Contains Nonbinding Recommendations
Medical Devices Containing Materials Derived from Animal Sources (Except for In Vitro Diagnostic Devices)
Guidance for Industry and Food and Drug Administration Staff
Document issued on March 15, 2019.
The draft of this document was issued on January 23, 2014.
This document supersedes “Medical Devices Containing Materials Derived from Animal Sources (Except for In Vitro Diagnostic Devices)” issued November 6, 1998.
U.S. Department of Health and Human Services Food and Drug Administration Center for Devices and Radiological Health
Contains Nonbinding Recommendations
Preface
Public Comment
You may submit electronic comments and suggestions at any time for Agency consideration to https://www.regulations.gov. Submit written comments to the Dockets Management Staff, Food and Drug Administration, 5630 Fishers Lane, Room 1061, (HFA-305), Rockville, MD 20852. Identify all comments with the docket number FDA-2013-D-1574. Comments may not be acted upon by the Agency until the document is next revised or updated.
Additional Copies
Additional copies are available from the Internet. You may also send an e-mail request to CDRH-Guidance@fda.hhs.gov to receive a copy of the guidance. Please use the document number 2206 to identify the guidance you are requesting
Contains Nonbinding Recommendations
Table of Contents
I. Introduction........................................................................................................................................1
II. Background ........................................................................................................................................2
III. Scope..................................................................................................................................................3
IV. Considerations When Using Animal-Derived Materials ...................................................................4
A. Control of Animal Tissue Collection..............................................................................................4
B. Manufacturing Controls for Animal Tissue Components..............................................................5
C. Sterilization ....................................................................................................................................6
D. Transmissible Spongiform Encephalopathy-Specific Issues.........................................................8
Contains Nonbinding Recommendations
Medical Devices Containing Materials Derived from Animal Sources (Except for In Vitro Diagnostic Devices)
1
Guidance for Industry and Food and Drug Administration Staff
This guidance represents the current thinking of the Food and Drug Administration (FDA or Agency) on this topic. It does not establish any rights for any person and is not binding on FDA or the public. You can use an alternative approach if it satisfies the requirements of the applicable statutes and regulations. To discuss an alternative approach, contact the FDA staff or Office responsible for this guidance as listed on the title page.
I. Introduction
The Food and Drug Administration (FDA) is issuing this guidance to update the policy regarding the use of animal-derived material in medical device manufacturing. The role of animal-derived material in medical devices is well established. However, these materials may carry a risk of transmitting infectious disease when improperly collected, stored, or manufactured. The purpose of this guidance is to provide further clarification and updated information on the use of International Organization for Standardization (ISO) 22442-1 “Medical devices utilizing animal tissues and their derivatives – Part 1: Application of risk management,” ISO 22442-2, “Medical devices utilizing animal tissues and their derivatives – Part 2: Controls on sourcing, collection and handling,” and ISO 22442-3 “Medical devices utilizing animal tissues and their derivatives – Part 3: Validation of the elimination and/or inactivation of viruses and transmissible spongiform encephalopathy (TSE) agents” to support applications to FDA. This guidance also provides recommendations regarding methods for controlling the sourcing of animal tissues with regard to viral pathogens and evaluating the ability of manufacturing methods to remove such pathogens from the final product. This guidance replaces “Medical Devices Containing Materials Derived from Animal Sources (Except for In Vitro Diagnostic Devices)” issued November 6, 1998 (“the 1998 guidance.”) For the current edition of the FDA-recognized standard(s) referenced in this document, see the FDA Recognized Consensus Standards Database. 1
Contains Nonbinding Recommendations
Throughout this guidance document, the term “we” refers to FDA staff from CDRH. “You” and “your” refers to the manufacturer.
FDA’s guidance documents, including this guidance, do not establish legally enforceable responsibilities. Instead, guidances describe the Agency’s current thinking on a topic and should be viewed only as recommendations, unless specific regulatory or statutory requirements are cited. The use of the word should in Agency guidance means that something is suggested or recommended, but not required.
II. Background
This guidance updates the 1998 guidance by addressing aspects of potential risk from the use of animal tissues and now includes recommendations related to viral pathogens and all transmissible spongiform encephalopathies (TSEs). The 1998 guidance addressed ways to reduce the potential for exposure to one specific TSE, bovine spongiform encephalopathy (BSE). This document continues to focus on the control of transmissible disease, and contains recommendations for documenting the source of animal tissue and conducting viral inactivation validation studies. Commercial production of animals as sources of bodily tissues used in medical devices can introduce several kinds of risks. The 1998 document primarily addressed geographical factors in the sourcing of the animal tissue. In addition to geographical factors, this document includes recommendations that recognize the role of appropriate animal husbandry to ensure safe tissue sources.
International Standard ISO 22442 series, “Medical devices utilizing animal tissues and their derivatives – Part 1: Application of risk management,” “Part 2: Controls on sourcing, collection and handling,” and “Part 3: Validation of the elimination and/or inactivation of viruses and transmissible spongiform encephalopathy (TSE) agents,” provides recommendations for selection and handling of animal tissues as well as evaluating the risk of pathogen contamination in medical devices. Used in concert with the ISO 22442 series of standards, this guidance is intended to help you identify the possible risks related to medical device components and/or manufacturing reagents that are sourced from animal tissues. We also recognize that an ISO standard is a document that undergoes periodic review and is subject to revision. Through the FDA standards recognition process, CDRH provides information regarding the extent of recognition of the ISO 22442 series of standards through Supplementary Information Sheets published on the FDA website.
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2 FDA will make updates to this guidance document as appropriate, should future revisions to the ISO 22442 series of standards result in significant changes to the recommendations in this document.
Contains Nonbinding Recommendations
III. Scope
The information in this guidance is applicable to all medical devices that contain or are exposed (e.g., through a manufacturing reagent) to animal-derived (e.g., bovine, ovine, porcine, avian) materials with the exception of in vitro diagnostic devices and materials generally recognized to be safe based on their method of manufacture (e.g., tallow derivatives as described in Annex C of ISO 22442-1: 2015). This guidance addresses the risks of human pathogens that could contaminate animal material and be present in a medical device. For devices that indirectly contact humans, this guidance considers the risk to patients (e.g., how might indirect contact result in pathogen exposure) and the healthcare provider who may handle device components that do not contact a patient.
This guidance provides:
1) information that FDA believes is important to document the safe and consistent manufacture of medical devices containing animal tissue;
2) information that should be included in a premarket submission for products within the scope of this guidance;
3) recommendations regarding how specific aspects of the Quality System (QS) Regulation
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3 should be applied to control and document the safe and consistent manufacture of medical devices containing animal tissue; and 4) additional information on specific approaches for determining the ability of manufacturing methods to eliminate viral contamination in the final product. In general, premarket submissions should include information on the specifics identified below or the methods by which the risks are mitigated. In addition, records at the manufacturing facility should continue to document this information on each lot of product manufactured consistent with the QS Regulation.
FDA has developed this guidance document to assist industry in preparing Premarket Approval (PMA) applications, Humanitarian Device Exemption (HDE) applications, Investigational Device Exemption (IDE) applications, Premarket Notification (510(k)) submissions, and De Novo requests for medical devices that contain device components derived from animal sources and come into direct or indirect contact with the human body. This guidance is not applicable to medical devices that are derived from human tissues because the potential contaminants associated with human donor tissues are considerably different than those that are found in animal tissues.
Should a manufacturer have questions about the applicability of this guidance to their specific product, we recommend consultation with FDA.
3 21 CFR part 820
Contains Nonbinding Recommendations
IV. Considerations When Using AnimalDerived Materials
A. Control of Animal Tissue Collection
To ensure the safety of medical devices containing or contacting animal tissue, FDA believes that it is important: 1) to document the sourcing and handling of animal tissues as well as 2) to understand the capabilities of the manufacturing and sterilization processes to eliminate human pathogens. Consequently, FDA recommends that you collect and document the information outlined below for animal tissue-derived materials that are used as either device components (e.g., pericardium, viscera, bone, hyaluronic acid, collagen) or manufacturing reagents (e.g., tissue culture media, enzymes). For devices prepared from animal tissues that have a reduced risk of human pathogen contamination (e.g., crustaceans), FDA recommends that you address the information outlined below if applicable to that particular source material. If determined not to be applicable, FDA recommends providing a scientific explanation (i.e., based on published literature or information from a recognized source (e.g., WHO, CDC, USDA)) that identifies the human pathogens that may be present in the animal species, and how your approach ensures device safety.
Premarket submissions should include information on the items identified below, consistent with ISO 22442-2 and the methods by which the risks are mitigated 4
4 if applicable. You may document this information in a premarket submission or by reference to other regulatory submissions (e.g., Master File, PMA, 510(k)).
· the animal species;
· the age of the animal at slaughter;
· the specific tissue(s) used (if multiple tissues are used, please identify all such tissues);
· the animals’ country of origin and residence (with more specific geographic information when appropriate) when such information is available;
· the status of the herd or collection of organisms (e.g., closed herd/group);
· the methods for actively monitoring the health of the herd and the health of specific animals from which tissues are collected (e.g., vaccinations with live modified viruses that can co-purify in the desired tissue, active surveillance for human pathogens);
· the methods and conditions for transporting animal tissue (e.g., tissue refrigeration and quarantine);
· the United States Department of Agriculture (USDA) status of the abattoir;
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· the tests performed (and release criteria) for permitting tissue to be further processed and/or combined with other tissues and device components (e.g., a Certificate of Analysis); and
· Material Safety Data Sheets may be helpful information to include in a regulatory submission, when available, because they provide an overview of the safety and
4
ISO 22442-1, Medical devices utilizing animal tissues and their derivatives – Part 1: Application of risk management
5 USDA status is not included in ISO 22442-2, however, will provide additional assurance regarding the safety of the tissue used.
Contains Nonbinding Recommendations
potential toxicities related to that component, including information on any reagents used in the processing of the tissue, to support biocompatibility assessments.
Certification of compliance with USDA Animal and Plant Health Inspection Service (APHIS) importation and/or USDA Food Safety and Inspection Service (FSIS) inspection requirements may be provided in lieu of any aforementioned items provided in these forms. In addition, the manufacturing facility should document 1) procedures for maintaining records on the above cited items
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and 2) all information outlined above on each lot of product manufactured (Device History Record).
7 If necessary to ensure the safety of the medical device, this information may be reviewed during inspection.
B. Manufacturing Controls for Animal Tissue Components FDA also recommends that you collect and document the information listed below for each animal-derived material (and facility) used in device manufacture. Premarket submissions should include information on the items identified below and the methods by which the risks are mitigated8
if applicable. You may document this information in a premarket submission or by reference to other regulatory submissions (e.g., Master File, PMA, 510(k)). The recommended information is:
· test methods and release criteria permitting animal tissues to be further processed and/or combined with other animal tissue(s) or device components for manufacture;
· quarantine procedures for tissues until they have met/failed release criteria;
· test methods and acceptance criteria for assessing in-process and final product bioburden or sterility; and
· methods for facility decontamination/sterilization so that cross-contamination is avoided. In addition, the manufacturing facility should document: 1) procedures for maintaining records on the above cited items;
9 2) all information outlined above on each lot of product manufactured (Device History Record);
10 and 3) information to validate the effectiveness of manufacturing equipment cleaning, decontamination, and sterilization relative to the specific pathogen exposure.
11 If necessary to ensure the safety of the medical device, this information may be reviewed during inspection.
The QS Regulation includes requirements related to the methods used in and the facilities and controls used for designing, manufacturing, packaging, labeling, storing, installing, and
6 21 CFR 820.70 7 21 CFR 820.184
8
ISO 22442-1, Medical devices utilizing animal tissues and their derivatives – Part 1: Application of risk management
9 21 CFR 820.70 10 21 CFR 820.184 11 21 CFR 820.75
Contains Nonbinding Recommendations
servicing of medical devices. Purchasing Controls, under 21 CFR 820.50, require final device manufacturers to establish procedures that ensure all purchased or otherwise received products and services conform to specified requirements, including those materials derived from animal sources. The controls applied to manufacturing materials are expected to be appropriate to the manufacturing material, the intended use, and the effect of the manufacturing materials on safety and effectiveness (61 FR 52602, 52624). Further information on the QS Regulation for certain premarket applications can be found in “Quality System Information for Certain
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Premarket Application Reviews; Guidance for Industry and FDA Staff.”
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C. Sterilization
Because the issues for validating the sterilization of devices containing animal tissue are sufficiently complex to require a case-by-case assessment, we recommend you review the following FDA-recognized consensus standards:
· ISO 11135, Sterilization of health-care products – Ethylene oxide – Requirements for the development, validation and routine control of a sterilization process for medical devices
· ISO 17665-1, Sterilization of health care products – Moist heat – Part 1: Requirements for the development, validation and routine control of a sterilization process for medical devices
· ISO 11137-1, Sterilization of health care products – Radiation – Part 1: Requirements for development, validation and routine control of a sterilization process for medical devices
· ISO 11737-1, Sterilization of medical devices – Microbiological methods – Part 1: Determination of a population of microorganisms on products
· ISO 11737-2, Sterilization of medical devices – Microbiological methods – Part
2: Tests of sterility performed in the definition, validation and maintenance of a sterilization process
· ISO 14160, Sterilization of health care products – Liquid chemical sterilizing agents for single-use medical devices utilizing animal tissues and their derivatives – Requirements for characterization, development, validation and routine control of a sterilization process for medical devices
· ISO 14937, Sterilization of health care products – General requirements for characterization of a sterilizing agent and the development, validation, and routine control of a sterilization process for medical devices
In addition, we recommend you contact the FDA staff responsible for reviewing your specific type of device to discuss your sterilization procedures further, if needed. 13
12 Available at https://www.fda.gov/downloads/MedicalDevices/DeviceRegulationandGuidance/GuidanceDocuments/ucm070899 .pdf
13 Please refer to FDA’s guidance, “Requests for Feedback on Medical Device Submissions: The Pre-Submission Program and Meetings with Food and Drug Administration Staff,” available at
Contains Nonbinding Recommendations
When a viral pathogen in an animal tissue is part of the risk to the public health for a medical device, we recommend that you consider the extent to which processing and sterilization can inactivate or remove the virus(es). FDA recommendations for validating viral inactivation methods are described below.
Virus Validation Studies
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You should assess the processing methods and sterilization techniques used in product manufacture for their ability to inactivate and remove viruses. Viral inactivation data are usually determined by comparing an estimate of the amount of virus in the unprocessed source material with the magnitude of virus inactivation /clearance provided by manufacturing and sterilization processes. As suggested in ISO 22442 Part 3 (Section 5), a review of the published literature should be performed to estimate the amount of virus in the unprocessed source material and to optimize the design of the viral inactivation/elimination study (e.g., selection of model viruses and processing steps to be evaluated). Such studies are generally performed using a scaled down version of specific production and sterilization steps (e.g., acid extraction of collagen or dry heat sterilization) with appropriate model viruses. The model viruses used in these studies should be selected to reflect the actual viral contaminants that may be present in the source animal tissue (e.g., DNA-based and RNA-based, enveloped and non-enveloped viruses).
The results of your viral inactivation studies should demonstrate that the sum of the log10 reduction in virus from selected processing steps and sterilization process(es) (i.e., the overall virus reduction factor) is sufficient to produce a safe product.14 For example, a device in which virus has been reduced by at least six logs greater than the virus concentration estimated in the unprocessed source material has historically been considered a safe device. A final report describing these studies should be submitted in your premarket submission. This report should discuss: 1) the animal species and tissue source material in the device as well as the amount of virus(es) that might be present in the source material (as identified by in-house research or published literature); 2) the appropriateness of the model viruses selected; 3) the relevance of the conditions used in the virus inactivation studies to the commercial manufacturing methods; and 4) why these studies demonstrate that the final product will be safe.
ISO 22442-3 and the referenced ICH document15 provide additional insight into the general design and interpretation of viral clearance studies. ISO 22442-3 also recommends, whenever possible, to determine kinetics of viral inactivation to determine the theoretical time necessary to inactivate the total virus population. While such information can be valuable in specific
https://www.fda.gov/MedicalDevices/DeviceRegulationandGuidance/GuidanceDocuments/UCM311176 , for more information regarding requesting FDA feedback through the Pre-Submission process.
14 ISO 22442-1, Medical devices utilizing animal tissues and their derivatives – Part 1: Application of risk management
15 Viral Safety Evaluation of Biotechnology Products Derived From Cell Lines of Human or Animal Origin Q5a(R1), available at http://www.ich.org/fileadmin/Public_Web_Site/ICH_Products/Guidelines/Quality/Q5A_R1/Step4/Q5A_R1__Gui deline.pdf
Contains Nonbinding Recommendations
circumstances, FDA has found that measurement of the extent of viral inactivation at a single time point, rather than the multiple time points required for a kinetic study, may provide adequate evidence of viral clearance provided that: 1) the model system conditions evaluating viral inactivation closely resemble the conditions of device manufacture; 2) the model viruses tested accurately reflect the sensitivity of viral contaminates within the tissue to the inactivation methods tested; and 3) the extent of viral clearance observed in the study is significantly greater than the concentration of any pathogen present in the source tissue.
While data demonstrating the viral inactivation properties associated with manufacturing and sterilization processes are often determined in laboratory studies with the intended product, published literature demonstrating the viral inactivation parameters of device manufacture/sterilization processes may be submitted in lieu of such testing when appropriate. FDA recommends that literature information be submitted when: 1) the publication contains sufficient information to evaluate the study results (e.g., test conditions, sample composition, and the control studies performed to validate the test conditions); 2) information is provided which explains why the published test samples accurately reflect your product; and 3) information is provided which explains why the published viral inactivation procedures accurately reflect your manufacturing/sterilization methods (e.g., reaction temperature, solution pH and ionic strength, and time of product exposure to the inactivation step as well as the concentration of proteins and other impurities in your product and the cited publication). Finally, please note that viral inactivation studies are not generally recognized to reflect the extent of prion contamination clearance or inactivation.
D. Transmissible Spongiform Encephalopathy-Specific Issues
BSE is a degenerative disease that affects the central nervous system of cattle and is similar to other transmissible spongiform encephalopathies (TSEs) found in sheep (scrapie), deer (chronic wasting disease),
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16 and humans (Creutzfeldt-Jakob Disease or CJD and similar less common diseases). Current data suggest that the incubation period of two to eight years after exposure is required before BSE symptoms are detectable. Currently, there are no treatments for TSE diseases and no validated screening tests that detect infection in a live animal or human. Diagnosis is achieved by post-mortem microscopic examination of brain tissue, as well as assays using ELISA, Western Blot, or other techniques that detect abnormal forms of the prion protein.
The BSE infectious agent is widely theorized to be a prion (i.e., an abnormally folded form of a normal protease-sensitive cellular prion protein [called PrPC or PrP(sen)]) that facilitates the
16 USDA’s Animal and Plant Health and Inspection Services website concerning CWD (Chronic Wasting Disease), available at https://www.aphis.usda.gov/aphis/ourfocus/animalhealth/sa_animal_disease_information/sa_alternate_livestock/sa _cervid_health/sa_cwd
Contains Nonbinding Recommendations
conversion of additional normal cellular proteins to an abnormal misfolded infection-associated protease-resistant prion structure (called PrP(res) or PrPTSE). PrP(res) has been detected in bovine brain, spinal cord, eye, ileum, lymph nodes, proximal colon, spleen, tonsil, dura mater, pineal gland, placenta, cerebrospinal fluid, pituitary, adrenal, distal colon, nasal mucosa, peripheral nerves, bone marrow, liver, lung, pancreas, and thymus.
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17 The detection of TSE infectivity in other tissues may occur in the future after data become available from more sensitive assays or larger animal studies. Transmission has been experimentally demonstrated in animal studies.18 The TSE agent is known to be extremely resistant to traditional forms of disinfection and sterilization. Please refer to FDA’s website regarding BSE, available at https://www.fda.gov/AnimalVeterinary/ComplianceEnforcement/BovineSpongiformEncephalo pathy/ucm2006517.htm , for the most current information.19
Given the long incubation times before disease onset, the absence of a validated screening test for live animals, and vCJD’s fatal outcome, we recommend that you collect and document the following information, in addition to the information listed in Sections A and B above, in your premarket submission for any material derived from ruminant animals (e.g., cattle, sheep, goats, cervids such as deer and elk) that have the potential to incubate a TSE infection:
· whether animals were sourced from a country with Negligible, Controlled or Unknown BSE risk (per OIE); 20,21
· information concerning the long-term health of the herd (e.g., documented breeding history, animal traceability, absence of TSE disease and the surveillance program to detect a TSE);
· the animal feed composition (e.g., animal feed history records, including recordation of commingling of feeds, and labeling of animal feed composition at distribution locations) (note that in 2008, FDA issued a final rule prohibiting certain material from being fed to ruminants, see 73 FR 22719);
· the animal stunning and slaughter methods that reduce the risk of cross contaminating non-TSE tissues with material from tissues that could contain TSE; and
· the specifics of the ante mortem and/or postmortem inspections (e.g., gross visual inspection, specific organs and anomalies exams, lab tests such as PrPTSE testing).
In addition, the manufacturing facility should document 1) procedures for maintaining records
17 WHO Tables on Tissue Infectivity Distribution in Transmissible Spongiform Encephalopathies (updated 2010), available at http://www.who.int/bloodproducts/tablestissueinfectivity.pdf
18 Hamir, et.al., “Experimental interspecies transmission studies of the transmissible spongiform encephalopathies to cattle comparison to bovine spongiform encephalopathy in cattle.” Journal of Veterinary Diagnostic Investigation, May 2011, 23(3):407-420
19 Additional resources include World Organization for Animal Health (OIE) “BSE Situation in the world and annual incidence rate,” available at http://www.oie.int/en/animal-health-in-the-world/bse-situation-in-the-worldand-annual-incidence-rate/ , and “Variant CJD Cases Worldwide,” available at http://www.cjd.ed.ac.uk/sites/default/files/worldfigs.pdf .
20 “OIE List of Bovine Spongiform Encephalopathy Risk Status of Member Countries,” available at http://www.oie.int/animal-health-in-the-world/official-disease-status/bse/list-of-bse-risk-status/ 21 78 FR 72979
Contains Nonbinding Recommendations
on the above cited items
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22 and 2) all information outlined above on each lot of product manufactured (Device History Record).
23 If necessary to ensure the safety of the medical device, this information may be reviewed during inspection.
Furthermore, it is important to keep in mind that the residence time of TSE-infectious material on surfaces is unknown and methods to completely assure removal of TSE-infectious material from surfaces have yet to be fully defined. Cleaning processes developed to remove surface contamination in abattoirs after exposure to potentially TSE-infected animals (e.g., cattle, sheep, cervids such as deer or elk) may not have been fully characterized or validated for more critical sites or equipment used to manufacture devices. Therefore, for facilities involved in device manufacture using tissue from potentially TSE-infected animals, your documentation should also identify when/whether any potentially TSE-infected material may have been previously processed in the facility and what steps were taken to address any potential contamination. This information could include the information previously discussed under “Manufacturing Controls for Animal Tissue Components” in section IV.B. of this guidance and the dates of previous tissue processing (see also 21 CFR 820.50).
Because screening assays cannot ensure TSE-free tissues from cows or other ruminant animals, the methods discussed above (e.g., monitoring animal feed, controlling animal husbandry, and tissue handling) reflect the best available approaches for preparing safe medical devices from animal tissue. However, when a TSE-screening assay is validated to accurately identify TSE-contaminated tissues, FDA will consider revising this guidance as appropriate and recommending that such a test be introduced into the standard operating procedures for tissue collection and processing.
Greetings again FDA CDRH-Guidance et al,
i kindly wish to address this issue once again, and express how concerning, that after all these decades, with the risk factors so high, that we are still discussing this issue as ''Nonbinding Recommendations''. simply is mind boggling imo...
i wish to kindly submit the following for ;
Medical Devices Containing Materials Derived from Animal Sources (Except for In Vitro Diagnostic Devices) Guidance for Industry and Food and Drug Administration Staff Document issued on March 15, 2019
and the risk factors from TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE, ALL OF THEM!
my submission will have old history and new peer review science and transmission studies. as follows;
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001 Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001
Date: Tue, 9 Jan 2001 16:49:00 -0800
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
######### Bovine Spongiform Encephalopathy #########
Greetings List Members,
I was lucky enough to sit in on this BSE conference call today and even managed to ask a question. that is when the trouble started.
I submitted a version of my notes to Sandra Blakeslee of the New York Times, whom seemed very upset, and rightly so.
"They tell me it is a closed meeting and they will release whatever information they deem fit. Rather infuriating."
and i would have been doing just fine, until i asked my question. i was surprised my time to ask a question so quick.
(understand, these are taken from my notes for now. the spelling of names and such could be off.)
[host Richard Barns] and now a question from Terry S. Singeltary of CJD Watch.
[TSS] yes, thank you, U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?
[no answer, you could hear in the back ground, mumbling and 'we can't. have him ask the question again.]
[host Richard] could you repeat the question?
[TSS] U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?
[not sure whom ask this] what group are you with?
[TSS] CJD Watch, my Mom died from hvCJD and we are tracking CJD world-wide.
[not sure who is speaking] could you please disconnect Mr. Singeltary
[TSS] you are not going to answer my question?
[not sure whom speaking] NO
from this point, i was still connected, got to listen and tape the whole conference. at one point someone came on, a woman, and ask again;
[unknown woman] what group are you with?
[TSS] CJD Watch and my Mom died from hvCJD we are trying to tract down CJD and other human TSE's world wide. i was invited to sit in on this from someone inside the USDA/APHIS and that is why i am here. do you intend on banning me from this conference now?
at this point the conference was turned back up, and i got to finish listening. They never answered or even addressed my one question, or even addressed the issue. BUT, i will try and give you a run-down for now, of the conference.
IF i were another Country, I would take heed to my notes, BUT PLEASE do not depend on them. ask for transcript from;
RBARNS@ORA.FDA.GOV 301-827-6906
he would be glad to give you one ;-)
Rockville Maryland, Richard Barns Host
BSE issues in the U.S., How they were labelling ruminant feed? Revising issues.
The conference opened up with the explaining of the U.K. BSE epidemic winding down with about 30 cases a week.
although new cases in other countries were now appearing.
Look at Germany whom said NO BSE and now have BSE.
BSE increasing across Europe.
Because of Temporary Ban on certain rendered product, heightened interest in U.S.
A recent statement in Washington Post, said the New Administration (old GW) has a list of issues. BSE is one of the issues.
BSE Risk is still low, minimal in U.S. with a greater interest in MBM not to enter U.S.
HOWEVER, if BSE were to enter the U.S. it would be economically disastrous to the render, feed, cattle, industries, and for human health.
(human health-they just threw that in cause i was listening. I will now jot down some figures in which they told you, 'no need to write them down'. just hope i have them correct. hmmm, maybe i hope i don't ???)
80% inspection of rendering
*Problem-Complete coverage of rendering HAS NOT occurred.
sizeable number of 1st time FAILED INITIAL INSPECTION, have not been reinspected (70% to 80%).
Compliance critical, Compliance poor in U.K. and other European Firms.
Gloria Dunason Major Assignment 1998 goal TOTAL compliance. This _did not_ occur. Mixed level of compliance, depending on firm.
Rendering FDA license and NON FDA license
system in place for home rendering & feed 76% in compliance 79% cross contamination 21% DID NOT have system 92% record keeping less than 60% total compliance
279 inspectors 185 handling prohibited materials
Renderer at top of pyramid, significant part of compliance. 84% compliance
failed to have caution statement render 72% compliance & cross contamination caution statement on feed, 'DO NOT FEED TO CATTLE'
56 FIRMS NEVER INSPECTED
1240 FDA license feed mills 846 inspected
"close to 400 feed mills have not been inspected"
80% compliance for feed.
10% don't have system.
