astrocytes, microglia, lysosomes, and synaptophysin, which, in part, implicates each of these in the neuropathology of FelCWD. In conclusion, this work illustrates the simultaneous role of both host and strain in the development of a unique FelCWD neuropathologic profile and that such a profile can be used to discriminate between FelCWD and FSE.

 

prion chronic wasting disease immunohistochemistry interspecies cat feline spongiform encephalopathy transmissible spongiform encephalopathy adaptation species barrier

 


 

Sunday, March 09, 2014

 

Lesion Profiling and Subcellular Prion Localization of Cervid Chronic Wasting Disease in Domestic Cats

 


 

Monday, August 8, 2011

 

*** Susceptibility of Domestic Cats to CWD Infection ***

 

Oral.29: Susceptibility of Domestic Cats to CWD Infection

 

Amy Nalls, Nicholas J. Haley, Jeanette Hayes-Klug, Kelly Anderson, Davis M. Seelig, Dan S. Bucy, Susan L. Kraft, Edward A. Hoover and Candace K. Mathiason†

 

Colorado State University; Fort Collins, CO USA†Presenting author; Email: ckm@lamar.colostate.edu

 

Domestic and non-domestic cats have been shown to be susceptible to one prion disease, feline spongiform encephalopathy (FSE), thought to be transmitted through consumption of bovine spongiform encephalopathy (BSE) contaminated meat. Because domestic and free ranging felids scavenge cervid carcasses, including those in CWD affected areas, we evaluated the susceptibility of domestic cats to CWD infection experimentally. Groups of n = 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD deer brain homogenate. Between 40–43 months following IC inoculation, two cats developed mild but progressive symptoms including weight loss, anorexia, polydipsia, patterned motor behaviors and ataxia—ultimately mandating euthanasia. Magnetic resonance imaging (MRI) on the brain of one of these animals (vs. two age-matched controls) performed just before euthanasia revealed increased ventricular system volume, more prominent sulci, and T2 hyperintensity deep in the white matter of the frontal hemisphere and in cortical grey distributed through the brain, likely representing inflammation or gliosis. PrPRES and widely distributed peri-neuronal vacuoles were demonstrated in the brains of both animals by immunodetection assays. No clinical signs of TSE have been detected in the remaining primary passage cats after 80 months pi. Feline-adapted CWD was sub-passaged into groups (n=4 or 5) of cats by IC, PO, and IP/SQ routes. Currently, at 22 months pi, all five IC inoculated cats are demonstrating abnormal behavior including increasing aggressiveness, pacing, and hyper responsiveness.

 

*** Two of these cats have developed rear limb ataxia. Although the limited data from this ongoing study must be considered preliminary, they raise the potential for cervid-to-feline transmission in nature.

 


 


 

AD.63:

 

Susceptibility of domestic cats to chronic wasting disease

 

Amy V.Nalls,1 Candace Mathiason,1 Davis Seelig,2 Susan Kraft,1 Kevin Carnes,1 Kelly Anderson,1 Jeanette Hayes-Klug1 and Edward A. Hoover1 1Colorado State University; Fort Collins, CO USA; 2University of Minnesota; Saint Paul, MN USA

 

Domestic and nondomestic cats have been shown to be susceptible to feline spongiform encephalopathy (FSE), almost certainly caused by consumption of bovine spongiform encephalopathy (BSE)-contaminated meat. Because domestic and free-ranging nondomestic felids scavenge cervid carcasses, including those in areas affected by chronic wasting disease (CWD), we evaluated the susceptibility of the domestic cat (Felis catus) to CWD infection experimentally. Cohorts of 5 cats each were inoculated either intracerebrally (IC) or orally (PO) with CWD-infected deer brain. At 40 and 42 mo post-inoculation, two IC-inoculated cats developed signs consistent with prion disease, including a stilted gait, weight loss, anorexia, polydipsia, patterned motor behaviors, head and tail tremors, and ataxia, and progressed to terminal disease within 5 mo. Brains from these two cats were pooled and inoculated into cohorts of cats by IC, PO, and intraperitoneal and subcutaneous (IP/SC) routes. Upon subpassage, feline-adapted CWD (FelCWD) was transmitted to all IC-inoculated cats with a decreased incubation period of 23 to 27 mo. FelCWD was detected in the brains of all the symptomatic cats by western blotting and immunohistochemistry and abnormalities were seen in magnetic resonance imaging, including multifocal T2 fluid attenuated inversion recovery (FLAIR) signal hyper-intensities, ventricular size increases, prominent sulci, and white matter tract cavitation. Currently, 3 of 4 IP/SQ and 2 of 4 PO inoculared cats have developed abnormal behavior patterns consistent with the early stage of feline CWD.

 

*** These results demonstrate that CWD can be transmitted and adapted to the domestic cat, thus raising the issue of potential cervid-to- feline transmission in nature.

 


 

www.landesbioscience.com

 

PO-081: Chronic wasting disease in the cat— Similarities to feline spongiform encephalopathy (FSE)

 


 


 


 

FELINE SPONGIFORM ENCEPHALOPATHY FSE

 


 


 

*** 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.

 


 

cwd exposure, and iatrogenic CJD, what if ???

 

*** our results raise the possibility that CJD cases classified as VV1 may include cases caused by iatrogenic transmission of sCJD-MM1 prions or food-borne infection by type 1 prions from animals, e.g., chronic wasting disease prions in cervid. In fact, two CJD-VV1 patients who hunted deer or consumed venison have been reported (40, 41). The results of the present study emphasize the need for traceback studies and careful re-examination of the biochemical properties of sCJD-VV1 prions. ***

 


 

snip...see full text ;

 


 

Thursday, January 2, 2014

 

*** CWD TSE Prion in cervids to hTGmice, Heidenhain Variant Creutzfeldt-Jacob Disease MM1 genotype, and iatrogenic CJD ??? ***

 


 

*** We hypothesize that both BSE prions and CWD prions passaged through felines will seed human recPrP more efficiently than BSE or CWD from the original hosts, evidence that the new host will dampen the species barrier between humans and BSE or CWD. The new host effect is particularly relevant as we investigate potential means of trans-species transmission of prion disease.

 


 

 

 

 

>>> There is no evidence that humans or livestock can get the disease, according to the Centers for Disease Control and Prevention.

 

 hang on now, what do you call this ;

 

 > First transmission of CWD to transgenic mice over-expressing bovine prion protein gene (TgSB3985)

 

 PRION 2014 - PRIONS: EPIGENETICS and NEURODEGENERATIVE DISEASES – Shaping up the future of prion research

 

 Animal TSE Workshop 10.40 – 11.05 Talk Dr. L. Cervenakova First transmission of CWD to transgenic mice over-expressing bovine prion protein gene (TgSB3985)

 


 

 FORGOT TO ADD THIS ONE...

 

 P.126: Successful transmission of chronic wasting disease (CWD) into mice over-expressing bovine prion protein (TgSB3985)

 

 Larisa Cervenakova,1 Christina J Sigurdson,2 Pedro Piccardo,3 Oksana Yakovleva,1 Irina Vasilyeva,1 Jorge de Castro,1 Paula Saá,1 and Anton Cervenak1 1American Red Cross, Holland Laboratory; Rockville, MD USA; 2University of California; San Diego, CA USA; 3Lab TSE/OBRR /CBER/FDA; Rockville, MD USA

 

 Keywords: chronic wasting disease, transmission, transgenic mouse, bovine prion protein

 

 Background. CWD is a disease affecting wild and farmraised cervids in North America. Epidemiological studies provide no evidence of CWD transmission to humans. Multiple attempts have failed to infect transgenic mice expressing human PRNP gene with CWD. The extremely low efficiency of PrPCWD to convert normal human PrPC in vitro provides additional evidence that transmission of CWD to humans cannot be easily achieved. However, a concern about the risk of CWD transmission to humans still exists. This study aimed to establish and characterize an experimental model of CWD in TgSB3985 mice with the following attempt of transmission to TgHu mice.

 

 Materials and Methods. TgSB3985 mice and wild-type FVB/ NCrl mice were intracranially injected with 1% brain homogenate from a CWD-infected Tga20 mouse (CWD/Tga20). TgSB3985 and TgRM (over-expressing human PrP) were similarly injected with 5% brain homogenates from CWD-infected white-tailed deer (CWD/WTD) or elk (CWD/Elk). Animals were observed for clinical signs of neurological disease and were euthanized when moribund. Brains and spleens were removed from all mice for PrPCWD detection by Western blotting (WB). A histological analysis of brains from selected animals was performed: brains were scored for the severity of spongiform change, astrogliosis, and PrPCWD deposition in ten brain regions.

 

 Results. Clinical presentation was consistent with TSE. More than 90% of TgSB3985 and wild-type mice infected with CWD/Tga20, tested positive for PrPres in the brain but only mice in the latter group carried PrPCWD in their spleens. We found evidence for co-existence or divergence of two CWD/ Tga20 strains based on biochemical and histological profiles. In TgSB3985 mice infected with CWD-elk or CWD-WTD, no animals tested positive for PrPCWD in the brain or in the spleen by WB. However, on neuropathological examination we found presence of amyloid plaques that stained positive for PrPCWD in three CWD/WTD- and two CWD/Elk-infected TgSB3985 mice. The neuropathologic profiles in CWD/WTD- and CWD/Elkinfected mice were similar but unique as compared to profiles of BSE, BSE-H or CWD/Tg20 agents propagated in TgSB3985 mice. None of CWD-infected TgRM mice tested positive for PrPCWD by WB or by immunohistochemical detection.

