Feed Safety and BSE/Ruminant Feed Ban Support Project (U18)
Synopsis Full Announcement Application
The synopsis for this grant opportunity is detailed below, following this paragraph. This synopsis contains all of the updates to this document that have been posted as of 05/07/2010 . If updates have been made to the opportunity synopsis, update information is provided below the synopsis. If you would like to receive notifications of changes to the grant opportunity click send me change notification emails . The only thing you need to provide for this service is your email address. No other information is requested.
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Document Type: Grants Notice Funding Opportunity Number: RFA-FD-10-002 Opportunity Category: Discretionary Posted Date: May 07, 2010 Creation Date: May 07, 2010 Original Closing Date for Applications: Jul 15, 2010 Current Closing Date for Applications: Jul 15, 2010 Archive Date: Funding Instrument Type: Cooperative Agreement
Category of Funding Activity: Agriculture Consumer Protection Disaster Prevention and Relief Education Employment, Labor and Training Environment Food and Nutrition Health Natural Resources Science and Technology and other Research and Development
Category Explanation: Expected Number of Awards: 12 Estimated Total Program Funding: $3,000,000 Award Ceiling: $250,000 Award Floor: $0 CFDA Number(s): 93.449 -- Ruminant Feed Ban Support Project Cost Sharing or Matching Requirement: No
Eligible Applicants State governments Native American tribal governments (Federally recognized) Others (see text field entitled "Additional Information on Eligibility" for clarification)
Additional Information on Eligibility: U.S. Territory *This cooperative agreement program is only available to State, Territory, and Tribal government agency feed safety and/or BSE/ruminant feed ban regulatory programs that undertake inspections and related activities under Section 702 of the FD&C Act and that are not currently funded under an existing cooperative agreement or contract. Eligible Individuals Any individual(s) with the skills, knowledge, and resources necessary to carry out the proposed research as the PD/PI is invited to work with his/her organization to develop an application for support. Individuals from underrepresented racial and ethnic groups as well as individuals with disabilities are always encouraged to apply for FDA support.
Agency Name Food & Drug Administration Description
1. Research Objectives The Food and Drug Administration (FDA), Office of Regulatory Affairs (ORA), Division of Federal-State Relations (DFSR) in coordination with the Center for Veterinary Medicine (CVM), is announcing the availability of cooperative agreements to further enhance the infrastructure of State, territorial, and tribal animal feed safety and bovine spongiform encephalopathy (BSE) prevention programs. These cooperative agreements are intended to fund additional personnel, equipment, supplies, and training to support activities related to the FDA ruminant feed ban (21 CFR parts 589.2000 - 2001, referred to as the BSE/ruminant feed ban) as well as other activities related to feed safety, in State, territory, and tribal governments. The goal of FDA’s ORA Cooperative Agreement Program is to enhance, complement, develop and improve State/territory/tribal animal feed safety and surveillance programs. This will be accomplished through the provision of funding for additional equipment, supplies, funding for personnel, training in current feed testing methodologies recognized by FDA, participation in proficiency testing to establish additional reliable laboratory sample analysis capacity, and analysis of surveillance samples as well as State/territorial/tribal government compliance inspections. This will also require extensive cooperation and coordination with FDA District Offices to minimize duplication of inspections. Under these cooperative agreements, the State, territory, and tribal governments would enhance their feed safety and/or BSE/ruminant feed ban programs to increase the ability to locate and visit firms involved in the manufacture, distribution, and transportation of animal feed and operations feeding livestock in their jurisdiction. Verification of compliance with the BSE/ruminant feed ban as well as other regulations related to feed safety will be conducted. In addition, funds could be used to increase State, territory, and tribal personnel dedicated to conducting these inspections. Funds could be used for supplies, training, and laboratory equipment for feed sample testing using analytical methods recognized by FDA. Funds could also be used to conduct educational outreach activities and to develop materials needed to further and enhance the industries' knowledge of and compliance with feed safety regulations and the BSE/ruminant feed ban. As a result of enhancing their feed safety and/or BSE/ruminant feed ban programs, an increase in State, territory, and tribal inspections under section 702 of the Federal Food, Drug, and Cosmetic Act (the FD&C Act) (21 U.S.C. 372) of