Wednesday, May 2, 2012

ARS FLIP FLOPS ON SRM REMOVAL FOR ATYPICAL L-TYPE BASE BSE RISK HUMAN AND ANIMAL HEALTH

ARS FLIP FLOPS ON SRM REMOVAL FOR ATYPICAL L-TYPE BASE BSE RISK HUMAN AND ANIMAL HEALTH




Research Project: STUDY OF ATYPICAL BSE




Location: Virus and Prion Research Unit




Project Number: 3625-32000-086-05
Project Type: Specific Cooperative Agreement






Start Date: Sep 15, 2004
End Date: Sep 14, 2009



Objective:




The objective of this cooperative research project with Dr. Maria Caramelli from the Italian BSE Reference Laboratory in Turin, Italy, is to conduct comparative studies with the U.S. bovine spongiform encephalopathy (BSE) isolate and the atypical BSE isolates identified in Italy. The studies will cover the following areas: 1. Evaluation of present diagnostics tools used in the U.S. for the detection of atypical BSE cases. 2. Molecular comparison of the U.S. BSE isolate and other typical BSE isolates with atypical BSE cases. 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species.






Approach:




This project will be done as a Specific Cooperative Agreement with the Italian BSE Reference Laboratory, Istituto Zooprofilattico Sperimentale del Piemonte, in Turin, Italy. It is essential for the U.S. BSE surveillance program to analyze the effectiveness of the U.S diagnostic tools for detection of atypical cases of BSE. Molecular comparisons of the U.S. BSE isolate with atypical BSE isolates will provide further characterization of the U.S. BSE isolate. Transmission studies are already underway using brain homogenates from atypical BSE cases into mice, cattle and sheep. It will be critical to see whether the atypical BSE isolates behave similarly to typical BSE isolates in terms of transmissibility and disease pathogenesis. If transmission occurs, tissue distribution comparisons will be made between cattle infected with the atypical BSE isolate and the U.S. BSE isolate. Differences in tissue distribution could require new regulations regarding specific risk material (SRM) removal.






http://www.ars.usda.gov/research/projects/projects.htm?accn_no=408490








Research Project: STUDY OF ATYPICAL BSE




Location: Virus and Prion Research Unit


 

2010 Annual Report

1a.Objectives (from AD-416)

The objective of this cooperative research project with Dr. Maria Caramelli from the Italian BSE Reference Laboratory in Turin, Italy, is to conduct comparative studies with the U.S. bovine spongiform encephalopathy (BSE) isolate and the atypical BSE isolates identified in Italy. The studies will cover the following areas: 1. Evaluation of present diagnostics tools used in the U.S. for the detection of atypical BSE cases. 2. Molecular comparison of the U.S. BSE isolate and other typical BSE isolates with atypical BSE cases. 3. Studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species.



1b.Approach (from AD-416)

This project will be done as a Specific Cooperative Agreement with the Italian BSE Reference Laboratory, Istituto Zooprofilattico Sperimentale del Piemonte, in Turin, Italy. It is essential for the U.S. BSE surveillance program to analyze the effectiveness of the U.S diagnostic tools for detection of atypical cases of BSE. Molecular comparisons of the U.S. BSE isolate with atypical BSE isolates will provide further characterization of the U.S. BSE isolate. Transmission studies are already underway using brain homogenates from atypical BSE cases into mice, cattle and sheep. It will be critical to see whether the atypical BSE isolates behave similarly to typical BSE isolates in terms of transmissibility and disease pathogenesis. If transmission occurs, tissue distribution comparisons will be made between cattle infected with the atypical BSE isolate and the U.S. BSE isolate. Differences in tissue distribution could require new regulations regarding specific risk material (SRM) removal.



3.Progress Report

This report documents research conducted under a Specific Cooperative Agreement between ARS and the IST ZOOPROFIL SPERIMENT PIEMONTE. Additional details for the research can be found in the report for the parent project 3625-32000-086-00D, TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES


The aim of the cooperative research project was to: 1. Evaluate present diagnostic tools used in the U.S. for the detection of atypical bovine spongiform encephalopathy (BSE) cases. 2. Perform molecular comparison of the U.S. BSE isolate and other typical BSE isolates with atypical BSE cases. 3. Support studies on transmissibility and tissue distribution of atypical BSE isolates in cattle and other species. To complete objectives 1 and 2 (i.e., to compare Italian and U.S. BSE confirmatory protocols for detection of classical (C-) and atypical (H- and L-type) BSE cases), samples of Italian C-BSE and Italian L-type BSE (BASE), both frozen and formalin fixed, were sent to USDA laboratories in Ames, Iowa, to undergo Western blot (WB) and immunohistochemistry (IHC) comparison studies for PrPSc detection according to U.S. and Italian methods. A Western blot expert from the cooperating Italian lab assisted ARS scientists in performing the protocols from each laboratory in parallel. A comparative IHC study between U.S. and Italian BSE confirmatory protocols was also performed when the collaborator sent a scientist to Ames to assist in performing the Italian IHC protocol on BSE samples chosen for the study.