 

 Conclusions. To our knowledge, this is the first established experimental model of CWD in TgSB3985. We found evidence for co-existence or divergence of two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice. Finally, we observed phenotypic differences between cervid-derived CWD and CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway to characterize these strains.

 

 TSS

 

 UPDATED CORRESPONDENCE FROM AUTHORS OF THIS STUDY I.E. COLBY, PRUSINER ET AL, ABOUT MY CONCERNS OF THE DISCREPANCY BETWEEN THEIR FIGURES AND MY FIGURES OF THE STUDIES ON CWD TRANSMISSION TO CATTLE ;

 

 CWD to cattle figures CORRECTION

 

 Greetings,

 

 I believe the statement and quote below is incorrect ;

 

 "CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures."

 

 Please see ;

 

 Within 26 months post inoculation, 12 inoculated animals had lost weight, revealed abnormal clinical signs, and were euthanatized. Laboratory tests revealed the presence of a unique pattern of the disease agent in tissues of these animals. These findings demonstrate that when CWD is directly inoculated into the brain of cattle, 86% of inoculated cattle develop clinical signs of the disease.

 


 

 " although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). "

 

 shouldn't this be corrected, 86% is NOT a low rate. ...

 

 kindest regards,

 

 Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

 

 Thank you!

 

 Thanks so much for your updates/comments. We intend to publish as rapidly as possible all updates/comments that contribute substantially to the topic under discussion.

 


 

 re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations

 

 1Institute for Neurodegenerative Diseases, University of California, San Francisco, San Francisco, California 94143 2Department of Neurology, University of California, San Francisco, San Francisco, California 94143 Correspondence: stanley@ind.ucsf.edu

 


 

 Mule deer, white-tailed deer, and elk have been reported to develop CWD. As the only prion disease identified in free-ranging animals, CWD appears to be far more communicable than other forms of prion disease. CWD was first described in 1967 and was reported to be a spongiform encephalopathy in 1978 on the basis of histopathology of the brain. Originally detected in the American West, CWD has spread across much of North America and has been reported also in South Korea. In captive populations, up to 90% of mule deer have been reported to be positive for prions (Williams and Young 1980). The incidence of CWD in cervids living in the wild has been estimated to be as high as 15% (Miller et al. 2000). The development of transgenic (Tg) mice expressing cervid PrP, and thus susceptible to CWD, has enhanced detection of CWD and the estimation of prion titers (Browning et al. 2004; Tamgüney et al. 2006). Shedding of prions in the feces, even in presymptomatic deer, has been identified as a likely source of infection for these grazing animals (Williams and Miller 2002; Tamgüney et al. 2009b). CWD has been transmitted to cattle after intracerebral inoculation, although the infection rate was low (4 of 13 animals [Hamir et al. 2001]). This finding raised concerns that CWD prions might be transmitted to cattle grazing in contaminated pastures.

 

 snip...

 


 

 ----- Original Message -----

 

 From: David Colby To: flounder9@verizon.net

 

 Cc: stanley@XXXXXXXX

 

 Sent: Tuesday, March 01, 2011 8:25 AM

 

 Subject: Re: FW: re-Prions David W. Colby1,* and Stanley B. Prusiner1,2 + Author Affiliations

 

 Dear Terry Singeltary,

 

 Thank you for your correspondence regarding the review article Stanley Prusiner and I recently wrote for Cold Spring Harbor Perspectives. Dr. Prusiner asked that I reply to your message due to his busy schedule. We agree that the transmission of CWD prions to beef livestock would be a troubling development and assessing that risk is important. In our article, we cite a peer-reviewed publication reporting confirmed cases of laboratory transmission based on stringent criteria. The less stringent criteria for transmission described in the abstract you refer to lead to the discrepancy between your numbers and ours and thus the interpretation of the transmission rate. We stand by our assessment of the literature--namely that the transmission rate of CWD to bovines appears relatively low, but we recognize that even a low transmission rate could have important implications for public health and we thank you for bringing attention to this matter. Warm Regards, David Colby -- David Colby, PhDAssistant Professor Department of Chemical Engineering University of Delaware

 

 ===========END...TSS==============

 

 SNIP...SEE FULL TEXT ;

 


 

 UPDATED DATA ON 2ND CWD STRAIN Wednesday, September 08, 2010 CWD PRION CONGRESS SEPTEMBER 8-11 2010

 


 

 Sunday, August 19, 2012

 

 Susceptibility of cattle to the agent of chronic wasting disease from elk after intracranial inoculation 2012

 

 Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES Location: Virus and Prion Research Unit

 


 

 Thursday, November 21, 2013

 

 *** Assessing the susceptibility of transgenic mice over-expressing deer prion protein to bovine spongiform encephalopathy

 

 The present study was designed to assess the susceptibility of the prototypic mouse line, Tg(CerPrP)1536+/- to bovine spongiform encephalopathy (BSE) prions, which have the ability to overcome species barriers. Tg(CerPrP)1536+/- mice challenged with red deer-adapted BSE resulted in a 90-100% attack rates, BSE from cattle failed to transmit, indicating agent adaptation in the deer.

 


 

 *** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies.

 


 

 NOW, what is the latest on human risk factors to CWD strains ???

 

 *** PPo3-7: Prion Transmission from Cervids to Humans is Strain-dependent

 

 *** Here we report that a human prion strain that had adopted the cervid prion protein (PrP) sequence through passage in cervidized transgenic mice efficiently infected transgenic mice expressing human PrP,

 

 *** indicating that the species barrier from cervid to humans is prion strain-dependent and humans can be vulnerable to novel cervid prion strains.

 

 PPo2-27:

 

 Generation of a Novel form of Human PrPSc by Inter-species Transmission of Cervid Prions

 

 *** Our findings suggest that CWD prions have the capability to infect humans, and that this ability depends on CWD strain adaptation, implying that the risk for human health progressively increases with the spread of CWD among cervids.

 

 PPo2-7:

 

 Biochemical and Biophysical Characterization of Different CWD Isolates

 

 *** The data presented here substantiate and expand previous reports on the existence of different CWD strains.

 


 

 Envt.07:

 

 Pathological Prion Protein (PrPTSE) in Skeletal Muscles of Farmed and Free Ranging White-Tailed Deer Infected with Chronic Wasting Disease

 

 ***The presence and seeding activity of PrPTSE in skeletal muscle from CWD-infected cervids suggests prevention of such tissue in the human diet as a precautionary measure for food safety, pending on further clarification of whether CWD may be transmissible to humans.

 


 

 >>>CHRONIC WASTING DISEASE , THERE WAS NO ABSOLUTE BARRIER TO CONVERSION OF THE HUMAN PRION PROTEIN<<<

 

 *** PRICE OF CWD TSE PRION POKER GOES UP 2014 ***

 

 Transmissible Spongiform Encephalopathy TSE PRION update January 2, 2014

 

 Wednesday, January 01, 2014

 

 Molecular Barriers to Zoonotic Transmission of Prions

 

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

 

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

 


 


 

 the prion gods at the cdc state that there is ;

 

 ''no strong evidence''

 

 but let's see exactly what the authors of this cwd to human at the cdc state ;

 

 now, let’s see what the authors said about this casual link, personal communications years ago. see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ????

 

 “Our conclusion stating that we found no strong evidence of CWD transmission to humans”

 

From: TSS (216-119-163-189.ipset45.wt.net)

 

Subject: CWD aka MAD DEER/ELK TO HUMANS ???

 

Date: September 30, 2002 at 7:06 am PST

 

From: "Belay, Ermias"

 

To:

 

Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"

 

Sent: Monday, September 30, 2002 9:22 AM

 

Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

 

Dear Sir/Madam,

 

In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.

 

That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.

 

Ermias Belay, M.D. Centers for Disease Control and Prevention

 

-----Original Message-----

 

From:

 

Sent: Sunday, September 29, 2002 10:15 AM

 

To: rr26k@nih.gov; rrace@niaid.nih.gov; ebb8@CDC.GOV

 

Subject: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS

 

Sunday, November 10, 2002 6:26 PM ......snip........end..............TSS

 

Thursday, April 03, 2008

 

A prion disease of cervids: Chronic wasting disease

 

2008 1: Vet Res. 2008 Apr 3;39(4):41

 

A prion disease of cervids: Chronic wasting disease

 

Sigurdson CJ.

 

snip...

 

*** twenty-seven CJD patients who regularly consumed venison were reported to the Surveillance Center***,

 

snip...

 

full text ;

 


 


 


 

 

PRION2013 CONGRESSIONAL ABSTRACTS CWD

 

Sunday, August 25, 2013

 

HD.13: CWD infection in the spleen of humanized transgenic mice

 

***These results indicate that the CWD prion may have the potential to infect human peripheral lymphoid tissues.

 

Oral.15: Molecular barriers to zoonotic prion transmission: Comparison of the ability of sheep, cattle and deer prion disease isolates to convert normal human prion protein to its pathological isoform in a cell-free system ***However, they also show that there is no absolute barrier to conversion of human prion protein in the case of chronic wasting disease.