NON-FDA licensed mills There is NO inventory on non licensed mills. approximately 6000 to 8000 Firms ??? 4,344 ever inspected. "FDA does not have a lot of experience with"
40% do NOT have caution statement 'DO NOT FEED'.
74% Commingling compliance
"This industry needs a lot of work and only half gotten to"
"700 Firms that were falitive, and need to be re-inspected, in addition to the 8,000 Firms."
Quote to do BSE inspection in 19 states by end of January or 30 days, and other states 60 days. to change feed status??? Contract check and ask questions and pass info.
At this time, we will take questions.
[I was about the third or fourth to ask question. then all B.S.eee broke loose, and i lost my train of thought for a few minutes. picked back up here]
someone asking about nutritional supplements and sourcing, did not get name. something about inspectors not knowing of BSE risk??? the conference person assuring that Steve Follum? and the TSE advisory Committee were handling that.
Some other Dr. Vet, whom were asking questions that did not know what to do???
[Dennis Wilson] California Food Agr. Imports, are they looking at imports?
[Conference person] they are looking at imports, FDA issued imports Bulletin.
[Linda Singeltary ??? this was a another phone in question, not related i don't think] Why do we have non-licensed facilities?
(conference person) other feed mills do not handle as potent drugs???
Dennis Blank, Ken Jackson licensed 400 non FDA 4400 inspected of a total of 6000 to 8000,
(they really don't know how many non licensed Firms in U.S. they guess 6000 to 8000??? TSS)
Linda Detwiler asking everyone (me) not to use emergency BSE number, unless last resort. (i thought of calling them today, and reporting the whole damn U.S. cattle herd ;-) 'not'
Warren-Maryland Dept. Agr. Prudent to re-inspect after 3 years. concerned of Firms that have changed owners.
THE END
TSS
############ http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
FROM New York TIMES
Subject: Re: BSE 50 STATE CONFERENCE CALL thread from BSE List and FDA Posting of cut version...
Date: Thu, 11 Jan 2001 22:02:47 -0700
From: "Sandy Blakeslee"
To: "Terry S. Singeltary Sr." References: 1
Hi terry -- thanks for all your help. I know it made a difference with the FDA getting out that release.
----- Original Message -----
From: "Terry S. Singeltary Sr."
To: Sent: Thursday, January 11, 2001 2:06 PM
Subject: BSE 50 STATE CONFERENCE CALL thread from BSE List and FDA Posting of cut version...
hi sandy,
From the New York Times NYTimes.com, January 11, 2001
Many Makers of Feed Fail to Heed Rules on Mad Cow Disease By SANDRA BLAKESLEE
Large numbers of companies involved in manufacturing animal feed are not complying with regulations meant to prevent the emergence and spread of mad cow disease in the United States, the Food and Drug Administration said yesterday.
The widespread failure of companies to follow the regulations, adopted in August 1997, does not mean that the American food supply is unsafe, Dr. Stephen Sundlof, director of the Center for Veterinary Medicine at the F.D.A., said in an interview.
But much more needs to be done to ensure that mad cow disease does not arise in this country, Dr. Sundlof said.
The regulations state that feed manufacturers and companies that render slaughtered animals into useful products generally may not feed mammals to cud-chewing animals, or ruminants, which can carry mad cow disease.
All products that contain rendered cattle or sheep must have a label that says, "Do not feed to ruminants," Dr. Sundlof said. Manufacturers must also have a system to prevent ruminant products from being commingled with other rendered material like that from chicken, fish or pork. Finally, all companies must keep records of where their products originated and where they were sold.
Under the regulations, F.D.A. district offices and state veterinary offices were required to inspect all rendering plants and feed mills to make sure companies complied. But results issued yesterday demonstrate that more than three years later, different segments of the feed industry show varying levels of compliance.
Among 180 large companies that render cattle and another ruminant, sheep, nearly a quarter were not properly labeling their products and did not have a system to prevent commingling, the F.D.A. said. And among 347 F.D.A.-licensed feed mills that handle ruminant materials - these tend to be large operators that mix drugs into their products - 20 percent were not using labels with the required caution statement, and 25 percent did not have a system to prevent commingling.
Then there are some 6,000 to 8,000 feed mills so small they do not require F.D.A. licenses. They are nonetheless subject to the regulations, and of 1,593 small feed producers that handle ruminant material and have been inspected, 40 percent were not using approved labels and 25 percent had no system in place to prevent commingling.
On the other hand, fewer than 10 percent of companies, big and small, were failing to comply with the record-keeping regulations.
The American Feed Industry Association in Arlington, Va., did not return phone calls seeking comment.
http://www.nytimes.com/2001/01/11/science/11COW.html
Subject: USDA/APHIS response to BSE-L--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001
Date: Wed, 10 Jan 2001 14:04:21 -0500
From: "Gomez, Thomas M."
Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@uni-karlsruhe.de
######### Bovine Spongiform Encephalopathy #########
USDA/APHIS would like to provide clarification on the following point from Mr. Singeltary's 9 Jan posting regarding the 50 state conference call.
[Linda Detwiler asking everyone (me) not to use emergency BSE number, unless last resort. (i thought of calling them today, and reporting the whole damn U.S. cattle herd ;-) 'not']
Dr. Detwiler was responding to an announcement made during the call to use the FDA emergency number if anyone wanted to report a cow with signs suspect for BSE. Mr. Singeltary is correct that Dr. Detwiler asked participants to use the FDA emergency number as a last resort to report cattle suspect for BSE. What Mr. Singeltary failed to do was provide the List with Dr. Detwiler's entire statement. Surveillance for BSE in the United States is a cooperative effort between states, producers, private veterinarians, veterinary hospitals and the USDA. The system has been in place for over 10 years. Each state has a system in place wherein cases are reported to either the State Veterinarian, the federal Veterinarian in Charge or through the veterinary diagnostic laboratory system. The states also have provisions with emergency numbers. Dr. Detwiler asked participants to use the systems currently in place to avoid the possibility of a BSE-suspect report falling through the cracks. Use of the FDA emergency number has not been established as a means to report diseased cattle of any nature.
############ http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############
Subject: Re: USDA/APHIS response to BSE-L--U.S. 50 STATE CONFERENCE CALL Jan.9, 2001
Date: Wed, 10 Jan 2001 13:44:49 -0800
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de References: 1
######### Bovine Spongiform Encephalopathy #########
Hello Mr. Thomas,
> What Mr. Singeltary failed to do was provide the List with Dr. Detwiler's entire statement.
would you and the USDA/APHIS be so kind as to supply this list with a full text version of the conference call and or post on your web-site? if so when, and thank you. if not, why not?
The system has been in place for over 10 years.
that seems to be a very long time for a system to be in place, and only test 10,700 cattle from some 1.5 BILLION head (including calf crop). Especially since French are testing some 20,000 weekly and the E.U. as a whole, are testing many many more than the U.S., with less cattle, same risk of BSE/TSEs.
Why does the U.S. insist on not doing massive testing with the tests which the E.U. are using? Why is this, please explain?
Please tell me why my question was not answered?
U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds?
It was a very simple question, a very important question, one that pertained to the topic of BSE/feed, and asked in a very diplomatic way. why was it not answered?
If all these years, we have been hearing that pharmaceutical grade bovines were raised for pharmaceuticals vaccines etc. But yet the USA cannot comply with feed regulations of the ruminant feed ban, PLUS cannot even comply with the proper labelling of the feed, cross contamination etc. Then how in the world can you Guarantee the feed fed to pharmaceutical grade bovine, were actually non ruminant feed?
Before i was ask to be 'disconnected', i did hear someone in the background say 'we can't'-- have him ask the question again.
could you please be so kind, as to answer these questions?
thank you, Terry S. Singeltary Sr. Bacliff, Texas USA
P.S. if you will also notice, i did not post that emergency phone number and do not intend on passing it on to anyone. I was joking when i said i should call and report the whole damn U.S. Herd. So please pass that on to Dr. Detwiler, so she can rest easily.
BUT, they should be reported, some are infected with TSE. The U.S. is just acting as stupid as Germany and other Countries that insist they are free of BSE.
TSS
Subject: Report on the assessment of the Georgraphical BSE-risk of the USA July 2000 (not good)
Date: Wed, 17 Jan 2001 21:23:51 -0800
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy To: BSE-L@uni-karlsruhe.de
######### Bovine Spongiform Encephalopathy #########
Greetings List Members and ALL EU Countries,
Because of this report, and the recent findings of the 50-state BSE Conference call, I respectfully seriously suggest that these Countries and the SSC re-evaluate the U.S.A. G.B.R. to a risk factor of #3.
I attempted to post this to list in full text, but would not accept...
thank you, kind regards, Terry S. Singeltary Sr., Bacliff, Texas USA
Report on the assessment of the Geographical BSE-risk of the USA July 2000
PART II
REPORT ON THE ASSESSMENT OF THE GEOGRAPHICAL BSE RISK OF THE UNITED STATES OF AMERICA
- 29 -
Report on the assessment of the Geographical BSE-risk of the USA July 2000
EXECUTIVE SUMMARY
snip...see full text;
U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001
Subject: BSE--U.S. 50 STATE CONFERENCE CALL Jan. 9, 2001
Date: Tue, 9 Jan 2001 16:49:00 -0800
From: "Terry S. Singeltary Sr."
Reply-To: Bovine Spongiform Encephalopathy
To: BSE-L@uni-karlsruhe.de
######### Bovine Spongiform Encephalopathy #########
40,000 human heart valves a year from BSE herds
Sun, 3 Sep 2000. Unpublished Inquiry documents obtained by CJD activist Terry S. Singeltary Sr. of Bacliff, Texas
Opinion (webmaster): Below are some shocking documents. Here is a British company preparing 40,000 heart valves a year from bovine pericardium, primarily for export, and they are not required to source this material from BSE-free herds even in peak epidemic years. It is amazing to watch health "authorities" grovelling on their bellies to wring petty concessions from middle management at obscure little companies. The main worry is not the practise of using 800 potentially infected cows a week for human heart transplant material but that the press or recipients will get wind of it, hurting business.
BSE wasn't the problem, it was awkward queries from importing countries like the US. The cows are stunned using brain penetration -- can't do anything about the chunks of bovine brain blasted into the circulatory system, it's the norm. Can't use younger lower-risk animals either, patch would not be big enough. It is fascinating to see the British government worrying about, but doing nothing, with pigs with BSE 10 years ago.
While scrapie was long used as an excuse for continuing with human use of BSE-tainted material, little sheep material was used medically. Bovine transplants, vaccines, insulin doeses, etc. are far more dangerous than dietary material as injections, and are done on a very wide scale. So scrapie was never a valid analogy to BSE, as MAFF knew full well.
The British government deferred to the manufacturer's rep for an opinion on how contaminated pericardium might be, just as this appeared showing that this tissue is extremely dangerous:
CJD in a patient who received homograft [was it really?] tissue for tympanic membrane closure.
Eur Arch Otorhinolaryngol 1990;247(4):199-201
Tange RA, Troost D, Limburg M
We report the case history of a 54-year-old man who developed a fatal neurological disorder 4 years after a successful tympanoplasty with homograft pericardium...
COMMERCIAL IN CONFIDENCE
Miss M Duncan From: Dr E Hoxey
Date: 29 January 1990
cc: Mr R Burton
Dr N Richardson
Ms K Turner
Ms J Dhell
Mr N Weatherhead
BOVINE SPONGIFORM ENCEPHALOPATHY
1. In your absence on sick leave, I chaired the STD BSE group meeting
on 26th January 1990.
2. The minutes of the meeting will be circulated shortly but I was asked
to bring to your attention the concerns of the group regarding the BMS
heart valve.
3. This concern arose from a number of points on the agenda:-
i) the______________decision to source all raw material for sutures
from Australasia from January 1990.
ii) the major cleandown and decontamination proposed for the
factory and the possibility of press interest that this may generate.
iii) the indication in the Tyrell Report on Research that the
infective agent may be induced to cross the species barrier by
intracerebral, intraperitoneal or intravenous injection.
4. As you are aware, the____________situation has been a model which we
have observed closely.
5. Reviewing the BMS situatien, we considered the incidence of BSE in
the herds used for materials, the processing received by the material
and the age of the cattle used. Given the number of uncertainties and
lack of definitive information on BSE, the_______________model was
still considered as a good one. The group were uncomfortable with the
position of BMS as the only company using UK sourced material.
6. The group considered that it may be worthwhile arranging a further
meeting with___________to confidentially make them aware that they
would now be the only company using UK sourced bovine material for
products of this type.
7. Clearly, __________and__________ are now in an exposed position in
this area and all the implications need te be considered. Could we have
your news on this proposal please?
Dr E V Hoxey
PD STD PG1A
716 RSQ
Ext 3356
90/01.29/19.1
==============
B.S.E. GUIDELINES ON BOVINE IMPLANTS & BLOOD CONTACT DEVICES -
MEETING WITH MANUFACTURERS
DATE: 8 DECEMBER 1989
DH REPRESENTATIVES Nigel Richardson
Will Burton
Eammon Hoxey
Jeremy Tinkler
Helen Campbell
Carol Bleakley
Bill Waine
The main purpose of the meeeting is to discuss the companies current
manufacturing procedures, future plans and their compliance with the
BSE guidelines. Their views were also sought as to the practical
feasibility of the guidelines with respect to the manufacturing
process, and any improvements that could be suggested.
The meetings were held separately with each company. Neither had
received any queries concerning BSE from countries to which their
products are exported.
CURRENT POSITION
1.__________ have brought in a microbiologist as a technical scientific
adviser, initially to inform them of the current understanding of
BSE. He is still available to them and keeps them up to date with new
developments.
2. At present they produce bovine pericardial heart valves, & (a sister
company) produces heparin coated products (from a porcine source). In
the future it is possible that they will introduce a bovine patch
produced from bovine pericardium from the same source. They will keep
the Department informed of any progress in this area.
SOURCE MATERIAL
3. The source material for the manufacture of heart valves is bovine
pericardial sacs. The cows used are 18-24 months old when slaughtered,
the majority around 18 months. BMS have no knowledge of the actual
age.
4. The cows are killed using brain penetration. Dr Bleakley made the
point that as far as she was aware this was the only method used in
this country. Meat inspectors are paid to obtain the bovine
pericardium. They are paid a set rate but bonuses are given for
increased yields. Mr Burton expressed concern as to the conflict of
interests that may arise as a result of this. Dr Bleakley did not
believe that this was the case because of the relationship BMS had
developed with the inspectors.
89/12.12/8.1
============
COMMENTS ON THE GUIDELINES
14. Dr. Bleakley believed that the pericardium would not allow the
replication of the causative agent, and does not present a risk.
15. She suggested that the guidelines were impossible to implement
from the point of view of the manufacturing process for the following
reasons:-
-It is not possible to use closed herds simply because of the numbers
of cattle involved. This is up to 800 each week.
-Calves under 6 months old cannot be used as the pericardium is too
thin to be incorporated into a valve.
-For cows this in the age group used brain penetration is the only
method of slaughtering used in this country.
PROPOSALS PUT FORWARD BY DR BLEAKLEY
16. The goverment should fund research in this area. For example,
investigating the presence or absence of the infectious agent in
other parts of the body, such as the pericardium. Also to look at how
the slaughtering process affects the spread of the disease.
17. Ideally the answer would be to take random tissue samples in
order to detect contaminated material. This is not currently feasible
with the length of time required to conduct titre testing.
COMMENTS ON THE REVIEW ON METHODS OF STERILIZATION FOR BSE
18. Everything present reflected the published material, but the
validity of some of this is questionable. It was pointed out that:-
-it was stated that different strains display different heat
sensitivity, but this does not appear to be chemically related
-the claim to be "effective' would depend on the type of material that
was being used and the time involved.
CURRENT POSITION
19.____________ manufacture porcine valves and bovine pericardial
patches. The possibility of producing porcine conduits is currently
being investigated. This has not yet progressed.
20. The material is obtained from 2 abattoires in this country:-
-Dorchester, where veal calves under 18 weeks are slaughtered for
sourcing pericardium for ________________. These are used to produce
small patches of less than 90mm diameter, this may be divided into 4
quadrants. This represents 80-90% of sales.
-Fairham where cows between 5 and 10 years old are slaughtered to
produce larger patches and strips of 100mm by 45mm.
89/12.12/8.2
=============
32. As a result of the concern voiced of direct inoculation of BSE
via sectioning instruments it was stated that it would be feasible to
use new blades with each carcass.
COMMENTS ON THE GUIDELINES
33. Dr Waine was not convinced of the need for sterile sectioning
equipment and separate packaging from the abattoire. He felt that
this would merely have a cosmetic effect.
34. He suggested that the possibility of bovine-human cross-infection
was very remote.
35. He did not believe that it was possible for manufacturers to
follow the guidelines as they stand.
PROPOSALS
36. Dr Waine felt that the steps taken by the Government had been
realistic to control the outbreak.
REVIEW
37. Dr Waine did not believe that any sterilization treatment
proposed would retain the surgical usage of the pericardium.
VALVES
38. The response has been that this problem is restricted to the U.K.
Thier material is obtained from the same Italian source as the
patches. There is no age specification on the cows but the preference
is for the larger valves which would therefore come from the older
animals.
PORCINE VALVES
39. There was a small discussion as to whether these products do fall
under the issued guidelines. The assumption had been made by the
company that they are not included as pigs are not known to be
susceptible to infection by a Scrapie-like agent. This was confirmed
by Dr Hoxey.
40. The pigs are electrocuted and the heart and pericardium obtained
prior to inspection.
41. One abattoire supplies them with most of their porcine requirments.
H Campbell
PG2C
Room 312 RSQ
Ext. 3212
12 December 1989
89/12.12/8.3
============
TIP740203/3 0241
Bovine Spongiform Meeting Held On Friday 26th January 1990
Present Dr E Hoxey {chairman)
Mr W Burton
Dr N Richardson
Mrs J Dhell
Ms K Turner
MS H Cambell
Mr N Weatherhead (secretary)
copies: Miss Duncan
1.Apologies
Apologies were received from Miss Duncan
2.Minutes of the last meeting.
The previous minutes were accepted.
3.Matters arising not on the agenda.
As agreed at the previous meeting the paper on "Inactivation of
Scrapie-like Agents" was sent with a Covering letter drafted by
Dr Hoxey to all companies that use Bovine or Porcine materiais.
4.Report on the STD meeting with ___________________
The minutes of the meeting were discussed by the committee it was
noted that:-
a} _____________ now meet DH Guidelines as the devices produced from
the calf material comply as that they are obtained from animals less
than 6 months old.The company had written to confirm that they now
source older animals from overseas.
b) _____________ are unable to meet the DH Guidelines.
and will not be doing so in the foreseeable future. The panel showed
concern over the stance that BMS are taking. The committee felt that it
was important to arrange a further meeting to inform them that they
are now the only company using UK sourced material. [see minutes of the
meeting dated 8/12/89 attached). Dr Hoxey agreed to write separatey
to Miss Duncan on this issue.
action: Dr Hoxey
5. Report on the CSM/MCA BSE working party meeting 10/1/90
Mr Burton had produced a note of the above meeting as the minutes had
as yet not been distributed. The committee noted that:-
90/01.26/20.1
=============
TIP740203/3 0242
1) _______________ has exceeded all expectations tn complying
with DH Guidelines. They will be sourcing all raw material from
Australasia from January 1990.
2) _______________ are using an international expert _______________
to advise them on factory decontamination at the change over of source.
3) The use of Dr Taylor and the factory decontamination may qenerate
press interest.
4) The offal ban has not yet been expanded to include Scotland.
5) The CSM/MCA BSE working group agrees with the approach that STD
are taking to Tissue Harvesting and wished to be kept updated.
The note of the meeting is attached for reference.
6. STD Database updating
Mr Burton drafted a minute for signature by Mr Worroll.The object of
the minute was to enable STD to keep a check on companies that use
animal material in their products.
The control manual committee amended the minute and agreed that the
audit report procedure should include (if it does not already) a
statement to the effect that the company information section should
include details of raw materials used.
The CMC suggested a sentence to the effect "Team leaders visiting
Blue Guide companies should additionally take account of Mr Worroll's
minute of Jan 1990." The committee agreed with this sentence and passed
it back for inclusion in the Base-line Documents.
action N Weatherhead
7. Review of the 'Interim Report of the Consultative Committee on
Research into BSE" (Tyrell committee report.)
Mrs Dhell presented a summarized Version of the above document to the
committee. It was noted that only the research studies catorqorised
high/medium priority would all somehow receive funding. The committee
expressed a wish to find out:-
1) Areas which have not been prioritised which have relevance to
STDS area of interest.
2) Has any party taken up the study "Investigation into the fate of
bovine and ovine tissues and product that could lead to infection by
as yet unrecognised routes."
90/01.26/20.2
==============
TIP740203/3 0243
3. The protocol of work being carried out by the Clinical Research
Laboratory in Harrow add proposed by the Neuropathogenesis unit in
Edinburgh:
a) Have they any plans to include pericardium. If not could PD suggest
that they miqht include it.
b) What controls are they using.
c) Will it be possible to arrange a visit.
4) It was suggested that Dr Pickles be contacted as the DH
representitive on the Tyrell committee, to enquire if comments on
this document were being sought by the committee, as PD has a number
of points it wishes to raise.
8. Incorporation of Guidance into Chemical Methods for the sterilization
of animal tissue Used in medical Devices.
The draft paper on methods of validation in chemical sterilization was
shown to the BGRP for comments, these were later received. A copy was
also forwarded to MCA and despite numerous reminders no reply had as
yet been received.
The committee recommended that the paper on "Chemical Methods for the
Sterilization of Animal Tissue Used in Medical Devices" should be
amended include Tissue Harvesting. The BGRP will be informed of this
and a copy of tbe document will be presented to the next CMS/MCA BSE
working group which is to be held on 4th July l99O.
Mrs Dhell to arrange a meeting to draft this ammendment.
Mrs Turner
action:Hr Tinkler
Mrs Dhell
Dr Hoxey
9. Possibility of sending STD paper 'Inactivation of Scrapie-like
Agents" to Dr Taylor and Dr Kimberlin for their comments.
The committee felt that the paper should be sent to Dr Taylor and
Dr Klmberlin and that they should be invited to comment. If they
subsequently required payment for this work the committee felt that
the Department should finance it if necessary.
Mrs Dhell will draft a letter to accompany the report for Miss Duncan
to sign.
action: Mrs Dhell
90/01.26/20.3
==============
TIP740203/3 0244
10. - presentation on current situation
Miss Duncan's report was passed over until the next meeting.
1l. Oral discussion on relevant media interest and media reports.
The discussion mainly revolved around _____________ and the exposed
position PD would be in if the media became involved. The possible
press coverage expected in relation to events at ___________ could also
raise the profile of BSE in "medical" products.
Mr Burton to obtain copies of any defensive briefings drafted
by MCA in responce to the ______________ situation.
N Weatherhead
90/01.26/20.4
WEDNESDAY, OCTOBER 31, 2018
PIG HEART VALVES and Potential Iatrogenic Transmissible Spongiform Encephalopathy TSE Prion Disease in Humans, what if?
THURSDAY, JANUARY 23, 2014
Medical Devices Containing Materials Derived from Animal Sources (Except for In Vitro Diagnostic Devices) [Docket No. FDA–2013–D–1574]
Terry S. Singeltary Sr. Submission [Docket No. FDA–2013–D–1574]
Medical Devices Containing Materials Derived from Animal Sources (Except for In Vitro Diagnostic Devices)
Draft Guidance for Industry and Food and Drug Administration Staff DRAFT GUIDANCE This guidance document is being distributed for comment purposes only. Document issued on January 23, 2014.
Friday, December 04, 2009
*** New guidance on decontamination of trial contact lenses and other contact devices has been revealed for CJD AND vCJD
Thursday, January 29, 2009
***Medical Procedures and Risk for Sporadic Creutzfeldt-Jakob Disease, Japan, 1999–2008 (WARNING TO Neurosurgeons and Ophthalmologists)
Wednesday, August 20, 2008 ***Tonometer disinfection practice in the United Kingdom: A national survey
FDA Singeltary submission 2001
Greetings again Dr. Freas and Committee Members,
I wish to submit the following information to the Scientific Advisors and Consultants Staff 2001 Advisory Committee (short version). I understand the reason of having to shorten my submission, but only hope that you add it to a copy of the long version, for members to take and read at their pleasure, (if cost is problem, bill me, address below). So when they realize some time in the near future of the 'real' risks i speak of from human/animal TSEs and blood/surgical products. I cannot explain the 'real' risk of this in 5 or 10 minutes at some meeting, or on 2 or 3 pages, but will attempt here:
snip...see full text ;
Subject: Prion Scientific Advisors and Consultants Staff Meeting Singeltary Submission Freas Monday, January 08,2001 3:03 PM
PLEASE be aware, my submission here has now been removed from the www, or changed to a different url that no one knows now, and does not come up in search engines anymore, after 17 years...wonder why that could be, i guess the truth just hurt to much$$$
Freas, William
From: Terry S. Singeltary Sr. [flounder@wt.net]
Sent: Monday, January 08,2001 3:03 PM
Subject: CJD/BSE (aka madcow) Human/Animal TSE’s--U.S.--Submission To Scientific Advisors and Consultants Staff January 2001 Meeting (short version)
CJD/BSE (aka madcow) Human/Animal TSE’s--U.S.--Submission To Scientific Advisors and Consultants Staff January 2001 Meeting (short version)
Greetings again Dr. Freas and Committee Members,
I wish to submit the following information to the Scientific Advisors and Consultants Staff 2001 Advisory Committee (short version).
I understand the reason of having to shorten my submission, but only hope that you add it to a copy of the long version, for members to take and read at their pleasure, (if cost is problem, bill me, address below). So when they realize some time in the near future of the 'real' risks i speak of from human/animal TSEs and blood/surgical products. I cannot explain the 'real' risk of this in 5 or 10 minutes at some meeting, or on 2 or 3 pages, but will attempt here:
remember AIDS/HIV, 'no problem to heterosexuals in the U.S.? no need to go into that, you know of this blunder:
DO NOT make these same stupid mistakes again with human/animal TSE's aka MADCOW DISEASE. I lost my Mom to hvCJD, and my neighbor lost his Mother to sCJD as well (both cases confirmed). I have seen many deaths, from many diseases. I have never seen anything as CJD, I still see my Mom laying helpless, jerking tremendously, and screaming "God, what's wrong with me, why can't I stop this". I still see this, and will never forget. Approximately 10 weeks from 1st of symptoms to death. This is what drives me. I have learned more in 3 years about not only human/animal TSE's but the cattle/rendering/feeding industry/government than i ever wished to.
I think you are all aware of CJD vs vCJD, but i don't think you all know the facts of human/animal TSE's as a whole, they are all very very similar, and are all tied to the same thing, GREED and MAN.
I am beginning to think that the endless attempt to track down and ban, potential victims from known BSE Countries from giving blood will be futile. You would have to ban everyone on the Globe eventually? AS well, I think we MUST ACT SWIFTLY to find blood test for TSE's, whether it be blood test, urine test, .eyelid test, anything at whatever cost, we need a test FAST.
DO NOT let the incubation time period of these TSEs fool you.
To think of Scrapie as the prime agent to compare CJD, but yet overlook the Louping-ill vaccine event in 1930's of which 1000's of sheep where infected by scrapie from a vaccine made of scrapie infected sheep brains, would be foolish. I acquired this full text version of the event which was recorded in the Annual Congress of 1946 National Vet. Med. Ass. of Great Britain and Ireland. from the BVA and the URL is posted in my (long version).
U.S.A. should make all human/animal TSE's notifiable at all ages, with requirements for a thorough surveillance and post-mortem examinations free of charge, if you are serious about eradicating this horrible disease in man and animal.