Results obtained showed the Italian and U.S. IHC procedures were alike in PrPSc detection regarding its tissue distribution, deposition pattern and intensity of staining on all the C-, L- and H-type BSE cases considered. In addition, the U.S. protocol evidenced the characteristic presence of plaques in the frontal cortex of the Italian BASE case similar to the Italian protocol. Data from studies on objectives 1 & 2 has been presented at several international meetings in 2008 and 2009, and has been finalized into manuscript form for publication in a peer-reviewed journal (Journal of Veterinary Diagnostic Investigation). In support of objective 3, the cooperators completed and published their transmissibility and tissue distribution work on BASE cases in a peer-reviewed journal in 2008 (PLoS Pathogens Volume 4, page e1000075). They reported that in all experimentally infected atypical BSE animals, no PrPSc was detected in peripheral tissues either by standard Western blot analysis or following phosphotungstic acid precipitation. Peripheral issues examined included cervical and mesenteric lymph nodes, spleen, thymus, liver, lung, peripheral nerves, and forelimb and hind limb muscles.




These findings support the conclusion there is no scientific evidence to expand the list of tissues included in the Specified Risk Material ban based on atypical BSE research data, thus confirming other studies indicating the pathogenesis of BSE in cattle is fundamentally different from that in sheep and mice, due to an exclusive intraneuronal spread of infectivity from the gut to the central nervous system. Methods used for monitoring included email, site visits, and periodic written reports.






http://www.ars.usda.gov/research/projects/projects.htm?ACCN_NO=408490&showpars=true&fy=2010





“ These findings support the conclusion there is no scientific evidence to expand the list of tissues included in the Specified Risk Material ban based on atypical BSE research data, thus confirming other studies indicating the pathogenesis of BSE in cattle is fundamentally different from that in sheep and mice, due to an exclusive intraneuronal spread of infectivity from the gut to the central nervous system. “







REALLY ???







October 2009 O.11.3





Infectivity in skeletal muscle of BASE-infected cattle





Silvia Suardi1, Chiara Vimercati1, Fabio Moda1, Ruggerone Margherita1, Ilaria Campagnani1, Guerino Lombardi2, Daniela Gelmetti2, Martin H. Groschup3, Anne Buschmann3, Cristina Casalone4, Maria Caramelli4, Salvatore Monaco5, Gianluigi Zanusso5, Fabrizio Tagliavini1 1Carlo Besta" Neurological Institute,Italy; 2IZS Brescia, Italy; 33FLI Insel Riems, D, Germany; 4CEA-IZS Torino, Italy; 5University of Verona, Italy




Background: BASE is an atypical form of bovine spongiform encephalopathy caused by a prion strain distinct from that of BSE. Upon experimental transmission to cattle, BASE induces a previously unrecognized disease phenotype marked by mental dullness and progressive atrophy of hind limb musculature. Whether affected muscles contain infectivity is unknown. This is a critical issue since the BASE strain is readily transmissible to a variety of hosts including primates, suggesting that humans may be susceptible.




Objectives: To investigate the distribution of infectivity in peripheral tissues of cattle experimentally infected with BASE. Methods: Groups of Tg mice expressing bovine PrP (Tgbov XV, n= 7-15/group) were inoculated both i.c. and i.p. with 10% homogenates of a variety of tissues including brain, spleen, cervical lymph node, kidney and skeletal muscle (m. longissimus dorsi) from cattle intracerebrally infected with BASE. No PrPres was detectable in the peripheral tissues used for inoculation either by immunohistochemistry or Western blot.




Results: Mice inoculated with BASE-brain homogenates showed clinical signs of disease with incubation and survival times of 175±15 and 207±12 days. Five out of seven mice challenged with skeletal muscle developed a similar neurological disorder, with incubation and survival times of 380±11 and 410±12 days. At present (700 days after inoculation) mice challenged with the other peripheral tissues are still healthy. The neuropathological phenotype and PrPres type of the affected mice inoculated either with brain or muscle were indistinguishable and matched those of Tgbov XV mice infected with natural BASE.




Discussion: Our data indicate that the skeletal muscle of cattle experimentally infected with BASE contains significant amount of infectivity, at variance with BSE-affected cattle, raising the issue of intraspecies transmission and the potential risk for humans. Experiments are in progress to assess the presence of infectivity in skeletal muscles of natural BASE.