 

PRION2013 CONGRESSIONAL ABSTRACTS CWD

 

Sunday, August 25, 2013

 

***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood, and mother to offspring transmission

 


 

Tuesday, November 04, 2014

 

*** Six-year follow-up of a point-source exposure to CWD contaminated venison in an Upstate New York community: risk behaviours and health outcomes 2005–2011

 


 

 

Sunday, December 28, 2014

 

*** CHRONIC WASTING DISEASE CWD TSE PRION DISEASE AKA MAD DEER DISIEASE USDA USAHA INC DECEMBER 28, 2014

 


 


 

Thursday, October 23, 2014

 

FIRST CASE OF CHRONIC WASTING DISEASE CONFIRMED IN OHIO ON PRIVATE PRESERVE

 


 

Sunday, December 21, 2014

 

Mucosal immunization with an attenuated Salmonella vaccine partially protects white-tailed deer from chronic wasting disease

 


 

 

 

Tuesday, October 21, 2014

 

Pennsylvania Department of Agriculture Tenth Pennsylvania Captive Deer Tests Positive for Chronic Wasting Disease CWD TSE PRION DISEASE

 


 

Tuesday, October 07, 2014

 

Wisconsin white-tailed deer tested positive for CWD on a Richland County breeding farm, and a case of CWD has been discovered on a Marathon County hunting preserve

 


 

Thursday, October 02, 2014

 

IOWA TEST RESULTS FROM CAPTIVE DEER HERD WITH CHRONIC WASTING DISEASE RELEASED 79.8 percent of the deer tested positive for the disease

 


 

Thursday, July 03, 2014

 

*** How Chronic Wasting Disease is affecting deer population and what’s the risk to humans and pets?

 


 

Tuesday, July 01, 2014

 

*** CHRONIC WASTING DISEASE CWD TSE PRION DISEASE, GAME FARMS, AND POTENTIAL RISK FACTORS THERE FROM

 


 

another reason that not testing all deer for CWD, OF ALL AGES, risk spreading CWD further, by ignoring the fact that young deer are susceptible to CWD ;

 

Saturday, February 04, 2012

 

*** Wisconsin 16 age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised

 

Approximately 4,200 fawns, defined as deer under 1 year of age, were sampled from the eradication zone over the last year. The majority of fawns sampled were between the ages of 5 to 9 months, though some were as young as 1 month.

 

*** Two of the six fawns with CWD detected were 5 to 6 months old.

 

All six of the positive fawns were taken from the core area of the CWD eradication zone where the highest numbers of positive deer have been identified. ...

 

snip...

 

"Finding CWD prions in both lymph and brain tissues of deer this young is slightly surprising," said Langenberg, "and provides information that CWD infection and illness may progress more rapidly in a white-tailed deer than previously suspected. Published literature suggests that CWD doesn't cause illness in a deer until approximately 16 months of age. Our fawn data shows that a few wild white-tailed deer may become sick from CWD or may transmit the disease before they reach that age of 16 months." ... see full text and more here ; Saturday, February 04, 2012

 

Wisconsin 16 MONTH age limit on testing dead deer Game Farm CWD Testing Protocol Needs To Be Revised

 


 

Therefore, in the USA, materials from cervids other than CWD positive animals may be used in animal feed and feed ingredients for non-ruminants.

 

The amount of animal PAP that is of deer and/or elk origin imported from the USA to GB can not be determined, however, as it is not specified in TRACES. It may constitute a small percentage of the 8412 kilos of non-fish origin processed animal proteins that were imported from US into GB in 2011.

 

Overall, therefore, it is considered there is a __greater than negligible risk___ that (nonruminant) animal feed and pet food containing deer and/or elk protein is imported into GB.

 

There is uncertainty associated with this estimate given the lack of data on the amount of deer and/or elk protein possibly being imported in these products.

 


 

2003D-0186 Guidance for Industry: Use of Material From Deer and Elk In Animal Feed

 

EMC 1 Terry S. Singeltary Sr. Vol #: 1

 


 


 

see my full text submission here ;

 


 

Conclusion

 

European red deer are susceptible to infection with the cattle BSE agent, not only by the intra-cerebral but also by the oral route, and although the clinical signs and spong- iform change are similar to those of CWD in the same species, these two infections can be easily differentiated. The lack of lymphoid involvement, the PrPd truncation pattern both "in vivo" and "in vitro", and the predominantly intracellular accumulation of PrPd are features of deer BSE that are in contrast with those of deer CWD. However, only one of six deer developed disease after alimentary exposure to 25 g of a BSE brain pool homogenate after an incubation period of nearly 5 years; this suggests a strong species barrier but if a TSE in European red deer should ever be identified then BSE/CWD discrimination would be an urgent priority. To determine whether there are potential naturally occurring BSE-like strains and to determine the degree to which there is strain variation, it would be necessary to examine many more naturally occurring CWD cases. These results will support the ongoing European surveillance for natural TSEs in red deer and the further assessment of potential risk to human health.

 

Published: 27 July 2009 BMC Veterinary Research 2009, 5:26 doi:10.1186/1746-6148-5-26 Received: 12 February 2009 Accepted: 27 July 2009 This article is available from: http://www.biomedcentral.com/1746-6148/5/26 © 2009 Martin et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

 


 

Sunday, December 15, 2013

 

*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE

 


 

Tuesday, December 23, 2014

 

*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION

 


 

Monday, June 23, 2014

 

PRION 2014 CHRONIC WASTING DISEASE CWD

 


 

*** 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.

 


 

 

 

>>>***>>>Here we show that a panel of sheep scrapie prions transmit to several tgHu mice models with an efficiency comparable to that of cattle BSE. The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions. <<<***<<<

 

Tuesday, December 16, 2014

 

Evidence for zoonotic potential of ovine scrapie prions

 

Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1, Affiliations Contributions Corresponding author Journal name: Nature Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014 Article tools Citation Reprints Rights & permissions Article metrics

 

Abstract

 

Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie prions remains unknown. Mice genetically engineered to overexpress the human ​prion protein (tgHu) have emerged as highly relevant models for gauging the capacity of prions to transmit to humans. These models can propagate human prions without any apparent transmission barrier and have been used used to confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie prions transmit to several tgHu mice models with an efficiency comparable to that of cattle BSE. The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.

 

Subject terms: Biological sciences• Medical research At a glance

 


 

see more here ;

 


 

2001

 

Suspect symptoms

 

What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?

 

28 Mar 01

 

Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.

 

Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.

 

"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb...

 

2001

 

Suspect symptoms

 

What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?

 

28 Mar 01

 

Like lambs to the slaughter

 

31 March 2001

 

by Debora MacKenzie Magazine issue 2284.

 

FOUR years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.

 

Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.

 

Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.

 

"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb. ...snip...end

 

 


 

see more here ;

 


 


 

 

Thursday, July 24, 2014

 

*** Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA

 


 

From: Terry S. Singeltary Sr.

 

Sent: Friday, January 13, 2012 4:19 PM

 

To: Terry S. Singeltary Sr.

 

Subject: deadstock downer cows NSLP

 

> > > Ackerman says downed cattle are 50 times more likely to have mad cow disease (also known as Bovine Spongiform Encephalopathy, or BSE) than ambulatory cattle that are suspected of having BSE. Of the 20 confirmed cases of mad cow disease in North America since 1993, at least 16 have involved downer cattle, he said. < < <

 

don’t forget the children...

 

PLEASE be aware, for 4 years, the USDA fed our children all across the Nation (including TEXAS) dead stock downer cows, the most high risk cattle for BSE aka mad cow disease and other dangerous pathogens.

 

who will watch our children for CJD for the next 5+ decades ???

 

WAS your child exposed to mad cow disease via the NSLP ???

 

Thursday, November 28, 2013

 

Department of Justice Former Suppliers of Beef to National School Lunch Program Settle Allegations of Improper Practices and Mistreating Cows

 


 

seems USDA NSLP et al thought that it would be alright, to feed our children all across the USA, via the NSLP, DEAD STOCK DOWNER COWS, the most high risk cattle for mad cow type disease, and other dangerous pathogens, and they did this for 4 years, that was documented, then hid what they did by having a recall, one of the largest recalls ever, and they made this recall and masked the reason for the recall due to animal abuse (I do not condone animal abuse), not for the reason of the potential for these animals to have mad cow BSE type disease (or other dangerous and deadly pathogens). these TSE prion disease can lay dormant for 5, 10, 20 years, or longer, WHO WILL WATCH OUR CHILDREN FOR THE NEXT 5 DECADES FOR CJD ???

