Recent comments

15 years later, and it still amazes me the bull shit the USDA puts out, of which most of the media follows. both of which are oblivious. very sad... OIE says the animal was sub-clinical ; http://web.oie.int/wahis/public.php?page=single_report&pop=1&reportid=11893 also, officials have confirmed it was a atypical L-type BASE BSE. I am deeply disturbed about the false and terribly misleading information that is being handed out by the USDA FDA et al about this recent case of the atypical L-type BASE BSE case in California. these officials are terribly misinformed (I was told they are not lying), about the risk factor and transmissibility of the atypical L-type BASE BSE. these are very disturbing transmission studies that the CDC PUT OUT IN 2012. I urge officials to come forward with the rest of this story. It is important to reiterate here, even though this animal did not enter the food chain, the fact that the USA now finds mad cow disease in samplings of 1 in 40,000 is very disturbing, and to add the fact that it was an atypical L-type BASE BSE, well that is very disturbing in itself. 1 out of 40,000, would mean that there were around 25 mad cows in the USA annually going by a National herd of 100 million (which now I don’t think the USA herd is that big), but then you add all these disturbing factors together, the documented link of sporadic CJD cases to atypical L-type BASE BSE, the rise in sporadic CJD cases in the USA of a new strain of CJD called ‘classification pending Creutzfeldt Jakob Disease’ cpCJD, in young and old, with long duration of clinical symptoms until death. the USA has a mad cow problem and have consistently covered it up. it’s called the SSS policy. ... see full text with updated transmission studies and science on the atypical L-type BASE BSE Jan. 2012 CDC. ... ***Oral Transmission of L-type Bovine Spongiform Encephalopathy in Primate Model ***Infectivity in skeletal muscle of BASE-infected cattle ***feedstuffs- It also suggests a similar cause or source for atypical BSE in these countries. ***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. now, for the rest of the story, the most updated science on the atypical BSE strains, and transmission studies... Thursday, April 26, 2012 Update from USDA Regarding a Detection of Bovine Spongiform Encephalopathy (BSE) in the United States WASHINGTON bulletin at 04/26/2012 10:11 PM EDT http://transmissiblespongiformencephalopathy.blogspot.com/2012/04/update-from-usda-regarding-detection-of.html 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. http://wwwnc.cdc.gov/eid/article/18/1/pdfs/11-1092.pdf http://transmissiblespongiformencephalopathy.blogspot.com/2011/12/oral-transmission-of-l-type-bovine.html 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. http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf 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. http://www.plosone.org/article/info:doi%2F10.1371%2Fjournal.pone.0003017 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. http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2 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... http://www.neuroprion.org/en/np-neuroprion.html 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. http://www.prion2009.com/sites/default/files/Prion2009_Book_of_Abstracts.pdf 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 http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm 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 ______________________________ http://www.fda.gov/bbs/topics/enforce/2006/ENF00968.html 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 ### http://www.fda.gov/bbs/topics/ENFORCE/2006/ENF00964.html 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 ### http://www.fda.gov/bbs/topics/enforce/2006/ENF00963.html 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 ### http://www.fda.gov/bbs/topics/enforce/2006/ENF00960.html please see full text ; http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html Tuesday, March 2, 2010 Animal Proteins Prohibited in Ruminant Feed/Adulterated/Misbranded Rangen Inc 2/11/10 USA http://madcowfeed.blogspot.com/2010/03/animal-proteins-prohibited-in-ruminant.html Monday, March 1, 2010 ANIMAL PROTEIN I.E. MAD COW FEED IN COMMERCE A REVIEW 2010 http://madcowfeed.blogspot.com/2010/03/animal-protien-ie-mad-cow-feed-in.html Tuesday, September 14, 2010 Feed Safety and BSE/Ruminant Feed Ban Support Project (U18) http://madcowfeed.blogspot.com/2010/09/feed-safety-and-bseruminant-feed-ban.html 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 http://madcowfeed.blogspot.com/2010/10/scientific-reasons-for-feed-ban-of-meat.html