There is histopathology reports describing o florid plaques" in CJD victims in the USA and some of these victims are getting younger. I have copies of such autopsies, there has to be more. PLUS, sub-clinical human TSE's will most definitely be a problem.
THEN think of vaccineCJD in children and the bovine tissues used in the manufacturing process, think of the FACT that this agent surviving 6OO*C. PNAS -- Brown et al. 97 (7): 3418 scrapie agent live at 600*C
Then think of the CONFIDENTIAL documents of what was known of human/animal TSE and vaccines in the mid to late 80s, it was all about depletion of stock, to hell with the kids, BUT yet they knew. To think of the recall and worry of TSE's from the polio vaccine, (one taken orally i think?), but yet neglect to act on the other potential TSE vaccines (inoculations, the most effective mode to transmit TSEs) of which thousands of doses were kept and used, to deplete stockpile, again would be foolish.
--Oral polio; up to 1988, foetal calf serum was used from UK and New Zealand (pooled); since 1988 foetal calf serum only from New Zealand. Large stocks are held.
--Rubella; bulk was made before 1979 from foetal calf serum from UK and New Zealand. None has been made as there are some 15 years stock.
--Diphtheria; UK bovine beef muscle and ox heart is used but since the end of 1988 this has been sourced from Eire. There are 1,250 litres of stock.
--Tetanus; this involves bovine material from the UK mainly Scottish. There are 21,000 litres of stock.
--Pertussis; uses bovine material from the UK. There are 63,000 litres of stock. --They consider that to switch to a non-UK source will take a minimum of 6-18 months and to switch to a non-bovine source will take a minimum of five years.
3. XXXXXXXXXXX have measles, mumps, MMR, rubella vaccines. These are sourced from the USA and the company believes that US material only is used.
89/2.14/2.1
============
BSE3/1 0251
4. XXXXXXXXXXX have a measles vaccine using bovine serum from the UK. there are 440,000 units of stock. They have also got MMR using bovine serum from the UK.
5. XXXXXXXXXXX have influenza, rubella, measles,' MMR vaccines likely to be used in children. Of those they think that only MMR contains bovine material which is probably a French origin.
6. XXXXXXXXXXX have diphtheria/tetanus and potasses on clinical trial. hese use veal material, some of which has come from the UK and has been ade by XXXXXXXXXXX (see above).
I have documents of imports from known BSE Countries, of ferments, whole blood, antiallergenic preparations,
2
human blood plasma, normal human blood sera, human immune blood sera, fetal bovine serum, and other blood fractions not elsewhere specified or included, imported glands, catgut, vaccines for both human/animal, as late as 1998. Let us not forget about PITUITARY EXTRACT. This was used to help COWS super ovulate. This tissue was considered to be of greatest risk of containing BSE and consequently transmitting the disease.
ANNEX 6
MEETING HELD ON 8 JUNE 1988 TO DISCUSS THE IMPLICATIONS OF BSE TO BIOLOGICAL PRODUCTS CONTAINING BOVINE - EXTRACTED MATERIAL
How much of this was used in the U.S.?
Please do not keep making the same mistakes; 'Absence of evidence is not evidence of absence'.
What are the U.S. rules for importing and manufacturing vaccines, medicines and medical devices?
Does the U.S.A. allow sourcing of raw material of ruminants from the U.S.A.?
U.S. cattle, what kind of guarantee can you give for serum or tissue donor herds? . The U.S. rendering system would easily amplify T.S.E.'s:
Have we increased the stability of the system (improved heat treatments) since the EU SSC report on the U.S.A. was published in july 2000?
What is done to avoid cross-contaminations in the U.S.A.?
How can the U.S. control absence of cross-contaminations of animal TSE's when pig and horse MBM and even deer and elk are allowed in ruminant feed, as well as bovine blood? I sadly think of the rendering and feeding policy before the Aug. 4, 1997 'partial' feed ban, where anything went, from the city police horse, to the circus elephant, i will not mention all the scrapie infected sheep. I am surprised that we have not included man 'aka soyent green'. It is a disgusting industry and nothing more than greed fuels it.
When will the U.S.. start real surveillance of the U.S. bovine population (not passive, this will not work)?
When will U.S. start removing SRMs?
Have they stopped the use of pneumatic stunners in the U.S.?
If so, will we stop it in all U.S. abattoirs or only in those abattoirs exporting to Europe?
If not, WHY NOT?
same questions for removal of SRM in the U.S.A., or just for export?
If not, WHY NOT?
How do we now sterilize surgical/dental instruments in the U.S.A.?
Where have we been sourcing surgical catgut?
(i have copies of imports to U.S., and it would floor you) hen will re-usable surgical instruments be banned?
'Unregulated "foods" such as 'nutritional supplements' containing various extracts from ruminants, whether imported or derived from
3
US cattle/sheep/cervids ("antler velvet" extracts!) should be forbidden or at least very seriously regulated. (neighbors Mom, whom also died from CJD, had been taking bovine based supplement, which contained brain, eye, and many other bovine/ovine tissues for years, 'IPLEX').
What is the use of banning blood or tissue donors from Germany, France, etc... when the U.S.A. continues exposing cattle, sheep and people to SRM, refuses to have a serious feed ban, refuses to do systematic BSE-surveillance?
The FDA should feel responsible for the safety of what people eat, prohibit the most dangerous foods, not only prohibit a few more donors - the FDA should be responsible for the safe sourcing of medical devices, not only rely on banning donors "from Europe", The 'real' risks are here in the U.S. as well, and nave been for some time.
We must not forget the studies that have proven infectivity in blood from TSE's.
The Lancet, November 9, 1985
Sir, --Professor Manuelidis and his colleagues (Oct 19, p896) report transmission to animals of Creutzfeldt-Jakob disease (CJD) from the buffy coat from two patients. We also transmitted the disease from, whole blood samples of a patient (and of mice) infected with CJD.l Brain, Cornea, and urine from this patient were also infectious, and the clinicopathological findings2 are summarised as follows.
snip...
Samples,were taken aseptically at necropsy. 10% crude homogenates of brain and cornea in saline, whole blood (after crushing a clot), and untreated CSF and urine were innoculated intracerebrally into CFl strain mice (20 ul per animal). Some mice showed emaciation, bradykinesia, rigidity of the body and tail, and sometimes tremor after long incubation periods. Tissues obtained after the animal died (or was killed) were studied histologically (table). Animals infected by various inocula showed common pathological changes, consisting of severe spongiform changes, glial proliferation, and a moderate loss of nerve cells. A few mice inoculated with brain tissue or urine had the same amyloid plaques found in patients and animals with CJD.3
snip...
Department of Neuropathology,. Neurological Institute, Faculty of Medicine, Kyushu University, Fukuoka812, Japan JUN TATEISHI
(full text-long version)
and
CWD and transmission to man will be no different than other TSE's.
"Clearly, it is premature to draw firm conclusions about CWD passing naturally into humans, cattle and sheep, but the present results suggest that CWD transmissions to humans would be as limited by PrP incompatibility as transmissions of BSE or sheep scrapie to humans. Although there is no evidence that sheep scrapie has affected humans, it is likely that BSE has
4
caused variant CJD in 74 people (definite and probable variant CJD cases to date according to the UK CJD Surveillance Unit). Given the presumably large number of people exposed to BSE infectivity, the susceptibility of humans may still be very low compared with cattle, which would be consistent with the relatively inefficient conversion of human PrP-sen by PrPBSE. Nonetheless, since humans have apparently been infected by BSE, it would seem prudent to take reasonable measures to limit exposure of humans (as well as sheep and cattle) to CWD infectivity as has been recommended for other animal TSEs,"
G.J. Raymond1, A. Bossers2, L.D. Raymond1, K.I. O'Rourke3, L.E. McHolland4, P.K. Bryant III4, M.W. Miller5, E.S. Williams6, M. Smits2 and B. Caughey1,7
or more recently transmission of BSE to sheep via whole blood Research letters Volume 356, Number 9234 16 September 2000
Transmission of BSE by blood transfusion in sheep
Lancet 2000; 356: 999 – 1000
F Houston, J D Foster, Angela Chong, N Hunter, C J Bostock
See Commentary
"We have shown that it is possible to transmit bovine spongiform encephalopathy (BSE) to a sheep by transfusion with whole blood taken from another sheep during the symptom-free phase of an experimental BSE infection. BSE and variant Creutzfeldt-Jakob disease (vCJD) in human beings are caused by the same infectious agent, and the sheep-BSE experimental model has a similar pathogenesis to that of human vCJD. Although UK blood transfusions are leucodepleted--a possible protective measure against any risk from blood transmission-- this report suggests that blood donated by symptom-free vCJD-infected human beings may represent a risk of spread of vCJD infection among the human population of the UK."
"The demonstration that the new variant of Creutzfeldt-Jakob disease (vCJD) is caused by the same agent that causes bovine spongiform encephalopathy (BSE) in cattle1 has raised concerns that blood from human beings in the symptom-free stages of vCJD could transmit infection to recipients of blood transfusions (full text long version)"
and...
"The large number of cases (1040), temporal clustering of the outbreaks (15 in the first 6 months of 1997), the high in-flock incidence, and the exceptional involvement of goats (390 cases), suggested an accidental infection. The source of the epidemic might have been TSE-contaminated meat and bonemeal, but eight flocks had never been fed any commercial feedstuff. Infection might have risen from the use of a formol-inactivated vaccine against contagious agalactia prepared by a single laboratory with brain and mammary gland homogenates of sheep infected with Mycoplasma agalactiae. Although clinical signs of TSE in the donor sheep have not been found, it is possible that one or more of them were harbouring the
5
infectious agent. Between 1995 and 1996, this vaccine was given subcutaneously to 15 of the affected flocks (to one flock in 1994) ; in these animals the disease appeared between 23 and 35 months after vaccination. No information is available for herd 13 because it was made up of stolen animals. Sheep from the remaining three flocks (1-3, figure) did not receive the vaccine, thus suggesting a naturally occurring disease.’’ (again, full text long version).
IN SHORT, please do under estimate this data and or human/animal TSE's including CWD in the U.S.A.
A few last words, please.
The cattle industry would love to have us turn our focus to CWD and forget about our own home grown TSE in Bovines. This would be easy to do. Marsh's work was from downer cattle feed, NOT downer deer/elk feed. This has been proven.
DO NOT MAKE THAT MISTAKE.
There should be NO LESS THAN 1,000,000 tests for BSE/TSE ' in 2001 for U.S.A. French are testing 20,000 a week. The tests are available. Why wait until we stumble across a case from passive surveillance, by then it is to late. IF we want the truth, this is a must???
United States Total ,Bovine Brain Submissions by State,
May 10 ,1990 thru October 31, 2000
Total 11,700
FROM 1.5 BILLION HEAD OF CATTLE since 1990 ???
with same feeding and rendering practices as that of U.K. for years and years, same scrapie infected sheep used in feed, for years and years, 950 scrapie infect FLOCKS in the U.S. and over 20 different strains of scrapie known to date. (hmmm, i am thinking why there is not a variant scrapie, that is totally different than all the rest)? just being sarcastic.
with only PARTIAL FEED BAN implemented on Aug. 4, 1997??? (you really need to reconsider that blood meal etc. 'TOTAL BAN')
AND PLEASE FOR GODS SAKE, STOP saying vCJD victims are the only ones tied to this environmental death sentence. "PROVE IT". It's just not true. The 'CHOSEN ONES' are not the only ones dying because of this man-made death sentence. When making regulations for human health from human/animal TSEs, you had better include ALL human TSE's, not just vCJD. Do NOT underestimate sporadic CJD with the 'prehistoric' testing available to date. This could be a deadly mistake. Remember, sCJD kills much faster from 1st onset of symptoms to death, and hvCJD is the fastest. Could it just be a higher titre of infectivity, or route or source, or all three?
Last, but not least. The illegal/legal harvesting of body parts and tissues will come back to haunt you. Maybe not morally, but due to NO background checks and human TSEs, again it will continue to spread.
Stupidity, Ignorance and Greed is what fuels this disease. You must stop all of this, and ACT AT ONCE...
Sent: Monday, January 08,2001 3:03 PM
FDA CJD BSE TSE Prion Scientific Advisors and Consultants Staff January 2001 Meeting Singeltary Submission
2001 FDA CJD TSE Prion Singeltary Submission
see search results for the original link;
another search here;
i wonder if the Government FDA et al, or whom ever removed my submission to fda from 2001 from the www after 17 years, where most every thing i said has come true, i wonder if the government wonders by removing my submission they will change the science and the truth?
reasons for Government FDA removal of Singeltary Submission materials to federal dockets;
see updated link;
-----Original Message-----
From: Terry S. Singeltary Sr. [mailto:flounder@wt.net]
Sent: Tuesday, February 18, 2003 12:45 PM
To: Freas, William Cc: Langford, Sheila
Subject: Re: re-vCJD/blood and meeting of Feb. 20, 2003
Greetings FDA, Variant Creutzfeldt-Jakob Disease Guidance Topic of Feb. 20 TSE Cmte. [Committee Meeting on February 20, 2003] FDA’s Transmissible Spongiform Encephalopathies Advisory Committee will meet Feb. 20 to hear updates on the implementation of the agency’s variant Creutzfeldt-Jakob Disease guidance and its effect on blood supply.
FULL SUBMISSION ;
Docket Management Docket: 02D-0073 - Guidance: Validation of Procedures for Processing of Human Tissues Intended for Transplantation Comment Number: EC -4 Accepted - Volume 1 2003-01-16 16:33:04
Docket: 02D-0073 - Guidance: Validation of Procedures for Processing of Human Tissues Intended for Transplantation
Greetings,
please be advised;
with the new findings from Collinge et al; that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype which is indistinguishable from type 2 PrPSc, the commonest sporadic CJD, i only ponder how many of the sporadic CJDs in the USA are tied to this alternate phenotype? these new findings are very serious, and should have a major impact on the way sporadic CJDs are now treated as opposed to the vCJD that was thought to be the only TSE tied to ingesting beef, in the medical/surgical arena. these new findings should have a major impact on the way sporadic CJD is ignored, and should now be moved to the forefront of research as with vCJD/nvCJD.
SNIP...FULL TEXT ;
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE)
Singeltary submission ;
FSIS, USDA, REPLY TO SINGELTARY
Animal and Plant Health Inspection Service (APHIS) Proposed Rule: Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived From Bovines
THURSDAY, FEBRUARY 25, 2016
U.S. Food & Drug Administration (FDA) FDA/CFSAN Cosmetics Update: Cosmetics Program; Import and Domestic and Transmissible Spongiform Encephalopathy TSE Prion Disease Risk Factors
***WARNING TO ALL CONSUMERS AND COUNTRIES AROUND THE WORLD***
***Note: FDA labs do not conduct BSE analysis and thus no sampling guidance is issued for BSE. ***
FDA MAY STRENGTHEN BSE FEED REGULATIONS
T U E S D A Y , A P R I L 1 9 , 2 0 1 6
Docket No. FDA-2013-N-0764 for Animal Feed Regulatory Program Standards
Singeltary Comment Submission Docket No. FDA-2013-N-07 64 for “Animal Feed Regulatory Program Standards.”
Singeltary Comment,
Greetings FDA et al,
I would kindly like to comment on ;
Docket No. FDA-2013-N-07 64 for “Animal Feed Regulatory Program Standards.”
I implore that we close the mad cow feed loopholes with cervid, and we must enforce existing feed regulations against the BSETSEPrion. we have failed terribly in this.
2019 UPDATE TSE PRION USA
USDA APHIS CDC FDA BSE CWD TSE PRION UPDATE 2019
THURSDAY, MARCH 14, 2019
USDA APHIS CDC FDA BSE TSE PRION UPDATE 2019
THURSDAY, MARCH 14, 2019
USDA APHIS CDC Cervids: Chronic Wasting Disease Specifics Updated 2019
FRIDAY, MARCH 15, 2019
Saskatchewan Chronic Wasting Disease TSE Prion 349 Cases Positive for 2018
SATURDAY, MARCH 16, 2019
Chronic Wasting Disease CWD TSE Prion United States of America Update March 16, 2019
FRIDAY, MARCH 15, 2019
USDA APHIS SCRAPIE TSE PRION Sheep and Goat Health Update 2019
Friday, December 14, 2012
DEFRA U.K. What is the risk of Chronic Wasting Disease CWD being introduced into Great Britain? A Qualitative Risk Assessment October 2012
snip.....
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.
snip.....
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.
snip.....
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).
snip.....
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.
snip.....
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.
snip.....
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.
snip.....
TUESDAY, APRIL 18, 2017
*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***
cwd scrapie pigs oral routes
***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <***
>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <***
***> Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%).
***> Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period.
This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.
Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
***> However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. <***
>*** Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health. <***
Scrapie Transmits To Pigs By Oral Route, what about the terribly flawed USA tse prion feed ban?
Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies Location: Virus and Prion Research
2017 Annual Report
1a. Objectives (from AD-416):
Objective 1: Investigate the mechanisms of protein misfolding in prion disease, including the genetic determinants of misfolding of the prion protein and the environmental influences on protein misfolding as it relates to prion diseases. Subobjective 1.A: Investigate the differences in the unfolded state of wild-type and disease associated prion proteins to better understand the mechanism of misfolding in genetic prion disease. Subobjective 1.B: Investigate the influence of metal ions on the misfolding of the prion protein in vitro to determine if environmental exposure to metal ions may alter disease progression. Objective 2: Investigate the pathobiology of prion strains in natural hosts, including the influence of prion source genotype on interspecies transmission and the pathobiology of atypical transmissible spongiform encephalopathies (TSEs). Subobjective 2.A: Investigate the pathobiology of atypical TSEs. Subobjective 2.B: Investigate the influence of prion source genotype on interspecies transmission. Objective 3: Investigate sampling methodologies for antemortem detection of prion disease, including the utility of blood sampling as a means to assess prion disease status of affected animals and the utility of environmental sampling for monitoring herd prion disease status. Subobjective 3.A: Investigate the utility of blood sampling as a means to assess prion disease status of affected animals. Subobjective 3.B: Investigate the utility of environmental sampling for monitoring herd prion disease status.
1b. Approach (from AD-416):
The studies will focus on three animal transmissible spongiform encephalopathy (TSE) agents found in the United States: bovine spongiform encephalopathy (BSE); scrapie of sheep and goats; and chronic wasting disease (CWD) of deer, elk, and moose. The research will address sites of protein folding and misfolding as it relates to prion disease, accumulation of misfolded protein in the host, routes of infection, and ante mortem diagnostics with an emphasis on controlled conditions and natural routes of infection. Techniques used will include spectroscopic monitoring of protein folding/misfolding, clinical exams, histopathology, immunohistochemistry, and biochemical analysis of proteins. The enhanced knowledge gained from this work will help understand the underlying mechanisms of prion disease and mitigate the potential for unrecognized epidemic expansions of these diseases in populations of animals that could either directly or indirectly affect food animals.
3. Progress Report:
All 8 project plan milestones for FY17 were fully met. Research efforts directed toward meeting objective 1 of our project plan center around the production of recombinant prion protein from either bacteria or mammalian tissue culture systems and collection of thermodynamic data on the folding of the recombinant prion protein produced. Both bacterial and mammalian expression systems have been established. Thermodynamic data addressing the denatured state of wild-type and a disease associated variant of bovine prion protein has been collected and a manuscript is in preparation. In research pertaining to objective 2, all studies have been initiated and animals are under observation for the development of clinical signs. The animal studies for this objective are long term and will continue until onset of clinical signs. In vitro studies planned in parallel to the animals studies have similarly been initiated and are ongoing. Objective 3 of the project plan focuses on the detection of disease associated prion protein in body fluids and feces collected from a time course study of chronic wasting disease inoculated animals. At this time samples are being collected as planned and methods for analysis are under development.
4. Accomplishments
1. Showed that swine are potential hosts for the scrapie agent. A naturally occurring prion disease has not been recognized in swine, but the agent of bovine spongiform encephalopathy does transmit to swine by experimental routes. Swine are thought to have a robust species barrier when exposed to the naturally occurring prion diseases of other species, but the susceptibility of swine to the agent of sheep scrapie has not been thoroughly tested. ARS researchers at Ames, Iowa conducted this experiment to test the susceptibility of swine to U.S. scrapie isolates by intracranial and oral inoculation. Necropsies were done on a subset of animals at approximately 6 months post inoculation (PI): the time the pigs were expected to reach market weight. Remaining pigs were maintained and monitored for clinical signs of transmissible spongiform encephalopathies (TSE) until study termination at 80 months PI or when removed due to intercurrent disease. Brain samples were examined by multiple diagnostic approaches, and for a subset of pigs in each inoculation group, bioassay in mice expressing porcine prion protein. At 6 months PI, no evidence of scrapie infection was noted by any diagnostic method. However, at 51 months of incubation or greater, 5 animals were positive by one or more diagnostic methods. Furthermore, positive bioassay results were obtained from all inoculated groups (oral and intracranial; market weight and end of study) suggesting that swine are potential hosts for the agent of scrapie. Although the current U.S. feed ban is based on keeping tissues from TSE infected cattle from contaminating animal feed, swine rations in the U.S. could contain animal derived components including materials from scrapie infected sheep and goats. These results indicating the susceptibility of pigs to sheep scrapie, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
2. Determined that pigs naturally exposed to chronic wasting disease (CWD) may act as a reservoir of CWD infectivity. Chronic wasting disease is a naturally occurring, fatal, neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of CWD disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Pigs were assigned to 1 of 3 groups: intracranially inoculated; orally inoculated; or non-inoculated. At market weight age, half of the pigs in each group were tested ('market weight' groups). The remaining pigs ('aged' groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by multiple diagnostic methods. Brain samples from selected pigs were bioassayed in mice expressing porcine prion protein. Some pigs from each inoculated group were positive by one or more tests. Bioassay was positive in 4 out of 5 pigs assayed. Although only small amounts of PrPSc were detected using sensitive methods, this study demonstrates that pigs can serve as hosts for CWD. Detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity. Currently, swine rations in the U.S. could contain animal derived components including materials from deer or elk. In addition, feral swine could be exposed to infected carcasses in areas where CWD is present in wildlife populations. The current feed ban in the U.S. is based exclusively on keeping tissues from TSE infected cattle from entering animal feeds. These results indicating the susceptibility of pigs to CWD, coupled with the limitations of the current feed ban, indicates that a revision of the feed ban may be necessary to protect swine production and potentially human health.
3. Developed a method for amplification and discrimination of the 3 forms of BSE in cattle. The prion protein (PrP) is a protein that is the causative agent of transmissible spongiform encephalopathies (TSEs). The disease process involves conversion of the normal cellular PrP to a pathogenic misfolded conformation. This conversion process can be recreated in the lab using a misfolding amplification process known as real-time quaking induced conversion (RT-QuIC). RT-QuIC allows the detection of minute amounts of the abnormal infectious form of the prion protein by inducing misfolding in a supplied substrate. Although RT-QuIC has been successfully used to detect pathogenic PrP with substrates from a variety of host species, prior to this work bovine prion protein had not been proven for its practical uses for RT-QuIC. We demonstrated that prions from transmissible mink encephalopathy (TME) and BSE-infected cattle can be detected with using bovine prion proteins with RT-QuIC, and developed an RT-QuIC based approach to discriminate different forms of BSE. This rapid and robust method, both to detect and discriminate BSE types, is of importance as the economic implications for different types of BSE vary greatly.
Review Publications
Hwang, S., Greenlee, J.J., Nicholson, E.M. 2017. Use of bovine recombinant prion protein and real-time quaking-induced conversion to detect cattle transmissible mink encephalopathy prions and discriminate classical and atypical L- and H-type bovine spongiform encephalopathy. PLoS One. 12(2):e0172391.
Moore, S., Kunkle, R., Greenlee, M., Nicholson, E., Richt, J., Hamir, A., Waters, W., Greenlee, J. 2016. Horizontal transmission of chronic wasting disease in reindeer. Emerging Infectious Diseases. 22(12):2142-2145. doi:10.3201/eid2212.160635.
Moore, S.J., West Greenlee, M.H., Smith, J.D., Vrentas, C.E., Nicholson, E.M., Greenlee, J.J. 2016. A comparison of classical and H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism in wild type and EK211 cattle following intracranial inoculation. Frontiers in Veterinary Science. 3:78.
Greenlee, J.J., Kunkle, R.A., Smith, J.D., West Greenlee, M.H. 2016. Scrapie in swine: a diagnostic challenge. Food Safety. 4(4):110-114. Kondru, N., Manne, S., Greenlee, J., West Greenlee, H., Anantharam, V., Halbur, P., Kanthasamy, A., Kanthasamy, A. 2017. Integrated organotypic slice cultures and RT-QuIC (OSCAR) assay: implications for translational discovery in protein misfolding diseases. Scientific Reports. 7:43155. doi:10.1038/srep43155.
Mammadova, N., Ghaisas, S., Zenitsky, G., Sakaguchi, D.S., Kanthasamy, A.G., Greenlee, J.J., West Greenlee, M.H. 2017. Lasting retinal injury in a mouse model of blast-induced trauma. American Journal of Pathology. 187(7):1459-1472. doi:10.1016/j.ajpath.2017.03.005.
Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES
Location: Virus and Prion Research
Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease
Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin
Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:
Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent. Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC. Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%).
Conclusions: This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge. CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease. Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.
CONFIDENTIAL
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...
we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.
May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...
3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...
But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....
snip...
It was not until . . . August 1990, that the result from the pig persuaded both SEAC and us to change our view and to take out of pig rations any residual infectivity that might have arisen from the SBOs.
4.303 The minutes of the meeting record that:
It was very difficult to draw conclusions from one experimental result for what may happen in the field. However it would be prudent to exclude specified bovine offals from the pig diet. Although any relationship between BSE and the finding of a spongiform encephalopathy in cats had yet to be demonstrated, the fact that this had occurred suggested that a cautious view should be taken of those species which might be susceptible. The 'specified offals' of bovines should therefore be excluded from the feed of all species. 17
http://web.archive.org/web/20031026084516/http://www.bseinquiry.gov.uk/files/yb/1990/09/07001001.pdf
IN CONFIENCE
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
1. CMO should be aware that a pig inoculated experimentally (ic, iv, and ip) with BSE brain suspension has after 15 months developed an illness, now confirmed as a spongiform encephalopathy. This is the first ever description of such a disease in a pig, although it seems there ar no previous attempts at experimental inoculation with animal material. The Southwood group had thought igs would not be susceptible. Most pigs are slaughtered when a few weeks old but there have been no reports of relevant neurological illness in breeding sows or other elderly pigs. ...see full text ;
IN CONFIDENCE
So it is plausible pigs could be preclinically affected with BSE but since so few are allowed to reach adulthood this has not been recognised through clinical disease. ...
CONFIDENTIAL
EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY
While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...
we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.
May I, at the outset, reiterate that we should avoid dissemination of papers relating to this experimental finding to prevent premature release of the information. ...
3. It is particularly important that this information is not passed outside the Department, until Ministers have decided how they wish it to be handled. ...
But it would be easier for us if pharmaceuticals/devices are not directly mentioned at all. ...
Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom.....
BSE TO PIGS NEWS RELEASE
CONFIDENTIAL
BSE: PRESS PRESENTATION
http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/20010001.pdf
http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25013001.pdf
http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25015001.pdf
INDUSTRY RESPONSE TYPICAL
DEFENSIVE BRIEFING
http://web.archive.org/web/20030820195733/http://www.bseinquiry.gov.uk/files/yb/1990/09/25016001.pdf
CONFIDENTIAL
pigs & pharmaceuticals
COMMERCIAL IN CONFIDENCE COMMITTEE ON SAFETY OF MEDICINE NOT FOR PUBLICATION BOVINE SPONGIFORM ENCEPHALOPATHY WORKING GROUP
There are only two products using porcine brain and these use corticotrophin BP, made from porcine pituitary, source from outside the UK.............
snip...