 

Saturday, September 21, 2013

 

Westland/Hallmark: 2008 Beef Recall A Case Study by The Food Industry Center January 2010 THE FLIM-FLAM REPORT

 


 

DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH RISK FOR MAD COW DISEASE ??? this recall was not for the welfare of the animals. ...tss you can check and see here ; (link now dead, does not work...tss)

 


 

try this link ;

 


 

Saturday, August 30, 2014

 

Maine Firm Recalls Ribeye and Carcass Products That May Contain Specified Risk Materials SRM TSE PRION aka mad cow type disease

 


 

Friday, December 19, 2014

 

Rancho Alleged Cancerous Eyeball Case Going To Trial

 


 

Tuesday, December 23, 2014

 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION

 


 

Sunday, December 15, 2013

 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE

 


 

Thursday, June 6, 2013

 

BSE TSE PRION USDA FDA MAD COW FEED COMPLIANCE REPORT and NAI, OAI, and VAI ratings as at June 5, 2013

 


 

Sunday, November 13, 2011

 

*** California BSE mad cow beef recall, QFC, CJD, and dead stock downer livestock

 


 

Thursday, February 13, 2014

 

HSUS VS USDA ET AL BAN DOWNER CALVES FOR HUMAN CONSUMPTION (*veal) and potential BSE risk factor there from

 


 

Saturday, November 10, 2012

 

Wisconsin Firm Recalls Beef Tongues That May Contain Specified Risk Materials Nov 9, 2012 WI Firm Recalls Beef Tongues

 


 

Saturday, July 23, 2011

 

CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE

 


 

Sunday, October 18, 2009

 

Wisconsin Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, October 17, 2009

 


 

Thursday, October 15, 2009

 

Nebraska Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, Oct 15, 2009

 


 

Thursday, June 26, 2008

 

Texas Firm Recalls Cattle Heads That Contain Prohibited Materials

 


 

Tuesday, July 1, 2008

 

Missouri Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs

 


 

Friday, August 8, 2008

 

Texas Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs 941,271 pounds with tonsils not completely removed

 


 

Saturday, April 5, 2008

 

SRM MAD COW RECALL 406 THOUSAND POUNDS CATTLE HEADS WITH TONSILS KANSAS

 


 

Wednesday, April 30, 2008

 

Consumption of beef tongue: Human BSE risk associated with exposure to lymphoid tissue in bovine tongue in consideration of new research findings

 


 

Wednesday, April 30, 2008

 

Consumption of beef tongue: Human BSE risk associated with exposure to lymphoid tissue in bovine tongue in consideration of new research findings

 


 

Friday, October 15, 2010

 

BSE infectivity in the absence of detectable PrPSc accumulation in the tongue and nasal mucosa of terminally diseased cattle

 


 

SPECIFIED RISK MATERIALS SRMs

 


 

 

Tuesday, December 30, 2014

 

*** TSEAC USA Reason For Recalls Blood products, collected from a donors considered to be at increased risk for Creutzfeldt-Jakob Disease (CJD), were distributed END OF YEAR REPORT 2014

 


 

Wednesday, December 11, 2013

 

*** Detection of Infectivity in Blood of Persons with Variant and Sporadic Creutzfeldt-Jakob Disease ***

 


 

BAD BLOOD AND TSE PRION DISEASE

 


 

atypical BSE a spontaneous event ???

 

if that's the case, then France is having one hell of an epidemic of atypical BSE, probably why they stopped testing for BSE $$$

 

Sunday, October 5, 2014

 

France stops BSE testing for Mad Cow Disease

 


 

Thursday, July 24, 2014

 

*** Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical BSE investigations

 


 

>>> The generally older age of the identified H-BSE and L-BSE cases, and their apparently low prevalence in the population, suggest that these Atypical BSE forms could be arising spontaneously.

 

if that is the case, then FRANCE has an exceedingly high rate of spontaneous atypical BSE cases.

 

*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;

 


 

Monday, December 1, 2014

 

Germany Bovine Spongiform Encephalopathy BSE CJD TSE Prion disease A Review December 1, 2014

 


 

SUMMARY REPORT CALIFORNIA ATYPICAL L-TYPE BOVINE SPONGIFORM ENCEPHALOPATHY CASE INVESTIGATION JULY 2012 CALIFORNIA

 

Summary Report BSE 2012

 

Executive Summary

 


 

Saturday, August 4, 2012

 

Final Feed Investigation Summary - California atypical L-type BSE Case - July 2012

 


 

Saturday, August 4, 2012

 

Update from APHIS Regarding Release of the Final Report on the BSE Epidemiological Investigation

 


 

Tuesday, December 16, 2014

 

Evidence for zoonotic potential of ovine scrapie prions

 

Scrapie from sheep could infect humans with 'mad cow disease', study finds

 


 


 

Tuesday, December 2, 2014

 

UK EXPORTS OF MBM TO WORLD Bovine Spongiform Encephalopathy BSE TSE Prion aka Mad Cow Disease

 

USA, NORTH AMERICA, MBM (or any potential TSE prion disease) EXPORTS TO THE WORLD (?) [protected by the BSE MRR policy] $$$

 


 

Sunday, December 28, 2014

 

*** Reverse Freedom of Information Act request rFOIA FSIS USDA APHIS TSE PRION aka BSE MAD COW TYPE DISEASE December 2014

 


 


 

 

2014

 

>>> The generally older age of the identified H-BSE and L-BSE cases, and their apparently low prevalence in the population, suggest that these Atypical BSE forms could be arising spontaneously.

 

if that is the case, then FRANCE has an exceedingly high rate of spontaneous atypical BSE cases.

 

snip...

 

see full text ;

 


 

*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;

 


 

Thursday, November 18, 2010

 

UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS

 

Dustin Douglass was indicted and charged with making a fraudulent application to the VA, in an effort to obtain benefits from injuries Douglas represented he suffered while deployed in Iraq. Based on his application, the VA provided benefits totaling $22,148.53. Douglass claimed he suffered various injuries and illnesses as a result of his service in combat. The investigation revealed Douglass had, in fact, been deployed to Iraq, but had served as a computer specialist, had never been in combat, and did not suffer the service-related injuries and illnesses he claimed to have suffered. Douglass was placed on supervised release for 3 years, and required to pay $22,148.53 in restitution. Galen Niehues, an inspector for the Nebraska Department of Agriculture, (NDA), was convicted of mail fraud for submitting falsified reports to his employer concerning inspections he was supposed to perform at Nebraska cattle operations. Niehues was tasked with performing inspections of Nebraska ranches, cattle and feed for the presence of neurological diseases in cattle including Bovine Spongiform Encephalopathy (BSE), also known as “Mad Cow Disease”. Niehues was to identify cattle producers, perform on-site inspections of the farm sites and cattle operations, ask producers specific questions about feed, and take samples of the feed. Niehues was to then submit feed samples for laboratory analysis, and complete reports of his inspections and submit them to the NDA and to the Federal Food and Drug Administration (FDA). An investigation by the FDA and NDA revealed Niehues had fabricated approximately 100 BSE inspections and inspection reports. When confronted, Niehues admitted his reports were fraudulent, and that had fabricated the reports and feed samples he submitted to the NDA. Niehues received a sentence of 5 years probation, a 3-year term of supervised release, and was required to pay $42,812.10 in restitution.

 


 


 

Thursday, July 24, 2014

 

*** Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical BSE investigations ***

 


 

Tuesday, December 23, 2014

 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION

 


 

Sunday, December 15, 2013

 

FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE

 


 

Thursday, June 6, 2013

 

BSE TSE PRION USDA FDA MAD COW FEED COMPLIANCE REPORT and NAI, OAI, and VAI ratings as at June 5, 2013

 


 

Saturday, December 6, 2014

 

Detection of Bovine Central Nervous System Tissues in Rendered Animal By-Products by One-Step Real-Time Reverse Transcription PCR Assay

 


 

Friday, December 5, 2014

 

SPECIAL ALERT The OIE recommends strengthening animal disease surveillance worldwide

 

OIE BSE TSE PRION AKA MAD COW DISEASE ?

 

‘’the silence was deafening’’ ...tss

 


 

Tuesday, December 30, 2014

 

TSEAC USA Reason For Recalls Blood products, collected from a donors considered to be at increased risk for Creutzfeldt-Jakob Disease (CJD), were distributed END OF YEAR REPORT 2014

 


 

UPDATE* NOVEMBER 16, 2014 vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???

 

Friday, January 10, 2014

 

Greetings again Friends, Neighbors, and Colleagues,

 

I would kindly like to follow up on ‘vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???’ ran across an old paper from 1984, that some might find interest in, and I will update the link with this old science paper from 1984, a 2010 paper from Japan, and some information on scrapie transmission. The paper from Japan first, then the 1984 paper, and then the scrapie transmission studies.

 

***The occurrence of contact cases raises the possibility that transmission in families may be effected by an unusually virulent strain of the agent.

 


 

From: Terry S. Singeltary Sr.

 

Sent: Saturday, November 15, 2014 9:29 PM

 

To: Terry S. Singeltary Sr.

 

Subject: THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE R. G. WILL 1984

 

THE EPIDEMIOLOGY OF CREUTZFELDT-JAKOB DISEASE

 

R. G. WILL

 

1984

 

snip...

 


 

Friday, January 10, 2014

 

vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???

 


 

Sunday, April 06, 2014

 

SPORADIC CJD and the potential for zoonotic transmission there from, either directly or indirectly via friendly fire iatrogenic mode, evidence to date

 


 

Sunday, November 23, 2014

 

Confirmed Variant Creutzfeldt-Jakob Disease (variant CJD) Case in Texas in June 2014 confirmed as USA case NOT European

 

‘’The specific overseas country where this patient’s infection occurred is less clear largely because the investigation did not definitely link him to a country where other known vCJD cases likely had been infected.’’