http://transmissiblespongiformencephalopathy.blogspot.com/2012/04/mad-cow-disease-usa-4th-case-documented.html 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 http://madcowfeed.blogspot.com/2010/11/tafs1-position-paper-on-position-paper.html Archive Number 20101206.4364 Published Date 06-DEC-2010 Subject PRO/AH/EDR> Prion disease update 2010 (11) PRION DISEASE UPDATE 2010 (11) http://www.promedmail.org/direct.php?id=20101206.4364 Sunday, February 5, 2012 February 2012 Update on Feed Enforcement Activities to Limit the Spread of BSE http://transmissiblespongiformencephalopathy.blogspot.com/2012/02/february-2012-update-on-feed.html Saturday, July 23, 2011 CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE http://transmissiblespongiformencephalopathy.blogspot.com/2011/07/cattle-heads-with-tonsils-beef-tongues.html IMPORT EXPORT BEEF, LIVE, PRODUCTS, CANADA AND USA http://bse-atypical.blogspot.com/2009/02/atypical-bse-north-america-update.html America's Mad Cow Crisis by John Stauber Permission granted to reprint this article: America's Mad Cow Crisis John Stauber Americans might remember that when the first mad cow was confirmed in the United States in December, 2003, it was major news. The United States Department of Agriculture (USDA) and the Food and Drug Administration (FDA) had been petitioned for years by lawyers from farm and consumer groups I worked with to stop the cannibal feeding practices that transmit this horrible, always fatal, human and animal dementia. When the first cow was found in Washington state, the government said it would stop such feeding, and the media went away. But once the cameras were off and the reporters were gone nothing substantial changed. In the United States, dairy calves are still taken from their mothers and fed the blood and fat of dead cattle. This is no doubt a way to infect them with the mad cow disease that has now been incubating here for decades, spread through such animal feeding practices. No one knows how the latest dairy cow was infected, the fourth confirmed in the United States. Maybe it was nursed on cow's blood. Perhaps it was fed feed containing cattle fat with traces of cattle protein. Or perhaps there is a mad cow disease in pigs in the United States, which simply has not been found yet, because pigs are not tested for it at all, even though pigs are fed both pig and cattle byproducts, and then the blood, fat and other waste parts of these pigs are fed to cattle. All these U.S. cattle feeding methods are long banned and illegal in other countries that suffered through but eventually dealt properly with mad cow disease. Here, rather than stopping the transmission of the disease by stopping the cannibal feeding, mad cow is simply covered up with inadequate testing and very adequate public relations. US cattle are still fed mammalian blood, fat and protein, risking human deaths and threatening the long term safety of human blood products, simply to provide the U.S. livestock industry with a cheap protein source and a cheap way to get rid of dead animal waste. I began researching this issue around 1989, long before the disease was confirmed to have jumped from cattle to the people eating them, as announced by the British government in 1996. In 1997 I co-authored <https://www.prwatch.org/books/madcow.html> Mad Cow USA, warning that the disease was likely already here and spreading, since the animal cannibalism that caused its outbreak in Britain and spread it to other countries was actually more widespread in the United States than anywhere. Some years ago responsible U.S. beef companies wanted to test their animals for mad cow disease and label their beef as being disease free, but they were forbidden under penalty of law from doing so. Only the USDA can test for mad cows in America. In 2004 and 2005, after two additional mad cows were discovered in Texas and Alabama, the United Sates government declared that obviously mad cow wasn't much of a problem and gutted it's anemic testing program. Today only about 40,000 cattle a year are tested, out of tens of millions slaughtered. It's amazing that the California cow was even detected given this pathetic testing program that seems well designed to hide rather than find mad cows. The prevention of mad cow disease is relatively simple. If your country has it, test each animal before it goes to slaughter to keep the diseased animals out of the food chain. Cheap, accurate and easy tests are now available in other countries but illegal here. Testing cattle both identifies the true extent of the disease, and keeps infected animals from being eaten in your sausage or hamburger. In this manner countries like Britain, Germany, France and Japan have controlled their problem through testing