renderers, protein blenders, feed mills that manufacture animal feeds, feed ingredient manufacturers, feed distributors an d transporters, salvagers of food and feed, and livestock feeders is expected. Animal feed and feed ingredients utilizing materials prohibited under the BSE/ruminant feed ban are of significant interest, although other work related to feed safety may also be conducted. Finally, the Feed Safety and BSE/Ruminant Feed Ban Support Project funds are intended to supplement, not replace, State funding for program improvement. All cooperative agreement projects that are developed at State, territorial, and tribal levels must have existing feed inspection and surveillance programs or propose in detail the development of a State/territory/tribal feed regulatory program. There are eight key project areas identified for this effort that must be addressed: (1) Hire and/or train State/territory/tribal personnel to conduct inspections. Training of State/territory/tribal personnel may be accomplished through the ORA University, training sponsored by the Association of American Feed Control Officials, or other training that meets State/territory/tribal and FDA requirements. New hires for this program must meet the State/territory/tribal agency’s qualifications for feed inspections and sampling techniques. (2) Hire and/or train laboratory personnel to conduct laboratory analyses of fe d samples. Laboratory analyses of samples collecte under this program must utilize methodologies recognized by the FDA, or other professional groups, such as the Association of Official Analytical Chemists International (AOACI). (3) Identify animal feed and feed ingredient manufacturers, including renderers, protein blenders, feed mills, ingredient manufacturers, feed salvagers, distributors (including retailers), transporters of animal feed and feed ingredients, and on-farm animal feed mixers, as well as ruminant feeders within the State/territory/tribal jurisdiction where such firms have not already been identified and/or inspected for compliance with feed safety requirements, such as the BSE/ruminant feed ban. (4) Inspect animal feed and feed ingredient manufacturers, including renderers, protein blenders, feed mills, ingredient manufacturers, feed salvagers, distributors (including retailers), transporters of animal feed and feed ingredients, and on-farm animal feed mixers, as well as ruminant feeders within the State/territory/tribal jurisdiction where such firms have not already been identified and/or inspected for compliance with feed safety requirements, such as the BSE/ruminant feed ban. These inspections would be conducted under section 702 of the FD&C Act, using and completing the appropriate inspection forms and following the appropriate guidance to verify compliance. For example, the FDA Ruminant Feed Ban Inspection Checklist and Ruminant Feed Ban Compliance Program would be used to verify compliance with the BSE/ruminant feed ban. These inspections would be conducted by officers and employees duly commissioned by FDA in accordance with section 702 of the FD&C Act. (5) Conduct surveillance sampling at establishments supplying ingredients or finished feed into the feed supply, including manufacturers, distributors, and livestock feeders. Samples should be tested for the presence of materials prohibited under the BSE/ruminant feed ban or other contaminants, such as drug and pesticide residues, mycotoxins, heavy metals or the presence of pathogenic microorganisms. This surveillance sampling would be conducted under section 702 of the FD&C Act and would be conducted by officers and employees duly commissioned by FDA in accor dance with section 702 of the FD&C Act. (6) Provide copies of all completed inspection reports, including any FDA Ruminant Feed Ban Inspection Checklists, analytical results for surveillance sampling, and reports of any other inspection work as a part of the mid-year program progress report to the FDA Project officer or designated office, as well as provide completed checklists and sample results in accordance with section 702 of the FD&C Act. (7) Be able to identify and quantify improvements to the existing State/territory/tribal feed safety and/or BSE/ruminant feed ban program or developing new programs (i.e., personnel hiring, personnel training, equipment upgrades, increase in inspections conducted) in the mi d-year report as a result of the cooperative agreement. (8) Conduct educational outreach activities and develop materials needed to further and enhance the industries' knowledge of and compliance with feed safety requirements, such as but not limited to the BSE/ruminant feed ban and medicated feed good manufacturing practice regulations, for example. FDA will support the projects covered by this notice under the authority of section 311 of the Public Health Security and Bioterrorism Preparedness and Response Act of 2002 (the Bioterrorism Act) (Public Law 107-188), which amends the FD&C Act by adding section 909 (21 U.S.C. 399). This program is described in the Catalog of Federal Domestic Assistance under number 93.449.