 


 

Sunday, December 14, 2014

 

ALERT new variant Creutzfeldt Jakob Disease nvCJD or vCJD, sporadic CJD strains, TSE prion aka Mad Cow Disease United States of America Update December 14, 2014 Report

 


 

Sunday, June 29, 2014

 

Transmissible Spongiform Encephalopathy TSE Prion Disease North America 2014

 


 

maybe it's time to start taking seriously about food production and the potential environmental contamination therefrom, in terms of the TSE prion disease.

 

what about the environment and tse prion, and using bovine blood, and or any animal blood, to spread across the land, and the potential risk factors therefrom for the environment.

 

how can practices such as this still be applied today, with what we now know about the TSE prion and blood with nvCJD, atypical TSE prion disease and infectivity therefrom, such as CWD, and or the atypical TSE prion disease in different species, and what we don't know yet, and the environment therefrom, and how long the tse prion can persist in the environment, and still practice such practices in 2015 and beyond?

 

environmental risk factors for the TSE prion disease

 

Cornell Waste Management Institute

 

Appendix A Characteristics of Raw Materials Table A.1

 

% N C:N ratio Moisture Bulk density

 

Material Type of value (dry weight) (weight to weight) content % (wet weight) (pounds per cubic yard)

 

Fish and meat processing

 

Blood wastes (slaughterhouse waste and dried blood)

 

Typical 13-14 3-3.5 10-78 -

 

snip...

 

Mixed slaughterhouse waste Typical 7-10 2-4 - -

 

Poultry carcasses Typical 2.4 b 5 65 -

 


 

see ;

 

The paunch contents, ‘paunch manure’ (partially digested feed), is estimated to range from 27 to 40 kg. The paunch can be handled in four ways:

 

1: Total dumping. All of the paunch contents is flushed away into the sewer. 2: Wet dumping. The paunch contents are washed out and the wet slurry is screened on the presence of gross solids, which are subsequently removed.

 

3: Dry dumping. The paunch contents are dumped for subsequent rendering or for disposal as solid waste without needless water flushing.

 

4: Whole paunch handling. The entire paunch may be removed, intact, for rendering or for disposal as solid waste.

 


 

2. SLAUGHTERHOUSES

 

Produced by: Agriculture and Consumer Protection Title: Management of Waste from Animal Product Processing...

 

2.1.1. Description of the slaughter process.

 

 Figure 1 presents a flow diagram of a red meat slaughterhouse.

 

Slaughtering

 

In slaughterhouses animals are received and kept around in stockyards and pens for 1 day. The animals are watered, but in most cases not fed unless they are kept more than 1 day.

 

The animals are then driven from the holding pens to the slaughtering area where the following activities take place:

 

- Stunning;

 

- Suspension from an overhead rail by the hind legs;

 

*** - Sticking and bleeding over a collecting trough. The collected blood may be sewered or processed;

 

Cattle Pigs

 

Denmark England U.S. Denmark Sweden U.S.* U.S.*

 

The percentages of by-products in some western countries are presented in Table 3.

 

Blood 3-4 3 4 3 4 3

 

snip...

 

2.3.2.1. Wastewater by red meat slaughtering

 

Major contribution to the total waste load.

 

Production of blood: Of all waste products, the waste in the form of blood has the highest polluting value. Blood itself has a high BOD: 150,000 - 200,000 mg/l, the extreme value being 405,000 mg/l. (Domestic wastewater has a BOD of 300 mg/l). In the killing, bleeding and skinning phases, blood is produced which, when completely sewered, leads to a total waste load of 10 kg BOD per ton of LWK. A waste load of up to 3.0 kg BOD per ton of LWK may occur in wastewater flowing out of the killing-area and the hide-removal-area.

 

In order to reduce the waste load, attempts should be made to collect and process blood (= drying). Drying of blood can be done by direct heating which produces large quantities of bloodwater (corresponding waste load approximately 1.3 kg BODper ton of LWK) but preferably it is done by indirect (external) heating (corresponding waste load approximately 0.3 kg BOD per ton of LWK).

 

Paunch: Paunch manure is the second most important source of pollution. It may substantially contribute to the total waste load if not properly handled. Dumping (sewering) of the entire paunch content gives a BOD of 2.5 kg per ton of LWK. There are several ways to handle paunch (see 2.1.1)

 

Minor contributions to the total waste load.

 

Stockyards and pens: Waste results from manure and urine, feed, livestock dirt, sanitizers and cleaning agents. The waste will reach the sewer by means of water overflowing from water troughs, by rain and snowwater and pen washdown water. The sewered raw waste, assuming that solid contaminants have been removed, has been estimated at 0.25 kg BOD per ton of LWK.

 

Slaughtering: During the slaughtering the following wastes are produced (Edible offals are excluded because these are considered as meat (by-products)):

 

- Blood and tissue produced during hide removal fall on the floor. External contamination of the hide with dirt and manure is a secondary source of pollutants. The waste load is also increased as a result of cleaning-up operations in this area. - Wastewater is produced from intentional overflow from scalding tanks that contain blood, dirt, manure and hair (0.15 kg BOD per ton of LWK). The fluming of the mechanically removed hair also results in wastewater containing residual hair, blood and dirt after recovery of the bulk of the hair (0.4 kg BOD per ton of LWK). Recovered hog hair may be be dumped as solid waste, washed and baled for marketing (0.7 kg BOD per ton of LWK) or it may be hydrolysed by pressure cooking (1 kg BOD per of LWK).

 

- Slime and casings from intestines. De-sliming and casing washing add 0.6 kg BOD per ton of LWK to the raw waste load;

 

- Inedible offals that are produced are hair, recovered from fluming water, heads and carcass trimmings, lungs and paunch. They also contribute to the amount of wastewater.

 

Meatpacking: Cutting and deboning operations produce trimmings, blood, bones and bone dust. The total of raw waste loads for meat processing plants (including cutting and deboning) has been estimated at 5.7 - 6.7 kg BOD per ton of product. Meatprocessing operations produce a raw waste load from:

 

- Blood, tissues and fat that reach the sewer during cleaning activities; - The curing of solutions containing sugar and salt. Pickling can cause a high chloride waste, only 25% of the curing brine remains in the product.

 

- Baking, smoking etc. and energy use (contributing to air pollution).

 

Edible Rendering: Both wet-rendering and continuous rendering at low temperatures produce polluted tank water containing residues of fat and protein (2 kg BOD per ton of LWK).

 

Table 9 summarizes the potential wastewater emissions of red meat slaughterhouses (no water prevention).

 

snip...

 


 

4. PROPERTIES OF WASTES RELEVANT TO AGRICULTURAL BENEFIT AND ENVIRONMENTAL IMPACT

 

4.2.2 Background

 

Wastes from abattoirs include blood, gut contents, wash waters and sludge from dissolved air flotation treatment where this process has been used to separate solids from liquid waste materials of the abattoir. Some wastes such as hoof parts and bone meal are recycled in other industries (e.g. fertiliser and glue). Landspreading of abattoir wastes is probably the best practicable environmental option for small-scale abattoirs but it is likely to be much less appropriate for modern large-scale abattoir operations.

 

Landspreading of blood and gut contents from abattoirs is liable to cause public nuisance due to odours and environmental concerns. If spread on the soil surface it is unsightly and there is potential for disease transmission. The material should be dealt with as for untreated sewage sludge and applied to the land by subsurface soil injection or else incorporated as soon as possible after spreading on the surface of the arable land. The land-use restrictions as for untreated sewage sludge should apply. The rate of application of the waste should be in accordance with crop requirements for nutrients.

 

4.2.3 Key Properties

 

Waste blood is produced in large quantities from abattoirs and has various uses including landspreading. Its high fertiliser value has been known for a long time, and it is one of the more traditional materials spread on land. Its nitrogen content is extremely high and its levels of potassium and phosphorus make it a good source of plant nutrients. Nutrients are also found to be more available than those found in other organic wastes.

 

Waste stomach contents consist predominantly of partially digested feed or vegetable matter. As with the blood waste, stomach contents usually contain high levels of nitrogen, potassium and phosphorus. These nutrients are generally in well balanced proportions with an N:P:K ratio of around 5:1:1. Moderately high ammonium nitrogen content is an added benefit.

 

As with many other food processing industries, large volumes of wash waters are produced, and the term is often used to describe a wide range of low solid waste materials. This category can contain dung and urine from animal holding areas and washings from distribution vehicles. As for the other abattoir wastes, the wash waters contain a mixture of nitrogen, potassium and phosphorus but at lower concentrations.

 

4.2.4 Potential Problems

 

From the data above, it is seen that abattoir wastes contain high levels of nitrogen, potassium and phosphorus. If applied in excess to plant requirements, these elements can cause potential water pollution problems, and may also pose a danger to plant health. These wastes also have a tendency to have a high BOD which makes the waste readily degradable by soil micro-organisms ; this can rapidly result in anaerobic soil conditions if over applied.