and a strict ban on cannibal feed. Once mad cow disease moves into the human population of a country, all bets are off as to what could happen next. It's a very slow disease, it develops invisibly over decades in someone who has been infected, and it is always fatal. We'll know a lot more in fifty years, but the future looks worrisome. In Britain people are dying from mad cow disease, people who never consumed infected meat. They used medical products containing human blood, and that blood was infected because it was from infected people. There is no test to identify infectious prions, the causal agent, in blood. Almost none of this information appeared in news stories about the California mad cow. Instead the headlines and the talking heads fed us the line that the United States fixed this problem long ago, and the fact that only 4 mad cows have been detected so far is proof of our success. Oprah Winfrey once tried via her talk show to warn about this, way back in 1996, but Texas cattlemen dragged her and her guest Howard Lyman into court and she had to spend many millions of dollars defending herself from the supposed crime of slandering meat. Oprah won her case, which was probably unfortunate for the rest of us because had she been convicted the ensuing appeals court trial might have gotten enough attention to wake up Americans to the truth. Instead Oprah learned her lesson - shut up and you won't get sued. Other media learned too that if the government and industry can silence Oprah, they can muzzle anyone. (One of the 4 confirmed U.S. mad cows was later found in Texas, appropriately enough.) There are a handful of dedicated activists such as Howard Lyman who have been sounding the alarm on this. They include the ecologist Dr. Michael Hansen of Consumers Union and Dr. Michael Greger, a physician. Terry Singeltary Sr., whose mom died of a version of the human form of mad cow disease, has been a relentless, unpaid activist on this issue. Despite their dedicated work, there is no indication that anything is going to change here in America. The U.S. government refuses to implement the feed ban and the animal testing necessary. It doesn't matter if the President is named Clinton, Bush or Obama because their bureaucrats in the USDA and FDA stay the course and keep the cover up going. Docile, eating what they are fed, trusting the rancher all the way to the slaughterhouse. Is that just the cows, or is it us too? -- John Stauber: <https://www.sourcewatch.org/index.php?title=John_Stauber> is an independent author and activist. He founded the Center for Media and Democracy in 1993, retiring in 2009. Way back in 1997 he co-authored Mad Cow USA. <https://www.prwatch.org/books/madcow.html> http://www.commondreams.org/view/2012/04/26-1?nocache=1 http://www.counterpunch.org/2012/04/26/americas-mad-cow-crisis/ http://transmissiblespongiformencephalopathy.blogspot.com/2012/04/americas-mad-cow-crisis-by-john-stauber.html Tell the USDA to Stop the Spread of Mad Cow Disease! Terry Singeltary P.O. Box 42 Bacliff, TX 77518-0042 April 25, 2012 Administrator Gregory Parham 12th & Jefferson Drive, SW Whitten Bldg., Room 313-E Washington, DC 20250 Re: Docket No. APHIS-2008-0010 Dear Administrator Parham: In order to stop the spread of bovine spongiform encephalopathy (BSE or mad cow disease), the US Department of Agriculture should adopt and enforce the same strict standards required by the European Union and Japan: * Mandatory testing for all cattle brought to slaughter, before they enter the food chain. * Ban the feeding of blood, manure, and slaughterhouse waste to animals. In the meantime, the USDA must stop harassing farmers and food processors who are interested in independently testing their own beef for mad cow disease. Ironically, the news that mad cow is still in our food supply comes at a time that the U.S. Department of Agriculture Animal and Plant Health Inspection Service (APHIS) is proposing to drop significant protections the U.S. has against the importation of cattle infected with mad cow disease. APHIS proposes to open United States' borders to cattle from countries that have had thousands of cases of BSE, and where new BSE cases continue to be found. The importation of a single infected cow from Canada in 2001 set in motion restrictions on U.S. beef exports that cost the beef industry billions of dollars and that still exist today in several major export markets. APHIS also proposes to drop important measures that have been used to protect U.S. consumers from these imported cattle and meat products (which have a much higher chance of being infected with BSE than U.S.