7 OF 10 LITTLE PIGGIES WENT ON TO DEVELOP BSE;
1: J Comp Pathol. 2000 Feb-Apr; 122(2-3): 131-43. Related Articles,
The neuropathology of experimental bovine spongiform encephalopathy in the pig.
Ryder SJ, Hawkins SA, Dawson M, Wells GA.
Veterinary Laboratories Agency Weybridge, Woodham Lane, New Haw, Addlestone, Surrey, KT15 3NB, UK.
In an experimental study of the transmissibility of BSE to the pig, seven of 10 pigs, infected at 1-2 weeks of age by multiple-route parenteral inoculation with a homogenate of bovine brain from natural BSE cases developed lesions typical of spongiform encephalopathy. The lesions consisted principally of severe neuropil vacuolation affecting most areas of the brain, but mainly the forebrain. In addition, some vacuolar change was identified in the rostral colliculi and hypothalamic areas of normal control pigs. PrP accumulations were detected immunocytochemically in the brains of BSE-infected animals. PrP accumulation was sparse in many areas and its density was not obviously related to the degree of vacuolation. The patterns of PrP immunolabelling in control pigs differed strikingly from those in the infected animals.
PMID: 10684682 [PubMed - indexed for MEDLINE]
snip...
In the United States, feeding of ruminant by-products to ruminants is prohibited, but feeding of ruminant materials to swine and poultry still occurs. The potential for swine to have access to scrapie-contaminated feedstuffs exists, but the potential for swine to serve as a host for replication/accumulation of the agent of scrapie is unknown. The purpose of this study was to perform oral and intracerebral inoculation of the U.S. scrapie agent to determine the potential of swine as a host for the scrapie agent and their clinical susceptibility.
see full text and more transmission studies here ;
Transgenic mice expressing porcine prion protein resistant to classical scrapie but susceptible to sheep bovine spongiform encephalopathy and atypical scrapie.
Emerg Infect Dis. 2009 Aug; [Epub ahead of print]
FRIDAY, APRIL 20, 2018
*** Scrapie Transmits To Pigs By Oral Route, what about the terribly flawed USA tse prion feed ban?
Research Project: Pathobiology, Genetics, and Detection of Transmissible Spongiform Encephalopathies
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...
FRIDAY, JUNE 29, 2018
Vaccines, TSE, Prion, risk factors?
Monday, May 19, 2008
*** SPORADIC CJD IN FARMERS, FARMERS WIVES, FROM FARMS WITH BSE HERD AND ABATTOIRS ***
BSE Inquiry
DFA 15 Monitoring and Enforcement of the SBO Specified Bovine Offal Regulations
TUESDAY, AUGUST 22, 2017
BSE INQUIRY DFA 16 MID 1995 TO THE FINAL DAYS
TUESDAY, AUGUST 1, 2017
BSE INQUIRY DFA 17 Medicines and medical devices
THURSDAY, AUGUST 3, 2017
BSE INQUIRY DFA 18 COSMETICS FDA OVERSIGHT WARNING The Honorable Frank Pallone, Jr.
***> see HISTORY great debate here <***
BSE, CJD, and Baby foods (the great debate 1999 to 2005)
Transmissible Spongiform Encephalopathies
Spongiform Encephalopathy in Captive Wild ZOO BSE INQUIRY
Sheep and cattle may be exposed to CWD via common grazing areas with affected deer but so far, appear to be poorly susceptible to mule deer CWD (Sigurdson, 2008). In contrast, cattle are highly susceptible to white-tailed deer CWD and mule deer CWD in experimental conditions but no natural CWD infections in cattle have been reported (Sigurdson, 2008; Hamir et al., 2006). It is not known how susceptible humans are to CWD but given that the prion can be present in muscle, it is likely that humans have been exposed to the agent via consumption of venison (Sigurdson, 2008). Initial experimental research suggests that human susceptibility to CWD is low and there may be a robust species barrier for CWD transmission to humans (Sigurdson, 2008), however the risk appetite for a public health threat may still find this level unacceptable.
***> Wednesday, January 23, 2019
***> CFIA SFCR Guidance on Specified risk material (SRM) came into force on January 15, 2019 <***
Prion Conference 2018
O5 Prion Disease in Dromedary Camels
Babelhadj B (1), Di Bari MA (2), Pirisinu L (2), Chiappini B (2), Gaouar SB (3), Riccardi G (2), Marcon S (2), Agrimi U (2), Nonno R (2), Vaccari G (2) (1) École Normale Supérieure Ouargla. Laboratoire de protection des écosystèmes en zones arides et semi arides University Kasdi Merbah Ouargla, Ouargla, Algeria; (2) Istituto Superiore di Sanità, Department of Food Safety, Nutrition and Veterinary Public Health, Rome, Italy (3) University Abou Bekr Bélkaid, Tlemcen, Algeria.
Prions are responsible for fatal and transmissible neurodegenerative diseases including CreutzfeldtJakob disease in humans, scrapie in small ruminants and bovine spongiform encephalopathy (BSE). Following the BSE epidemic and the demonstration of its zoonotic potential, general concerns have been raised on animal prions.
Here we report the identification of a prion disease in dromedary camels (Camelus dromedarius) in Algeria and designate it as Camel Prion Disease (CPD). In the last years, neurological symptoms have been observed in adult male and female dromedaries presented for slaughter at the Ouargla abattoir. The symptoms include weight loss, behavioral abnormalities and neurological symptoms such as tremors, aggressiveness, hyper-reactivity, typical down and upwards movements of the head, hesitant and uncertain gait, ataxia of the hind limbs, occasional falls and difficult getting up. During 2015 and 2016, symptoms suggestive of prion disease were observed in 3.1% of 2259 dromedaries presented at ante-mortem examination. Laboratory diagnosis was obtained in three symptomatic dromedaries, sampled in 2016 and 2017, by the detection of typical neurodegeneration and disease-specific prion protein (PrPSc) in brain tissues.
Histopathological examination revealed spongiform change, gliosis and neuronal loss preferentially in grey matter of subcortical brain areas. Abundant PrPSc deposition was detected in the same brain areas by immunohistochemistry and PET-blot. Western blot analysis confirmed the presence of PK-resistant PrPSc, whose N-terminal cleaved PK-resistant core was characterized by a mono-glycosylated dominant form and by a distinctive N-terminal cleavage, different from that observed in BSE and scrapie.
PrPSc was also detected, by immunohistochemistry, in all sampled lymph nodes (cervical, prescapular and lumbar aortic) of the only animal from which they were collected.
The PRNP sequence of the two animals for which frozen material was available, showed 100% nucleotide identity with the PRNP sequence already reported for dromedary camel.
Overall, these data demonstrate the presence of a prion disease in dromedary camelswhose nature, origin and spread need further investigations. However, our preliminary observations on the rather high prevalence of symptomatic dromedaries and the involvement of lymphoid tissues, are consistent with CPD being an infectious disease. In conclusion, the emergence of a new prion disease in a livestock species of crucial importance for millions of people around the world, makes urgent to assess the risk for humans and to develop policies able to control the spread of the disease in animals and to minimize human exposure.
CDC
New Outbreak of TSE Prion in NEW LIVESTOCK SPECIES
Mad Camel Disease
Volume 24, Number 6—June 2018 Research
Prion Disease in Dromedary Camels, Algeria
Abstract
Prions cause fatal and transmissible neurodegenerative diseases, including Creutzfeldt-Jakob disease in humans, scrapie in small ruminants, and bovine spongiform encephalopathy (BSE). After the BSE epidemic, and the associated human infections, began in 1996 in the United Kingdom, general concerns have been raised about animal prions. We detected a prion disease in dromedary camels (Camelus dromedarius) in Algeria. Symptoms suggesting prion disease occurred in 3.1% of dromedaries brought for slaughter to the Ouargla abattoir in 2015–2016. We confirmed diagnosis by detecting pathognomonic neurodegeneration and disease-specific prion protein (PrPSc) in brain tissues from 3 symptomatic animals. Prion detection in lymphoid tissues is suggestive of the infectious nature of the disease. PrPSc biochemical characterization showed differences with BSE and scrapie. Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.
SNIP...
The possibility that dromedaries acquired the disease from eating prion-contaminated waste needs to be considered.
Tracing the origin of prion diseases is challenging. In the case of CPD, the traditional extensive and nomadic herding practices of dromedaries represent a formidable factor for accelerating the spread of the disease at long distances, making the path of its diffusion difficult to determine. Finally, the major import flows of live animals to Algeria from Niger, Mali, and Mauritania (27) should be investigated to trace the possible origin of CPD from other countries.
Camels are a vital animal species for millions of persons globally. The world camel population has a yearly growth rate of 2.1% (28). In 2014, the population was estimated at ≈28 million animals, but this number is probably underestimated.. Approximately 88% of camels are found in Africa, especially eastern Africa, and 12% are found in Asia. Official data reported 350,000 dromedaries in Algeria in 2014 (28).
On the basis of phenotypic traits and sociogeographic criteria, several dromedary populations have been suggested to exist in Algeria (29). However, recent genetic studies in Algeria and Egypt point to a weak differentiation of the dromedary population as a consequence of historical use as a cross-continental beast of burden along trans-Saharan caravan routes, coupled with traditional extensive/nomadic herding practices (30).
Such genetic homogeneity also might be reflected in PRNP. Studies on PRNP variability in camels are therefore warranted to explore the existence of genotypes resistant to CPD, which could represent an important tool for CPD management as it was for breeding programs for scrapie eradication in sheep.
In the past 10 years, the camel farming system has changed rapidly, with increasing setup of periurban dairy farms and dairy plants and diversification of camel products and market penetration (13). This evolution requires improved health standards for infectious diseases and, in light of CPD, for prion diseases.
The emergence of another prion disease in an animal species of crucial importance for millions of persons worldwide makes it necessary to assess the risk for humans and develop evidence-based policies to control and limit the spread of the disease in animals and minimize human exposure. The implementation of a surveillance system for prion diseases would be a first step to enable disease control and minimize human and animal exposure. Finally, the diagnostic capacity of prion diseases needs to be improved in all countries in Africa where dromedaries are part of the domestic livestock.
***> IMPORTS AND EXPORTS <***
***SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN ***
ZOONOSIS OF SCRAPIE TSE PRION
O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations
Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France
Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases).
Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods.
*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period,
***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014),
***is the third potentially zoonotic PD (with BSE and L-type BSE),
***thus questioning the origin of human sporadic cases.
We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health.
===============
***thus questioning the origin of human sporadic cases***
===============
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
==============
***Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
***Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
***These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
PRION 2016 TOKYO
Saturday, April 23, 2016
SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016
Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online
Taylor & Francis
Prion 2016 Animal Prion Disease Workshop Abstracts
WS-01: Prion diseases in animals and zoonotic potential
Juan Maria Torres a, Olivier Andreoletti b, J uan-Carlos Espinosa a. Vincent Beringue c. Patricia Aguilar a,
Natalia Fernandez-Borges a. and Alba Marin-Moreno a
"Centro de Investigacion en Sanidad Animal ( CISA-INIA ). Valdeolmos, Madrid. Spain; b UMR INRA -ENVT 1225 Interactions Holes Agents Pathogenes. ENVT. Toulouse. France: "UR892. Virologie lmmunologie MolécuIaires, Jouy-en-Josas. France
Dietary exposure to bovine spongiform encephalopathy (BSE) contaminated bovine tissues is considered as the origin of variant Creutzfeldt Jakob (vCJD) disease in human. To date, BSE agent is the only recognized zoonotic prion... Despite the variety of Transmissible Spongiform Encephalopathy (TSE) agents that have been circulating for centuries in farmed ruminants there is no apparent epidemiological link between exposure to ruminant products and the occurrence of other form of TSE in human like sporadic Creutzfeldt Jakob Disease (sCJD). However, the zoonotic potential of the diversity of circulating TSE agents has never been systematically assessed. The major issue in experimental assessment of TSEs zoonotic potential lies in the modeling of the ‘species barrier‘, the biological phenomenon that limits TSE agents’ propagation from a species to another. In the last decade, mice genetically engineered to express normal forms of the human prion protein has proved essential in studying human prions pathogenesis and modeling the capacity of TSEs to cross the human species barrier.
To assess the zoonotic potential of prions circulating in farmed ruminants, we study their transmission ability in transgenic mice expressing human PrPC (HuPrP-Tg). Two lines of mice expressing different forms of the human PrPC (129Met or 129Val) are used to determine the role of the Met129Val dimorphism in susceptibility/resistance to the different agents.
These transmission experiments confirm the ability of BSE prions to propagate in 129M- HuPrP-Tg mice and demonstrate that Met129 homozygotes may be susceptible to BSE in sheep or goat to a greater degree than the BSE agent in cattle and that these agents can convey molecular properties and neuropathological indistinguishable from vCJD. However homozygous 129V mice are resistant to all tested BSE derived prions independently of the originating species suggesting a higher transmission barrier for 129V-PrP variant.
Transmission data also revealed that several scrapie prions propagate in HuPrP-Tg mice with efficiency comparable to that of cattle BSE. While the efficiency of transmission at primary passage was low, subsequent passages resulted in a highly virulent prion disease in both Met129 and Val129 mice.
Transmission of the different scrapie isolates in these mice leads to the emergence of prion strain phenotypes that showed similar characteristics to those displayed by MM1 or VV2 sCJD prion.
These results demonstrate that scrapie prions have a zoonotic potential and raise new questions about the possible link between animal and human prions.
***> 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
Title: Transmission of scrapie prions to primate after an extended silent incubation period)
*** In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS.
*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated.
*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains.
***> Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility. <***
Transmission of scrapie prions to primate after an extended silent incubation period
Emmanuel E. Comoy, Jacqueline Mikol, Sophie Luccantoni-Freire, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Valérie Durand, Capucine Dehen, Olivier Andreoletti, Cristina Casalone, Juergen A. Richt, Justin J. Greenlee, Thierry Baron, Sylvie L. Benestad, Paul Brown & Jean-Philippe Deslys Scientific Reports volume 5, Article number: 11573 (2015) | Download Citation
Abstract
Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie.
SNIP...
Discussion We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes. Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.
The second possibility is a laboratory cross-contamination. Three facts make this possibility equally unlikely. First, handling of specimens in our laboratory is performed with fastidious attention to the avoidance of any such cross-contamination. Second, no laboratory cross-contamination has ever been documented in other primate laboratories, including the NIH, even between infected and uninfected animals housed in the same or adjacent cages with daily intimate contact (P. Brown, personal communication). Third, the cerebral lesion profile is different from all the other prion diseases we have studied in this model19, with a correlation between cerebellar lesions (massive spongiform change of Purkinje cells, intense PrPres staining and reactive gliosis26) and ataxia. The iron deposits present in the globus pallidus are a non specific finding that have been reported previously in neurodegenerative diseases and aging27. Conversely, the thalamic lesion was reminiscent of a metabolic disease due to thiamine deficiency28 but blood thiamine levels were within normal limits (data not shown). The preferential distribution of spongiform change in cortex associated with a limited distribution in the brainstem is reminiscent of the lesion profile in MM2c and VV1 sCJD patients29, but interspecies comparison of lesion profiles should be interpreted with caution. It is of note that the same classical scrapie isolate induced TSE in C57Bl/6 mice with similar incubation periods and lesional profiles as a sample derived from a MM1 sCJD patient30.
We are therefore confident that the illness in this cynomolgus macaque represents a true transmission of a sheep c-scrapie isolate directly to an old-world monkey, which taxonomically resides in the primate subdivision (parvorder of catarrhini) that includes humans. With an homology of its PrP protein with humans of 96.4%31, cynomolgus macaque constitutes a highly relevant model for assessing zoonotic risk of prion diseases. Since our initial aim was to show the absence of transmission of scrapie to macaques in the worst-case scenario, we obtained materials from a flock of naturally-infected sheep, affecting animals with different genotypes32. This c-scrapie isolate exhibited complete transmission in ARQ/ARQ sheep (332 ± 56 days) and Tg338 transgenic mice expressing ovine VRQ/VRQ prion protein (220 ± 5 days) (O. Andreoletti, personal communication). From the standpoint of zoonotic risk, it is important to note that sheep with c-scrapie (including the isolate used in our study) have demonstrable infectivity throughout their lymphoreticular system early in the incubation period of the disease (3 months-old for all the lymphoid organs, and as early as 2 months-old in gut-associated lymph nodes)33. In addition, scrapie infectivity has been identified in blood34, milk35 and skeletal muscle36 from asymptomatic but scrapie infected small ruminants which implies a potential dietary exposure for consumers.
Two earlier studies have reported the occurrence of clinical TSE in cynomolgus macaques after exposures to scrapie isolates. In the first study, the “Compton” scrapie isolate (derived from an English sheep) and serially propagated for 9 passages in goats did not transmit TSE in cynomolgus macaque, rhesus macaque or chimpanzee within 7 years following intracerebral challenge1; conversely, after 8 supplementary passages in conventional mice, this “Compton” isolate induced TSE in a cynomolgus macaque 5 years after intracerebral challenge, but rhesus macaques and chimpanzee remained asymptomatic 8.5 years post-exposure8. However, multiple successive passages that are classically used to select laboratory-adapted prion strains can significantly modify the initial properties of a scrapie isolate, thus questioning the relevance of zoonotic potential for the initial sheep-derived isolate. The same isolate had also induced disease into squirrel monkeys (new-world monkey)9. A second historical observation reported that a cynomolgus macaque developed TSE 6 years post-inoculation with brain homogenate from a scrapie-infected Suffolk ewe (derived from USA), whereas a rhesus macaque and a chimpanzee exposed to the same inoculum remained healthy 9 years post-exposure1. This inoculum also induced TSE in squirrel monkeys after 4 passages in mice. Other scrapie transmission attempts in macaque failed but had more shorter periods of observation in comparison to the current study. Further, it is possible that there are differences in the zoonotic potential of different scrapie strains.
The most striking observation in our study is the extended incubation period of scrapie in the macaque model, which has several implications. Firstly, our observations constitute experimental evidence in favor of the zoonotic potential of c-scrapie, at least for this isolate that has been extensively studied32,33,34,35,36. The cross-species zoonotic ability of this isolate should be confirmed by performing duplicate intracerebral exposures and assessing the transmissibility by the oral route (a successful transmission of prion strains through the intracerebral route may not necessarily indicate the potential for oral transmission37). However, such confirmatory experiments may require more than one decade, which is hardly compatible with current general management and support of scientific projects; thus this study should be rather considered as a case report.
Secondly, transmission of c-BSE to primates occurred within 8 years post exposure for the lowest doses able to transmit the disease (the survival period after inoculation is inversely proportional to the initial amount of infectious inoculum). The occurrence of scrapie 10 years after exposure to a high dose (25 mg) of scrapie-infected sheep brain suggests that the macaque has a higher species barrier for sheep c-scrapie than c-BSE, although it is notable that previous studies based on in vitro conversion of PrP suggested that BSE and scrapie prions would have a similar conversion potential for human PrP38.
Thirdly, prion diseases typically have longer incubation periods after oral exposure than after intracerebral inoculations: since humans can develop Kuru 47 years after oral exposure39, an incubation time of several decades after oral exposure to scrapie would therefore be expected, leading the disease to occur in older adults, i.e. the peak age for cases considered to be sporadic disease, and making a distinction between scrapie-associated and truly sporadic disease extremely difficult to appreciate.
Fourthly, epidemiologic evidence is necessary to confirm the zoonotic potential of an animal disease suggested by experimental studies. A relatively short incubation period and a peculiar epidemiological situation (e.g., all the first vCJD cases occurring in the country with the most important ongoing c-BSE epizootic) led to a high degree of suspicion that c-BSE was the cause of vCJD. Sporadic CJD are considered spontaneous diseases with an almost stable and constant worldwide prevalence (0.5–2 cases per million inhabitants per year), and previous epidemiological studies were unable to draw a link between sCJD and classical scrapie6,7,40,41, even though external causes were hypothesized to explain the occurrence of some sCJD clusters42,43,44. However, extended incubation periods exceeding several decades would impair the predictive values of epidemiological surveillance for prion diseases, already weakened by a limited prevalence of prion diseases and the multiplicity of isolates gathered under the phenotypes of “scrapie” and “sporadic CJD”.
Fifthly, considering this 10 year-long incubation period, together with both laboratory and epidemiological evidence of decade or longer intervals between infection and clinical onset of disease, no premature conclusions should be drawn from negative transmission studies in cynomolgus macaques with less than a decade of observation, as in the aforementioned historical transmission studies of scrapie to primates1,8,9. Our observations and those of others45,46 to date are unable to provide definitive evidence regarding the zoonotic potential of CWD, atypical/Nor98 scrapie or H-type BSE. The extended incubation period of the scrapie-affected macaque in the current study also underscores the limitations of rodent models expressing human PrP for assessing the zoonotic potential of some prion diseases since their lifespan remains limited to approximately two years21,47,48. This point is illustrated by the fact that the recently reported transmission of scrapie to humanized mice was not associated with clinical signs for up to 750 days and occurred in an extreme minority of mice with only a marginal increase in attack rate upon second passage13. The low attack rate in these studies is certainly linked to the limited lifespan of mice compared to the very long periods of observation necessary to demonstrate the development of scrapie. Alternatively, one could estimate that a successful second passage is the result of strain adaptation to the species barrier, thus poorly relevant of the real zoonotic potential of the original scrapie isolate of sheep origin49. The development of scrapie in this primate after an incubation period compatible with its lifespan complements the study conducted in transgenic (humanized) mice; taken together these studies suggest that some isolates of sheep scrapie can promote misfolding of the human prion protein and that scrapie can develop within the lifespan of some primate species.
In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free... Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.
Chronic Wasting Disease CWD TSE Prion
Cervid to human prion transmission
Kong, Qingzhong Case Western Reserve University, Cleveland, OH, United States
We hypothesize that:
(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence;
(3) Reliable essays can be established to detect CWD infection in humans; and
(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.
(1) The classic CWD prion strain can infect humans at low levels in the brain and peripheral lymphoid tissues;
(2) The cervid-to-human transmission barrier is dependent on the cervid prion strain and influenced by the host (human) prion protein (PrP) primary sequence;
(3) Reliable essays can be established to detect CWD infection in humans; and
(4) CWD transmission to humans has already occurred. We will test these hypotheses in 4 Aims using transgenic (Tg) mouse models and complementary in vitro approaches.
ZOONOTIC CHRONIC WASTING DISEASE CWD TSE PRION UPDATE
here is the latest;
PRION 2018 CONFERENCE
Oral transmission of CWD into Cynomolgus macaques: signs of atypical disease, prion conversion and infectivity in macaques and bio-assayed transgenic mice
Hermann M. Schatzl, Samia Hannaoui, Yo-Ching Cheng, Sabine Gilch (Calgary Prion Research Unit, University of Calgary, Calgary, Canada) Michael Beekes (RKI Berlin), Walter Schulz-Schaeffer (University of Homburg/Saar, Germany), Christiane Stahl-Hennig (German Primate Center) & Stefanie Czub (CFIA Lethbridge).
To date, BSE is the only example of interspecies transmission of an animal prion disease into humans. The potential zoonotic transmission of CWD is an alarming issue and was addressed by many groups using a variety of in vitro and in vivo experimental systems. Evidence from these studies indicated a substantial, if not absolute, species barrier, aligning with the absence of epidemiological evidence suggesting transmission into humans. Studies in non-human primates were not conclusive so far, with oral transmission into new-world monkeys and no transmission into old-world monkeys. Our consortium has challenged 18 Cynomolgus macaques with characterized CWD material, focusing on oral transmission with muscle tissue. Some macaques have orally received a total of 5 kg of muscle material over a period of 2 years.
After 5-7 years of incubation time some animals showed clinical symptoms indicative of prion disease, and prion neuropathology and PrPSc deposition were detected in spinal cord and brain of some euthanized animals. PrPSc in immunoblot was weakly detected in some spinal cord materials and various tissues tested positive in RT-QuIC, including lymph node and spleen homogenates. To prove prion infectivity in the macaque tissues, we have intracerebrally inoculated 2 lines of transgenic mice, expressing either elk or human PrP. At least 3 TgElk mice, receiving tissues from 2 different macaques, showed clinical signs of a progressive prion disease and brains were positive in immunoblot and RT-QuIC. Tissues (brain, spinal cord and spleen) from these and pre-clinical mice are currently tested using various read-outs and by second passage in mice. Transgenic mice expressing human PrP were so far negative for clear clinical prion disease (some mice >300 days p.i.). In parallel, the same macaque materials are inoculated into bank voles.
Taken together, there is strong evidence of transmissibility of CWD orally into macaques and from macaque tissues into transgenic mouse models, although with an incomplete attack rate.
The clinical and pathological presentation in macaques was mostly atypical, with a strong emphasis on spinal cord pathology.
Our ongoing studies will show whether the transmission of CWD into macaques and passage in transgenic mice represents a form of non-adaptive prion amplification, and whether macaque-adapted prions have the potential to infect mice expressing human PrP.
The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD..
***> The notion that CWD can be transmitted orally into both new-world and old-world non-human primates asks for a careful reevaluation of the zoonotic risk of CWD. <***
https://prion2018.org/
READING OVER THE PRION 2018 ABSTRACT BOOK, LOOKS LIKE THEY FOUND THAT from this study ;
P190 Human prion disease mortality rates by occurrence of chronic wasting disease in freeranging cervids, United States
Abrams JY (1), Maddox RA (1), Schonberger LB (1), Person MK (1), Appleby BS (2), Belay ED (1) (1) Centers for Disease Control and Prevention (CDC), National Center for Emerging and Zoonotic Infectious Diseases, Atlanta, GA, USA (2) Case Western Reserve University, National Prion Disease Pathology Surveillance Center (NPDPSC), Cleveland, OH, USA..
SEEMS THAT THEY FOUND Highly endemic states had a higher rate of prion disease mortality compared to non-CWD
states.
AND ANOTHER STUDY;
P172 Peripheral Neuropathy in Patients with Prion Disease
Wang H(1), Cohen M(1), Appleby BS(1,2) (1) University Hospitals Cleveland Medical Center, Cleveland, Ohio (2) National Prion Disease Pathology Surveillance Center, Cleveland, Ohio..
IN THIS STUDY, THERE WERE autopsy-proven prion cases from the National Prion Disease Pathology Surveillance Center that were diagnosed between September 2016 to March 2017,
AND
included 104 patients. SEEMS THEY FOUND THAT The most common sCJD subtype was MV1-2 (30%), followed by MM1-2 (20%),
AND
THAT The Majority of cases were male (60%), AND half of them had exposure to wild game.
snip...
see more on Prion 2017 Macaque study from Prion 2017 Conference and other updated science on cwd tse prion zoonosis below...terry
https://prion2018.org/wp-content/uploads/2018/05/program.pdf
https://prion2018.org/
THURSDAY, OCTOBER 04, 2018
Cervid to human prion transmission 5R01NS088604-04 Update
http://grantome.com/grant/NIH/R01-NS088604-04
http://chronic-wasting-disease.blogspot.com/2018/10/cervid-to-human-prion-transmission.html
snip...full text;
SATURDAY, FEBRUARY 09, 2019
Experts: Yes, chronic wasting disease in deer is a public health issue — for people
***> This is very likely to have parallels with control efforts for CWD in cervids.
Rapid recontamination of a farm building occurs after attempted prion removal
Kevin Christopher Gough, BSc (Hons), PhD1, Claire Alison Baker, BSc (Hons)2, Steve Hawkins, MIBiol3, Hugh Simmons, BVSc, MRCVS, MBA, MA3, Timm Konold, DrMedVet, PhD, MRCVS3 and Ben Charles Maddison, BSc (Hons), PhD2
Abstract
The transmissible spongiform encephalopathy scrapie of sheep/goats and chronic wasting disease of cervids are associated with environmental reservoirs of infectivity.