CDC 2012




Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model




Nadine Mestre-Francés, Simon Nicot, Sylvie Rouland, Anne-Gaëlle Biacabe, Isabelle Quadrio, Armand Perret-Liaudet, Thierry Baron, and Jean-Michel Verdier




We report transmission of atypical L-type bovine spongiform encephalopathy to mouse lemurs after oral or intracerebral inoculation with infected bovine brain tissue. After neurologic symptoms appeared, transmissibility of the disease by both inoculation routes was confirmed by detection of disease-associated prion protein in samples of brain tissue.




snip...




Conclusions




We demonstrated that the agent of L-BSE can be transmitted by the oral route from cattle to mouse lemurs. As expected, orally inoculated animals survived longer than IC-inoculated animals. Orally inoculated lemurs had less severe clinical signs and symptoms, with no evidence of motor dysfunction. It was previously suggested that the agent of L-BSE might be involved in the foodborne transmission of a prion disease in mink (11,12), a species in which several outbreaks of transmissible mink encephalopathy had been identified, notably in the United States (13).




Our study clearly confirms, experimentally, the potential risk for interspecies oral transmission of the agent of L-BSE. In our model, this risk appears higher than that for the agent of classical BSE, which could only be transmitted to mouse lemurs after a first passage in macaques (14). We report oral transmission of the L-BSE agent in young and adult primates. Transmission by the IC route has also been reported in young macaques (6,7). A previous study of L-BSE in transgenic mice expressing human PrP suggested an absence of any transmission barrier between cattle and humans for this particular strain of the agent of BSE, in contrast to findings for the agent of classical BSE (9). Thus, it is imperative to maintain measures that prevent the entry of tissues from cattle possibly infected with the agent of L-BSE into the food chain.














P.9.21




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.










Subject: Atypical BSE (BASE) Transmitted from Asymptomatic Aging Cattle to a Primate




Atypical BSE (BASE) Transmitted from Asymptomatic Aging Cattle to a Primate




Emmanuel E. Comoy1*, Cristina Casalone2, Nathalie Lescoutra-Etchegaray1, Gianluigi Zanusso3, Sophie Freire1, Dominique Marcé1, Frédéric Auvré1, Marie-Magdeleine Ruchoux1, Sergio Ferrari3, Salvatore Monaco3, Nicole Salès4, Maria Caramelli2, Philippe Leboulch1,5, Paul Brown1, Corinne I. Lasmézas4, Jean-Philippe Deslys1




1 Institute of Emerging Diseases and Innovative Therapies, CEA, Fontenay-aux-Roses, France, 2 Istituto Zooprofilattico Sperimentale del Piemonte, Turin, Italy, 3 Policlinico G.B. Rossi, Verona, Italy, 4 Scripps Florida, Jupiter, Florida, United States of America, 5 Genetics Division, Brigham & Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America




Abstract Top Background




Human variant Creutzfeldt-Jakob Disease (vCJD) results from foodborne transmission of prions from slaughtered cattle with classical Bovine Spongiform Encephalopathy (cBSE). Atypical forms of BSE, which remain mostly asymptomatic in aging cattle, were recently identified at slaughterhouses throughout Europe and North America, raising a question about human susceptibility to these new prion strains.




Methodology/Principal Findings




Brain homogenates from cattle with classical BSE and atypical (BASE) infections were inoculated intracerebrally into cynomolgus monkeys (Macacca fascicularis), a non-human primate model previously demonstrated to be susceptible to the original strain of cBSE. The resulting diseases were compared in terms of clinical signs, histology and biochemistry of the abnormal prion protein (PrPres). The single monkey infected with BASE had a shorter survival, and a different clinical evolution, histopathology, and prion protein (PrPres) pattern than was observed for either classical BSE or vCJD-inoculated animals. Also, the biochemical signature of PrPres in the BASE-inoculated animal was found to have a higher proteinase K sensitivity of the octa-repeat region. We found the same biochemical signature in three of four human patients with sporadic CJD and an MM type 2 PrP genotype who lived in the same country as the infected bovine.




Conclusion/Significance




Our results point to a possibly higher degree of pathogenicity of BASE than classical BSE in primates and also raise a question about a possible link to one uncommon subset of cases of apparently sporadic CJD. Thus, despite the waning epidemic of classical BSE, the occurrence of atypical strains should temper the urge to relax measures currently in place to protect public health from accidental contamination by BSE-contaminated products.