-raised cattle), and intends to rely almost exclusively on slaughtering techniques, particularly the removal of specified risk materials (SRMs), which we know on occasion is not employed fully or effectively, and which has not been practiced long enough to determine whether it is indeed the panacea APHIS assumes, given the long gestation time of variant Creutzfeldt-Jakob Disease (vCJD) in humans. I support the view of R-CALF USA CEO Bill Bullard: "Seventy-six farm and consumer organizations, representing tens of millions of U.S. citizens, recently urged Secretary Vilsack to strengthen, not weaken, our already lax BSE policies by reversing the so-called 'over-thirty-month rule,' which allows Canadian cattle born during the time the BSE agent was known to be circulating in Canada's feed system to be imported into the United States. "Secretary Vilsack has again ignored our concerns and is putting the self-interests of corporate meatpackers that want access to more meat supplies regardless of risk to humans and livestock, ahead of the health and safety concerns of U.S. citizens. "The USDA is touting its proposed rule as a trade rule, claiming it will strengthen the United States' negotiating position in trade agreements. This is the same failed argument the Bush Administration used when it first relaxed our U.S. BSE policies in 2004, and the result of that failed argument is that many important export markets imposed long-lasting export restrictions on U.S. beef. "USDA's proposal amounts to a unilateral disarmament of essential disease protections for U.S. citizens and livestock. It will disadvantage U.S. producers in the global market because other major beef exporters, including Brazil, Australia, and India continue to maintain adequate import standards while the U.S. relaxes its own. This will create unnecessary and avoidable anxieties among other beef consuming nations for U.S. beef. "Exposing U.S. consumers and U.S. livestock to a heightened risk of BSE introduction is irresponsible and contrary to pledges made by the Obama Administration during his campaign." This is no time to relax our essential protections against the introduction of mad cow disease. so, USDA et al accidently find two atypical mad cows in Texas and Alabama during the infamous enhanced BSE cover up back in 2004 and 2005, and then shut the testing down to numbers so low, it's almost impossible to find another mad cow case, unless your country is to a point that mad cow disease can be found in 1 in 40,000, and STILL FIND MAD COW DISEASE, HOUSTON, WE HAVE A PROBLEM. ... PLEASE UNDERSTAND, the USDA et al are lying about atypical BSE being a spontaneous mutation, NOT caused by feed. spontaneous BSE has NEVER been proven in any natural field case of BSE. feed is the most likely route. ...tss As previously stated most of the characteristics of atypical BSE have not been defined. In addition to the origin, the risk to other cattle by means of natural transmission, the risk to humans and other animal species suck as chickens and pigs is still unknown as is the distribution of infectivity throughout the body of a bovine. There is little information on clinical manifestation if it occurs at all in certain of the cases. Documented L cases have been diagnosed from samples taken from older ''healthy'' cattle presented for routine slaughter. While additional surveillance and research is being conducted, it is important for policy make to consider the implications of atypical BSE. They may need to rethink what populations are appropriate targets. It would probably be unwise to prematurely lessen or discontinue the current BSE protection measures. SNIP... http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3291375/ http://creutzfeldt-jakob-disease.blogspot.com/2006/11/on-question-of-sporadic-or-atypical.html Atypical BSE: What is it and what is the significance Linda A. Detwiler, Paul Brown, Lisa M. McShane, and Gianluigi Zanusso When atypical cases were first reported there was some speculation that these may merely be protein accumulation disorders associated with old age. It has now been shown that both the Land H types of atypical BSE are at least experimentally transmissible. Homogenates from L cases have been transmitted to bovinized transgenic mice, humanized transgenic mice, Cynomolgus monkeys and 1 breed of cattle (Buschmann et al. 2006; Book of abstracts (2006), International Conference on Prion Diseases, Turin, Italy). H cases have been transmitted to bovinized transgenic (Tgbov) and ovinized transgenic mice (Béringue et al. 2006). The incubation times for atypical L cases of BSE were shorter in the Tgbov mice than classical BSE inoculated into Tgbov mice and the H cases had longer incubations. A variation or mutation of the classical BSE strain