Preventing environmental prions acting as a source of infectivity to healthy animals is of major concern to farms that have had outbreaks of scrapie and also to the health management of wild and farmed cervids.
Here, an efficient scrapie decontamination protocol was applied to a farm with high levels of environmental contamination with the scrapie agent.
Post-decontamination, no prion material was detected within samples taken from the farm buildings as determined using a sensitive in vitro replication assay (sPMCA).
A bioassay consisting of 25 newborn lambs of highly susceptible prion protein genotype VRQ/VRQ introduced into this decontaminated barn was carried out in addition to sampling and analysis of dust samples that were collected during the bioassay.
Twenty-four of the animals examined by immunohistochemical analysis of lymphatic tissues were scrapie-positive during the bioassay, samples of dust collected within the barn were positive by month 3.
The data illustrates the difficulty in decontaminating farm buildings from scrapie, and demonstrates the likely contribution of farm dust to the recontamination of these environments to levels that are capable of causing disease.
snip...
As in the authors' previous study,12 the decontamination of this sheep barn was not effective at removing scrapie infectivity, and despite the extra measures brought into this study (more effective chemical treatment and removal of sources of dust) the overall rates of disease transmission mirror previous results on this farm. With such apparently effective decontamination (assuming that at least some sPMCA seeding ability is coincident with infectivity), how was infectivity able to persist within the environment and where does infectivity reside? Dust samples were collected in both the bioassay barn and also a barn subject to the same decontamination regime within the same farm (but remaining unoccupied). Within both of these barns dust had accumulated for three months that was able to seed sPMCA, indicating the accumulation of scrapie-containing material that was independent of the presence of sheep that may have been incubating and possibly shedding low amounts of infectivity.
This study clearly demonstrates the difficulty in removing scrapie infectivity from the farm environment. Practical and effective prion decontamination methods are still urgently required for decontamination of scrapie infectivity from farms that have had cases of scrapie and this is particularly relevant for scrapiepositive goatherds, which currently have limited genetic resistance to scrapie within commercial breeds.24 This is very likely to have parallels with control efforts for CWD in cervids.
Acknowledgements The authors thank the APHA farm staff, Tony Duarte, Olly Roberts and Margaret Newlands for preparation of the sheep pens and animal husbandry during the study. The authors also thank the APHA pathology team for RAMALT and postmortem examination.
Funding This study was funded by DEFRA within project SE1865.
Competing interests None declared.
Saturday, January 5, 2019
Rapid recontamination of a farm building occurs after attempted prion removal
*** 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.
you can see more evidence here ;
Wednesday, May 24, 2017
PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh UPDATE 1
WEDNESDAY, SEPTEMBER 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
PRION 2010
International Prion Congress: From agent to disease September 8–11, 2010 Salzburg, Austria
Transmission Studies
Mule deer transmissions of CWD were by intracerebral inoculation and compared with natural cases {the following was written but with a single line marked through it ''first passage (by this route)}....TSS
resulted in a more rapidly progressive clinical disease with repeated episodes of synocopy ending in coma. One control animal became affected, it is believed through contamination of inoculum (?saline). Further CWD transmissions were carried out by Dick Marsh into ferret, mink and squirrel monkey. Transmission occurred in ALL of these species with the shortest incubation period in the ferret.
snip....
Prion Infectivity in Fat of Deer with Chronic Wasting Disease▿
Brent Race#, Kimberly Meade-White#, Richard Race and Bruce Chesebro* + Author Affiliations
In mice, prion infectivity was recently detected in fat. Since ruminant fat is consumed by humans and fed to animals, we determined infectivity titers in fat from two CWD-infected deer. Deer fat devoid of muscle contained low levels of CWD infectivity and might be a risk factor for prion infection of other species.
Prions in Skeletal Muscles of Deer with Chronic Wasting Disease
Here bioassays in transgenic mice expressing cervid prion protein revealed the presence of infectious prions in skeletal muscles of CWD-infected deer, demonstrating that humans consuming or handling meat from CWD-infected deer are at risk to prion exposure.
*** now, let’s see what the authors said about this casual link, personal communications years ago, and then the latest on the zoonotic potential from CWD to humans from the TOKYO PRION 2016 CONFERENCE.
see where it is stated NO STRONG evidence. so, does this mean there IS casual evidence ???? “Our conclusion stating that we found no strong evidence of CWD transmission to humans”
From: TSS (216-119-163-189.ipset45.wt.net)
Subject: CWD aka MAD DEER/ELK TO HUMANS ???
Date: September 30, 2002 at 7:06 am PST
From: "Belay, Ermias"
To: Cc: "Race, Richard (NIH)" ; ; "Belay, Ermias"
Sent: Monday, September 30, 2002 9:22 AM
Subject: RE: TO CDC AND NIH - PUB MED- 3 MORE DEATHS - CWD - YOUNG HUNTERS
Dear Sir/Madam,
In the Archives of Neurology you quoted (the abstract of which was attached to your email), we did not say CWD in humans will present like variant CJD.. That assumption would be wrong. I encourage you to read the whole article and call me if you have questions or need more clarification (phone: 404-639-3091). Also, we do not claim that "no-one has ever been infected with prion disease from eating venison." Our conclusion stating that we found no strong evidence of CWD transmission to humans in the article you quoted or in any other forum is limited to the patients we investigated.
Ermias Belay, M.D. Centers for Disease Control and Prevention
-----Original Message-----
From: Sent: Sunday, September 29, 2002 10:15 AM
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 ;
> However, to date, no CWD infections have been reported in people.
key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry
*** LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ ***
*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***
SEE; Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey
Monday, May 23, 2011
CDC Assesses Potential Human Exposure to Prion Diseases Travel Warning
Public release date: 23-May-2011
Contact: Francesca Costanzo adajmedia@elsevier.com 215-239-3249 Elsevier Health Sciences
CDC assesses potential human exposure to prion diseases Study results reported in the Journal of the American Dietetic Association
Philadelphia, PA, May 23, 2011 – Researchers from the Centers for Disease Control and Prevention (CDC) have examined the potential for human exposure to prion diseases, looking at hunting, venison consumption, and travel to areas in which prion diseases have been reported in animals. Three prion diseases in particular – bovine spongiform encephalopathy (BSE or “Mad Cow Disease”), variant Creutzfeldt-Jakob disease (vCJD), and chronic wasting disease (CWD) – were specified in the investigation. The results of this investigation are published in the June issue of the Journal of the American Dietetic Association.
“While prion diseases are rare, they are generally fatal for anyone who becomes infected. More than anything else, the results of this study support the need for continued surveillance of prion diseases,” commented lead investigator Joseph Y. Abrams, MPH, National Center for Emerging and Zoonotic Infectious Diseases, CDC, Atlanta.”But it’s also important that people know the facts about these diseases, especially since this study shows that a good number of people have participated in activities that may expose them to infection-causing agents.”
Although rare, human prion diseases such as CJD may be related to BSE. Prion (proteinaceous infectious particles) diseases are a group of rare brain diseases that affect humans and animals. When a person gets a prion disease, brain function is impaired. This causes memory and personality changes, dementia, and problems with movement. All of these worsen over time. These diseases are invariably fatal. Since these diseases may take years to manifest, knowing the extent of human exposure to possible prion diseases could become important in the event of an outbreak.
CDC investigators evaluated the results of the 2006-2007 population survey conducted by the Foodborne Diseases Active Surveillance Network (FoodNet). This survey collects information on food consumption practices, health outcomes, and demographic characteristics of residents of the participating Emerging Infections Program sites. The survey was conducted in Connecticut, Georgia, Maryland, Minnesota, New Mexico, Oregon, and Tennessee, as well as five counties in the San Francisco Bay area, seven counties in the Greater Denver area, and 34 counties in western and northeastern New York.
Survey participants were asked about behaviors that could be associated with exposure to the agents causing BSE and CWD, including travel to the nine countries considered to be BSE-endemic (United Kingdom, Republic of Ireland, France, Portugal, Switzerland, Italy, the Netherlands, Germany, Spain) and the cumulative length of stay in each of those countries. Respondents were asked if they ever had hunted for deer or elk, and if that hunting had taken place in areas considered to be CWD-endemic (northeastern Colorado, southeastern Wyoming or southwestern Nebraska). They were also asked if they had ever consumed venison, the frequency of consumption, and whether the meat came from the wild.
The proportion of survey respondents who reported travel to at least one of the nine BSE endemic countries since 1980 was 29.5%. Travel to the United Kingdom was reported by 19.4% of respondents, higher than to any other BSE-endemic country. Among those who traveled, the median duration of travel to the United Kingdom (14 days) was longer than that of any other BSE-endemic country.. Travelers to the UK were more likely to have spent at least 30 days in the country (24.9%) compared to travelers to any other BSE endemic country. The prevalence and extent of travel to the UK indicate that health concerns in the UK may also become issues for US residents.
The proportion of survey respondents reporting having hunted for deer or elk was 18.5% and 1.2% reported having hunted for deer or elk in CWD-endemic areas. Venison consumption was reported by 67.4% of FoodNet respondents, and 88.6% of those reporting venison consumption had obtained all of their meat from the wild. These findings reinforce the importance of CWD surveillance and control programs for wild deer and elk to reduce human exposure to the CWD agent. Hunters in CWD-endemic areas are advised to take simple precautions such as: avoiding consuming meat from sickly deer or elk, avoiding consuming brain or spinal cord tissues, minimizing the handling of brain and spinal cord tissues, and wearing gloves when field-dressing carcasses.
According to Abrams, “The 2006-2007 FoodNet population survey provides useful information should foodborne prion infection become an increasing public health concern in the future. The data presented describe the prevalence of important behaviors and their associations with demographic characteristics. Surveillance of BSE, CWD, and human prion diseases are critical aspects of addressing the burden of these diseases in animal populations and how that may relate to human health.”
###
The article is “Travel history, hunting, and venison consumption related to prion disease exposure, 2006-2007 FoodNet population survey” by Joseph Y. Abrams, MPH; Ryan A. Maddox, MPH; Alexis R Harvey, MPH; Lawrence B. Schonberger, MD; and Ermias D. Belay, MD. It appears in the Journal of the American Dietetic Association, Volume 111, Issue 6 (June 2011) published by Elsevier.
In an accompanying podcast CDC’s Joseph Y. Abrams discusses travel, hunting, and eating venison in relation to prion diseases. It is available at http://adajournal.org/content/podcast. ;
Thursday, May 26, 2011
Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey
Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.
Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey
Joseph Y. Abrams, MPH, Ryan A. Maddox, MPH , Alexis R. Harvey, MPH , Lawrence B. Schonberger, MD , Ermias D. Belay, MD
Accepted 15 November 2010. Abstract Full Text PDF References .
Abstract
The transmission of bovine spongiform encephalopathy (BSE) to human beings and the spread of chronic wasting disease (CWD) among cervids have prompted concerns about zoonotic transmission of prion diseases. Travel to the United Kingdom and other European countries, hunting for deer or elk, and venison consumption could result in the exposure of US residents to the agents that cause BSE and CWD. The Foodborne Diseases Active Surveillance Network 2006-2007 population survey was used to assess the prevalence of these behaviors among residents of 10 catchment areas across the United States. Of 17,372 survey respondents, 19.4% reported travel to the United Kingdom since 1980, and 29.5% reported travel to any of the nine European countries considered to be BSE-endemic since 1980. The proportion of respondents who had ever hunted deer or elk was 18.5%, and 1.2% had hunted deer or elk in a CWD–endemic area. More than two thirds (67.4%) reported having ever eaten deer or elk meat. Respondents who traveled spent more time in the United Kingdom (median 14 days) than in any other BSE-endemic country. Of the 11,635 respondents who had consumed venison, 59.8% ate venison at most one to two times during their year of highest consumption, and 88.6% had obtained all of their meat from the wild. The survey results were useful in determining the prevalence and frequency of behaviors that could be important factors for foodborne prion transmission.
PLUS, THE CDC DID NOT PUT THIS WARNING OUT FOR THE WELL BEING OF THE DEER AND ELK ;
Thursday, May 26, 2011
Travel History, Hunting, and Venison Consumption Related to Prion Disease Exposure, 2006-2007 FoodNet Population Survey
Journal of the American Dietetic Association Volume 111, Issue 6 , Pages 858-863, June 2011.
NOR IS THE FDA recalling this CWD positive elk meat for the well being of the dead elk ;
Wednesday, March 18, 2009
Noah's Ark Holding, LLC, Dawson, MN RECALL Elk products contain meat derived from an elk confirmed to have CWD NV, CA, TX, CO, NY, UT, FL, OK RECALLS AND FIELD CORRECTIONS: FOODS CLASS II
Transmissible Spongiform Encephalopathies
Spongiform Encephalopathy in Captive Wild ZOO BSE INQUIRY
THURSDAY, OCTOBER 04, 2018
Cervid to human prion transmission 5R01NS088604-04 Update
MONDAY, JANUARY 14, 2019
Evaluation of iatrogenic risk of CJD transmission associated with Chronic Wasting Disease TSE Prion in Texas TAHC TPWD
It is a dimension as vast as space and as timeless as infinity. It is the middle ground between light and shadow, between science and superstition, and it lies between the pit of man's fears and the summit of his knowledge. This is the dimension of imagination. It is NOT, an area which we call the Twilight Zone, but an area that believes junk science, and the very industries and lobbyist some Texas Hunters, the cervid industry, that insist on shoving the fake news down their throats, we call this ted nugent junk science, and in TEXAS, sometimes you just can't fix stupid, this is where the rubber meets the road, here's your sign!
chronic wasting disease cwd tse prion aka mad deer elk disease, if you consume a cwd tse prion positive cervid, then months, years, decades later, go on to have surgery, dental, ophthalmology, endoscopy, donate tissue, blood, organs, you then expose those medical theaters and tissue, blood, organs, that are incubating the infectious cwd tse prion disease, to everyone that comes in contact.
these are not memes, these are actual statements from hunters/industry in Texas about CWD tse prion.
God help them, and us...terry
''Got a call today from TPWD, I’ve got a mule deer that tested early positive for CWD. I’m soon to turn into a zombie because I have already been eating it. They advised not to consume any of the meat...too late! They want to come confiscate what meat is left once they get more results back from another lab.''
snip...
MONDAY, FEBRUARY 25, 2019
MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019
BSE INQUIRY EVIDENCE
Why did the appearance of new TSEs in animals matter so much? It has always been known that TSEs will transfer across species boundaries. The reason for this was never known until the genetic nature of the prion gene was fully investigated and found to be involved. The gene is found to have well preserved sites and as such there is a similar gene throughout the animal kingdom...and indeed a similar gene is found in insects! It is NOT clear that the precise close nature of the PrP gene structure is essention for low species barriers. Indeed it is probably easier to infect cats with BSE than it is to infect sheep. As such it is not clear that simply because it is possible to infect BSE from cattle into certain monkeys then other apes will necessarily be infectable with the disease. One factor has stood out, however, and that is that BSE, when inoculated into mice would retain its apparent nature of disease strain, and hence when it was inoculated back into cattle, then the same disease was produced. Similarly if the TSE from kudu was inoculated into mice then a similar distribution of disease in the brain of the mouse is seen as if BSE had been inoculated into the mouse. This phenomenon was not true with scrapie, in which the transmission across a species barrier was known to lose many of the scrapie strain phenomena in terms of incubation period or disease histopathology. This also suggested that BSE was not derived from scrapie originally but we probably will never know.
------------------------------------------------------------------------
TSE in wild UK deer? The first case of BSE (as we now realise) was in a nyala in London zoo and the further zoo cases in ungulates were simply thought of as being interesting transmissions of scrapie initially. The big problem started to appear with animals in 1993-5 when it became clear that there was an increase in the CJD cases in people that had eaten deer although the statistics involved must have been questionable. The reason for this was that the CJD Surveillance was well funded to look into the diet of people dying of CJD. This effect is not clear with vCJD...if only because the numbers involved are much smaller and hence it is difficult to gain enough statistics. They found that many other foods did not appear to have much association at all but that deer certainly did and as years went by the association actually became clearer. The appearance of vCJD in 1996 made all this much more difficult in that it was suddenly clearer that the cases of sporadic CJD that they had been checking up until then probably had nothing to do with beef...and the study decreased. During the period there was an increasing worry that deer were involved with CJD..
see references:
DEER BRAIN SURVEY
i have not updated my blogspot url with all this data archived, but i will work on it...but until then, i have updated this on the above links with live urls to the actual BSE Inquiry documents...
Subject: Re: DEER SPONGIFORM ENCEPHALOPATHY SURVEY & HOUND STUDY
Date: Fri, 18 Oct 2002 23:12:22 +0100
From: Steve Dealler
Reply-To: Bovine Spongiform Encephalopathy Organization: Netscape Online member
To: BSE-L@ References: <3daf5023 .4080804="" a="" class="yiv5273118069linkified" href="http://wt.net/" rel="noopener noreferrer" style="color: blue; cursor: pointer;" target="_blank">WT.NET
Dear Terry,
An excellent piece of review as this literature is desparately difficult to get back from Government sites.
What happened with the deer was that an association between deer meat eating and sporadic CJD was found in about 1993. The evidence was not great but did not disappear after several years of asking CJD cases what they had eaten. I think that the work into deer disease largely stopped because it was not helpful to the UK industry...and no specific cases were reported. Well, if you dont look adequately like they are in USA currenly then you wont find any!
Steve Dealler ===============
BSE Inquiry Steve Dealler
Management In Confidence
BSE: Private Submission of Bovine Brain Dealler
reports of sheep and calf carcasses dumped...
re-scrapie to cattle GAH Wells BSE Inquiry
https://web.archive.org/web/20090506043931/http://www.bseinquiry.gov.uk/files/yb/1993/12/09001001.pdf
Dr. Dealler goes rogue to confirm BSE
Confirmation BSE Dealler's mad cow
BSE vertical transmission
1993 cjd report finds relationship with eat venison and cjd increases 9 fold, let the cover up begin...tss
FINDINGS
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). ***
There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02)..
The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08).
snip...
It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05).
snip...
In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ...
snip...
In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS)
snip...see full report ;
GAME FARM INDUSTRY WANTS TO COVER UP FINDINGS OF INCREASE RISK TO CJD FROM CERVID
BSE INQUIRY
CJD9/10022
October 1994
Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane
BerksWell Coventry CV7 7BZ
Dear Mr Elmhirst,
CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT
Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.
The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended.. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.
The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.
The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.
I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.
THURSDAY, FEBRUARY 28, 2019
BSE infectivity survives burial for five years with only limited spread
SATURDAY, MARCH 2, 2019
MAD COW TSE PRION DISEASE AND THE PEER REVIEW PROCESS OF BSe Science $$$
MONDAY, FEBRUARY 25, 2019
MAD DOGS AND ENGLISHMEN BSE, SCRAPIE, CWD, CJD, TSE PRION A REVIEW 2019
Saturday, December 15, 2018
***> ADRD Summit RFI Singeltary COMMENT SUBMISSION BSE, SCRAPIE, CWD, AND HUMAN TSE PRION DISEASE December 14, 2018
SATURDAY, JANUARY 5, 2019
Low levels of classical BSE infectivity in rendered fat tissue
***> FRIDAY, DECEMBER 14, 2018 MAD COW USA FLASHBACK Texas Style
FRIDAY DECEMBER 14, 2018
THURSDAY, JANUARY 3, 2019
MAD COW USDA DISEASE BSE TSE Prion
THURSDAY, OCTOBER 22, 2015
Former Ag Secretary Ann Veneman talks women in agriculture and we talk mad cow disease USDA and what really happened
HOW TO COVER UP MAD COW DISEASE IN TEXAS
WEDNESDAY, AUGUST 29, 2018
OIE Bovine spongiform encephalopathy, United States of America Information received on 29/08/2018 from Dr John Clifford, Official Delegate, Chief Trade Advisor, APHIS USDA
''The event is resolved. No more reports will be submitted.''
well, so much for those herd mates exposed to this atypical BSE cow, and all those trace in and trace outs.
The OIE, USDA, and the BSE MRR policy is a joke, a sad, very sad joke...
Wednesday, January 23, 2019
CFIA SFCR Guidance on Specified risk material (SRM) came into force on January 15, 2019
ONE DECADE POST MAD COW FEED BAN OF AUGUST 1997...2007
2007
10,000,000 POUNDS REASON Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II PRODUCT
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007 CODE Cattle feed delivered between 01/12/2007 and 01/26/2007 RECALLING FIRM/MANUFACTURER Pfeiffer, Arno, Inc, Greenbush,
WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON Blood meal used to make cattle feed was recalled because it was cross- contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE 42,090 lbs. DISTRIBUTION WI
___________________________________
PRODUCT Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot- Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI - 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J - PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A- BYPASS ML W/SMARTA, Recall # V-025-2007
CODE The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007.
Firm initiated recall is complete.
REASON Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE 9,997,976 lbs. DISTRIBUTION ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
PAGE NOT FOUND
ALABAMA MAD COW FEED IN COMMERCE 2006
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6;
d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;
e) "Big Jim’s" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6
CODE
Product manufactured from 02/01/2005 until 06/06/2006
RECALLING FIRM/MANUFACTURER
Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.
REASON
Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE
125 tons
DISTRIBUTION
AL and FL
______________________________
PRODUCT
Bulk custom dairy feds manufactured from concentrates, Recall # V-113-6
CODE
All dairy feeds produced between 2/1/05 and 6/16/06 and containing H. J. Baker recalled feed products.
RECALLING FIRM/MANUFACTURER
Vita Plus Corp., Gagetown, MI, by visit beginning on June 21, 2006. Firm initiated recall is complete.
REASON
The feed was manufactured from materials that may have been contaminated with mammalian protein.
VOLUME OF PRODUCT IN COMMERCE
27,694,240 lbs
DISTRIBUTION
MI
______________________________
PRODUCT
Bulk custom made dairy feed, Recall # V-114-6
CODE
None
RECALLING FIRM/MANUFACTURER
Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006. Firm initiated recall is ongoing.
REASON
Custom made feeds contain ingredient called Pro-Lak, which may contain ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE
?????
DISTRIBUTION
KY
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
=====
PRODUCT
Bulk Whole Barley, Recall # V-256-2009
CODE
No code or lot number.
RECALLING FIRM/MANUFACTURER
Mars Petcare US, Clinton, OK, by telephone on May 21, 2009. Firm initiated recall is complete.
REASON
Product may have contained prohibited materials without cautionary statement on the label.
VOLUME OF PRODUCT IN COMMERCE
208,820 pounds
DISTRIBUTION
TX
END OF ENFORCEMENT REPORT FOR AUGUST 26, 2009
###
Subject: MAD COW FEED RECALL KY VOLUME OF PRODUCT IN COMMERCE ?????
Date: August 6, 2006 at 6:19 pm PST
PRODUCT Bulk custom made dairy feed, Recall # V-114-6
CODE None
RECALLING FIRM/MANUFACTURER Burkmann Feeds LLC, Glasgow, KY, by letter on July 14, 2006.
Firm initiated recall is ongoing. REASON Custom made feeds contain ingredient called Pro-Lak, which may contain ruminant derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE ?????
DISTRIBUTION KY
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248.128.67
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;
b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;
c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;
d) Feather Meal, Recall # V-082-6
CODE a) Bulk b) None c) Bulk d) Bulk
RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006.
Firm initiated recall is ongoing.
REASON Possible contamination of animal feeds with ruminent derived meat and bone meal..
VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons
DISTRIBUTION Nationwide
END OF ENFORCEMENT REPORT FOR July 12, 2006
###
Subject: MAD COW FEED BAN WARNING LETTER ISSUED MAY 17, 2006
Date: June 27, 2006 at 7:42 am PST Public Health Service Food and Drug Administration
New Orleans District 297 Plus Park Blvd. Nashville, TN 37217
Telephone: 615-781-5380 Fax: 615-781-5391
May 17, 2006
WARNING LETTER NO.. 2006-NOL-06
FEDERAL EXPRESS OVERNIGHT DELIVERY
Mr. William Shirley, Jr., Owner Louisiana.DBA Riegel By-Products 2621 State Street Dallas, Texas 75204
Dear Mr. Shirley:
On February 12, 17, 21, and 22, 2006, a U.S. Food & Drug Administration (FDA) investigator inspected your rendering plant, located at 509 Fortson Street, Shreveport, Louisiana. The inspection revealed significant deviations from the requirements set forth in Title 21, Code of Federal Regulations, Part 589.2000 [21 CFR 589.2000], Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE). You failed to follow the requirements of this regulation; products being manufactured and distributed by your facility are misbranded within the meaning of Section 403(a)(1) [21 USC 343(a)(1)] of the Federal Food, Drug, and Cosmetic Act (the Act).
Our investigation found you failed to provide measures, including sufficient written procedures, to prevent commingling or cross-contamination and to maintain sufficient written procedures [21 CFR 589.2000(e)] because:
You failed to use clean-out procedures or other means adequate to prevent carryover of protein derived from mammalian tissues into animal protein or feeds which may be used for ruminants. For example, your facility uses the same equipment to process mammalian and poultry tissues. However, you use only hot water to clean the cookers between processing tissues from each species. You do not clean the auger, hammer mill, grinder, and spouts after processing mammalian tissues.
You failed to maintain written procedures specifying the clean-out procedures or other means to prevent carryover of protein derived from mammalian tissues into feeds which may be used for ruminants.
As a result . the poultry meal you manufacture may contain protein derived from mammalian tissues prohibited in ruminant feed. Pursuant to 21 CFR 589.2000(e)(1)(i), any products containing or may contain protein derived from mammalian tissues must be labeled, "Do not feed to cattle or other ruminants." Since you failed to label a product which may contain protein derived from mammalian tissues with the required cautionary statement. the poultry meal is misbranded under Section 403(a)(1) [21 USC 343(a)(1)] of the Act.
This letter is not intended as an all-inclusive list of violations at your facility. As a manufacturer of materials intended for animal feed use, you are responsible for ensuring your overall operation and the products you manufacture and distribute are in compliance with the law. You should take prompt action to correct these violations, and you should establish a system whereby violations do not recur. Failure to promptly correct these violations may result in regulatory action, such as seizure and/or injunction, without further notice.
You should notify this office in writing within 15 working days of receiving this letter, outlining the specific steps you have taken to bring your firm into compliance with the law. Your response should include an explanation of each step taken to correct the violations and prevent their recurrence. If corrective action cannot be completed within 15 working days, state the reason for the delay and the date by which the corrections will be completed. Include copies of any available documentation demonstrating corrections have been made.
Your reply should be directed to Mark W. Rivero, Compliance Officer, U.S. Food and Drug Administration, 2424 Edenborn Avenue, Suite 410, Metairie, Louisiana 70001. If you have questions regarding any issue in this letter, please contact Mr. Rivero at (504) 219-8818, extension 103.
Sincerely,
/S
Carol S. Sanchez Acting District Director New Orleans District
PLEASE NOTE, THE FDA URLS FOR OLD WARNING LETTERS ARE OBSOLETE AND DO NOT WORK IN MOST CASES.. I LOOKED UP THE OLD ONE ABOVE AND FOUND IT, BUT HAVE NOT DONE THAT FOR THE OTHERS TO FOLLOW. THE DATA IS VALID THOUGH!
Subject: MAD COW PROTEIN IN COMMERCE USA 2006 RECALL UPDATE
From: "Terry S. Singeltary Sr." <[log in to unmask]>
Reply-To: SAFETY <[log in to unmask]>
Date: Mon, 9 Oct 2006 14:10:37 -0500
Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS
IN COMMERCE AL, TN, AND WV
Date: September 6, 2006 at 7:58 am PST
PRODUCT a) EVSRC Custom dairy feed, Recall # V-130-6; b) Performance Chick Starter, Recall # V-131-6; c) Performance Quail Grower, Recall # V-132-6; d) Performance Pheasant Finisher, Recall # V-133-6. CODE None RECALLING FIRM/MANUFACTURER Donaldson & Hasenbein/dba J&R Feed Service, Inc., Cullman, AL, by telephone on June 23, 2006 and by letter dated July 19, 2006.