 

In general, slaughterhouse wastes are a recognised source of environmental contamination by Salmonella and other zoonotic pathogens (Wray and Sojka 1977, Edel et al. 1978) Cryptosporidium may occur in gut contents although not necessarily in infective form. Veterinary ante-mortem inspection at slaughterhouses ensures that no animal suffering from European Commission-Directorate-General for Environment

 

WRc Ref: CO 4953-2/11768-1 July 2001 50

 

notifiable disease or any other disease likely to affect the fitness of meat is slaughtered for human consumption. However, slaughtered animals may be symptomless carriers of pathogenic bacteria and therefore slaughterhouse wastes should be used with caution and with restrictions on land for rearing livestock or grazing after application.

 

Strict statutory procedures are now enforced at abattoirs and renderers with the intention of removing, for separate disposal, components of cattle carcasses which might contain BSE.

 

snip...

 


 

Final report April 11

 

3.5.6. Abattoir wastes

 

3.5.6.1. Introduction

 

In this section, wastes from abattoirs include blood, gut contents, wash waters, and sludge from dissolved air flotation (DAF) treatment where this process has been used for the separation solids from any liquid waste materials of the abattoir (Davis and Rudd, 1999).

 

It has been reported that 21% of an animal is waste when processed (Gendebien et al., 2001). Some of the abattoir wastes, such as bones and hoof parts are recycled in other industries (e.g. fertiliser and gelatine). In the EU, between 5 to 10 % of abattoir waste is applied to land following composting or without any further treatment. This waste mainly consists of gut contents, wash waters and blood (Gendebien et al., 2001). For small-scale abattoirs, landspreading of the waste is probably the best environmental option but likely to be much less appropriate for large-scale operations (Mittal, 2007).

 

Whereas waste blood and stomach contents have a high fertilizer value due to their high nitrogen, phosphorus and potassium content, which makes them a good source of plants nutrients, wash waters contain lower levels of nutrients (Mittal, 2007). Abattoir wastes may also have a high conductivity and fat content (Davis and Rudd, 1999). Blood and gut content from abattoirs are included in the exempt industrial wastes for land application. Since most of the exempt wastes are not pre-treated or stored at the point of source, it can cause public nuisance due to odours, environmental concerns and if spread on the soil surface it is unsightly and may have the potential for disease transmission (Mittal, 2007). It is recommended that these wastes should be immediately incorporated into arable land, or applied to grassland by sub-surface injection following a 3 week period to allow the injection slots to close before the use of the grass for grazing or conservation (Davis and Rudd, 1999).

 

Blood

 

Waste blood is produced in large quantities from abattoirs and used to be applied onto land without further treatment as a source of nutrients. Nitrogen content in waste blood is extremely high, typically exceeding 15 kg/m3 total nitrogen and 2 kg/m3 of ammonium nitrogen. The high nitrogen content combined with potassium and phosphorus contents of 1 to 2 kg/m3, waste blood provides a good source of plant nutrients, which are in a more available form when compared to other organic wastes (Davis and Rudd, 1999). Potential disadvantages are if applied in excess to plant requirements, these high levels of elements might cause water pollution and pose a danger to plant health (Gendebien et al., 2001). Abattoir wastes also have a

 

The Food and Environment Research Agency 83

 

high biological oxygen demand (BOD) that makes it readily degradable by soil microorganisms and thus over application can result in anaerobic soil conditions (Davis and Rudd, 1999).

 

In the EU, however, from the 1st May 2003, the EU Animal By-products Regulations require that certain by-products need to be treated before disposal (Defra, 2003). Therefore, it is no longer permitted the disposal of untreated blood to sewers or landfill or to recover untreated blood via application on land.

 

 Other abattoir wastes

 

Other abattoir wastes include waste from where animals are temporarily kept (also known as lairage), wastes from biological treatment plants and fat (Davis and Rudd, 1999; WRc, 2009). Due to the amount of blood in wastes for treatment and disposal, the nitrogen content can be very high, in excess of 8 kg/m3 and ammonium nitrogen typically exceeding 1 kg/m3. Potassium, phosphorus and magnesium can be in excess of 1 to 2 kg/m3. Different types of abattoirs produce different types and amounts of fat, but chicken processing plants are sources of high fat materials. Adverse effects on plant growth following application of animal fat have been observed at relatively low fat percentages when compared to wastes containing other fats and oils (Davis and Rudd, 1999). These wastes should also be incorporated into the soil.

 

snip...

 

5.3.3. Pathogens

 

5.3.3.1. Sources

 

Animal manures contain pathogenic elements in variable quantities depending on the animal health. Pathogenic microorganisms such as Esherichia c. O157, Salmonella, Listeria, Campylobacter, Cryptosporidium and Giardia have all been isolated from cattle, pig and sheep manures (ADAS, Imperial College, JBA Consulting, 2005).

 

5.3.3.2. Upstream control measures

 

Veterinary medicines are administered to reduce certain harmful pathogens and diseases. Waste from infected animals with high risk diseases such as BSE should be disposed of separately and not spread on land. However, most pathogens of concern to human health do not affect animals and so are not treated with medicines.

 

Upstream measures to reduce pathogens in manures are presented below.

 

snip...

 


 

 

*** COMERCIAL IN CONFIDENCE

 

SPREADING OF UNPROCESSED BLOOD ON LAND

 


 

 

*** The BSE Inquiry / Statement No 19B (supplementary) Dr Alan Colchester Issued 06/08/1999 (not scheduled to give oral evidence) SECOND STATEMENT TO THE BSE INQUIRY Dr A Colchester BA BM BCh PhD FRCP Reader in Neurosciences & Computing, University of Kent at Canterbury; Consultant Neurologist, Guy’s Hospital London and William Harvey Hospital Ashford April 1999

 

snip...

 

88. Natural decay: Infectivity persists for a long time in the environment. A study by Palsson in 1979 showed how scrapie was contracted by healthy sheep, after they had grazed on land which had previously been grazed by scrapie-infected sheep, even though the land had lain fallow for three years before the healthy sheep were introduced. Brown also quoted an early experiment of his own (1991), where he had buried scrapie-infected hamster brain and found that he could still detect substantial infectivity three years later near where the material had been placed. 89. Potential environmental routes of infection: Brown discusses the various possible scenarios, including surface or subsurface deposits of TSE-contaminated material, which would lead to a build-up of long-lasting infectivity. Birds feeding on animal remains (such as gulls visiting landfill sites) could disperse infectivity. Other animals could become vectors if they later grazed on contaminated land. "A further question concerns the risk of contamination of the surrounding water table or even surface water channels, by effluents and discarded solid wastes from treatment plants. A reasonable conclusion is that there is a potential for human infection to result from environmental contamination by BSE-infected tissue residues. The potential cannot be quantified because of the huge numbers of uncertainties and assumptions that attend each stage of the disposal process". These comments, from a long established authority on TSEs, closely echo my own statements which were based on a recent examination of all the evidence. 90. Susceptibility: It is likely that transmissibility of the disease to humans in vivo is probably low, because sheep that die from scrapie and cattle that die from BSE are probably a small fraction of the exposed population. However, no definitive data are available.

 

91. Recommendations for disposal procedures: Brown recommends that material which is actually or potentially contaminated by BSE should be: 1) exposed to caustic soda; 2) thoroughly incinerated under carefully inspected conditions; and 3) that any residue should be buried in landfill, to a depth which would minimise any subsequent animal or human exposure, in areas that would not intersect with any potable water-table source.

 

92. This review and recommendations from Brown have particular importance. Brown is one of the world's foremost authorities on TSEs and is a senior researcher in the US National Institutes of Health (NIH). It is notable that such a respected authority is forthright in acknowledging the existence of potential risks, and in identifying the appropriate measures necessary to safeguard public health. Paper by SM Cousens, L Linsell, PG Smith, Dr M Chandrakumar, JW Wilesmith, RSG Knight, M Zeidler, G Stewart, RG Will, "Geographical distribution of variant CJD in the UK (excluding Northern Ireland)". Lancet 353:18-21, 2 nd January 1999 93. The above paper {Appendix 41 (02/01/99)} (J/L/353/18) examined the possibility that patients with vCJD (variant CJD) might live closer to rendering factories than would be expected by chance. All 26 cases of vCJD in the UK with onset up to 31 st August 1998 were studied. The incubation period of vCJD is not known but by analogy with other human TSEs could lie within the range 5-25 years. If vCJD had arisen by exposure to rendering products, such exposure might plausibly have occurred 8-10 years before the onset of symptoms. The authors were able to obtain the addresses of all rendering plants in the UK which were in production in 1988. For each case of vCJD, the distance from the place of residence on 1st January 1998 to the nearest rendering plant was calculated

 

snip...

 


 

Sunday, December 28, 2014

 

*** Reverse Freedom of Information Act request rFOIA FSIS USDA APHIS TSE PRION aka BSE MAD COW TYPE DISEASE December 2014

 


 


 


 


 


 


 


 


 


 


 


 


 


 

good luck, good health to all, respectfully,

 

Terry S. Singeltary Sr.