Link to Full Announcement NIH GUIDE ANNOUNCEMENT RFA-FD-10-002 If you have difficulty accessing the full announcement electronically, please contact: MARTIN BERNARD CONTRACT SPECIALIST 301-443-5869 MARTIN.BERNARD@FDA.HHS.GOV Synopsis Modification History There are currently no modifications for this opportunity.
Feed Safety and BSE/Ruminant Feed Ban Support Project (U18)
FOR IMMEDIATE RELEASE September 14, 2010
AGRICULTURE DEPARTMENT RECEIVES FEDERAL FUNDING TO PREVENT MAD COW DISEASE FDA cooperative agreement helps Illinois maintain food and feed inspections SPRINGFIELD, Ill. - The Illinois Department of Agriculture (IDOA) will receive more than a million dollars in federal funding to conduct important inspections for bovine spongiform encephalopathy (BSE), otherwise known as mad cow disease.
The U.S. Food and Drug Administration (FDA) has entered into a cooperative agreement with the department that will provide a total of $1,244,960 over the next five years to ensure cattle feed produced and used in Illinois does not contain ingredients that could transmit the rare brain-wasting disease. Illinois was one of twelve states to receive federal funding in this cooperative agreement.
"For nearly 20 years, our inspectors have been contracted by the FDA to inspect feed mills and feed manufacturing plants across the state," Agriculture Director Tom Jennings said. "But this agreement will allow us to maintain our expanded on-farm surveillance efforts. We believe these inspections provide additional assurance to consumers and our agricultural trading partners that Illinois beef is safe to eat."
Feed contaminated with tissue from the nervous system of infected cattle is believed to spread BSE. Therefore, the FDA has prohibited the use of ruminant protein in feed for cattle and other ruminant animals since 1997. The department enforces this prohibition in Illinois through regular inspections.
Over the past two years under a similar agreement, IDOA completed 300 on-farm inspections and 100 non-farm inspections. More than 1,000 cattle feed samples were collected and analyzed.
I suppose we have to give them E for effort. course it's like closing the barn doors after the mad cows got loose. ...TSS
Molecular characterization of BSE in Canada
Jianmin Yang1, Sandor Dudas2, Catherine Graham2, Markus Czub3, Tim McAllister1, Stefanie Czub1 1Agriculture and Agri-Food Canada Research Centre, Canada; 2National and OIE BSE Reference Laboratory, Canada; 3University of Calgary, Canada
Background: Three BSE types (classical and two atypical) have been identified on the basis of molecular characteristics of the misfolded protein associated with the disease. To date, each of these three types have been detected in Canadian cattle.
Objectives: This study was conducted to further characterize the 16 Canadian BSE cases based on the biochemical properties of there associated PrPres. Methods: Immuno-reactivity, molecular weight, glycoform profiles and relative proteinase K sensitivity of the PrPres from each of the 16 confirmed Canadian BSE cases was determined using modified Western blot analysis.
Results: Fourteen of the 16 Canadian BSE cases were C type, 1 was H type and 1 was L type. The Canadian H and L-type BSE cases exhibited size shifts and changes in glycosylation similar to other atypical BSE cases. PK digestion under mild and stringent conditions revealed a reduced protease resistance of the atypical cases compared to the C-type cases. N terminal- specific antibodies bound to PrPres from H type but not from C or L type. The C-terminal-specific antibodies resulted in a shift in the glycoform profile and detected a fourth band in the Canadian H-type BSE.
Discussion: The C, L and H type BSE cases in Canada exhibit molecular characteristics similar to those described for classical and atypical BSE cases from Europe and Japan. This supports the theory that the importation of BSE contaminated feedstuff is the source of C-type BSE in Canada. It also suggests a similar cause or source for atypical BSE in these countries.