Firm initiated recall is complete.
REASON Dairy and poultry feeds were possibly contaminated with ruminant based protein.
VOLUME OF PRODUCT IN COMMERCE 477.72 tons
DISTRIBUTION AL
______________________________
snip...
Subject: MAD COW FEED RECALLS ENFORCEMENT REPORT FOR AUGUST 9, 2006 KY, LA, MS, AL, GA, AND TN 11,000+ TONS
Date: August 16, 2006 at 9:19 am PST RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II
______________________________
snip...
______________________________
PRODUCT Bulk custom dairy pre-mixes, Recall # V-120-6
CODE None
RECALLING FIRM/MANUFACTURER Ware Milling Inc., Houston, MS, by telephone on June 23, 2006. Firm initiated recall is complete.
REASON Possible contamination of dairy animal feeds with ruminant derived meat and bone meal..
VOLUME OF PRODUCT IN COMMERCE 350 tons DISTRIBUTION AL and MS
______________________________
PRODUCT
a) Tucker Milling, LLC Tm 32% Sinking Fish Grower, #2680-Pellet, 50 lb. bags, Recall # V-121-6;
b) Tucker Milling, LLC #31120, Game Bird Breeder Pellet, 50 lb. bags, Recall # V-122-6;
c) Tucker Milling, LLC #31232 Game Bird Grower, 50 lb. bags, Recall # V-123-6;
d) Tucker Milling, LLC 31227-Crumble, Game Bird Starter, BMD Medicated, 50 lb bags, Recall # V-124-6;
e) Tucker Milling, LLC #31120, Game Bird Breeder, 50 lb bags, Recall # V-125-6;
f) Tucker Milling, LLC #30230, 30 % Turkey Starter, 50 lb bags, Recall # V-126-6;
g) Tucker Milling, LLC #30116, TM Broiler Finisher, 50 lb bags, Recall # V-127-6
CODE All products manufactured from 02/01/2005 until 06/20/2006
RECALLING FIRM/MANUFACTURER Recalling Firm: Tucker Milling LLC, Guntersville, AL, by telephone and visit on June 20, 2006, and by letter on June 23, 2006. Manufacturer: H. J. Baker and Brothers Inc., Stamford, CT. Firm initiated recall is ongoing.
REASON Poultry and fish feeds which were possibly contaminated with ruminant based protein were not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 7,541-50 lb bags
DISTRIBUTION AL, GA, MS, and TN
END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006
###
Subject: MAD COW FEED RECALL AL AND FL VOLUME OF PRODUCT IN COMMERCE 125 TONS
Products manufactured from 02/01/2005 until 06/06/2006
Date: August 6, 2006 at 6:16 pm PST
PRODUCT
a) CO-OP 32% Sinking Catfish, Recall # V-100-6;
b) Performance Sheep Pell W/Decox/A/N, medicated, net wt. 50 lbs, Recall # V-101-6;
c) Pro 40% Swine Conc Meal -- 50 lb, Recall # V-102-6; d) CO-OP 32% Sinking Catfish Food Medicated, Recall # V-103-6;
e) "Big Jim's" BBB Deer Ration, Big Buck Blend, Recall # V-104-6;
f) CO-OP 40% Hog Supplement Medicated Pelleted, Tylosin 100 grams/ton, 50 lb. bag, Recall # V-105-6;
g) Pig Starter Pell II, 18% W/MCDX Medicated 282020, Carbadox -- 0.0055%, Recall # V-106-6;
h) CO-OP STARTER-GROWER CRUMBLES, Complete Feed for Chickens from Hatch to 20 Weeks, Medicated, Bacitracin Methylene Disalicylate, 25 and 50 Lbs, Recall # V-107-6;
i) CO-OP LAYING PELLETS, Complete Feed for Laying Chickens, Recall # 108-6;
j) CO-OP LAYING CRUMBLES, Recall # V-109-6;
k) CO-OP QUAIL FLIGHT CONDITIONER MEDICATED, net wt 50 Lbs, Recall # V-110-6;
l) CO-OP QUAIL STARTER MEDICATED, Net Wt. 50 Lbs, Recall # V-111-6;
m) CO-OP QUAIL GROWER MEDICATED, 50 Lbs, Recall # V-112-6
CODE
Product manufactured from 02/01/2005 until 06/06/2006 RECALLING FIRM/MANUFACTURER Alabama Farmers Cooperative, Inc., Decatur, AL, by telephone, fax, email and visit on June 9, 2006. FDA initiated recall is complete.
REASON Animal and fish feeds which were possibly contaminated with ruminant based protein not labeled as "Do not feed to ruminants".
VOLUME OF PRODUCT IN COMMERCE 125 tons DISTRIBUTION AL and FL
END OF ENFORCEMENT REPORT FOR AUGUST 2, 2006
###
MAD COW FEED RECALL USA EQUALS 10,878.06 TONS NATIONWIDE Sun Jul 16, 2006 09:22 71.248..128.67
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE -- CLASS II
______________________________
PRODUCT
a) PRO-LAK, bulk weight, Protein Concentrate for Lactating Dairy Animals, Recall # V-079-6;
b) ProAmino II, FOR PREFRESH AND LACTATING COWS, net weight 50lb (22.6 kg), Recall # V-080-6;
c) PRO-PAK, MARINE & ANIMAL PROTEIN CONCENTRATE FOR USE IN ANIMAL FEED, Recall # V-081-6;
d) Feather Meal, Recall # V-082-6
CODE a) Bulk b) None c) Bulk d) Bulk
RECALLING FIRM/MANUFACTURER H. J. Baker & Bro., Inc., Albertville, AL, by telephone on June 15, 2006 and by press release on June 16, 2006.
Firm initiated recall is ongoing.
REASON Possible contamination of animal feeds with ruminent derived meat and bone meal.
VOLUME OF PRODUCT IN COMMERCE 10,878.06 tons
DISTRIBUTION Nationwide
END OF ENFORCEMENT REPORT FOR July 12, 2006
###
Product Details
Product Description:
CalDensity Black Label, CalDensity White Label with HA, packaged in white plastic 5, 15, 25, 40, 60 lb pails with plastic liner and white plastic lid. Reason for Recall:
During an FDA inspection it was found that the CalDensity Black label and CalDensity White Label with HA product containers did not include the precautionary statement DO NOT FEED TO CATTLE OR OTHER RUMINANTS
Product Quantity: 50,935 lbs
Recall Number: V-209-2012
Code Information: 042009, 051009, 061209, 071509, 091009, 011510, 030310, 031610, 052610, 092410, 120110, 011211, 020111, 030911, 050111, 071111 & 090111. Classification: Class II Event Details
Event ID: 61880
Voluntary / Mandated:
Voluntary: Firm Initiated
Product Type:
Veterinary
Initial Firm Notification of Consignee or Public:
E-Mail
Status:
Terminated
Distribution Pattern:
Nationwide distribution: AL, AR, AZ, CA, CO, FL, GA, IA, ID, IL, KY, LA, MD, MI, MN, MO, MS, NC, NE, NJ, NM, NY, OH, OK, PA, SC, TX, UT, VA, WA & WV. No shipments were made to foreign countries including Canada.
Recalling Firm:
Process Managers LLC
485 Gawthrope Dr
Winchester, KY 40391-8910
United States
Recall Initiation Date:
1/6/2012
Center Classification Date:
9/7/2012
Date Terminated:
1/24/2014
Product Details
Product Description:
Regular Chicken 50# Ingredients: Corn, Wheat, Oats, Oyster shells, Medium Grit, CCC, ADS, Plant Protein Products, Animal Protein Products, Processed Grain By-Products, Roughage Products, Animal Fat procession with DHA, etc
Reason for Recall:
During an FDA sample collection, the firms 50# Regular Chicken Feed was found to contain mammalian protein. The label does not contain the warning statement.
Product Quantity:
5400lbs (50lb bags)
Recall Number:
V-137-2013
Code Information:
8/6/2012
Classification:
Class III
Event Details
Event ID:
63743
Voluntary / Mandated:
Voluntary: Firm Initiated
Product Type:
Veterinary
Initial Firm Notification of Consignee or Public:
Other
Status:
Terminated
Distribution Pattern:
Midland MI area only.
Recalling Firm:
Cohoons Elevator Inc.
802 Townsend St
Midland, MI 48640-5362
United States
Recall Initiation Date:
11/21/2012
Center Classification Date:
2/8/2013
Date Terminated:
2/12/2013
V. Use in animal feed of material from deer and elk NOT considered at high risk for CWD
FDA continues to consider materials from deer and elk NOT considered at high risk for CWD to be acceptable for use in NON-RUMINANT animal feeds in accordance with current agency regulations, 21 CFR 589.2000.
Deer and elk not considered at high risk include:
(1) deer and elk from areas not declared by State officials to be endemic for CWD and/or to be CWD eradication zones; and
(2) deer and elk that were not at some time during the 60-month period immediately before the time of slaughter in a captive herd that contained a CWD-positive animal.
2017 Section 21 C.F.R. 589.2000, Animal Proteins Prohibited in Ruminant Feed
Subject: MICHIGAN FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE BREACH APRIL 4, 2017
MICHIGAN FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE BREACH APRIL 4, 2017
FDA BSE/Ruminant Feed Inspections Firms Inventory
11998 DET-DO MI 48846-847 OPR 4/4/2017 OAI
http://www.accessdata.fda.gov/scripts/BSEInspect/bseinspections.csv
NAI = NO ACTION INDICATED
OAI = OFFICIAL ACTION INDICATED
VAI = VOLUNTARY ACTION INDICATED
RTS = REFERRED TO STATE
OAI (Official Action Indicated) when inspectors find significant objectionable conditions or practices and believe that regulatory sanctions are warranted to address the establishment’s lack of compliance with the regulation. An example of an OAI classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not contaminated with prohibited material. Inspectors will promptly re-inspect facilities classified OAI after regulatory sanctions have been applied to determine whether the corrective actions are adequate to address the objectionable conditions...end...TSS
TUESDAY, APRIL 18, 2017
*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***
TUESDAY, JANUARY 17, 2017
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION
FY 2016 Inspectional Observation Summaries
4132 21 CFR 589.2000(d)(1) Protein blenders, feed manufacturers, distributors Products that contain or may contain prohibited material fail to bear the caution statement, "Do not feed to cattle or other ruminants." Specifically, *** 2
4131 21 CFR 589.2000(c)(1)(i) Renderers Products that contain or may contain prohibited material fail to bear a label containing the caution statement, "Do not feed to cattle or other ruminants." Specifically, *** 1
FY 2015 Inspectional Observation Summaries
4132 21 CFR 589.2000(d)(1) Protein blenders, feed manufacturers, distributors Products that contain or may contain prohibited material fail to bear the caution statement, "Do not feed to cattle or other ruminants." Specifically, *** 2
FY 2014 Inspectional Observation Summaries
4146 21 CFR 589.2000(e)(1) Written clean-out procedures Failure to maintain written clean-out procedures to prevent carryover of protein derived from mammalian tissues to animal protein or feeds that may be used for ruminants. Specifically, *** 2
4131 21 CFR 589.2000(c)(1)(i) Renderers Products that contain or may contain prohibited material fail to bear a label containing the caution statement, "Do not feed to cattle or other ruminants." Specifically, *** 1
4132 21 CFR 589.2000(d)(1) Protein blenders, feed manufacturers, distributors Products that contain or may contain prohibited material fail to bear the caution statement, "Do not feed to cattle or other ruminants." Specifically, *** 1
4145 21 CFR 589.2000(e)(1) Use of clean-out procedures Failure to use clean-out procedures or other means adequate to prevent carryover of protein derived from mammalian tissues to animal protein or feeds that may be used for ruminants. Specifically, *** 1
FY 2013 Inspectional Observation Summaries
4131 21 CFR 589.2000(c)(1)(i) 5 Renderers Products that contain or may contain prohibited material fail to bear a label containing the caution statement, "Do not feed to cattle or other ruminants." Specifically, ***
4132 21 CFR 589.2000(d)(1) 5 Protein blenders, feed manufacturers, distributors Products that contain or may contain prohibited material fail to bear the caution statement, "Do not feed to cattle or other ruminants." Specifically, ***
4145 21 CFR 589.2000(e)(1) 1 Use of clean-out procedures Failure to use clean-out procedures or other means adequate to prevent carryover of protein derived from mammalian tissues to animal protein or feeds that may be used for ruminants. Specifically, ***
4146 21 CFR 589.2000(e)(1) 1 Written clean-out procedures Failure to maintain written clean-out procedures to prevent carryover of protein derived from mammalian tissues to animal protein or feeds that may be used for ruminants. Specifically, ***
FY 2012 Inspectional Observation Summaries
4131 21 CFR 589.2000(c)(1)(i) 5 Renderers Products that contain or may contain prohibited material fail to bear a label containing the caution statement, "Do not feed to cattle or other ruminants." Specifically, ***
4132 21 CFR 589.2000(d)(1) 4 Protein blenders, feed manufacturers, distributors Products that contain or may contain prohibited material fail to bear the caution statement, "Do not feed to cattle or other ruminants." Specifically, ***
FY 2011 Inspectional Observation Summaries
4132 21 CFR 589.2000(d)(1) 5 Protein blenders, feed manufacturers, distributors Products that contain or may contain prohibited material fail to bear the caution statement, "Do not feed to cattle or other ruminants."Specifically, ***
4131 21 CFR 589.2000(c)(1)(i) 4 Renderers Products that contain or may contain prohibited material fail to bear a label containing the caution statement, "Do not feed to cattle or other ruminants."Specifically, ***
4146 21 CFR 589.2000(e)(1) 1 Written clean-out procedures Failure to maintain written clean-out procedures to prevent carryover of protein derived from mammalian tissues to animal protein or feeds that may be used for ruminants. Specifically, ***
FY 2010 Inspectional Observation Summaries
4131 21 CFR 589.2000(c)(1)(i) 3 Renderers Products that contain or may contain prohibited material fail to bear a label containing the caution statement, "Do not feed to cattle or other ruminants." Specifically, *** 4132 21 CFR 589.2000(d)(1) 3 Protein blenders, feed manufacturers, distributors Products that contain or may contain prohibited material fail to bear the caution statement, "Do not feed to cattle or other ruminants." Specifically, ***
4146 21 CFR 589.2000(e)(1) 1 Written clean-out procedures Failure to maintain written clean-out procedures to prevent carryover of protein derived from mammalian tissues to animal protein or feeds that may be used for ruminants. Specifically, ***
FY 2009 Inspectional Observation Summaries
4132 21 CFR 589.2000(d)(1) 10 Protein blenders, feed manufacturers, distributors Products that contain or may contain prohibited material fail to bear the caution statement, "Do not feed to cattle or other ruminants." Specifically, ***
4146 21 CFR 589.2000(e)(1) 4 Written clean-out procedures Failure to maintain written clean-out procedures to prevent carryover of protein derived from mammalian tissues to animal protein or feeds that may be used for ruminants. Specifically, ***
4145 21 CFR 589.2000(e)(1) 3 Use of clean-out procedures Failure to use clean-out procedures or other means adequate to prevent carryover of protein derived from mammalian tissues to animal protein or feeds that may be used for ruminants. Specifically, ***
FY 2008 Inspectional Observation Summaries
4132 21 CFR 589.2000(d)(1) 7 Protein blenders, feed manufacturers, distributors Products that contain or may contain prohibited material fail to bear the caution statement, "Do not feed to cattle or other ruminants." Specifically, ***
4145 21 CFR 589.2000(e)(1) 1 Use of clean-out procedures Failure to use clean-out procedures or other means adequate to prevent carryover of protein derived from mammalian tissues to animal protein or feeds that may be used for ruminants. Specifically, *** 4146 21 CFR 589.2000(e)(1) 1 Written clean-out procedures Failure to maintain written clean-out procedures to prevent carryover of protein derived from mammalian tissues to animal protein or feeds that may be used for ruminants. Specifically, ***
FY 2007 Inspectional Observation Summaries
4132 21 CFR 589.2000(d)(1) 3 Protein blenders, feed manufacturers, distributors Products that contain or may contain prohibited material fail to bear the caution statement, "Do not feed to cattle or other ruminants." Specifically, ***
4146 21 CFR 589.2000(e)(1) 3 Written clean-out procedures Failure to maintain written clean-out procedures to prevent carryover of protein derived from mammalian tissues to animal protein or feeds that may be used for ruminants. Specifically, ***
4131 21 CFR 589.2000(c)(1)(i) 2 Renderers Products that contain or may contain prohibited material fail to bear a label containing the caution statement, "Do not feed to cattle or other ruminants." Specifically, ***
4145 21 CFR 589.2000(e)(1) 1 Use of clean-out procedures Failure to use clean-out procedures or other means adequate to prevent carryover of protein derived from mammalian tissues to animal protein or feeds that may be used for ruminants. Specifically, ***
FY 2006 Inspectional Observation Summaries
4132 21 CFR 589.2000(d)(1) 6 Protein blenders, feed manufacturers, distributors Products that contain or may contain prohibited material fail to bear the caution statement, "Do not feed to cattle or other ruminants."Specifically, ***
4146 21 CFR 589.2000(e)(1) 5 Written clean-out procedures Failure to maintain written clean-out procedures to prevent carryover of protein derived from mammalian tissues to animal protein or feeds that may be used for ruminants. Specifically, ***
4145 21 CFR 589.2000(e)(1) 4 Use of clean-out procedures Failure to use clean-out procedures or other means adequate to prevent carryover of protein derived from mammalian tissues to animal protein or feeds that may be used for ruminants. Specifically, ***
4131 21 CFR 589.2000(c)(1)(i) 2 Renderers Products that contain or may contain prohibited material fail to bear a label containing the caution statement, "Do not feed to cattle or other ruminants." Specifically, ***
*** PLEASE SEE THIS URGENT UPDATE ON CWD AND FEED ANIMAL PROTEIN ***
Sunday, March 20, 2016
Docket No. FDA-2003-D-0432 (formerly 03D-0186) Use of Material from Deer and Elk in Animal Feed ***UPDATED MARCH 2016*** Singeltary Submission
SEE MAD COW FEED VIOLATIONS AFER MAD COW FEED VIOLATIONS ;
Tuesday, April 19, 2016
Docket No. FDA-2013-N-0764 for Animal Feed Regulatory Program Standards Singeltary Comment Submission
17 years post mad cow feed ban August 1997
Monday, October 26, 2015
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE October 2015
Tuesday, December 23, 2014
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2014 BSE TSE PRION
16 years post mad cow feed ban August 1997 2013
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
Saturday, August 29, 2009
FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009
Friday, September 4, 2009
FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009
Thursday, March 19, 2009
MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA WITH ONGOING 12 YEARS OF DENIAL NOW, WHY IN THE WORLD DO WE TO TALK ABOUT THIS ANYMORE $$$
Office of Inspector General Semiannual Report to Congress FY 2007 - 2nd Half
Two Texas Companies Sentenced and Fined for Misbranding Meat Products In April 2007, two closely held and related Texas companies pled guilty in Federal court and were sentenced to 12 months of probation and ordered to pay $10,250 in fines for misbranding meat products. One of the companies sold adulterated meat products to a retail store in New Mexico. Additionally, portions of the invoices failed to properly and consistently identify the meat products as being from cattle more than 30 months old at time of slaughter. This information is required to be disclosed because of bovine spongiform encephalopathy (BSE, or "mad cow disease") concerns. No adulterated meat reached consumers.
THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ;
CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006
In an article today for United Press International, science reporter Steve Mitchell writes:
Analysis: What that mad cow means
By STEVE MITCHELL UPI Senior Medical Correspondent
WASHINGTON, March 15 (UPI) -- The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.
The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.
These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.
"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."
Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.
USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.
"Everything they did on the Texas cow makes everything they did before 2005 suspect," Brown said.
Despite this, Brown said the U.S. prevalence of mad cow, formally known as bovine spongiform encephalopathy, or BSE, did not significantly threaten human or cattle health.
"Overall, my view is BSE is highly unlikely to pose any important risk either in cattle feed or human feed," he said.
However, Jean Halloran of Consumers Union in Yonkers, N.Y., said consumers should be troubled by the USDA's secrecy and its apparent plan to dramatically cut back the number of mad cow tests it conducts.
"Consumers should be very concerned about how little we know about the USDA's surveillance program and the failure of the USDA to reveal really important details," Halloran told UPI. "Consumers have to be really concerned if they're going to cut back the program," she added.
Last year the USDA tested more than 300,000 animals for the disease, but it has proposed, even in light of a third case, scaling back the program to 40,000 tests annually.
"They seem to be, in terms of actions and policies, taking a lot more seriously the concerns of the cattle industry than the concerns of consumers," Halloran said. "It's really hard to know what it takes to get this administration to take action to protect the public."
The USDA has insisted that the safeguards of a ban on incorporating cow tissue into cattle feed (which is thought to spread the disease) and removal of the most infectious parts of cows, such as the brain and spinal cord, protect consumers. But the agency glosses over the fact that both of these systems have been revealed to be inadequately implemented.
The feed ban, which is enforced by the Food and Drug Administration, has been criticized by the Government Accountability Office in two reports, the most recent coming just last year. The GAO said the FDA's enforcement of the ban continues to have weaknesses that "undermine the nation's firewall against BSE."
USDA documents released last year showed more than 1,000 violations of the regulations requiring the removal of brains and spinal cords in at least 35 states, Puerto Rico and the Virgin Islands, with some plants being cited repeatedly for infractions. In addition, a violation of similar regulations that apply to beef exported to Japan is the reason why Japan closed its borders to U.S. beef in January six weeks after reopening them.
Other experts also question the adequacy of the USDA's surveillance system. The USDA insists the prevalence of mad cow disease is low, but the agency has provided few details of its surveillance program, making it difficult for outside experts to know if the agency's monitoring plan is sufficient.
"It's impossible to judge the adequacy of the surveillance system without having a breakdown of the tested population by age and risk status," Elizabeth Mumford, a veterinarian and BSE expert at Safe Food Solutions in Bern, Switzerland, a company that provides advice on reducing mad cow risk to industry and governments, told UPI.
"Everybody would be happier and more confident and in a sense it might be able to go away a little bit for (the USDA) if they would just publish a breakdown on the tests," Mumford added.
UPI requested detailed records about animals tested under the USDA's surveillance plan via the Freedom of Information Act in May 2004 but nearly two years later has not received any corresponding documents from the agency, despite a federal law requiring agencies to comply within 30 days. This leaves open the question of whether the USDA is withholding the information, does not have the information or is so haphazardly organized that it cannot locate it.
Mumford said the prevalence of the disease in U.S. herds is probably quite low, but there have probably been other cases that have so far gone undetected. "They're only finding a very small fraction of that low prevalence," she said.
Mumford expressed surprise at the lack of concern about the deadly disease from American consumers. "I would expect the U.S. public to be more concerned," she said.
Markus Moser, a molecular biologist and chief executive officer of Prionics, a Swiss firm that manufactures BSE test kits, told UPI one concern is that if people are infected, the mad cow pathogen could become "humanized" or more easily transmitted from person to person.
"Transmission would be much easier, through all kinds of medical procedures" and even through the blood supply, Moser said.
© Copyright 2006 United Press International, Inc. All Rights Reserved
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency." ........TSS
Subject: USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half (bogus BSE sampling FROM HEALTHY USDA CATTLE)
Date: June 21, 2007 at 2:49 pm PST
Owner and Corporation Plead Guilty to Defrauding Bovine Spongiform Encephalopathy (BSE) Surveillance Program
An Arizona meat processing company and its owner pled guilty in February 2007 to charges of theft of Government funds, mail fraud, and wire fraud. The owner and his company defrauded the BSE Surveillance Program when they falsified BSE Surveillance Data Collection Forms and then submitted payment requests to USDA for the services. In addition to the targeted sample population (those cattle that were more than 30 months old or had other risk factors for BSE), the owner submitted to USDA, or caused to be submitted, BSE obex (brain stem) samples from healthy USDA-inspected cattle. As a result, the owner fraudulently received approximately $390,000. Sentencing is scheduled for May 2007.
snip...
Topics that will be covered in ongoing or planned reviews under Goal 1 include:
soundness of BSE maintenance sampling (APHIS),
implementation of Performance-Based Inspection System enhancements for specified risk material (SRM) violations and improved inspection controls over SRMs (FSIS and APHIS),
snip...
The findings and recommendations from these efforts will be covered in future semiannual reports as the relevant audits and investigations are completed.
4 USDA OIG SEMIANNUAL REPORT TO CONGRESS FY 2007 1st Half
OR, what the Honorable Phyllis Fong of the OIG found ;
Audit Report Animal and Plant Health Inspection Service Bovine Spongiform Encephalopathy (BSE) Surveillance Program  Phase II and Food Safety and Inspection Service
Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III
Report No. 50601-10-KC January 2006
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain
TUESDAY, JANUARY 17, 2017
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION
Thursday, November 16, 2017
Texas Natural Meats Recalls Beef Products Due To Possible Specified Risk Materials Contamination
PAGE NOT FOUND
IF you will notice, archived information has now been deleted before 2008. please be aware, 2006 was a banner year for tons and tons of banned mad cow protein fed out into commerce. i have some archived, but not all. the mad cow feed ban by the FDA et al was and is nothing but ink on paper...terry
TUESDAY, JANUARY 17, 2017
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEEDVIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE 2016 to 2017 BSE TSE PRION
FRIDAY, NOVEMBER 3, 2017
BSE MAD COW TSE PRION DISEASE PET FOOD FEED IN COMMERCE INDUSTRY VS TERRY S. SINGELTARY Sr. A REVIEW
''I have a neighbor who is a dairy farmer. He tells me that he knows of several farmers who feed their cattle expired dog food. These farmers are unaware of any dangers posed to their cattle from the pet food contents. For these farmers, the pet food is just another source of protein.''
IN CONFIDENCE
2017
FRIDAY, DECEMBER 22, 2017
Detection of PrPBSE and prion infectivity in the ileal Peyer’s patch of young calves as early as 2 months after oral challenge with classical bovine spongiform encephalopathy
WEDNESDAY, OCTOBER 4, 2017
EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR) of the United States of America (USA) a review 2017
TUESDAY, JULY 18, 2017
***> USDA announces Alabama case of Bovine Spongiform Encephalopathy Alabama
THURSDAY, JULY 20, 2017
***> USDA OIE Alabama Atypical L-type BASE Bovine Spongiform Encephalopathy BSE animal feeds for ruminants rule, 21 CFR 589..200
SUNDAY, JULY 23, 2017
***> atypical L-type BASE Bovine Amyloidotic Spongiform Encephalopathy BSE TSE PRION
SUNDAY, JULY 23, 2017
***> Experimental Infection of Cattle With a Novel Prion Derived From Atypical H-Type Bovine Spongiform Encephalopathy
''Atypical BSE is different, and it generally occurs in older cattle, usually 8 years of age or greater. It seems to arise rarely and spontaneously in all cattle populations.''
FALSE!
''The primary source of infection for classical BSE is feed contaminated with the infectious prion agent, such as meat-and-bone meal containing protein derived from rendered infected cattle. Regulations from the Food and Drug Administration (FDA) have prohibited the inclusion of mammalian protein in feed for cattle and other ruminants since 1997 and have also prohibited high risk tissue materials in all animal feed since 2009.''