 

P.O. Box 42

 

Bacliff, Texas USA 77518

 

--- ...- . .-. / .- -. -.. / --- ..- -

 

 

Tuesday, December 16, 2014

Evidence for zoonotic potential of ovine scrapie prions

Evidence for zoonotic potential of ovine scrapie prions

 

Hervé Cassard,1, n1 Juan-Maria Torres,2, n1 Caroline Lacroux,1, Jean-Yves Douet,1, Sylvie L. Benestad,3, Frédéric Lantier,4, Séverine Lugan,1, Isabelle Lantier,4, Pierrette Costes,1, Naima Aron,1, Fabienne Reine,5, Laetitia Herzog,5, Juan-Carlos Espinosa,2, Vincent Beringue5, & Olivier Andréoletti1, Affiliations Contributions Corresponding author Journal name: Nature Communications Volume: 5, Article number: 5821 DOI: doi:10.1038/ncomms6821 Received 07 August 2014 Accepted 10 November 2014 Published 16 December 2014 Article tools Citation Reprints Rights & permissions Article metrics

 

Abstract

 

Although Bovine Spongiform Encephalopathy (BSE) is the cause of variant Creutzfeldt Jakob disease (vCJD) in humans, the zoonotic potential of scrapie prions remains unknown. Mice genetically engineered to overexpress the human ​prion protein (tgHu) have emerged as highly relevant models for gauging the capacity of prions to transmit to humans. These models can propagate human prions without any apparent transmission barrier and have been used used to confirm the zoonotic ability of BSE. Here we show that a panel of sheep scrapie prions transmit to several tgHu mice models with an efficiency comparable to that of cattle BSE. The serial transmission of different scrapie isolates in these mice led to the propagation of prions that are phenotypically identical to those causing sporadic CJD (sCJD) in humans. These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.

 

Subject terms: Biological sciences• Medical research At a glance

 



see more here ;

http://www.nature.com/ncomms/2014/141216/ncomms6821/extref/ncomms6821-s1.pdf

 

 Scrapie from sheep could infect humans with 'mad cow disease', study finds

 

Tests find a link between the infectious agent behind scrapie with fatal human brain disease, sporadic CJD, which caused major health scare in 1990s

 

A ram being tested for Scrapie

 

A ram being tested for Scrapie Photo: Wayne HUTCHINSON / Alamy

 

By Press Association

 

12:01AM GMT 17 Dec 2014

 

The deadly brain condition known as "mad cow disease" could potentially be transmitted to humans by sheep carrying scrapie, new research suggests.

 

Scientists have concluded that scrapie - the sheep equivalent of mad cow disease, or BSE, in cows - has the potential to infect humans in a similar way to variant CJD (Creuzfeldt Jakob Disease), which caused a major health scare over beef in the 1990s.

 

Tests on mice found a link between the infectious agent behind scrapie with sporadic CJD (sCJD), a fatal human disease whose cause has never been known.

 

The scientists stress they have no proof that eating mutton or lamb infected with scrapie can lead to sCJD in humans.

 

But tests on humanised laboratory mice show that potentially scrapie is capable of infecting humans. And the way the infection spreads in the brain is identical to that seen in cases of sCJD.

 

Related Articles Mad cow infected blood 'to kill 1000’ Mad cow infected blood 'to kill 1,000’ 28 Apr 2013 NHS patients at risk of getting mad cow disease during surgery 24 Jul 2014 Vegetarian diagnosed with 'Mad Cow Disease' 23 Aug 2013

 

The scientists, led by Dr Olivier Andreoletti, from the National Veterinary School of Toulouse in France, wrote in the journal Nature Communications: "Our data on their own do not unequivocally establish a causative link between natural exposure to sheep scrapie and the subsequent appearance of sCJD in humans.

 

"However, our studies clearly point out the need to consider this possibility."

 

Both scrapie and different forms of CJD are caused by rogue misshapen prion proteins. Normal prions that come into contact with the defective versions are changed too and turn "bad". In this way the infection spreads, inflicting terrible damage to the brain.

 

Variant CJD first emerged in 1996 and was shown to be the human version of the cattle disease bovine spongiform encephalopathy (BSE).

 

The prions that caused the disease spread to humans in contaminated beef - especially burgers, cheap cuts and pies - and some cases were also traced to blood transfusions from infected donors.

 

However, fears of a catastrophic epidemic with thousands or even millions of people dying never materialised. To date, 177 UK deaths from vCJD have been recorded, most occurring in the late 1990s and early 2000s.

 

The mice in the new study were the same strain previously used to confirm the ability of BSE to break the species barrier and infect humans.

 

In the tests, the animals had scrapie prions injected straight into their brains. The authors point out that prion infection via non-direct routes, such as eating contaminated tissue, can have an incubation period running into decades.

 

They added: "Furthermore, it is crucial to bear in mind that sporadic sCJD in humans is a rare disease and that scrapie has been circulating in small ruminants populations used for food purposes for centuries.

 

"Consequently, it is our opinion that even if a causative link was established between sheep scrapie exposure and the occurrence of certain sCJD cases, it would be wrong to consider small ruminant (prion) agents as a new major threat for public health."

 

A Defra spokesperson, said: “There are existing measures in place to ensure that any clinically affected animals with this disease are not able to enter the food chain.

 

"Regular surveillance for the disease is carried out in abattoirs and in stock which have died. Scrapie has a very low prevalence within the UK and there are strict biosecurity procedures in place to prevent it entering the country.”

 


 

 

 

Suspect symptoms

 

What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?

 

28 Mar 01 Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.

 

Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.

 

"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb...

 

2001

 

Suspect symptoms

 

What if you can catch old-fashioned CJD by eating meat from a sheep infected with scrapie?

 

28 Mar 01

 

Like lambs to the slaughter

 

31 March 2001

 

by Debora MacKenzie Magazine issue 2284.

 

FOUR years ago, Terry Singeltary watched his mother die horribly from a degenerative brain disease. Doctors told him it was Alzheimer's, but Singeltary was suspicious. The diagnosis didn't fit her violent symptoms, and he demanded an autopsy. It showed she had died of sporadic Creutzfeldt-Jakob disease.

 

Most doctors believe that sCJD is caused by a prion protein deforming by chance into a killer. But Singeltary thinks otherwise. He is one of a number of campaigners who say that some sCJD, like the variant CJD related to BSE, is caused by eating meat from infected animals. Their suspicions have focused on sheep carrying scrapie, a BSE-like disease that is widespread in flocks across Europe and North America.

 

Now scientists in France have stumbled across new evidence that adds weight to the campaigners' fears. To their complete surprise, the researchers found that one strain of scrapie causes the same brain damage in mice as sCJD.

 

"This means we cannot rule out that at least some sCJD may be caused by some strains of scrapie," says team member Jean-Philippe Deslys of the French Atomic Energy Commission's medical research laboratory in Fontenay-aux-Roses, south-west of Paris. Hans Kretschmar of the University of Göttingen, who coordinates CJD surveillance in Germany, is so concerned by the findings that he now wants to trawl back through past sCJD cases to see if any might have been caused by eating infected mutton or lamb.

 

Scrapie has been around for centuries and until now there has been no evidence that it poses a risk to human health. But if the French finding means that scrapie can cause sCJD in people, countries around the world may have overlooked a CJD crisis to rival that caused by BSE.

 

Deslys and colleagues were originally studying vCJD, not sCJD. They injected the brains of macaque monkeys with brain from BSE cattle, and from French and British vCJD patients. The brain damage and clinical symptoms in the monkeys were the same for all three. Mice injected with the original sets of brain tissue or with infected monkey brain also developed the same symptoms.

 

As a control experiment, the team also injected mice with brain tissue from people and animals with other prion diseases: a French case of sCJD; a French patient who caught sCJD from human-derived growth hormone; sheep with a French strain of scrapie; and mice carrying a prion derived from an American scrapie strain. As expected, they all affected the brain in a different way from BSE and vCJD. But while the American strain of scrapie caused different damage from sCJD, the French strain produced exactly the same pathology.

 

"The main evidence that scrapie does not affect humans has been epidemiology," says Moira Bruce of the neuropathogenesis unit of the Institute for Animal Health in Edinburgh, who was a member of the same team as Deslys. "You see about the same incidence of the disease everywhere, whether or not there are many sheep, and in countries such as New Zealand with no scrapie." In the only previous comparisons of sCJD and scrapie in mice, Bruce found they were dissimilar.

 

But there are more than 20 strains of scrapie, and six of sCJD. "You would not necessarily see a relationship between the two with epidemiology if only some strains affect only some people," says Deslys. Bruce is cautious about the mouse results, but agrees they require further investigation. Other trials of scrapie and sCJD in mice, she says, are in progress.

 

People can have three different genetic variations of the human prion protein, and each type of protein can fold up two different ways. Kretschmar has found that these six combinations correspond to six clinical types of sCJD: each type of normal prion produces a particular pathology when it spontaneously deforms to produce sCJD.

 

But if these proteins deform because of infection with a disease-causing prion, the relationship between pathology and prion type should be different, as it is in vCJD. "If we look at brain samples from sporadic CJD cases and find some that do not fit the pattern," says Kretschmar, "that could mean they were caused by infection."

 

There are 250 deaths per year from sCJD in the US, and a similar incidence elsewhere. Singeltary and other US activists think that some of these people died after eating contaminated meat or "nutritional" pills containing dried animal brain. Governments will have a hard time facing activists like Singeltary if it turns out that some sCJD isn't as spontaneous as doctors have insisted.