THIS is just ONE month report, of TWO recalls of prohibited banned MBM, which is illegal, mixed with 85% blood meal, which is still legal, but yet we know the TSE/BSE agent will transmit blood. we have this l-BSE in North America that is much more virulent and there is much concern with blood issue and l-BSE as there is with nvCJD in humans. some are even starting to be concerned with sporadic CJD and blood, and there are studies showing transmission there as well. ... this is one month recall page, where 10 MILLION POUNDS OF BANNED MAD COW FEED WENT OUT INTO COMMERCE, TO BE FED OUT. very little of the product that reaches commerce is ever returned via recall, very, very little. this was 2007, TEN YEARS AFTER THE AUGUST 4, 1997, PARTIAL AND VOLUNTARY MAD COW FEED BAN IN THE USA, that was nothing but ink on paper. i have listed the tonnage of mad cow feed that was in ALABAMA in one of the links too, this is where the infamous g-h-BSEalabama case was, a genetic relation matching the new sporadic CJD in the USA. seems this saga just keeps getting better and better.......$$$
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
Cattle feed delivered between 01/12/2007 and 01/26/2007
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
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
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
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
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
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
Tuesday, March 2, 2010
Animal Proteins Prohibited in Ruminant Feed/Adulterated/Misbranded Rangen Inc 2/11/10 USA
Monday, March 1, 2010
ANIMAL PROTEIN I.E. MAD COW FEED IN COMMERCE A REVIEW 2010
Terry S. Singeltary Sr. (Submitted question): Monday, April 5, 2010
Update on Feed Enforcement Activities to Limit the Spread of BSE April 5, 2010
Friday, April 23, 2010
Upcoming BSE Webinar on Thursday, April 22, 2010 a review
Sunday, January 17, 2010
BSE USA feed inspection violations 01/01/2009 to 01/17/2010 FDA BSE/Ruminant Feed Inspections Firms Inventory Report
Friday, January 15, 2010
New York Firm Recalls Beef Carcass That Contains Prohibited Materials (BSE)
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
Saturday, August 29, 2009
FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009
C O N F I R M E D
----- Original Message ----- From: "Terry S. Singeltary Sr." To: Sent: Thursday, November 05, 2009 9:25 PM Subject: [BSE-L] re-FOIA REQUEST ON FEED RECALL PRODUCT contaminated with prohibited material Recall # V-258-2009 and Recall # V-256-2009
Thursday, November 12, 2009
BSE FEED RECALL Misbranding of product by partial label removal to hide original source of materials 2009
Thursday, March 19, 2009
MILLIONS AND MILLIONS OF POUNDS OF MAD COW FEED IN COMMERCE USA WITH ONGOING 12 YEARS OF DENIAL
CVM Annual Report Fiscal Year 2008: October 1, 2007-September 30, 2008
PUTTING LIPSTICK ON A PIG AND TAKING HER TO A DANCE...TSS
BSE Feed Rule Enforcement: A Decade of Success OFF TO A FAST START
Thursday, April 9, 2009
Docket No. FDA2002N0031 (formerly Docket No. 2002N0273) RIN 0910AF46 Substances Prohibited From Use in Animal Food or Feed; Final Rule: Proposed
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.
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.
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.
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).
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.
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 Bradleyâ€™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.
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.
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),
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
Monday, September 13, 2010
atypical BSE strains and sporadic CJD strains, is there a connection and why shouldn't there be $
Wednesday, September 08, 2010
Emerging Infectious Diseases: CJD, BSE, SCRAPIE, CWD, PRION, TSE Evaluation to Implementation for Transfusion and Transplantation September 2010
Saturday, September 04, 2010
ARS atypical BSE g-h-BSEalabama genetic susceptibility argues against a spontaneous origin for many atypical BSE cases July 2010
FEED, FEED, FEED, WHAT ABOUT ATYPICAL BSE AND FEED ??? why not??? have you seen the tonnage in Alabama ???