FALSE!
oh what webs of deceit we weave, when all we do is practice to deceive $$$
LET'S REVIEW RECENT AND PAST SCIENCE THAT SHOWS THE ABOVE TWO STATEMENTS ARE FAR FROM TRUE;
PRION 2018 CONFERENCE
P98 The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge
Greenlee JJ (1), Moore SJ (1), and West Greenlee MH (2) (1) United States Department of Agriculture, Agricultural Research Service, National Animal Disease Center, Virus and Prion Research Unit, Ames, IA, United States (2) Department of Biomedical Sciences, Iowa State University College of Veterinary Medicine, Ames, IA, United States.
reading up on this study from Prion 2018 Conference, very important findings ;
***> This study demonstrates that the H-type BSE agent is transmissible by the oronasal route.
***> These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.
PRION 2018 CONFERENCE ABSTRACT
P98 The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge Greenlee JJ (1), Moore SJ (1), and West Greenlee MH (2) (1) United States Department of Agriculture, Agricultural Research Service, National Animal Disease Center, Virus and Prion Research Unit, Ames, IA, United States (2) Department of Biomedical Sciences, Iowa State University College of Veterinary Medicine, Ames, IA, United States.
In 2006, a case of H-type bovine spongiform encephalopathy (BSE) was reported in a cow with a previously unreported prion protein polymorphism (E211K).
The E211K polymorphism is heritable and homologous to the E200K mutation in humans that is the most frequent PRNP mutation associated with familial Creutzfeldt-Jakob disease.
Although the prevalence of the E211K polymorphism is low, cattle carrying the K211 allele develop H-type BSE with a rapid onset after experimental inoculation by the intracranial route.
The purpose of this study was to investigate whether the agents of H-type BSE or H-type BSE associated with the E211K polymorphism transmit to wild type cattle or cattle with the K211 allele after oronasal exposure.
Wild type (EE211) or heterozygous (EK211) cattle were oronasally inoculated with either H-type BSE from the 2004 US Htype BSE case (n=3) or from the 2006 US H-type case associated with the E211K polymorphism (n=4) using 10% w/v brain homogenates.
Cattle were observed daily throughout the course of the experiment for the development of clinical signs.
At approximately 50 months post-inoculation, one steer (EK211 inoculated with E211K associated H-BSE) developed clinical signs including inattentiveness, loss of body condition, weakness, ataxia, and muscle fasciculations and was euthanized.
Enzyme immunoassay confirmed that abundant misfolded protein was present in the brainstem, and immunohistochemistry demonstrated PrPSc throughout the brain.
Western blot analysis of brain tissue from the clinically affected steer was consistent with the E211K H-type BSE inoculum.
With the experiment currently at 55 months post-inoculation, no other cattle in this study have developed clinical signs suggestive of prion disease. This study demonstrates that the H-type BSE agent is transmissible by the oronasal route.
These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.
WEDNESDAY, AUGUST 15, 2018
***> The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge
PLOS ONE Journal
IBNC Tauopathy or TSE Prion disease, it appears, no one is sure
Terry S. Singeltary Sr., 03 Jul 2015 at 16:53 GMT
***however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE.
***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.
*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***
http://www.plosone.org/annotation/listThread.action?root=86610
***Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.
*** IBNC Tauopathy or TSE Prion disease, it appears, no one is sure ***
http://www.plosone.org/annotation/listThread.action?root=86610
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;
MONDAY, JANUARY 09, 2017
Oral Transmission of L-Type Bovine Spongiform Encephalopathy Agent among Cattle
CDC Volume 23, Number 2—February 2017
*** Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.
*** Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.
TUESDAY, AUGUST 28, 2018
USDA finds BSE infection in Florida cow 08/28/18 6:43 PM
http://animalhealthreportpriontse..blogspot.com/2018/08/usda-finds-bse-infection-in-florida-cow.html
WEDNESDAY, AUGUST 29, 2018
USDA Announces Atypical Bovine Spongiform Encephalopathy Detection USDA 08/29/2018 10:00 AM EDT
WEDNESDAY, AUGUST 29, 2018
Transmissible Spongiform Encephalopathy TSE Prion Atypical BSE Confirmed Florida Update USA August 28, 2018
***> P.108: Successful oral challenge of adult cattle with classical BSE
Sandor Dudas1,*, Kristina Santiago-Mateo1, Tammy Pickles1, Catherine Graham2, and Stefanie Czub1 1Canadian Food Inspection Agency; NCAD Lethbridge; Lethbridge, Alberta, Canada; 2Nova Scotia Department of Agriculture; Pathology Laboratory; Truro, Nova Scotia, Canada
Classical Bovine spongiform encephalopathy (C-type BSE) is a feed- and food-borne fatal neurological disease which can be orally transmitted to cattle and humans. Due to the presence of contaminated milk replacer, it is generally assumed that cattle become infected early in life as calves and then succumb to disease as adults. Here we challenged three 14 months old cattle per-orally with 100 grams of C-type BSE brain to investigate age-related susceptibility or resistance. During incubation, the animals were sampled monthly for blood and feces and subjected to standardized testing to identify changes related to neurological disease. At 53 months post exposure, progressive signs of central nervous system disease were observed in these 3 animals, and they were euthanized. Two of the C-BSE animals tested strongly positive using standard BSE rapid tests, however in 1 C-type challenged animal, Prion 2015 Poster Abstracts S67 PrPsc was not detected using rapid tests for BSE. Subsequent testing resulted in the detection of pathologic lesion in unusual brain location and PrPsc detection by PMCA only.
***Our study demonstrates susceptibility of adult cattle to oral transmission of classical BSE.
We are further examining explanations for the unusual disease presentation in the third challenged animal.
***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
P.86: Estimating the risk of transmission of BSE and scrapie to ruminants and humans by protein misfolding cyclic amplification
Morikazu Imamura, Naoko Tabeta, Yoshifumi Iwamaru, and Yuichi Murayama
National Institute of Animal Health; Tsukuba, Japan
To assess the risk of the transmission of ruminant prions to ruminants and humans at the molecular level, we investigated the ability of abnormal prion protein (PrPSc) of typical and atypical BSEs (L-type and H-type) and typical scrapie to convert normal prion protein (PrPC) from bovine, ovine, and human to proteinase K-resistant PrPSc-like form (PrPres) using serial protein misfolding cyclic amplification (PMCA).
Six rounds of serial PMCA was performed using 10% brain homogenates from transgenic mice expressing bovine, ovine or human PrPC in combination with PrPSc seed from typical and atypical BSE- or typical scrapie-infected brain homogenates from native host species. In the conventional PMCA, the conversion of PrPC to PrPres was observed only when the species of PrPC source and PrPSc seed matched. However, in the PMCA with supplements (digitonin, synthetic polyA and heparin), both bovine and ovine PrPC were converted by PrPSc from all tested prion strains. On the other hand, human PrPC was converted by PrPSc from typical and H-type BSE in this PMCA condition.
Although these results were not compatible with the previous reports describing the lack of transmissibility of H-type BSE to ovine and human transgenic mice, our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals.
P.170: Potential detection of oral transmission of H type atypical BSE in cattle using in vitro conversion
***P.170: Potential detection of oral transmission of H type atypical BSE in cattle using in vitro conversion
Sandor Dudas, John G Gray, Renee Clark, and Stefanie Czub Canadian Food Inspection Agency; Lethbridge, AB Canada
Keywords: Atypical BSE, oral transmission, RT-QuIC
The detection of bovine spongiform encephalopathy (BSE) has had a significant negative impact on the cattle industry worldwide. In response, governments took actions to prevent transmission and additional threats to animal health and food safety. While these measures seem to be effective for controlling classical BSE, the more recently discovered atypical BSE has presented a new challenge. To generate data for risk assessment and control measures, we have challenged cattle orally with atypical BSE to determine transmissibility and mis-folded prion (PrPSc) tissue distribution. Upon presentation of clinical symptoms, animals were euthanized and tested for characteristic histopathological changes as well as PrPSc deposition.
The H-type challenged animal displayed vacuolation exclusively in rostral brain areas but the L-type challenged animal showed no evidence thereof. To our surprise, neither of the animals euthanized, which were displaying clinical signs indicative of BSE, showed conclusive mis-folded prion accumulation in the brain or gut using standard molecular or immunohistochemical assays. To confirm presence or absence of prion infectivity, we employed an optimized real-time quaking induced conversion (RT-QuIC) assay developed at the Rocky Mountain Laboratory, Hamilton, USA.
Detection of PrPSc was unsuccessful for brain samples tests from the orally inoculated L type animal using the RT-QuIC. It is possible that these negative results were related to the tissue sampling locations or that type specific optimization is needed to detect PrPSc in this animal. We were however able to consistently detect the presence of mis-folded prions in the brain of the H-type inoculated animal. Considering the negative and inconclusive results with other PrPSc detection methods, positive results using the optimized RT-QuIC suggests the method is extremely sensitive for H-type BSE detection. This may be evidence of the first successful oral transmission of H type atypical BSE in cattle and additional investigation of samples from these animals are ongoing.
Detection of PrPBSE and prion infectivity in the ileal Peyer’s patch of young calves as early as 2 months after oral challenge with classical bovine spongiform encephalopathy
Ivett Ackermann1 , Anne Balkema‑Buschmann1 , Reiner Ulrich2 , Kerstin Tauscher2 , James C. Shawulu1 , Markus Keller1 , Olanrewaju I. Fatola1 , Paul Brown3 and Martin H. Groschup1*
Abstract
In classical bovine spongiform encephalopathy (C-BSE), an orally acquired prion disease of cattle, the ileal Peyer’s patch (IPP) represents the main entry port for the BSE agent. In earlier C-BSE pathogenesis studies, cattle at 4–6 months of age were orally challenged, while there are strong indications that the risk of infection is highest in young animals. In the present study, unweaned calves aged 4–6 weeks were orally challenged to determine the earli‑ est time point at which newly formed PrPBSE and BSE infectivity are detectable in the IPP. For this purpose, calves were culled 1 week as well as 2, 4, 6 and 8 months post-infection (mpi) and IPPs were examined for BSE infectivity using a bovine PrP transgenic mouse bioassay, and for PrPBSE by immunohistochemistry (IHC) and protein misfolding cyclic amplifcation (PMCA) assays. For the frst time, BSE prions were detected in the IPP as early as 2 mpi by transgenic mouse bioassay and PMCA and 4 mpi by IHC in the follicular dendritic cells (FDCs) of the IPP follicles. These data indi‑ cate that BSE prions propagate in the IPP of unweaned calves within 2 months of oral uptake of the agent.
In summary, our study demonstrates for the frst time PrPBSE (by PMCA) and prion infectivity (by mouse bioassay) in the ileal Peyer’s patch (IPP) of young calves as early as 2 months after infection. From 4 mpi nearly all calves showed PrPBSE positive IPP follicles (by IHC), even with PrPBSE accumulation detectable in FDCs in some animals. Finally, our results confrm the IPP as the early port of entry for the BSE agent and a site of initial propagation of PrPBSE and infectivity during the early pathogenesis of the disease. Terefore, our study supports the recommendation to remove the last four metres of the small intestine (distal ileum) at slaughter, as designated by current legal requirements for countries with a controlled BSE risk status, as an essential measure for consumer and public health protection.
A study comparing preclinical cattle infected naturally with BSE to clinically affected cattle either naturally or experimentally infected with BSE by the oral route found the most abundant PrPSc in the brainstem area (39), which is consistent with ascension to the brain from the gut by sympathetic and parasympathetic projections (40). In our experiment, abundant prions were observed in the brainstem of cattle with clinical signs of BSE, which is similar to the amount in their thalamus or midbrain regions. Interestingly, prions in the brainstem of cattle with clinical evidence of BSE seeded the RT-QuIC reactions faster than any other brain region despite the brainstem area having lower EIA OD values (Table 2) in comparison to other brain regions. This suggests that higher concentrations of prions do not necessarily seed the reaction faster. Perhaps prions of the brainstem exist in a preferred conformation for better conversion despite being present in lower concentrations.
snip...
The 2004 enhanced BSE surveillance program was so flawed, that one of the top TSE prion Scientist for the CDC, Dr. Paul Brown stated ; Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.
see ;
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency."
OR, what the Honorable Phyllis Fong of the OIG found ;
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain
IT is of my opinion, that the OIE and the USDA et al, are the soul reason, and responsible parties, for Transmissible Spongiform Encephalopathy TSE prion diseases, including typical and atypical BSE, typical and atypical Scrapie, and all strains of CWD, and human TSE there from, spreading around the globe. I have lost all confidence of this organization as a regulatory authority on animal disease, and consider it nothing more than a National Trading Brokerage for all strains of animal TSE, just to satisfy there commodity. AS i said before, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization. JUST because of low documented human body count with nvCJD and the long incubation periods, the lack of sound science being replaced by political and corporate science in relations with the fact that science has now linked some sporadic CJD with atypical BSE and atypical scrapie, and the very real threat of CWD being zoonosis, I believed the O.I.E. has failed terribly and again, I call for this organization to be dissolved...
Monday, May 05, 2014
Member Country details for listing OIE CWD 2013 against the criteria of Article 1.2.2., the Code Commission recommends consideration for listing
Friday, December 5, 2014
SPECIAL ALERT The OIE recommends strengthening animal disease surveillance worldwide
O.4.3
Spread of BSE prions in cynomolgus monkeys (Macaca fascicularis) after oral transmission
Edgar Holznagel1, Walter Schulz-Schaeffer2, Barbara Yutzy1, Gerhard Hunsmann3, Johannes Loewer1 1Paul-Ehrlich-Institut, Federal Institute for Sera and Vaccines, Germany; 2Department of Neuropathology, Georg-August University, Göttingen, Germany, 3Department of Virology and Immunology, German Primate Centre, Göttingen, Germany
Background: BSE-infected cynomolgus monkeys represent a relevant animal model to study the pathogenesis of variant Creutzfeldt-Jacob disease (vCJD).
Objectives: To study the spread of BSE prions during the asymptomatic phase of infection in a simian animal model.
Methods: Orally BSE-dosed macaques (n=10) were sacrificed at defined time points during the incubation period and 7 orally BSE-dosed macaques were sacrificed after the onset of clinical signs. Neuronal and non-neuronal tissues were tested for the presence of proteinase-K-resistant prion protein (PrPres) by western immunoblot and by paraffin-embedded tissue (PET) blot technique.
Results: In clinically diseased macaques (5 years p.i. + 6 mo.), PrPres deposits were widely spread in neuronal tissues (including the peripheral sympathetic and parasympathetic nervous system) and in lymphoid tissues including tonsils. In asymptomatic disease carriers, PrPres deposits could be detected in intestinal lymph nodes as early as 1 year p.i., but CNS tissues were negative until 3 – 4 years p.i. Lumbal/sacral segments of the spinal cord and medulla oblongata were PrPres positive as early as 4.1 years p.i., whereas sympathetic trunk and all thoracic/cervical segments of the spinal cord were still negative for PrPres. However, tonsil samples were negative in all asymptomatic cases.
Discussion: There is evidence for an early spread of BSE to the CNS via autonomic fibres of the splanchnic and vagus nerves indicating that trans-synaptical spread may be a time-limiting factor for neuroinvasion. Tonsils were predominantly negative during the main part of the incubation period indicating that epidemiological vCJD screening results based on the detection of PrPres in tonsil biopsies may mostly tend to underestimate the prevalence of vCJD among humans.
P.4.23
Transmission of atypical BSE in humanized mouse models
Liuting Qing1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5, Qingzhong Kong1 1Case Western Reserve University, USA; 2Instituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University (Previously at USDA National Animal Disease Center), USA
Background: Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Atypical BSE cases have been discovered in three continents since 2004; they include the L-type (also named BASE), the H-type, and the first reported case of naturally occurring BSE with mutated bovine PRNP (termed BSE-M). The public health risks posed by atypical BSE were largely undefined.
Objectives: To investigate these atypical BSE types in terms of their transmissibility and phenotypes in humanized mice. Methods: Transgenic mice expressing human PrP were inoculated with several classical (C-type) and atypical (L-, H-, or Mtype) BSE isolates, and the transmission rate, incubation time, characteristics and distribution of PrPSc, symptoms, and histopathology were or will be examined and compared.
Results: Sixty percent of BASE-inoculated humanized mice became infected with minimal spongiosis and an average incubation time of 20-22 months, whereas only one of the C-type BSE-inoculated mice developed prion disease after more than 2 years. Protease-resistant PrPSc in BASE-infected humanized Tg mouse brains was biochemically different from bovine BASE or sCJD. PrPSc was also detected in the spleen of 22% of BASE-infected humanized mice, but not in those infected with sCJD. Secondary transmission of BASE in the humanized mice led to a small reduction in incubation time. The atypical BSE-H strain is also transmissible with distinct phenotypes in the humanized mice, but no BSE-M transmission has been observed so far.
Discussion: Our results demonstrate that BASE is more virulent than classical BSE, has a lymphotropic phenotype, and displays a modest transmission barrier in our humanized mice.
BSE-H is also transmissible in our humanized Tg mice.
The possibility of more than two atypical BSE strains will be discussed.
Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
P03.137
Transmission of BSE to Cynomolgus Macaque, a Non-human Primate; Development of Clinical Symptoms and Tissue Distribution of PrPSC
Yamakawa, Y1; Ono, F2; Tase, N3; Terao, K3; Tannno, J3; Wada, N4; Tobiume, M5; Sato, Y5; Okemoto-Nakamura, Y1; Hagiwara, K1; Sata, T5 1National Institure of Infectious diseases, Cell biology and Biochemistry, Japan; 2Corporation for Production and Research Laboratory Primates., Japan; 3National Institure of Biomedical Innovation, Tsukuba Primate Reserch Center, Japan; 4Yamauchi Univ., Veterinary Medicine, Japan; 5National Institure of Infectious diseases, Pathology, Japan
Two of three cynomolgus monkeys developed abnormal neuronal behavioral signs at 30-(#7) and 28-(#10) months after intracerebral inoculation of 200ul of 10% brain homogenates of BSE affected cattle (BSE/JP6). Around 30 months post inoculation (mpi), they developed sporadic anorexia and hyperekplexia with squeal against environmental stimulations such as light and sound. Tremor, myoclonic jerk and paralysis became conspicuous during 32 to 33-mpi, and symptoms become worsened according to the disease progression. Finally, one monkey (#7) fell into total paralysis at 36-mpi. This monkey was sacrificed at 10 days after intensive veterinary care including infusion and per oral supply of liquid food. The other monkey (#10) had to grasp the cage bars to keep an upright posture caused by the sever ataxia. This monkey was sacrificed at 35-mpi. EEG of both monkeys showed diffuse slowing. PSD characteristic for sporadic CJD was not observed in both monkeys. The result of forearm movement test showed the hypofunction that was observed at onset of clinical symptoms. Their cognitive function determined by finger maze test was maintained at the early stage of sideration. However, it was rapidly impaired followed by the disease progression. Their autopsied tissues were immunochemically investigated for the tissue distribution of PrPSc. Severe spongiform change in the brain together with heavy accumulation of PrPSc having the type 2B/4 glycoform profile confirmed successful transmission of BSE to Cynomolgus macaques. Granular and linear deposition of PrPSC was detected by IHC in the CNS of both monkeys. At cerebral cortex, PrPSC was prominently accumulated in the large plaques. Sparse accumulation of PrPSc was detected in several peripheral nerves of #7 but not in #10 monkey, upon the WB analysis. Neither #7 nor #10 monkey accumulated detectable amounts of PrPSc in their lymphatic organs such as tonsil, spleen, adrenal grands and thymus although PrPSc was barely detected in the submandibular lymph node of #7 monkey. Such confined tissue distribution of PrPSc after intracerebral infection with BSE agent is not compatible to that reported on the Cynomolgus macaques infected with BSE by oral or intra-venous (intra-peritoneal) routs, in which PrPSc was accumulated at not only CNS but also widely distributed lymphatic tissues.
P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany
Background: In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.
Aims: The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.
Methods: Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results: In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.
Conclusions: Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian vCJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfilment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).http://www.neuroprion.org/resources/pdf_docs/conferences/prion2007/abstract_book.pdf
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate.
WE know now, and we knew decades ago, that 5.5 grams of suspect feed in TEXAS was enough to kill 100 cows.
look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused 7% (1 of 14) of the cows to come down with BSE;
Risk of oral infection with bovine spongiform encephalopathy agent in primates
Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe Deslys Summary The uncertain extent of human exposure to bovine spongiform encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease (vCJD)--is compounded by incomplete knowledge about the efficiency of oral infection and the magnitude of any bovine-to-human biological barrier to transmission. We therefore investigated oral transmission of BSE to non-human primates. We gave two macaques a 5 g oral dose of brain homogenate from a BSE-infected cow. One macaque developed vCJD-like neurological disease 60 months after exposure, whereas the other remained free of disease at 76 months. On the basis of these findings and data from other studies, we made a preliminary estimate of the food exposure risk for man, which provides additional assurance that existing public health measures can prevent transmission of BSE to man.
snip...
BSE bovine brain inoculum
100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg
Primate (oral route)* 1/2 (50%)
Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) 1/15 (7%)
RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)
PrPres biochemical detection
The comparison is made on the basis of calibration of the bovine inoculum used in our study with primates against a bovine brain inoculum with a similar PrPres concentration that was inoculated into mice and cattle.8 *Data are number of animals positive/number of animals surviving at the time of clinical onset of disease in the first positive animal (%). The accuracy of bioassays is generally judged to be about plus or minus 1 log. ic ip=intracerebral and intraperitoneal.
Table 1: Comparison of transmission rates in primates and cattle infected orally with similar BSE brain inocula
Published online January 27, 2005
It is clear that the designing scientists must also have shared Mr Bradley’s surprise at the results because all the dose levels right down to 1 gram triggered infection.
it is clear that the designing scientists must have also shared Mr Bradleyâs surprise at the results because all the dose levels right down to 1 gram triggered infection.
I ask Professor Kong ;
Thursday, December 04, 2008 3:37 PM
Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment
IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....
Professor Kong reply ;
.....snip
As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete. Thanks for your interest.
Best regards, Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA
P.4.23 Transmission of atypical BSE in humanized mouse models
Liuting Qing1, Wenquan Zou1, Cristina Casalone2, Martin Groschup3, Miroslaw Polak4, Maria Caramelli2, Pierluigi Gambetti1, Juergen Richt5, Qingzhong Kong1 1Case Western Reserve University, USA; 2Instituto Zooprofilattico Sperimentale, Italy; 3Friedrich-Loeffler-Institut, Germany; 4National Veterinary Research Institute, Poland; 5Kansas State University (Previously at USDA National Animal Disease Center), USA
Background: Classical BSE is a world-wide prion disease in cattle, and the classical BSE strain (BSE-C) has led to over 200 cases of clinical human infection (variant CJD). Atypical BSE cases have been discovered in three continents since 2004; they include the L-type (also named BASE), the H-type, and the first reported case of naturally occurring BSE with mutated bovine PRNP (termed BSE-M). The public health risks posed by atypical BSE were argely undefined.
Objectives: To investigate these atypical BSE types in terms of their transmissibility and phenotypes in humanized mice.
Methods: Transgenic mice expressing human PrP were inoculated with several classical (C-type) and atypical (L-, H-, or Mtype) BSE isolates, and the transmission rate, incubation time, characteristics and distribution of PrPSc, symptoms, and histopathology were or will be examined and compared.
Results: Sixty percent of BASE-inoculated humanized mice became infected with minimal spongiosis and an average incubation time of 20-22 months, whereas only one of the C-type BSE-inoculated mice developed prion disease after more than 2 years. Protease-resistant PrPSc in BASE-infected humanized Tg mouse brains was biochemically different from bovine BASE or sCJD. PrPSc was also detected in the spleen of 22% of BASE-infected humanized mice, but not in those infected with sCJD. Secondary transmission of BASE in the humanized mice led to a small reduction in incubation time. The atypical BSE-H strain is also transmissible with distinct phenotypes in the humanized mice, but no BSE-M transmission has been observed so far.
Discussion: Our results demonstrate that BASE is more virulent than classical BSE, has a lymphotropic phenotype, and displays a modest transmission barrier in our humanized mice. BSE-H is also transmissible in our humanized Tg mice. The possibility of more than two atypical BSE strains will be discussed.
Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
see full text ;
>>> It is distinct from atypical BSE, which may develop spontaneously, according to information from the U.S. Centers for Disease Control and Prevention.
THIS IS A MYTH $$$
***atypical spontaneous BSE in France LOL***
FRANCE STOPS TESTING FOR MAD COW DISEASE BSE, and here’s why, to many spontaneous events of mad cow disease $$$
***so 20 cases of atypical BSE in France, compared to the remaining 40 cases in the remaining 12 Countries, divided by the remaining 12 Countries, about 3+ cases per country, besides Frances 20 cases. you cannot explain this away with any spontaneous BSe. ...TSS
Sunday, October 5, 2014
France stops BSE testing for Mad Cow Disease
Thursday, March 24, 2016
FRANCE CONFIRMS BOVINE SPONGIFORM ENCEPHALOPATHY BSE MAD COW (ESB) chez une vache dans les Ardennes
***atypical spontaneous BSE in France LOL***
FRANCE STOPS TESTING FOR MAD COW DISEASE BSE, and here’s why, to many spontaneous events of mad cow disease $$$
we have seen the spontaneous BSE epidemic in France, what about the other HIGH INCIDENCE ATYPICAL BSE COUNTRY OF POLAND, another atypical spontaneous event of high incidence. how can this be blamed on a happenstance of nothing, i.e. old age? goes against all junk science to date on the spontaneous atypical BSE i.e.
> In 2015, the OIE determined that atypical BSE occurred spontaneously at a low rate in all cattle populations and would be excluded for BSE risk. ...
>Atypical BSE occurs in older cattle, usually 8 years of age or greater, and does not appear to be associated with contaminated feed. Like classic or sporadic CJD in humans, it seems to arise rarely and spontaneously.
POLAND ATYPICAL BSE AND SPORADIC CJD
we have seen the spontaneous BSE epidemic in France, what about the other HIGH INCIDENCE ATYPICAL BSE COUNTRY OF POLAND, another atypical spontaneous event of high incidence. how can this be blamed on a happenstance of nothing, i.e. old age? goes against all junk science to date on the spontaneous atypical BSE i.e.
> In 2015, the OIE determined that atypical BSE occurred spontaneously at a low rate in all cattle populations and would be excluded for BSE risk. ...
>Atypical BSE occurs in older cattle, usually 8 years of age or greater, and does not appear to be associated with contaminated feed. Like classic or sporadic CJD in humans, it seems to arise rarely and spontaneously.
POLAND ATYPICAL BSE AND SPORADIC CJD
Atypical status of bovine spongiform encephalopathy in Poland: a molecular typing study
Summary
The aim of this study was to analyze molecular features of protease-resistant prion protein (PrPres) in Western blots of BSE cases diagnosed in Poland with respect to a possible atypical status. Confirmed cases were analyzed by Western blotting with several monoclonal antibodies directed at N-terminal and core epitopes of prion protein (PrP). Most cases showed the classical glycoprofile characterized by the dominance of the di- over the monoglycosylated PrPres band, yielding di-/mono- ratios well above 2 and by reactivity with antibodies having their epitopes in bovine PrP region 110–242 (C-type cases). Surprisingly, seven cases of BSE were atypical. Six were classified as L-type based on a slightly lower molecular mass (Mr) of the non- glycosylated band with respect to C-types and a conspicuously low di-/mono- ratio of glycosylated PrPres bands approaching unity. One case was classified as H-type because of a higher Mr of PrPres bands on the blot when compared with C-type cases. A characteristic epitope of H-type PrPres occurred in the 101–110 region of PrP for which only antibody 12B2 had a sufficient affinity. The occurrence of atypical cases only in animals 9 years of age and older raises questions about the mechanisms of prion diseases and the origin of BSE.
Atypical status of bovine spongiform encephalopathy in Poland: a molecular typing study
M. P. Polak1, J. F. Zmudzinski1, J. G. Jacobs2, J. P. M. Langeveld2
1 National Veterinary Research Institute, Pulawy, Poland
2 Central Institute for Animal Disease Control (CIDC-Lelystad), Lelystad, The Netherlands Received 24 April 2007; Accepted 27 August 2007; Published online 26 September 2007 # Springer-Verlag 2007
snip...