 

Deslys's work on macaques also provides further proof that the human disease vCJD is caused by BSE. And the experiments showed that vCJD is much more virulent to primates than BSE, even when injected into the bloodstream rather than the brain. This, says Deslys, means that there is an even bigger risk than we thought that vCJD can be passed from one patient to another through contaminated blood transfusions and surgical instruments.

 


 

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

 


 

1: J Infect Dis 1980 Aug;142(2):205-8

 

Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to nonhuman primates.

 

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

 

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of sheep and goats were transmitted to squirrel monkeys (Saimiri sciureus) that were exposed to the infectious agents only by their nonforced consumption of known infectious tissues. The asymptomatic incubation period in the one monkey exposed to the virus of kuru was 36 months; that in the two monkeys exposed to the virus of Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and that in the two monkeys exposed to the virus of scrapie was 25 and 32 months, respectively. Careful physical examination of the buccal cavities of all of the monkeys failed to reveal signs or oral lesions. One additional monkey similarly exposed to kuru has remained asymptomatic during the 39 months that it has been under observation.

 

snip...

 

The successful transmission of kuru, Creutzfeldt-Jakob disease, and scrapie by natural feeding to squirrel monkeys that we have reported provides further grounds for concern that scrapie-infected meat may occasionally give rise in humans to Creutzfeldt-Jakob disease.

 

PMID: 6997404

 


 

Recently the question has again been brought up as to whether scrapie is transmissible to man. This has followed reports that the disease has been transmitted to primates. One particularly lurid speculation (Gajdusek 1977) conjectures that the agents of scrapie, kuru, Creutzfeldt-Jakob disease and transmissible encephalopathy of mink are varieties of a single "virus". The U.S. Department of Agriculture concluded that it could "no longer justify or permit scrapie-blood line and scrapie-exposed sheep and goats to be processed for human or animal food at slaughter or rendering plants" (ARC 84/77)" The problem is emphasised by the finding that some strains of scrapie produce lesions identical to the once which characterise the human dementias"

 

Whether true or not. the hypothesis that these agents might be transmissible to man raises two considerations. First, the safety of laboratory personnel requires prompt attention. Second, action such as the "scorched meat" policy of USDA makes the solution of the acrapie problem urgent if the sheep industry is not to suffer grievously.

 

snip...

 

76/10.12/4.6

 


 

Nature. 1972 Mar 10;236(5341):73-4.

 

Transmission of scrapie to the cynomolgus monkey (Macaca fascicularis).

 

Gibbs CJ Jr, Gajdusek DC.

 

Nature 236, 73 - 74 (10 March 1972); doi:10.1038/236073a0

 

Transmission of Scrapie to the Cynomolgus Monkey (Macaca fascicularis)

 

C. J. GIBBS jun. & D. C. GAJDUSEK

 

National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland

 

SCRAPIE has been transmitted to the cynomolgus, or crab-eating, monkey (Macaca fascicularis) with an incubation period of more than 5 yr from the time of intracerebral inoculation of scrapie-infected mouse brain. The animal developed a chronic central nervous system degeneration, with ataxia, tremor and myoclonus with associated severe scrapie-like pathology of intensive astroglial hypertrophy and proliferation, neuronal vacuolation and status spongiosus of grey matter. The strain of scrapie virus used was the eighth passage in Swiss mice (NIH) of a Compton strain of scrapie obtained as ninth intracerebral passage of the agent in goat brain, from Dr R. L. Chandler (ARC, Compton, Berkshire).

 


 


 

Sunday, December 12, 2010

 

EFSA reviews BSE/TSE infectivity in small ruminant tissues News Story 2 December 2010

 


 

Wednesday, January 18, 2012

 

Selection of Distinct Strain Phenotypes in Mice Infected by Ovine Natural Scrapie Isolates Similar to CH1641 Experimental Scrapie

 

Journal of Neuropathology & Experimental Neurology: February 2012 - Volume 71 - Issue 2 - p 140–147

 


 

Thursday, July 14, 2011

 

Histopathological Studies of "CH1641-Like" Scrapie Sources Versus Classical Scrapie and BSE Transmitted to Ovine Transgenic Mice (TgOvPrP4)

 


 

Wednesday, January 18, 2012

 

BSE IN GOATS CAN BE MISTAKEN FOR SCRAPIE

 

February 1, 2012

 


 

Thursday, December 23, 2010

 

Molecular Typing of Protease-Resistant Prion Protein in Transmissible Spongiform Encephalopathies of Small Ruminants, France, 2002-2009

 

Volume 17, Number 1 January 2011

 


 

Thursday, November 18, 2010

 

Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep

 


 

Monday, December 14, 2009

 

Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease Are Encoded by Distinct Prion Types

 

(hmmm, this is getting interesting now...TSS)

 

Sporadic CJD type 1 and atypical/ Nor98 scrapie are characterized by fine (reticular) deposits,

 

see also ;

 

All of the Heidenhain variants were of the methionine/ methionine type 1 molecular subtype.

 


 

see full text ;

 

Monday, December 14, 2009

 

Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease Are Encoded by Distinct Prion Types

 


 

Thursday, July 21, 2011

 

A Second Case of Gerstmann-Sträussler-Scheinker Disease Linked to the G131V Mutation in the Prion Protein Gene in a Dutch Patient Journal of Neuropathology & Experimental Neurology:

 

August 2011 - Volume 70 - Issue 8 - pp 698-702

 


 

Friday, March 09, 2012

 

Experimental H-type and L-type bovine spongiform encephalopathy in cattle: observation of two clinical syndromes and diagnostic challenges

 

Research article

 


 

Thursday, June 23, 2011

 

Experimental H-type bovine spongiform encephalopathy characterized by plaques and glial- and stellate-type prion protein deposits

 


 

Thursday, February 14, 2013

 

*** The Many Faces of Mad Cow Disease Bovine Spongiform Encephalopathy BSE and TSE prion disease

 


 

Tuesday, March 5, 2013

 

Use of Materials Derived From Cattle in Human Food and Cosmetics; Reopening of the Comment Period FDA-2004-N-0188-0051 (TSS SUBMISSION)

 

FDA believes current regulation protects the public from BSE but reopens comment period due to new studies

 


 

Tuesday, March 05, 2013

 

A closer look at prion strains Characterization and important implications

 

Prion 7:2, 99–108; March/April 2013; © 2013 Landes Bioscience

 


 

Thursday, January 26, 2012

 

Facilitated Cross-Species Transmission of Prions in Extraneural Tissue

 

Science 27 January 2012: Vol. 335 no. 6067 pp. 472-475 DOI: 10.1126/science.1215659

 


 

Saturday, February 11, 2012

 

Prion cross-species transmission efficacy is tissue dependent

 


 

Thursday, January 26, 2012

 

The Risk of Prion Zoonoses

 

Science 27 January 2012: Vol. 335 no. 6067 pp. 411-413 DOI: 10.1126/science.1218167

 


 

Monday, April 25, 2011

 

Experimental Oral Transmission of Atypical Scrapie to Sheep

 

Volume 17, Number 5-May 2011

 


 

Sunday, April 18, 2010

 

SCRAPIE AND ATYPICAL SCRAPIE TRANSMISSION STUDIES A REVIEW 2010

 


 

Thursday, November 18, 2010

 

Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep

 


 

Wednesday, January 19, 2011

 

EFSA and ECDC review scientific evidence on possible links between TSEs in animals and humans Webnachricht 19 Januar 2011

 


 

Monday, June 27, 2011

 

Comparison of Sheep Nor98 with Human Variably Protease-Sensitive Prionopathy and Gerstmann-Sträussler-Scheinker Disease

 


 

Thursday, November 18, 2010

 

Increased susceptibility of human-PrP transgenic mice to bovine spongiform encephalopathy following passage in sheep

 


 

Tuesday, September 24, 2013

 

NORDION (US), INC., AND BIOAXONE BIOSCIENCES, INC., Settles $90M Mad Cow TSE prion Contamination Suit Cethrin(R)

 

Case 0:12-cv-60739-RNS Document 1 Entered on FLSD Docket 04/26/2012 Page 1 of 15

 


 

with great sadness and disgust, I must inform you that our federal government has failed us again, and chose the industry over sound science, with regards to TSE prion disease, aka mad cow type disease...tss

 

Saturday, November 2, 2013

 

APHIS Finalizes Bovine Import Regulations in Line with International Animal Health Standards while enhancing the spread of BSE TSE prion mad cow type disease around the Globe

 


 

Wednesday, November 13, 2013

 

Atypical Scrapie Prions from Sheep and Lack of Disease in Transgenic Mice Overexpressing Human Prion Protein

 


 


 

Friday, December 5, 2014

 

SPECIAL ALERT The OIE recommends strengthening animal disease surveillance worldwide

 


 

Tuesday, December 16, 2014

 

Texas 84th Legislature 2015 H.R. No. 2597 Kuempel Deer Breeding Industry TAHC TPWD CWD TSE PRION

 


 

Saturday, December 13, 2014

 

Terry S. Singeltary Sr. Publications TSE prion disease

 

for my files...tss

 

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

 

Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA

 

snip...

 


 

Sunday, December 14, 2014

 

ALERT new variant Creutzfeldt Jakob Disease nvCJD or vCJD, sporadic CJD strains, TSE prion aka Mad Cow Disease United States of America Update December 14, 2014 Report

 


 

TSS