ALABAMA MAD COW g-h-BSEalabama
In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
(see mad cow feed in COMMERCE IN ALABAMA...TSS)
Wednesday, July 28, 2010
re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE July 28, 2010
Sunday, September 6, 2009
MAD COW USA 1997 SECRET VIDEO
U.S.A. HIDING MAD COW DISEASE VICTIMS AS SPORADIC CJD ? see video at bottom
The EMBO Journal (2002) 21, 6358 - 6366 doi:10.1093/emboj/cdf653
BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein
Emmanuel A. Asante1, Jacqueline M. Linehan1, Melanie Desbruslais1, Susan Joiner1, Ian Gowland1, Andrew L. Wood1, Julie Welch1, Andrew F. Hill1, Sarah E. Lloyd1, Jonathan D.F. Wadsworth1 and John Collinge1
1.MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK Correspondence to:
John Collinge, E-mail: firstname.lastname@example.org
Received 1 August 2002; Accepted 17 October 2002; Revised 24 September 2002
Variant Creutzfeldt–Jakob disease (vCJD) has been recognized to date only in individuals homozygous for methionine at PRNP codon 129. Here we show that transgenic mice expressing human PrP methionine 129, inoculated with either bovine spongiform encephalopathy (BSE) or variant CJD prions, may develop the neuropathological and molecular phenotype of vCJD, consistent with these diseases being caused by the same prion strain. Surprisingly, however, BSE transmission to these transgenic mice, in addition to producing a vCJD-like phenotype, can also result in a distinct molecular phenotype that is indistinguishable from that of sporadic CJD with PrPSc type 2. These data suggest that more than one BSE-derived prion strain might infect humans; it is therefore possible that some patients with a phenotype consistent with sporadic CJD may have a disease arising from BSE exposure.
Keywords:BSE, Creutzfeldt–Jakob disease, prion, transgenic
Monday, August 9, 2010
Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein or just more PRIONBALONEY ?
FRIENDLY FIRE FROM ALL OF THE ABOVE ;
Wednesday, August 18, 2010
Incidence of CJD Deaths Reported by CJD-SS in Canada as of July 31, 2010
Monday, August 9, 2010
National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010)
(please watch and listen to the video and the scientist speaking about atypical BSE and sporadic CJD and listen to Professor Aguzzi)
Thursday, August 12, 2010
USA Blood products, collected from a donor who was at risk for vCJD, were distributed July-August 2010
*****see farmers and farmers wives with BSE HERDS, that came down with sporadic CJD*****
Thursday, July 10, 2008
A Novel Human Disease with Abnormal Prion Protein Sensitive to Protease update July 10, 2008 Friday, June 20, 2008
STUPID IS, AS STUPID DOES, AND SOME TIMES, YOU JUST CAN'T FIX STUPID $$$
STRICTLY PRIVATE AND CONFIDENTIAL 25, AUGUST 1995
To minimise the risk of farmers' claims for compensation from feed compounders.
To minimise the potential damage to compound feed markets through adverse publicity.
To maximise freedom of action for feed compounders, notably by maintaining the availability of meat and bone meal as a raw material in animal feeds, and ensuring time is available to make any changes which may be required.
MAFF remains under pressure in Brussels and is not skilled at handling potentially explosive issues.
5. Tests _may_ show that ruminant feeds have been sold which contain illegal traces of ruminant protein. More likely, a few positive test results will turn up but proof that a particular feed mill knowingly supplied it to a particular farm will be difficult if not impossible.
6. The threat remains real and it will be some years before feed compounders are free of it. The longer we can avoid any direct linkage between feed milling _practices_ and actual BSE cases, the more likely it is that serious damage can be avoided. ...
SEE full text ;
AND RAMIFICATIONS THERE FROM ;
Tuesday, September 14, 2010
Transmissible Spongiform Encephalopathies Advisory Committee; Notice of
Meeting October 28 and 29, 2010 (COMMENT SUBMISSION)
----- Original Message -----
From: Terry S. Singeltary Sr.
Cc: email@example.com ; Emery, Bryan (CBER)
Sent: Tuesday, September 14, 2010 11:15 AM
SNIP...SEE FULL TEXT ;
Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518