Clarification of whether these atypical cases represent genuine strains of BSE would be accomplished by transmission studies in mice. Such studies have already been performed in France, Germany and Italy [3, 5, 14, 15]. For H-type cases in France, successful transmission was achieved in both wild-type, and transgenic mice expressing bovine and ovine PrPC. In Germany, successful transmission of both an L-type and an H-type case to transgenic mice overexpressing bovine PrPC has been described. PrPres from those mice was identical to the inoculum used in the study, proving the existence of distinct strains of BSE. All atypical features of those isolates were maintained in the inoculated mice, indicating the existence of several prion strains in cattle, or alternatively a possible evolution to a single BSE strain, as suggested from data obtained by Capobianco et al. with wild-type inbred mice [15]. This second hypothesis could fit with data from the United Kingdom, where over 180,000 cases of BSE were diagnosed by passive surveillance. British and European experience based on tissue analysis from clinically affected animals showed consistent characteristics of BSE agent not only on histological sections from cattle brains but also when inoculating mice, pointing to the existence of one uniform strain of BSE. Therefore, it is possible that a sporadic form of BSE present in the cattle population at a very low rate in the past could have spread to naive animals via contaminated meatand-bone meals. Spontaneous BSE, if it occurs, must be a very rare phenomenon. However, data for Poland, where 14% of all cases comprised an atypical form of BSE, seems to be in contradiction to this hypothesis. But when the average age of all positive cases in Poland is taken into account, BSE is generally found in older animals (mean age of 7.7). Analysis of the age structure of cattle in Poland in the period of 2002–2006 shows that 56–60% of all animals were 7 years old and above. A much larger number of cattle should be tested to get better insight into the real prevalence of atypical BSE. However, current tendencies based on economic analysis point to a decrease in the number of tests performed rather than expanding this scheme any further. It would be sensible to maintain a certain level of testing focused on the older age group to distinguish between a stable, thus sporadic-based, situation of BSE, or alternatively a fade-out, thus epidemic-based, situation. Exploring the subject of spontaneous BSE in the cattle population may be ceased for economic reasons, and it may never be known while this answer is in our reach thanks to great financial efforts in recent years.
Poland is Proof atypical BSE is NOT an old cow spontaneous disease...tss
Number of reported cases of bovine spongiform encephalopathy (BSE) in farmed cattle worldwide* (excluding the United Kingdom) Country/Year
Poland
89 90 91 92 93 94 95 96 97 98 99 00 01 02 03 04 05 06 07 08 09 10 11 12 13 14 15 16
0 0 0 0 0 0 0 0 0 0 0 0 0 4f 5 11 19 10 9 5 4 2 1m 3 1 0 0 0
Source: USDA, APHIS, VS
What is the level of passenger traffic arriving in the United States from Poland?
A total of 188,946 passengers arrived at US airports on direct flights from Poland in fiscal year 2000.
An undetermined number of passengers arrived in the US from Poland via indirect flights.
Under APHIS-PPQ’s agricultural quarantine inspection monitoring, 451 air passengers from Poland were sampled for items of agricultural interest in fiscal year 2000.
Thirteen (13) of these passengers, or 2.9 percent, carried a total of 26.2 kg of meat 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 Department of Transportation, and APHIS-PPQ Agricultural Quarantine Inspection data base CEI’s plans for follow up: CEI has no plans to provide additional information on this situation. If you need more information or wish to comment, you may contact Judy Akkina at (970) 490-7852 or Carol Tuszynski at (970) 490-7893.
What measures has USDA-APHIS taken to prevent the introduction of BSE? To prevent BSE from entering the United States, APHIS has restricted the importation of live ruminants and certain ruminant products from countries where BSE is known to exist.
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.
PRION 2018 CONFERENCE
P98 The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge
Greenlee JJ (1), Moore SJ (1), and West Greenlee MH (2) (1) United States Department of Agriculture, Agricultural Research Service, National Animal Disease Center, Virus and Prion Research Unit, Ames, IA, United States (2) Department of Biomedical Sciences, Iowa State University College of Veterinary Medicine, Ames, IA, United States.
reading up on this study from Prion 2018 Conference, very important findings ;
***> This study demonstrates that the H-type BSE agent is transmissible by the oronasal route.
***> These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.
PRION 2018 CONFERENCE ABSTRACT
WEDNESDAY, OCTOBER 24, 2018
Experimental Infection of Cattle With a Novel Prion Derived From Atypical H-Type Bovine Spongiform Encephalopathy
MONDAY, JANUARY 09, 2017
Oral Transmission of L-Type Bovine Spongiform Encephalopathy Agent among Cattle
CDC Volume 23, Number 2—February 2017
*** Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.
*** Consumption of L-BSE–contaminated feed may pose a risk for oral transmission of the disease agent to cattle.
SPONTANEOUS ATYPICAL BOVINE SPONGIFORM ENCEPHALOPATHY
***> Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.***
MONDAY, JANUARY 21, 2019
Bovine Spongiform Encephalopathy BSE TSE Prion Surveillance FDA USDA APHIS FSIS UPDATE 2019
TUESDAY, MARCH 12, 2019
***> Early preclinical detection of prions in the skin of prion-infected animals
***> prepare for the storm....
TUESDAY, NOVEMBER 20, 2018
CDC Eyes of CJD patients show evidence of prions concerns for iatrogenic transmission
***> prepare for the storm....
MONDAY, DECEMBER 03, 2018
Prion Seeds Distribute throughout the Eyes of Sporadic Creutzfeldt-Jakob Disease Patients
Eye procedure raises CJD concerns
BySTEVE MITCHELL, Medical Correspondent
WASHINGTON, Nov. 18 (UPI) -- A New York man who died from a rare brain disorder similar to mad cow disease in May underwent an eye procedure prior to his death that raises concerns about the possibility of transmitting the fatal disease to others, United Press International has learned.
The development comes on the heels of the announcement Thursday by U.S. Department of Agriculture officials of a possible second case of mad cow disease in U.S. herds.
Richard Da Silva, 58, of Orange County, N.Y., died from Creutzfeldt Jakob disease, an incurable brain-wasting illness that strikes about one person per million.
Richard's wife Ann Marie Da Silva told UPI he underwent a check for the eye disease glaucoma in 2003, approximately a year before his death. The procedure involves the use of a tonometer, which contacts the cornea -- an eye tissue that can contain prions, the infectious agent thought to cause CJD.
Ann Marie's concern is that others who had the tonometer used on them could have gotten infected.
A 2003 study by British researchers suggests her concerns may be justified. A team led by J.W. Ironside from the National Creutzfeldt-Jakob Disease Surveillance Unit at the University of Edinburgh examined tonometer heads and found they can retain cornea tissue that could infect other people -- even after cleaning and decontaminating the instrument.
"Retained corneal epithelial cells, following the standard decontamination routine of tonometer prisms, may represent potential prion infectivity," the researchers wrote in the British Journal of Ophthalmology last year. "Once the infectious agent is on the cornea, it could theoretically infect the brain."
Prions, misfolded proteins thought to be the cause of mad cow, CJD and similar diseases, are notoriously difficult to destroy and are capable of withstanding most sterilization procedures.
Laura Manuelidis, an expert on these diseases and section chief of surgery in the neuropathology department at Yale University, agreed with the British researchers that tonometers represent a potential risk of passing CJD to other people.
Manuelidis told UPI she has been voicing her concern about the risks of corneas since 1977 when her own study, published in the New England Journal of Medicine, showed the eye tissue, if infected, could transmit CJD.
At the time the procedure was done on Richard Da Silva, about a year before he died, she said it was "absolutely" possible he was infectious.
The CJD Incidents Panel, a body of experts set up by the U.K. Department of Health, noted in a 2001 report that procedures involving the cornea are considered medium risk for transmitting CJD. The first two patients who have a contaminated eye instrument used on them have the highest risk of contracting the disease, the panel said.
In 1999, the U.K. Department of Health banned opticians from reusing equipment that came in contact with patients' eyes out of concern it could result in the transmission of variant CJD, the form of the disease humans can contract from consuming infected beef products.
Richard Da Silva was associated with a cluster of five other cases of CJD in southern New York that raised concerns about vCJD.
None of the cases have been determined to stem from mad cow disease, but concerns about the cattle illness in the United States could increase in light of the USDA announcement Thursday that a cow tested positive on initial tests for the disease. If confirmed, this would be the second U.S. case of the illness; the first was detected in a Washington cow last December. The USDA said the suspect animal disclosed Thursday did not enter the food chain. The USDA did not release further details about the cow, but said results from further lab tests to confirm the initial tests were expected within seven days.
Ann Marie Da Silva said she informed the New York Health Department and later the eye doctor who performed the procedure about her husband's illness and her concerns about the risk of transmitting CJD via the tonometer.
The optometrist -- whom she declined to name because she did not want to jeopardize his career -- "didn't even know what this disease was," she said.
"He said the health department never called him and I called them (the health department) back and they didn't seem concerned about it," she added. "I just kept getting angrier and angrier when I felt I was being dismissed."
She said the state health department "seems to have an attitude of don't ask, don't tell" about CJD.
"There's a stigma attached to it," she said. "Is it because they're so afraid the public will panic? I don't know, but I don't think that the answer is to push things under the rug."
New York State Department of Health spokeswoman Claire Pospisil told UPI she would look into whether the agency was concerned about the possibility of transmitting CJD via tonometers, but she had not called back prior to story publication.
Disposable tonometers are readily available and could avoid the risk of transmitting the disease, Ironside and colleagues noted in their study. Ann Marie Da Silva said she asked the optometrist whether he used disposable tonometers and "he said 'No, it's a reusable one.'"
Ironside's team also noted other ophthalmic instruments come into contact with the cornea and could represent a source of infection as they are either difficult to decontaminate or cannot withstand the harsh procedures necessary to inactivate prions. These include corneal burrs, diagnostic and therapeutic contact lenses and other coated lenses.
Terry Singletary, whose mother died from a type of CJD called Heidenhain Variant, told UPI health officials were not doing enough to prevent people from being infected by contaminated medical equipment.
"They've got to start taking this disease seriously and they simply aren't doing it," said Singletary, who is a member of CJD Watch and CJD Voice -- advocacy groups for CJD patients and their families.
U.S. Centers for Disease Control and Prevention spokeswoman Christine Pearson did not return a phone call from UPI seeking comment. The agency's Web site states the eye is one of three tissues, along with the brain and spinal cord, that are considered to have "high infectivity."
The Web site said more than 250 people worldwide have contracted CJD through contaminated surgical instruments and tissue transplants. This includes as many as four who were infected by corneal grafts. The agency noted no such cases have been reported since 1976, when sterilization procedures were instituted in healthcare facilities.
Ironside and colleagues noted in their study, however, many disinfection procedures used on optical instruments, such as tonometers, fail. They wrote their finding of cornea tissue on tonometers indicates that "no current cleaning and disinfection strategy is fully effective."
Singletary said CDC's assertion that no CJD cases from infected equipment or tissues have been detected since 1976 is misleading.
"They have absolutely no idea" whether any cases have occurred in this manner, he said, because CJD cases often aren't investigated and the agency has not required physicians nationwide report all cases of CJD.
"There's no national surveillance unit for CJD in the United States; people are dying who aren't autopsied, the CDC has no way of knowing" whether people have been infected via infected equipment or tissues, he said.
Ann Marie Da Silva said she has contacted several members of her state's congressional delegation about her concerns, including Rep. Sue Kelly, R-N.Y., and Sen. Charles Schumer, D-N.Y.
"Basically, what I want is to be a positive force in this, but I also want more of a dialogue going on with the public and the health department," she said.
Cadaver corneal transplants -- without family permission Houston, Texas channel 11 news 28 Nov 99
Repoorted by Terry S. Singeltary Sr.son of CJD victim
"It was a story about how the Lions eye bank were harvesting corneas from victims in the Morgue, without their consent. Under Texas law, this appears to be legal (remember Texas has the Veggie liable law). Even if Family says no, this appears to happen, from what the news story said.
They said the only way to prevent this, is to fill out a form, stating not to have this done. So if you don't fill out the form, they can do this. How many people don't know about the form?
This is not only disgusting and appalling, it could be highly infectious. Without proper background checking of the donors, on their physical history, checking on past dementia, and/or family history, some of these unfortunate victims, could be passing a human TSE.
Response Jill Spitler Clevelland Eye Bank:
"No, we are not stealing.........Yes, you do have such a law in the state of Texas, but not all your state Eye Banks utilize the law. The Eye Bank that you're speaking of is only one of 43 certified Eye Bank throughout the USA.
And there are measure taken per the Medical Standards of the Eye Bank Association of America, the certifying body for eye banks and per FDA regulations to address those concerns that you speak of.
I would suggest that those interested/concern with transplant contact their local agencies. The Eye Bank Association of America has a web. site . Further if anyone has problems contacting or finding out about their local organization(s), call me or e-mail me I would be glad to help. My e-mail address is jill@clevelandeyebank.org"
Terry Singeltary responds:
"Explain this to the family in Houston who went to their loved ones funeral, only to find out that the loved one that was in the casket, had their corneas removed without their permission, without the consent of the victim or it's family. They would not have known it, only for the funny look the victim had. So, they questioned, only to find out, the corneas, had in fact, been removed without consent.
I call that stealing, regardless what the law states. This type of legal grave robbing is not a logical thing to do without knowing any type of background of the victims medical past, which really will not prove anything due to the incubation period. Eye tissue being potentially a highly infective source, there are risks here.
Should they not at least know of the potential ramifications of TSE's (the person receiving the corneas)?
Should there not be some sort of screening?
Should there be some sort of moral issue here?
If this is the case, and in fact, they can come take your corneas, without your consent, then what will they start taking next, without your consent?
Lets look at a hypothetical situation:
What would happen if my Mom (DOD 12-14-97 hvCJD) would have gotten into a car wreck and died, before the symptoms of CJD appeared. Not much money, so there was no autopsy. What would have happened to that recipient of those infecting corneas?"
Comment (webmaster): Actual transmission of CJD by means of corneal transplant may or may not be rare. The incidence of infectivity in older people could be fairly high; this is not to be confused with the lower incidence of symptomatic (clinical) CJD. It is very unlikely that familial CJD would have been diagnosed in earlier generations; however, without interviewing the family even known kindreds would not be excluded.
In blood donation, a much stricter policy is followed, even though corneal transplant may be far more dangerous (being a direct link to the brain and not going through purification steps).
Since highly sensitive tests for pre-clinical CJD are now available, it would make sense to screen corneas for CJD, just as they are screened for AIDS, hepatitus, and a host of other conditions.
Friday, December 04, 2009
New guidance on decontamination of trial contact lenses and other contact devices has been revealed for CJD AND vCJD
SUNDAY, JANUARY 17, 2016
Of Grave Concern Heidenhain Variant Creutzfeldt Jakob Disease
TUESDAY, AUGUST 1, 2017
Could Insulin be contaminated with and potentially spread, Transmissible Spongiform Encephalopathy TSE Prion, what if?
Friday, January 10, 2014
vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???
Greetings Friends, Neighbors, and Colleagues,
Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease
*** Singeltary comment PLoS ***
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT
IN CONFIDENCE
5 NOVEMBER 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
[9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication.
There are also results to be made available shortly
(1) concerning a farmer with CJD who had BSE animals,
(2) on the possible transmissibility of Alzheimer’s and
(3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.]
snip...see full Singeltary Nature comment here;
re-Evidence for human transmission of amyloid-? pathology and cerebral amyloid angiopathy Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015)
I would kindly like to comment on the Nature Paper, the Lancet reply, and the newspaper articles.
First, I applaud Nature, the Scientist and Authors of the Nature paper, for bringing this important finding to the attention of the public domain, and the media for printing said findings.
Secondly, it seems once again, politics is getting in the way possibly of more important Transmissible Spongiform Encephalopathy TSE Prion scientific findings. findings that could have great implications for human health, and great implications for the medical surgical arena. but apparently, the government peer review process, of the peer review science, tries to intervene again to water down said disturbing findings.
where have we all heard this before? it's been well documented via the BSE Inquiry. have they not learned a lesson from the last time?
we have seen this time and time again in England (and other Country's) with the BSE mad cow TSE Prion debacle.
That 'anonymous' Lancet editorial was disgraceful. The editor, Dick Horton is not a scientist.
The pituitary cadavers were very likely elderly and among them some were on their way to CJD or Alzheimer's. Not a bit unusual. Then the recipients, who got pooled extracts injected from thousands of cadavers, were 100% certain to have been injected with both seeds. No surprise that they got both diseases going after thirty year incubations.
That the UK has a "system in place to assist science journalists" to squash embargoed science reports they find 'alarming' is pathetic.
Sounds like the journalists had it right in the first place: 'Alzheimer's may be a transmissible infection' in The Independent to 'You can catch Alzheimer's' in The Daily Mirror or 'Alzheimer's bombshell' in The Daily Express
if not for the journalist, the layperson would not know about these important findings.
where would we be today with sound science, from where we were 30 years ago, if not for the cloak of secrecy and save the industry at all cost mentality?
when you have a peer review system for science, from which a government constantly circumvents, then you have a problem with science, and humans die.
to date, as far as documented body bag count, with all TSE prion named to date, that count is still relatively low (one was too many in my case, Mom hvCJD), however that changes drastically once the TSE Prion link is made with Alzheimer's, the price of poker goes up drastically.
so, who makes that final decision, and how many more decades do we have to wait?
the iatrogenic mode of transmission of TSE prion, the many routes there from, load factor, threshold from said load factor to sub-clinical disease, to clinical disease, to death, much time is there to spread a TSE Prion to anywhere, but whom, by whom, and when, do we make that final decision to do something about it globally? how many documented body bags does it take? how many more decades do we wait? how many names can we make up for one disease, TSE prion?
Professor Collinge et al, and others, have had troubles in the past with the Government meddling in scientific findings, that might in some way involve industry, never mind human and or animal health.
FOR any government to continue to circumvent science for monetary gain, fear factor, or any reason, shame, shame on you.
in my opinion, it's one of the reasons we are at where we are at to date, with regards to the TSE Prion disease science i.e. money, industry, politics, then comes science, in that order.
greed, corporate, lobbyist there from, and government, must be removed from the peer review process of sound science, it's bad enough having them in the pharmaceutical aspect of healthcare policy making, in my opinion.
my mother died from confirmed hvCJD, and her brother (my uncle) Alzheimer's of some type (no autopsy?). just made a promise, never forget, and never let them forget, before I do.
I kindly wish to remind the public of the past, and a possible future we all hopes never happens again. ...
2012
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Background
Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.
Methods
Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.
Results
I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.
Conclusions
There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.
end...tss
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
source references ...end...tss
Hello Nicole,
by all means, please do use my poster. but I thought this was already taken care of, and I could not attend for my poster presentation, therefore, it was not going to be presented. I have some health issues and could not make the trip.
please see old correspondence below...
From: Nicole Sanders Sent: Tuesday, April 10, 2012 5:37 PM To: Terry S. Singeltary Sr. Subject: RE: re-submission
Dear Terry,
The decline of proposal number 30756 is registered in the system. Thank you for your consideration.
Best Regards,
Nicole
Nicole Sanders
Senior Specialist, Membership & Conference Programming
______________________________________
From: xxxx
To: Terry Singeltary
Sent: Saturday, December 05, 2009 9:09 AM
Subject: 14th ICID - abstract accepted for 'International Scientific Exchange'
Your preliminary abstract number: 670
Dear Mr. Singeltary,
On behalf of the Scientific Committee, I am pleased to inform you that your abstract
'Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009'
WAS accepted for inclusion in the INTERNATIONAL SCIENTIFIC EXCHANGE (ISE) section of the 14th International Congress on Infectious Diseases. Accordingly, your abstract will be included in the "Intl. Scientific Exchange abstract CD-rom" of the Congress which will be distributed to all participants.
Abstracts accepted for INTERNATIONAL SCIENTIFIC EXCHANGE are NOT PRESENTED in the oral OR poster sessions.
Your abstract below was accepted for: INTERNATIONAL SCIENTIFIC EXCHANGE
#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
Author: T. Singeltary; Bacliff, TX/US
Topic: Emerging Infectious Diseases Preferred type of presentation: International Scientific Exchange
This abstract has been ACCEPTED.
#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
Authors: T. Singeltary; Bacliff, TX/US
Title: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
Body: Background
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods
12 years independent research of available data
Results
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries.
I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
Keywords: Transmissible Spongiform Encephalopathy Creutzfeldt Jakob Disease Prion
page 114 ;
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
http://www.isid.org/14th_icid/
http://www.isid.org/publications/ICID_Archive.shtml
http://ww2.isid.org/Downloads/IMED2009_AbstrAuth.pdf
TUESDAY, DECEMBER 12, 2017
Creutzfeldt Jakob Disease CJD National Prion Disease Pathology Surveillance Center Cases Examined to December 14, 2017
http://creutzfeldt-jakob-disease.blogspot.com/2017/12/creutzfeldt-jakob-disease-cjd-national.html
Tuesday, December 12, 2017
Neuropathology of iatrogenic Creutzfeldt–Jakob disease and immunoassay of French cadaver-sourced growth hormone batches suggest possible transmission of tauopathy and long incubation periods for the transmission of Abeta pathology
http://tauopathies.blogspot.com/2017/12/neuropathology-of-iatrogenic.html
MONDAY, OCTOBER 02, 2017
Creutzfeldt Jakob Disease United States of America USA and United Kingdom UK Increasing and Zoonotic Pontential From Different Species
http://creutzfeldt-jakob-disease.blogspot.com/2017/10/creutzfeldt-jakob-disease-united-states.html
THURSDAY, AUGUST 17, 2017
*** Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States revisited 2017
Singeltary et al
http://creutzfeldt-jakob-disease.blogspot.com/2017/08/monitoring-occurrence-of-emerging-forms.html
Background
Alzheimer’s disease and Transmissible Spongiform Encephalopathy disease have both been around a long time, and was discovered in or around the same time frame, early 1900’s. Both diseases are incurable and debilitating brain disease, that are in the end, 100% fatal, with the incubation/clinical period of the Alzheimer’s disease being longer (most of the time) than the TSE prion disease. Symptoms are very similar, and pathology is very similar.
Methods
Through years of research, as a layperson, of peer review journals, transmission studies, and observations of loved ones and friends that have died from both Alzheimer’s and the TSE prion disease i.e. Heidenhain Variant Creutzfelt Jakob Disease CJD.
Results
I propose that Alzheimer’s is a TSE disease of low dose, slow, and long incubation disease, and that Alzheimer’s is Transmissible, and is a threat to the public via the many Iatrogenic routes and sources. It was said long ago that the only thing that disputes this, is Alzheimer’s disease transmissibility, or the lack of. The likelihood of many victims of Alzheimer’s disease from the many different Iatrogenic routes and modes of transmission as with the TSE prion disease.
Conclusions
There should be a Global Congressional Science round table event set up immediately to address these concerns from the many potential routes and sources of the TSE prion disease, including Alzheimer’s disease, and a emergency global doctrine put into effect to help combat the spread of Alzheimer’s disease via the medical, surgical, dental, tissue, and blood arena’s. All human and animal TSE prion disease, including Alzheimer’s should be made reportable in every state, and Internationally, WITH NO age restrictions. Until a proven method of decontamination and autoclaving is proven, and put forth in use universally, in all hospitals and medical, surgical arena’s, or the TSE prion agent will continue to spread. IF we wait until science and corporate politicians wait until politics lets science _prove_ this once and for all, and set forth regulations there from, we will all be exposed to the TSE Prion agents, if that has not happened already.
end...tss
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
source references ...end...tss
Hello Nicole,
by all means, please do use my poster. but I thought this was already taken care of, and I could not attend for my poster presentation, therefore, it was not going to be presented. I have some health issues and could not make the trip.
please see old correspondence below...
From: Nicole Sanders Sent: Tuesday, April 10, 2012 5:37 PM To: Terry S. Singeltary Sr. Subject: RE: re-submission
Dear Terry,
The decline of proposal number 30756 is registered in the system. Thank you for your consideration.
Best Regards,
Nicole
Nicole Sanders
Senior Specialist, Membership & Conference Programming
______________________________________
From: xxxx
To: Terry Singeltary
Sent: Saturday, December 05, 2009 9:09 AM
Subject: 14th ICID - abstract accepted for 'International Scientific Exchange'
Your preliminary abstract number: 670
Dear Mr. Singeltary,
On behalf of the Scientific Committee, I am pleased to inform you that your abstract
'Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009'
WAS accepted for inclusion in the INTERNATIONAL SCIENTIFIC EXCHANGE (ISE) section of the 14th International Congress on Infectious Diseases. Accordingly, your abstract will be included in the "Intl. Scientific Exchange abstract CD-rom" of the Congress which will be distributed to all participants.
Abstracts accepted for INTERNATIONAL SCIENTIFIC EXCHANGE are NOT PRESENTED in the oral OR poster sessions.
Your abstract below was accepted for: INTERNATIONAL SCIENTIFIC EXCHANGE
#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
Author: T. Singeltary; Bacliff, TX/US
Topic: Emerging Infectious Diseases Preferred type of presentation: International Scientific Exchange
This abstract has been ACCEPTED.
#0670: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
Authors: T. Singeltary; Bacliff, TX/US
Title: Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
Body: Background
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods
12 years independent research of available data
Results
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries.
I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
Keywords: Transmissible Spongiform Encephalopathy Creutzfeldt Jakob Disease Prion
page 114 ;
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
http://www.isid.org/14th_icid/
http://www.isid.org/publications/ICID_Archive.shtml
http://ww2.isid.org/Downloads/IMED2009_AbstrAuth.pdf
TUESDAY, DECEMBER 12, 2017
Creutzfeldt Jakob Disease CJD National Prion Disease Pathology Surveillance Center Cases Examined to December 14, 2017
http://creutzfeldt-jakob-disease.blogspot.com/2017/12/creutzfeldt-jakob-disease-cjd-national.html
Tuesday, December 12, 2017
Neuropathology of iatrogenic Creutzfeldt–Jakob disease and immunoassay of French cadaver-sourced growth hormone batches suggest possible transmission of tauopathy and long incubation periods for the transmission of Abeta pathology
http://tauopathies.blogspot.com/2017/12/neuropathology-of-iatrogenic.html
MONDAY, OCTOBER 02, 2017
Creutzfeldt Jakob Disease United States of America USA and United Kingdom UK Increasing and Zoonotic Pontential From Different Species
http://creutzfeldt-jakob-disease.blogspot.com/2017/10/creutzfeldt-jakob-disease-united-states.html
THURSDAY, AUGUST 17, 2017
*** Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States revisited 2017
Singeltary et al
http://creutzfeldt-jakob-disease.blogspot.com/2017/08/monitoring-occurrence-of-emerging-forms.html
Tuesday, March 20, 2018
Variably protease-sensitive prionopathy (VPSPr), sporadic creutzfeldt jakob disease sCJD, the same disease, what if?
SUNDAY, APRIL 8, 2018
Transmissible Spongiform Encephalopathy TSE Prion Disease Global Pandemic Urgent Update April 9, 2018
SATURDAY, OCTOBER 06, 2018
Evaluation of iatrogenic risk of CJD transmission associated with corneal transplantation
SATURDAY, SEPTEMBER 22, 2018
Emerging Diseases, Infection Control & California Dental Practice Act
WEDNESDAY, SEPTEMBER 26, 2018
A new variant of Creutzfeldt-Jakob disease in the UK 1995 revisited 2018 a review of science
SUNDAY, MARCH 10, 2019
National Prion Disease Pathology Surveillance Center Cases Examined¹ Updated Feb 1, 2019 Variably protease-sensitive prionopathy VPSPr
Terry S. Singeltary Sr., Bacliff, Texas USA, 77518 flounder9@verizon.net Galveston Bay, on the bottom...