Citation: Comoy EE, Casalone C, Lescoutra-Etchegaray N, Zanusso G, Freire S, et al. (2008) Atypical BSE (BASE) Transmitted from Asymptomatic Aging Cattle to a Primate. PLoS ONE 3(8): e3017. doi:10.1371/journal.pone.0003017




Editor: Neil Mabbott, University of Edinburgh, United Kingdom




Received: April 24, 2008; Accepted: August 1, 2008; Published: August 20, 2008




Copyright: © 2008 Comoy et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.




Funding: This work has been supported by the Network of Excellence NeuroPrion.




Competing interests: CEA owns a patent covering the BSE diagnostic tests commercialized by the company Bio-Rad.




* E-mail: emmanuel.comoy@cea.fr




snip...




In summary, we have transmitted one atypical form of BSE (BASE) to a cynomolgus macaque monkey that had a shorter incubation period than monkeys infected with classical BSE, with distinctive clinical, neuropathological, and biochemical features; and have shown that the molecular biological signature resembled that seen in a comparatively uncommon subtype of sporadic CJD. We cannot yet say whether BASE is more pathogenic for primates (including humans) than cBSE, nor can we predict whether its molecular biological features represent a clue to one cause of apparently sporadic human CJD. However, the evidence presented here and by others justifies concern about a potential human health hazard from undetected atypical forms of BSE, and despite the waning epizoonosis of classical BSE, it would be premature to abandon the precautionary measures that have been so successful in reversing the impact of cBSE. We would instead urge a gradual, staged reduction that takes into account the evolving knowledge about atypical ruminant diseases, and both a permanent ban on the use of bovine central nervous system tissue for either animal or human use, and its destruction so as to eliminate any risk of environmental contamination.








Wednesday, March 31, 2010




Atypical BSE in Cattle




To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.




This study will contribute to a correct definition of specified risk material (SRM) in atypical BSE. The incumbent of this position will develop new and transfer existing, ultra-sensitive methods for the detection of atypical BSE in tissue of experimentally infected cattle.








Thursday, August 12, 2010




Seven main threats for the future linked to prions




First threat




The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.




***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.




Second threat




snip...









full text ;




atypical L-type BASE BSE











let's take a closer look at this new prionpathy or prionopathy, and then let's look at the g-h-BSEalabama mad cow.




This new prionopathy in humans? the genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like this, ......wait, it get's better. this new prionpathy is killing young and old humans, with LONG DURATION from onset of symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and the plaques are very similar in some cases too, bbbut, it's not related to the g-h-BSEalabama cow, WAIT NOW, it gets even better, the new human prionpathy that they claim is a genetic TSE, has no relation to any gene mutation in that family. daaa, ya think it could be related to that mad cow with the same genetic make-up ??? there were literally tons and tons of banned mad cow protein in Alabama in commerce, and none of it transmitted to cows, and the cows to humans there from ??? r i g h t $$$




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)









now, what about that mad cow feed and atypical BSE $$$





LET’S see how that mad cow triple firewall aka mad cow feed ban is working out $$$






*** BANNED MAD COW FEED IN THE USA IN COMMERCE TONS AND TONS




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




___________________________________




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










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)




BANNED MAD COW FEED IN COMMERCE IN ALABAMA




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




______________________________








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




###










please see full text ;










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








Tuesday, September 14, 2010




Feed Safety and BSE/Ruminant Feed Ban Support Project (U18)








Friday, October 8, 2010




Scientific reasons for a feed ban of meat-and-bone meal, applicable to all farmed animals including cattle, pigs, poultry, farmed fish and pet food














Saturday, November 6, 2010




TAFS1 Position Paper on Position Paper on Relaxation of the Feed Ban in the EU




Berne, 2010 TAFS INTERNATIONAL FORUM FOR TRANSMISSIBLE ANIMAL DISEASES AND FOOD SAFETY a non-profit Swiss Foundation










Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR>




Prion disease update 2010 (11) PRION DISEASE UPDATE 2010 (11)










Sunday, February 5, 2012




February 2012 Update on Feed Enforcement Activities to Limit the Spread of BSE








Saturday, July 23, 2011




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








IMPORT EXPORT BEEF, LIVE, PRODUCTS, CANADA AND USA










Saturday, June 12, 2010


PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05 Study of Atypical Bse




Wednesday, July 28, 2010


re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE July 28, 2010




P.9.21


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.







CONSUMERS UNION



Tuesday, May 1, 2012


BSE MAD COW LETTERS TO USDA (Tom Vilsack, Secretary of Agriculture) and FDA (Magaret Hamburg, Commissioner of FDA) May 1, 2012










kind regards,


terry




senior layperson Smile

No comments:

Post a Comment